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Psychopathology

Research, Assessment, and Treatment in Clinical

Psychology

THIRD EDITION

GRAHAM DAVEY
University of Sussex
Brighton, UK
Acknowledgements

Once again I'd like to begin by thanking the Wiley commissioning and production team. Without their
hard work, skills, and persistence this new edition would not have been possible. I would also like to
thank all of those people who advised me on the first and second editions of the book by making
sensible suggestions about content, providing me with materials, and reviewing drafts. These include
Chris Brewin, Alison Brown, Kate Cavanagh, Roger Cocks, Rudi Dallos, Suzanne Dash, Thomas
Ehring, Andy Field, Daniel Freeman, Theresa Gannon, David Green, Richard Hastings, Marko Jelicic,
Jo Johnson, Fergal Jones, Nick Lake, Ruth Mann, Charlie Martin, Lance McCracken, Fran Meeten,
Michael Morgan, Peter Muris, Filip Raes, Ben Smith, Helen Startup, Emma Veitch, Brendan Weekes,
and Leonora Wilkinson. Those who have advised me on aspects of the third edition include Kate
Cavanagh, Ann Cook, Alan Frances, Samei Huda, Lucy Johnstone, Nick Lake, Frances Meeten, Paul
Salkovskis, and Adrian Whittington.
Also, a big thank you to all my family and friends who have endured me talking about very little else
than finishing this new edition for over the last 6 months! Especially my mother Betty and daughters
Kate and Lizzie.
If you have time on your hands you can read my thoughts about mental health and other issues on my
blogs at http://www.papersfromsidcup.com and
https://www.psychologytoday.com/gb/experts/graham‐cl‐davey‐phd and follow me on Twitter at
http://twitter.com/GrahamCLDavey
Finally, I finished the last few pages of this third edition during the second week of the first coronavirus
lockdown in the UK. I would like to dedicate this book to all NHS health professionals and staff whose
tireless and courageous work under extreme circumstances has been doing so much for the country
under what are unprecedented and very difficult circumstances.

Graham Davey
Brighton, April 2020
Preface to Third Edition

It feels like a significant landmark to have published the third edition of Psychopathology. Students still
want to study psychology in their tens of thousands, and a significant proportion of those still enter
university with the intention of becoming professional psychologists, and more specifically, with a view
to learning about mental health and becoming clinical psychologists.
And there is no more important time than now when it comes to learning about mental health. We live
in times when mental health problems are more high profile than they've ever been, more people are
becoming aware of their mental health and seeking help and support for their problems, and there are
many researchers and clinicians who would claim that we live in times when many common mental
health problems have reached epidemic proportions.
Over the three editions of its life so far, this textbook has been refined to provide the enquiring student
with access to most aspects of mental health and clinical psychology, and I hope this new edition is in a
form that is easily accessible and engaging and facilitates learning.
One of the main aims of this third edition was to update the research database in the book, and we've
included a total of over 1,100 new references spread across all 17 chapters. This enables Psychopathology
to act as a sourcebook for students and instructors wanting to access the most recent evidence‐based
research on the causes and treatments of mental health problems.
So, has our understanding of mental health problems changed over the 5 years since the publication of
the second edition? Yes, there have been many significant developments in the science, treatment, and
conceptualisation of mental health problems over recent years and many of these are represented in this
third edition. These developments include the growth in alternative evidence‐based approaches to
diagnosing and categorising mental health problems; the surge in research in epigenetics and the
possibility that many forms of early experience may moderate the expression of genes in ways that
affect mental health symptoms; the continuing advancement of the neurodiversity movement, which
promotes the idea that there is not just one ‘normal’ or ‘healthy’ type of brain; the growing importance
of network analyses showing how mental health symptoms interact; and the greater understanding of
how mental health problems develop out of the socioeconomic conditions in which people live and are
not in any simple way about biological or even psychological dysfunction.
The book continues to provide multiple perspectives on mental health problems from a range of
psychological, sociological, biological, and genetic approaches and to emphasise the importance of
experimental psychopathology to good clinical psychology research. It is also associated with a wide
variety of supplementary material, available for both students and instructors. In this third edition, these
resources have been expanded and updated.
Just like the first and second editions, this third edition is supplemented by a range of features designed
to facilitate effective teaching and learning. These include:
Focus Point Boxes: These provide more in‐depth discussion of particular topics that are conceptually
important, controversial, or simply of contemporary interest. Whenever possible these are linked to
everyday examples—such as high‐profile news items—that allow the reader to consider the issues in a
contemporary, everyday context.
Research Methods Boxes: These features contain detailed descriptions of methods utilised in
psychopathology research and describe the pros and cons of individual methods and their potential
uses. These examples act to supplement the general material provided on research methods in Chapter
3. Like most researchers, those involved in clinical psychology research are often imaginative in their use
of research methods, and many of the examples provided in research methods boxes attempt to convey
how methods from other areas of psychology and science generally can be adapted to study issues
relevant to psychopathology.
Case Histories: Most chapters contain example case histories describing the symptoms, experiences
and life circumstances encountered by individuals experiencing particular psychopathologies. Many of
these examples conclude with a clinical commentary that is designed to link the detail of that specific case
history to the general facts to be learned in the text.
The Client's Perspective: Many chapters also contain examples of an individual's own descriptions
of the experience of psychopathology. These are designed to provide the reader with an insight into the
phenomenology of different psychopathologies and the way that symptoms affect moods, experiences,
and everyday living—including social, occupational, and educational functioning. These descriptions
are also supplemented by the personal accounts of psychopathologies that begin each chapter. As with case
histories, client's perspective features usually conclude with a clinical commentary that links the personal
experiences of the psychopathology to the academic content of the text.
Treatment in Practice Boxes: These boxes attempt to provide the reader with a more detailed
insight into how individual treatments and interventions are conducted in practice. It is often difficult for
a student to understand, for example, how a therapy is conducted in practice from descriptions given in
academic texts. These boxes provide some specific examples of how a practitioner might implement the
principles of a treatment in a specific case.
Self‐Test Questions: Throughout each chapter the reader will encounter self‐test questions. These are
designed to test the reader's absorption of basic factual and conceptual knowledge. Instructors and
teachers can also use these questions as a basis for discussing key material in class or in small group
discussions.
Glossary: At the end of each chapter there is a list of key terms used in the chapter. When each term
first appears in the text, it is highlighted in bold and is either described or defined at that point.
Highlighting these terms makes them easy to locate, and the list of key terms can serve as a revision
checklist—especially for students due to take multiple‐choice questionnaire assessments.
Finally, I hope you find this third edition readable, accessible, and enlightening and a worthwhile
addition to your teaching and learning activities. To all who have used the earlier editions, thank you so
much for your support, and I wish you well with your teaching and learning. Good luck!

Graham Davey
Brighton
April 2020
About the Companion Website

This book is accompanied by Student and Instructor companion websites.

www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter ReferencesVideos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
Part I
Introducing
Psychopathology: Concepts,
Procedures, and Practices
1 An Introduction to Psychopathology: Concepts, Paradigms, and Stigma
2 Classification and Assessment in Clinical Psychology
3 Research Methods in Clinical Psychology
4 Treating Psychopathology
5 Clinical Practice
1
An Introduction to Psychopathology: Concepts,
Paradigms, and Stigma

ROUTE MAP OF THE CHAPTER

This first chapter introduces the reader to a number of basic issues concerned with the
definition and explanation of psychopathology—including the issue of ‘stigma’ that can often
be an outcome of how psychopathology is conceptualised and portrayed. The first section
describes a brief history of how mental health problems have been conceived and treated
followed in the second section by a discussion of how psychopathology can be defined, and how
we identify behaviour that is in need of support and treatment. The third section describes
some of the most common explanatory approaches that have been developed to help us
understand psychopathology, and these approaches are ones that the reader will encounter
frequently throughout this book. Finally, the fourth section takes a close look at mental health
stigma, how it is manifested, why it is important, and how stigma can be dealt with.

CHAPTER OUTLINE
1.1 A BRIEF HISTORY OF PSYCHOPATHOLOGY
1.2 DEFINING PSYCHOPATHOLOGY
1.3 EXPLANATORY APPROACHES TO PSYCHOPATHOLOGY
1.4 MENTAL HEALTH AND STIGMA
1.5 CONCEPTS, PARADIGMS, AND STIGMA REVISITED

LEARNING OUTCOMES
When you have completed this chapter, you should be able to:
1. Discuss the pros and cons of a number of different approaches to defining
psychopathology.
2. Describe important developments in the history of our understanding and response to
mental health problems.
3. Describe and evaluate the nature and causes of mental health stigma.
4. Compare and contrast approaches to the explanation of psychopathology, including
historical approaches, the medical model, and psychological models.
Am I crazy? I don't know what is wrong with me. I did have depression in the past and what I am going through
doesn't feel a lot like what I had before. My moods change every 30 minutes at times. I have been like this for a
while. I started out about once a week I would have a day where I was going from one extreme to the next. In the
past few weeks it has gotten worse. It seems like my moods change for no reason at all. There are times that I will
just lay down and cry for what appears to be no reason at all and then 2 hours later I will be happy. I find myself
yelling at my son for stupid reasons and then shortly after I am fine again. I truly feel that I am going crazy and
the more I think about it the worse I get. I am not sleeping or eating much and when I do eat I feel like I will be
sick.
Joan's Story

Ten years ago after a pub brawl I was beaten and left for dead outside a pub. Following the attack, my physical
recovery from a broken collarbone and broken ribs was slow. From that day on, I lost my confidence and was
scared of going out in case I was attacked again as the attackers were never caught; scared that I would lose my
rag and end up in prison. I started getting panic attacks and getting easily upset by noise, spending most of the
time in my room on my own. I was unable to stop thinking about the beating and it played in my mind almost
constantly like a film. Sometimes, I went crazy, I lost the sense of where I was and it felt like the assault was
happening all over again—the footsteps behind me, the whack on my head, the sense of falling on my face
thinking ‘This is it, I'm in for it’. I started smoking cannabis because that was the only way to numb my feelings
and get me to sleep but I woke soon after with nightmares of being chased and would wake up shouting and
soaked in sweat.
Ten years on and little has changed. I'm stuck in a rut and don't know how to get out. My life is worthless. I'm a
failure for letting this get on top of me.
Adapted from Davey GCL, Lake N & Whittington A (2015) Clinical Psychology. Routledge
Peter's Story

I found it hard at secondary school to make friends and not having a lot of money meant I was singled out. While
it wasn't physical, mainly name calling and being spat at, it reinforced the feeling that I didn't deserve to be here.
By now I was hearing ‘inside’ voices in my head telling me I was useless, shouting words like ‘Bitch!’ and ‘Die!’.
I was having severe mood swings. I thought about self‐harming and became controlling about my food intake. At
age 14 I started taking drugs and drinking alcohol. Between 14 and 21 I had a cannabis and cocaine addiction
which I overcame. At age 24 I was planning my suicide when my father died. Within 3 days I was having
extreme audio and visual hallucinations such as whispering and people calling my name and seeing deceased
people, dead bodies and shadows as well as everyday objects. People also transformed into other people in front of
me leading me to believe they were possessed by the dead. I also heard menacing voices issuing commands. I
experienced strange smells, tasting poison in my food and on one occasion felt someone stroking my hair. It sounds
crazy, but I thought that my mind was being controlled, that I could communicate with the dead and that, because
of this, the government was spying on me and plotting to kill me.
Adapted from Davey GCL, Lake N & Whittington A (2015) Clinical Psychology. Routledge
Jo's Story
 I started using cocaine at 13. Before, I was using marijuana and alcohol and it didn't really work for me, so I
wanted to step it up a level. I started using heroin when I was 15. I began using it to come down from cocaine
and get some sleep. But I started liking the heroin high and started using it straight. Every day, after a while.
Along with cocaine, I also began taking prescription drugs when I was thirteen. They were so easy to get. I never
had to buy them or get them from a doctor. I would just get them from friends who had gone through their parent's
medicine cabinet. I also thought that prescription drugs were “safer” than other drugs. I figured that it was okay
for people to take them, and if they were legal, I was fine. Like I said, prescription drugs were incredibly easy to
get from friends, and it always seemed to be a last‐minute thing. Heroin was also easy to get—all I had to do was
go into town and buy it. My heroin use started spiraling out of control. I stopped going to school. I was leaving
home for days at a time. My whole life revolved around getting and using drugs—I felt like I was going crazy.
Erica's Story

Introduction
We begin this book with personal accounts from four very different individuals. Possibly the only
common link between these four accounts is that they each use the word ‘crazy’ in relating their story.
Joan questions whether she is going crazy, Peter feels he's going crazy as he relives the trauma he
experienced, Jo experienced auditory and visual hallucinations that in retrospect seem crazy, and Erica's
life gets so out of control that she too felt like she was ‘going crazy’. We tend to use words like ‘crazy’,
‘madness’, and ‘insanity’ regularly—as if we knew what we meant by those terms. However, we do tend
to use these terms in a number of different circumstances—for example, (a) when someone's behaviour
deviates from expected norms, (b) when we are unclear about the reasons for someone's actions, (c)
when a behaviour seems to be irrational, or (d) when a behaviour or action appears to be maladaptive
or harmful to the individual or others. You can try seeing whether these different uses of the term
‘crazy’ or ‘mad’ apply to each of our personal accounts, but they probably still won't capture the full
meaning of why they each used the word ‘crazy’ in their vignettes. Trying to define our use of everyday
words like ‘crazy’, ‘madness’, and ‘insanity’ leads us on to thinking about those areas of thinking and
behaving that seem to deviate from normal or everyday modes of functioning and cause distress to those
exhibiting these behaviours. For psychologists the study of these phenomena is known as
psychopathology, and the branch of psychology responsible for understanding and treating
psychopathology is known as clinical psychology.

psychopathology The in-depth study of mental health problems

clinical psychology The branch of psychology responsible for understanding and treating
psychopathology.

But before we go any further, let's quickly unpack what is meant by the term psychopathology. A
traditional definition of psychopathology based on the linguistic origins of the term is that it is ‘the
scientific study of mental disorders’—a definition that harks back to the days when the medical or illness
model of mental health problems was the most influential. But as we'll see in this chapter, in current
usage the term psychopathology has a much broader meaning covering the in‐depth study of mental
health problems generally, and many contemporary approaches to mental health problems do not
conceive of them as disorders or illnesses but as the product of perfectly healthy psychological processes
in response to stressful or extreme life experiences. In this way, psychopathology has become a term that
describes a general scientific approach that embraces attempts to understand the causes of mental
health problems, how we should classify them, and how we can successfully fix them. If you're interested
in how the nature of mental health terms can change over time, see the descriptions of ‘concept creep’
in clinical psychology terminology discussed by Haslam (2016) and McGrath, Randall‐Dzerdz, Wheeler,
Murphy, & Haslam (2019).
With this broader, eclectic meaning of psychopathology in mind, let's examine our four personal
accounts a little closer. In each case, the individual finds what is happening to them distressing, and to
some extent out of their control. Joan is distressed because she appears to have no control over her
moods. She feels depressed; she shouts at her son, she feels sick when she eats. Peter is plagued by
continually reliving the horrors of a traumatic assault and feels his life is now stuck in a rut and is
worthless. In response to severe bullying at school and then the death of her father, Jo developed
unusual ways of interpreting events around her, hearing voices and experiencing visual hallucinations
—interpretations of the world that many other people might label as crazy. Finally, Erica's behaviour has
become controlled by her need for drugs. She feels out of control and all other activities in her life—
such as her education‐ are suffering severely because of this.
These four cases are all ones that are likely to be encountered by clinical psychologists and although
very different in their detail, they do all possess some commonalities that might help us to define what
represents a mental health problem. For example, (a) both Joan and Peter experience debilitating distress,
(b) both Joan and Erica feel that important aspects of their life (such as their moods or cravings) are out
of their control and they cannot cope, (c) both Joan and Erica find that their conditions have resulted in
them failing to function properly in certain spheres of their life (e.g., as a mother or as a student), and (d)
Jo's life appears to be controlled by interpretations of the world that are extreme and are probably not
real. As we shall see later, these are all‐important aspects of psychopathology and define to some extent
what will be the subject matter of clinical practice.
However, deciding what are proper and appropriate examples of psychopathology is not easy. Just
because someone's behaviour deviates from accepted norms or patterns does not mean they are
suffering from a mental health problem, and just because we might use the term ‘crazy’ to describe
someone's behaviour does not mean that it is the product of disordered thinking. Similarly, as we
alluded to earlier, we cannot attempt to define psychopathology on the basis that some ‘normal’
functioning (psychological, neurological, or biological) has gone wrong. This is because (a) we are still
some way from understanding the various processes that contribute to mental health problems, and (b)
many forms of behaviour that require treatment by clinical psychologists are merely extreme forms of
what we would call ‘normal’ or ‘adaptive’ behaviour. For example, we all worry and we all get depressed
at some times, but in most cases these activities do not significantly interfere with our everyday living.
However, for some other people, their experience of these activities may be so extreme or so chronic as
to cause them significant distress and prevent them from undertaking normal daily activities such as
looking after a family or earning a living (Focus Point 1.1).

FOCUS POINT 1.1 IS THERE A MODERN‐DAY MENTAL

HEALTH EPIDEMIC?

There has been a general concern in recent decades that the prevalence of mental health
problems is increasing, to almost epidemic proportions. This concern has been expressed in the
media generally (https://www.bbc.co.uk/news/health‐41125009), by blogging health
journalists (https://www.thenational.ae/lifestyle/wellbeing/the‐fear‐factor‐1.640564), by heads
of mental health agencies (e.g., https://www.telegraph.co.uk/health‐fitness/mind/mental‐
health‐crisis‐among‐children‐selfie‐culture‐sees‐cases/), and by health practitioners and
researchers (Davey, 2018a; The Lancet, 2018b).
But is there an epidemic? Well it's very hard to find longitudinal data to confirm this. In part
this is because reliable data on prevalence rates has been patchy over the last 3–4 decades, and
when data are reported they are often reported in different ways using different methods of
data collection.
The Adult Psychiatric Morbidity Survey carried out in England by the National Health Service
(NHS) uses validated mental health screening and assessment tools to gauge the level of mental
health problems in a sample of the general population, and this survey provides prevalence data
for years 1993, 2000, 2007, and 2014 (NHS Digital, 2016). Key findings suggest that between
2007 and 2014, the number of adults aged 16–74 years accessing mental health treatment in
the UK with conditions such as anxiety or depression had increased significantly from 24% to
39%. In addition, in 2014 around one in six adults met the criteria for a common mental health
problem such as anxiety or depression, and this number has increased modestly over the 4 years
of sampling since 1993—but these increases are probably not statistically significant (Spiers et
al., 2016). However, what these figures do suggest is that while there may not be a substantial
increase in diagnosable common mental health problems, there does appear to be a sizable
increase in the number of people accessing mental health services for these conditions.

Prevalence of common mental health problems (anxiety or depression) in England between 1993 and 2014 (data
from NHS Digital, 2016).
Similarly, the picture on more severe diagnosable mental health problems such as
schizophrenia, autism, and eating disorders does not obviously indicate a growing mental health
epidemic. The following table shows data on the global prevalence of mental health problems
as collected by the Global Burden of Disease 2017 study (The Lancet, 2018a). To be sure, this
indicates that a significant number of people worldwide (970.8 million) are suffering from a
diagnosable mental health problem, and on current population figures that amounts to one in
seven people globally (14.2%). But a comparison of figures between 1990 and 2017 suggests a
small decrease in reported mental health problems in both males (−2.1%) and females (−3.0%)
over this time. This evidence for a relative stability of mental health problems over time is also
supported by systematic reviews and meta‐analyses, which suggest at best only a modest
increase in the prevalence of mental health problems since at least the 1970s (Richter, Wall,
 Bruen, & Whittington, 2019).
Global Prevalence of Mental Health Problems 2017 (The Lancet, 2018a)
Mental Health Problem Prevalence (million)
All mental health problems 970.8
Anxiety disorders 284.3
Depressive disorders 264.4
Substance use disorders 175.5
Bipolar disorder 45.5
Autism spectrum disorders 31.1
Schizophrenia 19.7
Eating disorders 15.8
So what is driving talk of a mental health epidemic? Perhaps people are becoming more aware
of the immense scale of existing levels of mental health problems (the NHS Psychiatric
Morbidity Survey for 2014 suggests that one in six people in the UK will be suffering a
diagnosable common mental health problem at any one time (NHS Digital, 2016). People may
also be growing more aware of when they themselves are suffering mental health symptoms.
They may be more able to identify these symptoms and have a better knowledge of how to
access mental health services for treatment.
In addition, there may be a real growth of mental health problems in specific demographic
groups and a growth in numbers of individuals experiencing only specific conditions. For
example, there may be a growing recognition of mental health problems in children and
adolescents—especially common mental health problems such as anxiety, depression, and self‐
harm (e.g., Creswell, Waite, & Cooper, 2013), and the number of young people experiencing
severe emotional disorders in England has increased from 3.9% in 2004 to 5.8% in 2017 (NHS
Digital, 2017). Also, the 2017 Global Burden of Disease study indicates that anxiety has
overtaken depression as the predominant mental health condition globally—the ‘silent
epidemic’ may have eclipsed the ‘black dog’ (Davey, 2018a). The following figure shows the
Google trends results on searches for ‘depression’ (blue line) and ‘anxiety’ (red line) over the
years from 2004 to 2019, indicating that there has been a relative increase in interest in the
term ‘anxiety’ relative to ‘depression’ during this time.

Before we continue to discuss individual mental health problems in detail, it is important to discuss how
the way we define these problems has evolved over time.

1.1 A BRIEF HISTORY OF PSYCHOPATHOLOGY

Throughout history, we have been willing to label behaviour as ‘mad’, ‘crazy’, or ‘insane’ if it appears
unpredictable, irrational, harmful, or if it simply deviates from accepted contemporary social norms.
Characters from history who have been labelled in such a way include the Roman Emperor Caligula,
King George III, Vincent Van Gogh, King Saul of Israel, and Virginia Woolf, to name just a few. But
the term ‘madness’ does not imply a cause—it simply re‐describes the behaviour as something that is
unusual. Views about what causes ‘mad’ behaviour have changed significantly over the course of history,
and it is instructive to understand how the way we attribute the causes of mental health problems have
developed over time. We begin by looking at an historical perspective on explaining psychopathology,
which is known as demonic possession. We then describe how the medical model of
psychopathology developed and finish with a discussion of the transition from asylums to
community care.

demonic possession Historical explanations of psychopathology such as ‘demonic

possession’ often alluded to the fact that the individual had been ‘possessed’ in some way.

medical model An explanation of psychopathology in terms of underlying biological or

medical causes.

asylums In previous centuries asylums were hospices converted for the confinement of
individuals with mental health problems.

community care Care that is provided outside a hospital setting.

1.1.1 Demonic Possession

Many forms of psychopathology are accompanied by what appear to be changes in the individuals'
personality, and these changes in personality or behaviour are some of the first symptoms that are
noticed. The reserved person may become manic and outgoing, and the gregarious person withdrawn
and sombre. They may start behaving in ways that mean they neglect important daily activities (such as
parenting or going to work) or may be harmful to themselves or others. The fact that an individual's
personality seems to have changed (and in some cases may do so very suddenly) has historically tended
people towards describing those exhibiting symptoms of psychopathology as being ‘possessed’ in some
way. That is, their behaviour has changed in such a way that their personality appears to have been
taken over and replaced by the persona of someone or something else.
Explanations of psychopathology in terms of ‘possession’ have taken many forms over the course of
history, and it is a form of explanation that has meant that many who have been suffering debilitating
and distressing psychological problems have been persecuted and physically abused rather than offered
the support and treatment they need. Many ancient civilizations, such as those in Egypt, China,
Babylon, and Greece believed that those exhibiting symptoms of psychopathology were possessed by
bad spirits (this is known as demonic possession), and the only way to exorcise these bad spirits was
with elaborate ritualised ceremonies that frequently involved direct physical attacks on the sufferer's
body in an attempt to force out the demons (e.g., through torture, flogging, or starvation). Not
surprisingly, such actions usually had the effect of increasing the distress and suffering of the victim.
 demonic possession Historical explanations of psychopathology such as ‘demonic
possession’ often alluded to the fact that the individual had been ‘possessed’ in some way.

In Western societies demonology survived as an explanation of mental health problems right up until
the eighteenth century, when witchcraft and demonic possession were common explanations for
psychopathology, and analyses of examples of demonic possession from the Middle Ages have identified
symptoms of psychosis, mood disorders, neurosis, and personality disorders in those believed to be
possessed (Forcén & Forcén, 2014). Today, demonic possession is still a common explanation of
psychopathology in some less developed areas of the world—especially where witchcraft and voodoo
are still important features of the local culture such as Haiti and some areas of Western Africa
(Desrosiers & Fleurose, 2002). The continued adoption of demonic possession as an explanation of
mental health problems (especially in relation to psychotic symptoms) is often linked to local religious
beliefs (Hanwella, de Silva, Yoosuf, Karunaratne, & de Silva, 2012; Ng, 2007), and may often be
accompanied by exorcism as an attempted treatment—even in individuals with a known history of
diagnosed psychotic symptoms (e.g., Tajima‐Pozo et al., 2011) (Focus Point 1.2).

FOCUS POINT 1.2 SPIRIT POSSESSION AS A TRAUMA‐

RELATED PHENOMENON IN UGANDAN CHILD SOLDIERS
Even today, many cultures still believe that unusual behaviour that may be symptomatic of
psychopathology is caused by spirit possession—especially in some less developed areas of the
world where such beliefs are still important features of the local culture. Interestingly, beliefs
about spirit possession are not simply used to try to explain the effects of psychopathology‐
related experiences, but are also regularly used to control and coerce individuals.
Neuner et al. (2012) carried out a study investigating the prevalence of cen, a local variant of
spirit possession, in youths aged between 12 and 25 years in war‐affected regions of Northern
Uganda. They compared youths who had been abducted and forced to fight as child soldiers in
the so‐called Lord's Resistance Army—a group that had waged a long and brutal campaign to
overthrow the government of Uganda—with youths who had never been abducted.
Cen is a form of spirit possession where the ‘ghost of a deceased person is believed to visit the
affected individual and replaces his or her identity’. Neuner and colleagues found that reporting
of spirit possession is significantly higher in former abducted child soldiers than in non‐
abductees. They also found that reports of spirit possession were related to trauma exposure
(such as sexual assault and being forced to kill), to psychological distress, and to higher rates of
suicide and post‐traumatic stress disorder (PTSD).
Neuner et al. (2012) concluded that in many of the areas of the world where beliefs about spirit
possession are widely held, such beliefs are a standard consequence of psychological trauma and
may be a way of explaining the dissociative symptoms that often accompany intense traumatic
 experiences (see Chapter 14). These beliefs about spirit possession can then be used by various
local agencies to manipulate the behaviour of individuals—even to the extent of coercing them
into acts of extreme brutality.

1.1.2 The Medical or Disease Model

As cultures develop, then so too do the types of causes that they attribute behaviour to. By the middle of
the seventeenth century, religious, spiritual, and superstitious explanations of psychopathology were
being replaced by more objective, medical explanations as a consequence of the new empirical scientific
methods being pioneered across Europe by thinkers and scientists such as Isaac Newton, René
Descartes, and Galileo. In particular, the body‐mind dualism of René Descartes introduced some
significant reorientations in the explanation of mental health phenomena. According to Descartes,
because minds could not be diseased, mental health problems must be located in the body, and more
specifically in the brain. It's at this point that psychopathology moved from being a concern of theology
or demonology to being in the realm of medicine (Davey, 2018b).
The medical model of psychopathology was a significant development because it introduced scientific
thinking into our attempts to understand psychopathology and shifted explanations away from those
associated with cultural and religious beliefs. The medical model has given rise to a large body of
scientific knowledge about psychopathology that is based on medicine, and this profession is known as
psychiatry, and the primary approach of the medical model is to identify the biological causes of
psychopathology and treat them with medication or surgery. As we shall see in later chapters, there are
many explanations of psychopathology that allude to biological causes, and these attempt to explain
symptoms in terms of such factors as brain abnormalities (e.g., in dementia, autism) biochemical
imbalances (especially imbalances of brain neurotransmitters) (e.g., major depression, bipolar disorder,
schizophrenia), genetic factors (e.g., learning disabilities, autism, schizophrenia), chromosome disorders
(e.g., intellectual disabilities), congenital risk factors (such as maternal infections during pregnancy) (e.g.,
intellectual disorders, attention‐deficit‐hyperactivity disorder [ADHD]), abnormal physical development
(e.g., autism), and the physical effects of pathological activities (e.g., the effect of hyperventilation in
panic disorder) amongst others. However, while such biological factors may play a role in the aetiology
of some psychopathologies, biological explanations are not the only way in which psychopathology can
be explained, nor is biological dysfunction necessarily a factor underlying all psychopathology. As we
shall see later—it is often a person's experiences that are problematic, not their biological substrates.

psychiatry A scientific method of treatment that is based on medicine, the primary approach
of which is to identify the biological causes of psychopathology and treat them with medication
or surgery.

However, despite its obvious importance in developing a scientific view of psychopathology and
providing some influential treatments, the medical model of psychopathology has some important
implications for the way we conceive mental health problems.
First, an obvious implication is that it implies that medical or biological causes underlie
psychopathology. This is by no means always the case, and bizarre behaviour can be developed by
perfectly normal learning processes. For example, children with autism or intellectual disabilities often
learn disruptive, challenging or self‐harming behaviours through normal learning processes that have
nothing to do with their intellectual deficits (see Treatment in Practice Box 17.1). Furthermore, in
contrast to the medical model, both psychodynamic and contemporary cognitive accounts of
psychopathology argue that many psychological problems are the result of the individual acquiring
dysfunctional ways of thinking and acting, and they acquire these characteristics through normal,
functional learning processes. In this sense, it is not the individual or any part of their biology that is
dysfunctional, it is the experiences they have had that are dysfunctional and has led to them thinking and
acting in the way they do.
Second, the medical model adopts what is basically a reductionist approach by attempting to reduce the
complex psychological and emotional features of psychopathology to simple biology. If you look at the
personal accounts provided at the beginning of this chapter, it is arguable whether the phenomenology
(i.e., the personal experience of psychopathology) or the complex cognitive factors involved in many
psychological problems can be reduced to simple biological descriptions. Biological reductionism cannot
easily encapsulate the distress felt by sufferers, nor can it easily explain the dysfunctional beliefs and
forms of thinking that are characteristic of many psychopathologies. In addition, complex mental
health problems are often not just biological or even simply reducible to psychological problems and
processes, they are influenced by the socio‐economic situation in which the individual lives (Lund et al.,
2018), their potential for employment and education, and the support they are given that will provide
hope for recovery and support for social inclusion (this broad ranging approach to understanding and
treating mental health problems is known as the recovery model and is discussed in more detail in
Chapter 5, Section 5.3.3). All of these factors arguably contribute to a full understanding and
explanation of psychopathology.

recovery model Broad-ranging treatment approach which acknowledges the influence and
importance of socio-economic status, employment and education and social inclusion in helping
to achieve recovery from mental health problems.

Finally, as we have mentioned already, there is an implicit assumption in the medical model that
psychopathology is caused by ‘something not working properly’. For example, this type of explanation
may allude to brain processes not functioning normally, brain or body biochemistry being imbalanced,
or normal physical development being impaired. This ‘something is broken and needs to be fixed’ view
of psychopathology is problematic for a number of reasons:
1. Rather than reflecting a dysfunction, psychopathology might just represent a more extreme form
of normal behaviour. We all get anxious, we all worry, and we all get depressed. Yet anxiety, worry,
and depression in their extreme form provide the basis of many of the common mental health
problems we will cover in this book. If we take the example of worry, we can all testify to the fact
that we worry about something at some time. However, for some of us it may become such a
prevalent and regular activity that it becomes disabling, and may lead to a diagnosis of generalised
anxiety disorder (GAD, see Chapter 6). Nevertheless, there is no reason to suppose that the
cognitive mechanisms that generate the occasional worry bout in all of us are not the same ones
that generate chronic worry in others (Davey & Meeten, 2016). In this sense, psychopathology can
be viewed as being on a dimension rather than being a discrete phenomenon that is separate from
normal experience, and there is accumulating evidence that common psychopathology symptoms
such as anxiety and depression are on a dimension from normal to distressing, rather than being
qualitatively distinct (e.g., Haslam, Holland, & Kuppens, 2011; Lupien et al., 2017).
2. By implying that psychopathology is caused by a normal process that is broken, imperfect or
dysfunctional, the medical model may have an important influence on how we view people
suffering from mental health problems, and indeed, how they might view themselves. At the very
least it can be stigmatising to be labelled as someone who is biological or psychologically imperfect,
and people with mental health problems are often viewed as second‐class citizens—even when
their symptoms are really only more prominent and persistent versions of characteristics that we all
possess (see Section 1.4).

1.1.3 From Asylums to Community Care

Prior to the eighteenth century hospitals and asylums were few and far between, and those that were
established were often devoted to very specific and often highly infectious illnesses (such as leprosy).
‘Madness’ was considered to be a local or domestic problem, and individuals suffering mental health
problems would either be cared for by their families or by their local parish authorities. However, as
many traditional infectious diseases became less common, many hospices for these diseases were
converted into asylums for the confinement of individuals with mental health problems.
Because in many countries there was no coordinated government response to mental health issues until
the nineteenth century, individual privately funded hospitals or ‘madhouses’ began to appear prior to
this time, and in the UK the most famous of these was the Bethlem Hospital in Moorfields, London
that in 1676 had a capacity for 100 inmates (Porter, 2006). Life in these asylums was often cruel and
inhumane, and because “madhouses” were essentially businesses established for financial profit, many
expanded to take more and more sufferers in conditions that were not subject to inspection under the
relevant legislation of the time (MacKenzie, 1992). Any medical treatments provided were usually crude
and often painful (e.g., drawing copious quantities of blood from the brain, hot and cold baths, mercury
pills, or administration of the opiate laudanum to pacify inmates), and the nature of the inmates often
expanded to include not just those with mental health problems, but paupers and individuals from poor
backgrounds—especially young pregnant women, who were considered to be ‘wayward’ or ‘morally
degenerate’. This growing hotchpotch of inmates in eighteenth and nineteenth century asylums gave
rise to ad hoc approaches to mental health care that were based around combating moral degeneration
and ‘social weakness’, and such approaches probably represent the roots of the modern‐day stigma that
is associated with mental health problems. Indeed, in Victorian times, the public could buy tickets to
view the inmates of asylums, a process that will have increased the conception that individuals with
mental health problems were objects of curiosity excluded from everyday society.

Bethlem Hospital One of the first psychiatric hospitals originally established in Moorfields,
London

However, in the nineteenth century there was a gradual movement towards more humane treatments
for individuals in asylums, and these developments were led by a number of important reforming
pioneers. Philippe Pinel (1745–1826) is often considered to be the first to introduce more humane
treatments during his time as the superintendent of the Bicêtre Hospital in Paris. He began by removing
the chains and restraints that had previously been standard ways of shackling inmates and started to
treat these inmates as sick human beings rather than animals. Further enlightened approaches to the
treatment of asylum inmates were pioneered in the US by Benjamin Rush of Philadelphia, and by the
Quaker movement in the UK. The latter developed an approach known as moral treatment, which
abandoned contemporary medical approaches in favour of understanding, hope, moral responsibility,
and occupational therapy (Digby, 1985).

moral treatment Approach to the treatment of asylum inmates, developed by the Quaker
movement in the UK, which abandoned contemporary medical approaches in favour of
understanding, hope, moral responsibility, and occupational herapy.

Even into the twentieth century and up until the 1970s in both the UK and the US, hospitalisation was
usually the norm for individuals with severe mental health problems, and lifelong hospitalisation was not
uncommon for individuals with chronic symptoms. However, it became clear that custodial care of this
kind was neither economically viable nor was it providing an environment in which patients had an
opportunity to improve (Photo 1.1). Because of the growing numbers of inpatients diagnosed with
mental health problems, the burden of care came to rest more and more on nurses and attendants who,
because of lack of training and experience, would resort simply to restraint as the main form of
intervention. This would often lead to deterioration in symptoms, with patients developing what was
called social breakdown syndrome, consisting of confrontational and challenging behaviour,
physical aggressiveness, and a lack of interest in personal welfare and hygiene (Gruenberg, 1980).
Between 1950 and 1970, these limitations of hospitalisation were being recognised and there was some
attempt to structure the hospital environment for patients. The first attempts were known as milieu
therapies, which were the first attempts to create a therapeutic community on the ward that would
develop productivity, independence, responsibility, and feelings of self‐respect. This included mutual
respect between staff and patients and the opportunity for patients to become involved in vocational
and recreational activities. Patients exposed to milieu therapy were more likely to be discharged from
hospital sooner and less likely to relapse than patients who had undergone traditional custodial care
(Cumming & Cumming, 1962; Paul & Lentz, 1977). A further therapeutic refinement of the hospital
environment came in the 1970s with the development of token economy programmes (Ayllon &
Azrin, 1968; see Hackenberg, 2018, for a review of research and application). These were programmes
based on operant reinforcement, where patients would receive tokens (rewards) for emitting desired
behaviours. These desired behaviours would usually include social and self‐help behaviours (e.g.,
communicating coherently to a nurse or other patient, or washing, or combing hair), and tokens could
subsequently be exchanged for a variety of rewards such as chocolate, cigarettes, and hospital privileges.
A number of studies have demonstrated that token economies can have significant therapeutic gains.
For example, Gripp and Magaro (1971) showed that patients in a token economy ward improved
significantly more than patients in a traditional ward, and Gershone, Errickson, Mitchell, and Paulson
(1977) found that patients in a token economy scheme were better groomed, spent more time in
activities and less time in bed, and made fewer disturbing comments than patients on a traditional ward.
Patients on token economy schemes also earn discharge significantly sooner than patients who are not
on such a scheme or have been involved in a milieu therapy programme (Hofmeister, Schneckenbach, &
Clayton, 1979; Paul & Lentz, 1977). However, despite the apparent success of token economies, their
use in the hospital setting has been in serious decline since the early 1980s (Dickerson, Tenhula, &
Green‐Paden, 2005). There were a number of reasons for this decline, and these include the legal and
ethical difficulties of withholding desired materials and events so they can be used as reinforcers, and a
lack of consensus on whether behaviours nurtured in token economy schemes were maintained after the
scheme ended and whether they generalised to other environments and settings (Davey, 1998; Glynn,
1990).
PHOTO 1.1 This photograph shows a ward in Cardiff City Mental Hospital, Whitchurch, UK, in the early twentieth
century. Beds are crowded close together allowing little personal space for patients, who were often hospitalised for much of
their life.
https://www.bbc.co.uk/news/uk‐wales‐south‐east‐wales‐35766956.

milieu therapies The first attempts to structure the hospital environment for patients, which
attempted to create a therapeutic community on the ward in order to develop productivity,
independence, responsibility and feelings of self-respect.

token economy A reward system which involves participants receiving tokens for engaging in
certain behaviours, which at a later time can be exchanged for a variety of reinforcing or
desired items.

In 1963, the US Congress passed a Community Mental Health Act that specified that, rather than be
detained and treated in hospitals, people with mental health problems had the right to receive a broad
range of services in their communities. These services included outpatient therapy, emergency care,
preventative care, and aftercare. Growing concerns about the rights of mental health patients and a
change in social attitudes away from the stigma associated with mental health problems meant that
other countries around the world swiftly followed suit in making mental health treatment and aftercare
available in the community (Hafner & van der Heiden, 1988). These events led to the development of a
combination of services usually termed assertive community treatment or assertive outreach, and, in the
US alone, by the 1990s this had led to around a 10‐fold decrease in the number of people being treated
in hospital for mental health problems (Torrey, 2001).
Given these developments, treatment and care of individuals diagnosed with severe mental health
problems has moved away from long‐term hospitalisation to various forms of community care.
However, the psychiatric hospital is still an important part of the treatment picture for those displaying
severe and distressing symptoms—especially since it will often be the environment in which treatment
takes place for an individual's first acute experience (e.g., a first psychotic episode). However, length of
stay in hospital for individuals has been significantly reduced as a result of the development of more
effective early intervention treatments and supportive community care and outreach programmes, and
even for individuals diagnosed with a serious mental health problem, length of stay typically ranges
from a few days to just a few weeks depending on the nature of the diagnosis (Jacobs et al., 2015).
Nevertheless, even when living back in their communities, it was clear that many individuals diagnosed
with mental health problems would often need support and supervision. They would need help
maintaining their necessary medication regime, finding and keeping a job or applying for and securing
welfare benefits. They may also need help with many aspects of normal daily living that others would
take for granted, such as personal hygiene, shopping, feeding themselves, managing their money, and
coping with social interactions and life stressors. Today in the UK, these outreach services are delivered
by a Community Mental Health Team (CMHT) that can include psychiatrists, clinical
psychologists, social workers, and nurses, and in more complex cases a Care Programme Approach
(CPA) might be applied where an individual care plan is developed to provide ongoing support (NHS
England, 2019). Many mental health services also have Assertive Outreach Teams whose function is
to help individuals with mental health problems who find it difficult to work with mental health services
or have related problems such as violence, self‐harm, homelessness, or substance abuse. Assertive
outreach staff would expect to meet their clients in their own environments, whether that is a home,
café, park, or street, with the aim of building up a long‐term relationship between the client and mental
health services (Photo 1.2). (Video https://www.youtube.com/watch?v=zBcmTUMJZfI shows how
crisis mental health services are delivered in parts of London using dedicated teams of mental health
professionals). (Treatment in Practice 1.1).
PHOTO 1.2 Assertive Outreach staff try to meet their clients in their own environments, and for many homeless
individuals suffering psychotic symptoms this may mean parks, streets, and cafes. The aim of such programmes is to help
individuals with their medication regimes, provide assistance in dealing with everyday life and its stressors and securing
welfare benefits. These programmes also aim to help build a long‐term relationship between the individual and local mental
health services.
https://www.julianhouse.org.uk/life‐as‐an‐outreach‐worker.

CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 1.1

THE PROS AND CONS OF HOSPITALISATION
 From https://www.mind.org.uk/information‐support/guides‐to‐support‐and‐services/crisis‐
services/treatment‐in‐hospital/#.XS70Yi2ZPxo
Read Claire's Blog about her experiences of going into hospital during a crisis:
https://www.mind.org.uk/information‐support/your‐stories/in‐crisis‐my‐
experience/#.XS73pS2ZPxr

1.1.4 Summary
This section has provided an historical perspective on the way in which people have attempted to
understand and explain mental health problems and also describes how people with mental health
problems have been treated over the centuries. Today, most models of mental health provision espouse
compassion, support, understanding, and empowerment for individuals suffering mental health
problems (Repper & Perkins, 2006), but it has been a long journey to get to this point. It has required us
to understand that individuals with mental health problems are not ‘possessed’, they do not need to have
‘demons’ exorcised or driven from their bodies by physical force, they do not need to be incarcerated in
asylums, and nor do they need lifelong custodial care in psychiatric institutions. However, while most of
the physical constraints and impositions imposed on individuals with mental health problems have been
lifted, attitudes to mental health problems have been slower to evolve, and the stigma and discrimination
associated with mental health problems remain a significant issue in need of resolution (see Section 1.4).

SELF‐TEST QUESTIONS
Why was demonic possession such a popular way of explaining psychopathology in
historical times?
What are the pros and cons of the medical model of psychopathology?
How has care for people with mental health problems developed from the times of
asylums to the present day?

SECTION SUMMARY

1.1 A BRIEF HISTORY OF PSYCHOPATHOLOGY

Historical explanations of psychopathology such as ‘demonic possession’ often alluded to
the fact that the individual had been ‘possessed’ in some way.
The medical model attempts to explain psychopathology in terms of underlying biological or
medical causes.
Historically individuals with mental health problems were often locked away in asylums or
given lifelong custodial care in psychiatric hospitals.
Current models of mental health care espouse compassion, support, understanding, and
empowerment.
1.2 DEFINING PSYCHOPATHOLOGY
The personal accounts at the beginning of this chapter have been chosen to represent rather different
and contrasting examples of mental health problems. However, it is not hard to believe that the
experiences reported by Joan, Peter, Jo, and Erica are ones for which they would be happy to receive some
structured help and support. So how do we define what is a problem that should be considered suitable
for support and treatment and what is not? Unlike medicine, we can't simply base our definitions on the
existence of a pathological cause. This is because we have already argued that psychological problems
often do not have underlying physical or biological causes; and second, knowledge of the aetiology of
many psychopathologies is still very much in its infancy, so we are not yet in a position to provide a
classification of psychopathologies that is based on causal factors. This leads us to try to define
psychopathology in ways that are independent of the possible causes of such problems—and, as we
shall see, many attempts to do this have important ethical and practical implications.
The problems of defining psychopathology not only revolve around what criteria we use to define
psychopathology, but also what terminology we use. For example, there are still numerous
psychopathology courses and textbooks that use the title abnormal psychology. Merely using this
title implies that people suffering from mental health problems are in some way ‘abnormal’ either in the
statistical or the functional sense. But the term ‘abnormal’ also has more important ramifications
because it implies that those people suffering psychopathology are in some way ‘not normal’ or are
inferior members of society. In this sense, the ‘abnormal’ label may affect our willingness to fully include
such individuals in everyday activities and may lead to us treating such individuals with suspicion rather
than respect (see Section 1.4 for a fuller account of mental health stigma and how this affects people
suffering with mental health problems). Individuals with mental health problems have become
increasingly vocal about how psychopathology and those who suffer from it are labelled and perceived
by others, and examples of groups set up to communicate these views include service user groups
(groups of individuals who are end users of the mental health services provided by, for example,
government agencies such as the NHS) (see Rose et al., 2016, for a discussion of how mental health
service‐user led organisations interact with mental health decision makers to bring about change),
charitable organisations such as Mind and Rethink, that champion the rights of mental health service
users (https://www.mind.org.uk and https://www.rethink.org), and ‘Time to Change’ a national UK
programme aiming to promote awareness of mental health problems and to combat stigma and
discrimination (http://www.time‐to‐change.org.uk).

abnormal psychology An alternative definition of psychopathology, albeit with stigmatizing

connotations relating to not being ‘normal’.

service user groups Groups of individuals who are end users of the mental health services
provided by, for example, government agencies such as the NHS.

So, when considering how to define psychopathology we must consider not only whether a definition is
useful in the scientific and professional sense but also whether it provides a definition that will minimise
the stigma experienced by sufferers and facilitate the support they need to function as inclusive members
of society. Let us bear this in mind as we look at some potential ways of identifying and defining
psychopathology.

1.2.1 Deviation from the Statistical Norm

We can use statistical definitions to decide whether an activity or a psychological attribute deviates
substantially from the statistical norm, and in some areas of clinical psychology this has been used as
a means of deciding whether a particular disorder meets diagnostic criteria. For example, in the area of
intellectual disability, if an IQ score is approximately two standard deviations or more below the
population mean, this is taken as an indicator of intellectual disability (see Chapter 17, Table 17.6).
Figure 1.1 shows the distribution of IQ scores in a standard population, and this indicates that the
percentage of individuals with IQ scores below 70 would be relatively rare (i.e., around 2.5%–3% of the
population) (Figure 1.1). However, there are at least two important problems with using deviations from
statistical norms as indications of psychopathology. First, in the intellectual disability case, an IQ of less
than 70 may be statistically rare, but rather than simply forcing the individual into a diagnostic category,
a better approach would be to evaluate the specific needs of individuals with intellectual disabilities in a
way that allows us to suggests strategies, services, and supports that will optimise individual functioning.
Second, as we can see from Figure 1.1, substantial deviation from the norm does not necessarily imply
psychopathology because individuals with exceptionally high IQs are also statistically rare—yet we
would not necessarily be willing to consider this group of individuals as candidates for psychological
intervention. We might feel that adopting a definition of psychopathology that is statistically based lends
some objectivity and measurability to our definition. However, where we draw our cut‐off points
between ‘normality’ and ‘abnormality’ will still be a subjective judgement.

statistical norm The mean, average or modal example of a behaviour.

FIGURE 1.1 This figure represents a normal distribution curve for IQ scores. From this distribution it can be seen that
68% of people score between 84 and 116 points, while only 2.27% of people have an IQ score below 68 points. This
graph suggests that around 2–3% of the population will have IQs lower than the 70 points that is the diagnostic criterion
for intellectual development disorder. However, the problem for basing a definition of psychopathology on scores that deviate
substantially from the norm is that high IQ also is very rare. Only 2.27% of the population have an IQ score greater than
132 points.
Finally, emotions such as anxiety and depression that underlie the most common mental health
problems are not statistically rare emotions. They are experienced almost daily by most people, and this
represents another reason why deviation from the statistical norm does not make a good basis on which
to define psychopathology.

1.2.2 Deviation from Social and Political Norms

There is often a tendency within individual societies for the members of that society to label a
behaviour or activity as indicative of psychopathology if it is far removed from what we consider to be
the social norms for that culture. We assume (perhaps quite wrongly) that socially normal and
acceptable behaviours have evolved to represent adaptive ways of behaving and that anyone who
deviates from these norms is exhibiting psychopathology. However, it is very difficult to use deviation
from social norms, or even violations of social norms, as a way of defining psychopathology.
First, different cultures often differ significantly in what they consider to be socially normal and
acceptable. For example, in the Soviet Union during the 1970s and 1980s, political dissidents who were
active against the communist regime were regularly diagnosed with schizophrenia and incarcerated in
psychiatric hospitals. At first, we might think that this is a cynical method of political repression used to
control dissent, but amongst many in the Soviet Union at the time it represented a genuine belief that
anti‐Soviet activity was indeed a manifestation of psychopathology (i.e., ‘surely anyone who wanted to
protest against the perfect social system must be suffering from mental health problems!’). Soviet
psychiatrists even added to the official symptoms of schizophrenia by including disorders that appear to
consist of ‘revisionist’ views and beliefs. For example, ‘reformist delusions’ was a label for beliefs that an
improvement in social conditions can be achieved only through the revision of people's attitudes, in
accordance with the individual's own ideas for the transformation of reality, and ‘litigation mania was a
conviction, which does not have any basis in fact, that the individual's own rights as a human being are
being violated and flouted’ (Goldacre, 2002). However, since the collapse of the Soviet system, few
would suspect that these kinds of beliefs and activities are representative of psychopathology.
Second, it is difficult to use cultural norms to define psychopathology because cultural factors seem to
significantly affect how psychopathology manifests itself. For example, (a) social and cultural factors will
affect the vulnerability of an individual to causal factors (e.g., poor mental health is more prevalent in
low income countries) (Bryant, 2019), and (b) culture can produce ‘culture‐bound’ symptoms of
psychopathology which seem confined to specific cultures and can influence how stress, anxiety, and
depression manifest themselves. Two examples of such ‘culture‐bound’ effects are described in Focus
Point 1.3, and these are known as Ataque de nervios, a form of panic disorder found mainly in
Latinos from the Caribbean (Moitra, Duarte‐Velez, Lewis‐Fernàndez, Weisberg, & Keller, 2018; Salman
et al., 1998), and Seizisman, a state of psychological paralysis found in the Haitian community
(Nicolas, DeSilva, Grey, & Gonzalez‐Eastep, 2006) (Focus Point 1.3).

ataque de nervios A form of panic disorder found in Latinos from the Caribbean.

seizisman A state of psychological paralysis found in the Haitian community.

FOCUS POINT 1.3 PSYCHOPATHOLOGY AND CULTURE

Psychopathology can manifest itself in different forms in different cultures, and this can lead to
some disorders that are culture‐specific (i.e., have a set of symptoms which are found only in
 that particular culture). Two such examples are Ataque de Nervos, which is an anxiety‐based
disorder found almost exclusively amongst Latinos from the Caribbean (Salman et al., 1998),
and Seizisman, a state of psychological paralysis found in the Haitian community (Nicolas et al.,
2006).

Ataque de Nervos
Its literal translation is ‘attack of nerves’, and symptoms include trembling, attacks of crying,
screaming uncontrollably, and becoming verbally or physically aggressive. In some cases, these
primary symptoms are accompanied by fainting bouts, dissociative experiences, and suicide
attempts.
Research on Ataque de Nervos has begun to show that it is found predominantly in women, those
over 45 years of age, and from low socio‐economic backgrounds and disrupted marriages
(Guarniccia, De La Cancela, & Carrillo, 1989), The symptoms appear to resemble many of
those found in panic disorder, but with a coexisting affective disorder characterised by
emotional lability and anger (Salman et al., 1998).
From this research, it appears that Ataque de Nervos may be a form of panic disorder brought on
by stressful life events (such as economic or marital difficulties), but whose expression is
determined by the social and cultural norms within that cultural group. In particular, Latino
cultures place less emphasis on self‐control and emotional restraint than other Western cultures,
and so the distress of panic disorder in Latinos tends to be externalised in the form of
screaming, uncontrolled behaviour and aggression. In contrast, in Western cultures the distress
of panic disorder is usually coped with by adopting avoidance and withdrawal strategies—
hence the common diagnosis of panic disorder with agoraphobia.

Seizisman
The name literally means ‘seized‐up‐ness’ and refers to a state of paralysis usually brought on
by rage, anger, or sadness, and in rare cases happiness. Events that can cause Seizisman include
a traumatic event (such as receiving bad news), a family crisis, and verbal insults from others.
Individuals affected by the syndrome become completely dysfunctional, disorganised, and
confused and unresponsive to their surroundings (Laguerre, 1981). The following quote
illustrates how viewing traumatic events while working within a Haitian community that is
attuned to the symptoms of this syndrome can actually give rise to these culture‐bound
symptoms:
‘I remember over and over, when I was a UN Human Rights Monitor and I was down there in
Port‐au‐Prince viewing cadaver after cadaver left by the Haitian army, people would say, “Now
go home and lie down or you will have Seizisman”. And I never really had a problem, you
know? I never threw up or fainted no matter what I saw, but I started to feel “stressed,” which is
an American illness defined in an American way. After viewing one particularly vile massacre
scene, I went home and followed the cultural model I had been shown. I lay down, curled up,
and went incommunicado. “Ah‐hah! Seizisman!” said the people of my household’ (From
Nicolas et al., 2006, p. 705).

1.2.3 Maladaptive Behaviour and Harmful Dysfunction

It is often tempting to define psychopathology in terms of whether it renders the individual incapable of
adapting to what most of us would consider normal daily living. That is, whether a person can
undertake and hold down a job, can cope with the demands of being a parent, develop loving
relationships, or function socially. In its extreme form, maladaptive behaviour might involve behaving in
a way that is a threat to the health and well‐being of the individual and to others. It is certainly the case
that current diagnostic criteria, such as those in the Diagnostic and Statistical Manual of Mental Disorders, 5th
Edition (DSM‐5), do use deficits in social, occupational, and educational functioning as one criterion for
defining many mental health problems, but it is by no means the only criterion by which those
conditions are defined. The problem with defining psychopathology solely in terms of maladaptive
behaviour is also apparent when we discuss forms of behaviour that we might call maladaptive, but we
would not necessarily want to label as psychopathology. The behaviour of many people convicted of
murder or terrorist acts, for example, is maladaptive in the sense that it is harmful to others, but it is by
no means the case that all murderers or terrorists commit their crimes because they have mental health
problems. On the other side of the coin, it can be argued that many forms of psychopathology may not
be representative of maladaptive behaviour but instead serve a protective or adaptive function. For
example, a case can be made for suggesting that specific phobias such as height phobia, water phobia,
snake and spider phobia are adaptive responses which could protect us from exposure to potentially life‐
threatening situations (e.g., Seligman, 1971; see Chapter 6).
A similar approach is to assume that mental health problems can be defined as harmful dysfunction
(Wakefield, 1997). This view assumes that psychopathology is defined by the ‘dysfunction’ of a normal
process that has the consequence of being in some way harmful. For example, ‘hearing voices’ during
episodes of psychosis may be caused by the brain's inability to turn off unwanted thoughts, and these
may give rise to potentially harmful consequences such as the extreme behaviours which are
consequences of severe paranoia (see Chapter 8, Section 8.5.2). The problem with this type of
definition is that we still know very little about the brain mechanisms that generate psychopathology
symptoms (both biological and psychological mechanisms), so it is very difficult to know what ‘normal’
process might be dysfunctioning. In addition, there are now a number of taxometric studies suggesting
that many common mental health problems are best considered as dimensional rather than categorical
(e.g., Haslam et al., 2011; Olatunji, Williams, Haslam, Abramowitz, & Tolin, 2008). That is, distressing
mental health symptoms are just more extreme versions of normal emotions and behaviours and are
not in any way qualitatively different from normal behaviour as the harmful dysfunction model would
imply.

harmful dysfunction Assumption that psychopathology is defined by the ‘dysfunction’ of a

normal process that has the consequence of being in some way harmful.

1.2.4 Distress and Disability

In Chapter 2 we will look at some of the ways in which psychologists and psychiatrists have attempted
to classify psychopathology, and in order to be diagnosed as a mental health problem one of the most
common requirements is that the symptoms must cause ‘clinically significant distress or impairment in
social, academic, or occupational functioning’. It is clearly the case that many individuals with severe
symptoms of psychopathology do suffer considerable personal distress—often to the point of wanting to
take their own lives. Defining psychopathology in terms of the degree of distress and impairment
expressed by the sufferer is useful in a number of ways. First, it allows people to judge their own
‘normality’ rather than subjecting them to judgements about their ‘normality’ made by others in society
such as psychologists or psychiatrists. Many people who are diagnosed with mental health problems
originally present themselves for treatment because of the distress and impairment caused by their
symptoms, and to some degree this makes them judges of their own needs. Second, defining
psychopathology in terms of the degree of distress and impairment experienced can be independent of
the type of lifestyle chosen by the individual. This means we do not judge whether someone has a
psychopathology purely on the basis of whether they are perceived as productively contributing to
society or not, or whether they actively violate social norms but on the basis of how they are able to
cope with the life they are living. In addition to this, there is plenty of evidence that psychological
distress is closely associated with poor quality of life and a lowered ability to cope with stress and life
problems (Arvidsdotter, Marklund, Kylén, Taft, & Ekman, 2016; Atkins, Naismith, Luscombe, & Hickie,
2013)—factors that would offer additional good reason for providing support and help for individuals
experiencing distress.
However, as attractive as this definition for defining psychopathology seems, it does have a number of
difficulties. First, this approach does not provide any standards by which we should judge behaviour
itself. For example, in Erica's Story she does admit that her substance dependency is beginning to cause
her some distress, but should we consider that a teenager's drug addiction is in need of treatment only if
they express unhappiness about their situation? In addition, psychopathology classification schemes do
include diagnostic categories in which diagnosis does not require that the sufferer necessarily reports any
personal distress or impairment. A good example of this is that group of disorders known as personality
disorders (see Chapter 12). For example, individuals diagnosed with antisocial personality disorder
frequently exhibit behaviour that is impulsive, emotional, threatening, and harmful to themselves and
others. Yet they are rarely willing to admit that their behaviour is unusual or problematic.

1.2.5 Summary
None of these individual ways of defining psychopathology is ideal. They may fail to include examples
of behaviour that we intuitively believe are representative of mental health problems (the distress and
impairment approach), they may include examples we intuitively feel are not examples of
psychopathology (e.g., the statistical approach, the deviation from social norms approach), or they may
represent forms of categorisation that would lead us simply to imposing stigmatising labels on people
rather than considering their individual needs (e.g., the statistical approach). In practice, classification
schemes tend to use an amalgamation of all these approaches with emphasis being placed on individual
approaches depending on the nature of the symptoms and disorder being classified.

SELF‐TEST QUESTIONS
What are the problems with using the normal curve to define psychopathology?
How do cultural factors make it difficult to define psychopathology in terms of deviations
from social norms?
What are the pros and cons of using maladaptive behaviour or distress and impairment as
means of defining psychopathology?

SECTION SUMMARY

1.2 DEFINING PSYCHOPATHOLOGY

Potential ways of defining psychopathology include deviation from the statistical norm, deviation
from social norms, exhibiting maladaptive behaviour, and experiencing distress and impairment.

1.3 EXPLANATORY APPROACHES TO PSYCHOPATHOLOGY

Despite the fact that symptoms of mental health problems seemed baffling to many people, there was
still a strong desire to understand psychopathology, to describe its causes, and as a consequence, to
develop effective interventions. Section 1.1 has described some of the important milestones in the
history of psychopathology and how an understanding of mental health problems has evolved from the
level of primitive beliefs, through an application of scientific knowledge, to current models of care. This
section introduces you to the main contemporary explanatory approaches to psychopathology, and these
are ones that you will encounter regularly in the following chapters.
At this point it is important to understand what an explanatory paradigm is and why we can
explain mental health problems in many different ways within a number of different paradigms. First,
human beings are multifaceted organisms, they consist of a genetically propagated biological substrate
which serves as a basis for behaviour and a whole range of psychological processes, such as thinking,
learning, remembering, perceiving, etc. These genetic, biological, behavioural, and psychological
processes are interdependent and together make up our conception of the complete thinking and
behaving human being. But genetic, biological, behavioural, and psychological processes can also be
studied independently, they have their own language of description, and researchers may be skilled in
studying people only within one of these basic paradigms. Second, this view also applies to
psychopathology. For example, symptoms of psychosis might be explained genetically (in terms of the
inheritance of genes that give rise to a predisposition for these symptoms), biologically (in terms of
abnormalities in brain function that generate symptoms), behaviourally (in terms of how symptomatic
behaviours are learnt through experience), and psychologically (in terms of how symptoms might be
generated by unusual or biased ways of thinking). In many cases, a specific psychopathology can be
explained at all these different levels. Furthermore, these explanations within different paradigms are
not mutually exclusive they supplement each other and provide a fuller, richer understanding of that
psychopathology.
The following sections introduce you to some examples of these different paradigms and how they each
contribute to our broad understanding of psychopathology.

1.3.1 Biological Models

Genetics and neuroscience are two of the most important biological paradigms through which
researchers attempt to understand psychopathology. The discipline of genetics provides us with a variety
of techniques that allow an assessment of whether psychopathology symptoms are inherited or not, and
neuroscience techniques allow us to determine whether psychopathology symptoms are associated with
abnormalities or differences in brain or central nervous system functioning.

Genetics
Genetics is a fast growing and important branch of science, and collaborations such as the Human
Genome Project are attempting to identify those genes that may be responsible for human
characteristics, disorders, and diseases (Collins & McKusick, 2001; Lander, 2011). People are biological
organisms who come into the world with a biological substructure that will be significantly determined
by the genes they have inherited from their ancestors. It is therefore almost a truism to say that
behaviour—and mental health problems too—will therefore have at least some genetic component. In
some cases the genetic component may be extremely influential (e.g., in Huntington's disease—see Focus
Point 1.4), in others it may be a necessary component but may not always be sufficient to trigger a
mental health problem, in still other cases the genetic component may be relatively nonspecific and less
important to the development of a mental health problem than the experiences that an individual may
have during their lifetime.

Genetics The study of heredity and the variation of inherited characteristics.

 FOCUS POINT 1.4 THE GENETICS OF INHERITING MENTAL
HEALTH PROBLEMS

Huntington's disease is a degenerative neurological conditioning that can often give rise to
dementia, and it is caused by a dominant mutation in a gene on the fourth chromosome. Each
person has two copies of this gene (each one called an allele), one inherited from each parent.
In the case of Huntington's disease an individual needs only one copy of the mutant allele to
develop the disease. Parents randomly give one of their two alleles to their offspring, so a child
of a parent who has Huntington's disease has a 50% chance of inheriting the mutant version of
the gene from their parent. A grandchild of a person with Huntington's disease has a 25%
chance of inheriting the mutant gene and so developing the disease.

The gene for Huntington's disease is dominant, and so the disease can be inherited only if one
parent has the mutant gene. In this case, inheriting the mutant gene is the primary factor in the
affected individual developing the disease. In other mental health problems where genetic
factors have been found to be important (e.g., schizophrenia), inheritance is only one of a
number of factors that has been found to contribute to the development of symptoms, and this
has led researchers to advocate a diathesis–stress model in which inherited factors provide a
vulnerability to develop symptoms, but these symptoms do not appear unless the individual
encounters stressful life experiences.

The way in which genetics might influence psychopathology can be studied in a variety of ways: (a) by
studying psychopathology symptoms across different family members who may differ in the extent to
which they are genetically related to each other. These studies are known as concordance studies,
where the probability of symptoms occurring can be related to the degree to which different family
members share genes in common; (b) twin studies compare the probability with which monozygotic
(MZ) and dizygotic (DZ) twins both develop psychopathology symptoms. MZ twins (identical twins)
share 100% of their genetic material, whereas DZ twins (nonidentical twins) share only 50% of their
genes, so a genetic explanation of psychopathology would predict that there would be greater
concordance in the diagnosis of a mental health problem in MZ than in DZ twins (see Chapter 8 for
some examples of this approach); and (c) Because both families and twins are likely to share similar
environments as well as genes, interpretation of family and twin studies can be difficult. However, many
of these difficulties of interpretation can be overcome by studying the offspring of MZ and DZ twins
rather than the twins themselves (Gottesman & Bertelsen, 1989; see McAdams et al., 2018, for methods
of exploring intergenerational genetic associations). If one MZ twin develops psychopathology
symptoms and the other does not, any genetic element in symptoms should still show up in the children
of either of the two MZ twins. That is, the children of the MZ twins should still exhibit similar rates of
risk for the psychopathology (because they have inherited the same predisposition)—even though one of
their parents developed the symptoms and the other did not.

concordance studies Studies designed to investigate the probability with which family
members or relatives will develop a psychological disorder depending on how closely they are
related – or, more specifically, how much genetic material they have in common.

twin studies Studies in which researchers have compared the probability with which
monozygotic (MZ) and dizygotic (DZ) twins both develop symptoms indicative of a
psychopathology inorder to assess genetic contributions to that sychopathology.

However, in the vast majority of psychopathologies we will describe in this book, people do not solely
inherit a mental health problem through their genes; a mental health problem develops because of an
interaction between a genetic predisposition and our interactions with the environment (Shenk, 2010).
This is basically what is known as a diathesis–stress model of psychopathology, where ‘diathesis’
refers to an inherited predisposition and ‘stress’ refers to a variety of experiences that may trigger the
inherited predisposition (this is a model that is particularly important in the understanding of psychosis,
see Chapter 8). (see https://www.youtube.com/watch?v=yuMi50PrwIM). This interaction between
genes and experiences gives rise to the notion of heritability. Heritability is a measure of the degree to
which symptoms can be accounted for by genetic factors; this ranges from 0 to 1, and the nearer this
figure is to 1, the more important are genetic factors in explaining the symptoms. In the case of
Huntington's disease described in Focus Point 1.4, the heritability of Huntington's symptoms is very
close to 1 because if you inherit the dominant gene for this disorder that is sufficient to ensure that the
individual will develop the disease.

diathesis-stress model Model that suggests a mental health problem develops because of an
interaction between a genetic predisposition and our interactions with the environment.

Heritability A measure of the degree to which symptoms can be accounted for by genetic
factors. It ranges from 0 to 1, and the nearer this figure is to 1, the more important are genetic
factors in explaining the symptoms.

Not only do genetic approaches to psychopathology attempt to estimate the heritability of individual
disorders, the area of molecular genetics also seeks to identify individual genes that may be involved
in transmitting psychopathology symptoms (see Uher & Zwicker, 2017, for a review of genetic
approaches to understanding psychopathologies). One method of identifying individual genes that has
been particularly applied to psychopathology is genetic linkage analysis. Linkage analysis works by
comparing the inheritance of characteristics for which gene location is known (e.g., eye colour) with the
inheritance of psychopathology symptoms. For example, if the inheritance of eye colour follows the
same pattern within a family as particular psychopathology symptoms, then it can reasonably be
concluded that the gene controlling the psychopathology symptoms can probably be found on the same
chromosome as the gene controlling eye colour. While such methods are extremely valuable, it should
be pointed out that it is very rare that psychopathology symptoms can be traced to an individual gene,
and very often symptoms are associated with multiple genes, which testifies to the complex and often
heterogenous nature of mental health problems (e.g., Badner & Gershon, 2002; Faraone et al., 2007;
Levinson, Lewis, & Wise, 2002). Finally, an alternative means of identifying psychopathology‐relevant
genes is to use nonhuman animals. For example, researchers can manipulate specific genes in animals
with some accuracy, and in mice studies can even delete individual genes. This then enables the
researcher to determine whether that gene is linked to any changes in the animal's behaviour that might
be indicative of psychopathology (e.g., by observing more anxious behaviour) (Gross et al., 2002).

molecular genetics Genetic approach that seeks to identify individual genes that may be
involved in transmitting psychopathology symptoms.

genetic linkage analysis A method of identifying individual genes by comparing the

inheritance of characteristics for which gene location is known (e.g. eye colour) with the
inheritance of psychopathology symptoms.

FIGURE 1.2 The heritability gap.

Source: From Uher & Zwicker (2017).
However, we must be cautious about how heritability estimates are calculated. Different methods can
often provide very different heritability estimates, and this phenomenon is known as the ‘heritability
gap’. Figure 1.2 shows dramatic differences in the heritability estimates for some common
psychopathologies when we compare heritability estimates based on concordance measures with
estimates based on molecular genetic analyses. The most likely explanation for this ‘heritability gap’ is
that twin studies may often erroneously attribute genetic effects to individuals growing up in the same
family or environment (i.e., MZ twins) whereas this factor is not a confound when molecular studies are
carried out on unrelated individuals (Uher & Zwicker, 2017).
Finally, one new area of genetics highly relevant to psychopathology is epigenetics. We know that
aspects of psychopathology and mental health can be influenced by genetics and hereditary factors, and
we also know that personal experiences can also influence psychopathology. However, recent research in
the developing area of epigenetics suggests that the way that parents behaved or what they ate can also
affect the subsequent behaviour of their offspring by influencing their offspring's genetic heritage, either
by changing the nature of their DNA or triggering or inhibiting the expression of genes that may
represent risk factors for psychopathology. Similarly, the early experiences of an individual may either
trigger or inhibit the expression of genes they may possess that make them vulnerable to mental health
problems such as anxiety or depression, and in this way there can be a direct interaction between
environmental factors and inherited factors. For example, early life stress can enable the expression of
genes that control the neuroendocrinology of PTSD, which then puts such individuals at higher risk of
developing PTSD after highly traumatic life experiences (Yehuda et al., 2010). This has important
implications for our understanding of how mental health problems develop and the aetiology of those
disorders (Guintivano & Kaminsky, 2016; Kofink, Boks, Timmers, & Kas, 2013).

Neuroscience
The neuroscience paradigm seeks an understanding of psychopathology by identifying aspects of the
individual's biology that may contribute to symptoms. The main focus of this paradigm is on brain
structure and function, although the broader activity of the neuroendocrine system has also been
implicated in some psychopathology symptoms, especially mood disorders (the neuroendocrine system
involves interactions between the brain and the endocrine system that produces hormone secretions in
the body).

neuroscience The scientific study of the nervous system.

Brain structure and function

The brain is the organ that controls and organises most of a person's behaviour—including their actions
and their thoughts, so it is not surprising that the brain has been a focus for attempting to understand
psychopathology. The brain is divided into two mirror‐image hemispheres that are connected by a set of
nerve fibres called the corpus callosum. The outer convoluted area of the brain is known as the
cerebral cortex, and the large troughs in the convolutions are called fissures (see Figure 1.3). The
lateral and central fissures divide the cerebral cortex into four lobes: the frontal, occipital, temporal, and
parietal lobes, and these areas serve various specific functions. The occipital lobe is the area for visual
perception, the temporal lobe is considered to be a focus for memory processes, and the parietal
lobe is associated with visuo‐motor coordination (Kolb & Whishaw, 2009). However, the frontal lobes
are especially important and are the areas of the brain that are considered to make us uniquely human.
The frontal lobes are known to be important in executive functions such as planning and decision
making, error correction and troubleshooting, novel situations, and inhibiting habitual and impulsive
responses (Miller & Cummings, 2017). Given the important functions of the frontal lobes, it is an area
of the brain where deficits or abnormalities have been implicated in many types of psychopathology,
including attention disorders, perseveration and stereotyped behaviour patterns, lack of drive and
motivation, inability to plan ahead, and apathy and emotional blunting. Alternatively, because the
frontal lobes also control response inhibition, deficits in this area can also be associated with personality
disorders, impulsivity, euphoria, aggressive behaviour, and deficits in emotional regulation (Falquez et
al., 2015; Sebastian et al., 2014).

corpus callosum A set of nerve fibres which connects the two mirror-image hemispheres of
the brain.
cerebral cortex The outer, convoluted area of the brain.

occipital lobe Brain area associated with visual perception.

temporal lobe The areas of the brain that lie at the side of the head behind the temples and
which are involved in hearing, memory, emotion, language, illusions, tastes and smells.

parietal lobe Brain region associated with visuomotor coordination.

Frontal lobes One of four parts of the cerebrum that control voluntary movement, verbal
expressions, problem solving, will power and planning.
FIGURE 1.3 The neuroanatomy of the brain. (a) The cerebral cortex. (b) The limbic system.
A further set of brain areas that are often implicated in psychopathology are collectively known as the
limbic system. The limbic system comprises the hippocampus, mammillary body, amygdala,
hypothalamus, fornix, and thalamus. It is situated beneath the cerebral cortex (see Figure 1.3) and is
thought to be critically involved in emotion and learning. For example, the hippocampus is involved
in spatial learning and the amygdala is an important region coordinating attention to emotionally‐
relevant stimuli (e.g., threatening or fear‐relevant stimuli). Because of its function in regulating
emotional responses, the amygdala is an important brain structure in understanding many aspects of
psychopathology. It is involved in the formation and storage of emotion‐relevant stimuli and provides
feedback to the thalamus that results in appropriate motor action (Del Casale et al., 2012). Because of
this role, the amygdala is important in activating phobic fear (Ahs et al., 2009), and depressed
individuals show more activity in the amygdala when viewing emotional stimuli than nondepressed
individuals (Sheline et al., 2001).

limbic system A brain system comprising the hippocampus, mamillary body, amygdala,
hypothalamus, fornix and thalamus. It is situated beneath the cerebral cortex and is thought to
be critically involved in emotion and learning.
 hippocampus A part of the brain which is important in adrenocorticotropic hormone
secretion and is also critical in learning about the context of affective reactions.

amygdala The region of the brain responsible for coordinating and initiating responses to fear.

Brain neurotransmitters
These are the chemicals that help neurones to communicate with each other and thus are essential
components of the mechanisms that regulate efficient and effective brain functioning. During synaptic
transmission, neurones release a neurotransmitter that crosses the synapse and interacts with receptors
on neighbouring neurones, and most neurotransmitters relay, amplify and modify signals between
neurones (see Figure 1.4). There are many different types of neurotransmitters that can be grouped
according to either their chemical structure or to their function, and a number of different
neurotransmitters have been implicated in psychopathology, including dopamine, serotonin,
norepinephrine, and gamma‐aminobutyric acid(GABA). Abnormalities in levels of serotonin
and norepinephrine have been implicated in the symptoms of mood disorders (see Chapter 7),
dopamine is central to important theories of schizophrenia and psychotic symptoms (see Chapter 8,
Section 8.5), and norepinephrine and GABA may play a role in anxiety symptoms (Kaur & Singh,
2017; Liu, Zhao, & Guo, 2018; Monaco, Coley, & Gao, 2016). Even so, the functions of
neurotransmitters are often not simple or easy to define. For example, dopamine has many functions in
the brain, including important roles in regulating voluntary movement, motivation, and reward and is
critically involved in mood, attention, and learning. Similarly, early theories of the role of
neurotransmitters in psychopathology symptoms tended to assume that symptoms were caused by either
too little or too much of a particular neurotransmitter. This picture, however, is much too simple, and
more recent theories suggest that symptoms may be associated with much more complex interactions
between different neurotransmitters (e.g., Carlsson et al., 2001; Devor et al., 2017).

dopamine A compound that exists in the body as a eurotransmitter and as a precursor of

other substances including adrenalin.
FIGURE 1.4 Neurons, neurotransmitters, and nerve impulses. The cells in the brain are called neurons and consist of
(a) the cell body, (b) dendrites, and (c) one or more axons of varying length. When a neuron sends a signal to another
neuron, a nerve impulse travels down the axon to the synapse between the two neurons. The end of the axon contains
synaptic vesicles which are small structures filled with neurotransmitters. When the neurotransmitter is released into the
synapse, some of the molecules reach the receptor and a message is sent to the postsynaptic cell. Once a presynaptic neuron
has sent its signal, the synapse then has to return to its normal state by either breaking down any remaining neurotransmitter
in the synapse or taking it back into the axon through a process called reuptake.

serotonin An important brain neurotransmitter where low levels are associated with
depression.

norepinephrine A neurotransmitter thought to play a role in anxiety symptoms.

gamma-aminobutyric acid (GABA) A neurotransmitter thought to play a role in anxiety

symptoms.

Summary
Most chapters of this book have a section on biological explanations of psychopathology where
explanations of the causes of symptoms are discussed in terms of genetics, brain structure and function,
and brain neurotransmitters. Because behaviour and thought cannot occur in the absence of a
biological substrate, it is clear that biological explanations of psychopathology will be highly relevant.
They will tell us whether all or some of the symptoms of a mental health problem are inherited or not,
and they will also provide us with information about whether abnormalities in brain function or
neurotransmitter activity is associated with psychopathology. There are some clear advantages to the
biological approach—especially in terms of treatments. One prominent example is that if we can
identify associations between psychopathology and imbalances in neurotransmitters, then we can
develop pharmaceutical products that might resolve this imbalance—and this has been particularly the
case with mood disorders and psychotic symptoms. However, mental health problems cannot always be
reduced simply to biological descriptions, and a full understanding of the causes and experience of
mental health problems will require description and explanation at other levels (e.g., how a person's
experiences influence their thoughts and behaviour, how their interpretation of events affect their
emotions, and how distress is experienced and manifested). We discuss some of these alternative—but
complimentary—paradigms later in the chapter. But for a fuller introductory coverage of neuroscience,
the brain and behaviour, see Ward and King (2018).

1.3.2 Psychological Models

Moving away from the biological model of psychopathology, some approaches to understanding and
explaining mental health problems still see mental health problems as symptoms produced by an
underlying cause (what is known as the pathology model), but that the causes are psychological rather
than biological or medical. These approaches often view the cause as a perfectly normal and adaptive
reaction to difficult or stressful life conditions (such as the psychoanalytic view that psychopathology is a
consequence of perfectly normal psychodynamic processes that are attempting to deal with conflict). As
such, psychological models of psychopathology tend to view mental health symptoms as normal
reactions mediated by intact psychological or cognitive mechanisms and not the result of processes that
are abnormal, ‘broken’, or malfunctioning.
The following sections describe in brief some of the main psychological approaches to understanding
and explaining psychopathology.

The psychoanalytical or psychodynamic model

This approach was first formulated and pioneered by the Viennese neurologist Sigmund Freud
(1856–1939). He collaborated with the physician Josef Breuer in an attempt to understand the causes of
mysterious physical symptoms such as hysteria and spontaneous paralysis—symptoms which appeared
to have no obvious medical causes. Freud and Breuer first tried to use hypnosis as a means of
understanding and treating these conditions, but during these cases clients often began talking about
earlier traumatic experiences and highly stressful emotions. In many cases, simply talking about these
repressed experiences and emotions under hypnosis led to an easing of symptoms. Freud built on these
cases to develop his influential theory of psychoanalysis, which was an attempt to explain both
normal and abnormal psychological functioning in terms of how various psychological mechanisms
help to defend against anxiety and depression by repressing memories and thoughts that may cause
conflict and stress. Freud argued that three psychological forces shape an individual's personality and
may also generate psychopathology. These are the id (instinctual needs), the ego (rational thinking), and
the superego (moral standards).

Sigmund Freud An Austrian neurologist and psychiatrist who founded the psychoanalytic
school of psychology.

psychoanalysis An influential psychological model of psychopathology based on the

theoretical works of Sigmund Freud.
 id In psychoanalysis, the concept used to describe innate instinctual needs – especially sexual
needs.

The concept of the id was used to describe innate instinctual needs—especially sexual needs. He noted
that from a very early age, children obtained pleasure from nursing, defecating, masturbating, and other
‘sexually’ related activities and that many forms of behaviour were driven by the need to satisfy the
needs of the id.
As we grow up, Freud argued that it becomes apparent to us that the environment itself will not satisfy
all our instinctual needs, and we develop a separate part of our psychology known as the ego. This is a
rational part of the psyche that attempts to control the impulses of the id, and ego defence
mechanisms develop by which the ego attempts to control unacceptable id impulses and reduce the
anxiety that id impulses may arouse.

ego In psychoanalysis, a rational part of the psyche that attempts to control the impulses of the
id.

ego defence mechanisms Means by which the ego attempts to control unacceptable id
impulses and reduce the anxiety that id impulses may arouse.

superego Key concept in Sigmund Freud’s psychoanalytic theory. The superego develops out
of both the id (innateinstinctual needs) and ego (a rational part of the psyche that attempts to
control the impulses of the id), and represents our attempts to integrate ‘values’ that we learn
from our parents or society.

The superego develops out of both the id and ego, and represents our attempts to integrate ‘values’
that we learn from our parents or society. Freud argued that we will often judge ourselves by these values
that we assimilate and if we think our behaviour does not meet the standards implicit in these values we
will feel guilty and stressed.
According to Freud, the id, ego, and superego are often in conflict, and psychological health is
maintained only when they are in balance. However, if these three factors are in conflict then behaviour
may begin to exhibit signs of psychopathology. Individuals attempt to control conflict between these
factors and also reduce stress and conflict from external events by developing defence mechanisms,
and Table 1.1 describes some of these defence mechanisms together with some examples of how they
are presumed to prevent the experience of stress and anxiety.

defence mechanisms In psychoanalysis, the means by which individuals attempt to control

conflict between the id, ego and superego and also reduce stress and conflict from external
events.

A further factor that Freud believed could cause psychopathology was how children negotiated various
stages of development from infancy to maturity. He defined a number of important stages through
which childhood development progressed, and each of these stages was named after a body area or
erogenous zone. If the child successfully negotiated each stage then this led to personal growth and a
psychologically healthy person. If, however, adjustment to a particular stage was not successful, then the
individual would become fixated on that early stage of development. For example, Freud labelled the
first 18 months of life as the oral stage because of the child's need for food from the mother. If the
mother fails to satisfy these oral needs, the child may become fixated at this stage and in later life
display ‘oral stage characteristics’ such as extreme dependence on others. Other stages of development
include the anal stage (18 months to 3 years), the phallic stage (3–5 years), the latency stage (5–12 years),
and the genital stage (12 years to adulthood).

stages of development Progressive periods of development from infancy to maturity.

oral stage According to Sigmund Freud, the first 18 months of life based on the child’s need
for food from the mother. If the mother fails to satisfy these oral needs, the child may become
fixated at this stage and in later life display ‘oral stage characteristics’ such as extreme
dependence on others.

TABLE 1.1 Defence mechanisms in psychoanalytic theory

Each of the Freudian defence mechanisms described here function to reduce the amount of stress or
conflict that might be caused by specific experiences.
Denial
The individual denies the source of the anxiety exists (e.g., I didn't fail my exam, it must be a mistake).
Repression
Suppressing bad memories, or even current thoughts that cause anxiety (e.g., repressing thoughts about
liking someone because you are frightened that you may be rejected if you approach them).
Regression
Moving back to an earlier developmental stage (e.g., when highly stressed you abandon normal coping
strategies and return to an early developmental stage, for example by smoking if you are fixated at the
oral stage).
Reaction formation
Doing or thinking the opposite to how you feel (e.g., the person who is angry with their boss may go
out of their way to be kind and courteous to them).
Projection
Ascribing unwanted impulses to someone else (e.g., the unfaithful husband who is extremely jealous of
his wife might always suspect that she is being unfaithful).
Rationalisation
Finding a rational explanation for something you've done wrong. (e.g., you didn't fail the exam because
you didn't study hard enough but because the questions were unfair).
Displacement
Moving an impulse from one object (target) to another (e.g., if you've been told off by your boss at
work, you go home and shout at your partner or kick the dog).
Sublimation
Transforming impulses into something constructive (e.g., redecorating the bedroom when you're
feeling angry about something).
There is no doubt that the psychoanalytical model has been extremely influential, both in its attempts to
provide explanations for psychopathology and in the treatments it has helped to develop. Psychoanalysis
was arguably the first of the ‘talking therapies’ and in 2010 as many as 18% of modern practicing
clinical psychologists identified themselves at least in part with a psychoanalytical or psychodynamic
approach to psychopathology (Norcross & Karpiak, 2012). Psychoanalysis was also the first approach to
introduce a number of perspectives on psychopathology that are still important today, including (a) the
view that psychopathology can have its origins in early experiences rather than being a manifestation of
biological dysfunction, and (b) the possibility that psychopathology may often represent the operation of
‘defence mechanisms’ that reflect attempts by the individual to suppress stressful thoughts and memories
(see, for example, cognitive theories of chronic worrying in Chapter 6 and theories of dissociative
disorders in Chapter 14). Theorists in the psychoanalytic tradition have elaborated on Freud's original
theory, and we will see many examples of psychodynamic explanations applied to specific
psychopathologies presented later in this book. However, psychoanalytic theory does have many
shortcomings, and it is arguably no longer the explanation or treatment of choice for most psychological
problems, nor is it a paradigm in which modern evidence‐based researchers attempt to understand
psychopathology. This is largely because the central concepts in psychoanalytic theory are hard to
objectively define and measure. Because concepts such as the id, ego, and superego are difficult to
observe and measure, it is therefore difficult to conduct objective research on them to see if they are
actually related to symptoms of psychopathology in the way that Freud and his associates describe
(Fonagy, 2003).

The behavioural model

Most psychological models have in common the view that psychopathology is caused by how we
assimilate our experiences and how this is reflected in thinking and behaviour. The behavioural model
adopts the broad view that many examples of psychopathology reflect our learned reactions to life
experiences. That is, psychopathology can be explained as learned reactions to environmental
experiences, and this approach was promoted primarily by the behaviourist school of psychology.
During the 1950s and 1960s, many clinical psychologists became disillusioned by psychoanalytic
approaches to psychopathology and sought an approach that was more scientific and objective. They
turned to that area of psychology known as learning theory, and argued that just as adaptive
behaviour can be acquired through learning, then so can many forms of dysfunctional behaviour
(Davey, 1998). The two important principles of learning on which this approach was based are classical
conditioning and operant conditioning. Classical conditioning represents the learning of an
association between two stimuli, the first of which (the conditioned stimulus, CS) predicts the
occurrence of the second (the unconditioned stimulus, UCS). The prototypical example of this form of
learning is Pavlov's experiment in which a hungry dog learns to salivate to a bell (the CS) that predicts
subsequent delivery of food (the UCS), and this is represented schematically in Figure 1.5. In contrast,
operant conditioning represents the learning of a specific behaviour or response because that
behaviour has certain rewarding or reinforcing consequences. A prototypical example of operant
conditioning is a hungry rat learning to press a lever to obtain food in an experimental chamber called a
Skinner Box (see Photo 1.3).

learning theory The body of knowledge encompassing principles of classical and operant
conditioning (and which is frequently applied to explaining and treating psychopathology).

Classical conditioning The learning of an association between two stimuli, the first of
which (the conditioned stimulus, CS) predicts the occurrence of the second (the unconditioned
stimulus, UCS).
FIGURE 1.5 Classical conditioning.(a) Before conditioning takes place, Pavlov's dog salivates only to the
presentation of food and not to the presentation of the bell; (b) pairing the bell with food then enables
the dog to learn to predict food whenever it hears the bell, and (c) this results in the dog subsequently
salivating whenever it hears the bell. This type of learning has frequently been used to explain
psychopathology, and one such example is the acquisition of specific phobias where the phobic stimulus
(the CS) elicits fear because it has been paired with some kind of trauma (the UCS) (see Figure 6.1).
 operant conditioning The modification of behaviour as a result of its consequences.
Rewarding consequences increase the frequency of the behaviour, punishing consequences
reduce its frequency.

These two forms of learning have been used to explain a number of examples of psychopathology.
First, classical conditioning has been used to explain the acquisition of emotional disorders including
many of those with anxiety‐based symptoms (see Chapter 6). For example, some forms of specific
phobias appear to be acquired when the sufferer experiences the phobic stimulus (the CS) in association
with a traumatic event (the UCS), and such experiences might account for the acquisition of dog phobia
(in which dogs have become associated with, for example, being bitten or chased by a dog), accident
phobia (in which travelling in cars has become associated with being in a traumatic car accident), and
dental phobia (when being at the dentist has become associated with a traumatic dental experience)
(Davey, 1989; Doogan & Thomas, 1992; Kuch, 1997). Classical conditioning processes have also been
implicated in a number of other forms of psychopathology, including the acquisition of PTSD (see
Chapter 6), the acquisition of paraphilias (see Chapter 11), and substance dependency (see Chapter 9).
Operant conditioning has been used extensively to explain why a range of psychopathology‐relevant
behaviours may have been acquired and maintained. Examples you will find in this book include
learning approaches to understanding the acquisition of bizarre behaviours in schizophrenia (Ullman
& Krasner, 1975), how the stress‐reducing or stimulant effects of nicotine, alcohol, and many illegal
drugs may lead to substance dependency (e.g., Runegaard, Jensen, Wörtwein, & Gether, 2018; Schacter,
1982), how hypochondriacal tendencies and somatoform disorders may be acquired when a child's
illness symptoms are reinforced by attention from parents (Latimer, 1981), and how the disruptive, self‐
harming, or challenging behaviour exhibited by individuals with intellectual or developmental
disabilities may be maintained by attention from family and carers (Machalicek et al., 2014).
PHOTO 1.3 Operant Conditioning. In operant conditioning, the rat learns to press the lever in this Skinner Box because
it delivers food, and food acts to reinforce that behaviour so that it occurs more frequently in the future (known as operant
reinforcement). Operant reinforcement has been used to explain how many behaviours that are typical of psychopathology are
acquired and maintained. That is, many bizarre and disruptive behaviours may be acquired because they actually have
positive or rewarding outcomes.
The behavioural approach led to the development of important behavioural treatment methods,
including behaviour therapy and behaviour modification. For example, if psychopathology is
learned through normal learning processes, then it should be possible to use those same learning
processes to help the individual ‘unlearn’ any maladaptive behaviours or emotions. This view enabled
the development of treatment methods based on classical conditioning principles (such as flooding,
systematic desensitisation, aversion therapy, see Chapter 4) and operant conditioning principles (e.g.,
functional analysis, token economies, see Chapter 4). Furthermore, learning principles could be used to
alter psychopathology symptoms even if the original symptoms were not necessarily acquired through
conditioning processes themselves, and so the behavioural approach to treatment had a broad appeal
across a very wide range of symptoms and disorders.

behaviour therapy A term currently used for all interventions that attempt to change the
client’s behaviour (and have largely been based on principles from learning theory).

behaviour modification Behavioural treatment methods based on operant conditioning

principles, which assume that learnt psychopathology could be ‘unlearnt’ using normal learning
processes.
As influential as the behavioural approach has been over the years, it too has limitations. For example,
many psychopathologies are complex and symptoms are acquired gradually over many years (e.g.,
obsessive‐compulsive disorder, substance dependence, somatoform disorders, etc.). It would be almost
impossible to trace the reinforcement history of such symptoms across time in an attempt to verify that
reinforcement processes had shaped these psychopathologies. Second, learning paradigms may simply
not represent the most ideal conceptual framework in which to describe and understand some quite
complex psychopathologies. For example, many psychopathologies are characterised by a range of
cognitive factors such as information processing biases, belief schemas and dysfunctional ways of
thinking, and learning theory jargon is probably not the best framework in which to describe these
phenomena accurately and inclusively. The cognitive approaches we describe next are probably more
suited to describing and explaining these aspects of psychopathology.

The cognitive model

Perhaps the most widely adopted current psychological model of psychopathology is the cognitive
model, and roughly one in three modern clinical psychologists would describe their approach as
cognitive (Norcross & Karpiak, 2012). Primarily, this approach considers psychopathology to be the
result of individuals acquiring irrational beliefs, developing dysfunctional or unusual ways of thinking,
and processing information in biased ways. It was an approach first pioneered by Albert Ellis (1962) and
Aaron Beck (1967). Albert Ellis argued that emotional distress (such as anxiety or depression) is caused
primarily because people develop a set of irrational beliefs by which they need to judge their behaviour.
Some people become anxious, for example, because they make unrealistic demands on themselves. The
anxious individual may have developed unrealistic beliefs such as ‘I must be loved by everyone’, and the
depressed individual may believe “I am incapable of doing anything worthwhile.” Judging their
behaviour against such ‘dysfunctional’ beliefs causes distress. Aaron Beck developed a highly successful
cognitive therapy for depression based on the view that depressed individuals have developed unrealistic
distortions in the way they perceive themselves, the world, and their future (see Chapter 7). For example,
Beck's cognitive approach argues that depression results from the depressed individual having
developed negative beliefs about themselves (e.g., ‘I am worthless’), the world (e.g., ‘bad things always
happen’), and their future (e.g., ‘I am never going to achieve anything’), and these beliefs act to maintain
depressive thinking (Strauss, 2019).
The view that dysfunctional ways of thinking generate and maintain symptoms of psychopathology has
been applied across a broad range of psychological problems, including both anxiety disorders and
mood disorders, and has also been applied to the explanation of specific symptoms, such as paranoid
thinking in schizophrenia (Morrison, 2001), antisocial and impulsive behaviour in personality disorders
(Young, Klosko, & Weishaar, 2003), dysfunctional sexual behaviour in sex offenders and paedophiles
(Ward, Hudson, Johnston, & Marshall, 1997), and illness reporting in hypochondriasis and somatoform
disorders (Warwick, 1995) to name but a few.
The cognitive approach has also been highly successful in generating an influential approach to
treatment. If dysfunctional thoughts and beliefs maintain the symptoms of psychopathology, then these
dysfunctional thoughts and beliefs can be identified, challenged, and replaced by more functional
cognitions. This has given rise to a broad‐ranging therapeutic approach known as cognitive
behaviour therapy(CBT), and many examples of the use of this approach will be encountered in
this book (see also https://www.babcp.com/public/What‐is‐CBT.aspx; Rakovshik, 2019)

cognitive behaviour therapy (CBT) An intervention for changing both thoughts and
behaviour. CBT represents an umbrella term for many different therapies that share the
common aim of changing both cognitions and behaviour.

As successful as the cognitive approach seems to have been in recent years, it too also has some
limitations. For example, rather than being a cause of psychopathology, it has to be considered that
dysfunctional thoughts and beliefs may themselves simply be just another symptom of psychopathology.
For example, we have very little knowledge at present about how dysfunctional thoughts and beliefs
develop. Are they the product of childhood experiences? Do they develop from the behavioural and
emotional symptoms of psychopathology (i.e., do depressed people think they are worthless because of
their feelings of depression)? Or are they merely post hoc constructions that function to help the
individual rationalise the way they feel? These are all potentially fruitful areas for future research.

The humanist‐existential approach

Some approaches to psychopathology believe that insights into emotional and behavioural problems
cannot be achieved unless the individual is able to gain insight into their lives from a broad range of
perspectives. People not only acquire psychological conflicts and experience emotional distress, they also
have the ability to acquire self‐awareness, develop important values and a sense of meaning in life, and
pursue freedom of choice. If these latter abilities are positively developed and encouraged, then conflict,
emotional distress, and psychopathology can often be resolved. This is the general approach adopted by
humanistic and existential models of psychopathology, and the aim is to resolve psychological problems
through insight, personal development, and self‐actualisation.
Because such approaches are interested primarily in insight and personal growth when dealing with
psychopathology, they are relatively uninterested in aetiology and the origins of psychopathology but
more interested in ameliorating symptoms of psychopathology through encouraging personal
development. An influential example of the humanistic‐existential approach is client‐centred
therapy developed by Carl Rogers (1951, 1987; Joseph, 2017). This approach stresses the goodness of
human nature and assumes that if individuals are unrestricted by fears and conflicts, they will develop
into well‐adjusted, happy individuals. The client‐centred therapist will try to create a supportive climate
in which the client is helped to acquire positive self‐worth. The therapist will use empathy to help
them understand the client's feelings and unconditional positive regard, by which the therapist
expresses their willingness to totally accept the client for who he or she is.

client-centred therapy An approach to psychopathology stressingthe goodness of human

nature, assuming that if individuals areunrestricted by fears and conflicts, they will develop into
well-adjusted, happy individuals.

empathy An ability to understand and experience a client’s own feelings and personal
meanings, and a willingness to demonstrate unconditional positive regard for the client.

unconditional positive regard Valuing clients for who they are without judging them.

As we said earlier, this type of approach to psychopathology does not put too much emphasis on how
psychopathology was acquired but does try to eradicate psychopathology by moving the individual from
one phenomenological perspective (e.g., one that contains fears and conflicts) to another (e.g., one that
enables the client to view themselves as worthy, respected and achieving individuals). Approaches such
as humanistic and existentialist ones are difficult to evaluate. For example, some controlled studies have
indicated that clients undergoing client‐centred therapy tend to fair no better than those undergoing
nontherapeutic control treatments (Greenberg, Watson, & Lietaer, 1998; Patterson, 2000), whereas some
other studies suggest a significant effectiveness of person‐centred counselling over a 5‐year period when
compared with a waiting list control group (Gibbard & Hanley, 2008). Even so, exponents of existential
therapies believe that experimental methodologies are inappropriate for estimating the effectiveness of
such therapies, because such methods either dehumanise the individuals involved or are incapable of
measuring the kinds of existential benefits that such approaches claim to bestow (May & Yalom, 1995;
Walsh & McElwain, 2002). Nevertheless, such approaches to treatment are still accepted as having some
value and are still used at least in part by clinical psychologists, counselling psychologists, and
psychotherapists.

Summary
The four psychological paradigms we have discussed in this section have tended to evolve historically
from explanatory paradigms that have represented different ‘schools’ of psychology generally, but all
have a relevant place in explaining psychopathology—either at different levels of explanation (e.g.,
cognitive vs behavioural), or using different philosophical approaches to explaining human behaviour
and psychopathology (e.g., the hypothetical constructs developed by the psychoanalytical approach vs.
the learning paradigm developed by behaviourist approaches). In addition to pure psychological
paradigms, clinical psychologists are continually developing new ways of conceptualising and studying
the factors that influence the development of mental health problems, and one approach of growing
importance is to consider how sociocultural factors might affect the acquisition of psychopathology.
Some examples of this latter approach are discussed in Focus Point 1.5.

FOCUS POINT 1.5 SOCIOCULTURAL FACTORS AND

PSYCHOPATHOLOGY

There is a growing realisation that sociocultural factors can influence both the acquisition of
mental health problems and the way that psychopathology is expressed. These factors include
gender, culture, ethnicity, and socioeconomic factors such as poverty and deprivation, and we
discuss some examples of these here.

Gender
Your gender is likely to be a significant factor in whether you are likely to be diagnosed with a
particular mental health problem. For example, the prevalence of major depression is twice as
high in women as it is in men (Kuehner, 2016); women are significantly more likely to develop
anxiety‐based problems such as social anxiety disorder, panic disorder, or GAD, and to suffer
trauma‐ and stress‐related mental health problems (see Chapter 6). Women are also significantly
more likely to be diagnosed with eating disorders such as anorexia nervosa or bulimia nervosa
(Zayas et al., 2018; see Chapter 10), but males are more likely to be diagnosed with conduct
disorders, ADHD (see Chapter 16), and antisocial personality disorder (Chapter 12). How
gender differentially affects the acquisition of these various disorders is far from clear and could
be linked to gender‐based biological differences, for example, sex hormone differences (Li &
Graham, 2017), to factors associated with the gender roles that males and females adopt in
different societies (e.g., women's roles in society may be more stressful than men's and so
increase the risk of mental health problems) (Mayor, 2015), or differences in gender‐based
coping practices (e.g., women ruminate more than men, whereas men frequently react to stress
by distracting themselves, Just & Alloy, 1997). A comprehensive discussion of the many possible
explanations for gender differences in diagnosis and prevalence rates is provided by Hartung
and Lefler (2019).

Culture
The culture in which you live can also be a factor that will determine whether you will be
diagnosed with a particular mental health problem and also how that problem will manifest
itself. For example, prevalence rates for many common mental health problems differ
significantly across the world. In the case of major depression, prevalence rates can vary
between 1.5% and 19% (Weissman et al., 1996), with some of the highest prevalence estimates
for depression being found in some of the wealthiest countries in the world (Kessler & Bromet,
2013). These cultural‐demographic differences may be caused by the stigma associated with
reporting symptoms in some societies, cultural differences in diagnosing symptoms, and
depression being expressed in more physical terms in some societies (called somatisation), or
simply by cultural difference in the way people report their depression or the methodologies
used to collect data about depression (Compton et al., 1991; Huang, Beshai, & Mabel, 2016;
Patten, 2003). Eating disorders are another example where prevalence rates are higher in most
Western cultures but in the past have only rarely been reported in less socio‐economically
developed societies (Keel & Klump, 2003). However, in recent times, ‘Westernisation’,
industrialisation, and urbanisation of underdeveloped countries do seem to be associated with
rises in the levels of eating disorders reported in those countries (Pike & Dunne, 2015). Finally,
some combinations of mental health problems may be found only in certain specific cultures
and may be examples of the culturally specific ways in which stress and trauma are manifested.
Two specific examples of this are provided in Focus Point 1.3.

Ethnicity
The frequency of diagnosis of many mental health problems also differs across different
ethnicities. For example, schizophrenia is more frequently diagnosed in individuals of African
descent than of White European origin. Conversely, specific types of eating disorders—such as
anorexia nervosa—have been diagnosed more commonly in White women than Black women
(Walcott, Pratt, & Patel, 2003). In some of these cases, there may be a genetic component, for
example, individuals of Asian descent inherit a gene which makes drinking large amounts of
alcohol aversive and so makes them less likely to develop alcohol dependency and abuse
problems (Li, Zhao, & Gelernter, 2012), but equally it may be the case that diagnostic criteria
are either wittingly or unwittingly applied differently to people from different ethnic
backgrounds (e.g., it is caused by a cultural bias in assessment—see Section 2.2.6, Chapter 2).
For example, Black Americans with severe depression are significantly more likely than other
racial or ethnic groups to be misdiagnosed with schizophrenia (Gara, Minsky, Silverstein,
Miskimen, & Strakowski, 2019), and such differential effects may reflect differential diagnoses
driven by implicit racial and ethnic stereotyping.

Socio‐economic Conditions
Finally, the socio‐economic conditions in which an individual is either raised or lives in are an
important contributor to the development of psychopathology (Lund et al., 2018). Obvious
examples include the development of conduct disorders, some personality disorders such as
antisocial personality disorder, and substance abuse and dependency problems, many of which
are associated with poverty and low socio‐economic conditions (Karriker‐Jaffe, 2013; Walsh et
al., 2013). However, poverty is also a risk factor for the development of many common mental
health problems such as depression (Freeman et al., 2016), and the development of anxiety
disorders in women—but not necessarily men (Mwinyi et al., 2017). Reasons for the association
between poor socio‐economic conditions and psychopathology may include the additional
stressors and traumas that accompany poverty, such as unemployment, substandard
accommodation, and neglect, and poverty also brings with it feelings of a lack of control over
one's own life and an inability to access the resources that could actively change poor living
conditions (Evans & Kim, 2012). Indeed, so specific are many of the stressors that afflict people
living in poverty, that it may be necessary to develop interventions that are tailored to the
specific sociocultural experiences of low‐income families (Goodman, Pugach, Skolnik, & Smith,
2013).

SELF‐TEST QUESTIONS
What are the main approaches to understanding psychopathology that are advocated by
the biological approach?
What are the pros and cons of attempting to explain mental health problems in terms of
genetics?
Can you describe the basic concepts underlying psychoanalytic and psychodynamic
approaches to psychopathology?
What are the learning principles on which the behavioural approach to psychopathology is
based?
Who were the main founders of the cognitive approach to psychopathology, and what
were their main contributions?
How do humanistic‐existential approaches to psychopathology differ from most of the
others?
 SECTION SUMMARY

1.3 EXPLANATORY APPROACHES TO PSYCHOPATHOLOGY

Psychological models view psychopathology as caused primarily by psychological rather than
biological processes
Influential psychological models of psychopathology include biological models, the
psychoanalytical model, the behavioural model, the cognitive model, and the humanist‐existential model.
Biological models attempt to explain psychopathology in terms of processes such as genetics
and brain structure and function.
Psychoanalytical models attempt to discuss psychopathology in terms of the psychological
mechanisms that help to defend against anxiety and depression
Behavioural models use processes of learning such as classical conditioning and operant conditioning
to understand how psychopathology might be acquired.
The cognitive model considers psychopathology to be the result of individuals acquiring
irrational beliefs, developing dysfunctional ways of thinking, and processing information in
biased ways.
The humanist‐existential approach attempts to help the individual to gain insight into their lives
from a broad range of perspective and develop a sense of meaning in life.

1.4 MENTAL HEALTH AND STIGMA

There are still attitudes within most societies that view symptoms of psychopathology as threatening and
uncomfortable, and these attitudes frequently foster stigma and discrimination towards people with
mental health problems. Reactions to people often change when they suffer a mental health problem,
and this can lead to a loss of respect and consideration. Such reactions are common when people are
brave enough to admit they have a mental health problem, and they can often lead on to various forms
of exclusion or discrimination—either within social circles or within the workplace (Client's Perspective
1.1) (Video—five young people share their experiences of mental health problems and stigma:
https://www.youtube.com/watch?v=vzmfdECUvxM). In the following sections we look at (a) what
mental health stigma is, (b) Who holds stigmatising beliefs and attitudes?, (c) What causes stigma? (d)
Why does stigma matter? and (e) How can we eliminate stigma?
 CLIENT'S PERSPECTIVE 1.1

Lewis is a university lecturer who has suffered from depression for much of his life. Here is his
view of the mental health stigma he encountered:
‘There can be no doubt that there is considerable stigma associated with depression. I am
repeatedly congratulated for being so brave, even courageous, in talking so openly about my
depression. I, in fact, am a “performer” and there is no bravery, but these comments show how
others view depression and that it is highly stigmatised. An example of how stigma can present
a particularly difficult problem for sportsmen is provided by the case of a professional footballer,
Stan Collymore who played for England. He had a severe depression and his career went into a
rapid decline. He says that he can never forgive the Aston Villa manager for the way he reacted
to his depression. He told him to pull his socks up and that his idea of depression was that of a
woman living on a 20th floor flat with kids. The Sun newspaper said that he should be kicked
out of football as how could anyone be depressed when he is earning so much money. He
bitterly remarks that if you suffer from an illness that millions of others suffer from, but it is a
mental illness which leads many to take their own lives, then you are called spineless and weak.’

(From Wolpert, 2001, Stigma of depression—a personal view. British Medical Bulletin, 57, 221–224.

1.4.1 What Is Mental Health Stigma?

Mental health stigma can be divided into a number of distinct types: social stigma is
characterised by prejudicial attitudes and discriminating behaviour directed towards individuals with
mental health problems as a result of the psychiatric label they have been given. In contrast,
internalised stigma, perceived stigma, or self‐stigma is the internalising by the mental health
sufferer of their perceptions of discrimination where perceived stigma can significantly affect feelings of
shame and lead to poorer treatment outcomes (Link, Cullen, Struening, & Shrout, 1989; Perlick et al.,
2001). A third type of mental health stigma is associative stigma which is the prejudice and
discrimination experienced by families because of their relationship with the person with mental health
problems (Corrigan & Nieweglowski, 2019).

Mental health stigma Mental health stigma can be divided into two distinct types: social
stigma is characterised by prejudicial attitudes and discriminating behaviour directed towards
individuals with mental health problems. Perceived stigma or self-stigma is the internalising by
the mental health sufferer of their perceptions of discrimination. This can significantly affect
feelings of shame and lead to poorer treatment outcomes.

social stigma Stigma characterised by prejudicial attitudes and discriminating behaviour

directed towards individuals with mental health problems as a result of the psychiatric label they
have been given.
 perceived stigma/self-stigma The internalising by the mental health sufferer of their
perceptions of discrimination. This can significantly affect feelings of shame and lead to poorer
treatment outcomes. See also Mental health stigma.

In relation to social stigma, studies have suggested that stigmatising attitudes towards people with
mental health problems are widespread and commonly held (Byrne, 1997; Crisp, Gelder, Rix, Meltzer,
& Rowlands, 2000; Heginbotham, 1998). In a survey of over 1,700 adults in the UK, Crisp et al. (2000)
found that (a) the most commonly held belief was that people with mental health problems were
dangerous—especially those with schizophrenia, alcoholism, and drug dependence; (b) people believed
that some mental health problems such as eating disorders and substance abuse were self‐inflicted; and
(c) respondents believed that people with mental health problems were generally hard to talk to. People
tended to hold these negative beliefs regardless of their age, regardless of what knowledge they had of
mental health problems, and regardless of whether they knew someone who had a mental health
problem. More recent studies of attitudes to individuals with a diagnosis of schizophrenia or major
depression convey similar findings. In both forms of psychopathology, a significant proportion of
members of the public considered that people with mental health problems such as depression or
schizophrenia were likely to lose control, be unpredictable, and be dangerous, and they would be less
likely to employ someone with a mental health problem (Mannarini & Rossi, 2019; Reavley & Jorm,
2011; Wang & Lai, 2008). Importantly, mental health stigma is an almost universal phenomenon that
can be found in most cultures, and similar forms of mental health prejudice and discrimination can be
found regardless of significant differences in cultural backgrounds (Abdullah & Brown, 2011; Grover et
al., 2017; Mannarini, Boffo, Rossi, & Balottin, 2018)
Finally, while many forms of mental health stigma are overt and represent discriminatory beliefs and
opinions openly held by many members of society, unconscious negative beliefs about mental health
problems can often be found using implicit bias tasks with participants who claim not to hold
stigmatising beliefs about mental health problems (Mannarini & Buffo, 2014; Schlier & Lincoln, 2019)
(similar findings are often found with racist beliefs which may exist as unconscious implicit biases). Such
implicit biases operating outside of an individual's conscious control appear to reflect stigmatisation
based on ‘in‐group’ versus ‘out‐group’ distinctions, where those with mental health problems are
implicitly categorised as members of an ‘out‐group’ (Schlier & Lincoln, 2019). The fact that such
stigmatising beliefs can operate outside of conscious awareness poses some significant challenges for
interventions designed to alleviate mental health stigma.

1.4.2 Who Holds Stigmatising Beliefs About Mental Health Problems?

Perhaps surprisingly, stigmatising beliefs about individuals with mental health problems are held by a
broad range of individuals within society, regardless of whether they know someone with a mental
health problem, have a family member with a mental health problem, or have a good knowledge and
experience of mental health problems (Crisp et al., 2000; Moses, 2010; Wallace, 2010). For example,
Moses (2010) found that stigma directed at adolescents with mental health problems came from family
members, peers, and teachers. 46% of these adolescents described experiencing stigmatisation by family
members in the form of unwarranted assumptions (e.g., the sufferer was being manipulative), distrust,
avoidance, pity, and gossip, 62% experienced stigma from peers which often led to friendship losses and
social rejection (Connolly, Geller, Marton, & Kutcher (1992), and 35% reported stigma perpetrated by
teachers and school staff, who expressed fear, dislike, avoidance, and underestimation of abilities.
Mental health stigma is even widespread in the medical profession including amongst nursing students
(Chang et al., 2017), medical students and qualified medical doctors (Wallace, 2012). These
discriminatory beliefs may exist because ‘the stigma of mental illness thrives in the medical profession as
a result of the culture of medicine and medical training, perceptions of physicians and their colleagues,
and expectations and responses of health care systems and organizations’ (Wallace, 2010, p. 3)—quite a
list of potential culprits!
1.4.3 What Factors Cause Stigma?
The social stigma associated with mental health problems almost certainly has multiple causes. We've
seen in the section on historical perspectives that throughout history people with mental health
problems have been treated differently, excluded, and even brutalised. This treatment may come from
the misguided views that people with mental health problems may be more violent or unpredictable
than people without such problems, or somehow just ‘different’ (i.e., for some people individuals with
mental health problems belong to a social ‘out‐group’), but none of these beliefs has any basis in fact
(e.g., Swanson, Holzer III, Ganju, & Jono, 1990; Varshney, Mahapatra, Krishnan, Gupta, & Deb, 2016).
Similarly, early beliefs about the causes of mental health problems, such as demonic or spirit possession,
were ‘explanations’ that would almost certainly give rise to reactions of caution, fear, and
discrimination. Even the medical model of mental health problems is itself an unwitting source of
stigmatising beliefs. First, the medical model implies that mental health problems are on a par with
physical illnesses and may result from medical or physical dysfunction in some way (when many may not
be simply reducible to biological or medical causes). This itself implies that people with mental health
problems are in some way ‘different’ from ‘normally’ functioning individuals (e.g., Read & Harré, 2001)
(Focus Point 1.6). Second, the medical model implies diagnosis, and diagnosis implies a label that is
applied to a ‘patient’. That label may well be associated with undesirable attributes (e.g., ‘mad’ people
cannot function properly in society, or can sometimes be violent) or with influencing the view that this
person is a member of an ‘out‐group’ of some kind, and this again will perpetuate the view that people
with mental health problems are different and should be treated with caution.

FOCUS POINT 1.6 CREATING MENTAL HEALTH PROBLEMS

THROUGH THE ‘MEDICALISATION OF NORMALITY’
It is worth considering when an everyday ‘problem in living’ becomes something that should be
categorised as a mental health problem. It is a fact of life that we all have to deal with difficult
life situations. Sometimes these may make us anxious or depressed, sometimes we might feel as
though we are ‘unable to cope’ with these difficulties. But they are still problems that almost
everyone encounters. Many people have their own strategies for coping with these problems,
some get help and support from friends and family and in more severe cases perhaps seek help
from their doctor or GP. However, at what point do problems of living cease to be everyday
problems and become mental health problems? In particular, we must be wary about
 ‘medicalising’ problems in daily living so that they become viewed as ‘abnormal’, symptoms of
illness or disease, or even as characteristics of individuals who are ‘ill’ or in some way ‘second
class’.
A 2018 survey of over 1,000 GPs by the Mental Health Charity Mind found that over 40% of
consultations with patients seen by GPs involved mental health issues (Mind, 2018), and
experiencing depression is one of the most common reasons for consulting a doctor or GP in
the UK (Singleton et al., 2001). In order for GPs to be able to provide treatment for such
individuals, there is often a tendency for patients to present distress as depression in order to
secure support or medication (Middleton, Shaw, Hull, & Feder, 2005), and doctors and GPs
may even misdiagnose symptoms as depression when validated assessments would not indicate
a diagnosis (Carey et al., 2014). For example, while epidemiological studies in the early 2000s
suggested that the prevalence rates for depression in the general population were fairly constant,
there was at the same time a significant increase in depression being diagnosed by GPs and
physicians, and a significant increase in the prescription of antidepressant medications (Dowrick
& Frances, 2013).
Effects such as this may have contributed to the common view expressed by lay people that
depression is a ‘disease’ rather than a normal consequence of everyday life stress (Lauber,
Falcato, Nordt, & Rossler, 2003). If lay people already view depression as a ‘disease’ or
biological illness, and GPs are more than willing to diagnose it, then we run the risk of the
‘medicalisation’ of normal everyday negative emotions such as mild distress or even
unhappiness (Shaw & Woodward, 2004).

We discuss ways in which stigma can be addressed later, but it must also be acknowledged here that the
media regularly play a role in perpetuating stigmatising stereotypes of people with mental health
problems. Media portrayals of mental health problems have long been recognised as being misleading
and stigmatising, and the popular press is a branch of the media that is frequently criticised for
perpetuating these stereotypes. A study of mental health‐related stories in nine UK newspapers
published in 2017 found that over half of the articles were negative in tone, and 18.5% indicated an
association with violence (Chen & Lawrie, 2017). But maybe there is some positive movement on this.
Bowen and Lovell (2019) explored how UK newspapers had represented mental health issues on their
Twitter feeds between 2014 and 2017. They did identify a significant decrease in the proportion of
mental health tweets that were characterised as ‘bad news’ over that period. But even in 2017, 24% of
these tweets were still considered as ‘bad news’.
Blame can also be levelled at the entertainment media. For example, cinematic depictions of
schizophrenia are often stereotypic and characterised by misinformation about symptoms, causes and
treatment. In an analysis of English‐language movies released between 1990 and 2010 that depicted at
least one character with schizophrenia, Owen (2012) found that most schizophrenic characters displayed
violent behaviour, one third of these violent characters engaged in homicidal behaviour, and a quarter
committed suicide. This suggests that negative portrayals of schizophrenia in contemporary movies are
common and are sure to reinforce biased beliefs and stigmatising attitudes towards people with mental
health problems. While the media may be getting better at increasing their portrayal of anti‐stigmatising
material over recent years, studies suggest that there has been only a minimal decrease in the news
media's publication of stigmatising articles, suggesting that the media is still a significant source of
stigma‐relevant misinformation (Thornicroft et al., 2013).

1.4.4 Why Does Stigma Matter?

Stigma is a form of social discrimination and prejudice, the social effects of which include exclusion,
poor social support, poorer subjective quality of life, and low self‐esteem (Livingston & Boyd, 2010). As
well as its effect on the quality of daily living, stigma also has a detrimental effect on treatment
outcomes and so hinders efficient and effective recovery from mental health problems (Perlick et al.,
2001). In particular, self‐stigma is correlated with a number of negative outcomes including poorer
employment success, increased social isolation (Yanos, Roe, & Lysaker, 2010), negative attitudes towards
treatment seeking (Sickel, Seacat, & Nabors, 2019), poorer adherence to medication regimes (Farabee,
Hall, Zaheer, & Joshi, 2019), and poorer ability to regulate emotions (Burton, Wang, & Pachankis,
2018). These factors alone represent significant reasons for attempting to eradicate mental health stigma
and ensure that social inclusion is facilitated and recovery can be efficiently achieved.

1.4.5 How Can We Eliminate Stigma?

We now have a good knowledge of what mental health stigma is and how it affects sufferers, both in
terms of their role in society and their route to recovery. It is not surprising, then, that attention has
most recently turned to developing ways in which social stigma and discrimination can be reduced. As
we have already described, people tend to hold these negative beliefs about mental health problems
regardless of their age, regardless of what knowledge they have of mental health problems, and
regardless of whether they know someone who has a mental health problem. The fact that such
negative attitudes appear to be so entrenched and often represent implicit biases in attitudes toward
those with mental health problems suggests that campaigns to change these beliefs will have to be
multifaceted, will have to do more than just impart knowledge about mental health problems, and will
need to challenge existing negative stereotypes especially as they are portrayed in the general media
(Pinfold et al., 2003). In the UK, the ‘Time to Change’ campaign is one of the biggest programmes
attempting to address mental health stigma and is supported by both charities and mental health service
providers (http://www.time‐to‐change.org.uk). This programme provides blogs, videos, TV
advertisements, and promotional events to help raise awareness of mental health stigma and the
detrimental effect this has on mental health sufferers. However, raising awareness of mental health
problems simply by providing information about these problems may not always be effective alone—
especially since individuals who are most knowledgeable about mental health problems (e.g.,
psychiatrists, mental health nurses) regularly hold strong stigmatising beliefs about mental health
themselves! (Caldwell & Jorm, 2001; Wallace, 2010). As a consequence, attention has turned towards
some methods identified in the social psychology literature for improving inter‐group relations and
reducing prejudice (Brown, 2010). These methods aim to promote events encouraging mass
participation social contact between individuals with and without mental health problems and to
facilitate positive intergroup contact and disclosure of mental health problems (one example is the ‘Time
to Change’ Roadshows, which set up events in prominent town centre locations with high footfall). Analysis
of these kinds of intergroup events suggests that they (a) improve attitudes towards people with mental
health problems, (b) increase future willingness to disclose mental health problems, and (c) promote
behaviours associated with anti‐stigma engagement (Evans‐Lacko et al., 2012; Thornicroft, Brohan,
Kassam, & Lewis‐Holmes, 2008).

Time to Change A national UK programme aiming to promote awareness of mental health

problems and to combat stigma and discrimination.

As well as the need to inform and educate members of the public about mental health stigma, there is
also a need to create interventions that will reduce internalised stigma in those suffering from mental
health problems. A variety of methodologies have been successfully employed to reduce internalised
stigma, and these include (a) psychoeducational interventions, (b) CBT interventions aimed at modifying
self‐stigmatising beliefs, (c) interventions based on understanding the causes of mental health problems,
and (d) multifaceted interventions that combine several of the above (Alonso, Guillen, & Munoz, 2019).
Such interventions have been shown to reduce measures of internalised stigma, facilitate subjective
measures of recovery or coping, and improve self‐efficacy and insight (e.g., Wood, Byrne, Varese, &
Morrison, 2016).
 SELF‐TEST QUESTIONS
What are the different types of mental health stigma?
What kinds of factors may be responsible for causing and maintaining mental health
stigma?
What kinds of interventions have been developed to try and reduce mental health stigma?

SECTION SUMMARY

1.4 MENTAL HEALTH AND STIGMA

Social stigma is characterised by prejudicial attitudes and discriminating behaviour directed
towards individuals with mental health problems
Internalised stigma, perceived stigma, or self‐stigma is the internalising by the mental health
sufferer of their perceptions of discrimination
Stigmatising beliefs about people with mental health are held by a broad range of
individuals within society, including family members, peers, teachers, and members of the
medical profession.
The popular media often play a role in perpetuating stigmatising stereotypes of people
with mental health problems.
Stigma has a detrimental effect on treatment outcome for people with mental health
problems, as well as on employment prospects, and increased social isolation.
Campaigns to challenge mental health stigma will usually be multifaceted and will need to
challenge existing stereotypes of people with mental health problems.

1.5 CONCEPTS, PARADIGMS, AND STIGMA REVISITED

This chapter has introduced the reader to the important concepts and paradigms that surround
psychopathology. We have set the scene with a brief history of psychopathology, looking at traditional
ways in which people have tried to understand and explain mental health problems and how people
with mental health problems have been treated. This has given us a backdrop by which to discuss the
many contemporary ways in which psychopathology can be defined and the explanatory paradigms that
are used in modern day scientific study of psychopathology. Defining exactly what kinds of symptoms
or behaviour should be considered as examples of psychopathology is also problematic. The four type
of definition that we discussed (deviation from the statistical norm, deviation from social norms,
maladaptive behaviour, and distress and impairment) all have limitations. Some fail to cover examples
of behaviour that we would intuitively believe to be representative of mental health problems, others
may cover examples that we intuitively feel are not examples of psychopathology, or they may represent
forms of categorisation that would lead us to imposing stigmatising labels on people suffering from
psychopathology. In practice, classification schemes end up using an amalgamation of these different
approaches to definition, and we will discuss some of these issues in Chapter 2. Finally, this chapter has
introduced the notion of mental health stigma, described what it is and how it affects individuals with
mental health problems. Stigma and discrimination are currently important targets for change, and
programmes designed to challenge both social stigma and internalised stigma are a valuable component
of most mental health services.

This book is accompanied by Student and Instructor companion websites.

www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter References
Videos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
2
Classification and Assessment in Clinical Psychology

ROUTE MAP OF THE CHAPTER

This chapter describes the various ways in which clinicians gather information about a client's
problems. This information can then be used to help them classify the person's problems,
understand the causes of those problems, and treat their problems. The chapter begins by
discussing classification of mental health problems, the most recent developments found in the
classification system Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM‐5), and
some developing alternatives to DSM‐5. We then continue by discussing the benefits and
limitations of clinical interviews, psychological tests, biologically based assessments, and clinical
observation and introduce the reader to the concepts of reliability and validity. The chapter
ends by discussing cultural biases in clinical assessments and the popular use of case
formulations as a means of understanding the client's problems and developing a strategy for
treatment.

CHAPTER OUTLINE
2.1 CLASSIFYING PSYCHOPATHOLOGY
2.2 METHODS OF ASSESSMENT
2.3 CASE FORMULATION
2.4 CLASSIFICATION AND ASSESSMENT IN CLINICAL PSYCHOLOGY
REVISITED

LEARNING OUTCOMES
When you have completed this chapter, you should be able to:
1. Compare and contrast the pros and cons of DSM as a means of classifying and diagnosing
psychopathology.
2. Describe a range of clinical assessment methods and evaluate the benefits and limitations
of each.
3. Describe the concepts of reliability and validity as applied to clinical assessment methods.
4. Critically analyse some of the sources of cultural bias that may influence the process of
clinical assessment.
5. Explain what a case formulation is, and provide some examples from different
psychological approaches.
 I saw Ann Smith, aged 39, in my clinic today. She met criteria for depression, with a 5‐month history of low
mood. This was triggered by an argument with her husband during the Christmas period. Despite receiving a lot
of support from her husband, Ann continues to experience ‘black spells’, which can go on for 5 days per episode.
In March she expressed some suicidal thoughts, which precipitated her referral to psychiatric services.
At interview Ann was well presented, clear, and articulate. However, both her eye contact and concentration were
poor, and she reported having lost 10 lbs in weight. This is the first time she has been referred to psychiatric
services but has been prescribed antidepressant medication on three previous occasions by her GP. She states that
she has experienced low times throughout her life.
She is the middle child of three and stated that she missed a lot of schooling due to the combination of having
chronic asthma and an overprotective mother. She left school without qualifications, feeling she has not realised her
potential in any area. She married Michael 14 years ago. Owing to his job as a vicar, they entertain frequently.
She finds the entertaining difficult. I would welcome your assessment of this case, with a view of taking her on for
therapy.
Ann's Story (as told by Blackburn, James, & Flitcroft, 2006)

Introduction
Ann has low mood. She has been prescribed antidepressant medication by her GP, who subsequently
referred her to a psychiatrist. Following an interview with the psychiatrist, the latter sent the referral
letter to a clinical psychologist. The referral letter immediately raises a number of questions, the main
one being ‘Can we help this person?’ But this question itself raises a number of other questions that will
need answering. These questions include (a) are Ann's symptoms typical of a specific psychological
problem (e.g., depression)? (b) do they meet the criteria for formal diagnosis of a mental health problem?
(c) what has led this person to have these problems? (d) are there specific events that trigger her
symptoms? (e) how can we help this person? and (f) by what criteria will we judge that we have
successfully helped this person to recover? These are all questions that the clinical psychologist must
answer by gathering a variety of information about the client, and this information is often gathered
using a range of different clinical tools and techniques. Clinical assessment procedures are formal ways
of finding answers to these questions, especially ‘Precisely what problems does this person have?’, ‘What
has caused their problems?’, ‘What is the best way to treat their problems?’, and ‘Were our support and
interventions successful?’
Clinicians use a wide range of assessment procedures to gather this information. In many cases, the
types of techniques they use will depend on their theoretical orientation to psychopathology. For
example, the cognitive‐behavioural clinician may want to find out quite different information to a
psychodynamic clinician—largely because their conceptions of the causes of psychopathology are
different and because the kinds of therapeutic techniques they employ are different. The cognitive
therapist will want to know what kinds of cognitions may trigger symptoms so that these cognitions can
be addressed in therapy, whereas a psychodynamic therapist may want to explore the client's history of
conflicts and defence mechanisms in order to assess their suitability for psychodynamic therapy
(Marzillier & Marzillier, 2008).
In this chapter we describe the range of assessment techniques available to clinicians that enables them
to answer the basic questions about a case that we have just raised. These techniques are an aid to
diagnosis, an aid to determining the best intervention for a client, and a help in establishing whether
treatment has successfully dealt with the client's symptoms. We discuss these assessment types
individually, but to gain a complete picture of the client's condition, the clinician will usually use a range
of different assessments (Antony & Barlow, 2012; Meyer et al., 2001). The chapter begins by discussing
the ways in which we currently classify and diagnose mental health problems, because many forms of
assessment are structured in ways that enable classification. We then move on to discussing different
types of assessment, including the interview, psychological tests, biologically based tests, and
observation. Finally we discuss some issues relating to diagnosis and how diagnosis can be associated
with the development of a treatment plan (known as formulation).

2.1 CLASSIFYING PSYCHOPATHOLOGY

In Chapter 1 we discussed the difficulties associated with defining what is and is not a mental health
problem. Given the inherent difficulties surrounding this question you may be saying to yourself ‘Why
try to define and classify psychopathology at all?’ Nevertheless, there are some good reasons for wanting
to do this. First, as a social and biological science, psychology will want to try to understand the causes
of mental health problems. This is important so that we can develop effective treatments that address
the root causes of psychopathology and also develop prevention strategies designed to reduce the risk of
individuals developing symptoms of psychopathology. Most sciences use classification to group
phenomena into categories according to their similarities. Categorisation and classification is thus an
important first stage in the pursuit of knowledge about causes and aetiology, and it would be difficult to
discuss aetiology in this book if there were not some form of classification that enabled us to understand
how different causes relate to different symptoms. Secondly, classification is necessary if we are to
effectively organise services and support for sufferers. For example, the needs of individuals with
intellectual disabilities, major depression, an anxiety‐based disorder, or substance dependency are all
very different and require different approaches and different means of support and intervention. We
need to have some basis for differentiating between these different kinds of problems and determining
the different kinds of support that each might need, and classification systems provide a common
language for reporting and monitoring mental health problems which allows the world to share and
compare data in a consistent way. Third, how do we decide if our interventions and support for
sufferers have been effective unless we have some objective way of defining what constitutes the
symptoms of psychopathology? One important and objective way of determining whether an individual
is responding to treatment is to see if there has been any improvement in objectively defined and
measurable symptoms. Classification systems based on clusters of symptoms may help us to do this.
Finally, whether we like it or not, modern day society requires that we assess and classify people for a
number of reasons, and this is also the case with psychopathology. For example, we might want to know
whether a person is psychologically fit to stand trial for a criminal offence, whether a child has
disabilities that will require special educational needs, or whether financial compensation or damages
should be awarded to an individual because of psychological symptoms caused by the actions of others.
All of these requirements of modern society necessitate a form of assessment and classification that can
adequately and objectively deal with these kinds of issues.

2.1.1 The Development of Classification Systems

Arguably the first person to develop a comprehensive classification system for psychopathology was the
German psychiatrist Emil Kraepelin (1883–1923). He suggested that psychopathology, like physical
illness, could be classified into different and separate pathologies, each of which had a different cause
and could be described by a distinct set of symptoms that he called a syndrome. Kraepelin's work
provided some hope at the time that mental health problems could be described and successfully treated
in much the same way as other medical illnesses.
Following on from Kraepelin's scheme, the first extensive system for classifying psychopathology was
developed by the World Health Organization (WHO), who added psychological disorders to the
International List of Causes of Death(ICD) in 1939. Despite this development, the mental
disorders section in the ICD was not widely accepted, and in 1952 the American Psychiatric
Association(APA) published their first Diagnostic and Statistical Manual(DSM). In 1968 the
APA produced a second version of their diagnostic manual (DSM‐II) and in 1969 the WHO published
a new classification system, which was more widely accepted, while in the UK a glossary of definitions
was produced to accompany the WHO system (General Register Office, 1968). However, the WHO
system was simply a listing of diagnostic categories, and while DSM‐II and the British Glossary of
Mental Disorders provide more information on which to base diagnoses, the actual practice of
diagnosing psychopathology varied widely. However, in 1980, the APA produced a substantially revised
and expanded DSM‐III which has come to be accepted as the most influential diagnostic system for
both clinical and research purposes. The most recent version that is used in this book is DSM‐5 ‐
published in 2013. The ICD system (now known as the International Classification of Diseases) is currently in
its tenth edition (ICD‐10) with ICD‐11 having been accepted by WHO's World Health Assembly
(WHA) in May 2019 and will come into effect on 1st January 2022. Most revisions of the DSM have
been coordinated with the ICD to ensure some consistency of diagnosis across systems, but the ICD is
usually considered as the classification system used most in daily clinical work, whereas the DSM has
uses for both clinical diagnosis and research purposes. Use of ICD‐10 is most common in Europe,
whereas DSM‐5 use is almost universal in the United States (Clark, Cuthbert, Lewis‐Fernandez,
Narrow, & Reed, 2017). For convenience and consistency, we will be using only the DSM diagnostic
system in this book, mainly because it is the most widely used classification system in clinical psychology
research (see Cooper, 1994, for a guide to the ICD‐10 classification system, and you can browse the
most recent version of ICD‐11 here: https://icd.who.int/browse11/l‐m/en.)

Diagnostic and Statistical Manual (DSM) First published in 1952 by the American
Psychiatric Association (APA), the DSM extended the World Health Organisation’s (WHO)
International List of Causes of Death (ICD) classification system to include a more widely
accepted section on mental disorders.

2.1.2 Diagnostic and Statistical Manual (DSM)

Defining and diagnosing psychopathology

Before attempting to classify individual psychopathologies it was necessary for DSM to consider what
should be the definition of a mental health problem generally. As we have already seen in Chapter 1 this
is not a simple matter. However, DSM does make some attempt to rule out behaviours that are simply
socially deviant as examples of psychopathology, and puts the emphasis on distress and disability as
important defining characteristics. Distress relates to the chronic experience of pain or distressing
emotions, and disability refers to the fact that distress can lead to impairment in one or more important
areas of functioning, such as education, employment, and dealing with family and social responsibilities.
It is also important to try and define at this point what exactly the DSM system is designed to do.
Wakefield (1997) argues that DSM has four basic objectives: (a) it must provide necessary and sufficient
criteria for correct differential diagnosis, (b) it should provide a means of distinguishing ‘true’
psychopathology from non‐disordered human conditions that are often labelled as everyday ‘problems
in living’ (examples of the latter being everyday experiences of emotions such as stress or sadness), (c) it
should provide diagnostic criteria in a way that allows them to be applied systematically by different
clinicians in different settings, and (d) the diagnostic criteria it provides should be theoretically neutral,
in the sense that they do not favour one theoretical approach to psychopathology over another. Whether
DSM can achieve these four objectives will be to some extent the measure of its success as a diagnostic
tool.
DSM classification systems also provide the following information: (a) essential features of the disorder
(those that ‘define’ the disorder and allow for consistent diagnosis across clinicians), (b) associated features
(i.e., those that are usually, but not always, present), (c) diagnostic criteria (a list of symptoms that must be
present for the patient to be given this diagnostic label), and (d) information on differential diagnosis (i.e.,
information on how to differentiate this disorder from other, similar disorders). Finally, as we mentioned
earlier, an important feature of DSM is that it avoids any suggestion about the cause of a disorder
unless the cause has been definitely established. This means that diagnosis is made almost entirely on
the basis of observable behavioural symptoms rather than any supposition about the underlying cause
of the symptoms. In this sense, diagnostic categories in DSM are descriptive constructs based on groups of
symptoms that define a diagnostic category, and they are not definitions of diseases nor do they have
any explanatory significance (in terms of helping to understand the causes of those symptoms) (Table
2.1).

General problems with classification

While classification systems such as DSM attempt to provide an objective and reliable set of criteria by
which psychopathology symptoms can be diagnosed, they are in many senses imperfect.
First, we have already mentioned that DSM does not classify psychopathology according to its causes
but does so merely on the basis of symptoms. This can be problematic in a number of different ways.
For example, psychopathologies that look the same on the surface may have different causes, and as a
consequence require different forms of treatment. Also, diagnosis on the basis of symptoms gives the
illusion of explanation, when it is nothing more than a re‐description of the symptoms (Carson, 1996).
So, to say that ‘she hears voices because she has schizophrenia’ sounds like an explanation, but within
DSM, schizophrenia is merely a collective term for the defining symptoms.
TABLE 2.1 Chapters in DSM‐5

Neurodevelopmental disorders
Schizophrenia spectrum and other psychotic disorders
Bipolar and related disorders
Depressive disorders
Anxiety disorders
Obsessive‐compulsive and related disorders
Trauma‐ and stressor‐related disorders
Dissociative disorders
Somatic symptom disorders
Feeding and eating disorders
Elimination disorders
Sleep‐wake disorders
Sexual dysfunctions
Gender dysphoria
Disruptive, impulse control, and conduct disorders
Substance use and addictive disorders
Neurocognitive disorders
Personality disorders
Paraphilic disorders
Other disorders
The number of total disorders in DSM‐5 has not increased significantly, but some disorders have now had their
importance recognised by being allocated separate chapter headings (e.g., obsessive‐compulsive disorder). The chapter
on neurodevelopmental disorders is a new heading containing autism spectrum disorders, intellectual development
disorder, and attention/hyperactivity disorder (ADHD). The chapter on substance use and addictive behaviours now
includes gambling disorder. The importance of both bipolar disorder and depressive disorders is recognised by them
being allocated to separate chapters.
Second, simply using DSM criteria to label people with a disorder can be stigmatising and harmful. We
saw in Chapter 1 that individuals with a mental health diagnosis tend to be viewed and treated
differently within society (Perkins et al., 2018). In addition, diagnostic labels may encourage individuals
to adopt a ‘sick’ role and can result in people adopting a long‐term role as an individual with what they
perceive as a debilitating illness (Scheff, 1975).
Third, DSM diagnostic classification tends to define disorders as discrete entities (i.e., after being assessed,
you will either be diagnosed with a disorder or you will not). However, much recent evidence has begun
to suggest that many common mental health problems such as anxiety and depression may be
dimensional rather than discrete (Krueger & Piasecki, 2002; den Hollander‐Gijsman et al., 2012; Clark et
al. 2017). That is, symptoms diagnosed as a disorder may just be more extreme versions of everyday
behaviour. For example, at times we all worry about our own life problems—some more than others. In
extreme cases worry can become so regular and persistent that it will interfere with our daily living and
may meet DSM criteria for diagnosis as a disorder (e.g., generalised anxiety disorder, GAD, see Chapter
6). However, chronic worrying and GAD symptoms appear to be dimensional and range in frequency
and intensity across the general population (Niles, Lebeau, Liao, Glenn, & Craske, 2012), and in such
circumstances, the cut‐off point for defining an activity such as worrying as a disorder becomes
relatively arbitrary. DSM had traditionally attempted to deal with this problem by adding a clinical
significance criterion to many diagnostic categories which required that symptoms cause ‘significant
distress or impairment in social, occupational, or other important areas of functioning’ (Spitzer &
Wakefield, 1999), and the purpose of this was to try to differentiate symptoms that reflect normal
reactions to stress that the individual may be able to cope with from those that may require intervention
and treatment to restore functioning. However, with growing evidence that psychopathology symptoms
are on a dimension, DSM‐5 has included simple dimensional measures of disorder severity to
accompany more specific diagnostic criteria. For example, in the case of GAD, dimensional measures
such as per cent of the day spent worrying can provide an indication of symptom severity on a
dimensional scale.
Fourth, DSM conceptualises psychopathology as a collection of hundreds of distinct categories of
disorders, but what happens in practice provides quite a different picture. For example, the discrete,
differentially defined disorders listed in DSM regularly co‐occur. This is known as comorbidity, where
an individual client will often be diagnosed with two or more distinct disorders (e.g., an anxiety disorder
such as obsessive‐compulsive disorder and major depression). What is interesting is that comorbidity is
so common that it is the norm rather than the exception. For example, surveys suggest that up to 79%
of individuals diagnosed with a disorder at some point during their lifetime will have a history of more
than one disorder (Kessler et al., 1994). The frequency of comorbidity suggests that most disorders as
defined by DSM may indeed not be independent discrete disorders but may represent symptoms of
either hybrid disorders (e.g., a disorder that contains elements of a number of different disorders) or
a more broad ranging syndrome or disorder spectrum that represents a higher‐order categorical
class of symptoms (Kotov et al., 2017; Widiger & Samuel, 2005). An example of a hybrid disorder is
mixed anxiety‐depressive disorder, and many people exhibit symptoms of both anxiety and
depression, yet do not meet the threshold for either an anxiety or a depression diagnosis (Möller, et al.,
2016; Barlow & Campbell, 2000). Examples such as this suggest that because DSM defines disorders as
numerous individual discrete entities, it fails to recognise when combinations of discrete symptoms may
each not reach a level significant enough for diagnosis but may collectively be causing significant
distress. There is also a broader theoretical implication to the fact that comorbidity is so common, and
this is that psychopathology may occur in a spectrum that has a hierarchical structure rather than
consisting merely of numerous discrete disorders (e.g., Conway, et al., 2019, see Section 2.1.4 for further
detail).

comorbidity The co-occurrence of two or more distinct psychological disorders.

hybrid disorders Disorders that contain elements of a number of different disorders.

disorder spectrum The frequency of comorbidity suggests that most disorders as defined by
DSM may indeed not be independent discrete disorders, but may represent symptoms of a
disorder spectrum that represents a higher-order categorical class of symptoms.

Mixed anxiety-depressive disorder An example of a hybrid disorder whereby people

exhibit symptoms of both anxiety and depression, yet do not meet the threshold for either an
anxiety or a depression diagnosis.

One final problem with DSM is that it can be conceived as a ‘hodgepodge’ collection of disorders that
have been developed and refined in a piecemeal way across a number of revisions (see Focus Point 2.1) –
and this makes it almost impossible to frame a definition of what a mental health problem actually is.
Frances & Widiger (2012) characterise this ‘hodgepodge’ view in the following quotation:
The current list of mental disorders certainly constitutes a hodgepodge collection. Some describe short‐term states, others
life‐long personality. Some reflect inner misery, others bad behaviour. Some represent problems rarely or never seen in
normals, others are just slight accentuations of the everyday. Some reflect too little self‐control, others too much. Some are
quite intrinsic to the individual; others are defined against varying and changing cultural mores and stressors. Some begin
in infancy, others in old age. Some affect primarily thought; others emotions, behaviors, or inter‐personal relations; and
there are complex combinations of all these. Some seem more biological, others more psychological.
(Frances & Widiger, 2012, p. 111)

FOCUS POINT 2.1 CRITICISMS OF THE DSM DEVELOPMENT

PROCESS

DSM regularly undergoes an intensive revision process to take account of new research on
mental health problems and to refine the diagnostic categories from earlier versions of the
system. One would assume that this would be a deliberate and objective process that could only
further our understanding of psychopathology, and that is certainly the intention of the
majority of those involved. However, at least some people argue that the process of developing
a classification system such as DSM can never be entirely objective, free from bias, or free from
corporate or political interests. Allen Frances and Thomas Widiger were two individuals who
were prominent in the development of the fourth edition of the DSM, and they have written a
fascinating account of the lessons they believe should be learned from previous attempts to
revise and develop mental health classification systems (Frances & Widiger, 2012). They make
the following points:
1. Just as the number of mental health clinicians grows, so too will the number of life
conditions that work their way into becoming disorders. This is because the proliferation
of diagnostic categories tends to follow practice rather than guide it.
2. Because we know very little about the true causes of mental health problems, it is easier
and simpler to proliferate multiple categories of disorder based on relatively small
differences in descriptions of symptoms.
3. Most experts involved in developing DSM are primarily worried about false negatives (i.e.,
the missed diagnosis or patient who does not fit neatly into the existing categorisations),
and this leads to either more inclusive diagnostic criteria or even more diagnostic
categories. Unfortunately, experts are relatively indifferent to false positives (patients who
receive unnecessary diagnosis, treatment, and stigma) and so are less likely to be concerned
about over‐diagnosis.
4. Political and economic factors have also shaped the ‘medical model’ view of
psychopathology on which DSM is based, and also contributed to the establishment and
proliferation of diagnostic categories. For example, the pharmaceutical industry benefits
significantly from the sale of medications for mental health problems, and its profits will be
dependent on both (a) conceptions of mental health based on a medical model that implies
a medical solution, and (b) a diagnostic system that will err towards overdiagnosis rather
than underdiagnosis (see Pilecki, Clegg, & McKay, 2011).

While DSM is not ideal, it is the most comprehensive classification system we have available, and while
we have just listed a number of criticisms of DSM we must also remember that classification in and of
itself does also have some advantages (see Section 2.1).
2.1.3 DSM‐5
DSM‐5 arguably represents the most comprehensive revision of the DSM so far (Table 2.1), and it has
involved many years of deliberation and field trials to determine what changes to mental health
classification and diagnosis are essential and empirically justifiable. The main changes between DSM‐5
and its predecessor (DSM‐IV‐TR) are listed in Table 2.2 (see Blashfield, Keeley, Flanagan, & Miles,
2014, for a review of changes in the DSM from DSM‐I to DSM‐5).
However, while these most recent changes to the DSM have been extensively discussed and researched,
many of the revisions have been received critically, and it is worth discussing some of these criticisms
because they provide an insight into the difficulties of developing a classification system for
psychopathology that is fair and objective.
First, many of the diagnostic changes in DSM‐5 have reduced the number of criteria necessary to
establish a diagnosis. This is the case with attenuated psychosis syndrome, major depression, and
generalised anxiety disorder, and this runs the risk of increasing the number of people that are likely to
be diagnosed with common mental health problems such as anxiety and depression. It is a debatable
point whether increases in the number of diagnosed cases is a good or a bad thing, but it is likely to have
the effects of ‘medicalising’ many everyday emotional experiences (such as ‘grief ’ following a
bereavement, or worry following a stressful life event), and may create “false‐positive” epidemics
(Frances, 2010; Wakefield, 2016). This is a process that many clinicians critical of DSM claim is ‘eating
up normality’, and ‘none of the new mental disorders added to DSM‐5 passes any of the three
necessary tests for a new diagnosis: a low false positive rate, an effective treatment, and safety. Future
DSMs should stick to well defined mental disorders that have clear treatment implications and can be
easily distinguished from normality’ (Frances, 2015, p. 179)
TABLE 2.2 Summary of changes in DSM‐5

Axes I, II, and II will be combined

Disorders no longer categorised as acute or lifelong
New chapters for OCD and trauma and stress‐related disorders
Confirms the growing importance of these types of disorder as possibly independent of
other anxiety‐based problems
Autism spectrum disorder will incorporate many previously separate labels (e.g., Asperger’s
disorder)
New disruptive mood dysregulation disorder
Diagnoses children with persistent irritability
Binge eating disorder, hoarding disorder, and skin‐picking disorder included
All recognised as new independent disorder categories
Personality disorders retained with added dimensional scales
PTSD included in new chapter on stress
Emphasises the importance of trauma‐related disorders
Removal of bereavement exclusion in major depression
Allows bereavement to be included as a contributor to major depression
Substance use disorder combines substance abuse and substance dependence
Second, DSM‐5 has introduced disorder categories that are designed to identify populations that are at
risk for future mental health problems, and these include mild neurocognitive disorder (which is
intended to diagnose cognitive decline in the elderly) and attenuated psychosis syndrome (seen as
a potential precursor to psychotic episodes). Once again, these initiatives run the risk of medicalising
states that are not yet full‐blown disorders and could facilitate the diagnosis of normal developmental
processes as psychological disorders. Introducing diagnostic categories that attempt to identify
individuals at risk for future mental health problems seems to be a trend diametrically opposed to what
has been happening in the rest of medicine, which in recent times has tended to move away from
screening and early diagnosis, having discovered through research and experience that these can often
cause patients more harm than good (e.g., Adami, Kalager, Valdimarsdottir, Bretthauer, & Ioannidis,
2018).

mild neurocognitive disorder DSM-5 has introduced disorder categories that are designed
to identify populations that are at risk for future mental health problems, and these include mild
neurocognitive disorder, which diagnoses cognitive decline in the elderly.

attenuated psychosis syndrome DSM-5 has introduced disorder categories that are
designed to identify populations that are at risk for future mental health problems. Attenuated
psychosis syndrome is seen as a potential precursor to psychotic episodes.

Third, there are concerns that changes in diagnostic criteria will result in lowered rates of diagnosis for
some particularly vulnerable populations. For example, 5 years after the implementation of DSM‐5
criteria for autism spectrum disorder(ASD), a comprehensive review and meta‐analysis suggests
there has been a significant decrease of at least 20% in the number of individuals being diagnosed with
ASD using DSM‐5 criteria compared to using DSM‐IV‐TR criteria (Kulage et al. 2019). In addition,
many researchers believe that introducing a single autism diagnostic dimension in DSM‐5 risks
marginalising future research on the different subtypes of autism that constituted specific diagnostic
categories in DSM‐IV‐TR (Tsai, 2015). Similar concerns have been voiced about changes to specific
learning disorder diagnostic criteria in DSM‐5, and the possibility that deletion of the term dyslexia
as a diagnostic label will disadvantage individuals with specific phonologically based, developmental
reading disabilities.
Finally, two enduring criticisms of DSM generally that have continued to be fired specifically at DSM‐5
have been that (a) DSM‐5 has continued the process of attempting to align its diagnostic criteria with
developments and knowledge from neuroscience (Regier, Narrow, Kuhl, & Kupfer, 2011), but
neuroscience may never be able to provide a comprehensive basis for diagnosis because its approach is
too reductionist and by its very nature it will be unable to capture the social and cultural factors that
indisputably contribute to the symptoms of mental health problems (e.g., de Macedo, 2017); and (b)
most mental health problems (and psychological distress generally) are now viewed as dimensional, so
any criteria defining a diagnostic cut‐off point will be entirely arbitrary. DSM‐5 has attempted to
recognise the importance of the dimensionality of symptoms by introducing dimensional severity rating
scales for individual disorders. But as we have seen from the previous discussion, each iteration change
in DSM diagnostic criteria changes the number and range of people who will receive a diagnosis, and
this makes it increasingly hard to accept diagnostic categories as valid constructs (e.g., Kendler, Kupfer,
Narrow, Phillips, & Fawcett, 2009).

2.1.4 Developing Alternatives to DSM

Both DSM and ICD take a very medically oriented approach to diagnosing psychopathology by
splitting mental health problems into numerous discrete diagnostic categories each defined on the basis
of different clusters of symptoms. But this is exactly what we might expect if medically trained
professionals—who already considered mental health problems to be forms of illness or disease—were
the people who originally devised these diagnostic schemes. However, many modern‐day clinical
psychologists object to this medically oriented form of classification, and some even object to any form
of psychopathology classification at all. So what are the alternatives? In the remainder of this section,
we take a brief look at some alternatives to DSM that have emerged over the last decade or so.

Research domains criteria (RDoC)

Both DSM and ICD are diagnostic systems based on descriptions of symptoms and neither classifies
mental health problems in terms of their aetiology or their causes. This raises the question of how
researchers should go about discovering the causes of psychopathology. What has happened in the past
is that researchers have attempted to understand the causes of psychopathology using the diagnostic
categories in either DSM or ICD—but these diagnostic categories are defined only in terms of clusters
of symptoms, and this does not imply that each diagnostic category will have its own distinctive set of
causal factors. A more sensible approach to classifying psychopathologies in terms of their causes would
be to start from scratch by researching causes and then relating them to observable symptoms. This is
the approach adopted by the Research Domain Criteria (RDoC) initiative. This programme of research
was launched by the US National Institute of Mental Health (NIMH) in 2009, and is a “vision for the
future” rather than a closely specified research programme. It represents an attempt to understand the
causes of psychopathology in terms of the neurological, biological, psychological, social, and cultural
structures and processes that underlie mental health problems (Insel, 2009), and conceives of
psychopathologies as “disorders of brain circuits” that can be experimentally explored using the tools of
neuroscience (Insel et al., 2010). This knowledge of causality would then serve as the basis for a new
classification framework for mental health problems (see Clark et al. 2017, for a comparison of DSM,
ICD, and RDoC).
RDoC provides researchers with a two‐dimensional matrix that offers a basis for guiding research.
Figure 2.1 shows this five‐by‐seven matrix and its environmental and neurological contexts. There are
seven neurodevelopmental units of analysis from basic to more complex (genes, molecules, cells, circuits,
physiology, behaviour, self‐reports), and these units of analysis are intersected by five domains that
correspond to constructs relevant to psychopathology—negative valence systems (e.g., threat, loss),
positive valence systems (e.g., responsiveness to reward), cognitive systems (e.g., attention, memory),
social processes (e.g., theory of mind), and arousal/regulatory systems. The aim of this approach is to
provide a framework for understanding the neurobiology of mental health problems and in particular to
understand the relationships between different causal factors operating at different levels of analysis.
There are some potential limitations to the RDoC initiative. First, it was originally based on the
assumption that psychopathologies are ‘disorders of brain circuits’. Certainly, most mental health
problems are manifestations of brain activity, but they are not necessarily dysfunctions of the brain.
That is, at least some mental health problems may be the product of brain and neural processes
reacting normally to harsh or extreme environmental experiences (Lilienfeld & Treadway, 2016).
Second, RDoC focuses almost entirely on intra‐individual variables to the detriment of extra‐individual
variables such as the social, developmental, or cultural context of mental health problems (Shankman &
Gorka, 2015). Third, if RDoC is going to provide an alternative classification system for
psychopathology, then it will be a long‐term project requiring detailed and intensive research at many
different levels of analysis, and so a classification system based on RDoC is still a long way off.
FIGURE 2.1 The framework of the National Institute of Mental Health's Research Domain Criteria. This figure
depicts the five‐by‐seven RDoC matrix and its environmental and neurodevelopmental contexts.
From Clark, Cuthbert, Lewis‐Fernandez, Narrow, & Reed, 2017.

Hierarchical Taxonomy of Psychopathology (HiTOP)

Both DSM and ICD are categorical classification systems that have difficulty explaining two things: (a)
why comorbidity between diagnoses should be the norm rather than the exception, and (b) why it is that
some symptoms are often better described in dimensional rather than categorical terms. HiTOP is a
recently developed hierarchical classification of psychopathology symptoms that helps to predict
comorbidity and also higher‐order dimensions that reflect associations between lower‐order dimensions.
HiTOP is an evidence‐based consensual model of symptom taxonomy drawn up by a group of
psychopathology researchers and clinicians (Conway et al., 2019). Figure 2.2 shows a working model of
the HiTOP taxonomy. This has five levels, with very specific symptom components at the bottom and
broad, heterogeneous constructs near the top, and the hierarchy is organised on the basis of evidence
from statistical modelling, validation studies, and the observed covariation of symptoms (Kotov et al.,
2017). The model deals with comorbidity by identifying higher‐order dimensions that predict
associations between disorders and symptoms on lower levels and can encompass both narrowly defined
symptoms (e.g., obsessions) and broader clusters of psychological conditions (such as internalising). In
particular, the model is consistent with empirical evidence from a number of different levels of analysis,
including genetics, neurobiology, and environmental risk studies (Conway et al., 2019), and has an
underlying structure that is stable across countries and cultures (de Jonge et al., 2018).
HiTOP is a work in progress, and research is still needed to incorporate psychopathologies not currently
included in the model (such as autism spectrum disorder), and one potential limitation of the model is
that it still relies on DSM/ICD diagnostic categories at the level of syndromes and disorders. If the
diagnostic categories listed in DSM/ICD turn out to be unreliable, then so too will be the HiTOP
model.

Network analyses
DSM defines psychological disorders in terms of a series of co‐occurring symptoms, yet does not specify
how these symptoms are caused. One way to try to explain how these symptoms co‐occur is to assume
that there is some kind of underlying cause or latent variable that connects the symptoms together
(Reise & Waller, 2009). For example, a lung tumour can explain why an individual experiences bloody
sputum, chest pains, and a chronic cough, and so in psychopathology it may be that an underlying
hypothetical process called ‘depression’ can explain the co‐occurrence of criteria symptoms for
depression such as insomnia, sadness, and loss of interest. However, the thing we call ‘depression’ may
not be a separate entity that causes symptoms in the same way that a lung tumor is an identifiable entity
that is separate from its symptoms and causes its symptoms. For example, clinicians and
psychometricians have proposed a radically different way of understanding what makes up a collection
of symptoms such as depression. Instead of being an underlying cause of the symptoms, ‘depression’ is
the name given to the dynamic causal interactions between defining symptoms themselves, and this has
given rise to network analysis of symptoms indicative of mental health problems (Borsboom &
Cramer, 2013). This approach assumes that disorders emerge from the causal interactions between
symptoms themselves, and understanding the causal relationships between symptoms will enable us to
define individual clusters of symptoms that define individual disorders. In this way, depression is not a
causal entity but merely a name for the network of symptoms that interact to cause the syndrome we
call ‘depression’.
FIGURE 2.2 HiTOP consortium working model. Constructs higher in the figure are broader and more general, whereas
constructs lower in the figure are narrower and more specific. Dashed lines denote provisional elements requiring further
study. At the lowest level of the hierarchy (i.e., traits and symptom components), conceptually related signs and symptoms
(e.g., phobia) are indicated in bold for heuristic purposes, with specific manifestations indicated in parenthesis. ADHD =
attention‐deficit/hyperactivity disorder, BPD = bipolar disorder, GAD = generalised anxiety disorder, HiTOP =
Hierarchical Taxonomy of Psychopathology; IED = intermittent explosive disorder, MDD = major depressive disorder;
OCD = obsessive‐compulsive disorder, ODD = oppositional defiant disorder; SAD = separation anxiety disorder; PD =
personality disorder; PTSD = post‐traumatic stress disorder.
From Conway et al., 2019.
Networks of interacting symptoms can be identified using statistical methods that measure the strength
of the associations between symptoms and the centrality of symptoms within the network (i.e. how
important a symptom is in affecting other symptoms) (e.g., Fried, Epskamp, Nesse, Tuerlinckx, &
Borsboom, 2016). Focus Point 2.2 provides a detailed description of a network analysis of depression
symptoms and its implications (Focus Point 2.2).
The benefits of a network analysis approach are that it provides an objective measure of how symptoms
are interrelated and can identify symptoms that are centrally important in defining a disorder and
affecting other symptoms (i.e., have ‘high centrality’) (Contreras, Nieto, Valiente, Espinosa, & Vazquez,
2019). Identifying symptoms with high centrality that trigger other symptoms means that these
symptoms can then be prime targets for clinical interventions. Network analysis can also help to explain
comorbidity. For example, McNally, Mair, Mugno, and Riemann (2017) found that a network analysis
revealed that sadness was the one symptom that connected obsessive‐compulsive disorder (OCD)
symptoms with depression in clients with comorbid OCD and depression. However, network analysis is
a cross‐sectional analysis of relationships between symptoms and as yet does not provide information on
causal relationships between symptoms that may occur over different time scales, and experimental lab‐
based studies of individual symptoms may be necessary to complement the statistical analyses. A useful
introduction to network analysis is provided by McNally (2016), and a review and future directions by
Robinaugh, Hoekstra, Toner, and Borsboom (2019).

FOCUS POINT 2.2 A NETWORK ANALYSIS OF DEPRESSION

SYMPTOMS

Network analyses can be created by collecting data about symptoms in a variety of ways
and subjecting these data to statistical analyses that provide information about the
connectedness between symptoms (Borsboom & Cramer, 2013). First, it is important to identify
the elements or symptoms that will function as nodes, and these can be taken from diagnostic
manuals such as the DSM, or from clinician‐rated or client‐rated assessment tools such as the
Inventory of Depressive Symptomatology if you are studying depressive symptoms (IDS‐C,
IDS‐SR, Trivedi et al., 2004). Even greater detail can be achieved by asking clinicians and
clients to rate the direction of causality of symptoms.
These data can then be used to create a visual representation of the network of symptoms that
consists of nodes and edges. Nodes represent symptoms, and edges represent associations
between symptoms. The centrality of a node can then be calculated by such details as the
number of edges connected to it and the strength with which it will activate associated nodes.
Nodes (symptoms) with high centrality are those of greatest importance in the network.

The figure shows an example of a network analysis carried out on depression symptoms by
Fried, Epskamp, Nesse, Tuerlinckx, and Borsboom (2016). On the left is the representation of
the network. Green lines represent positive associations between symptoms and red lines
negative ones. The thickness and brightness of the connecting edges indicate the strength of the
association between nodes. The four sleep symptoms are closely connected (hyp, in1, in2, in3) but
only weakly associated with other symptoms. The DSM core depression criteria symptoms of
“diminished interest in pleasure” (int, ple) were closely associated. On the right of the figure is
the centrality strength of each node, with DSM core symptoms of sadness, interest loss and
pleasure loss all having high centrality, meaning they are symptoms which will have a significant
influence on other symptoms, and the centrality of these symptom nodes validates their use as
core diagnostic criteria in DSM‐5. In addition, the fact that anxiety (anx) is also a significant
node in the network is consistent with the high comorbidity rates found between depression and
anxiety (Kessler, Chiu, Demler, Merikangas, & Walters, 2005), and this provides a way of
showing how depression and anxiety may be connected when the two are comorbid. (From
Fried EI, Epskamp S, Nesse RM, Tuerlinckx F & Borsboom D (2016) What are ‘good’
depression symptoms? Comparing the centrality of DSM and non‐DSM symptoms of
depression in a network analysis. Journal of Affective Disorders, 189, 314‐320.)
The Power Threat Meaning (PTM) framework
In 2018 the British Psychological Society published the Power Threat Meaning Framework. This project was
funded by the Division of Clinical Psychology and developed over 5 years by a team of leading clinical
psychologists and service users in the UK. The framework is a scholarly document aimed at promoting
discussion and debate by offering a fundamentally different perspective on the origins, experience and
expression of mental health problems
(https://www.bps.org.uk/sites/bps.org.uk/files/Policy/Policy%20‐%20Files/PTM%20Summary.pdf). It
represents an attempt to move away from primarily biological and medical models of mental health
problems that are based on psychiatric diagnosis and the assumption that mental health problems are
disorders of biology and are ‘pathological’. Instead, the framework takes a broad view of the causes of
psychopathology and views people as social beings whose experiences of distress and troubling
behaviour are inseparable from their material, social, environmental, socio‐economic, and cultural
contexts. In effect, those aspects of life that are labelled as mental health problems can be viewed as
quite natural reactions to stressful and threatening life events, examples of which include poverty,
discrimination, and inequality, and traumatic experiences such as abuse and violence, along with more
subtle pressures such as social norms and expectations. These events can be indicative of the adverse
operation of ‘Power’ (coercive, legal, economic, ideological, social/cultural, or interpersonal), and the
‘Threat’ that the negative operation of power may pose. As a consequence this gives rise to learned and
evolved threat responses that can range from automatic physiological reactions to consciously selected
actions such as hyper‐vigilance, self‐injury, or compulsive behaviour which are currently considered as
symptoms of mental health problems. A significant feature of the framework is the importance of
offering ‘Meaning’ to the client, and helping them to construct a nondiagnostic, nonblaming,
demystifying story about strength and survival and that such experiences and reactions are perfectly
natural attempts to survive the negative impacts of power.
Instead of asking ‘What is wrong with you?’, the framework replaces this type of question with four
others:
‘What has happened to you?’ (How has Power operated negatively in your life?)
‘How did it affect you?’ (What kinds of Threats did it pose?)
‘What sense did you make of it?’ (What is the Meaning of these situations and experiences to you?)
‘What did you have to do to survive?’ (What kinds of Threat Response are you using?)
Translated into clinical practice, two additional questions need to be asked:
‘What are your strengths?’
‘What is your story?’
The latter two questions can form the basis for giving meaning to the client's experiences and providing
a road map to recovery.
The PTM Framework is basically a radical nondiagnostic and dimensional approach to what are
currently called mental health problems. It is dimensional in that reactions to stressors and threats are
seen as perfectly normal attempts to survive such events, and its purpose is to offer a way of helping
people to create more hopeful narratives or stories about the difficulties in their lives instead of seeing
themselves as blameworthy, weak, deficient or ‘mentally ill’.
However, there is still some way to go because at present PTMF only offers a theoretical framework for
approaching and resolving mental health problems in a nondiagnostic way, and more is needed to
translate this framework into clinical practice. Also, because of its radical anti‐diagnostic approach, the
framework has generated a good deal of controversy and discussion amongst mental health
professionals and service users alike (e.g.,
https://www.mentalhealthtoday.co.uk/blog/diagnosis/challenging‐narratives‐the‐power‐threat‐
meaning‐framework; Johnstone, et al., 2019).
2.1.5 Conclusions
Despite its conceptual difficulties and its many critics, DSM is still the most widely adopted classification
and diagnostic system for clinical practice and clinical research. Such a system can be useful for a
number of reasons, including determining the allocation of resources and support for mental health
problems, for circumstances that require a legal definition of mental health problems, and providing a
common language that allows the world to share and compare data on mental health problems. Having
said this, there are still many significant problems associated with DSM, and diagnosing and labelling
people with specific psychological disorders raises other issues to do with stigma and discrimination.
Indeed, we should be clear that diagnostic systems are not a necessary requirement for helping people
with mental health problems to recover, and many clinical psychologists prefer not to use diagnostic
systems such as DSM or ICD, but instead prefer to treat each client as someone with a unique mental
health problem that can best be described and treated using other means such as case formulation
(see Section 2.3 for a fuller description and examples of case formulation). In recent years, the
imperfections in DSM and in particular the criticisms of DSM‐5 have led clinicians and researchers to
attempt to develop alternative evidence‐based classification systems to the DSM (e.g., RDoC, HiTOP,
and network analysis) or to offer theoretical frameworks for clinical practice that do not require
diagnostic classification at all (e.g., the PTM Framework).

case formulation The use of clinical information to draw up a psychological explanation of

the client’s problems and to develop a plan for therapy.

SELF‐TEST QUESTIONS
Briefly describe the history of the development of psychopathology classification systems.
What is the DSM classification system primarily designed to do?
DSM is not an ideal classification system. Describe at least four problems associated with
this method of classification.
What are the main alternatives to DSM‐5 that are being developed by clinical
psychologists?

SECTION SUMMARY

2.1 CLASSIFYING PSYCHOPATHOLOGY

The two most influential classification systems are the American Psychiatric Association
(APA) Diagnostic and Statistical Manual and the World Health Organization (WHO)
International Classification of Diseases (ICD).
Currently, the most widely adopted classification system is DSM‐5.

2.2 METHODS OF ASSESSMENT

This section describes in some detail a range of assessment tools that clinical psychologists can use to aid
diagnosis, determine the best forms of intervention for an individual's problems, and assess their
progress towards recovery. But first, it is important to be sure that a method of assessment is both
reliable and valid.

2.2.1 The Reliability and Validity of Assessment Methods

In order for assessment methods to provide objective information about clients we need to be sure about
two things. First, we need to be sure that the method has high reliability. That is, that the method will
still provide the same result when used by different clinicians on different occasions. Second, we also
need to be sure that the assessment has validity. That is, that it actually does measure what it claims to
measure (e.g., if it is a test measuring anxiety, then scores on the test should correlate well with other
ways of measuring anxiety).

reliability The extent that an assessment method will still provide the same result when used
by different clinicians on different occasions.

validity The extent that an assessment method actually does measure what it claims to be
measuring.

Reliability
Reliability refers to how consistently an assessment method will produce the same results, and reliability
can be affected by a number of different factors. First, test‐retest reliability refers to the extent that
the test will produce roughly similar results when the test is given to the same person several weeks or
even months apart (as long as no treatments or interventions have occurred in between). As we indicated
earlier, most psychological tests are based on the assumption that most traits and personal
characteristics are relatively stable and can be reliably measured. If the test has high test‐retest reliability
then when an individual is given the test on two separate occasions, the two scores should be highly
correlated.

test–retest reliability The extent that a test will produce roughly similar results when the test
is given to the same person several weeks or even months apart (as long as no treatments or
interventions have occurred in between).

Second, interrater reliability refers to the degree to which two independent clinicians will actually
agree when interpreting or scoring a particular test. Most highly structured tests, such as personality
inventories, will have high interrater validity because the scoring system is clearly defined and there is
little room for individual clinician judgements when interpreting the test. However, some other tests
have much lower interrater reliability, especially where scoring schemes are not rigidly defined, and
projective tests are one example of this (see Section 2.2.3).

interrater reliability The degree to which two independent clinicians or researchers actually
agree when interpreting or scoring a particular test.

Third, many assessment tests have multiple items (e.g., personality and trait inventories), and internal
consistency within such tests is important. Internal consistency refers to the extent to which all the
items in the test consistently relate to each other. For example, if there are 20 items in a test, then we
would expect scores on each of those 20 items to correlate highly with each other. If one item does not
correlate highly with the others, then it may lower the internal consistency of the test. The internal
consistency of a questionnaire or inventory can usually be assessed by using a statistical test called
Cronbach's α, and this test will also indicate whether any individual item in the test is significantly
reducing the internal consistency of the test (Field, 2017, pp. 821‐830).

Internal consistency The extent to which all the items in a test consistently relate to one
another.

Cronbach’s α Statistical test used to assess the internal consistency of a questionnaire or

inventory.

Validity
It is important to be sure that an assessment method actually measures what it claims to be measuring,
and this is covered by the concept of test validity. However, validity is a complex concept, and we
begin by discussing some of the more obvious issues surrounding this problem.
To determine whether a test actually measures what it claims to measure, we need to establish the
concurrent validity of the test. That is, we need to see if scores on that test correlate highly with
scores from other types of assessment that we know also measure that attribute. For example, the Spider
Phobia Questionnaire (SPQ) purports to be a measure of the spider phobic's anxious reaction to spiders
(Watts & Sharrock, 1984), but in order to establish the concurrent validity of this questionnaire, we
might need to be sure that scores actually correlate highly with other measures of spider fear such as the
magnitude of physiological anxiety measures taken while the individual is viewing a spider.

concurrent validity A measure of how highly correlated scores of one test are with scores
from other types of assessment that we know also measure that attribute.

A particular assessment method may appear to be valid simply because it has questions which intuitively
seem relevant to the trait or characteristic being measured. This is known as face validity, but just
because a test has items that seem intuitively sensible does not mean that the test is a valid measure of
what it claims to be. For example, a questionnaire measuring health anxiety may ask about how
frequently the respondent visits a doctor. Although this would be a characteristic of health anxiety, it is
also a characteristic of individuals who are genuinely ill or have chronic health problems.

face validity The idea that a particular assessment method may appear to be valid simply
because it has questions which intuitively seem relevant to the trait or characteristic being
measured.

For an assessment method to have high predictive validity it must be able to help the clinician to
predict future behaviour and future symptoms, and so be valuable enough to help with the planning of
care, support or treatment for that individual. For example, a good measure of depression would predict
that certain types of antidepressant medication will help to alleviate the symptoms. Some assessment
measures are predictive in the sense that they help us to understand the kinds of factors that might pose
as risk factors for subsequent psychopathology. For example, assessments that allow us to gather reliable
information about childhood abuse and neglect will indicate that such individuals are likely to suffer a
range of possible psychopathologies in later life (see Table 16.2).
 predictive validity The degree to which an assessment method is able to help the clinician
predict future behaviour and future symptoms.

Finally, construct validity is also an important concept in clinical assessment. A construct is a

hypothetical or inferred attribute that may not be directly observable or directly measurable.
Hypothetical constructs are used frequently in the study of psychopathology to help understand some
of the cognitive factors that may cause or maintain mental health problems, and so being able to
measure them is a useful tool in diagnosis and subsequent treatment. For example, individuals with
OCD tend to have inflated conceptions of their own responsibility for preventing harm, and this
inflated responsibility appears to be an important vulnerability factor in developing OCD
(Salkovskis, 1985; Purdon, 2019). However, inflated responsibility is not directly observable, but has to
be inferred from indirect measures of the individual's behaviour, and so questionnaires such as the
Obsessive Beliefs Questionnaire (OBQ) have been developed to measure beliefs about inflated
responsibility (see Chapter 6, Section 6.6.3). The more that independent evidence that can be gathered
to show that a measure of a construct like inflated responsibility is related to other similar measures (e.g.,
compulsive perseveration at checking tasks, or high scores in groups diagnosed with OCD than
nonclinical control participants) the greater the construct validity of the measure.

construct validity Independent evidence showing that a measure of a construct is related to

other similar measures.

inflated responsibility The belief that one has power to bring about or prevent subjectively
crucial negative outcomes. These outcomes are perceived as essential to prevent. They may be
actual: that is, having consequences in the real world, and/or at a moral level.

2.2.2 Clinical Interviews

The nature of clinical interviews

We have all probably been interviewed at some point in our lives. This may be for a job, a place at
university, or by our GP who is enquiring about symptoms of an illness. An interview usually represents
an informal, relatively unstructured conversation between two or more people, the purpose of which is
to gather some information about one or more of those people in the interview. The clinical interview is
probably the first form of contact that a client will have with a clinician, and the clinical psychologist
will usually be trying to gain a broad insight into the client and their problems. Questions may relate to
the nature of the symptoms the client experiences, their past history, and their current living and
working circumstances. The type of questions that will be asked in a clinical interview will depend very
much on the theoretical orientation of the clinician. For example, psychodynamic clinicians are likely to
want to ask questions about the client's childhood history and their memories of past events and to take
note of any strong emotional responses that may indicate unconscious processes (see Chapter 1). In
contrast, the behavioural interviewer will want to explore any relationships between the client's
symptoms and environmental events, such as the consequences of symptoms that may reinforce them.
Finally, the cognitive clinician will want to try and discover whether the client holds any assumptions or
beliefs that may maintain or influence their problems.
In general, those conducting clinical interviews must be skillful in guiding the client towards revealing
the kinds of information they are looking for. They must be able to establish a good rapport with their
client, they must gain their trust, they must be able to convince the client of the value of the theoretical
approach they are taking, and in most cases they must be able to empathise with their clients in order to
encourage them to elaborate on their concerns and to provide information that they may otherwise be
reluctant to give. The clinical interviewer can encounter a number of difficulties when conducting an
interview and these will often require all their experience and skill to overcome. For example, (a) many
clients will want to withhold information about themselves, especially if it involves painful or
embarrassing memories, or if the information concerns illegal or unsocial activities (such as illegal drug
use or illegal sexual activities), and (b) clients may well have poor self‐knowledge, and so be unable to
answer questions accurately or with any real insight into why they behave or feel the way they do. It is
the skilled interviewer's job to find ways to deal with these problems and to reveal the reliable
information that they need to form a diagnosis, to understand the causes of the client's problems, and to
formulate a treatment programme.

Structured interviews
The clinician can also use the interview method to acquire the kinds of standardised information they
need to make a diagnosis or to construct a case formulation (see Section 2.3), but this requires that they
conduct the interview in a structured way. The normal clinical interview would probably contain many
open questions such as ‘Tell me something about yourself and what you do’, and the direction of the
interview will be to some extent determined by the client's responses to these open questions. However,
structured interviews can be used to enable the clinician to make decisions about diagnosis and
functioning. One such structured interview technique is known as the Structured Clinical Interview
for DSM‐5 (SCID‐5) (First, Williams, Karg, & Spitzer, 2016), which can be used for determining
diagnoses using DSM‐5 criteria. The SCID is a branching, structured interview in which the client's
response to one question will determine the next question to be asked. This enables the clinician to
establish the main symptoms exhibited by a client, their severity, and whether a combination of these
symptoms and severity meet DSM‐5 criteria for a particular disorder, and the SCID‐5 has been shown
to provide highly reliable diagnoses and severity ratings for many disorders (e.g., Shankman et al., 2018;
Somma et al., 2018). In clinical practice, most clinical psychologists are skilled enough to reach
diagnostic decisions about a client without a structured interview such as the SCID‐5, but the reliability
of a diagnosis tends to be much higher when a structured interview is used (Garb, 2005).

structured interview An interview in which questions to be asked, their sequence and

detailed information to be gathered are all predetermined.

Structured Clinical Interview for DSM-5 (SCID) A branching, structured interview in

which the client’s response to one question will determine the next question to be asked.

Structured interviews can also be used to determine overall levels of psychological and intellectual
functioning, especially in older people who may be suffering from degenerative disorders such as
dementia. One such structured interview is the Mini Mental State Examination(MMSE), which is
a structured test that takes 10 minutes to administer and can provide reliable information on the client's
overall levels of cognitive and mental functioning. A fuller description of this structured interview is
given in Chapter 15 (see Focus Point 15.2).

Mini Mental State Examination (MMSE) A structured test that takes 10 minutes to
administer and can provide reliable information on a client’s overall levels of cognitive and
mental functioning.
Limitations of the clinical interview
The clinical interview is usually a good way of beginning the process of assessment, and it can provide a
range of useful information for the clinician. However, there are limitations to this method. First, the
reliability of clinical interviews is probably quite low. That is, no matter how skilled they may be, two
different clinicians are quite likely to end up with rather different information from an unstructured
interview. For example, clients are likely to give different information to an interviewer who is ‘cold’ and
unresponsive than to one who is ‘warm’ and supportive (Hersen & Thomas, 2007; Eisenthal, Koopman,
& Lazare, 1983), and a teenage client is likely to respond differently to a young interviewer who is
dressed casually than to an older interviewer who is dressed formally. There is also significant evidence
that an interviewer's race and sex will influence a client's responses (Paurohit, Dowd, & Cottingham,
1982). As we have already mentioned, many clients may have quite poor self‐awareness, so only a skilled
interviewer will be able to glean the information they require by inferring information from the client's
responses. Interviewers are also prone to biases that may affect the conclusions they draw from an
interview. For example, they may rely too heavily on first impressions (the primacy effect), or give
priority only to negative information (Meehl, 1996), and may be influenced by irrelevant details such as
the client's biological sex, race, skin colour or sexual orientation. Interestingly, diagnoses are most likely
to be correct when relevant diagnostic information is presented last (a recency effect)(Cwik & Margraf,
2017). Finally, there are some mental health problems in which sufferers may intentionally mislead the
interviewer or lie to them, and these can mean that the client can manipulate the interview or
deliberately provide misleading information. This can occur in the case of personality disorders or
sexual disorders such as paedophilia that may involve illegal behaviours (see Chapters 11 and 12)
(Activity Box 2.1).

2.2.3 Psychological Tests

Psychological tests represent highly structured ways of gathering information about an individual. They
usually take the form of a written questionnaire in which the client has to respond to a series of
questions or stimuli. However, they can be given verbally by the clinician or completed on a computer.
The psychological test is one of the most common forms of assessment in clinical psychology and it is
considerably more structured than the interview method. Psychological tests have a number of
advantages as methods of assessment:
1. They usually assess the client on one or more specific characteristics or traits (e.g., levels of anxiety,
depression, IQ , cognitive functioning, or individual psychopathology traits such as
hypochondriasis, paranoia, conversion hysteria, etc.).
2. They will usually (but not always) have very rigid response requirements so that the questions can
be scored according to a preconceived scoring system—Table 2.3 provides an example of the
question format for a measure of trait anxiety—the State‐Trait Anxiety Inventory (STAI)
(Spielberger, Gorsuch, Lushene, Vagg, & Jacobs, 1983)—and this is a test format common to many
psychometric tests.
3. Once data from these tests have been collected from large numbers of participants, statistical
norms for the tests can be established. This is known as standardisation, and it allows the
clinician to see where an individual client's score on the test falls in relation to the normal
distribution of scores for that test (see, for example, Figure 1.1). It also means that the clinician may
be able to use the score on a particular test to estimate whether a client might meet the diagnostic
criteria for a psychological disorder. For example, scores on a test such as the Clark‐Beck Obsessive
Compulsive inventory (Clark & Beck, 2003) (CBOCI) can be used to estimate the probability with
which a client might meet DSM‐5 diagnostic criteria for OCD.
 standardisation The establishment of statistical norms for clinical tests, which allows the
clinician to see where an individual client’s score on the test falls in relation to the normal
distribution of scores for that test.

4. Unlike the ad hoc quizzes and questionnaires you might find in popular magazines, most
structured psychological tests are rigorously tested to ensure that they are both valid and reliable
(see Section 2.2.1). That is, they are tested to ensure that they are a valid measure of what they
claim to be measuring (e.g., that scores on a written psychological test claiming to measure anxiety
actually correlate with behavioural measures of anxiety) and that the test is reliable in the sense
that it yields consistent scores when it is given to the same person on different occasions.

TABLE 2.3 Measuring state and trait anxiety using a questionnaire

The Spielberger STAI‐Y2 is a well‐known psychometric test for measuring levels of state and trait
anxiety. Its questions take the following format, and this format is one that is regularly used in
psychological tests of this kind (Spielberger, Gorsuch, Lushene, Vagg, & Jacobs, 1983).
A number of statements which people have used to describe themselves are given below. Read each
statement and then circle the appropriate number to the right of the statement to indicate how you
generally feel. There are no right or wrong answers. Do not spend too much time on any one statement
but give the answer which seems to describe how you generally feel.
1 = Almost never
2 = Sometimes
3 = Often
4 = Almost always
1. I feel pleasant 1 2 3 4
2. I feel nervous and restless 1 2 3 4
3. I feel satisfied with myself 1 2 3 4
4. I wish I could be as happy as others seem to be 1 2 3 4
5. I feel like a failure 1 2 3 4
6. I feel rested 1 2 3 4
The scale of 1 to 4 is known as a Likert scale where the client has to specify their level of agreement
with each statement. Some items will be reversed so that the respondent cannot simply endorse each
item in the same way (for example, Q3 is a reversed item in which the anxious individual would
endorse a low number rather than a high number). The clinician can then create a total score for a
client by adding together the individual scores that the client has circled (but remembering to reverse
score any reversed items—for example, on Q3 4 would be scored as 1, 3 as 2, and so on). When data
have been collected from a large number of participants from differing age groups and demographic
backgrounds statistical norms for the test can be established, and this is known as standardisation. This
allows the clinician to compare the score of their client with the normal distribution of scores that
occur in the population in general.
Most psychological tests are based on the psychometric approach. That is, the test assumes that
there are stable underlying characteristics or traits (e.g., anxiety, depression, compulsiveness, worry, etc.)
that exist at different levels in everyone. The psychological tests we will discuss below can take a number
of different forms and serve a number of different functions. For example, some tests stick rather rigidly
to the structured question, response, and scoring format similar to that shown in Table 2.3 (personality
inventories, specific symptom inventories), while others (such as projective tests) may closely define the
questions or stimuli to be presented to the client, but allow a much wider range of potential responses.
The clinical psychologist will use psychological tests for a variety of different purposes, including the
assessment of psychopathology symptoms, intelligence, and neurological or cognitive deficits.

psychometric approach The idea that a psychological test assumes that there are stable
underlying characteristics or traits (e.g. anxiety, depression, compulsiveness, worry) that exist at
different levels in everyone.

Personality inventories
The most well known of the personality inventories used by clinical psychologists and psychiatrists
is the Minnesota Multiphasic Personality Inventory(MMPI). This was originally developed in
the 1940s by Hathaway and McKinley (1943) and was updated in 1989 by Butcher et al. (1989) (known
as the MMPI‐2). The MMPI‐2 consists of 567 self‐statements to which the client has to respond on a 3‐
point scale by replying either ‘true’, ‘false’ or ‘cannot say’. The questions cover topics such as mood,
physical concerns, social attitudes, psychological symptoms, and feelings of well‐being. The original
authors asked around 800 psychiatric patients to indicate whether the questions were true for them and
compared their responses with those from 800 nonpsychiatric patients. They then included in the
inventory only those questions that differentiated between the two groups. The test has 4 validity scales
and 10 clinical scales, and examples of these are shown in Table 2.4. The test provides scores for each
scale between 0 and 120, and scores above 70 on a scale are considered to be indicative of
psychopathology. The scores from the various scales can be displayed on a graph to give a distinctive
profile indicating the client's general personality features, potential psychopathology, and emotional
needs. The validity scales are particularly useful, because they allow the clinician to estimate whether a
client has been providing false information on the test. Clients might provide false information for a
number of reasons: (a) because they want to ‘look good’ and so respond in a socially acceptable way
(measured by the lie scale), (b) because they may want to fake psychopathology symptoms in order to
receive attention and treatment (measured by the F scale) (Rogers, Sewell, Martin, & Vitacco, 2003), (c)
because they are being evasive or simply having difficulty reading or interpreting the questions
(measured by the ? scale), or (d) because they are defensive and want to avoid appearing incompetent
(measured by the K scale).

Minnesota Multiphasic Personality Inventory (MMPI) A well-known personality

inventory used by clinical psychologists and psychiatrists.
TABLE 2.4 Subscales and sample items from the MMPI
Subscale What the scale measures Sample item
? Evasiveness or difficulty interpreting the (number of items left unanswered)
question
L (lie scale) Tendency of respondent to respond in a ‘I approve of every person I meet’
socially acceptable way
F Respondent is trying to fake ‘Everything tastes sweet’
psychopathology symptoms
K Respondent is defensive and trying not ‘Things couldn’t be going any better for
to look incompetent me’
Hypochondriasis Abnormal concern with bodily ‘I am often aware of tingling feelings in my
(HS) sensations body’
Depression (D) Pessimism and hopelessness ‘Life never feels worthwhile to me’
Conversion Uses physical symptoms to avoid ‘My muscles often twitch for no apparent
Hysteria (Hy) conflicts and responsibilities reason’
Psychopathy Emotional shallowness and disregard ‘I don’t care about what people think of
(Pd) for social norms me’
Masculinity‐ Identifies respondents with ‘I like to arrange flowers’
Femininity (Mf) nontraditional gender characteristics
Paranoia (Pa) Pathological suspiciousness or delusions ‘There are evil people trying to influence
of grandeur or persecution my mind’
Psychasthenia Identifies respondents with obsessions, ‘I save everything I buy, even after I have
(Pt) compulsions, guilt, and irrational fears no use for it’
Schizophrenia Identifies bizarre sensory experiences ‘Things around me do not seem real’
(Sc) and beliefs
Hypomania Identifies emotional excitement, ‘Sometimes I have a strong impulse to do
(Ma) hyperactivity, and impatience something that others will find appalling’
Social Identifies someone who is shy, modest, ‘I am easily embarrassed’
Introversion (Si) and prefers solitary activities
Clinical research has indicated that the MMPI has good internal reliability, and scores on the MMPI
appear to have excellent clinical validity by corresponding accurately with clinical diagnoses and ratings
of symptoms made by both clinicians and members of the client's own family (Ganellan, 1996;
Graham, 1990; Vacha‐Hasse, Kogan, Tani, & Woodall, 2001). One limitation of the MMPI is the time
that it takes to administer, and answering 567 questions requires some stamina on the part of both the
client and the overworked clinician. However, a streamlined version is available which retains only 338
of the original 567 items (MMPI‐2‐RF) (Ben‐Porath, 2012) and has been shown to exhibit construct
validity and reliability equal to or better than the original longer version (Tellegen & Ben‐Porath, 2008).
Another widely used personality questionnaire is the Big Five Inventory‐2 (BFI‐2) which consists of
60 items and measures personality on five broad scales that have been derived using factor analysis of
verbal descriptions of human behaviour—these scales are extraversion, agreeableness,
conscientiousness, neuroticism, and open‐mindedness (Soto & John, 2012). These five domains of
personality have subsequently been found to subsume most known personality traits and may represent
the basic structure behind all personality traits (O'Connor, 2002). Common mental health problems
such as anxiety and depression have been closely linked with scales such as neuroticism, and high
neuroticism scores have been shown to be a risk factor for subsequent anxiety and depression (Cuijpers
et al., 2010) as well as a number of other mental health problems such as psychosis and substance abuse
(Jeronimus, Kotov, Riese, & Ormel, 2016).
Specific trait inventories
While personality inventories such as the MMPI and the Big Five Inventory assess characteristics of the
client across a range of different traits and domains, other inventories have been developed simply to
measure functioning in one specific area or one specific psychopathology. Such tests may measure
emotional functioning, such as levels of anxiety, depression, or anger, or they may measure aspects of
behaviour such as social skills. More recently, other tests have been developed in an attempt to measure
cognitive functioning or cognitive constructs that are relevant to psychopathology. One such example is
the Obsessive Belief Questionnaire (OBQ) (Steketee et al., 2005) which was designed to assess beliefs
and appraisals considered critical to the acquisition and maintenance of obsessions. This measures six
cognitive constructs thought to play a role in OCD including (a) intolerance of uncertainty, (b)
overestimation of threat, (c) control of thoughts, (d) importance of thoughts, (e) beliefs about inflated
responsibility, and (f) perfectionism, and you may want to look at Section 6.6.3 to understand how these
cognitive constructs are relevant to the aetiology of OCD.
Specific tests such as these can be used to measure variables that are directly observable and
measurable, such as characteristics found in observable behaviour. But they are becoming increasingly
used to measure hypothetical constructs that are not necessarily directly observable but have to be
inferred from the answers given to a range of questions. For example, the degree to which an individual
cannot tolerate uncertainty (a factor that has been implicated in the acquisition and maintenance of a
number of anxiety disorders) is assessed on the OBQ by asking respondents to endorse statements such
as ‘If I am uncertain there is something wrong with me’ or ‘I should be 100% certain that everything
around me is safe’. Taken together, such questions provide an estimate of how much the individual is
able to ‘tolerate’ uncertainty. Hypothetical constructs such as ‘intolerance of uncertainty’ are often
constructs that emerge from clinical experience with a client group when clinical psychologists begin to
see consistent cognitive traits that appear to be associated with certain diagnoses or symptoms.

hypothetical constructs Constructs that are not necessarily directly observable but have to
be inferred from other data.

Because of their potential diagnostic and theoretical value (such inventories can also be used as research
tools to help us understand the causes of psychopathology), the number of specific trait inventories
available to clinicians and researchers has burgeoned in the past 20 years. While some are very valuable
and have good face validity, many others are relatively underdeveloped. For example, unlike the MMPI,
a majority of specific trait inventories fail to include any questions to indicate whether respondents are
faking responses or are merely being careless with their answers, and many are not subjected to
stringent standardisation, validation, and reliability tests. There is even a view that researchers may
simply create a specific trait inventory to serve their own theoretical purposes and to give their own
theoretical perspective a façade of objective credibility (i.e., they may create an inventory simply to
‘measure’ a construct that they themselves have invented) (Davey, 2003).

Projective tests
This group of tests usually consists of a standard fixed set of stimuli that are presented to the client but
are ambiguous enough for the client to put their own interpretation on what the stimuli represent. This
often allows for considerable variation in responses between clients and also considerable variation
between clinicians in how the responses should be interpreted. The most widely used of the projective
tests are the Rorschach Inkblot Test, the Thematic Apperception Test (TAT), and the Sentence
Completion Test. Projective tests were originally based on the psychodynamic view that people's
intentions and desires are largely unconscious and must be inferred indirectly (Dosajh, 1996). Most
projective tests were designed during the mid‐twentieth century and were extremely popular for
assessment purposes right up to the turn of the century. However, as we shall see later because they are
open‐ended tests that allow significant variation in client responding, they are significantly less reliable
and valid than more structured tests. Nevertheless, even though their popularity has declined in recent
years (Piotrowski, Belter, & Keller, 1998), many clinicians still use these types of tests to give them some
first impressions of a client’s symptoms or as part of a larger battery of assessment procedures (Garb,
Wood, Lilienfeld, & Nezworski, 2002).

projective tests A group of tests usually consisting of a standard fixed set of stimuli that are
presented to clients, but which are ambiguous enough for clients to put their own interpretation
on what the stimuli represent.

The Rorschach Inkblot Test was originally developed by the Swiss psychiatrist Hermann Rorschach.
He created numerous inkblots by dropping ink onto paper and then folding the paper in half to create a
symmetrical image. He discovered that everyone he showed them to saw designs and shapes in the blots,
and he assumed that their responses revealed information about the individual's psychological
condition. Most versions of the Rorschach Inkblot Test now use around 10 official inkblots of which 5
are black ink on white, 2 are black and red ink on white, and 3 are multicoloured. An example of a
black and white and multicoloured inkblot are given in Figure 2.3. The clinician will have available to
them a highly structured scoring system (e.g., Exner & Weiner, 1995) that allows them to compare the
scores the client provides with a set of standardised personality norms, that may provide indications of
underlying psychopathology. However, if the test is used as a formal assessment procedure, it is still
heavily dependent on the clinician's interpretation of the client's responses. For example, if certain
themes keep appearing in the client's responses they may provide evidence of underlying conflicts, such
as the repeated perception of ‘eyes’ on the inkblots perhaps providing evidence of paranoia the clinician
may want to explore further. Nevertheless, the Rorschach test can be a valid and reliable test for the
detection of thought disorders that may be indicative of schizophrenia or people at risk of developing
schizophrenia (Lilienfeld, Wood, & Garb, 2000; Mondal & Prakash, 2015).

Rorschach Inkblot Test A projective personality test using inkblots created by dropping ink
onto paper and then folding the paper in half to create a symmetrical image.
FIGURE 2.3 The Rorschach Inkblot Test. The Rorschach Inkblot Test usually consists of 10 official
inkblots. Five inkblots are black ink on white. Two are black and red ink on white. Three are multicoloured, and the pictures
give examples of a black and white inkblot and a multicoloured one. The clinician shows the inkblots in a particular order
and asks the client: ‘What might this be?’ (a free association phase). After the client has seen and responded to all the
inkblots, the clinician then presents them again one by one to study (the inquiry phase). The client is asked to list everything
they see in each blot, where they see it, and what there is in the blot that makes it look like that. The blot can also be
rotated. The clinician also times the client, which then factors into the overall assessment. Methods of interpretation differ.
The most widely used method in the United States is based on the work of John E. Exner (Exner & Weiner, 1995). In
this system, responses are scored systematically with reference to their level of vagueness or synthesis of multiple images in
the blot, the location of the response, which of a variety of determinants is used to produce the response (for example,
whether the shape of the inkblot, its colour, or its texture is primary in making it look like what it is said to resemble), the
form quality of the response (to what extent a response is faithful to how the actual inkblot looks), the contents of the
response (what the respondent actually sees in the blot), the degree of mental organising activity that is involved in producing
the response, and any illogical, incongruous, or incoherent aspects of responses.
The Thematic Apperception Test (TAT) is a projective personality test consisting of 30 black and
white pictures of people in vague or ambiguous situations (Morgan & Murray, 1935) (Figure 2.4). The
client is asked to create a dramatic story around the picture, describing what they think is happening in
the picture; what events preceded it; what the individuals in the picture are saying, thinking, or feeling;
and what the outcome of the situation is likely to be. Many clinicians claim that this test is particularly
useful for eliciting information about whether the client is depressed, has suicidal thoughts, or strong
aggressive impulses (Rapaport, Gill, & Shaefer, 1968). Clients usually identify with one of the characters
in the pictures (known as the ‘hero’) and the picture then serves as a vehicle for the client to describe
their own feelings and emotions as if they were involved in the ambiguous scene. The TAT may also
allow the clinician to determine the client's expectations about relationships with peers, parents, other
authority figures, and romantic partners. However, there is some doubt about how valid the TAT is as a
clinical diagnostic tool, with one study indicating that clinicians classified individuals as clinical or
nonclinical cases at close to chance level when using the TAT alone (Wildman & Wildman, 1975).
Nevertheless, it can be a useful tool after a client has been formally diagnosed in order to match them
with a suitable form of psychotherapy.

Thematic Apperception Test (TAT) A projective personality test consisting of 30 black and
white pictures of people in vague or ambiguous situations.

FIGURE 2.4 The Thematic Apperception Task (TAT). The Thematic Apperception Test consists of 30
black and white pictures similar to the one in the figure. The client is asked to create a dramatic story around the picture.
Clients will usually identify with one of the characters in the picture which enables them to express their own feelings and
emotions as if they were involved in the scene.
Finally, the Sentence Completion Test is a useful open‐ended assessment test that was first
developed in the 1920s and provides clients with the first part of an uncompleted sentence, such as ‘I
like. . . .’, ‘I think of myself as. . .’, ‘I feel guilty when. . .’, which the client then completes with words of
their own. This test allows the clinician to identify topics that can be further explored with the client,
and can also help to identify ways in which an individual's psychopathology might bias their thinking
and the way they process information. Research Methods in Clinical Psychology Box 2.1 shows how the
sentence completion task has been used to identify trauma‐relevant thinking biases in combat veterans
with post‐traumatic stress disorder (PTSD) (Kimble et al., 2002). Such thinking biases help to maintain
emotional problems, and using the sentence completion task can help the clinician to identify ways of
thinking that can be targeted during treatment (Research Methods Box 2.1).

Sentence Completion Test An open-ended projective personality test that provides clients
with the first part of an uncompleted sentence which they complete with words of their own.
As we mentioned earlier, the popularity of projective tests has declined steadily over the years. There are
a number of reasons for this:
1. Such tests are mainly based on revealing information that is relevant to psychodynamic approaches
to psychopathology, and the role of psychodynamic approaches in the assessment and treatment of
psychopathology has itself declined over the past 30 years.
2. Even though standardised procedures for scoring projective tests have developed over recent years,
the reliability of such tests is still disappointingly low (Lilienfeld, Wood, & Garb, 2000), and
different clinicians will often interpret the same responses in quite different ways (Wildman &
Wildman, 1975).
3. Even with highly standardised scoring methods, some projective tests such as the Rorschach Test
often result in psychopathology being inferred when other evidence for such a conclusion is sparse.
For example, Hamel, Shaffer, & Erdberg (2000) administered the Rorschach Test to 100 school
children—none of whom had any history of mental health problems. However, the results of the
test were interpreted in almost all cases as evidence of faulty reasoning that might be indicative of
schizophrenia or mood disorder.
4. Projective tests such as the TAT have intrinsic cultural biases. For instance, in the traditional set of
TAT pictures there are no ethnic minority characters even though the client is expected to identify
with one of the characters in the picture. In some cases, this has been overcome by developing
more contemporary TAT pictures that contain figures from ethnic minorities (Constantino,
Flanagan, & Malgady, 2001).

cultural biases The phenomenon of interpreting and judging phenomena in terms

particular to one’s own culture.

RESEARCH METHODS IN CLINICAL PSYCHOLOGY BOX

2.1 THE SENTENCE COMPLETION TEST

The sentence completion task is an open‐ended assessment test that provides the client
with the first part of a sentence which the client then has to complete in their own words.
This is a useful projective test that allows the clinician to identify topics that are important
to the client, and to identify any biases in the way that a client tends to think about things.
For example, incomplete sentences such as ‘My greatest fear. . . .’, ‘I feel. . . . .’, ‘I need. . . ’
etc. can give the clinician an insight into some of the client’s emotional responses.
Similarly, questions such as ‘My father. . . .’, ‘Other pupils. . .’, ‘Most girls. . .’ will provide
some insight into the client's feelings about others.
The sentence completion task can also be used successfully as an important research tool.
For example, Kimble et al. (2002) used a sentence completion task to assess interpretation
biases in combat veterans who were diagnosed with PTSD (see Chapter 6). They gave their
participants 33 sentences to complete. Each item was generated so that it could be
completed with words of military or nonmilitary content. Examples included:

‘He was almost hit by a. ..’

‘The night sky was full of. . .’
‘The air was heavy with the smell of. . .’
‘The silence was broken by the. . .’
 For example, ‘He was almost hit by a…’ could be completed with the word ‘rock’ or the
word ‘bullet’. The figure shows that veterans with PTSD completed sentences with
significantly more ‘war’ or trauma‐relevant words than veterans without PTSD. These
findings suggest that individuals diagnosed with PTSD have biases in the accessibility,
encoding, and retrieval of trauma‐relevant information (Bomyea, Johnson, & Lang, 2017)
and that sentence completion tasks of this kind might help to differentiate individuals with
a diagnosable mental health condition from those without.

5. Most projective tests are labour intensive for the limited amount of objective information they
provide. Clinicians need extensive training in order to administer tests such as the Rorschach and
TAT, and they are time consuming to administer, interpret, and score. Given the development of
more objective and easily scored inventories, this has inevitability led to a decline in the popularity
of projective tests.

Computerised adaptive testing (CAT)

In this modern age of computing and cloud computer environments, psychological tests do not need to
be lengthy pencil and paper tests completed by the client and then scored or interpreted by the
clinician. Assessment tests can be administered via computer, scored by the computer, and interpreted
by the computer. This is known as computerised adaptive testing (CAT) and is of growing value
to the clinician who needs to assess a client. CAT does not simply present existing paper and pencil tests
to clients but uses existing data to streamline and individualise the measurement process optimally
selecting questions from a large bank of questions and responses (Unick, Shumway, & Hargreaves,
2008). This means there is no response‐set bias due to repeated administration of the same items over
time because CAT items are optimised to the client's symptoms and the severity of those symptoms, and
therefore uses different items on repeated administration of the test. The utility of CAT has already
been demonstrated in the assessment of common mental health problems such as depression and
anxiety (Fliege et al., 2005; Walter et al., 2007), and computerised adaptive diagnosis has been shown to
reproduce trained clinician diagnoses in a small fraction of the time of a clinical interview (1 minute
versus 1 hour)(Gibbons, Weiss, Frank, & Kupfer, 2016).

Intelligence tests
Intelligence tests are regularly used by clinicians in a variety of settings and for a variety of reasons. IQ
(intelligence quotient) tests, as they are now generally known, were first devised in the early part of
the twentieth century as a means of comparing intellectual ability in specific groups of people (e.g.,
army recruits). Arguably the first IQ test was that produced by the French psychologist Alfred Binet in
1905, a test that purported to measure intelligence across a number of verbal and nonverbal skills. From
early tests such as this there are now over 100 tests of intelligence available, most of which are
standardised to have a score of 100 as the mean and a score of 15 or 16 as the standard deviation (see
Figure 1.1). As you can see from Figure 1.1, 68% of the population will score between 84 and 116 (one
standard deviation from the mean) on IQ tests, and around 2–3% of the population will have IQ scores
less than 2 standard deviations from the mean (e.g., less than 70). Because of their continued
development over the previous 100 years, IQ tests have high internal consistency (i.e., a client will score
roughly the same on different items that measure the same ability), high test‐retest reliability (i.e., a client
who takes the same test twice but some months or years apart will achieve roughly the same score both
times), and good validity (i.e., the tests are good at predicting intellectual ability or future educational
performance) (Sparrow & Davies, 2000).

IQ (intelligence quotient) tests Tests used as a means of estimating a person’s intellectual

ability.

Intelligence tests are used by clinicians in a number of contexts. For example, they are used with other
measures of ability to diagnose intellectual and learning disabilities, and the cardinal DSM‐5 diagnostic
criterion for intellectual disability is based primarily on an IQ score two standard deviations below the
mean (e.g., an IQ score of between 65 and 75, see Chapter 17). IQ tests are also used to try to assess the
needs of individuals with learning, developmental, or intellectual disabilities so that support can be
provided in any specific areas of need. Tests that provide scores on a range of different ability scales are
best suited for this purpose, and one such example is the Weschler Adult Intelligence Scale, now in
its fourth edition (WAIS‐IV) (Weschler, 2008). This contains scales that measure vocabulary, arithmetic
ability, digit span, information comprehension, letter‐number sequencing, picture completion ability,
reasoning ability, symbol search, and object assembly ability (Photo 2.1). Tests such as the WAIS‐IV can
also be used as part of a battery of tests to assess whether an individual is eligible for special educational
needs, and it will provide information that will suggest strategies, services, and supports that will
optimise the individual's functioning within society. Intelligence tests are frequently used as part of a
battery of assessments used in neurological evaluations (see Chapter 15, Section 15.1.2) and can help to
detect when a client has brain damage caused by traumatic injury or cerebral infection or has a
degenerative brain disorder such as Alzheimer's disease.
PHOTO 2.1 The Weschler Adult Intelligence Scale (WAIS‐IV). The WAIS‐IV is one of the tests of intellectual ability
most commonly used by clinicians. It comprises a range of verbal and performance tests that measure intellectual ability on
a variety of subscales including vocabulary, arithmetic ability, digit span, information comprehension, letter‐number
sequencing, picture completion ability, reasoning ability, symbol search, and object assembly ability

Weschler Adult Intelligence Scale A test designed to measure intelligence in adults and
older adolescents. It contains scales that measure vocabulary, arithmetic ability, digit span,
information comprehension, letternumber sequencing, picture completion ability, reasoning
ability, symbol search and object assembly ability.

However, despite their practical benefits across a range of clinical contexts, intelligence tests still have a
number of limitations. First, intelligence is an inferred construct. That is, it does not objectively exist in
the same way that physical attributes such as heart rate or blood pressure exist but is a hypothetical
construct that has been developed by psychologists to help us try to understand how well individuals can
adapt to various problems. This has led some skeptical psychologists to suggest that there is no clear
definition of intelligence but that ‘intelligence is merely what IQ tests measure’! Second, if the latter
statement is true, then our conception of whether someone is intelligent or not will depend on the
reliability and validity of the individual IQ test we use to measure their intelligence, and this can raise
some difficulties. For example, many IQ tests are culturally biased and appear to be based on middle‐
class, majority ethnic background views of what is adaptive (Gopaul‐McNicol & Armour‐Thomas,
2002), and so will disadvantage those from lower socio‐economic backgrounds, from ethnic minorities,
or from poorer quality educational backgrounds (Walker, Batchelor, & Shores, 2009). While attempts
have been made over the years to eradicate cultural bias of this kind, it is difficult to eliminate it entirely.
For instance, a test question may ask whether a cup goes with a bowl, a spoon, or a saucer, but a child
from a low socio‐economic background may never have drunk from a cup with a saucer and may be
more likely to associate a cup or mug with a spoon. Even so, because it is widely known that some ethnic
minorities perform relatively poorly on IQ tests, this knowledge alone can interfere with test
performance in that group (Spencer, Steele, & Quinn, 1999). Third, we assume that intelligence tests
mainly tend to be rather ‘static’ tests of intellectual ability (but see the next point) and provide a
snapshot of ability at any point in time. What they do not usually appear to measure is the individual's
capacity to learn or their potential to acquire new cognitive abilities (Grigorenko & Sternberg, 1998).
Fourth, IQ scores may not be as static as we originally imagined, and between 1932 and 1978 there has
been a 13.8‐point increase in IQ scores (Flynn, 1984). This is known as the Flynn effect and although
the rate of this IQ increase has slowed in recent years, it is still apparent (Trahan, Stuebing, Hiscock, &
Fletcher, 2014). It is not clear what has been causing this increase in IQ scores over time, but one
implication is that a test will overestimate an individual's IQ score by an average of about 0.3 points per
year between the year the test was normed and the year in which the test was administered. This has
important implications for psychopathologies such as intellectual disabilities which use the IQ measure
as a criterion for disability and, as a consequence, a criterion for access to services and support. Fifth,
many researchers argue that our current conception of intelligence as measured by IQ tests is too
narrow. There are many other skills that are not usually included in our conceptions of, and measures of
intelligence, and these include music ability; physical skill; the ability to perceive, understand, and
express emotion (known as ‘emotional intelligence’); and the ability to implement solutions to real‐world
problems (Gardner, 1998; Mayer, Salovey, & Caruso, 2000). For example, are Lionel Messi's footballing
skills as much an intelligent skill as arithmetic or verbal ability (Bishop, Wright, Jackson, & Abernathy,
2013)? (Photo 2.2).
PHOTO 2.2 ‘The Little Maestro’. Are Lionel Messi's footballing skills as much an intelligent skill as arithmetic or
verbal ability?
Source: Reuters / Darren Staples ‐ stock.adobe.com

Neurological impairment tests

Many psychological and cognitive problems are not caused by problematic life experiences or by
dysfunctional ways of thinking but are caused by damage to the structure and functioning of the brain
and the central nervous system. Such damage can be caused by traumatic injury (such as might be
received in a car accident), cardiovascular accidents such as a stroke, cerebral infection (such as
meningitis), a brain tumour, or they may be the result of a degenerative brain disorder such as
Alzheimer's disease. In such cases damage to the brain can cause both changes in personality (e.g.,
change someone from a passive into an aggressive individual) and cause deficits in cognitive functioning
depending on the areas of the brain that are affected. These issues are discussed more thoroughly in
Chapter 15, but at this point we will mention the value of neurological assessment tests in enabling the
clinician to determine the nature of any cognitive deficits (e.g., memory deficits, deficits in language
skills, etc.), to identify whether such deficits are the result of brain damage, and in many cases to identify
the area of the brain that has been affected. Clinicians will usually employ a battery of tests when
assessing for possible neurological deficits, and these may include electroencephalogram analyses, brain
scans such as positron emission tomography (PET) scans and functional magnetic resonance
imaging scans (see next section), blood tests (to assess potential inherited or genetic components to a
disorder), and chemical analyses of cerebrospinal fluids. But of equal importance in this overall
assessment is the use of neurological tests that measure cognitive, perceptual and motor performance as
indicators of underlying brain dysfunction (Rao, 2000). The rationale behind the use of such
neurological tests is that different psychological functions (such as motor skills, memory, language,
planning, and executive functioning) are localised in different areas of the brain (see Table 15.2), so
discovering a specific cognitive deficit can help to identify the area of the brain where any damage may
be localised. In addition, collecting such information is also crucial for identifying the focus of
rehabilitation strategies and in patient care and planning for the client (Veitch & Oddy, 2008). Tests that
are commonly used by clinical neuropsychologists in this respect are the Adult Memory and
Information Processing Battery (AMIPB) (Coughlan & Hollins, 1985), the Halstead‐Reitan
Neuropsychological Test Battery (Broshek & Barth, 2000), and the MMSE. Each of these tests is
described in more detail in Chapter 15 (Section 15.1.2), and their administration and scoring is an
important part of the day‐to‐day tasks undertaken by clinical neuropsychologists (Hodges, 2017)

positron emission tomography (PET) A neuroimaging technique which allows

measurement of both brain structure and function by utilising radiation emitted from the
participant to develop images.

Adult Memory and Information Processing Battery (AMIPB) A neuropsychological

test in wide use in the UK, comprising two tests of speed of information processing, verbal
memory tests (list learning and story recall) and visual memory tests (design learning and figure
recall).

Halstead–Reitan Neuropsychological Test Battery A common neuropsychological

test used in the USA, compiled to evaluate brain and nervous system functioning across a fixed
set of eight tests. The tests evaluate function across visual, auditory and tactile input, verbal
communication, spatial and sequential perception, the ability to analyse information, and the
ability to form mental concepts, make judgements, control motor output and to attend to and
memorise stimuli.

2.2.4 Biologically Based Assessments

In many cases, information about biological structures and biological functioning can help to inform the
assessment and diagnosis of psychological problems. There are two main types of biologically based
assessment that we describe here, psychophysiological tests and brain imaging.

Psychophysiological tests
There are a number of psychophysiological tests that can be used to provide information about
potential psychological problems. For example, anxiety causes increased activity in the sympathetic
nervous system and is regularly accompanied by changes in physiological measures such as heart rate,
blood pressure, body temperature, and electrodermal responding. Similarly, anger is usually associated
with physiological changes in blood pressure and heart rate. So, psychophysiological tests can provide
useful information related to emotionally‐based psychological problems.
One important measure of physiological activity is electrodermal responding, sometimes known as
the galvanic skin response (GSR) or skin conductance response (SCR). Emotional responses such as
anxiety, fear, or anger increase sweat‐gland activity, and changes in this activity can be recorded with the
use of electrodes that would normally be attached to the fingers of the participant. Traditionally,
changes in skin conductance caused by sweat‐gland activity have been measured as changes on a
polygraph—a pen that records changes in skin conductance on a continually moving roll of graph
paper, but this has now been superseded by direct computer analysis of skin conductance which is
displayed on a computer screen (see Photo 2.3). Skin conductance measures have been used in a variety
of contexts: (a) to assess the kinds of stimuli or events that elicit anxiety in a client (Cuthbert et al., 2003;
Alpers, Wilhelm, & Roth, 2005), (b) to assess autonomic or physiological reactivity in certain diagnostic
groups (e.g., individuals diagnosed with antisocial personality disorder tend to have less reactive
autonomic nervous systems than nonclinical samples) (Lykken, 1995), (c) to assess the ability of clients to
cope following treatment interventions (Bobadilla & Taylor, 2007; Grillon et al., 2004), and (d) whether
autonomic indices of anxiety or arousal correspond with appropriate changes in behaviour (e.g., in
panic disorder, avoidance responses may be triggered by physiological changes indicative of anxiety)
(Karekla, Forsyth, & Kelly, 2004).

electrodermal responding A psychophysiological measure which uses electrodes attached to

the fingers of participants to test emotional responses such as anxiety, fear or anger by
measuring changes in sweat gland activity.

Other useful examples of psychophysiological measurement techniques include the electromyogram

(EMG) that measures the electrical activity in muscles, and the electrocardiogram (ECG) for
measuring heart rate. Although measures such as electrodermal responding can indicate emotional
changes indicative of anxiety, fear or anger, it is not always foolproof. Rather than specifically indicating
the presence of these discrete emotions, skin conductance is more properly an indicator of general
physiological arousal, and this can be caused by a variety of factors, including simply orienting towards
or attending to an event (Siddle, 1983). This issue is nowhere better illustrated than in the history of the
use of lie detectors. Lie detectors use changes in autonomic responding in an attempt to identify
whether an individual is lying in response to specific preset questions, and this technique has often been
used in criminal prosecutions and employment screening—especially in the US (Krapohl, 2002).
However, while a polygraph may detect anxiety or arousal caused by the participant lying, it is also
likely to detect changes in arousal caused by factors other than lying (e.g., the question simply being a
stressful or unusual one), and so may represent an anxious—but innocent—participant as one who may
appear to be guilty (Raskin & Honts, 2002). As a result, findings from lie detector tests in the US are
now used significantly less as evidence of criminal guilt (Daniels, 2002), and no defendant or witness can
be forced to undergo the test.

electromyogram (EMG) A psychophysiological measurement technique that measures the

electrical activity in muscles.

electrocardiogram (ECG) A psychophysiological measurement technique used for

measuring heart rate.
 Lie detectors The measurement of changes in autonomic responding used to identify whether
an individual is lying in response to specific preset questions. This is a controversial technique
that has often been used in criminal prosecutions and employment screening.

PHOTO 2.3 Polygraph machine. The polygraph is a device used to measure changes in physiological responding that may
indicate emotional changes such as anxiety, fear, or anger. The polygraph works by recording physiological measures (such as
skin conductance or heart rate) on a continually moving roll of graph paper. In more recent times, these measures can be
analysed directly by computer and the output displayed on the computer screen.
Finally, another important psychophysiological assessment measure is the electroencephalogram
(EEG). This involves electrodes being attached to the scalp that record underlying electrical activity and
can help to localise unusual brain patterns in different areas of the brain. Abnormal electrical patterns
detected by EEG can indicate a number of problems, including epilepsy, brain tumours, or brain injury
(Cuthill & Epsie, 2005)

electroencephalogram (EEG) A psychophysiological assessment measure which involves

electrodes being attached to the scalp that record underlying electrical activity and can help to
localise unusual brain patterns in different areas of the brain.

Neuroimaging techniques
Many behavioural, cognitive, and psychological problems may be linked to abnormalities in brain
functioning, and while neurological tests can indicate that possible brain dysfunction may be involved,
we will usually need to use techniques that provide images of the brain to confirm this. There are a
range of neuroimaging or brain imaging techniques now available, and some provide the clinician with
anatomical and structural information about the brain (e.g., whether a brain tumour is present) while
others provide information about brain activity and brain functioning (e.g., whether specific brain areas
are fully functioning).
Computerised axial tomography, or CAT scan machines, are sophisticated versions of X‐ray
machines and can be used to form a three dimensional picture of the brain. Figure 2.5 shows a CAT
scan machine. The patient lies down on a platform which then moves through a large doughnut‐like
ring. The ring turns so that with each turn a narrow ‘slice’ of the brain is X‐rayed, and a computer uses
this information to construct two‐dimensional cross‐sections of the brain and these many separate
images can also be combined to provide a three‐dimensional image of the brain. CAT scan images can
help to detect abnormal growths in the brain such as tumours or enlargement of the ventricles in the
brain that can indicate tissue degeneration typical of dementia or schizophrenia.
Positron emission tomography, or PET scan allows measurement of both brain structure and
function. A PET scan can provide pictures of chemical activity in the brain either at rest or when the
participant is undertaking cognitive tasks such as language, learning, remembering, or sensory
processing. The PET scanner utilises radiation emitted from the participant to develop images. Each
participant is given a minute amount of a radioactive drug that closely resembles a natural substance
used by the body. Gamma radiation produced by the radioactive drug is detected by the PET scanner
and shows in fine detail the metabolism of glucose in the brain. The PET scanner's computer uses this
detail to produce colour pictures of the functioning brain. Brightly coloured areas represent areas of the
brain where metabolic rates are high, and represent high levels of brain activity. Figure 2.5 illustrates a
series of PET scans taken of a human infant's brain at intervals from 1 to 12 months, and these images
clearly show the increase in brain activity with early development (Figure 2.6). Because the PET scan
provides images of the brain indicating both levels of activity and areas of activity, it is a useful tool for
assessing cognitive functioning, and provides information about brain functioning in degenerative
diseases such as Alzheimer's disease, and brain functioning in intellectual disabilities such as Down
syndrome. In Chapter 8, Figure 8.3 also provides an example of the use of PET scans in assessing brain
functioning in schizophrenia.
A more recent and less expensive way of measuring chemical activity in the brain is Single‐Photon
Emission Computed Tomography (SPECT). Like PET, SPECT requires injecting a radioisotope
into the bloodstream but is able to provide a 3‐D image of neurotransmitter activity in the brain
(Pagani, Carletto, & Ostacoli, 2019).
FIGURE 2.5 Computerised Axial Tomography or ‘CAT’ Scan. The top picture shows a CAT scan
machine. The client lies down on the platform with their head positioned within the large doughnut‐like ring. The ring turns
to X‐ray individual thin ‘slices’ of the brain, and a computer is used to turn these individual images into either a two‐
dimensional or three‐dimensional picture of the brain. The lower picture shows an example CAT scan of a ‘slice’ of a
normal brain next to one that reveals a large brain tumour (the darker area).
One further imaging technique that has been developed is known as magnetic resonance imaging,
or MRI. MRI scanning involves the participant being placed inside a large circular magnet which
causes the hydrogen atoms in the body to move. This then produces an electromagnetic signal that is
converted by the scanner's computer into visual pictures of the brain. Pictures of the brain produced by
MRI scanning are highly detailed and allow the detection of even the smallest of lesions or tumours. A
subsequent development of MRI technology is known as functional magnetic resonance
imaging, or fMRI. This allows the clinician to take brain images so quickly that tiny changes in brain
metabolism can be detected and can provide minute‐to‐minute information about actual brain activity.
This technology can be used to measure changing brain activity while the participant is undertaking
particular tasks, such as a memory task or viewing an emotional film. Figure 2.7 provides an example of
an fMRI scan of individuals diagnosed with PTSD who are asked to recall an autobiographical
memory that gives rise to flashbacks. fMRI analyses allow the researcher to identify which areas of the
brain are involved in this activity and the sequential activation of brain areas that are specific to
experiencing a distressing ‘flashback’.

FIGURE 2.6 PET Scan of a Developing Infant Brain. These images are of PET scans showing the
increase in brain activity which accompanies the growth of the brain, in the same infant, from the age of 1 to 12 months.
This can be used, for instance, to pinpoint developmental problems in children much earlier than other tests would. Brightly
coloured areas represent areas of the brain where metabolic rates are high and indicate high levels of brain activity.

magnetic resonance imaging (MRI) A neuroimaging technique which involves the

participant being placed inside a large circular magnet that causes the hydrogen atoms in the
body to move. This produces an electromagnetic signal that is converted by the scanner’s
computer into visual pictures of the brain.

functional magnetic resonance imaging (fMRI) A development of MRI technology

which allows the clinician to take brain images so quickly that tiny changes in brain metabolism
can be detected and can provide minute-to-minute information about actual brain activity.

The use of modern brain imaging technology has been useful in providing detailed evidence of brain
abnormalities and dysfunction in relation to a number of psychopathology problems, and as we shall see
in Chapter 3, these techniques are not only valuable for assessment purposes but are also a useful
research tool. However, the use of brain imaging methodology to understand mental health problems is
not without its problems, and as yet there are still many mental health problems for which we have so
far failed to find any significant brain biomarkers – either in the form of dysfunctional brain processes
or normal brain processes that are indicators of specific disorders (Lozupone et al., 2017).
2.2.5 Clinical Observation
A further method of collecting useful clinical information is by direct observation of a client's behaviour.
This can supplement information from interviews and psychological tests and often allows an
assessment of behaviour in its natural context, such as the home, school classroom, or community
setting. Direct observation can provide an objective assessment of the frequency of particular behaviours
(e.g., aggressive behaviours) when this may not be so easily obtained from reports given by the client
themselves, their family, or carers. It also allows behaviour to be assessed in the context of events that
precede the behaviour (and so may trigger the problem behaviour) and events that immediately follow the
behaviour (and may represent the consequences of the behaviour that reinforce its occurrence). In
Chapter 17, Treatment in Practice Box 17.1 provides a detailed example of how an observational
technique can be used to identify what factors might be triggering and maintaining challenging
behaviour in an individual with intellectual disabilities. This example used an ABC chart that requires
the observer to note what happens before the target behaviour occurs (A), what the individual did (B),
and what the consequences of the behaviour were (C). Focus Point 2.2 provides some examples of how
behaviours and events can be coded when undertaking a clinical observation (Nock & Kurtz, 2005),
and which type of coding method you use will depend largely on what you want to find out (e.g., do you
want to just find out how frequently a behaviour occurs, or do you want to know more about the
context in which a behaviour is enacted?) (Focus Point 2.3).

FIGURE 2.7 Functional Magnetic Resonance Imaging (fMRI). fMRI scans allow the researcher to
measure brain activity while the participant is completing various behavioural or cognitive tasks. In this example,
individuals with a diagnosis of PTSD were asked to recall autobiographical memories that might give rise to distressing
‘flashbacks’ of their trauma, and researchers were able to track the brain activity that accompanied this experience.
From Whalley et al., 2013.
 ABC chart An observation method that requires the observer to note what happens before the
target behaviour occurs (A), what the individual did (B), and what the consequences of the
behaviour were (C).

There are a number of advantages to using observational techniques. First, if the observer is
appropriately trained, observation can provide important objective measures of the frequency of
behaviours and those events that precede and follow them, and the latter information will often provide
an insight into the purpose the problematic behaviour serves (e.g., in Treatment in Practice Box 17.1,
systematic observation reveals that the purpose of Andy's self‐injurious behaviour is to enable him to be
removed from noisy and crowded situations) (Kahng et al., 2014; Hastings & Noon, 2005). Second,
observational data has greater external or ecological validity than self‐reports or other forms of
testing because such data provide a measurement of the behaviour as it is actually occurring in a
context. Third, observation of behaviour in a context can often suggest workable answers to problem
behaviour as can clearly be seen in Treatment in Practice Box 17.1. Once it was established that Andy's
self‐injurious behaviour was functioning to get him removed from a stressful environment, staff could
look out for signs that he was becoming overstimulated and remove him from the room before he began
to injure himself.

ecological validity The extent to which conditions imulated in the laboratory reflect real-life
conditions.

Having listed these advantages of clinical observation, it also has a number of drawbacks. First, it is one
of the more time‐consuming forms of assessment, not just in terms of the amount of time required to
simply observed behaviour but also in terms of the amount of time needed to properly train observers
in the use of the various coding systems (e.g., Hawes, Dadds, & Pasalich, 2013) (see Focus Point 2.3).
This is especially so if members of the client's family need to be trained to make systematic observations
in the home setting. Second, observation will usually take place in a specific setting (e.g., the school
classroom or the home), and behaviour in this specific context may not be typical of behaviour in other
contexts (Nock & Kurtz, 2005). Third, the presence of an observer may lead those involved in the
observation setting to behave differently to how they would normally behave (Kazdin, 1978; Skinner,
Dittmer, & Howell, 2000), and this may often be the case with children, who will show dramatic
improvements in behaviour when they are aware they are being observed. This problem can often be
overcome by videorecording behaviour without an observer present and then analysing this at a later
time. Similarly, the clinician may want to undertake analogue observations in a controlled
environment that allows surreptitious observation of the client. For example, children can be observed
interacting in a playroom while the observer is situated behind a two‐way mirror. Fourth, unless
observers are properly trained in the coding methods used, there may be poor interobserver reliability
(Kamphaus & Frick, 2002). That is, two different observers assessing the same participant may focus on
quite different aspects of behaviour and context and arrive at quite different conclusions about the
frequency and causes of behaviour. Fifth, as in all observational procedures, the data can be influenced
by the observer's expectations. Observer expectations can cause biases in the way that information is
viewed and recorded and this can be caused by the theoretical orientation of the observer and what
they already know about the person being observed.

analogue observations Clinical observations carried out in a controlled environment that

allows surreptitious observation of the client.

FOCUS POINT 2.3 OBSERVATIONAL CODING FORMS

FIGURE 1 Sample descriptive coding form.

FIGURE 2 Sample checklist for coding child behaviour.

FIGURE 3 Sample interval coding form.

 FIGURE 4 Sample interval coding form with antecedents, behaviours, and consequences.

In the figure are four different types of observational coding forms and the one that a clinician
would use would depend on the type of data they want to collect. Figure 1 is a simple coding
scheme in which the observer merely describes the behaviours they observe plus the antecedents
and consequences of these behaviours. Because the observer is describing the behaviours in
their own words, there is likely to be poor inter‐rater reliability using this scheme. Figure 2
provides a coding system that simply measures the frequency of selected behaviours. Figure 3
extends this by providing the frequency of selected behaviours over a period of time. This will
allow the clinician to see if there is anything interesting in the sequence or order that
behaviours are emitted. Finally, Figure 4 provides a coding scheme that allows the recording of
quite complex information, including the behaviour of the client in relation to others in the
situation, such as teacher and peers.

(From Nock & Kurtz, 2005)

One final form of clinical observation that is frequently used is known as self‐observation or self‐
monitoring. This involves asking the client to observe and record their own behaviour, perhaps by
using a diary or a smartphone to note when certain behaviours or thoughts occur and in what contexts
they occur. (Focus Point 2.4—Apps for Self‐Monitoring). This has the benefit of collecting data in real
time and overcomes problems associated with poor and biased recall of behaviour and events when
using retrospective recall methods (Strongman & Russell, 1986). The increasing use of electronic diaries
for self‐observation has come to be known as ecological momentary assessment(EMA) (Stone &
Shiffman, 1994; Dunton, 2017), and such methods have been used to gather information about client's
day‐to‐day experiences, to aid diagnosis, to plan treatment, and to evaluate the effectiveness of
treatment (Piasecki, Hufford, Solham, & Trull, 2007). In addition, self‐monitoring itself can have
beneficial effects on behaviour even prior to any attempts at intervention. For example, many
problematic behaviours (e.g., smoking, illicit drug use, excessive eating) can occur without the individual
being aware of how frequently they happen and in what circumstances they happen, and self‐
monitoring can begin to provide some self‐knowledge that can be acted on by the individual. As a result,
self‐monitoring often has the effect of increasing the frequency of desirable behaviours and decreasing
the frequency of undesirable behaviours (McFall & Hammen, 1971; Maas, Hietbrink, Rinck, & Keijers,
2013). This is known as reactivity, and clinicians can often take advantage of this process to facilitate
behaviour change (Figure 2.8).

self-observation A form of clinical observation that involves asking clients to observe and
record their own behaviour, perhaps by using a diary or a smartphone to note when certain
behaviours or thoughts occur and in what contexts they occur.
 self-monitoring A form of clinical observation that involves asking clients to observe and
record their own behaviour, to note when certain behaviours or thoughts occur, and in what
contexts they occur.

ecological momentary assessment (EMA) The use of diaries for self- observation or self-
monitoring, perhaps by using an electronic diary or a palmtop computer.

2.2.6 Cultural Bias in Assessment

A majority of the most widely used assessment methods have been developed on populations consisting
largely of people from a single cultural background and with a limited ethnic profile—that is, most tests
have been developed on White European or White American populations. Because of this fact, many
tests and assessment methods may be culturally biased and provide a less than accurate picture of the
mental health of individuals from different cultural backgrounds. As we shall see, these biases can
manifest in many different ways, and the clinician must be aware that such biases may affect both their
judgements and their diagnoses.

Examples of cultural anomalies in assessment and diagnosis

Cultural anomalies can be identified in a number of different ways. First, some ethnic groups score
differently on assessment tests than others. For example, American Asians tend to score significantly
higher on most scales of the MMPI than White Americans (McNulty, Graham, Ben‐Porath, & Stein,
1997). Second, Black Americans have a higher rate of diagnosis of disorders such as alcoholism or
schizophrenia whereas White Americans are more likely to be given the less stigmatising diagnosis of
major depression (Garb, 1998). Similarly, it was clear during the 1970s that West Indian immigrants to
the UK were significantly more likely to be hospitalised with a diagnosis of schizophrenia than
nonimmigrants or immigrants from other areas of the world (Cochrane, 1977). While this might be
considered as an ethnic difference in susceptibility to some psychiatric disorders, subsequent studies
suggested that many West Indian immigrants who had been hospitalised with a diagnosis of
schizophrenia lacked the symptoms commonly regarded as primary indicators for the disorder
(Littlewood, 1992), and this suggests that popular ethnic stereotypes may often be carried over into
medical and psychiatric practice (Arnold et al., 2004). As well as the apparent bias in assessment and
diagnosis in ethnic minorities, individuals from low socio‐economic groups may also experience bias.
For example, many clinicians tend to view clients from lower socio‐economic backgrounds as more
disturbed than those from higher socio‐economic groups (Betancourt & Lopez, 1993; Robins & Regier,
1991), and this may result from the clinician's stereotypes of different socio‐economic groups being able
to influence judgments made during unstructured interviews (Garb, 1997).

FOCUS POINT 2.4 APPS FOR SELF‐MONITORING

Smartphone apps are increasingly used by clinical psychologists and researchers to facilitate
patient and participant self‐monitoring of behaviours, symptoms, and moods. They are
convenient to carry and easy to use and provide information that can be sent electronically
from the smartphone to the relevant data collection point at any time. Two commercial
examples of apps for self‐monitoring are MoodPanda and MoodKit. MoodPanda allows the
individual to record their mood wherever they are, post the data to a central collection point,
and—if need be—collate data into a graphical format to view progress. The figure shows an
example of a mood chart produced by MoodKit.

However, even with sophisticated apps, self‐reporting of mood can still be very unreliable, and
apps are now being developed that can record mood changes throughout the day by detecting
telltale changes in a person's voice that indicate the emotional state they are in. Miller (2012)
provides a detailed review of previous psychological research using mobile electronic devices,
and Lv, Su, and Martin (2016) review a number of recent apps and provide evidence‐based
recommendations for the development of future apps.
FIGURE 2.8 Self‐Monitoring of Smoking Behaviour. This figure shows the results of a smoking self‐
monitoring task undertaken by a college student. The student was asked to record what they were doing each time a cigarette
was smoked and each time they were given random prompts by a palm‐top computer. Comparing the base rates (random
prompts) with smoking rates when in various situations allows the clinician to see whether certain situations are triggers for
smoking. In this case comparisons suggest that low grades and doing schoolwork represent triggers for smoking, whereas
being with family or partner usually elicits no cigarette smoking.
From Piasecki, Hufford, Solhan, & Trull, 2007.

Causes of cultural anomalies in assessment and diagnosis

The reasons for cultural differences in assessment and diagnosis are multifaceted and not simply due to
the fact that most structured assessment tools were developed without regard to cultural diversity. We
discuss some of the factors next, and these include (a) the fact that mental health symptoms may
manifest differently in different cultures, (b) language differences between client and clinician, (c) the
effect of cultural differences in religion and spiritual beliefs on the expression and perception of
psychopathology, (d) the way that cultural differences affect client–clinician relationships, and (e) the role
of cultural stereotypes in the perception of ‘normality’ and ‘abnormality’ in ethnic groups.
First, we saw in Chapter 1 that stress and mental health problems can actually manifest quite differently
in different cultures and Focus Point 1.3 provides two examples of this. Since the diagnosis of
psychopathology is based almost entirely on the presence of observable symptoms (especially in DSM)
then this will complicate and confuse the process of diagnosis when assessing clients from different
cultural backgrounds.
Second, language differences and difficulties can also create biases in assessment and diagnosis. For
example, a number of studies have suggested that the diagnosis that a client receives may depend
critically on whether they are assessed in their first or second language. Interestingly, when a client is
interviewed in their second language their symptoms are often assessed as significantly less severe than if
they are interviewed in their first language (Malgady & Costantino, 1998), and this appears to be
because undertaking an interview in a second language requires the client to organise their thoughts
better and therefore appear more coherent. However, this is not the only distortion that can affect
assessment and diagnosis. Some other studies have suggested that undertaking a diagnostic interview in
the client's second language can also result in symptoms being assessed as significantly more severe than
if it was in their first language, and this distortion seems to be caused by the client's misuse of words,
hesitations, and misunderstanding of questions suggesting a lack of coherent thought (Cuellar, 1998).
Third, differences in spiritual or religious beliefs between cultures can affect assessment and diagnosis.
For example, behaviour that may be considered as a symptom of psychopathology in one culture may
be seen as relatively normal or to have non‐psychological causes in other cultures. We saw in Chapter 1
that some cultural beliefs view unusual behaviour as evidence that the individual is possessed by evil
spirits rather than suffering mental health problems (Focus Point 1.2). Similarly, in some other cultures
visual or auditory hallucinations with a religious content may be considered to be a normal part of
religious experience rather than a sign of psychopathology, and the clinician may be faced with a client
who is not necessarily exhibiting the early symptoms of schizophrenia but is merely indulging in
religious experiences common to their culture (e.g., Rogler & Hollingshead, 1985).
Fourth, when facing a clinician who is a member of an ethnic majority, the client who is from an ethnic
minority is quite likely to experience apprehension and timidity, and this can affect the way that the
client presents themselves at interview and can also affect the clinicians view of their symptoms (Terrell
& Terrell, 1984; Whaley, 1998). For example, apprehension and timidity can often make the client seem
incoherent or withdrawn, and this would need to be disentangled from any similar symptoms that were
a true manifestation of psychopathology. In more extreme examples, the client from an ethnic minority
may be distrustful of a clinician from an ethnic majority, and clinicians in such a position need to be
flexible in their approach to assessment and diagnosis and to build a helpful therapeutic relationship by
candidly exploring issues of apprehension, timidity, and distrust (Whaley, 1997).
Finally, just like any other social interaction, a discussion between a client and clinician can be
influenced by racial and ethnic stereotypes. For example, stereotypes can significantly affect how
ambiguous information in an interview or a case report is interpreted. In an analogue study, Rosenthal
& Berven (1999) gave White American students a vignette providing unfavourable information about a
hypothetical client. For half the participants the client was described as White American, for the other
half he was described as African American. Subsequently, participants were given more favourable
information about the client. For those who believed the client to be White American, the more
favourable information influenced their final judgment, but for those who though he was a Black
American, the positive information failed to change their original negative view. Common stereotypes
held about African American and Hispanic clients by clinicians are that they are violent, hostile and
unmotivated for treatment (Pavkov, Lewis, & Lyons, 1989; Whaley, 1998), and these perceptions
undoubtedly affect their clinical judgments. Garb (1996) called this a confirmatory bias, whereby
clinicians ignore information that does not support their initial hypotheses or stereotypes, and they
interpret ambiguous information as supporting their hypotheses. In some cases these biased judgments
are the result of direct racism, but more often they are probably manifestations of indirect racism in
which the clinician is unaware of their stereotype biases. Whether direct or indirect racism is involved,
clinicians have a responsibility to learn about and eradicate their own stereotypes and prejudices and to
provide an honest and unbiased assessment process for clients from ethnic minorities (Hollar, 2001;
Adebimpe, 1994). To partially address these biases, most clinical psychology training courses now
incorporate cultural competency training to alert clinicians to potential cultural biases in assessment and
diagnosis (Benuto, Casas, & O'Donohue, 2018).

confirmatory bias A clinical bias whereby individuals with a mental health problem ignore
information that does not support their beliefs and they interpret ambiguous information as
supporting their beliefs.

Addressing cultural anomalies in assessment and diagnosis

Clinicians need to work hard to eliminate cultural bias from their assessment and diagnostic processes,
and this needs to be addressed at a number of levels, including eradicating bias from existing assessment
tools, developing new culture‐free assessments, adopting assessment procedures that minimise cultural
bias, and training clinicians to identify cultural and racial bias in their own thinking and in the
assessment processes that they use.
DSM has made some attempt to identify potential cultural anomalies in diagnosis by including a specific
section on Culture, Age and Gender factors within most diagnostic categories. For example, we note in
Chapter 16 that when diagnosing conduct disorder the clinician is asked to take account of the social
background of the client. In certain deprived inner‐city areas, behaviours characteristic of conduct
disorder may be seen as being protective and may represent the norm for that environment. They may
also serve an adaptive function in dealing with poverty and the threatening behaviour of others rather
than being symptoms of an underlying pathology.
In addition to this, clinicians need proper education and training when required to assess and diagnose
minority persons (Hall, 1997; Aklin & Turner, 2006). They would need to understand minorities'
construction of self, their understanding of illness, and their attitudes to mental health provision and
medicine in general (Littlewood, 1992). Sadly, clinicians from minority groups are often as ill equipped
to deal with the diagnosis of clients from minority groups as are their non‐minority colleagues, largely
because they have been trained in the same programmes (Turner, Herson, & Heiser, 2003), but the
increasing adoption of cultural competency training in clinical training courses is addressing this
problem by providing clinicians with appropriate awareness of cultural issues, relevant knowledge about
these effects, and practical skills in working with individuals from diverse cultural backgrounds (Moleiro,
2018).
Finally, we can attempt to aspire to culture‐free assessment methods by making tests and assessments
more valid and reliable. Aklin and Turner (2006) have advocated the development of structured
interviews to replace the current unstructured interview that is frequently the main vehicle for diagnosis,
and support for this view comes from studies indicating there are fewer problems with the assessment of
ethnic minorities when structured rather than unstructured methods of interviewing are used (Widiger,
1997). In addition, in 2010 the International Test Commission released guidelines for translating
assessments and tests from one language into another that would help avoid cultural anomalies resulting
from the translation process (International Test Commission, 2017). Sadly, however, studies suggest that
these guidelines are still frequently ignored (Rios & Sireci, 2014).

Summary
You can see from the preceding sections that cultural bias in assessment and diagnosis is a complex and
pervasive phenomenon. The clinician needs to be aware of the sources of any cultural bias in these
processes and should be reflective about their own potential stereotypes of ethnic minorities and the
effect this might have on their clinical judgments.
SELF‐TEST QUESTIONS
Define what is meant by test‐retest reliability, interrater reliability and internal reliability.
Define what is meant by concurrent validity, face validity, predictive validity, and construct
validity.
What are the main benefits and limitations of the clinical interview?
What is a structured interview? Can you provide an example of one?
What are the advantages of psychological tests as methods of assessment?
Can you describe a detailed example of a personality inventory?
How do projective tests differ from other types of psychological test?
Can you describe the features of at least one projective test?
What are the benefits and limitations of intelligence tests?
Can you name and describe at least two psychophysiological tests that might be used for
clinical assessment?
Can you name and describe three different neuroimaging techniques?
What are the benefits and limitations of clinical observation techniques?
What is ecological momentary assessment (EMA)?
Can you provide at least three examples of cultural bias in assessment and diagnosis?
Can you describe at least two studies that have identified some of the causes of cultural
bias in assessment and diagnosis?
 SECTION SUMMARY

2.2 METHODS OF ASSESSMENT

Test reliability measures whether the test will provide the same result when used by different
clinicians on different occasions.
Test validity measures whether an assessment method actually measures what it claims to
measure.
An unstructured clinical interview is probably the first contact a client will have with a clinician.
Structured interviews can be used to help make decisions about diagnosis and functioning.
One such example is the Structured Clinical Interview for DSM‐5 (SCID‐5).
Psychological tests are a highly structured way of gathering information about the client.
The most well‐known personality inventories are the Minnesota Multiphasic Personality
Inventory (MMPI) and the Big Five Inventory‐2.
Specific trait inventories are used to measure functioning in one specific area (e.g., depression).
Projective tests include the Rorschach Inkblot Test, the Thematic Apperception Test (TAT), and the
Sentence Completion Test.
Both IQ tests and tests of general ability, such as the Weschler Adult Intelligence Scale (WAIS),
are regularly used by clinicians.
Neurological impairment tests are used to measure deficits in cognitive functioning that may be
caused by abnormalities in brain functioning.
Psychophysiological tests can be used to measure emotional responding.
Neuroimaging techniques generate images of the brain that provide information on any
abnormalities in brain functioning.
Important neuroimaging techniques include computerised axial tomography (CAT), positron
emission tomography (PET), Single‐Photon Emission Computed Tomography (SPECT), magnetic
resonance imaging (MRI), and functional magnetic resonance imaging (fMRI).
Clinical observation techniques can be used to gather objective information about the
frequency of behaviours or the contexts in which behaviours occur.
Because assessment methods have usually been developed on populations from a single
cultural background, they often result in biased assessments when applied to individuals
from a different cultural background.

2.3 CASE FORMULATION

The various forms of assessment we have described in the previous section are all used by clinicians to
gather useful information about the client and their problems. Some clinicians use this information to
establish a psychiatric diagnosis (e.g., to determine whether the client's symptoms meet DSM‐5 criteria
for a specific disorder), whereas others use this information to draw up a psychological explanation of
the client's problems and to develop a plan for therapy. The latter approach, known as case
formulation, has been increasingly adopted over the past 25 years by clinicians who consider that
each client's problems are uniquely different and so require an individualised approach (Persons, 1989).
It is an approach also championed by those who view the psychiatric diagnostic model of
psychopathology as unhelpful in practice and stigmatising to clients (e.g., Boyle, 2007; Johnstone, 2017).

case formulation The use of clinical information to draw up a psychological explanation of

the client’s problems and to develop a plan for therapy.

Many practicing clinical psychologists will usually develop a case formulation when dealing with a
client, and this is an attempt to work towards explaining the client's problems in established theoretical
terms. In most cases, the explanation developed will also suggest interventions that may be successful in
resolving those problems, and it will be a precise account of the patient's problems that is a collaborative
exercise with the client, and is not imposed on the client (as psychiatric diagnosis might be). Persons
(1989) has described case formulation as having six components: (a) creating a list of the client's
problems, (b) identifying and describing the underlying psychological mechanisms that might be
mediating these problems (and the nature of the mechanisms described will depend on the theoretical
orientation of the clinical psychologist—see below), (c) understanding the way in which the
psychological mechanisms generate the client's problems, (d) identifying the kinds of events that may
have precipitated the client's problems, (e) identifying how these precipitating events may have caused
the current problems through the proposed psychological mechanisms, and (f) developing a scheme of
treatment based on these explanations and predicting any obstacles to treatment.
How a case formulation is constructed will depend on the theoretical orientation of the clinical
psychologist and, within an individual formulation, explanation of the client's problems will be couched
in terms of the psychologist's own preferred theoretical approach. For example, those who work within a
cognitive or behavioural model of psychopathology (see Chapter 1, Section 1.3.2) will attempt to find
explanations for the client's problems based on cognitive and behavioural causes—sometimes known as
an ABC approach. That is, they will attempt to identify the antecedents (A) to the problems, describe the
beliefs (B) or cognitive factors that are triggered by these antecedents, and the consequences (C) of these
events. For example, if a client suffers from panic attacks, the case formulation may discover that (a)
these occur in situations where there are crowds of people (antecedents); (b) that the client believes that
feeling hot, sweaty, and faint are signals for an impending heart attack (beliefs); and (c) the client
indulges in certain ‘safety’ behaviours designed to keep her ‘safe’—such as avoiding going out of the
house—but which reinforce the symptoms and beliefs (consequences) (Tarrier & Johnson, 2015). Based
on this knowledge, the clinical psychologist can begin to understand the factors that are causing and
maintaining these problems (e.g., the faulty beliefs and the ‘safety’ behaviours) and develop therapeutic
interventions to try and deal with these.
In contrast, psychologists who hold a psychodynamic perspective use formulations to address the way
that current problems reflect underlying unconscious conflicts and early developmental experiences and
will couch their formulations in these kinds of ways. For those psychologists who believe that a holistic
or systemic view of a person's problems is important (e.g., their problems can only be fully understood
within a family or social context), the formulation will be developed in terms of the important
relationships between the client and important other people in their life. For example, within the context
of the family, someone with a psychological problem may be seen as a weak and dependent person, and
this may influence how other members of the family treat the client, and determine what demands the
client may make on their family. Thus, the client's problems can be formulated as interactions between
various ‘actors’ (the family members) that may maintain the client's problems (Marzillier & Marzillier,
2008; Dallos & Draper, 2005). Figure 2.9 provides a simple example of a systemic formulation that
attempts to explain how a client's problems are maintained by the relationships between him and other
members of his family. Johnstone & Dallos (2013) provide a comprehensive guide to the different
approaches to case formulation, and the British Psychological Society's Division of Clinical Psychology
has provided a good practice guide on the use of psychological formulation (British Psychological
Society, 2011).
In many cases clinicians prefer to represent their formulations in a diagrammatic form that permits easy
identification of factors that may be causing the client's problems, and it also enables the clinician to
clearly explain the formulation to the client. Activity Box 2.1 provides a detailed and structured
example of how a formulation based on a cognitive‐behavioural approach could be attempted, and
provides an example of a formulation interview that the reader can attempt to interpret in terms of the
theoretical model provided. This example shows how the case formulation for a client suffering panic
disorder would be interpreted by a cognitive‐behavioural psychologist in terms of existing cognitive
models of panic disorder (see Chapter 6, Section 6.4). Once the diagram is completed this should
suggest some possible targets for interventions (e.g., using cognitive behaviour therapy to change
misinterpretations of bodily sensations and to prevent the use of safety behaviours, see Chapter 6)
(Activity Box 2.2).

FIGURE 2.9 A Systemic Case Formulation. Jack has problems with both drugs and drink. He
later became involved in petty crime, and was diagnosed as depressed. He also began to exhibit
paranoia and delusional ideation. This simple formulation shows how the reactions of Jack and his
mother and sister reinforce Jack's feelings of rejection and his abuse of drink and drugs.
From Dallos & Stedman, 2006.
Tarrier (2006) lists the various advantages of the case formulation approach: (a) it allows a flexible and
idiosyncratic understanding of each client's individual problems irrespective of individual diagnoses
they may have been given (i.e. in clinical practice, a client's problems do not usually fall into simple
diagnostic categories but may reflect a range of problems unique to that individual); (b) it is
collaborative and treats the client with regard; (c) it is firmly based on a theoretical understanding of
psychopathology (unlike diagnosis which is based entirely on a description of symptoms); (d) it can
include information about a client's past history (e.g., their exposure to risk factors) and the client's
personal, social, and family history; and (5) it allows the development of treatment strategies that can be
moulded to the specific needs of that individual client, and is especially advantageous in treating
complex cases that do not easily conform to standard diagnostic categories. Finally, there is growing
empirical support that the case formulation approach has genuine therapeutic benefits with comparison
studies suggesting that clients receiving case formulation approaches may have better outcomes than
those that have not received either an initial case formulation or frequent monitoring of progress based
on the formulation (Jacqueline & Lisa, 2015; Persons & Hong, 2015)

SELF‐TEST QUESTIONS
What are the main components of a case formulation?
Can you describe how a cognitive‐behavioural clinician and a psychodynamic clinician
might approach case formulation differently?

SECTION SUMMARY

2.3 CASE FORMULATION

A case formulation is used by clinicians to draw up a psychological explanation of a client's
problems and to develop a plan for therapy.
The clinicians' theoretical approach will determine how they explain the client's problems
and what information they require during the case formulation process.

2.4 CLASSIFICATION AND ASSESSMENT IN CLINICAL

PSYCHOLOGY REVISITED
This chapter began by discussing the reasons for wanting to classify mental health problems—it enables
sharing of knowledge about mental health and it enables sufferers to receive support that is appropriate
for their specific problems. However, with classification comes diagnosis, and there is still a lively debate
about whether classification and diagnostic systems such as DSM‐5 are valid (i.e., do they define ‘real’
problems or are they merely an artificial way of arbitrarily classifying symptoms?) or indeed useful (does
labelling someone with a psychiatric diagnosis help or hinder their recovery?)
This chapter has also reviewed the diverse and varied ways in which clinicians gather information by
which they can classify, understand, and treat the mental health problems brought to them by their
clients. This information is used to address a number of questions, including ‘Precisely what problems
does this person have?’, ‘What has caused their problems?’, ‘What is the best way to treat their
problems?’, and ‘Did our treatment work?’ By far the most common assessment method is the clinical
interview, and this may be entirely unstructured or may have a very rigid structure depending on the
nature of the information the clinician wants to gather (Activity Box 2.2 provides a good example of a
structured interview designed to gather very specific information about a client). However, as well as
benefits, the clinical interview also has many limitations. Its reliability is quite low, depends on the
client's willingness to provide valid information about themselves and their problems, and is prone to
cultural bias when clinician and client are from differing ethnic backgrounds. More structured ways of
gathering information include psychological tests, and under this heading we have reviewed personality
inventories, specific trait inventories, projective tests, and intelligence tests. Biologically based
assessments such as psychophysiological tests and brain neuroimaging techniques can be valuable for
confirming the validity of interview or pencil and paper tests and can often identify whether any
impairments in brain functioning may be underlying the client's problems. Finally, we have discussed the
use of case formulations, which have become a popular tool for clinicians of many theoretical
persuasions. The case formulation allows the clinician to draw up a psychological explanation of the
client's problems and to develop a plan for therapy, and this allows a flexible and personal
understanding of each client's individual problems.

This book is accompanied by Student and Instructor companion websites.

www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter References
Videos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
3
Research Methods in Clinical Psychology

ROUTE MAP OF THE CHAPTER

This chapter begins by describing what research is and then discusses a number of ways in
which research can be conducted, with special attention being paid to the role of scientific
method in clinical psychology research. The chapter then describes why clinical psychologists
might want training in research and what kinds of questions they are interested in addressing.
The bulk of the chapter is concerned with describing and evaluating a range of research
designs used by clinical psychology researchers. Finally, a chapter on research would not be
complete without a full discussion of the ethical issues that clinical psychologists are likely to
encounter while undertaking research.

CHAPTER OUTLINE
3.1 RESEARCH AND SCIENCE
3.2 CLINICAL PSYCHOLOGY RESEARCH—WHAT DO WE WANT TO FIND
OUT?
3.3 RESEARCH DESIGNS IN CLINICAL PSYCHOLOGY
3.4 ETHICAL ISSUES IN CLINICAL PSYCHOLOGY RESEARCH
3.5 RESEARCH METHODS IN CLINICAL PSYCHOLOGY REVISITED

LEARNING OUTCOMES
When you have completed this chapter, you should be able to:
1. Describe and evaluate a range of research methods that can be used in clinical psychology
research.
2. Describe the types of research questions that are central to clinical psychology research.
3. Critically evaluate the ethical issues relevant to clinical psychology research.
 I am a clinical psychologist. Among the health care professions, clinical psychology is one of the few to provide
extensive research training, and a clinical psychologist can be involved in both basic and applied research. Because
of the breadth of their training in research methods, clinical psychologists are well suited to design, implement, and
evaluate research and to conduct evaluations of the services provided by mental health care agencies. When you are
a practicing clinical psychologist, finding time to conduct research of any kind is difficult. But when I am involved
it helps me to satisfy my curiosity, to generate new knowledge on which more effective treatments may be based, and
to evaluate whether the current services we offer are effective.
Sarah's Story

Introduction
Why might a profession whose main aim is arguably to alleviate mental health problems want to do
research or be involved in research? Why are clinical psychologists given such a rigorous training in
research methods anyway—shouldn't they simply be taught how to help people recover from their
mental health problems? The personal account opening the chapter goes some way to answering these
questions. Even if they are simply offering a treatment‐based service, clinical psychologists should be
able to evaluate whether their services are effective and successful, and to do this with any degree of
objectivity requires a knowledge of scientific method. Sarah's Story reflects a widely‐held view that the
clinical psychologist should be thought of as a scientist‐practitioner or an applied scientist—
someone who is competent as both a researcher and a practitioner (Overholser, 2010). This view arose
in the early twentieth century when psychology was thought of as an experimental science. However, as
the discipline of psychology developed from being a pure research subject to an applied profession,
clinical psychology still maintained its links with universities and the academic world (Davey, 2019).
Indeed, in the UK, almost all clinical psychology training courses are based in university psychology
departments and have substantial research training components to them. The current view of the link
between research and practice that is held in the UK tends to be one in which scientific method is
systematically integrated into clinical work (Barker, Pistrang, & Elliott, 2015). Shapiro (1985) defined this
applied scientist view of clinical psychologists as (a) applying the findings of general psychology to the
area of mental health, (b) using only methods of assessment that have been scientifically validated, and
(c) doing clinical work within the framework of scientific method (see also Overholser, 2010). However,
this view of clinical psychologists, their approach to research, and how they use research is not as clear
cut as it sounds, and in order to understand how research is used by clinicians and integrated into their
role as mental health professionals we need to spend a little time understanding what is meant by (a)
research and (b) scientific method, and also we need to look at what value research might have within
the broader scope of psychopathology. For example, some researchers simply want to understand what
causes psychopathology, others want to know whether there is empirical evidence supporting the
efficacy of specific treatments, and others simply want a systematic way of understanding and
interpreting the symptoms of their clients.

scientist-practitioner Someone who is competent as both a researcher and a practitioner.

applied scientist Someone who is competent as both a researcher and a practitioner.

3.1 RESEARCH AND SCIENCE

3.1.1 What Is Research?

If you are a psychology student, you have probably already encountered a course designed to teach you
about research. You will probably have undertaken some practical classes designed to teach you about
research methods, and you will also have learned about the role that statistics plays in interpreting
research data. But did anyone actually tell you what research is in the first place? In general, psychology
considers itself to be either a biological or a social science, so the emphasis is on using scientific method
to understand human behaviour. But research can mean much more than this. In its broadest sense,
research is a form of investigation aimed at discovering some facts about a topic or about furthering
understanding of that topic through careful consideration or study. In this respect, research does not
necessarily have to adhere to scientific principles, and understanding of a topic may be enhanced in
many other ways. For example, we can learn a lot about human behaviour and human nature from
literature and the way that many classical authors describe everyday experiences and their
consequences. Many clinicians and psychotherapists claim that they gain understanding and knowledge
from their own clinical experiences that they can use systematically and successfully when treating their
clients (Morrow‐Bradley & Elliott, 1986). Even historical research can be used to further understanding
of psychopathology. In a systematic search of the historical literature on spiders and how humans have
perceived them over the centuries, Davey (1994) found that spiders had been traditionally linked with
the spread of disease and illness—a finding which may help us to understand why spider fear is so
prevalent in Western societies today. What is common to these different approaches is that they are
attempts to understand an issue through systematic and careful consideration of the relevant facts.
However, how we collect the facts that are relevant to our considerations can vary considerably.
Literature collects facts usually through the author's observations of life and everyday living which are
then presented within an unfolding story; historical research collects facts by accumulating evidence
from historical documents or artefacts; and the practicing clinician gathers facts from their everyday
experiences with clients. In each case, these facts can then be considered systematically in an attempt to
enhance our understanding.
In contrast, scientific method advocates that facts are collected in rather specific ways. Usually this
means that we should collect our facts for consideration in a systematic way defined by objectivity and
precise measurement (usually so that our collecting of facts can be replicated by others and our
conclusions verified by them). Because the scientific method is used predominantly in psychological
research and clinical psychology research, we discuss this approach in detail next.

3.1.2 Scientific Method

Scientific method espouses the pursuit of knowledge through systematic and thorough observation. It
also requires that research findings are replicable and testable.
By replicable, we mean that the results of the research have been collected under controlled
conditions that will allow any other researcher to reproduce those exact same findings. Researchers
using the scientific method attempt to achieve this by precise measurement of stimuli and behaviour
and accurate and complete description of the methods by which the data were collected. Replicability is
essential to the progress of scientific knowledge because it means that different researchers can be sure
that a research finding is a legitimate fact that can be relied upon when developing explanations of a
phenomenon. This is especially true in the case of human behaviour, where the subject matter is often
complex and may differ significantly from situation to situation. Activity Box 3.1 provides a discussion
of one of the seminal research papers in human psychopathology—the attempt by Watson and Rayner
(1920) to condition a phobia in an 9‐month‐old infant (see Chapter 6, Section 6.2.3). You will see from
this discussion that although this paper is often considered to be one of the founding pieces of scientific
research in psychopathology, the ability of other contemporary researchers to replicate it was limited—
largely because Watson and Rayner were less than systematic in the way they collected their data and
reported it.

SELF‐TEST QUESTIONS
Can you describe the main principles of the scientific method?
What is the difference between a theory and a hypothesis?
What do we mean when we say that decisions about the effectiveness of an intervention
should be evidence based?
What are the benefits and drawbacks with clinical psychology using the scientific method
as a model for research?
What is the ‘replication crisis’ in psychology?
What is social constructionism and how does it offer a different research approach to the
scientific method?

However, although we are one hundred years on from the ‘Little Albert’ experiment and we would have
expected experimental methods to have been refined and data reporting to be fully standardised, we are
still experiencing what is known as a ‘replication crisis’. This is an ongoing methodological crisis in
many sciences in which it has been found that many scientific studies are difficult or impossible to
replicate (Pashler & Wagenmakers, 2012). Focus Point 3.1 discusses some of the issues that this
replication crisis raises for clinical psychology research in particular.
As well as being replicable, research findings also need to be testable. By testable, we mean that a
scientific explanation is couched in such a way that it clearly suggests ways in which it can be tested and
potentially falsified. Scientific method often relies on the construction of theories to explain phenomena,
and a theory is a set of propositions that usually attempt to explain a phenomenon by describing the
cause–effect relationships that contribute to that phenomenon. Theories are expected to be able to take
into account all relevant research findings on a phenomenon and be articulated in such a way that they
will also have predictive value. That is, they should be able to predict what might happen in as yet
untested situations. Thus, a good theory will allow the researcher to generate hypotheses about what
might happen and to test these hypotheses in other research studies. If the hypotheses are confirmed in
these other studies the theory is upheld, but if the hypotheses are disconfirmed then the theory is either
wrong or needs to be changed in detail to explain the new facts. This process illustrates one of the
important distinctions between science and so‐called nonscience. Karl Popper (1959) proposed that
science must be able to formulate hypotheses that are capable of refutation or falsification, and if it is
not possible to falsify a theory by generating testable hypotheses, then that theory is not scientific, and in
Popper's view is of little explanatory value (this is a specific criticism that has been directed at Sigmund
Freud and his theory of psychoanalysis, see Chapter 1, Section 1.3.2).

theory A set of propositions that usually attempt to explain a phenomenon by describing the
cause–effect relationships that contribute to that phenomenon.
SECTION SUMMARY
3.1 RESEARCH AND SCIENCE
Research is about furthering understanding of a topic through careful consideration or
study.
Scientific method espouses the pursuit of knowledge through systematic observation, and
requires that research findings are replicable and testable.
The ‘replication crisis’ is an ongoing methodological crisis in many sciences in which it has
been found that many scientific studies are difficult or impossible to replicate.
A theory is a set of propositions that attempt to explain a phenomenon.
There is growing pressure for mental health services to recommend treatments whose
efficacy is evidence based.
Social constructionism is one research approach in clinical psychology that is an alternative to
the scientific method.

FOCUS POINT 3.1 IS THERE A REPLICATION CRISIS IN

CLINICAL PSYCHOLOGY?

The replication crisis in science emerged in the early 2010s when it was discovered that a
mixture of questionable research practices (QRPs) had been contributing to difficulties in
replicating many scientific studies (Pashler & Wagenmakers, 2012; Simmons, Nelson &
Simonsohn, 2011), and psychology was one of the major disciplines implicated in this
replication crisis.
Psychological research is at the centre of this controversy for a number of reasons. These
include (a) questionable research practices involving dubious ‘flexibility’ in data collection and
reporting, (b) not publishing data that do not fit in with expected results, (c) choosing when to
stop data collection (e.g., when statistical significance has been achieved), (d) manipulation of
outliers (arbitrarily deciding whether to leave in or take out outliers depending on the
hypotheses being tested), and (e) capitalising on grey areas of acceptable scientific practice (e.g.,
arbitrarily deciding how to measure constructs that are not directly observable). Astonishingly,
in one survey, a majority of over 2000 psychologists admitting using at least one of these
questionable research practices (Leslie, Loewenstein, & Prelec, 2012). These practices
individually and collectively have contributed to generating a ‘publication bias’ in which papers
with statistically significant effects are more likely to be published, and so this may motivate
researchers to use questionable research practices to establish significant effects that in reality
are either very weak or nonexistent—and therefore very difficult to replicate.
Clinical psychology research has been less implicated in this replication crisis than have other
areas of psychology, and there may be some positive reasons for this. For example, Tackett,
Brandes, King, and Markon (2019) mention that (a) sample sizes used in studies in clinical
psychology journals tend to be much larger (and so generate more statistical power) than studies
published in other areas of psychology (Fraley & Vazire, 2014), and (b) some of the areas of
research relevant to clinical psychology (such as personality psychology) do have high
replication rates, at least partially because of the large body of research that underlies the
 conceptualisation and measurement of personality traits (Soto, 2018).
However, Tackett et al. (2019) do mention some areas of concern within clinical psychology
research. These include (a) the fact that clinically related research that is expensive and time
consuming tends to use relatively small sample sizes (examples include clinical neuroscience and
treatment/intervention research such as randomised controlled trials, RCTs, see Chapter 4,
Section 4.2.2), and this can only raise the chances of unreliable research results caused by a lack
of statistical power (Button et al., 2013; Cuijpers, 2016); (b) much clinical psychology research
uses the Diagnostic and Statistical Manual of Mental Disorders (DSM) diagnostic criteria to define
participant groups, and we know that interrater reliability using DSM criteria is itself poor; (c)
there is a consistent publication bias towards significant results in intervention studies (e.g.,
randomised controlled trials, RCTs) resulting in a likely overestimation of treatment effects for
many categories of mental health problems; and (d) many randomised controlled trials testing
the efficacy of individual treatments or interventions often show what are known as ‘allegiance
effects’ (the tendency of treatment studies to support the theoretical orientation of the authors),
with some critics arguing that such authors may often wittingly or unwittingly use questionable
research practices (QRPs) to influence the outcomes of their studies (Leichsenring et al., 2017).
Attempts to eradicate questionable research practices and increase the transparency and
replicability of scientific research also need to be applied to clinical psychology research
(Tackett et al., 2019). Ways of doing this include ensuring that the materials used in research
(e.g., questionnaires, computer software) and the raw data collected are openly available for
scrutiny by others. One way of preventing questionable research practices during the research
process is to ensure that researchers preregister the details of their studies, such as how they will
be conducted and analysed. Finally, multiple collaborations can be utilised for both replications
and original research—ensuring that acceptable research practices are shared across different
research sites and centres (Open Science Collaboration, 2015).

hypotheses Tentative explanations for a phenomenon used as a basis for further investigation
or predicting the outcome of a scientific study.

Activity Box 3.2 provides an example of a psychological theory that attempts to explain why some
people develop panic disorder (see Chapter 6, Section 6.4). This is a theory that can be represented
schematically as a series of cause–effect relationships, and the sequence of cause–effect relationships
described in this theory are assumed to precipitate regular panic attacks in those diagnosed with panic
disorder. This relatively simple theory is constructed in such a way that we can generate a number of
testable hypotheses from it, and so we could potentially falsify the theory according to Popper's criteria
(Focus Point 3.2).

3.2 CLINICAL PSYCHOLOGY RESEARCH—WHAT DO WE WANT

TO FIND OUT?

3.2.1 How Does Clinical Psychology Research Help Us to Understand

Psychopathology?
Clinical psychology researchers use research methods in a variety of different ways to answer a number
of different questions. We will describe the range of research methods available to clinical psychologists
in the next section, but first let's briefly look at how research can help us understand psychopathology.
Research can have a number of immediate goals. These goals include description, prediction, control
and understanding (explanation), and a clinical psychology researcher may be using research methods to
achieve any one or more of these goals.
For example, description involves the defining and categorising of events and relationships, and a
researcher may simply want to find suitable ways of describing and categorising psychopathology. To
some extent this is what is represented in DSM‐5 (the categorising of psychopathology), but other
researchers have used research methods to discover whether different symptoms are related or co‐occur
(e.g., Conway et al., 2019). For example, Figure 2.2 in Chapter 2 provides an example of how research
methods have been used to understand how psychopathology symptoms are related, and such
categorisation of symptoms is a first step towards defining the biological or psychological mechanisms
that link different mental health problems.

description The defining and categorising of events and relationships relevant to

psychopathology.

FOCUS POINT 3.2 SCIENTIFIC METHOD AS A MODEL FOR

CLINICAL PSYCHOLOGY RESEARCH: THE PROS AND CONS

We have described what the scientific method is, but is it the best model by which to conduct
clinical psychology research? In many countries of the world, clinical psychology has either
explicitly or implicitly adopted the scientist practitioner model described in Section 3.1.2, with
the implication that practicing clinical psychologists are willing to at least call themselves
scientists by training even if they do not regularly practice as scientists. Nevertheless, in many
countries there is a growing pressure for mental health services to provide scientific evidence
that treatments and therapies are effective and economical. In the UK, one such agency that
attempts to assess and recommend effective forms of treatment for mental health problems is
the National Institute for Health and Clinical Excellence (known as NICE,
www.nice.org.uk). It does this primarily by recommending treatments whose efficacy can be
labelled as ‘evidence‐based. That is, whose efficacy has been proven through research using
the scientific method. There is thus some pressure from these agencies for clinical psychologists
to accept the scientific method—at least as a way of assessing the effectiveness of therapies—
and as a way of assessing the cost effectiveness of individual interventions, which is an
important consideration for agencies providing psychological services (e.g., Crow et al., 2013;
Radhakrishnan et al., 2013). However, as we shall see on numerous occasions throughout this
book, many forms of therapy are not couched in ways that make them amenable to assessment
through a traditional scientific approach (e.g., psychoanalysis). As a result, at least some
clinicians view processes designed to scientifically assess treatments (such as those reported by
NICE) as being ways in which those clinicians who support therapies derived from traditional
scientific approaches can impose their own view of what treatments are effective (Elliott, 1998;
Roth & Fonagy, 1996). Let us look at some of the benefits and costs of clinical psychology
adopting the scientific method in its research.

National Institute for Health & Clinical Excellence (NICE) An independent

UK organisation responsible for providing national evidence-based guidance on
promoting good health and preventing and treating ill health.
 evidence-based Treatments whose efficacy has been proven through research using
the scientific method.

There are a number of benefits to clinical psychology using the scientific method as a model for
research, and there is no doubt that clinical psychology has used its scientific status as a means
of acquiring prestige and establishing its status as an independent discipline within the field of
mental health (Davey, 2019; Lavender, 1996). However, clinical psychologists often consistently
fail to use research evidence to inform their treatments and instead rely on anecdotal clinical
experience (Dawes, 1994), with evidence suggesting that many clinical psychologists are not
consistently utilising NICE guidelines for evidence‐based best practice (Court, Cooke, &
Scrivener, 2016). If this is so, then there becomes a thin line between a clinician who bases their
interventions on unvalidated experience and a bogus psychotherapist who invents a so‐called
therapy whose basic tenets are not amenable to objective assessment. Keeping abreast of recent
developments in evidence‐based research is therefore an important component of good practice
for clinical psychologists, and scientific method provides the theoretical and empirical
developments by which the clinician can achieve this (Singer, 1980).
In contrast, at least some clinicians have argued that the scientific method in its strictest form
may not be suitable for clinical psychology research or practice. First, some writers claim that to
base clinical psychology research on strict scientific method aligns it too closely to the medical
model of psychopathology and invites many of the problems associated with a strict medical
model of psychopathology (see Chapter 1, Section 1.1.2) (Corrie & Callahan, 2000). Second,
while the scientist‐practitioner model is often seen as the model for clinical psychology, it is
seldom an ideal that is fulfilled in practice (Barlow, Hayes, & Nelson, 1984). For the clinical
psychologist, the need to alleviate a client's psychological problems is often more pressing than
the need to be scientifically rigorous. Similarly, the demands placed on overworked clinicians in
underresourced mental health services means that they are rarely likely to engage in any
meaningful research independently of their clinical practice (Head & Harmon, 1990) and will
certainly rank research as a priority significantly lower than their service commitment (Allen,
1985; Corrie & Callahan, 2000). The pressures of their work mean that they will often view the
research literature (whether based on scientific method or not) as irrelevant to their professional
practice (Barlow et al., 1984). Third, in contrast to scientific method, an alternative approach to
research in clinical psychology is one based on social constructionism (Burr, 1995;
McCann, 2016). This approach emphasises that reality is a social construction, and so there are
no basic ‘truths’ of the kind that we seek to discover using the scientific method. Instead,
knowledge consists of multiple realities that are constructed by people and may be historically
and culturally specific. It is claimed this approach has particular relevance in clinical psychology
because psychopathology frequently involves individuals creating their own realities (e.g., the
paranoid individual creates a reality in which everyone is against them, and the depressed
individual creates a reality in which they view themselves as worthless). These various realities
can be accessed through analysing language and social interactions, and so those who advocate
a social constructionist approach argue that the study of language and discourse is the only
means of understanding human experience and, as a consequence, human psychopathology
(Lofgren, Hewitt, & das Nair, 2014).

Social constructionism An approach to research in clinical psychology emphasising

that reality is a social construction, and so there are no basic ‘truths’ of the kind that we
seek to discover using the scientific method.

Despite the fact that at least some clinicians have adopted alternative frameworks (e.g., the
social constructionist approach), scientific method is still the most favoured model for research
in most areas of clinical psychology, including research on the causes of psychopathology
 (aetiology), research pursuing the development of new forms of treatment, and research
assessing the efficacy and cost effectiveness of treatments. Even though each person may
develop their own individual psychological reality, the fact that human beings are evolved
biological organisms means that there are almost certain to be general ‘truths’ or processes
common to all humans that can be discovered using scientific method. As a consequence, there
are also likely to be a set of general ‘truths’ or processes common to psychopathology across all
individuals.

Once we have been able to describe and categorise psychopathology then we are one step away from
prediction. A logical next stage is to use these descriptions and categorisations to help us predict
psychopathology. For example, we may know that certain childhood or developmental experiences may
increase the risk of developing psychopathology later in life, and one such list of these risk factors is
provided in Table 16.1 in Chapter 16. This table indicates how various forms of childhood abuse or
neglect can raise the risk of developing a range of psychopathologies (as one example, childhood
physical and sexual abuse increases the risk of developing adolescent eating disorders). However, while
research may have identified such experiences as risk factors, this does not imply a direct causal
relationship between the risk factor and the psychopathology—it merely indicates that the early
experience in some as yet unknown way increases the possibility that a psychopathology will occur.

prediction A statement (usually quantitative) about what will happen under specific conditions
as a logical consequence of scientific theories.

risk factors Factors that may increase the risk of developing psychopathology later in life.

The next aim of research would move beyond describing and categorising events to actually trying to
control them in a way that (a) provides us with a clear picture of the causal relationships involved, and
(b) allows us to develop methods of changing events for the better. In the case of psychopathology, this
latter aim would include using our knowledge of the causal relationships between events to control
behaviour so that we could change it—the basic tenet of many forms of treatment and psychotherapy.
One of the main tools for discovering causal relationships between events is the experimental method
that we will describe in more detail in Section 3.3. This approach is generally known as experimental
psychopathology because it is an experimental attempt to control individual variables in a way that
allows us to define the causal relationships underlying psychopathology (van den Hout, Engelhard, &
McNally, 2016). For example, a number of studies have indicated that experimentally inducing a bias to
interpret ambiguous events as threatening causes an increase in experienced anxiety (Wilson, MacLeod,
Mathews, & Rutherford, 2006). As a consequence this research suggests that if we can decrease this
interpretation bias in anxious individuals, it should significantly reduce the anxiety they experience (see,
for example, Treatment in Practice Box 6.4).

control Using our knowledge of the causal relationships between events to manipulate
behaviour or cognitions.

The final aim of research is understanding. That is, once we have described and categorised
psychopathology, and once we have begun to identify some of the causal factors affecting
psychopathology, we are probably at a point where we want to describe how all these factors interact,
and this will provide us with a theory or model of the phenomenon we are trying to explain. Activity
Box 3.2 provides a useful example of how researchers believe the various causal factors involved in
panic disorder interact, and it is the development of models such as this (describing the
interrelationships between events) that can add significantly to our understanding of psychopathology
and suggest practical ways of alleviating and treating symptoms.
 understanding A full description of how the causal factors affecting psychopathology
interact.

model A hypothetical description of a process or mechanism (such as a process or

psychological mechanism involved in psychopathology).

3.2.2 What Questions Do Clinical Psychologists Use Research to Try to

Answer?
Potentially we can use research methods to try to understand any aspect of psychopathology that might
interest us. Arguably, the primary aim of clinical psychology research is to further our knowledge and
understanding of psychopathology and its treatment, and one important aspect of this is an
understanding of the causes of psychopathology, and especially an understanding of the aetiology of
psychological and mental health problems. Although the term aetiology is mainly used in medical
settings to refer to the causes of diseases or pathologies, it is also a term widely used in mental health
research to describe the causes or origins of mental health symptoms. We will discuss in detail research
that has led to an understanding of aetiology in sections specifically set aside for this in later chapters
(see sections on Adult Mental Health and Child and Adolescent Psychopathology). One practical
implication of research into the aetiology of mental health problems is that understanding the causes of
psychopathology will inevitably suggest methods of intervention that might be used to alleviate those
problems. Once again, Activity Box 3.2 provides a useful example that illustrates this. The model of
panic disorder displayed in this box describes the causal factors that generate a panic attack that have
been identified using controlled research methods (Clark, 1986). Clearly, in this model, panic attacks are
precipitated by the individual catastrophically misinterpreting ambiguous bodily sensations. This implies
that attempting to control and change this tendency to catastrophically misinterpret bodily sensations
should help to reduce the frequency and intensity of panic attacks in panic disorder, and over the years,
interventions of this kind have been refined to a point where they offer successful treatment for many
suffering panic disorder (Waddington, 2019; Wells, 2006).

aetiology A term widely used in psychopathology to describe the causes or origins of

psychological symptoms.

To be useful in helping to understand psychopathology, research does not necessarily have to be carried
out on those who have mental health problems or who display symptoms of psychopathology. In
Chapter 1 we discussed the possibility that much of what is labelled as psychopathology is often just an
extreme form of common and accepted behaviours. That is, symptoms diagnosed as a psychological
disorder may just be more extreme versions of everyday behaviour. One good example is worrying.
Worrying is usually viewed as a perfectly normal reaction to the challenges and stressors encountered in
daily life and the activity of worrying may often help us to cope with these problems by enabling us to
think them through. However, once uncontrollable worrying becomes a chronic reaction to even minor
stressors it then begins to cause distress and interfere with normal daily living. Because symptoms
diagnosed as a disorder may just be more extreme versions of everyday behaviour, then what we find
out about activities such as worrying in nonclinical populations will probably provide some insights into
the aetiology of pathological worrying when it is a significant indicator of a psychological disorder such
as generalised anxiety disorder (GAD). Undertaking research on healthy, nonclinical populations in
order to shed light on the aetiology of psychopathology is known as analogue research, and such
research makes an important contribution to the understanding of psychopathology (Davey, 2003, 2017;
Vredenburg, Flett, & Krames, 1993).
Another important function of clinical psychology research is to determine the efficacy of treatments
and interventions. This includes testing the effectiveness of newly developed drug, surgical or
psychological treatments. Research may even try to compare the effectiveness of two different types of
treatment for a psychological disorder (e.g., comparing a drug treatment for depression with a
psychological treatment for depression). Such studies are not quite as simple as they may initially seem
because the researcher will have to compare those who undergo the treatment with those who do not,
and they will also have to control for extraneous factors that might influence improvement that are not
directly due to the therapy being tested (e.g., how attentive the therapist is, or the degree to which the
client participating in the study “expects” to get better). We will discuss therapy outcome research of this
kind in more detail in Chapter 4, but the interested reader may want to have a look at Mendelberg
(2018), or Clark et al. (2006) as examples of how intervention outcome research is conducted and
evaluated, and at Smith & Thew (2017) for consideration of the difficulties encountered when
attempting to conduct research in clinical practice.

analogue research Research on healthy, non-clinical populations in order to shed light on the
aetiology of psychopathology.

Finally, practicing clinical psychologists often have pressing questions that, for various reasons, they need
to answer. Very often these are questions of a practical nature related to their employment as mental
health professionals working in organisations that provide mental health services. For example, in the
UK, most National Health Service (NHS) service providers will want to ensure that the service they are
offering is effective, and this is known as evaluation research or clinical audit. Clinical audit uses
research methods to determine whether existing clinical knowledge, skills and resources are effective and
are being properly used, and the kind of questions addressed will include ‘what is the service trying to
achieve?’ and ‘how will we know if the service has achieved what it is trying to achieve’ (Barker et al.,
2015). In this sense, clinical audit does not add to the body of knowledge about psychopathology but is
an attempt to ensure that current knowledge is being effectively used. In particular, clinical audit is
intended to influence the activities of a local team of clinicians, rather than influencing clinical practice
generally (Cooper, Turpin, Bucks, & Kent, 2005), and clinical audit uses research methods to assess how
much end users value the services on offer, their satisfaction with these services, and what is perceived as
good and bad about the services offered (see Tulett, Jones, & Lavender, 2006, for an example).

evaluation research See Clinical audit.

clinical audit The use of research methods to determine whether existing clinical knowledge,
skills and resources are effective and are being properly used. Also known as evaluation research.

These, then, are some of the reasons why clinical psychologists do research. They include attempts to
answer pressing practical problems (e.g., what treatments are effective?) and attempts to add to the body
of knowledge about psychopathology (e.g., what causes specific mental health problems?). The next
section introduces you to some of the research methods that can be used to answer these questions.

SELF‐TEST QUESTIONS
Can you name four main goals of research?
What does the term aetiology mean?
What is analogue research?
What is clinical audit?
 SECTION SUMMARY

3.2 CLINICAL PSYCHOLOGY RESEARCH—WHAT DO WE WANT TO

FIND OUT?
The main goals of research are description, prediction, control, and understanding.
Clinical psychology research is often aimed at understanding the aetiology, or causes of
psychopathology.
Analogue research involves using healthy nonclinical participants or nonhuman animal studies
to understand psychopathology.

3.3 RESEARCH DESIGNS IN CLINICAL PSYCHOLOGY

There is a whole range of research designs that are relevant to clinical psychology research and the type
of method you choose will be determined by a number of factors, including (a) the nature of the
question you are asking (e.g., do you want to find out whether one event causes another or whether these
events are merely correlated?), (b) the nature of the population you are studying (e.g., is the
psychopathology you are studying rare, and so you only have access to a few participants?), and (c)
whether your research is at an early or advanced stage (e.g., you may simply want to be able to describe
some of the phenomena associated with a psychopathology rather than to explain its causes in detail).
The following represent examples of the main research designs used in clinical psychology research, and
other more specific examples can be found in the specialised Research Methods Boxes found in
individual chapters.

3.3.1 Correlational Designs

Correlational designs are among those most commonly used in clinical psychology research. The
aim of this methodology is to try and determine whether there is a relationship between two or more
variables. For example, is trait anxiety associated with worrying? Is body dissatisfaction associated with
excessive dieting in eating disorders? Is the availability of drugs associated with substance abuse in
adolescents? As long as we have valid and reliable ways of measuring the variables we want to study (see
Chapter 2, Section 2.2.1), then we can undertake a correlational analysis. Basically a correlational
analysis will tell you whether two variables co‐vary. That is, if the value of one measure is higher, then
does the value of the other measure also increase? In the examples we have just given, a positive
correlation between trait anxiety and worrying would indicate that, as trait anxiety increased worry
would also increase, and a positive correlation between body dissatisfaction and dieting would indicate
that as body dissatisfaction increased so too would dieting behaviour. Note that this does not imply a
causal relationship between the two variables and does not explain why they are related, it only indicates
that scores on one variable co‐vary with scores on the other variable. So, for example, a positive
correlation between trait anxiety and worrying could mean any of the following: (a) that increases in
worrying cause an increase in trait anxiety, (b) that increases in trait anxiety cause an increase in
worrying, or (c) that some other variable causes similar changes in both worry and trait anxiety (for
example, increases in depression could cause both increases in worrying and increases in trait anxiety).
So a correlational analysis is often a method that is used at the very beginning of a research programme
to simply try to map out how the relevant variables involved in a particular phenomenon inter‐relate.

Correlational designs Research designs which enable a researcher to determine if there is a

relationship or association between two or more variables.

To undertake a correlational analysis the researcher needs to obtain pairs of scores on the variables
being studied. For example, if you are interested in whether there is a relationship between trait anxiety
and worrying, you can ask participants to complete questionnaires measuring worry and trait anxiety.
You will then have two scores for each participant, and these scores can be entered into a spreadsheet
for a computer statistical package such as IBMStatistical Package for the Social Sciences(SPSS)
(Field, 2017), or the R programming language for statistical computing (Field, Miles, & Field,
2012). This will then compute a correlation coefficient (denoted by the symbol r) that measures the
degree of relationship between the two variables. The correlation coefficient can range from +1.00
through 0.00 to −1.00, with 1.00 denoting a perfect positive correlation between the two variables
(i.e., as scores on one variable increase, then scores on the other variable will increase), and − 1.00
denoting a perfect negative correlation between the two variables (i.e., as scores on one variable
increase, then scores on the other variables will decrease). A correlation coefficient of 0.00 indicates that
the two variables are completely unrelated. The relationship between two variables can also be
represented graphically in what is known as a scattergram, and Figure 3.1 provides three examples of
scattergrams representing three different types of relationships between variables. These scattergrams
show how the line of best fit differs with the nature of the relationship between the two variables
concerned. The statistical package that calculates the correlation coefficient and prints out the
scattergram for you will also provide you with an indication of the statistical significance of your
results. A researcher will want to know the degree to which their results occurred by chance, and if the
probability of their results occurring by chance is low then they can be relatively assured that the finding
is a reliable one. Traditionally, a correlation is considered statistically significant if the probability of it
occurring by chance is less than 5 in 100, and this is written as p < .05 (p stands for probability). From
the examples given in Figure 3.1 you can see that the correlations in both Figures a and b are
statistically significant (because the p values are less than .05). However, the correlation in Figure c is not
significant (because the p value is higher than .05), meaning there is probably no important relationship
between the two variables. (see also Focus Point 3.3 for a discussion of probability levels and effect sizes).

Statistical Package for the Social Sciences (SPSS) A computer program specifically
developed for statistical analysis for the social sciences.

positive correlation A relationship between two variables in which a high score on one
measure is accompanied by a high score on the other.

negative correlation A relationship between two variables in which a high score on one
measure is accompanied by a low score on the other.

scattergram A graphical representation showing the relationship between two variables.

line of best fit A straight line used as a best approximation of a summary of all the points in
a scattergram.
 statistical significance The degree to which the outcome of a study is greater or smaller
than would be expected by chance.

Correlational designs are valuable for clinical psychology researchers in a variety of ways. First, they
allow the researcher to begin to understand what variables may be interrelated and this provides a useful
first step towards understanding a particular phenomenon. Second, correlational designs are useful for
researching how individual differences and personality factors may relate to psychopathology. For
example, it would allow us to determine whether a personality factor, such as perfectionism, was related
to a psychopathology, such as obsessive‐compulsive disorder (e.g., Tolin, Woods, & Abramowitz, 2003).
Third, it would also allow us to determine whether certain experiences were associated with specific
psychopathologies, such as whether the experience of stressful events is associated with depression (e.g.,
Brown & Harris, 1978).
FIGURE 3.1 Correlation scattergrams.
In a questionnaire study, 132 female college student participants were asked to fill in valid and reliable questionnaires
measuring (a) the extent to which they worried, (b) their level of trait anxiety, (c) the degree of positive mood they exhibited
over the past 6 months, (d) their level of dissatisfaction with their body shape, (e) their current level of depression, and (f)
their height.
(a) This scattergram shows the relationship between worry scores and trait anxiety scores for the 132 participants. This
exhibits a positive correlation, and the line of best fit (the straight line) indicates this by showing an increasing trend.
The correlation coefficient calculated by SPSS was r = .66, and this was significant at p < .001.
(b) This scattergram shows the relationship between measures of positive mood and body dissatisfaction for the 132
participants. This exhibits a negative correlation, and the line of best fit (the straight line) indicates this by showing a
decreasing trend. The correlation coefficient calculated by SPSS was r = −.40, and this was significant at p < .001.
(c) This scattergram shows the relationship between measures of height and depression for the 132 participants. This
indicates that these variables are unrelated with the line of best fit (the straight line) showing neither an increasing nor
decreasing trend. The correlation coefficient calculated by SPSS was r = .01, with p > .80, and this was nonsignificant.
However, as we indicated earlier, correlational designs are limited. They certainly do not allow us to
draw any conclusions about causality, and they usually provide very little insight into the mechanism or
process that might mediate the relationship between the two variables that are correlated (see Focus
Point 3.3). We need to use other designs (such as the experimental design) to help us answer the question
of how the two variables are related.
3.3.2 Longitudinal Studies and Prospective Designs
An alternative form of correlational design is known as the longitudinal study or prospective
design. In the traditional correlational design, all measures are taken at the same point in time (known
as a cross‐sectional design, because the study simply takes a sample of measures as a ‘cross‐section’
of ongoing behaviour). However, in longitudinal or prospective designs, measures are taken at two or
more different times. In a longitudinal study, measures are taken from the same participants on different
occasions usually over extended periods of time. This may extend over many years, or in more long‐
term studies, over a participant's whole lifetime. Prospective studies take measures of the relevant
variables at a particular point in time (usually called time 1), and then go back to the same participants
at some future time and take the same or similar measures again (usually called time 2). Both
longitudinal and prospective designs enable the researcher to specify more precisely the time‐order
relationships between variables that are correlated. That is, because measures are taken from the same
participant at both times 1 and 2, the researcher can not only see whether there are correlations
between variables X and Y but also whether variable X measured at time 1 predicts changes in measures
of variable Y that occurred between times 1 and 2. A detailed example of a prospective design is give in
Research Methods Box 7.2 (Chapter 7) where a measure of negative attributional style at time 1 was
shown to predict increases in depression scores between times 1 and 2. This type of design enables the
researcher to understand the time course of relationships between two variables, and to determine
whether one variable predicts changes in a second variable. In the case given in Research Methods Box
7.2, a negative attributional style predicts future increases in depression, and can therefore be identified
as a risk factor for depression.

longitudinal study Research that takes measures from the same participants at two or more
different times in order to specify the time relationships between variables. This may extend
over many years or over a participant’s whole lifetime.

prospective designs Research that takes measures from the same participants at two or more
different times in order to specify the time relationships between variables.

cross-sectional design A research design that involves the collection of data from a sample
at just one point in time.

FOCUS POINT 3.3 CORRELATION AND CAUSATION

A significant positive correlation between two variables does not imply causation, nor does it
provide any real insight into why or how the two variables are related. Take the following
example:
There is a significant positive correlation between body piercings and measures of negative
mood (Skegg, Nada‐Raja,Paul & Skegg, 2007). Does this mean that body piercing causes
negative mood, or that negative mood causes a person to have body piercings? We certainly
can't tell from the correlation alone. However, the significant relationship between these two
variables may not even represent a causal relationship between them at all, but that they may
both be caused by some other third variable that was not measured in the correlational study. In
this case, both having body piercings and negative mood may be caused by some other variable,
such as (a) being young, and so being more likely to indulge in body piercing and experience
adolescent depression (Caliendo, Armstrong, & Roberts, 2005), (b) a tendency to indulge in risk‐
taking behaviours, and so more likely to be less socially conformist but negatively affected by
unusual experiences (Carroll, Riffenburgh, Roberts, & Myhre, 2002), or (c) substance abuse, and
so likely to be drawn to socially nonconformist cultures that might include body piercing as a
fashion statement as well as experiencing the negative emotions that are associated with
substance abuse (Forbes, 2001).
And it's not just correlational studies where we should be careful about assigning causality. We
should also not assume causality when we choose two different groups of participants on the
basis of differing characteristics (a mixed design, see Section 3.3.5). For example, in the summer
 of 2019 The Times and The Daily Mail newspapers ran stories about a study that they claimed
showed that “people with body ink (tattoos) were more likely to make impulsive decisions”
(Pinkstone, 2019; Ruffle & Wilson, 2019). The study asked 1,104 respondents whether they had
tattoos or not and then asked them to complete some short tests that measured impulsivity and
their tendency to engage in short‐sighted behaviours (i.e., accept a small immediate reward
instead of waiting a while for a larger reward). The study found that those with tattoos scored
significantly higher on the impulsivity tests than those without tattoos and also tended to exhibit
short‐sighted behaviour by accepting the immediate smaller reward rather than wait for the
larger reward. But what can we conclude about these results? We can conclude only that the
two groups differ on measures of impulsivity—but we don't know why from this one study. We
can't make the causal assumption, for example, that impulsive people are more likely to get
tattoos than nontattooed people. The reason for this is that while the two groups have been
selected on the basis of one characteristic (tattooed or not tattooed), they may also differ
significantly on many other characteristics (e.g., gender, wealth, employment type, age, etc.), and
it may be one of these other characteristics that plays a causal role in someone getting tattooed.

One example of a longitudinal study is the Dunedin Multidisciplinary Health and Development Study
—a longitudinal investigation of health and behaviour in a complete birth cohort
(http://dunedinstudy.otago.ac.nz). Participants in the study were born in Dunedin, New Zealand,
between April 1972 and March 1973, and over 1,000 of these individuals then participated in follow‐up
assessments at ages 3, 5, 7, 9, 11, 13, 15, 18, 21, 26, 32, 38, and 44 years (a future assessment is
scheduled for age 50 years). The study has enabled researchers to understand the time‐order
relationships between variables associated with health and psychopathology, and to understand how
some variables can be identified as predictors or risk factors for later behaviour. For example, using
prospective data from the Dunedin study, Reichenberg et al. (2010) found that children who grow up to
develop adult schizophrenia enter primary school struggling with verbal reasoning and lag further
behind peers in working memory, attention, and processing speed as they grow older.

3.3.3 Epidemiological Studies

Epidemiology is the study of the frequency and distribution of conditions such as mental health
problems within specific populations over a specified period of time. In this sense, epidemiological
research usually takes the form of a large‐scale survey, and tends to be descriptive in the sense that it
attempts to provide details primarily about the prevalence of mental health problems. However, it can
also be used to gather information about the factors that correlate with mental health problems, and this
can provide information about how a specific psychopathology affects people, whether it is more
prevalent in young people or old people, men or women, etc. It can also help us to understand what
some of the risk factors are for a specific psychopathologies, and whether the incidence of a mental
health problem is increasing or decreasing over time (see Focus Point 1.1). Epidemiological studies
are usually large‐scale ones, and need to have enough respondents in the survey to ensure that the
sample is representative of all types of person in the population being studied.

prevalence The number of instances of a given disease or psychopathology in a given

population at a designated time.

Epidemiological studies Research which takes the form of a large-scale survey used to study
the frequency and distribution of disorders within specific populations over a specified period of
time.
One of the main uses of epidemiological studies is to determine the prevalence rates of various mental
health problems, and prevalence rates can be described in a number of different ways. For example,
respondents in an epidemiological study can be asked (a) ‘Have you ever experienced symptoms of a
specific psychopathology in your lifetime?’ (Providing information on the lifetime prevalence rate of
a disorder), (b) ‘Have you experienced symptoms of a specific psychopathology in the last year?’
(Providing information on the one‐year prevalence rate of a disorder, e.g., Regier et al., 1993), or (c)
‘Are you experiencing symptoms of a specific psychopathology at the present time?’ (Providing
information on what is known as the point prevalence of a disorder, that is, the frequency of a
disorder in the population at any one point in time). You can see from these examples that prevalence
rates represent incidence x duration, and it is important to view prevalence in this way because some
disorders are of high incidence but low duration (e.g., bouts of depression), and some others are of low
incidence but long duration (e.g., schizophrenia). DSM usually provides information on either the
lifetime prevalence rates of a disorder or its point prevalence, and these are the kinds of statistics we will
be using when considering specific disorders in later chapters.

prevalence rates The representation of incidence by duration of a particular disorder.

lifetime prevalence The frequency of a disorder within a lifetime.

one-month prevalence The frequency of occurrence of a disorder in a population within

the past month.

point prevalence The frequency of a disorder in the population at any one point in time.

The benefits of epidemiological studies are that they provide information about the frequency of
mental health problems that can be used for planning health care services. They may also provide
information about the risk factors for various psychological disorders, which will help health service
providers to identify those who may be at risk of developing a mental health problem and so introduce
programmes designed to help prevent those problems. For example, excessive alcohol consumption in
pregnant mothers is a risk factor for infant fetal alcohol syndrome in the offspring, and prevention
programmes aim to identify those women at risk of alcohol abuse during pregnancy and to provide
interventions or alcohol‐reduction counselling (Floyd, O'Connor, Bertrand, & Sokol, 2006; Montag,
2016).
However, like all research approaches, there are some limitations to epidemiological studies. For
example, to provide valid descriptions of the prevalence rates of mental health problems in a particular
population, the sample used must be truly representative of that population. This is often difficult to
achieve because such studies will never attain a 100% response rate, and many respondents will often
refuse to take part. Studies suggest that those who are most likely to refuse to take part in an
epidemiological survey are men, individuals of low socio‐economic status, and individuals from ethnic
minority populations (Fischer, Dornelas & Goether, 2001), and this is likely to mean that the samples
used in most epidemiological studies are not fully representative of the population being studied.

3.3.4 Experimental Designs

Arguably one of the most powerful research designs is the experiment. This is a design in which the
researcher manipulates a particular variable and observes the effect of this manipulation on some
outcome, such as the participant's behaviour. For example, if we want to know whether negative mood
makes people worry, we can experimentally manipulate participants' moods and see if this changes the
extent to which they worry in the way we predicted. One important advantage of the experimental
design over many of the other research designs we will discuss is that it does allow the researcher to
determine whether there is a causal relationship between variables, and to identify the direction of the
causal effect. This is an important step in developing theories and models about the aetiology of
psychopathologies (Davey, 2019; Field & Davey, 2005).

experiment A design in which the researcher manipulates a particular variable and observes
the effect of this manipulation on some outcome, such as the participant’s behaviour.

Basic features of the experimental method

In most experiments the researcher manipulates one particular variable to assess its effects on a
particular outcome. Usually, the experimenter begins with an experimental hypothesis or
experimental prediction about what will happen. For example, we may predict that if we increase
negative mood, our participants will worry more, and this hypothesis is derived either from (a) an
existing academic or scientific theory about worrying, (b) our observations of worrying in everyday life,
(c) the existing research literature on worrying, or (d) the outcomes of other studies we have conducted
on worrying. The variable we are manipulating (in this case mood) is known as the independent
variable, and the outcome variable we are measuring (in this case worrying) is known as the
Dependent Variable (DV). However, imagine that our experiment involves simply increasing
negative mood and finding out that this increases the participants' tendency to worry. This is not as
informative as it seems because (a) simply changing a participant's mood in any direction (positive or
negative) may cause them to worry more; (b) if we use sad music to put our participants into a negative
mood, maybe is it just listening to music that makes them worry more (regardless of whether it is sad
music); or, more radically, (c) any participant taking part in any experiment may simply worry more.
This clearly indicates that to be able to make some valid conclusions about the effect of our
manipulation, we will have to compare our manipulation with some other conditions that control for
any confounding effects. These comparisons are known as control conditions. For example, suitable
control conditions in our example experiment would be to have a group of participants who undergo a
mood manipulation that increases positive rather than negative mood, and perhaps a third group who
undergo a similar manipulation that does not change mood at all. So, our experimental group may
listen to sad music that makes their mood more negative, our first control group may listen to happy
music that makes their mood more positive, and our second control group may listen to neutral music
that does not change their mood in either direction. Suppose now that, after the music manipulation,
participants in our experimental group worry more than participants in both the positive and neutral
control groups. This allows us to conclude that negative mood causes an increase in worrying, and
allows us to discount our other potential confounding explanations. For example, the increase in
worrying in the negative group is not a result of (a) a change in mood in any direction (because the
positive mood group did not show a similar increase in worrying), (b) simply listening to music (because
all three groups listened to music, but only the negative group showed an increase in worry), or (c)
simply being in an experiment (because our positive and neutral mood groups did not increase their
worry as much as the negative mood group). It is still possible, however, that the differences in worrying
between our three groups have occurred by chance, and just as much as the researcher using
correlational designs needs to conduct a statistical analysis to rule this out, so does the researcher using
experimental designs. This means that we need to have an objective way of measuring the outcome
(dependent variable) so that the data from the experiment can be subjected to an analysis using
inferential statistics, and we can then gauge how important the differences in worry between our groups
are (see Focus Point 3.4). In this case we need to find a way of objectively measuring the amount of
worrying that each participant indulges in after the mood manipulation.
experimental hypothesis A prediction about what the outcome of an experimental
manipulation might be.

independent variable (IV) The variable that is manipulated in an experiment.

Dependent Variable (DV) The outcome variable that is measured in an experiment.

control conditions Conditions within an experiment that control for any effects other than
that produced by the independent variable.

experimental group A group of participants who experience the independent variable in an

experimental study.

control group A group of participants who experience manipulations other than the
independent variable being investigated.

FOCUS POINT 3.4 FROM STATISTICAL SIGNIFICANCE TO

EFFECT SIZES

Traditionally, inferential statistics has used a very specific method for testing whether differences
between experimental groups are statistically significant (and are therefore unlikely to have
occurred by chance). This is known as null hypothesis significance testing (Field, 2017),
and the statistical tests we use tell us the degree to which the pattern of results we got could
have occurred by chance (the null hypothesis). In an experiment where we decide to look at
whether manipulating negative mood increases worrying and we find that measures of worry
are higher in the group that experienced negative mood we can create two simple hypotheses:
 null hypothesis significance testing The use of inferential statistics to establish
whether differences between experimental groups are statistically significant (and are
therefore unlikely to have occurred by chance).

null hypothesis A pattern of findings which is a result of chance rather than

experimental manipulation.

Null hypothesis: Increased levels of worrying were nothing to do with negative mood.
Alternative hypothesis: Increased levels of worrying were caused by negative mood.
When using statistics, you can only show that the null hypothesis is likely to be wrong (you can
never prove your alternative hypothesis). Traditionally, researchers have adopted a significance
level of p < .05 to decide whether the null hypothesis can be rejected. If p < .05, it means that
there is only a 1 in 20 chance that your experimental results occurred by chance, so are more
likely to have been caused by your experimental manipulation.
One problem with null hypothesis significance testing is that it led researchers to believe that
either an experimental effect existed (if p < .05) or it did not exist (if p > .05). However, selecting a
p level of .05 by which to reject the null hypothesis is entirely arbitrary, it merely tells us that the
null hypothesis is unlikely—it does not tells us that our experimental hypothesis is correct. In
addition, the p value calculated with inferential statistics can be influenced by many factors that
are not directly related to your manipulation. For example, the more participants you test in
your experiment, the more likely you are to get a p of less than .05—even when the measured
differences between the groups in your experiment are quite small (Cohen, 1990).
More recently, less emphasis has been placed on the importance of the actual p value (and
whether the null hypothesis might be rejected) and more on effect size. An effect size is simply
an objective and standardised measure of the magnitude of the difference between your
experimental condition and the control conditions. The larger the effect size, the more likely it
is that your results did not occur by chance. This provides a dimensional scale by which to judge
the importance of your results rather than an arbitrary categorical “all‐or‐none” decision
provided by null hypothesis significance testing. Many measures of effect size are used in
contemporary clinical psychology research, with the most common being Cohen's d and
Pearson's correlation coefficient r (Field, 2017, see also a special issue of Behaviour Research &
Therapy for discussion of best practice guidelines for modern statistical methods in applied
clinical research, Brown & Field, 2017).

effect size An objective and standardized measure of the magnitude of the effect
observed in a research study.

One other feature of designing experiments is in the assignment of participants to the various
conditions or groups in the experiment. Typically, researchers use random assignment of
participants to experimental conditions. This is to ensure that at the outset of the experiment, all groups
have participants with similar characteristics. In our example experiment, the findings of our study
would be compromised if we happened to have participants in our negative mood group who naturally
worried more than the participants in the other two control groups—even before we had completed our
experimental manipulations. This can usually be prevented by the random assignment of participants to
groups, and this should normally ensure that there are no statistical differences between the groups at
the outset of the experiment on characteristics that may influence the dependent variable.
 random assignment Assignment of participants to different treatments, interventions or
conditions according to chance.

Finally, both the experimenter and the participant may introduce bias into an experiment that can affect
the validity of the findings. For example, during an experiment, a participant may begin to think about
the purpose of the experiment and behave in a way that is consistent with these thoughts. When this
occurs, the participant is said to be responding according to the demand characteristics of the
experiment (i.e., what they think the experiment is about) rather than to the stimuli and events in the
experiment. Equally, the experimenter may unwittingly bias the results of an experiment. Because the
experimenter may know which of the experimental conditions a participant is in, and also knows what
the experimental predictions are for these conditions, the experimenter may provide subtle cues that
lead the participant to behave in the predicted way. To avoid experimenter bias of this kind a double‐
blind procedure can be used in which neither the experimenter nor the participant is aware of which
group the participant is in (i.e., a second experimenter may be employed simply to assign participants to
experimental conditions without the first experimenter, who runs the experiment, knowing). An
interesting example of implicit experimenter bias that we encountered in our lab when researching the
relationship between cognitions and OCD symptoms is related in my blog at
https://www.papersfromsidcup.com/graham‐daveys‐blog/an‐effect‐is‐not‐an‐effect‐until‐it‐is‐
replicated‐pre‐cognition‐or‐experimenter‐demand‐effects.

demand characteristics The features of an experiment which are the result of participants
acting according to what they believe is expected of them.

double-blind An experimental procedure in which neither the experimenter nor the

participant is aware of which experimental condition the participant is in.

Activity Box 3.3 introduces you to the kinds of questions that someone undertaking an experimental
study needs to ask when designing and analysing their experiment, and you should ensure you
understand the various concepts described in this section before attempting this activity.

Uses of the experiment in clinical psychology research

Experimental designs are used extensively in research into the aetiology of psychopathology (known as
experimental psychopathology). This is because the experiment is a powerful technique that allows the
researcher to establish the direction of causal relationships between events, and this is critical for our
understanding of the causes of psychopathology. Many research methods do allow us to say that two
variables may be significantly associated, but that is all—they do not tell us whether there is a causal
relationship between these events. For example, we know that depression is associated with low levels of
the brain neurotransmitter serotonin. But do low levels of serotonin cause depression, or does
depression cause a reduction in brain serotonin levels, or is some third factor involved in affecting both?
Only properly controlled experiments can answer some of these questions. However, having said this, it
is often difficult to carry out experiments with individuals with mental health problems. Experiments
involve manipulating critical variables, and this may mean exposing already vulnerable and distressed
individuals to even greater distress. Imagine doing our experiment on the effect of negative mood on
worrying with individuals diagnosed with GAD. These are people who already suffer chronic
uncontrollable worry at distressing levels, and our negative mood manipulation could make this even
worse. In order to avoid these ethical difficulties, many clinical psychology researchers carry out their
research in what are known as analogue experiments using analogue populations (see Davey,
2003, 2019). As we mentioned earlier (Section 3.2.2) analogue populations are usually participants
without any mental health problems and often consist of a normal sample of healthy, student
participants. However, for experiments on psychopathology undertaken with analogue populations to be
valuable we need to consider what makes them valid analogues of psychopathology processes. There
are at least three ways in which we can argue that analogue studies are valid:

analogue populations Populations that participate in mental health research but do not have
mental health diagnoses; they may be human or non-human animals.

1. It is being increasingly argued that psychopathology is dimensional rather than discrete. That is,
symptoms diagnosed as a psychological disorder may just be extreme versions of normal, everyday
behaviours and reactions (Krueger & Piasecki, 2002; Niles, Lebeau, Liao, Glenn, & Craske, 2012;
Olatunji, Williams, Haslam, Abramowitz, & Tolin, 2008). If so, then what we find out about these
behaviours and reactions in nonclinical populations will tell us something about the processes that
cause the more severe reactions found in clinical populations.
2. In the laboratory, we can use experimental manipulations to simulate mild psychopathology
symptoms in nonclinical participants. For example, in Chapter 6, the attention bias modification
procedure described in Treatment in Practice Box 6.4 demonstrates how nonclinical participants
might be made “anxious” by establishing in them a threat interpretation bias, which can then be
used to study how this “anxiety” might be alleviated (e.g., MacLeod & Mathews, 2012).
3. Nonclinical participants can be selected for an experimental study because they are similar to
individuals with psychopathology. For example, a good deal of research has been carried out on
college students who score high on measures of depression but at subclinical levels (Vredenburg et
al., 1993). Such participants do not usually have levels of depression that is clinically significant,
but it does allow an experimenter to compare how college students scoring high or low on
measures of depression might react to an experimental manipulation (see Davey, 2017, and van
den Hout, Engelhard & McNally, 2016, for further discussion of the use of human analogue
participants in experimental psychopathology).
Finally, analogue populations do not even have to be human to provide valuable information about
psychopathology. Animal studies are also a valuable source of information about basic processes that
might underlie psychopathology, especially when attempting to understand how brain function may
influence psychopathology (Belzung & Lemoine, 2011; Stewart & Kalueff, 2015). Animal models
allow researchers to experimentally investigate such factors as the genetics of a psychopathology (using
intensive breeding programmes), changes in brain biochemistry associated with specific
psychopathologies (such as changes in brain neurotransmitter levels associated with psychotic‐like
symptoms), and the effects of drugs on psychopathology (such as the effect of antidepressants on brain
biochemistry and behaviour) (e.g., Lavi‐Avnon, Yadid, Overstreet & Weller, 2005; Porsolt, Leipchon &
Jalfre, 1977). Animal studies have the advantage of having complete control over the organism's
developmental history (and so controlling genetic factors and factors affected by feeding and living
experiences), and permit the use of some experimental methods that would be considered too intrusive
to use with human participants (such as assessing the effects of electrical stimulation of the brain, and
the sampling of brain neurotransmitters). Nevertheless, even though many types of animal research are
legally licensed by governments, it is an area of research that has become increasingly controversial
because of changing views on the ethical implications of using nonhuman animals in scientific
experiments (Guidelines for the Use of Animals, 2018; Rollin, 2006).

Animal models The use of laboratory animals in research to simulate processes comparable
to those occurring in humans.

Another important use of the experimental design in psychopathology research is in studies testing the
effectiveness of treatments for mental health problems. These types of studies are often known as
clinical trials, and attempt to test whether (a) a treatment is more effective than no treatment, (b)
whether treatment A is more effective than treatment B, or (c) whether a newly developed treatment is
more effective than existing treatments. In a standard treatment efficacy experiment, researchers will
allocate clients or patients with a specific psychopathology (e.g., depression) to different experimental
conditions. The experimental group will receive the treatment manipulation whose efficacy is being
tested (e.g., a form of psychotherapy), and control groups will undergo other manipulations depending
on what comparisons need to be made. For example, if the researchers want to discover if the
psychotherapy treatment is more effective than a drug treatment, then a control group will receive the
drug instead of psychotherapy. The researchers will then measure symptoms at various points in time
after the two treatments to assess which is more effective (e.g., Leff et al., 2000; Ward et al., 2000).
Sometimes, researchers may want to assess whether a particular intervention is more effective than
simply doing nothing. However, this is not as simple a comparison as it sounds. Logically you would
imagine that a researcher would subject half the participants to the intervention, and allocate the other
half to a control condition in which they receive no treatment. Suppose the researcher wants to assess
the effectiveness of a drug treatment for depression. Just giving the experimental group a pill containing
the drug and giving the control group nothing has a number of problems. First, the experimental group
may get better simply because they are being giving a pill and this leads them to expect to get better. This
is known as a placebo effect, where a participant may improve simply because the procedure they are
undergoing leads them to believe they should or might get better. To control for this possibility, a
control group should be included in which the participants are given a pill that contains an inactive
substance (such as a sugar pill). This is known as a placebo control condition that controls for the
possibility that participants may improve simply because they are being given a pill regardless of what is
in the pill (Gupta & Verma, 2013). Nevertheless, suffice it to say here that the experimental method does
provide a useful paradigm for assessing the effectiveness of different interventions, but we will discuss
the complexities and limitations of this approach when we discuss treatment methods more thoroughly
in the next chapter.

clinical trials Experimental research studies used to test the effectiveness of treatments for
mental health problems.

placebo effect The effect when participants in a clinical trial show improvement even though
they are not being given a theoretically structured treatment.

placebo control condition A control group that is included in a clinical trial to assess the
effects of participant expectations.

Summary
The experiment is arguably the most powerful research tool that we have because it allows us to draw
conclusions about the direction of causality between variables, and this is the first step towards putting
together theories and models of how psychopathology is caused. However, in order to provide valid
results, experiments must be carefully designed and well controlled. Experiments are more than just
data collection exercises, and the experimenter needs to manipulate important variables in order to
discover causal relationships between events and behaviour. This means that in some cases the
experiment can be too intrusive for use with clients suffering psychopathology, and this means that many
of our studies investigating psychopathology need to be conducted on analogue populations such as
healthy volunteers and nonhuman animals.
3.3.5 Mixed Designs
One of the basic principles of experimental design is that participants must be assigned to different
groups on a random basis. However, this principle can be set aside if the research question being tackled
requires a mixed design. For example, suppose we wanted to see whether negative mood caused anxious
individuals to worry more than depressed individuals. In an experiment of this kind, we would still be
experimentally inducing negative mood (the experimental manipulation), but we would not be assigning
participants randomly to the experimental groups, we would want to ensure that in one experimental
group we only had anxious individuals and in a second experimental group we only had depressed
individuals. We would select the participants pre‐experimentally on the basis of these attributes and
assign them nonrandomly to each group. This is known as a mixed design because (a) we are
adopting elements from the experimental approach (i.e., we are manipulating an independent variable),
but (b) we are assigning our participants nonrandomly to the experimental groups. This is a design that
is used quite frequently in psychopathology research because the clinical psychology researcher may
often want to know if a particular variable will affect individuals with different psychopathologies in
similar or different ways. An example of a mixed design is a study by Sanderson, Rapee, and Barlow
(1989) investigating the effects of expectations on panic disorder. They preselected two groups of
participants: one group consisted of individuals diagnosed with panic disorder and the other group
consisted of individuals with no psychiatric diagnosis. They then subjected both groups to an
experimental manipulation. In this case, they asked all participants to inhale compressed air but told
them they were inhaling CO2 that could induce a panic attack. Even though the compressed air itself
could not have induced a panic attack, participants diagnosed with panic disorder were significantly
more likely to have a panic attack after the manipulation, suggesting that in such individuals the mere
expectation of a panic attack is likely to induce one.

mixed design Research which uses the non-random assignment of participants to groups in
an experiment.

Mixed designs are frequently used in treatment outcome studies, where the effectiveness of a particular
intervention is being assessed on individuals with different psychiatric diagnoses or with different
severity of symptoms. Figure 3.2 shows the results of a mixed design study carried out by Huppert et al.
(2004) designed to assess the effects of administering a placebo pill to three different groups of
participants, each diagnosed with a different psychiatric condition. In this study they found that their
experimental manipulation (the administration of a placebo pill) significantly reduced the severity of
reported symptoms in individuals diagnosed with social phobia and panic disorder, but not in
individuals diagnosed with OCD.
This example illustrates how useful the mixed design can be when attempting to assess how individuals
with different diagnoses or groups of symptoms will react to an experimental manipulation (such as a
treatment intervention). However, we must always be aware of the fact that one of the variables in a
mixed design (in this case the diagnostic groups) is not manipulated, and so we cannot infer a direct
causal relationship between the diagnostic category and the effects of the manipulation. For example, in
Figure 3.2 we cannot infer that the failure of the OCD group to improve after being given a placebo is
caused by the specific fact that they are suffering from OCD because we have not explicitly manipulated
that variable. It could be that some other variable related to OCD is causing the failure to respond,
such as having less faith in drug treatments generally, or individuals with OCD may be more resistant to
any treatment than those in the other groups (see also Focus Point 3.3).
FIGURE 3.2 Example of a Mixed Design. Differential response to placebo among patients with social phobia, panic
disorder, and obsessive‐compulsive disorder. American Journal of Psychiatry, 161, 1485–1487.
From Huppert, Schultz, Foa, & Barlow (2004).

3.3.6 Natural Experiments

Most experiments are the result of a deliberate manipulation carried out under controlled conditions by
an experimenter. However, in the case of clinical psychology research, nature may sometimes provide us
with the opportunity to observe the effects on behaviour of a natural manipulation. Natural
experiments usually allow us to collect data on the effects of events that we would not usually be able
to manipulate in the laboratory, and such events include natural disasters such as earthquakes and
floods, traumatic disasters or accidents such as the Grenfell Tower fire in London in 2017, or terrorist
attacks, such as those on the New York Trade Center of 11th September 2001 or the suicide bombing
attack on the Manchester Arena in 2017. For example, van Griensven et al. (2006) studied survivors of
the 2004 tsunami in southern Thailand, and found that the event had caused elevated rates of
symptoms of post‐traumatic stress disorder (PTSD), anxiety and depression in survivors of this event.
Other studies have used naturally occurring disasters as a tool to assess whether such events increase
psychopathology only in individuals with particular characteristics. For instance, Weems et al. (2007)
found that PTSD symptoms in children following the devastation caused by Hurricane Katrina in the
southern US in 2005 was highest in those children who had high levels of trait anxiety prior to the
disaster (Photo 3.1).

Natural experiments Research which allows researchers to observe the effects on behaviour
of a naturally occurring ‘manipulation’ (such as an earthquake).

Other variables that may play a part in the development of psychopathology include poverty and social
deprivation, and these are clearly factors that we could not easily manipulate in a controlled experiment.
However, Costello, Compton, Keeler, and Angold (2003) took advantage of the opening of a casino in
an American Indian reservation to study how poverty and conduct disorder in children might be linked
(see Chapter 16, Section 16.2.2). The introduction of the casino provided income that moved many of
the local families out of poverty, and Costello et al. found that this resulted in a significant decrease in
the symptoms of conduct disorder in local children—but only in those children whose families had
benefited financially from the introduction of the casino, suggesting either a direct or indirect link
between poverty and symptoms of childhood conduct disorder.
PHOTO 3.1 The Grenfell Tower fire 2017. Natural disasters and accidents—such as the 2017 Grenfell Tower fire in
London ‐ can be studied as ‘natural’ experiments in the sense that they allow clinical psychology researchers to collect data
on the psychological effects of events that we would not be able to manipulate in laboratory settings (e.g., Strelitz, Lawrence,
Lyons‐Amos, & Macey, 2018).

3.3.7 Single‐Case Studies

For a variety of reasons, clinical psychology researchers may study just one individual, and gather the
information and knowledge they require from detailed description and analysis of a single case. This
may take the form of a comprehensive case study in which the clinician gathers detailed information
about the individual, including details of symptoms, family history, medical history, details of personal
experiences, educational background, etc., and then attempts to ascertain what light these details may
cast on an understanding of the individual's psychopathology (Morley, 2017). In some respects, the case
formulation that clinical practitioners undertake when conducting therapy is a form of case study, in
which they attempt to understand the causes of an individual client's symptoms in terms of that
person's cognitions, experiential history, or personal relationships (see Chapter 2, Section 2.3). An
alternative form of the single‐case study is the single‐case experiment, in which a participant's
behaviour is observed and measured both before and after an experimental manipulation. The
researcher can then make some assumptions about what is happening by comparing the participant's
behaviour before the manipulation with their behaviour after the manipulation, and that individual then
acts as both experimental participant and control participant.
 case study An in-depth investigation of an individual participant.

single-case experiment A single case study in which a participant’s behaviour is observed

and measured both before and after an experimental manipulation.

Case studies
Before the development of sophisticated research designs, the case study was one of the most widely
used methods of collecting information about psychopathology, and knowledge collected in this way
often served as the basis for the development of early theories of psychopathology. One famous
exponent of the case study was Sigmund Freud himself, and many important features of psychoanalytic
theory were based on Freud's detailed observation and analysis of individual cases. One such example is
the famous case of Little Hans, a 5‐year‐old boy who had a fear of horses. In Chapter 6, Focus Point 6.1
describes how Freud studied this single case in detail and how it enabled him to develop his view that
many childhood fears were caused by a subconscious Oedipus Complex. In a different example in the
1940s, case studies of disturbed children provided the Austrian psychiatrist Leo Kanner with a set of
observations indicating a consistent set of symptoms that he called infantile autism, and which gave rise to
the symptom classification that we currently know as autistic spectrum disorder (see Chapter 17).
Case studies are valuable in a number of different circumstances. They are useful when there are only a
few instances of a particular psychopathology available for study. This was the case when dissociative
identity disorder (DID) (multiple personalities) was first reported as a specific disorder in the 1950s and
1960s, and an example of the use of case histories in the first descriptions of this disorder is provided in
Case History 14.1 in Chapter 14. Case studies are also valuable for providing new insights into existing
psychopathologies, and the detailed information that a case study can offer can often provide new ways
of looking at a particular problem and new facts that can subsequently be subjected to more rigorous
research methods (Davison & Lazarus, 1995), and the example of Kanner's discovery of infantile autism
through meticulous case studies of individual children is one such example. The case study can also
provide detailed information that may disprove existing theories. We saw in Section 3.1.2 that scientific
hypotheses can often be refuted or falsified by a single finding, and case histories are capable of
providing individual findings that are inconsistent with existing theories or explanations of a
psychopathology. For example, some theories of eating disorders such as anorexia nervosa propose that
dissatisfaction with body shape is a critical factor in developing an eating disorder. However, it would
only take one case history describing an individual who developed anorexia without exhibiting any body
dissatisfaction to question the universality of this theory.
Despite these benefits, the case study also has a significant number of limitations. First, and most
important, case studies lack the objectivity and control provided by many other research methods. For
example, the information collected by a clinical researcher in a case study is likely to be significantly
influenced by that clinician's theoretical orientation. Arguably, the detailed information on Little Hans
collected by Freud was significantly influenced by Freud's own theoretical views on psychopathology,
and it was quite likely that he collected and used only that information that was consistent with his
existing views. Freud clearly spent much time finding out about Little Hans' childhood whereas more
cognitively or behaviourally oriented psychologists would focus on current cognitions or those current
environmental factors that might be maintaining Little Hans' behaviour (see Chapter 1, Section 1.3.2).
Second, case studies are usually low on external validity. That is, the findings from one case are
rarely generalisable to other cases. For instance, because of the subjective nature of the information
collected by a clinician in a case study, how can we be sure the supposed causes of psychopathology in
that case study will also be true for other individuals with similar psychopathologies?
 external validity The extent to which the results of a study can be extrapolated to other
situations.

Finally, we have just argued that the case study can be valuable in providing evidence that could
disprove a theory, but because of the uncontrolled way in which case studies are collected it is not
particularly useful for providing evidence to actually support theories. For example, a case study may
indicate that a young woman with an eating disorder is dissatisfied with her body shape. This is
information that is consistent with theories of eating disorders that assume a role for body dissatisfaction,
but it is not evidence that differentially favours that theory because the case study does not (a) rule out
other explanations, or (b) indicate that body dissatisfaction plays a critical role in causing the eating
disorder.

Single‐Case experiments
The single‐case experiment has a particular value in psychopathology research and is used relatively
frequently. The main value of this method is that it enables the researcher (a) to undertake an
experimental manipulation (and so potentially make some inferences about causal relationships between
variables), and (b) to use one individual as both experimental and control participant. There is a
particular advantage to using a single participant and subjecting that individual to both experimental
and control conditions. First, in many psychopathology studies the use of a control group may mean
denying individual participants a treatment that they need. For example, if a researcher is attempting to
assess the efficacy of a particular treatment, they would have to compare the treatment with a control
group who did not receive that treatment. This obviously raises ethical issues about withholding
treatment from clients who may benefit from it. Second, some psychopathologies are quite rare, and it
can be quite difficult to gather enough participants to form groups of experimental and control
participants, and conducting an experiment on a single participant may be a necessity.
The single case experiment allows the experimenter to take some baseline measures of behaviour (the
control condition) before introducing the experimental manipulation (the experimental condition), and
behaviour during baseline can then be compared with behaviour following the manipulation. Most
single‐case experiments use variations of what are known as the ABA or ABAB design. In the ABA
design, an initial baseline stage involves the observation and measurement of behaviour without any
intervention (A), this is then followed by a treatment or manipulation stage where the experimental
manipulation is introduced and its effect on behaviour observed and measured (B), subsequently a final
return‐to‐baseline stage is then introduced (A) in which behaviour is once more observed in the absence
of the treatment or manipulation. The second baseline stage is included to ensure that any behaviour
change that occurs in stage B is caused by the manipulation and not any confounding factor such as a
natural drift in behaviour over time. In the ABAB design (sometimes known as a reversal design), a
second treatment or manipulation stage is introduced and provides extra power in demonstrating that
any changes in behaviour are explicitly due to the manipulation or treatment. Figure 3.3 provides an
example of the use of an ABAB design. This demonstrates the effectiveness of providing a social story
conveying information about appropriate mealtime behaviour for an individual with autism spectrum
disorder (Bledisoe et al., 2007). In this example, the effectiveness of the manipulation was demonstrated
by the fact that behaviours returned to baseline levels following the withdrawal of the manipulation (the
second A stage), and across all four stages the frequency of the measured behaviour fluctuated in
accordance with whether the experimental manipulation was present (B) or not (A).
 ABA design A single-case experiment which involves an initial baseline stage of observation
and measurement of behaviour without any intervention (A), followed by a treatment or
manipulation stage where the experimental manipulation is introduced and its effect on
behaviour observed and measured (B). A final returnto-baseline stage is then introduced (A) in
which behaviour is once more observed in the absence of the treatment or manipulation.

FIGURE 3.3 Example of a single‐case experimental ABAB design. The participant in this study was a 13‐year‐old
male with Asperger's syndrome and attention deficit hyperactivity disorder (ADHD) (see Chapter 17) who exhibited a
number of eating‐related problems (e.g., talking with mouth full, spilling food, talking in a loud voice, etc.). Days 1–7
show the baseline levels of spills (a ‘bad’ response) and mouthwipes (a ‘good’ response) (The first ‘A’ phase). The
intervention used (phase ‘B’) was a social story provided to the participant to help him improve his eating habits. The figure
shows how good eating behaviours tended to increase and bad behaviours tended to decrease in frequency during the
intervention phases, but return to normal during baseline phases.
From Bledsoe et al. (2007).

ABAB design A single-case experiment, similar to the ABA design, with the addition of a
second treatment or manipulation stage, providing extra power in demonstrating that any
changes in behaviour are explicitly due to the manipulation or treatment.

One disadvantage to the ABAB design is that it alternates periods of treatment with non‐treatment, and
this may be problematic if the study is assessing the effectiveness of a treatment that has important
benefits for the participant (e.g., it prevents self‐injurious behaviour or alleviates distress). This can be
overcome by using a multiple‐baseline design (e.g., Coon & Rapp, 2017). There are two variations
to this procedure: (a) using a single participant, the researcher can select two or more behaviours to
measure and can target the treatment or manipulation on one behaviour but allow the other behaviours
to act as control comparisons; or (b) the researcher can use multiple participants by first taking baseline
measures from each (stage A), and then introducing the treatment or manipulation (B) successively
across the participants. The multiple baseline design means that each individual within the study can
receive the treatment for a maximum amount of time without compromising the experimental balance
of the study (e.g., Thompson, Kearns, & Edmonds, 2006).

multiple-baseline design An experimental design in which the researcher studies several

behaviours at a time.

While the single‐case experiment has a number of significant benefits, it too has some limitations. Most
important, it is still a single case study, so it may be difficult to generalise the results to other individuals
with similar psychopathologies—just because a treatment works for just one person, does not necessarily
mean it will work for another. Group designs overcome this problem by using statistical inference across
a number of participants to determine the probability that the findings from the study will be
generalisable to a larger population. However, the problem of generalisability can be overcome to some
extent by using more than one participant. If the treatment or manipulation is effective across more
than one participant then this increases the chances that it will be generalisable to other individuals.

3.3.8 Mediators and Moderators

We have previously described how experiments are powerful means of determining whether there is a
causal relationship between the independent variable (IV, the variable that we are manipulating in the
experiment) and the dependent variable (DV, the outcome variable that we are measuring) (see Section
3.3.4). However, statistical analyses now make it possible for us to determine whether a third variable
actually mediates the relationship between the IV and the DV that we discovered in our experiment (the
mediator). These analyses even allow us to discover whether a third variable is mediating the
relationship we might find between two variables in a simple correlational study (Baron & Kenny, 1986).
For example, in an experiment we may manipulate negative mood and discover that increases in
negative mood cause an increase in measures of worry frequency. We may also find that a measure of
the type of worry rule that a participant uses that we have taken during the experiment fully mediates
this causal relationship between negative mood and worrying (Dash & Davey, 2012). Mediation analysis
works by partialling out the relationship between the IV and the mediator from the relationship between
the IV and the DV, and after this, if there is no remaining significant relationship between the IV and
the DV, then the mediator fully accounts for the relationship between the IV and the DV (Hayes, 2018).
In this sense, the mediation analysis is an attempt to explain ‘how’ or ‘why’ an effect occurs.
A slightly different concept is the notion of a moderator. A moderating variable is one that affects the
strength of the relationship between the IV and the DV. For example, it is well known that stress affects
quality of life, yet the relationship between stress and quality of life depends on the amount of social
support an individual receives—someone who experiences a lot of stress but has good social support will
score higher on measures of quality of life than someone who has low social support (Cohen & Willis,
1985). In this case, social support is a moderating variable because it affects the strength of the
relationship between the predictor and outcome variables.
Understanding how causal relationships between variables are mediated and moderated is one of the
first steps to building up more complex theoretical models of how psychopathology symptoms are
caused, and Figure 3.4 provides a diagrammatic representation of the differences between mediators
and moderators. (See also https://www.youtube.com/watch?v=WZr1jlKi_s0 for a helpful description
of the differences between mediators and moderators).
FIGURE 3.4 Mediators and moderators. Illustration of variable M mediating the relationship between variables X and
Y where variable Z moderates the path from X to M, M to Y, and/or the path from X to Y (see text for further
elaboration).
Adapted from Tyron (2018).

3.3.9 Meta‐Analyses and Systematic Reviews

Many different researchers frequently conduct studies investigating the same or similar phenomena, so it
is usually the case that we end up with many studies providing information on the same issue. For
example, we may want to know whether cognitive behaviour therapy (CBT) is a successful treatment for
depression, and many different researchers may end up conducting studies and experiments to this end.
Some of these studies may convincingly demonstrate that CBT is effective, some others may suggest
that its effectiveness is marginal, and still others may fail to provide any evidence for its effectiveness. So
how do we decide which studies to believe, and how do we try to make an informed decision about the
effectiveness of CBT in treating depression? Traditionally, this task would have been undertaken in
review articles in which the reviewer would collect together all the relevant studies, and try to make an
informed judgement across the whole range of studies and their results (e.g., Brewin, 1996; Laidlaw,
2001; Marcotte, 1997). However, this approach is likely to be highly subjective, and one reviewer may
significantly disagree with another about the importance of individual studies and some researchers
with vested interests in particular types of treatment may consciously or unconsciously bias the way they
interpret findings (e.g., those favouring drug treatments for depression are likely to be less convinced by
studies demonstrating the effectiveness of CBT than others) (Field, 2013).
These problems with subjective reviews have led to attempts to develop more objective reviews using
standardised review procedures and statistical methods. Meta‐analysis and systematic reviews are
the outcome of this process, and are now becoming accepted ways of objectively assessing the strength
of findings across different studies. A systematic review is a review of a clearly formulated question that
uses systematic and explicit methods to identify, select, and critically appraise relevant research, and to
collect and analyse data from the studies that are included in the review. Guidelines for collecting and
reporting clinically‐relevant systematic reviews are provided by groups such as PRISMA (Preferred
Reporting Items for Systematic Reviews & Meta‐Analyses, http://www.prisma‐statement.org),
QUORUM (Quality of Reporting Meta‐Analyses) (Moher, Liberati, Tetzlaff, Altman, & The PRISMA
Group, 2009), and the American Psychological Association (MARS, Meta‐Analysis Reporting
Standards) (Cooper & Hedges, 2019). Figure 3.5 provides an example of a flow‐chart provided by
PRISMA for recording and reporting how studies for a systematic review were sourced and collated.

Meta-analysis A statistically accepted way of assessing the strength of a particular finding

across a number of different studies.

systematic review A review of a clearly formulated question that uses systematic and explicit
methods to identify, select, and critically appraise relevant research, and to collect and analyse
data from the studies that are included in the review.

In addition to a systematic review, a meta‐analysis attempts to detect trends across studies found through
systematic review that may have used different procedures, different numbers of participants, different
types of control procedures, and different forms of measurement, and it does this by comparing effect
sizes across studies. An effect size is an objective and standardised measure of the magnitude of the
effect observed in a study (i.e., the difference in measured outcome between participants in a treatment
or experimental group and those in appropriate control conditions) (see Focus Point 3.4), and the fact
that it is standardised means that we can use this measure to compare the outcomes of studies that may
have used different forms of measurement. Meta‐analyses are now an almost accepted way of
overviewing an area of studies that address the same or a similar research issue, and are particularly
popular as a statistical tool for assessing the effectiveness of interventions for psychopathology (for
examples see Cuijpers, Cristea, Karyotaki, Reijnders, & Huibers, 2016; De Maat, Dekker, Schoevers, &
De Jonghe, 2006; Hanrahan, Field, Jones, & Davey, 2013).

effect size An objective and standardised measure of the magnitude of the effect observed in a
research study.

While many meta‐analyses have been carried out specifically on the effectiveness of individual
treatments and interventions, the basis of comparison can be other factors such as type of
psychopathology being treated or the comparison of drug treatments generally versus psychotherapy
interventions. One of the earliest meta‐analyses was a large‐scale study carried out by Smith, Glass, &
Miller (1980) assessing whether psychotherapies were more effective than no treatment at all. From the
results of their meta‐analyses they concluded that (a) a very wide range of psychotherapies were more
effective at reducing symptoms of psychopathology than no treatment at all, and (b) perhaps more
controversially, that effect sizes did not differ significantly across different types of psychotherapies—
implying that all psychotherapies were equally effective (see also Focus Point 4.4)!
Nevertheless, while a meta‐analysis may seem like an objective solution to the problem of reviewing the
findings from groups of studies, this method too has its limitations. First, meta‐analyses frequently rely
almost entirely on analysing the results of published studies, and published studies are much more likely
to have significant results than nonsignificant results (Dickersin, Min, & Meinert, 1992). This means that
meta‐analyses are likely to overestimate mean effect sizes because they are unlikely to include
unpublished studies that are probably nonsignificant. The result is that they are probably biased towards
claiming that a variable or treatment is effective when it may not be (Field, 2013). Second, effect sizes
will be influenced by the quality of the research (e.g., whether the control conditions are adequate or
whether outcome measures are accurate and sensitive), but meta‐analyses include all studies equally and
do not take into account the quality of individual studies. The researcher undertaking a meta‐analysis
can overcome this problem by comparing effect sizes in ‘well‐conducted’ and ‘badly conducted’ studies
(Field, 2013), but this then involves the researcher in making some subjective judgements about what is
‘good’ and ‘bad’ research (Eysenck, 1994). There is even the possibility that meta‐analyses might
become a self‐perpetuating form of analysis, with at least some studies now attempting meta‐analyses of
meta‐analyses (e.g., Butler, Chapman, Forman, & Beck, 2006)!

FIGURE 3.5 An example of a flow chart for recording and reporting how studies for a systematic review are sourced
and selected.
From Moher et al. (2009). For more information, visit http://www.prisma‐statement.org.
3.3.10 Qualitative Methods
So far we have mainly discussed those research methods that place an important emphasis on accurate
and valid measurement of behaviour and attempt to draw conclusions from their studies on the basis of
statistical inference. These methods tend to be collectively known as quantitative methods, but there
is a growing body of research methodologies in clinical psychology that do place less emphasis on exact
measurement and statistical analysis, and these are known as qualitative methods. Instead of
emphasising mathematical analyses of data, the raw material for qualitative research is ordinary
language, and any analysis is verbal rather than statistical. The raw data in qualitative studies are
usually the participant's own descriptions of themselves, their experiences, their feelings and thoughts,
their ways of communicating with others, and their ways of understanding the world. Study samples are
often small, and data are collected using unstructured or semi‐structured interview techniques that can
be analysed in a variety of nonstatistical ways. Qualitative methods are particularly suited to clinical
psychology research because they enable the researcher to gain an insight into the full experience of
psychopathology, including the sufferer's feelings, ways of coping, and the specific ramifications that the
psychopathology has on everyday life (see Research Methods in Clinical Psychology Box 3.1). In recent
years, qualitative methods have provided information relevant to scale development, informed theories
of psychopathology, and provided explanations for unusual research findings and unusual case histories
(Harper, 2017; Harper & Thompson, 2011; Nelson & Quintana, 2005; Rennie, Watson, & Monteiro,
2002; Willott & Larkin, 2011;).

quantitative methods Research methods that place an important emphasis on accurate and
valid measurement of behaviour and attempt to draw conclusions from their studies on the
basis of statistical inference.

qualitative methods Research methods that rely on the analysis of verbal reports rather than
on statistical analyses of quantifiable data.

RESEARCH METHODS IN CLINICAL PSYCHOLOGY BOX 3.1

A QUALITATIVE STUDY OF DENTAL PHOBIA
This example is based on a paper by Abrahamsson, Berggren, Hallberg, and Carlsson (2002)
and gives you an insight into how qualitative methods might be used in clinical psychology
research. The following sections describe the aims of the study, how it was conducted, and how
the results were analysed to provide a theoretical perspective on the experience of dental
phobia.

AIMS
To explore the situation of dental phobic patients and to investigate (a) how their dental phobia
interferes with their normal routines, their daily functioning and their social activities and
relationships, (b) what factors contribute to the maintenance of their phobia, and (c) how they
cope with their fear.

STUDY SAMPLE
18 patients applying for treatment at a specialised dental fear clinic in Gőteborg, Sweden. All
patients were currently refusing dental treatment because of their phobia.

IN‐DEPTH INTERVIEWS
Audiotaped, open‐ended interviews were conducted with each participant. The purpose of
using open‐ended interviews was to explore the situation of dental phobics as expressed by the
participants themselves. An interview guide was used as a basic checklist to make sure that
relevant topics were covered. These included onset of dental fear, family, experiences in dental
care, health and effects on everyday life, coping strategies. Interviews were introduced with
questions such as ‘Does your dental fear have an impact on your daily life?’, ‘In what way?’,
‘What do you do?’, ‘feel?’, etc.

ETHICAL ISSUES
It was stressed that participation was voluntary, all data collected would be confidential, and the
participant had the right to end participation at any time. All participants completed and signed
an informed consent form.

ANALYSIS OF DATA
Interview transcripts were analysed using grounded theory (seeSection 3.3.10). The aim of this
method is to focus on different qualities of phenomenon in order to generate a model or a
theory. Different qualities of phenomena might include psychosocial processes, existing
problems caused by dental phobia, how participants coped with their problems, etc. This
process should be conducted with the original aims of the study clearly in mind. The interviews
were analysed line by line and broken down into segments reflecting their content, segments
with similar contents were then grouped together to form more abstract categories

EXAMPLES OF FORMING ABSTRACT CATEGORIES

One participant expressed the following: ‘What I'm most afraid of is that infections will spread. I've had
a lot of colds in the last year… I don't know if it has anything to do with my teeth. I only know that I've waited
much to long’. Another participant said ‘The idea of having false teeth at 45, then I'd be at rock bottom…I
don't know if I could handle it psychologically’. Similar comments made by a number of participants
led the researchers to create the abstract category Threat to own health to describe this
group of responses.
Similarly, participants also provided responses of the following kind: ‘My worries about going to the
dentist are a matter for me and me alone…maybe I could tell someone but they probably wouldn't care at all’
and ‘A friend said he had booked an appointment for me [at the dentist] and I went completely cold. When the
time got nearer [for the appointment] I saw the date couldn't be right and understood that it was a joke’. These
and similar responses were grouped into the abstract category of Lack of social support
and understanding.

CONCLUSIONS
This analysis allowed the researchers to construct a model or theory of the experience of dental
phobia which is represented schematically below. Four main categories of experience were
developed: threat to self‐respect and well‐being, avoidance, readiness to act, and ambivalence in
coping. This provides a rich description of how dental fear affects the daily lives of these
individuals and how social and psychological factors interact to determine how they cope with
this fear.
 Taken from Abrahamsson, Berggson, Hallberg, and Carlsson (2002).

Barker, Pistrang, and Elliott (2002) provide a succinct illustration of the difference between qualitative
and quantitative research:
A simplified illustration of the difference between the quantitative and the qualitative approach is shown in the differing
responses to the question ‘How are you feeling today?’ A quantitative oriented researcher might ask the participant to
respond on a seven‐point scale, ranging from 1=‘very unhappy’ to 7=‘very happy’, and receive an answer of 5,
signifying ‘somewhat happy’. A qualitative researcher might ask the same person the same question, ‘How are you
feeling today?’, but request an open‐ended answer, which could run something like ‘Not too bad, although my knee is
hurting me a little, and I've just had an argument with my boyfriend. On the other hand, I think I might be up for
promotion at work, so I'm excited about that’. In other words, the quantitative approach yields data which are relatively
simple to process, but are limited in depth and hide ambiguities; the qualitative approach yields a potentially large
quantity of rich, complex data which may be difficult and time consuming to analyse.
(Barker et al. (2002), p. 73

This example shows how qualitative methods are nonquantitative, usually open ended (in the sense that
the researcher does not know before the study exactly what data they may collect), and enable the
researcher to begin to understand an individual's lived experiences, the feelings they have about their
experiences, and the perceptions and meaning they give to their experiences (Nelson & Poulin, 1997;
Polkinghorne, 1983). Given these characteristics, a typical qualitative study will involve detailed
interviewing of participants to identify themes involving feelings and the meaning that those
participants give to their feelings.
The advantages of using qualitative methods are: (a) some aspects of psychopathology are difficult to
express numerically, and a qualitative approach allows data to be collected about more complex aspects
of experience; (b) they permit intensive and in‐depth study of individuals or small groups of individuals;
(c) because interviewing techniques are usually open ended, the researcher may discover interesting
things about a psychopathology that they were not originally looking for; and (d) they can be an
extremely valuable source of information at the outset of a research programme and provide the
researcher with a rich source of information which may lead them to construct hypotheses suitable for
study using quantitative methods.
Conducting and analysing qualitative methods
Qualitative studies are not entirely unstructured, and qualitative techniques specify ways in which data
should be collected and analysed. First, unlike quantitative methods that tend to emphasise the random
selection of participants and allocation to experimental groups, qualitative methods tend to deliberately
specify groups of participants for sampling depending on the phenomenon or psychopathology the
researcher is interested in. For example, these may include individuals who have suffered childhood
abuse, families with a member who is suffering a mental health problem, parents of autistic children,
etc. (Creswell, 1998). Once selected, participants will then usually take part in a semistructured, open‐
ended interview in a relaxed and comfortable interaction (McGrath, Palmgren, & Liljedahl, 2018). All
interview questions would normally be related back to the original research question(s) posed prior to
the study. For instance, a research question might be ‘How do individuals with panic disorder cope with
day‐to‐day living?’. In this example, the interviewer can ask very general questions or more specific
questions that are derived from the original research question. A general question might be ‘What
problems do you encounter each day because of your panic attacks, and how do you cope with them?’.
A more specific question might be ‘How do you feel about not being able to leave the house because of
the possibility you might have a panic attack?’ In this kind of structure, the participant has the
opportunity to respond to both general and specific questions. The general questions allow the
participant to create their own picture of their experiences, and the specific questions allow the
researcher to obtain detailed information that is relevant to the original research question.
Once detailed responses from the interview have been collected, the researcher has the task of making
sense of the data, picking out consistent themes that emerge in the participant's responding, and
deciding how these themes might relate to the original research question that was posed. The first step is
to break up the interview transcript into manageable and meaningful units. There are a number of
ways to do this (Giorgi, 1985; Merleau‐Ponty, 1962), but for simplicity we will describe a commonly
used approach known as grounded theory (see Heydarian, 2016, for a summary of developing theory
with the grounded theory approach). Grounded theory is an approach to qualitative analysis that was
developed by Glaser & Strauss (1967). It involves identifying consistent categories or themes within the
data, and then building on these to provide more abstract theoretical insights into the phenomenon
being studies. Research Methods Box 3.1 provides a detailed specific example of how grounded theory
has been used to understand how dental phobics cope with their psychopathology and how it affects
their day‐to‐day living. As we can see, this study was able to identify a number of consistent themes that
emerged from the interview data and provided a rich insight into the every‐day experiences and feelings
of individuals with dental phobia. The study also provided some higher‐level theoretical insights by
suggesting how several psychological and social factors interact to determine how dental phobics cope
with their fear (Abrahamsson et al. 2002). Grounded theory can be used with data collected in a
number of forms, including interviews, focus groups, observation of participants, and diary material. It
is also an approach that allows a constant dynamic interaction between research and theory. For
example, the study reported in Research Methods Box 3.1 provided some theoretical insights into how
dental phobics coped with their fear, this theoretical insight can then provide the basis of a refined
research question and a subsequent qualitative study pursuing this issue in further detail.

Grounded theory An approach to qualitative analysis which involves identifying consistent

categories or themes within the data, then building on these to provide more abstract theoretical
insights into the phenomenon being studied.

Summary
Qualitative methods lend themselves particularly well to understanding and describing many aspects of
psychopathology, and are becoming increasingly used in clinical psychology research. They are useful
for collecting data on everyday feelings and experiences associated with psychopathology, and data
collected in this way can make a significant contribution to theory. In this section of the chapter it has
not been possible to convey the full range of qualitative methods available to the researcher, nor to
convey the important philosophical and epistemological underpinnings of many of these techniques (see
Howitt, 2019; Sullivan & Forrester, 2018). However, qualitative methods are not just an alternative to
quantitative methods; the two can be combined in a useful and productive way in clinical psychology
research. Examples include using qualitative data to clarify quantitative findings, beginning research in a
new area with qualitative research but moving this on using quantitative methods, or using qualitative
data to develop quantitative measures (Barker et al., 2015).

3.3.11 Summary of Research Designs in Clinical Psychology

This section of the book has reviewed the various research methodologies that are available to the
clinical psychology researcher. All of these methodologies include ways of collecting information and, in
many cases, ways of interpreting that information. As we indicated at the outset of this section, the type
of research method you adopt will depend very much on (a) the nature of the research question you are
asking (do I want to discover whether there are causal relationships between variables, or do I just want
to know if two variables are related in some way), (b) the nature of the population you are studying (e.g.,
do you have lots of participants available or just a few?), and (c) whether your research is at an early or
advanced stage (if it is the former you may want to use qualitative methods, if the latter, then
quantitative methods may be more appropriate).
SELF‐TEST QUESTIONS
What are the main aims of correlational designs?
What is the difference between a positive and negative correlation?
Can you identify how a scattergram can tell us how two variables are related (see Figure
3.1)?
How do longitudinal and prospective studies differ from correlational studies?
Can you describe the different ways in which prevalence rates can be measured?
Which research design is the most effective for identifying causal relationships between
variables?
Can you describe what an independent variable (IV) and a dependent variable (DV) are?
Experimental designs use control groups. What are they and how would you design one?
What are the demand characteristics of an experiment?
What are clinical trials?
What is a placebo control condition?
Can you describe what a mixed design is?
What are the advantages and drawbacks of using case studies in research?
What is an ABAB design?
How do multiple‐baseline designs differ from ABAB designs?
How is effect size used to overview studies in a meta‐analysis?
What is the difference between a mediator and a moderator?
What are the main differences between quantitative and qualitative research methods?
What is grounded theory?
 SECTION SUMMARY

3.3 RESEARCH DESIGNS IN CLINICAL PSYCHOLOGY

Correlational designs enable the researcher to determine if there is a relationship between two
or more variables.
A correlation coefficient can range from +1.00 through 0.00 to −1.00 with +1.00 referring
to a perfect positive correlation between two variables, and −0.1.00 denoting a perfect negative
correlation.
Both longitudinal and prospective studies take measures from the same participants at two or
more different times in order to specify the time‐relationships between variables.
Epidemiological studies provide details about the prevalence of psychological disorders.
Experiments involve the researcher manipulating one of the variables (the independent variable)
and then measuring the effect of this on behaviour (the dependent variable).
To be valid, experimental studies need to use appropriately designed control conditions.
Clinical trials are types of experiments that are used to test the effectiveness of treatments.
A placebo effect is when a participant in a clinical trial shows improvement even though they
are not being given an effective treatment.
Mixed designs use the non‐random assignment of participants to groups in an experiment.
Natural experiments allow researchers to observe the effects on behaviour of a naturally
occurring ‘manipulation’ (such as an earthquake).
Single‐case studies allow researchers to collect data from just one individual.
The single‐case experiment uses ABA, ABAB or multiple‐baseline designs to carry out
controlled experiments on individual participants.
A mediator is a variable that mediates the relationship between the independent variable
and the dependent variable (DV), and a moderator is a variable that affects the strength of
the relationship between the IV and the DV.
Meta‐analyses are statistically accepted ways of assessing the strength of a particular finding
across a number of different studies.
Systematic reviews are reviews that use systematic and explicit methods to identify, select, and
critically appraise relevant research.
Qualitative methods use ordinary language as their raw material and adopt verbal rather than
statistical analyses.
Grounded theory is one particular example of a qualitative method that is used extensively in
clinical psychology research.

3.4 ETHICAL ISSUES IN CLINICAL PSYCHOLOGY RESEARCH

It would be almost impossible to do psychological research in general, and clinical psychology research
in particular, without those individuals who are needed to act as participants. However, the people that
we recruit as participants have rights that need to be protected, they have a dignity that needs to be
preserved, and their well‐being needs to be maintained. These all form part of the ethical deliberations
that need to be fully considered before we begin a particular piece of research. Examples of ethical
issues that might be encountered in clinical psychology research include ‘Is it harmful to induce panic
attacks in an experiment?’ ‘What will be the effect of inducing a negative mood in my participants, and
how can I ensure this doesn't affect them after the experiment?’ ‘Is giving a participant a placebo pill
instead of an active drug tantamount to with‐holding treatment?’ ‘Does my experiment involve
deceiving the participants in any way?’ ‘How can I be sure that my participants' involvement in the
study is truly voluntary?’ Most organisations that host clinical psychology research (such as universities
or hospitals) now have ethical committees that are required to vet all research proposals to see that they
meet basic ethical standards and protect the participants in the research. Ethical issues in clinical
psychology research fall under three main headings: (a) informed consent, (b) causing distress or
withholding benefits, and (c) privacy and confidentiality.

3.4.1 Informed Consent

Researchers should always properly inform participants about what it is they will be participating in,
what they will be asked to do, and what experiences they might have while taking part in the study. This
information needs to be detailed enough for the researcher to be sure that the potential participant can
make a rational and informed decision about whether to participate or not. This means that the
information provided about the study should be as detailed as possible, and—importantly—couched in
a language that the participant will understand, and does not include technical jargon that is only likely
to be comprehensible to the researcher. This information should also include (a) details of the purpose
of the experiment, (b) a description of the procedures the participant will encounter, (c) the duration of
the study, (d) who will know about the participant's involvement in the study and whether confidentiality
will be maintained, (e) whether participation is voluntary or a payment is being offered, and (f) clear
indication to the participant that they can withdraw from the study at any time and without prejudice if
they so wish. Participants should also be given the opportunity to ask questions about the study in order
to enable them to make an informed decision about participation, and they should also be given
sufficient time to reflect on this information.
All of this information is usually provided in a written informed consent form that the participant
must then sign to acknowledge that they understand what the study involves and that they formally
consent to take part in the study. A simple example of an informed consent form is provided in Table
3.1. Consent forms may be more or less detailed depending on the complexity of the study and the
nature of the participants required for the study. For example, if the study is one that requires the
participation of individuals already undergoing treatment for mental health problems, then the
participant may need to know how their involvement in the study might affect their treatment and
whether it might have an adverse effect on their existing mental health condition. In such circumstances,
informed consent forms might also want to include further details such as (a) the identity of the
researchers and their contact details, (b) a clear description of any complex procedures (e.g., any
procedures that may be invasive), (c) the identity of others who might be directly or indirectly associated
with the research (e.g., organisations that might be funding the research, such as drug companies or
mental health charities), (d) reasons why the participant has been selected (in case the participant may
feel stigmatised by being approached to participate), (e) the possible harms and benefits of the
procedure (especially if the participant has an existing mental health problem), and (f) details of any
future use of the data that are collected from the study.

informed consent form See Informed consent.

The issue of informed consent becomes problematic when an individual's understanding of the
information provided in a consent form is limited. This is particularly so with children and certain
categories of adults—for example, those who have learning disabilities or exhibit psychotic symptoms
(Bersoff & Bersoff, 1999; Fisher, Cea, Davidson, & Fried, 2006). In the case of children and adolescents
below the age of 17 years, then the written consent of the parent or guardian is required as well as
either the verbal or written agreement of the child.

informed consent Detailed information about an experiment is given to potential

participants to enable them to make an informed decision to participate.

Obtaining full informed consent of a participant also becomes somewhat problematic if informing the
participant of all the details of the study is likely to significantly affect the results. For example,
participants who are in a control condition in many drug treatment studies are given placebo pills to
assess what improvement might occur if they believe they are receiving a drug but in fact are not. This
involves some deception on the part of the researcher in the sense that they have not told those taking
the placebo that it is not an active drug. At the very least, this means that the participant is not being
given all the information about what is happening in a study, and if this is the case, can they then make
an informed decision about whether to participate? This is a moot point, and it is important because
many psychological studies depend for the validity of their findings on deceptions of this kind. Many
researchers overcome this problem by withholding some information from participants if providing that
information is likely to affect the outcome of the study. They will then offer the participant a full
debriefing at the end of the study, explaining any deception and offering any withheld information. If
the participant is unhappy about this, the researcher can then offer them the opportunity to withdraw
their consent to use their data (Bersoff & Bersoff, 1999).

deception The act of deceiving.

Finally, it is worth reiterating that all efforts should be made to ensure that a participant's involvement in
a study should be truly voluntary. There should be no explicit or implicit coercion. How often has a
student trying to finish off their undergraduate project gone into the corridor or coffee bar and tried to
persuade someone to take part in their experiment ‐ ‘I only need half a dozen more people’, they plead!
Is anyone approached in this way a genuine volunteer if they agree to take part? Probably not, because
at least some will feel obliged to participate in order to ‘help’ the student out. Similar problems in
obtaining truly voluntary consent are found in many other situations, such as studies that involve
hospital inpatients, prisoners, and even undergraduate psychology students who have to take part in
research studies to gain course credits for their degree programme! Some service providers (such as the
NHS) have developed a more imaginative and inclusive way of seeking participant involvement in
clinical research, and this is by involving service users (e.g., clients and patients) in the whole research
process, from design, through participation to the reporting of findings. Also, at a national level,
INVOLVE is a group dedicated to facilitating public participation in research designed to improve well‐
being and reduce social problems generally (www.involve.org.uk).

voluntary Of one’s own free will or design; not forced or compelled.

TABLE 3.1 Informed consent form

3.4.2 Causing Distress or Withholding Benefits

In many cases it is difficult to do clinical psychology research without asking someone with a mental
health problem to describe or experience their symptoms during the study. In other cases we
intentionally try to recreate the conditions that cause psychopathology symptoms in order to understand
the causes of that psychopathology. Both of these cases involve the researcher in important ethical
considerations. In clinical psychology research, distress to the participant can be caused in a number of
ways, for instance by (a) asking them to relate or relive distressing memories or experiences (e.g., in a
study looking retrospectively at experiences that may have preceded a mental health problem), (b)
subjecting them to experimental manipulations that may cause stress, anxiety or negative feelings
generally (e.g., a mood induction procedure), (c) requiring a participant to reveal information about
themselves that may be embarrassing or humiliating (e.g., in questionnaire studies investigating sexual
behaviour), (d) presenting physically aversive stimuli such as electric shocks or loud noises (e.g., in fear
conditioning studies), or (e) subjecting the participant to circumstances and situations that may be a
threat to their self‐image or self‐esteem (e.g., in situations where participants may be given real or false
feedback suggesting their performance on a task is poor or substandard). Even asking a participant to
complete a validated questionnaire measuring trait characteristics such as anxiety or depression might
be distressing. For example, answering questions about the frequency of suicidal ideation in a
questionnaire such as the Beck Depression Inventory (BDI) may trigger distressing thoughts for someone
who is either currently depressed or knows someone who has attempted suicide.
Because of these potential harms that could affect participants, researchers have an obligation to be
vigilant throughout a study for any indication that the participant might be experiencing distress. If the
researcher does notice indications of distress, they should terminate the study or suspend data collection
until the participant feels able to continue. A basic rule is that at the end of the study the participant
should certainly be in no worse a psychological or physical state than when they started it. In
experimental studies that are likely to cause stress (such as fear conditioning studies, negative mood
manipulations, studies involving negative or threatening materials) the experimenter should always ask
the participant at the end of the study how they are feeling. If they claim they feel distressed, stressed,
anxious, sad, or have other negative feelings, then the experimenter should be able to actively offer some
means of dealing with these feelings. This may include offering the opportunity to listen to a relaxation
tape or music designed to induce positive mood, or in more severe cases the experimenter may want to
provide information about counselling services that can be made available to the participant (e.g., if it is
a study taking place on a university campus, the experimenter may be able to provide the location and
phone number of the university counselling service). Clearly, making people distressed in a research
study is not an acceptable end in itself, and the researcher must always weigh up whether the potential
benefits of their research (in terms of its contribution to knowledge) outweighs the potential distress that
may be caused to some participants.
On the other side of the coin, a study may not cause distress but may involve the active withholding of
benefits for the participant. This is especially the case with studies attempting to assess the effectiveness
of treatments for psychopathology. For example, let us assume a researcher is attempting to find out if a
new psychotherapy is effective for treating depression. The study would involve participants diagnosed
with depression and some would be allocated to the experimental condition and receive the new
psychotherapy while for comparison purposes others would need to be allocated to control conditions
that did not receive the new psychotherapy. This raises a significant ethical issue. Should we withhold
effective treatment for someone suffering depression simply because we need to allocate them to a no
treatment control condition? A similar issue is that such studies also have very narrow inclusion
criteria. That is, to be able to interpret their results clearly, the researcher would want to ensure that
the study only included participants who had a single diagnosis of depression. Interpreting the data
would be complicated if the study also included participants who were diagnosed with other disorders
that were comorbid with depression. This means that those with more complex psychopathologies are
likely to be excluded from treatment outcome studies and so denied access to the treatment programme
associated with the study. Researchers tend to try and overcome the ethical issues involved in allocating
a patient to a no treatment condition by adopting what are called waiting‐list controls. That is, they
use patients who are on a waiting list for treatment as their no treatment control condition. Such
individuals would not be receiving treatment anyway during the time that they are on the waiting list.
This may be a suitable way out of this particular ethical dilemma, but as the reader is probably aware, it
is a solution that paradoxically is available only as long as service providers are unable to offer
immediate treatment!
 no treatment control condition The allocation of participants to a control condition, in
which they do not receive the treatment under investigation.

3.4.3 Privacy and Confidentiality

All participants in psychological research have a right to privacy and confidentiality. Privacy means
that participants can decide not to provide some forms of information to the researcher if they so wish
(e.g., their age or sexual orientation), and confidentiality means participants in psychological research
have a right to expect that information they provide will be treated confidentially. For example, if a
piece of research is eventually published in a scientific journal, participants who contributed to the study
should not be identifiable. In the event that confidentiality and/or anonymity cannot be guaranteed, the
participant must be warned of this in advance of agreeing to participate. Indeed, according to
legislation in many countries ‐such as the Data Protection Act 2018 and General Data Protection
Regulation (GDPR) in the UK ‐ information obtained about a participant during a study is confidential
unless otherwise agreed in advance. In many cases, such as questionnaire studies, researchers will ensure
that all data collected is anonymous, and participants will usually only have to provide basic
demographic information (e.g., sex, age, etc.) that will not usually allow them to be identified. In some
other circumstances (such as longitudinal studies, where participants may have to be contacted to
provide data on more than one occasion) it may be necessary to retain some information that will
identify the participant over the course of the study, but this should be erased once all the data are
collected. In studies where personal or sensitive information is being collected (such as studies involving
participants with mental health problems), the informed consent form should clearly state who will have
access to the data and the findings of the study. If interviews with participants are audiotaped or
videotaped, it should be clear to the participant who will hold those tapes and how long they will be
retained before being destroyed.

Privacy The right of participants to decide not to provide some forms of information to the
researcher if they so wish (e.g. their age or sexual orientation).

confidentiality The right of participants in psychological research to expect that information

they provide will be treated in confidence.

However, issues of confidentiality and anonymity become problematic when the participant discloses
information about illegal activities or events or circumstances that may be detrimental to an individual's
psychological or physical health. For example, what should a researcher do if a participant tells them
about suicidal intentions, serious drug abuse, criminal activities, physical or sexual abuse, etc.? Certainly,
a researcher has a legal and moral obligation to consider appropriate action if they believe a crime has
been committed or is intended, and in some countries it is mandatory by law, for example, to report
information about criminal activities such as child abuse (Becker‐Blease & Freyd, 2006). Perhaps it is
important to be clear that confidentiality is not the same as secrecy, and is therefore not absolute. If the
researcher believes that a study might reveal information about illegal or immoral activities, then they
might inform participants at the outset of the study that (a) confidentiality is not absolute, and (b) the
researcher will inform the participant if confidentiality is broken. However, providing such information
at the outset of a study is likely to mean that participants will be significantly less willing to provide
sensitive information (Bersoff & Bersoff, 1999; Koocher, 2013).
Finally, what should a researcher do when a participant provides information that they are likely to
harm themselves or others or are seriously distressed? This obviously requires a judgement on the part
of the researcher, and no one can morally turn a blind eye knowing that others may be harmed or an
individual is in a state of life‐threatening distress. Because of their knowledge of psychopathology and
the provision of treatments, most clinical psychology researchers are usually in the privileged position of
being able to offer at least some kind of support and guidance to those disclosing information indicating
serious distress. As a consequence, a researcher may be able to suggest treatment or referral to an
appropriate support service immediately after the study.

3.4.4 Summary of Ethical Issues

No description of research using human participants is complete without a thorough discussion of
ethical issues. Proper ethical procedures are designed to protect the rights, dignity and well‐being of
participants in research, and are a necessary part of any clinical psychology research project. Ethical
issues can be grouped under three broader headings, namely (a) informed consent (e.g., are the
participants fully informed about the study and can they freely and voluntary give their informed
consent to participate?), (b) causing distress or withholding benefits (e.g., what is the risk that a research
procedure will cause a participant harm or distress, and how can we avoid this?), and (c) privacy and
confidentiality (e.g., are the participants rights to privacy and confidentially being properly respected?).

SELF‐TEST QUESTIONS
What is informed consent?
What ethical issues need to be considered when a research study may cause distress to a
participant or lead to the withholding of benefits?
How should issues of privacy and confidentiality be considered when designing and
conducting a research study?

SECTION SUMMARY

3.4 ETHICAL ISSUES IN CLINICAL PSYCHOLOGY RESEARCH

Participants in clinical psychology research have rights that need to be protected, a dignity
that needs to be preserved, and a well‐being that needs to be maintained.
The informed consent of participants should always be obtained before they take part in a
study.
Participation in any research study should be voluntary.
Researchers have an obligation to be vigilant throughout a study for any indication that
the participant might be experiencing distress.
All participants in psychological research have a right to privacy and confidentiality.

3.5 RESEARCH METHODS IN CLINICAL PSYCHOLOGY REVISITED

Research is an important and central feature of clinical psychology. Research techniques allow us to (a)
describe the symptoms of psychopathologies and the feelings and experiences of those who suffer with
mental health problems, (b) understand the causes of psychopathologies, (c) assess the efficacy of
interventions developed to treat psychopathology, and (d) assess the effectiveness of services provided to
treat and support those with mental health problems (known as evaluation research or clinical audit).
Different research methods may be based on different theories of knowledge, and a theory of
knowledge represents a way of trying to understand the world. Many of the research methods we have
described in this chapter are based on the scientific method espoused by Karl Popper and require that
research results should be replicable and theories should be experimentally testable. However, even
within the realm of clinical psychology there are many who feel that the scientific method is not well
suited to exploring many of the important aspects of mental health problems such as the
phenomenology of psychopathology.
We have then described in detail a range of research methods that are available to the clinical
psychology researcher, and the type of method adopted will usually depend very much on the nature of
the research question being asked. For example, correlational and longitudinal methods are useful for
determining if there is a relationship between two or more variables, the experimental method is useful
for identify causal relationships between variables, case studies provide important ways of studying a
phenomenon when the number of available participants is restricted, and qualitative methods are useful
for gaining an insight into the full experience of psychopathology or beginning new research in an area.
The final and essential part of a description of research methods in clinical psychology is a discussion of
ethical issues, and these are vital in the protection of the rights, dignity, and well‐being of those who
participate in clinical psychology research.

This book is accompanied by Student and Instructor companion websites.

www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter References
Videos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
4
Treating Psychopathology

ROUTE MAP OF THE CHAPTER

This chapter discusses the reasons for treating psychopathology, the different theoretical
approaches to treatment, and how we attempt to evaluate whether treatment is successful or
not. The first section describes six different theoretical approaches to treatment and the basic
principles on which each of these approaches are based. We then discuss some of the modes of
treatment delivery, many of which have been developed in recent years and are the result of
new digital technologies. Finally, we discuss ways of evaluating treatment and cover issues about
what constitutes a therapeutic gain, how long it may take to achieve a successful outcome, and
how therapeutic gains should be measured. We end the chapter by describing some of the
methodologies that are currently used to objectively assess the effectiveness of treatments for
psychopathology, and discuss whether all types of treatment interventions are equally effective
(known as the ‘Dodo Bird Verdict’).

CHAPTER OUTLINE
4.1 THE NATURE AND FUNCTION OF TREATMENTS FOR
PSYCHOPATHOLOGY
4.2 EVALUATING TREATMENT
4.3 TREATING PSYCHOPATHOLOGY REVIEWED

LEARNING OUTCOMES
When you have completed this chapter, you should be able to:
1. Describe some of the reasons for wanting to treat psychopathology symptoms.
2. Describe and compare and contrast the basic theoretical principles on which at least four
different types of psychotherapy are based.
3. Describe and evaluate at least three to four different modes of delivery for treatments of
psychopathology.
4. Critically assess methods for determining the effectiveness of treatments for
psychopathology.
 I was a 22‐year‐old trainee working for a publishing company in London, and I was obsessed with food. I made
a pact with myself to limit myself to less than 700 calories a day. This worked well for a while, but then I
started binge eating, and my fear of gaining weight led to me to make myself sick. Sometimes up to 5 or 6 times a
day. This left me totally drained—both emotionally and physically, and my relationship with my partner began to
go downhill rapidly. I really hated myself, and I felt fat and disgusting most days. If only I felt thinner I would
feel better about myself. My GP eventually referred me to a clinical psychologist, who helped me to understand how
my thinking was just plain wrong. He explained to me how I evaluated my self‐worth purely on the basis of my
weight and body shape. My thinking was also ‘black and white’—I believed that foods were either ‘good’ or if
not, they were ‘bad’. During therapy I learned to identify and challenge my irrational thoughts about food and
eating, this helped me to begin to eat relatively normally again, and I began to feel less anxious and worthless.
What amazed me most was that eating normally didn't mean I put on weight, and I felt in control again—the
first time for years. All this as so wonderful that I became anxious about the possibility of therapy ending and that
I'd simple go back to starving and bingeing. But I was encouraged to practice a number of coping strategies and
learned what I should do in circumstances where I felt I might relapse back into my old ways.
Elly's Story

Introduction
Psychopathology can take many forms and involve anxiety, depression, worthlessness, guilt, and feelings
of lack of control, amongst others. For many people these feelings become so intense that they cause
personal distress and significantly impair normal daily functioning. Some people are able to deploy
adaptive coping strategies that allow them to successfully negotiate such periods in their life (e.g., by
seeking help and support from friends and family, or using problem‐solving strategies to deal with life
problems that may be causing their symptoms). Others may be less able to cope constructively and
choose less adaptive means of dealing with their symptoms, such as resorting to substance abuse and
dependency or deliberate self‐harm. Whatever route an individual may take, the distress and disruption
that symptoms of psychopathology cause will often lead an individual to seek professional help and
support for their problems. The first port of call is usually the individual's doctor or GP, and the GP
may be able to offer sufficient help to deal with acute bouts of psychopathology such as those involving
depression, stress and anxiety‐based problems. In most cases, this support will usually be in the form of
suitable medication, but it may also take the form of access to stress‐management courses, short‐term
counselling or psychotherapy, access to self‐help information or even computerised cognitive behaviour
therapy (CCBT) (e.g., Andersson, 2016; Fairburn & Patel, 2017). In other cases, it may be necessary for
the individual to be referred for more specific and specialised treatment, and the nature of this
treatment may often depend on the nature and severity of that person's symptoms. This is a fairly
standardised route by which individuals suffering psychopathology come into contact with the treatment
methods required to alleviate their symptoms and their distress. Others may simply decide to bypass the
health services available in their community and directly approach an accredited counsellor or
psychotherapist who can privately supply the treatment services they require. Whichever route is
followed, the aim is to find a suitable specialist who can help the individual to recover by successfully
alleviating the symptoms of psychopathology and easing the distress that is experienced.

4.1 THE NATURE AND FUNCTION OF TREATMENTS FOR

PSYCHOPATHOLOGY
Elly's Story provides her personal account of how therapy helped to alleviate her eating problems,
provided her with insight into the thought patterns that gave rise to her psychopathology, and how she
learnt to cope with situations that might give rise to relapse. Based on the example in Elly's Story,
treatments for psychopathology will usually possess some, if not all, of the following characteristics: (a)
they can provide relief from the distress caused by symptoms, (b) they can provide the client with self‐
awareness and insight into their problems, (c) they enable the client to acquire coping and problem‐
solving skills that will help them to manage any similar problems occurring in the future, and (d) they
attempt to identify and resolve the causes of the psychopathology, whether those causes are recognised
as problematic ways of behaving, problematic ways of thinking, or problematic ways of dealing with or
assimilating life experiences. Many treatments possess only some of these characteristics. For example,
many drug treatments for psychopathology will have a palliative effect (i.e., reduce the severity of
symptoms and so alleviate distress), but they may only rarely provide the client with insight into their
problems. Some other therapies may serve the primary purpose of helping the client to achieve insight
into their problems (e.g., psychodynamic psychotherapies), but it does not always follow that this insight
will bring about behaviour change or provide suitable coping skills (Lindfors et al., 2019; Prochaska &
Norcross, 2001). Still other therapies may provide effective ways of changing behaviour (such as many
behaviour therapies) but do not necessarily provide the client with insight into the causes of their
problems.

palliative effect The reduction of the severity of symptoms and alleviation of distress.

The treatment that is provided for a psychopathology will depend on at least two factors: (a) the
theoretical orientation and training of the therapist, and (b) the nature of the psychopathology. First, a
therapist will tend to adopt those treatment practices that they have most experience with and were
originally trained to use. This will often involve therapies with a specific theoretical approach (e.g., a
psychodynamic approach, a client‐centred approach, a cognitive approach or a behavioural approach—
see Section 1.3.2 in Chapter 1), and these theoretical approaches will not just advocate different
treatment procedures but will also advocate quite different approaches to understanding and explaining
psychopathology. Most accredited therapists will now also have to demonstrate that they have
periodically engaged in continuing professional development(CPD). That is, they must
demonstrate that they regularly update their knowledge of recent developments in treatment
techniques. If a therapist is unable to demonstrate that they are actively engaged in CPD, then they may
be in danger of losing their status as a legally registered practitioner. This has meant that practitioners
have become much more eclectic in the types of treatment they will offer as they learn new treatment
methods through the need to demonstrate their continuing professional development. While some
practicing therapists may also use the research literature as a way of updating their therapeutic skills,
most rely on information from less formal sources, such as colleagues, supervision, personal therapy,
professional newsletters, workshops and conferences (Goldfried & Wolfe, 1996; Hill, Spiegel, Hoffman,
Kivlighan, & Gelso, 2017).

continuing professional development (CPD) The demonstration by accredited therapists

that they regularly update their knowledge of recent developments in treatment techniques.

Second, treatments may be chosen largely on the basis that they are effective at treating a certain type
of psychopathology. In the UK, the National Institute for Health & Clinical Excellence(NICE)
(https://www.nice.org.uk/guidance/lifestyle‐and‐wellbeing/mental‐health‐and‐wellbeing) recommends
treatments for specific psychopathologies on the basis that their effectiveness is evidence‐based and
empirically supported by scientifically rigorous research (see also Focus Point 3.2 in Chapter 3), and we
will discuss some of these recommendations in later chapters when we discuss treatment programmes
for specific psychopathologies (see Chapters 6–17). Nowadays, most types of theoretical approach have
been adapted to treat most psychopathologies, or at least some aspect of most psychopathologies and
these will be discussed in detail in the treatment sections of each ensuing chapter.
4.1.1 Theoretical Approaches to Treatment
Traditionally, popular treatments have been developed around a relatively small number of important
theoretical approaches. We discussed these theoretical approaches in some detail in Chapter 1 (Section
1.3), and you may want to return to this section in order to refresh your memory about how these
different theoretical models conceptualise and explain psychopathology. This section continues with a
summary of how these theoretical approaches are adapted to treat psychopathology.

Psychodynamic approaches
The aim of most psychodynamic therapies is to reveal unconscious conflicts that may be causing
symptoms of psychopathology. Most psychodynamic approaches assume that unconscious conflicts
develop early in life, and part of the therapy is designed to identify life events that may have caused
these unconscious conflicts. Once these important developmental life events and unconscious conflicts
have been identified, the therapist will help the client to acknowledge the existence of these conflicts,
bring them into conscious awareness, and work with the client to develop strategies for change. One
important form of psychodynamic therapy is psychoanalysis, and this is a type of therapy based on
the theoretical works of Sigmund Freud (1856–1939). The aim of psychoanalysis is to bring any
unconscious conflicts into awareness, to help the individual understand the source of these conflicts
(perhaps by identifying past experiences or discussing the nature of important relationships), and to help
the individual towards a sense of control over behaviour, feelings and attitudes. There are a number of
basic techniques used by psychoanalysts to achieve these goals:
1. Free association: here the client is encouraged to verbalise all thoughts, feelings, and images that
come to mind while the analyst is normally seated behind them, and this process functions to bring
into awareness any unconscious conflicts or associations between thoughts and feelings.

Free association A technique used in psychoanalysis where the client is encouraged to

verbalise all thoughts, feelings and images that come to mind.

2. Transference: Here the analyst is used as a target for emotional responses, and the client behaves
or feels towards the analyst as they would have behaved towards an important person in their lives.
This allows the client to achieve understanding of their feelings by acting out any feelings or
neuroses that they have towards that person.

Transference A technique used in psychoanalysis where the analyst is used as a target for
emotional responses: clients behave towards the analyst as they would have behaved
towards an important person in their lives.

3. Dream Analysis: Freud believed that unconscious conflicts often revealed themselves in symbolic
forms in dreams, and this made the analysis of dream content an important means of accessing
unconscious beliefs and conflicts.

Dream analysis The analysis of dream content as a means of accessing unconscious

beliefs and conflicts.

4. Interpretation: Finally, the skilled psychoanalyst has to interpret information from all of the
above sources and help the client to identify important underlying conflicts and help the client
develop ways of dealing with these conflicts.
 Interpretation In psychoanalysis, helping the client to identify important underlying
conflicts.

Frosh (2012, p. 100) summarises Freud's conception of psychoanalysis as a therapeutic process in the
following way:
Psychoanalysis is a way of exploring the unconscious that might have therapeutic effects, but it is
not solely or necessarily therapeutic in its aims.
The assumption that psychological conflict arises from unconscious complexes suggests that if
psychoanalysis brings unconscious material into consciousness, it will have the effect of lessening
psychological disturbance.
Freud was cautious about the power of psychoanalysis to make a significant difference but
nevertheless believed that the movement from “unconscious to conscious” was an important step in
advancing individual well‐being as well as social life.
Psychological disturbance is caused by a complex array of phenomena, but at its core is the
relationship between anxiety and repression, which produces a variety of strategies aimed at
keeping troubling unconscious material out of awareness.
The different strategies (defences) adopted by different people and in different circumstances (see
Table 1.1, Chapter 1) characterise the various forms of psychological disturbance—neurosis,
psychosis, and so on.
Psychoanalysis as a mode of therapy aims to produce insight. Its main methods of therapeutic
activity are focussed on interpretation and transference.
As a form of treatment, psychoanalysis may take up to three to five sessions a week and change is
expected to take place at a normal maturational rate, and so may require anything between three and
seven years for the full therapeutic benefits of the therapy to be recognised. Other forms of
psychodynamic therapy may be briefer and less intensive than psychoanalysis and may draw on
techniques from other sources, such as family therapy (see Section 4.1.1). Primarily, psychoanalysis
represents a quest for self‐knowledge, where an individual's problems are viewed in the context of the
whole person, and in particular, any conflicts they may have repressed. It can be a helpful treatment for
many people with moderate to severe anxiety or depression‐based problems—especially when other,
more conventional, therapies have failed. In studies where the effects of long‐term psychoanalytic
therapy have been measurable, it has been shown to only be more effective than control treatments that
do not possess a specialised psychotherapy component, suggesting that the evidence for the effectiveness
of long‐term psychoanalytic therapy for psychopathology is still limited and at best conflicting (e.g.,
Lindfors et al., 2019; Smit et al., 2012).

Behaviour therapy
In the 1940s and 1950s there was a growing dissatisfaction with the medical or disease model of
psychopathology and also with the unscientific approaches to psychopathology being generated by
many psychodynamic theories. These dissatisfactions led psychologists to look towards the developing
area of experimental psychology for objective knowledge that might be used to inform treatment and
therapy. The body of knowledge that psychologists turned to was that of conditioning (see Section
1.3.2, Chapter 1), and this gave rise to the development of what came to be known as behaviour
therapies. First, such therapies stressed the need to treat symptoms of psychopathology as bona fide
behavioural problems rather than the mere symptoms of some other, hidden underlying cause.
Secondly, at the time, many psychologists believed that numerous psychological disorders were the result
of what was called ‘faulty learning’, and that symptoms were acquired through simple conditioning
processes. For example, it was believed that anxiety symptoms could be acquired through classical
conditioning (see Figure 6.1), and behavioural problems might be acquired through processes of
operant conditioning—e.g., bizarre and inappropriate behaviours might be acquired because they have
been reinforced or rewarded in the past (see Focus Point 8.5). The reasoning here was that, if
psychological problems were acquired through learning, then conditioning principles could be used to
develop therapies that effectively helped the individual to ‘unlearn’ those problematic associations. Two
distinctive strands of behaviour therapy developed from these assumptions. The first was a set of
therapies based on the principles of classical conditioning and the second based on principles of
operant conditioning. While the former group of therapies continues to be known as behaviour
therapy, the latter group has also come to be known as behaviour modification or behaviour
analysis. The term behaviour therapy is often used even more eclectically nowadays to refer to any
treatment that attempts to directly change behaviour (rather than, say, cognitions), whether the
underlying principles are based on conditioning or not.

conditioning A form of associative learning on which ehaviour therapies are based.

faulty learning A view that the symptoms of psychological disorders are acquired through the
learning of pathological responses.

behaviour analysis An approach to psychopathology based on the principles of operant

conditioning (also known as behaviour modification).

Therapies based on classical conditioning principles

Behaviour therapy effectively originates from the writings of Wolpe (1958)—who argued that many
forms of emotional disorder could be treated using the classical conditioning principle of extinction.
The assumption was that if emotional problems such as anxiety disorders were learned through classical
conditioning, they could be ‘unlearned’ by disrupting the association between the anxiety‐provoking
cues or situations and the threat or traumatic outcomes that they have become associated with. In
practice, this means ensuring that the anxiety‐provoking stimulus, event, or situation is experienced in
the absence of accompanying trauma so that the former no longer comes to evoke the latter. The most
famous behaviour therapy techniques to apply extinction principles are flooding,
counterconditioning, and systematic desensitisation, and they have collectively come to be
known as exposure therapies (Craske, Liao, Brown, & Vervliet, 2012; Foa & McLean, 2016; Richard
& Lauterbach, 2007), because they are all based on the need to expose the client to the events and
situations that evoke their distress and anxiety—so that they can learn that they are no longer
threatening (see Davey, 1998). Wolpe (1958) also introduced the principle of reciprocal inhibition, in
which an emotional response is eliminated not just by extinguishing the relationship between the
emotion‐inducing cue and the threatening consequence but also by attaching a response to the emotion‐
inducing cue which is incompatible with anxiety (e.g., relaxation). It has often been assumed that these
techniques can be applied only to the treatment of emotional problems such as anxiety disorders, but
they have in fact been applied to a range of disorders including addictive disorders (O'Leary & Wilson,
1975), marital conflict (Jacobson & Weiss, 1978), and sexual dysfunction (Mathews et al., 1976).

extinction The classical conditioning principle which assumes emotional problems can be
‘unlearnt’ by disrupting the association between the anxietyprovoking cues or situations and the
threat or traumatic outcomes with which they have become associated.
 flooding A form of exposure therapy for the treatment of phobias and related disorders in
which the patient is repeatedly exposed to highly distressing stimuli.

counterconditioning A behaviour therapy technique designed to use conditioning techniques

to establish a response that is antagonistic to the psychopathology.

systematic desensitisation A behaviour therapy based on classical conditioning used in the

treatment of phobias and anxiety disorders, during which the client overcomes their fears
through gradual and systematic exposure.

Exposure therapy Treatment in which sufferers are helped by the therapist to confront and
experience events and stimuli relevant to their trauma and their symptoms.

reciprocal inhibition A principle of behaviour therapy in which anxiety is eliminated not

just by extinguishing the relationship between the anxiety-inducing cue and the threatening
consequence, but also by attaching a response to the anxietyinducing cue which is incompatible
with anxiety.

Aversion therapy is another treatment based on classical conditioning but is rather different from the
proceeding therapies because it attempts to condition an aversion to a stimulus or event to which the
individual is inappropriately attracted. For example, aversion therapy is most widely used in the
treatment of addictive behaviours such as alcoholism, and in these procedures the taste of alcohol is
paired with aversive outcomes (e.g., sickness inducing drugs) in order to condition an aversive reaction to
alcohol (e.g., Lemere & Voegtlin, 1950; Voegtlin & Lemere, 1942) (see Chapters 8 and 10 for discussion
of the use of aversion therapy in the treatment of substance abuse and paraphilias). Since the 1950s
and 1960s, this type of procedure has been used to treat a wide variety of problems, including
inappropriate or distressing sexual activities (e.g., Feldman & MacCulloch, 1965), drug and alcohol
addiction (McRae, Budney, & Brady, 2003), and even obsessions and compulsions associated with
anxiety (Lam & Steketee, 2001). Aversion therapy was popularised in the 1971 cult film ‘A Clockwork
Orange’ where the lead character's excessive violence was treated by ‘conditioning’ him to vomit
whenever he saw a violent act (Photo 4.1). However, while aversion therapy for some problems (e.g.,
alcoholism, sexual offending) has been shown to have some therapeutic gains when used in conjunction
with broader community support programmes (Azrin, 1976) or social skills training (Maletzky, 1993),
substance abuse or sexual offending responses are often very resistant to this form of treatment, and
there is very little evidence that aversion therapy alone has anything other than short‐lived effects (e.g.,
Wilson, 1978) and does not significantly reduce reoffending in sexual offenders (Dennis et al., 2012;
Marques, Wiederanders, Day, Nelson, & van Ommeren, 2005).

Aversion therapy A treatment based on classical conditioning which attempts to condition an

aversion to a stimulus or event to which the individual is inappropriately attracted.

Therapies based on operant conditioning principles

The principles of operant conditioning offer some rather different approaches to treatment and therapy
than do those of classical conditioning. Operant conditioning is concerned with influencing the
frequency of a behaviour by manipulating the consequences of that behaviour. For example, if a
behaviour is followed by rewarding or reinforcing consequences, it will increase in frequency. If it is
followed by punishing or negative consequences, it will decrease in frequency (Davey, 1989). Operant
conditioning principles have mainly been used in therapy in three specific ways: (a) to try and
understand what rewarding or reinforcing factors might be maintaining an inappropriate or
maladaptive behaviour—this is known as functional analysis (e.g., trying to understand what factors
might be maintaining challenging or aggressive behaviours in individuals with intellectual disabilities);
(b) to use reinforcers and rewards to try to establish new or appropriate behaviours (e.g., to establish self‐
help or social behaviours in individuals who have become withdrawn because of their psychopathology);
and (c) to use negative or punishing consequences to try and suppress or eliminate problematic
behaviours in need of urgent attention (e.g., to eliminate or suppress self‐injurious behaviours in
individuals with intellectual disabilities or severe autistic symptoms) (see Sections 17.3 and 17.4 in
Chapter 17).

PHOTO 4.1 Alex, the leading character in the 1971 film A Clockwork Orange undergoes aversion therapy to cure his
violent tendencies.
A functional analysis is where the therapist attempts to identify consistencies between problematic
behaviours and their consequences—especially to try to discover whether there might be a consistent
event or consequence that appears to be maintaining the behaviour by rewarding it. For example, self‐
injurious or challenging behaviours may be maintained by a range of reinforcing consequences, such as
the attention the behaviour may attract or the sensory stimulation it provides (see Treatment in Practice
Box 17.1). Identifying the nature of the consequence allows the therapist to disrupt the reinforcement
contingency and, if necessary, reduce the frequency of that behaviour through extinction (Wacker et al.,
1990). Functional analysis has been adopted across a range of clinical settings and has been successfully
applied to managing aggressive/challenging behaviour (Delgado‐Casas, Navarro, Garcia‐Gonzalez‐
Gordon, & Marchena, 2014), tantrums (Wilder, Chen, Atwell, Pritchard, & Weinstein, 2006), attention‐
deficit‐hyperactivity disorder (Fabiano et al., 2008), depression (Ferster, 1985; Kanter, Cautilli, Busch, &
Baruch, 2011), eating problems (Meyer, 2008), and self‐injurious behaviour (Hastings & Noone, 2005).

functional analysis A detailed analysis of behaviour to identify the contingencies of

reinforcement that maintain a behaviour

Other influential interventions based on operant conditioning principles include the token economy,
response shaping, and behavioural self‐control. In the psychiatric setting, a token economy involves
participants receiving tokens (a generalised reinforcer) for engaging in behaviours defined by the
programme, and at a later time, these tokens can then be exchanged for a variety of reinforcing or
desired items (e.g., access to the hospital grounds, a visit to the cinema, etc.) (Hackenberg, 2018). In
psychiatric care, the token economy was first used to foster prosocial or self‐help behaviours (e.g.,
combing hair, bathing, brushing teeth, etc.) in previously withdrawn patients. However, despite the
apparent success of token economies, their use in the hospital setting has been in serious decline since
the early 1980s (Dickerson, Tenhula, & Green‐Paden, 2005). There were a number of reasons for this
decline, and these include the legal and ethical difficulties of withholding desired materials and events so
they can be used as reinforcers, and a lack of consensus on whether behaviours nurtured in token
economy schemes were maintained after the scheme ended and whether they generalised to other
environments and settings (Davey, 1998; Glynn, 1990).
Response shaping is a procedure that can be used to encourage new behaviours that are not already
occurring at a reasonable frequency. This may be especially a problem with withdrawn individuals or
individuals with restricted behavioural repertoires (such as those with severe intellectual disabilities).
However, the technique of response shaping by successive approximations is a way around this problem.
Here, the therapist will first reinforce a behaviour that does occur quite frequently and is an
approximation to the specific target response. Once this general response is established, reinforcement is
given only for closer and closer approximations to the target response.

Response shaping A reinforcement procedure that is used to develop new behaviours.

Finally, the use of operant conditioning principles for behaviour change purposes does not have to be
overseen or administered by a therapist. The principles are quite clear and can be used by any
individual to manage their own behaviour. This personal use of operant conditioning principles has
come to be known as behavioural self‐control training (e.g., Thoresen & Mahoney, 1974), and has
since been developed into multifaceted behavioural programmes to deal with a variety of personal
problems which include addiction, habits, obsessions, and other behavioural problems (Lutzker &
Martin, 1981; Miller & Munoz, 2013). An early programme developed by Stuart (1967) provides a good
example of a multifaceted behavioural self‐control scheme designed to address obesity by managing
behaviours contributing to overeating. The main elements of this programme were (a) recording the
time and quantity of food consumption (self‐observation); (b) weighing in before each meal and before
bedtime (helping the individual to discriminate how eating might have contributed to weight gain); (c)
removal of food from all places in the house except the kitchen (so that only the kitchen comes to act as
a cue for eating); (d) pairing eating with no other activity that might make eating enjoyable, and so
reinforce it (e.g., eating should not occur while watching an enjoyable TV programme); (e) setting a
weight loss goal of 1‐2 pounds/week (setting clearly attainable goals); (f) slowing down the pace of
eating (defining appropriate responses), and (g) substituting other activities for between‐meal eating
(programming acceptable competing responses). These principles are relatively easy to apply to your
own behaviour, and Activity Box 4.1 (available on the website) provides some suggestions as to how you
might develop your own behavioural self‐control programme to promote an activity such as studying.

behavioural self-control The personal use of operant conditioning principles to change or

control one’s own behaviour.
Cognitive therapies

The origins of cognitive therapy

In the past 40 years one of the most impressive developments in our understanding of psychopathology
has been our evolving insight into the cognitive factors that play important roles in causing and
maintaining psychopathology. For example, some psychopathologies are caused by dysfunctional ‘ways
of thinking’—either about the self or the world (e.g., in major depression). In other cases,
psychopathologies are characterised by dysfunctional ways of processing and interpreting incoming
information. For example, many anxiety disorders are characterised by a bias towards processing
threatening or anxiety‐relevant information (e.g. generalised anxiety disorder, GAD) or to interpreting
ambiguous information negatively (e.g., panic disorder, see Figure 6.4). In both cases these biases act to
develop and maintain anxiety. If such cognitive factors are maintaining psychopathology, then
developing treatments that try to address and change these dysfunctional cognitive features is important.
Two early forms of cognitive therapy based on these assumptions were Rational Emotive Therapy
(RET) and Beck's Cognitive Therapy.
How people construe themselves, their life and the world is likely to be a major determinant of their
feelings, and Rational Emotive Therapy (RET) developed by Albert Ellis (1962) was one of the first
cognitive therapies to address these factors. In particular, Ellis believed that people carry around with
them a set of implicit assumptions which determines how they judge themselves and others, and that
many of these implicit assumptions may be irrational and cause emotional distress. For example, two
irrational beliefs include (a) demanding perfection from oneself and from others, and (b) expecting
approval from others for everything one does. Clearly, there will be many occasions when these goals are
not met, and this will cause anxiety, depression and emotional discomfort. RET attempts to challenge
these irrational beliefs and to persuade the individual to set more attainable life goals. As such, RET is a
good example of a group of therapies which attempt to change a set of core beliefs about the world that
may be dysfunctional (i.e., either fallacious or a source of conflict and emotional distress). However,
make no mistake about it, changing an individual's core beliefs—which have been developed and
refined over a period of many years—is no easy thing. This is why highly structured cognitive therapies
are required for successful treatment, and these therapies will normally go through a process of
challenging existing dysfunctional beliefs, replacing these with more rational beliefs, and then getting the
individual to test out this new set of beliefs in structured behavioural exercises.

cognitive therapies Therapeutic interventions which seek to help the patient overcome
difficulties by identifying and changing dysfunctional thinking, behaviour, and emotional
responses. They include rational emotive therapy (RET), Beck’s cognitive therapy, and cognitive
behaviour therapy (CBT).

Rational Emotive Therapy (RET) A cognitive therapy technique developed by Albert Ellis
(1962) which addresses how people construe themselves, their life and the world.

Aaron Beck's cognitive theory of depression is outlined in more detail in Chapter 7, and from this
theory he developed a cognitive therapy for depression (see Whittington, 2019, and Strauss, 2019). Beck
argues that depression results when the individual develops a set of cognitive schemas (or beliefs) which
bias the individual towards negative interpretations of the self, the world and the future, and any
therapy for depression must therefore address these schemas, deconstruct them and replace them with
more rational schemas which do not always lead to negative interpretations. Beck's Cognitive
Therapy does this by engaging the depressed individual in an objective assessment of their beliefs, and
requires them to provide evidence for their biased views of the world. This enables the individual to
perceive their existing schemas as biased, irrational, and overgeneralised (see Section 7.1.2, Chapter 7).

Beck’s Cognitive Therapy An intervention derived from Beck’s view that depression is
maintained by a ‘negative schema’ that leads depressed individuals to hold negative views about
themselves, their future and the world (the ‘negative triad’).

Out of these early pioneering cognitive therapies developed what is now known as cognitive
behaviour therapy (CBT), which is an intervention for changing both thoughts and behaviour and
represents an umbrella term for many different therapies that share the common aim of changing both
cognitions and behaviour. A CBT intervention usually possesses most of the following characteristics: (a)
the client is encouraged to keep a diary noting the occurrence of significant events and associated
feelings, moods, and thoughts in order to demonstrate how events, moods and thoughts might be
interlinked; (b) with the help of the therapist, the client is urged to identify and challenge irrational,
dysfunctional, or biased thoughts or assumptions; (c) clients are given homework in the form of
‘behavioural experiments’ to test whether their thoughts and assumptions are accurate and rational; and
(d) clients are trained in new ways of thinking, behaving, and reacting in situations that may evoke their
psychopathology. As an example, Treatment in Practice Box 6.3 in Chapter 6 demonstrates how a
cognitive behaviour therapist would conduct an interview designed to identify and challenge irrational
and dysfunctional beliefs in an individual diagnosed with panic disorder.

cognitive behaviour therapy (CBT) An intervention for changing both thoughts and
behaviour. CBT represents an umbrella term for many different therapies that share the
common aim of changing both cognitions and behaviour.

‘Waves’ of CBT
CBT has not been a static treatment innovation, and just like any other knowledge‐based development,
new forms of CBT have evolved out of earlier ones. These progressive developments have come to be
known as ‘waves’, and at the present time we are experiencing what is called the third wave of CBT
techniques. The ‘first wave’ occurred during the 1950s and 1960s and was represented largely by
behaviour therapy techniques based on learning theory and conditioning principles (see Section 4.1.1).
The ‘second wave’ developed in the 1970s and 1980s when it became clear that what we do is not just
influenced by our learning and conditioning experiences but also by what and how we think
(cognitions), and how the way we think affects our emotions. This gave rise to the traditional forms of
CBT initially developed by therapists such as Aaron Beck and described in the previous section.
However, a ‘third wave’ or ‘third generation’ of CBT methods have developed which emphasise
mindfulness, acceptance, and a greater concern with the individual's relationship with their
psychopathology experiences and aim to reduce distress by changing the function of the experience
rather than necessarily changing the experience (for example, instead of attempting to eliminate the
hearing of voices in individuals with a diagnosis of schizophrenia, third‐wave CBT for psychosis
attempts to change the individual's beliefs about their voices and their relationship with those voices)
(Culpitt, 2018). Important examples of third‐wave CBT therapies include Dialectical Behaviour
Therapy (DBT) (to be discussed more fully in Chapter 12), MBCT, ACT, and Behavioural Activation
(BA).
Mindfulness‐based cognitive therapy (MBCT) is a direct extension of traditional CBT in which
treatments emphasise achieving a mental state characterised by present‐moment focus and
nonjudgmental awareness (Bishop et al., 2004; Kabat‐Zinn, 2003). The purpose of this is to improve
emotional well‐being by increasing awareness of how automatic cognitive and behavioural reactions to
thoughts, sensations, and emotions can cause distress. Clients are encouraged to acknowledge and
accept their thoughts and feelings, and by focussing on the present rather than the past or future, the
individual can learn to deal more effectively with life stressors and challenges that generate anxiety or
depression (Activity Box 4.2 – available on the website – provides a series of instructions for a simple 5–
10 minute mindfulness exercise that will facilitate bodily awareness). Mindfulness interventions are
considered to reduce symptoms of common mental health problems such as anxiety and depression by
countering avoidance strategies, helping the individual to respond reflectively rather than reflexively to
stressors, and reducing physical symptoms by advocating the use of meditation and yoga exercises
(Kabat‐Zinn, 1982). Since it's early development, mindfulness has now been successfully applied to a
wide range of mental health problems, including anxiety and stress, depression, pain relief, post‐
traumatic stress disorder (PTSD), and psychosis (Chadwick, Hughes, Russell, Russell, & Dagnan, 2009;
Goyal et al., 2014; Vujanovic, Niles, Pietrefesa, Schmertz, & Potter, 2011; Williams & Kuyken, 2012;
Zeidan & Vago, 2017). A description of the science of mindfulness given by Mark Williams can be
found at https://www.youtube.com/watch?v=0wBZjb8u95o.

Mindfulness-based cognitive therapy (MCBT) A direct extension of traditional CBT in

which treatments emphasize achieving a mental state characterised by present-moment focus
and nonjudgemental awareness

Acceptance and commitment therapy (ACT) is also a third‐wave CBT intervention that has
grown in popularity over recent years (Hayes, Strosahl, & Wilson, 2016). It is an approach that adopts
some aspects of mindfulness, but has developed more from the behaviour analysis or Skinnerian
approach to understanding behaviour (see Chapter 1, Section 1.3.2). ACT differs from traditional CBT
in that, rather than getting individuals to manage and change their thoughts and the way they think, it
teaches them to ‘just notice’, accept, and embrace private events such as thoughts (especially thoughts
that may be intrusive, distressing, or unwanted). As such, it aims to help the individual clarify their
personal values, to take action on them, and to increase their psychological flexibility (Hayes, Luoma,
Bond, Masuda, & Lillis, 2006; Zettle, 2005). Systematic reviews and meta‐analyses suggest that ACT is
probably efficacious for chronic pain disorders, depression, some psychotic symptoms, obsessive‐
compulsive disorder (OCD), and some forms of substance abuse, but effect sizes found in randomised
controlled trials (RCTs) tend to be relatively small and there may be insufficient evidence yet to
conclude that ACT for anxiety‐based problems is efficacious (Hacker, Stone, & McBeth, 2016; Öst,
2014; but see Atkins et al., 2017, for a response to these reviews by Hayes and colleagues). On the
book’s website, Activity Box 4.3 provides you with an example of how ACT attempts to help you
distance yourself from negative or distressing thoughts.

Acceptance and commitment therapy (ACT) A third wave CBT intervention that adopts
some aspects of mindfulness, but has developed more from the Skinnerian approach to
understanding behaviour.

randomised controlled trials (RCTs) Comparison of the effectiveness of a treatment

being assessed with a variety of control conditions, and with other forms of therapy and
treatment (if necessary).

Behavioural activation (BA) is a third‐wave therapy that encourages individuals with depression to
approach activities they may have been avoiding. The rationale is that depression is a condition caused
in part by avoiding particular activities or situations that in the past were positively reinforcing. Together
with the client, the therapist defines goals to be achieved and draws up a schedule of activities to achieve
these goals and so reestablish activities that are rewarding and pleasurable. For example, if one of the
goals of the client is to be a compassionate person, the client and therapist might draw up a schedule of
activities such as volunteering, helping out a friend, or donating to charity. BA has its origins in 1970s
behaviourism, which argued that depression was at least in part the result of the depressed individual no
longer engaging in activities that were positively reinforcing (Lewinsohn, 1974). After conducting a
component analysis of CBT, Jacobson and colleagues developed the BA approach to therapy by arguing
that the behavioural activation component of CBT was sufficient enough to account for its success
when treating depression (Jacobson et al., 1996). Subsequent meta‐analyses of random controlled trials
have generally reported significantly better effects of BA in treating depression than appropriate control
conditions (Ekers et al., 2014), but there is less consensus on whether BA is superior to other treatments
such as CBT or antidepressant medication (Dimijian et al., 2016).
While ‘new‐wave’ developments bring new and exciting ways of delivering CBT across a range of
disorders, these new approaches are still being evaluated. Studies suggest that third‐wave therapies such
as MBCT, ACT, and BA should not be considered as separate from the growing body of CBT
approaches (Hofman, Sawyer, & Fang, 2010), may have their successful therapeutic effects through
similar mechanisms to CBT (Dimijian et al., 2016; Hofman & Asmundson, 2008) and are generally
equally effective as each other (Gaudiano, 2009; Öst, 2008). CBT in general is perceived as an evidence‐
based and cost‐effective form of treatment that can be successfully applied to a very broad range of
psychopathologies (Butler, Chapman, Forman, & Beck, 2006; Cuijpers, Cristea, Karyotaki, Reijnders, &
Huibers, 2016), is equally as effective as other forms of psychotherapy, and superior to many other
forms of psychotherapy when treating anxiety and depressive disorders (Tolin, 2010).

Humanistic therapies
Throughout the twentieth century, many psychotherapists felt that psychological therapy was becoming
too focussed on psychological and behavioural mechanisms, or on psychological structures (such as
personality), and was losing sight of both the feelings of the individual and the individual themselves. As
a consequence, a number of what are called ‘humanistic’ therapies developed, including Gestalt therapy
(Perls, 1969), existential therapies (Cooper, 2003), primal therapy (Janov, 1973), narrative therapy
(Freedman & Combs, 1996), and transpersonal therapy (Wellings & McCormick, 2000) and, arguably
the most successful of these is client‐centred therapy (Rogers, 1961). These therapies had a number of
factors in common: (a) they espoused the need for the therapist to develop a more personal relationship
with the client in order to help the client reach a state of realisation that they can help themselves; (b)
they were holistic therapies, in that they emphasised the need to consider the ‘whole’ person and not
just those ‘bits’ of the person that manifest psychopathology; (c) therapy should be seen as a way of
enabling the individual to make their own decisions and to solve their own problems rather than
imposing structured treatments or ways of thinking on the individual; (d) humanistic therapies
espouse the need for the therapist‐client relationship to be a genuine reciprocal and empathetic one,
rather than the limited skilled professional‐referred client relationship that exists in many forms of
psychological therapy; and (e) increasing emotional awareness is a critical factor in alleviating
psychological distress, and is necessary before the client can begin to resolve life problems (Focus Point
4.1).

holistic therapies Therapies which emphasise the need to consider the ‘whole’ person, not
just those ‘bits’ of the person that manifest psychopathology.

humanistic therapies Therapies that attempt to consider the ‘whole’ person and not just the
individual symptoms of psychopathology.
 FOCUS POINT 4.1 GESTALT THERAPY

Gestalt therapy is a popular existential humanistic therapy that was originally developed by
Fritz Perls and colleagues in the 1940s and 1950s (Perls, 1947; Perls, Hefferline, & Goodman,
1951). It focuses on an individual's experiences in the present moment, the therapist‐client
relationship, and the contexts in which the individual lives their life. It emphasises that the most
helpful focus of psychotherapy is on what a person is doing, thinking, and feeling at the present
moment, rather than on what was, might be, or could be. It is also a method of awareness
practice very similar to mindfulness (see Section 4.1.1) in which current perceiving, feeling and
acting are helpful to interpreting, explaining, and conceptualising experience. Much of the
Gestalt approach is about the client exploring their relationship with themselves, and one
method of achieving this is by using the role‐playing empty‐chair technique, which involves
the client addressing the empty chair as if another person was in it and acting out the two sides
of a discussion.
Gestalt therapy is often considered a good method for managing tension, depression and
anxiety, and uncontrolled outcome studies suggest that Gestalt therapy provides participants
with better emotional well‐being and a heightened sense of hope (Leung, Leung, & Ng, 2013).
At least some psychotherapists believe that the methods deployed by Gestalt therapy might be
productively integrated with more conventional interventions such as cognitive therapy
(Tonnesvang, Sommer, Hammink, & Sonne, 2010) and might make a useful contribution to
modern psychiatric practice (Clegg, 2010).

Client‐centred therapy focuses on the individual's immediate conscious experience, and critical to
this form of humanistic therapy is the creation of a therapeutic climate that allows the client to progress
from a state of rigid self‐perception to one which encourages the client to become independent, self‐
directed, and to pursue self‐growth. For Carl Rogers (1902–1987), empathy (‘putting yourself in
someone else's shoes’) was the central important feature of any therapist‐client relationship, and it is this
ability that is essential in guiding the client towards resolving their own life problems. Empathy has at
least two main components in this context: (a) an ability to understand and experience the client's own
feelings and personal meanings, and (b) a willingness to demonstrate unconditional positive regard
for the client. This latter feature involves valuing the client for who they are and refraining from judging
them. Another important feature of client‐centred therapy is that it is not directive. The therapist acts
primarily as an understanding listener who assists the client by offering advice only when asked. The
overriding goal is to develop the client through empathy, congruence, and unconditional positive regard
to a point where they are successful in experiencing and accepting themselves and are able to resolve
their own conflicts and difficulties.

Client-centred therapy An approach to psychopathology stressing the goodness of human

nature, assuming that if individuals are unrestricted by fears and conflicts, they will develop into
welladjusted, happy individuals.

In much the same way that psychoanalysis has evolved, client‐centred therapy has developed not just as
a therapy but also as a process for fostering personal self‐growth. The general approach places relatively
little emphasis on how the psychopathology was acquired but attempts to eliminate symptoms by
moving the client from one phenomenological state (e.g., a state of anxiety, depression, etc.) to another
(e.g., one that enables the client to view themselves as worthy and respected individuals).
Family and systemic therapies
Family therapy is a form of intervention that is becoming increasingly helpful as a means of dealing
with psychopathology that may result from the relationship dynamics within the family (Dallos &
Draper, 2015). Family therapy has a number of purposes: (a) it helps to improve communications
between members of the family—especially where communication between individuals might be the
cause of psychopathology in one or more family members, (b) it can resolve specific conflicts—for
example between adolescents and their parents, and (c) it may apply systems theory (attempting to
understand the family as a social system) to treatment by trying to understand the complex relationships
and alliances that exist between family members, and then attempting to remould these relationships
into those expected in a well‐functioning family (the latter may usually involve ensuring that the primary
relationship in the family—between the two parents—is strong and functional) (Minuchin, 1985).

Family therapy A form of intervention involving family members that is helpful as a means
of dealing with psychopathology that may result from the relationship dynamics within the
family.

systems theory Approach that attempts to understand the family as a social system.

In family therapy, the therapist or family therapy team meets with those members of the family willing
to participate in discussion about a topic or problem raised by one or more members of the family. In
the case of an adolescent eating disorder, the parents may have raised the issue of how their child's
eating disorder affects family functioning, and this may be explored with the family over a series of
meetings. Family therapists are usually quite eclectic in the range of approaches they may bring to
family therapy, and these may include cognitive‐behavioural methods, psychodynamic approaches, and
systemic analyses depending on the nature of the problem and its underlying causes. In many cases,
family therapists may focus on how patterns of interaction within the family maintain the problem (e.g.,
an eating disorder) rather than trying to identify the cause (the latter may be seen as trying to allocate
blame for the problem within the family). Over a period of between 5 and 20 sessions, the family
therapist will attempt to identify family interaction patterns that the family may not be aware of, and to
suggest to family members different ways of responding to each other. Family therapy has been shown
to be an effective intervention for a number of psychopathologies in both children and adults, including
conduct disorder, substance abuse, depression, and eating disorders (Stratton, 2016; Sydow, Beher,
Schweitzer, & Retzlaff, 2010). A case example of the use of family therapy with an adolescent with an
eating disorder is provided in Treatment in Practice Box 10.1 in Chapter 10.

Drug treatments
Pharmacological or drug treatments are regularly used to alleviate some of the symptoms of
psychopathologies. They are often the first line of treatment provided by GPs and doctors to tackle
anxiety and mood‐based problems and may be sufficient to enable an individual to see through an acute
bout of anxiety or depression. Some of the most commonly used drug treatments include
antidepressant drugs to deal with symptoms of depression and mood disorder, anxiolytic drugs
to treat symptoms of anxiety and stress, and antipsychotic drugs prescribed for symptoms of
psychosis and schizophrenia.

antidepressant drugs Drug treatments intended to treat symptoms of depression and mood
disorder.
 anxiolytic drugs Drug treatments intended to treat symptoms of anxiety and stress.

antipsychotic drugs Drug treatments intended to treat symptoms of psychosis and

schizophrenia spectrum disorders

Drug treatments for depression

Drug treatments for depression were first developed in the 1960s and the first class of drugs were called
tricyclic antidepressants (because of their chemical structure). These drugs increase the amount of
norepinephrine and serotonin available for synaptic transmission. Other antidepressants introduced
during this period were monoamine oxidase inhibitors (MAOIs) (such as phenelzine and
tranylcypromine), and MAOIs are effective for some people with major depression who do not respond
to other antidepressants. They are also prescribed for the treatment of panic disorder and bipolar
depression. More recently, we have seen the development of the first ‘designer drugs’ for depression,
and these include fluoxetine (Prozac), sertraline (Lustral), and citalopram (Cipramil). These newer drugs
are collectively called selective serotonin reuptake inhibitors or SSRIs because they selectively
affect the uptake of only one neurotransmitter—usually serotonin. Serotonin and norepinephrine
reuptake inhibitors(SNRIs) are among the most recently developed antidepressants and, as the
name implies, they block the reuptake of both serotonin and norepinephrine (see Table 4.1 for examples
of antidepressant medications).

tricyclic antidepressants Antidepressant drugs developed in the 1960s which have their
effect by increasing the amount of norepinephrine and serotonin available for synaptic
transmission.

monoamine oxidase inhibitors (MAOIs) Antidepressants which are effective for some
people with major depression who do not respond to other antidepressants.

Selective serotonin reuptake inhibitors (SSRIs) A recent group of antidepressant drugs

that selectively affect the uptake of only one neurotransmitter – usually serotonin.

Serotonin–norepinephrine reuptake inhibitors (SNRIs) A recent group of drugs for

anxiety-based symptoms which selectively inhibit norepinephrine and serotonin reuptake and
have been shown to be effective and well tolerated in individuals with anxiety disorders.

Comparisons of antidepressant drugs with placebo controls suggest that most antidepressants are more
effective in treating depression symptoms than placebos (e.g., Cipriani et al., 2018), but not everyone
benefits from the use of antidepressants. The Royal College of Psychiatrists estimates that 50–65% of
people will see an improvement in symptoms, but some studies suggest that only one in three depression
sufferers will achieve full symptom relief after using antidepressants (Trivedi et al., 2006), and in other
studies only around 40% of people achieve sustained recovery (Arroll, Macgillivray, Ogston, Reid, &
Sullivan, 2005; Nelson, Portea, & Leon, 2006). Some studies suggest that antidepressants are more
effective than placebos for people with moderate to severe depression during the acute phase of their
depression (Undurraga & Baldessarini, 2011) but not for those with subthreshold or mild depression
(Fournier et al., 2010). These issues are compounded by the fact that almost 40% of those who are
prescribed with antidepressants stop taking the drug within the first month—often because of the side
effects (Olfson, Blanco, Liu, Moreno, & Laje, 2006). The length of antidepressant use varies, with
around half of those with a first diagnosis of depression terminating use after around 7 months, but
around a third continue use for 1 year or more (Coupland et al., 2015), and many individuals continue
with long‐term use of antidepressants at least in some cases because their continuing need for
medication use has not been adequately reviewed (Sinclair, Aucott, Lawton, Reid, & Cameron, 2014).
Finally, although antidepressants do appear to hasten recovery from an episode of depression, relapse is
common after the drug is discontinued (Reimherr, Strong, Marchant, Hedges, & Wender, 2001),
although this tendency to relapse is less so with SSRIs than with other forms of antidepressant (Sim,
Lau, Sim, Sum, & Baldessarini, 2015).
Interestingly, there has been a dramatic increase in the prescribing of antidepressants in the past 10–15
years, and in the UK there has been a doubling in the number of prescriptions in 10 years between
2007 and 2017 (Royal College of Psychiatrists, 2019), with a similar dramatic increase being reported in
the United States (Dorick & Frances, 2013). In the year 2017 one in six adults were given at least one
antidepressant prescription in the UK, and individuals over 60 years of age were twice as likely as those
in their twenties to be using an antidepressant (Royal College of Psychiatrists, 2019). Part of this
increase in prescribing may be due to an increase in the diagnosing of depression during this period
(e.g., Sarginson et al., 2017), and there is some evidence that the rate particularly accelerated between
2008 and 2012, during the period of financial recession. But at least some of this increase may be the
result of increased awareness of the symptoms of depression by the public generally (but see also Focus
Point 1.6 in Chapter 1 on the Medicalisation of Normality).
There is no clear conception of how antidepressants work and the original view that antidepressants
correct a chemical imbalance in the brain is an oversimplification. The assumption has been that
antidepressants target monoamine neurotransmitter function and increase serotonin or noradrenaline
availability in the brain (see Chapter 7 for discussion of the role of neurotransmitters in depression). But
there is a lack of evidence that antidepressants cure a deficiency of monoamines that is thought to be
causing depression (Healy, 2015; Huda, 2019). What is perplexing is that the main supposed effect of
antidepressants of inhibiting the reuptake of monoamines such as serotonin and noradrenaline occurs
immediately the individual begins taking the medication, but improvements in depression symptoms
rarely begin until several weeks after drug commencement (Harmer, Duman, & Cowen, 2017). More
recent conceptions of how antidepressants work claim that these medications may help to build up
neural plasticity which may have been eroded by stress, and that this may account in part for the
delayed onset of recovery (e.g., McEwen et al., 2015). In addition, there is evidence that antidepressants
decrease processing of negative emotional stimuli and increase attention to positive emotional stimuli
(Godlewska & Harmer, 2019; Harmer, Goodwin, & Cowen, 2009) and this eventually leads to
improvement in mood consistent with cognitive theories of depression (see Chapter 7).
TABLE 4.1 Common antidepressant medications
Category Generic name Brand Common side
name effects
Selective serotonin reuptake inhibitors (SSRIs) Fluoxetine Prozac Feeling sick
Headaches
Sleep problems
Diarrhoea
Feeling tired
Citalopram Cipramil Dry mouth
Sweating
Sleep problems
Tiredness
Sertraline Lustral Feeling sick
 Headaches
Sleep problems
Diarrhoea
Dry mouth
Dizziness
Feeling Tired
Serotonin‐noradrenaline reuptake inhibitors Duloxetine Cymbalta Nausea
(SNRIs) Yentreve Dry mouth
Constipation
Fatigue
Sleep Problems
Venlafaxine Efexor Feeling sick
Headaches
Sweating
Dry mouth
Sleep problems
Feeling dizzy
Constipation
Tricyclic Antidepressants (TCAs) Amitriptyline Tryptizol Constipation
Nausea
Appetite or weight
changes
Itching or rash
Decreased sex drive
Imipramine Tofranil Dry mouth
Blurred vision
Tiredness
Dizziness
Constipation
Nausea
Stomach cramps
Weight gain/loss
Monoamine oxidase inhibitors (MAOIs) Tranylcypromine Parnate Vision problems
Headaches
Fast heartbeats
Nausea
Dizziness
Phenelzine Nardil Headaches
Chest pain
Weight gain
Agitation/Unusual
thoughts

Drug treatments for anxiety

There are a number of psychological disorders that are characterised by chronic, high levels of anxiety.
The more prevalent of these include clinically diagnosable specific phobias, panic disorder, GAD, OCD,
and PTSD (see Chapter 6). The symptoms of these disorders can usually be treated with anxiolytics
(tranquillisers) such as the benzodiazepines (which include the well‐known tranquilliser, valium), and
they have their effect by increasing the level of the neurotransmitter gamma‐aminobutyric acid (GABA)
at synapses in the brain. Benzodiazepines are usually prescribed for only short periods because they can
encourage dependence if taken over a longer period and can also be abused if available in large doses.
However, it is important to be aware that anxiolytics will usually offer only symptom relief and do not
address the psychological and cognitive factors that may be maintaining the anxiety, and as a result
symptoms often return when the individual stops taking the drug. Benzodiazepines can have important
cognitive and physical side effects such as memory lapses and drowsiness, and these effects can have
real‐world consequences such as an increased risk of car accidents while taking the drug (Baldwin et al.,
2014).

benzodiazepines A group of anxiolytics which have their effect by increasing the level of the
neurotransmitter GABA at synapses in the brain.

Nowadays, the first choice medications for anxiety‐based problems are antidepressants, and in particular
SSRIs or SNRIs (Hoffman & Mathews, 2008). SSRIs and SNRIs have been shown to be an effective
and well tolerated treatment in individuals with anxiety disorders (Dell'Osso, Buoli, Baldwin, &
Altamura, 2010; Slee et al., 2019), making them superior to benzodiazepines in terms of significantly
reduced side effects and less likelihood of withdrawal symptoms following discontinuation (Schweizer,
Rickels, Case, & Greenblatt, 1990).

Drug treatments for psychosis

Drug treatments for psychosis and schizophrenia have radically changed the way that individuals with a
diagnosis of schizophrenia are treated and cared for. The use of effective antipsychotic drugs became
common in the 1960s and 1970s, and this had the effect of drastically reducing the number of
individuals with psychotic symptoms who needed long‐term institutionalised care, and has enabled
many experiencing such symptoms to achieve a level of functioning that permits relatively normal day‐
to‐day functioning. Prior to the 1980s, it was estimated that two out of three individuals with a diagnosis
of schizophrenia would spend most of their lives in a psychiatric institution; beyond the 1980s the
average length of stay is down to as little as two months (Lamb, 1984), and the number of National
Health Service (NHS) psychiatric beds has fallen from a high of 150,000 in the 1950s to less than
30,000 currently (Tyrer & Johnson, 2011).
Antipsychotic medications can be divided into first‐ and second‐generation drugs (see Table 4.2). The
first‐generation drugs were the first to be developed in the 1940s and 1950s, and certainly helped to
reduce many of the positive and disorganisational symptoms of psychosis (such as hallucinations,
delusions, confused thought, movement disorders) but had little effect on the negative symptoms (such as
apathy, loss of motivation, poverty of speech and thought, and lack of social interest). There is some
evidence that these first‐generation drugs reduced relapse (Leucht et al., 2012), but they were not a cure.
Around 30% of individuals with a diagnosis of schizophrenia do not respond favourably to first‐
generation drugs and many still have difficulty with day‐to‐day functioning (Lieberman et al., 2015).
Most important, these first‐generation drugs often had quite severe side effects that led to over half
those taking the drug quitting after a year (Lieberman et al., 2015). In particular, these side effects
included extrapyramidal effects (physical symptoms such as tremor and slurred speech similar to
symptoms found with Parkinson's disease, see Chapter 15). Blood sugar problems were often another
side effect that could give rise to type 2 diabetes.
Because first‐generation antipsychotic drugs did not represent a cure for psychosis, there was a drive in
the 1970s and 1980s to develop more effective drugs and this has given rise to the second generation of
antipsychotics. Early comparisons of first‐ and second‐generation drugs suggested that the second‐
generation medications resulted in a greater percentage of clients responding well to treatment, there
was a small but significant improvement in negative symptoms as well as positive symptoms, and a
reduction in extrapyramidal side‐effects (Kane, Honigfeld, Singer, & Meltzer, 1988). Second‐generation
drugs have also been found to be marginally superior to their first‐generation counterparts in improving
cognitive deficits (Davis, Chen, & Glick, 2003; Veselinović et al., 2019).
TABLE 4.2 Antipsychotic medications
Category Generic name Brand name Side effects
First‐Generation Drugs Chlorpromazine Largactil Common side effects:
Fluphenazine Modecate Restlessness
Dry mouth
Halperidol Dozic, Haldol Blurred vision
Trifluoperazine Stelazine Constipation
Weight gain
Second‐Generation Clozapine Clozaril, Denapine, Sexual dysfunction
Drugs Zaponex Rarer serious side‐effects:
Aripipazole Abilify Fever
Olanzapine Zypadhera, Zyprexa Sweating
Muscle stiffness
Risperidone Risperdal, Risperdal Consta Diabetes
Amisulpride Solian Irregular heart beats
Tremors and speech
Quetiapine Seroquel
slurring
Antipsychotics are thought to have their effects by reducing the activity of dopamine type 2 receptors,
and this is assumed to be the factor that reduces psychotic symptoms in those that respond to
antipsychotic drugs (Kapur, Agid, Mizrahi, & Ming, 2006, see Chapter 8). This not only reduces the
major positive symptoms (such as thought disorder and hallucinations) but can also reduce the major
negative symptoms (such as social withdrawal) when second‐generation drugs are used.
While antipsychotic drugs do not represent a cure for psychosis, there is evidence that their long‐term
use is associated with clinical benefits over the longer term—but this benefit may only be a lack of
worsening of symptoms rather than an improvement in symptoms when compared with placebos
(Takeuchi et al., 2017). Thus, even second‐generation antipsychotics are far from perfect. They do not
represent a cure, may only prevent a worsening of symptoms, and still have side effects that result in a
significant percentage of sufferers abandoning the medication within the first year of use. Are we
anywhere near a third generation of antipsychotics that will improve on those already available?
Seemingly not. As Owens and Johnstone (2018) point out in their recent review of the development of
antipsychotic drugs ‘the pipeline of new antipsychotics has dried to a trickle and international pharma
has moved on. The story of antipsychotics is a sobering rollercoaster’ (Owens & Johnstone, 2018, p. 1).

Problems with drug treatments

Despite the fact that appropriate medication can often provide relief from the symptoms of
psychopathology, there is a view that interventions using drugs alone may be problematic for a number
of reasons. First, prescribing drugs for some mild psychopathology symptoms may effectively
‘medicalise’ what are merely everyday problems of living and lead people to believe that acute bouts of
anxiety or depression are ‘diseases’ that will not be alleviated until medical treatment has been sought
(Shaw & Woodward, 2004; see Focus Point 1.6 in Chapter 1). Similarly, many drugs are tested for their
effectiveness on individuals with severe symptoms, and some recent studies suggest that they may be
ineffective for people with only mild symptoms (Fournier et al., 2010; Kirsch et al., 2008). Second, long‐
term prescription of drugs for a psychopathology may lead sufferers to believe that their symptoms are
unchangeable and that their psychological and social functioning will depend on them continuing to
take their medication. This can often prevent such individuals from trying to understand their
symptoms and from gaining insight into symptoms that may be primarily psychological rather than
medical in nature (Bentall, 2003). Finally, there is some evidence that while drug treatment of
psychopathology may alleviate the immediate symptoms, it may worsen the long‐term course of a
disorder. For example, while antidepressant drugs may alleviate the immediate symptoms of depression,
there is evidence that some may also increase vulnerability to relapse over the longer term (Fava, 2003).
This may be a result of drug tolerance effects as a result of continued drug use plus the fact that drug
treatment alone may not facilitate the kinds of beneficial insights into the psychopathology that
psychological therapies may provide. This account is consistent with the fact that when drug treatments
are successful over the longer term, this is more likely to be the case if drug treatment is combined with
psychological treatment (e.g., CBT) (Cuijpers et al., 2014; Hollon & Beck, 1994).

Summary of theoretical approaches to treatment

Each of the treatment approaches we have discussed in this section can be used to treat a range of
different psychopathologies, and we look more closely at how to evaluate their success later in this
chapter. Each of these approaches differs not only in the basic intervention procedures they use, but also
in the way they attempt to explain psychopathology (see Chapter 1). Contemporary practitioners may
well be skilled in using more than one of these approaches, and, indeed, a combination of approaches
may be used to address specific psychopathologies (e.g., the use of both drug treatment and CBT to
treat depression).

4.1.2 Modes of Treatment Delivery

The standard and traditional mode of psychotherapy delivery is in one‐to‐one, face‐to‐face meetings or
sessions between a therapist and a client, and this is still the most prevalent mode of delivery today.
However, with the pressing need to treat ever increasing numbers of individuals referred with symptoms
of psychopathology, over‐stretched clinicians and service providers often look to find more cost‐effective
and efficient ways to delivery treatment interventions. The following section looks briefly at some of the
modes of delivery that have been developed to supplement the traditional one‐to‐one therapist‐client
model.

Group therapy
Therapy can also be undertaken in a group and not just on a one‐to‐one therapist‐client basis. Group
therapy can be useful (a) when a group of individuals share similar problems or psychopathologies (e.g.,
self‐help groups), or (b) when there is a need to treat an individual in the presence of others who might
have a role in influencing the psychopathology (e.g., family therapy). Group therapies can have a
number of advantages, especially when individuals (a) may need to work out their problems in the
presence of others (e.g., in the case of emotional problems relating to relationships, feelings of isolation,
loneliness and rejection), (b) may need comfort and support from others, and (c) may acquire
therapeutic benefit from observing and watching others. There are now many different types of group
therapy (Block & Crouch, 1987), and these include experiential groups and encounter groups
(which encourage therapy and self‐growth through disclosure and interaction) and self‐help groups
(which bring together people who share a common problem, in an attempt to share information and
help and support each other—e.g., Alcoholics Anonymous, http://www.alcoholics‐anonymous.org.uk,
see Focus Point 9.2 in Chapter 9). However, interventions that have traditionally been used only in one‐
to‐one client‐therapist situations are now being adapted to group settings, and two of these include CBT
and mindfulness (Arch et al., 2013; Wolgensinger, 2015). Adapting interventions for groups is likely to be
a cost‐effective solution for service providers as well as an effective way of helping clients to manage
symptoms of psychopathology.
 encounter groups Group therapy which encourages therapy and self-growth through
disclosure and interaction.

self-help groups Group therapy which brings together people who share a common problem
in an attempt to share information and help and support one another.

Counselling
Counselling is still a developing and evolving profession that has burgeoned in the past 20–30 years,
and its expansion has partly resulted from the increasing demand for trained specialists able to provide
immediate support and treatment across a broad range of problems and client groups. Counsellors
receive specialised training in a range of support, guidance, and intervention techniques, and their levels
of training are monitored and accredited by professional bodies such as the British Association for
Counselling and Psychotherapy (BACP) in the UK, or Division 17 (Counselling Psychology) of the
American Psychological Association. Arguably, the primary task for counselling is to give the client an
opportunity to explore, discover, and clarify ways of living more satisfyingly and resourcefully, and to
‘help clients to understand and clarify their views of their lifespace, and to learn to reach their self‐
determined goals through meaningful, well‐informed choices and through resolution of problems of an
emotional or interpersonal nature.’ (Burks & Stefflre, 1979, p. 14). These definitions indicate that
counselling is a profession that aims to both promote personal growth and productivity and to alleviate
any personal problems that may reflect underlying psychopathology. In order to achieve these aims,
counsellors tend to adopt a range of theoretical approaches, with the main ones being psychodynamic,
cognitive—behavioural, and humanistic (Galbraith, 2018). Counsellors with different theoretical
orientations may often focus on different outcomes. Humanistic counsellors tend to promote self‐
acceptance and personal freedom, psychodynamic counsellors focus primarily on insight, and cognitive‐
behavioural counsellors are mainly concerned with the management of behaviour and symptoms of
psychopathology (Galbraith, 2018). Some counsellors specialise in areas such as marital breakdown,
rape, bereavement, or addictions, and their specialised roles may be recognised by the use of titles such
as mental health counsellor, marriage counsellor or student counsellor. Counselling
agencies have been established in a range of organisations to supplement community mental health
services and provide more direct and immediate access to support for vulnerable or needy individuals.
Counselling services may be directed towards people with particular medical conditions such as HIV
positive and cancer and also to the carers of individuals suffering these illnesses, and these services are
often provided by voluntary and charitable organisations set up specifically for these purposes. Even
individual companies and organisations may have set up their own in‐house counselling services to help
people through difficulties and anxieties associated with their work.

Counselling A profession that aims both to promote personal growth and productivity and to
alleviate any personal problems that may reflect underlying psychopathology.

mental health counsellor A counsellor who specialises in mental health problems

marriage counsellor A counsellor who specialises in marriage problems.

 student counsellor A counsellor who specialises in students’ problems.

Digital technologies
The availability of digital technologies offers new ways of providing psychological treatments for
mental health problems through computers, the Internet, mobile devices such as smartphones, and
mobile software applications (apps). The value of these types of interventions lies in the fact that they
reduce the need for continual therapist–client face‐to‐face therapeutic interactions at a time when
referrals for mental health problems are rising dramatically, and mental health services resources are
often severely stretched. In this section we cover a number of these developing technologies, including
computer‐based treatments, mental health apps, e‐therapy via the Internet, and virtual reality based
exposure.
There are already many well‐established computer‐based treatments for common mental health
problems such as anxiety and depression, and most are designed to be used on their own or with some
form of support (Fairburn & Patel, 2017). For example, because a treatment such as CBT has a highly
organised structure, it lends itself well to delivery by other modes and as a package that might be used
independently by the client. In recent years, computerised CBT (CCBT) has been developed as an
alternative to therapist‐delivered CBT, and consists of highly developed software packages that can be
delivered via an interactive computer interface on a personal computer, over the Internet or via the
telephone using interactive voice response (IVR) systems (Moritz, Schilling, Hauschildt, Schröder, &
Treszl, 2012). Examples of CCBT packages for depression and anxiety are ‘Beating the Blues’,
‘MoodGYM’, and ‘Fear Fighter’: (a) Beating the Blues® as an option for delivering computer‐based CBT
in the management of mild and moderate depression; (b) MoodGYM was developed by the Centre for
Mental Health Research at the Australian National University and is an online self‐help programme
that provides CBT training to help individuals manage symptoms of anxiety and depression
(Christensen, Griffiths, & Groves, 2004); and (c) Fear Fighter™ is an option for delivering computer‐based
CBT in the management of panic, agoraphobia and specific phobia. For example, Beating the Blues
consists of a 15‐minute introductory video and eight 1‐hour interactive sessions, including homework to
be completed between sessions. The programme helps the client identify thinking errors, challenge
negative thoughts, identify core negative beliefs, and provides help and advice on more adaptive
thinking styles (www.beatingtheblues.co.uk; see also Treatment in Practice Box 7.1).

computerised CBT (CCBT) Developed as an alternative to therapist delivered CBT, CCBT

consists of highly developed software packages that can be delivered via an interactive computer
interface on a personal computer, over the internet or via the telephone using interactive voice
response (IVR) systems.

Digital CBT is recommended by the UK National Institute for Health & Clinical Excellence as a
suitable intervention for adults and young people with mild depression (National Institute for Health
and Clinical Excellence, 2019), and early studies comparing CCBT with other forms of support and
intervention were relatively supportive, and suggested that CCBT along with other guided self‐help
programmes could be a valuable and effective way of treating individuals with common mental health
problems (Cuijpers et al., 2009; Kaltenthaler, Parry, Beverley, & Ferriter, 2008). For example, Proudfoot
et al. (2004) found that Beating the Blues provided a more effective treatment for depression and anxiety
than GP treatment as usual, and in a review of 16 studies exploring the efficacy of CCBT, Kaltenthaler,
Parry, and Beverley (2004) found that five studies showed CCBT to have equivalent outcomes to
therapist led CBT, and four studies found CCBT to be more effective than GP treatment as usual.
CCBT offers a number of advantages to both clients and service providers, including increased flexible
access to evidence‐based treatments, reduction of waiting lists, and savings in therapist time
(Learmonth, Trosh, Rai, Sewell, & Cavanagh, 2008; Titov, 2007).
However, there are still issues surrounding the usefulness and effectiveness of CCBT. First, clients may
often find it difficult to engage with CCBT without support. For example, clients need to have a
minimum knowledge of computers, and may often view CCBT as both mechanical and impersonal
(Beattie, Shaw, Kaur, & Kessler, 2009). CCBT may also lack many of the ingredients for successful
therapy that are a function of the therapeutic relationship between therapist and client (Dogg‐
Helgadottir, Menzies, Onslow, Packman, & O'Brian, 2009), but there are some indications that it may
be possible to incorporate these important ‘alliance’ ingredients into self‐help programmes such as
CCBT (Barazzone, Cavanagh, & Richards, 2012; Ormrod, Kennedy, Scott, & Cavanagh, 2010).
Second, and more important, recent large‐scale long‐term RCTs of CCBT have failed to find any
superiority for CCBT (e.g., MoodGYM) over GP care as usual, and relatively low uptake of CCBT is
found when it has been offered (Gilbody et al., 2015). However, the Gilbody et al. (2015) study was
conducted entirely within primary care settings, and was in contrast to many previous studies that had
demonstrated a superiority of CCBT that had targeted their participants through the Internet or
specialist referral centres where participants are directly supervised while using the CCBT package.
Much of the most recent evidence on the efficacy of CCBT suggests that support is critical for CCBT
to be effective or fully engaged with (e.g., with the help of a telephone support worker who provides a
programme of weekly telephone calls explaining the process and introducing the principles of CBT)
(Fairburn & Patel, 2017; Gilbody et al., 2017). To this extent, CCBT is still a work in progress, with
researchers still searching for the optimal conditions that will make CCBT both a significant help with
managing symptoms of mental health problems while being suitably cost effective.
Intervention programmes can also be delivered via mobile phones, and there has been a rapid growth in
the number of mental health apps made available in recent years. This has fuelled a belief that
mental health apps might be able to provide help to those with mental problems without imposing
substantial pressures on already squeezed mental health resources (e.g., Donker et al., 2013) (see also
Focus Point 2.4 in Chapter 2). However, there is still a significant amount of work required to evaluate
the usefulness of a rapidly expanding body of mental health apps. In 2013 there were 1,536 mental
health apps for depression available for download, but only 32 published articles evaluating their
efficacy (Martínez‐Pérez, de la Torre‐Díez, & López‐Coronado, 2013). Unfortunately, many apps have
no reliable evidence base to support the principles they use in their programmes and often cannot
provide data from controlled trials to support the efficacy of their application—and this is also true of
apps accredited and recommended by mental health organisations such as the NHS
(https://www.nhs.uk/apps‐library/category/mental‐health/) (Leigh & Flatt, 2015). What evidence is
available does indicate some hope for the usefulness of mental health apps. A meta‐analysis of RCTs by
Firth et al. (2017) found a significant small to moderate positive effect for apps on depressive symptoms
compared to controls, but this effect was restricted to those with only mild to moderate depression.
These findings are promising and suggest that apps may be helpful for those with subclinical depression
symptoms and may help to prevent worsening mood symptoms over time.
The rapid growth of the Internet over the past 30 years has meant people now have almost immediate
access to information about mental health problems and email provides another potential form of e‐
therapy communication between therapists and clients. As a result many therapists and practitioners
use email as an integral part of the treatment they provide (Hsiung, 2002). Email is a useful adjunct to
face‐to‐face sessions in a number of ways: (a) it may be used to enhance weekly sessions, monitor
treatment from a distance, monitor behaviour daily, communicate with the client's family members, or
intervene in a crisis (Yager, 2002; Yellowlees, 2002); (b) it allows clients to initiate contact with therapist
more easily, and this may make the client feel safer, and because the communication is online, more
secure (Ainsworth, 2002); (c) it allows clients who may be withdrawn or shy in personal face‐to‐face
interviews (such as adolescents with eating disorders) to be more open and compliant (Yager, 2002); and
(d) it enables clients to contact therapists more regularly in areas where resources are more difficult to
access in person, or when clients are living in remote and inaccessible areas (Gibson, Morley, & Romeo‐
Wolff, 2002). However, there are also a number of limitations to email communication, including
miscommunication because neither party to the communication is able to see the nonverbal cues being
given by the other, it is very difficult to ensure the confidentiality of online communications, and online
communication makes it very difficult to intervene effectively in severe emergencies when, for example,
a client may have suicidal intentions. Nevertheless, in recent years psychotherapy through Internet
communications has become a fast growing intervention channel—especially when Internet
communication has been combined with the client's use of an app or Internet programme. The
expansion of the use of internet‐based forms of therapist‐client communication ‐ especially video‐based
communication ‐ has also been a necessary consequence of the COVID‐19 pandemic lockdowns in
2020 and 2021, and is likely to be a form of therapist‐client communication much used in future years.
Recent reviews suggest that e‐therapy has been used successfully in the treatment of a broad range of
psychopathologies, and has been found to be cost effective for both clients and mental health service
providers (Kumar, Sattar, Bseiso, Khan, & Rutkofsky, 2017).

e-therapy A treatment method which involves the use of email and internet technology.

Finally, it is around 20 years since the first virtual reality exposure treatments were conducted, and since
then the use of virtual reality environments to assess and treat a range of mental health problems
has become significantly more widespread (Photo 4.2). Virtual reality is an interactive computer
environment that allows the user to experience a particular environment and also interact with that
environment, usually by wearing a head‐mounted display, headphones, and a position tracker that
allows the user to view changes in the environment in real time with head movements. Problems
interacting with the world are at the centre of many mental health problems, and virtual reality
exposure (VRE) is useful in helping the therapist to identify environmental factors that may trigger
symptoms and is predominantly used as a ‘safe’ form of exposure therapy that will allow clients to think,
react and behave differently in the simulated environments that are of concern to them (Freeman et al.,
2017). VRE therapies have now been successfully used in the treatment of a range of
psychopathologies, including anxiety disorders (Carl et al., 2019), symptoms of psychosis, such as
paranoia (Freeman et al., 2016), PTSD (Peskin et al., 2018), and eating disorders (Cesa et al., 2013).
PHOTO 4.2 Virtual reality exposure (VRE) therapies were first established to treat anxiety‐based problems such as fear
of heights, fear of flying, spider phobia, and post‐traumatic stress disorder (PTSD), and allowed clients to encounter their
fears and develop less fearful responses in the relative “safety” of a virtual environment.
Virtual reality has been used imaginatively during treatment to create helpful virtual environments,
some of which would be difficult to simulate in real life. For example, Freeman et al. (2014) used virtual
reality to manipulate a client's height in order to influence their self‐esteem and help them manage their
paranoia, Girard, Turcotte, Bouchard, and Girard (2009) attempted to reduce cravings for cigarette
smoking by getting clients to crush virtual cigarettes, and Keizer, van Elburg, Helms, and Dijkerman
(2016) used virtual reality to help clients with anorexia nervosa to experience ownership of a healthy
body mass index (BMI).
Studies suggest that VRE is significantly more effective than waiting list or placebo control conditions
(e.g., Carl et al., 2019), has dropout rates that are not significantly different from those found in in vivo
treatment, and can be used successfully to supplement and enhance more traditional forms of therapy
such as CBT (see special issue of the Journal of Anxiety Disorders, Powers & Rothbaum, 2019). Currently,
VRE treatments have tended to be used with a therapist present, and so it remains to be seen whether
VRE treatments will work effectively as a stand‐alone digital intervention that a client can successfully
use without a therapist.
In summary, emerging digital technologies offer a variety of new ways to deliver psychological
treatments for mental health problems, although most of these still need conclusive evidence endorsing
their effectiveness. CCBT has warranted much research and is now commercially available in a number
of different forms, although there is a growing consensus that some form of professional supervision
may be critical for its effectiveness to be achieved. Mental health apps are very much in their infancy,
and although they can often be useful in helping to manage subclinical mood‐based problems, there is
an urgent need for more controlled trials to establish evidence for their effectiveness—especially over the
longer term. Ever since the establishment of the Internet, therapist–client communications via email
have proven to be a helpful means of e‐therapy—especially in circumstances where geographic and social
factors make it difficult for direct face‐to‐face therapist‐client interaction. Finally, developing virtual reality
packages are proving to be effective in helping to treat a broad range of mental health problems. They
can be readily adapted to the very specific symptoms of the client and help to deliver exposure‐like
therapy in relative safety.

Improving access to psychological therapies (IAPT)

It is now clear that mental health problems are far from uncommon. One in four people will suffer a
diagnosable mental health problem in their lifetime (Bebbington et al., 2007), and one in six people in
the UK will be diagnosed with either chronic anxiety or depression (National Health Service, 2016).
These statistics have implications for the well‐being of those who suffer these disabilities, their families,
the agencies that are attempting to provide services for those with mental health problems, and also the
contribution that sufferers can make to the economic prosperity of the countries in which they live.
Mental health is the largest single cause of disability in the UK and the economic costs are estimated to
be over £77 billion, including the costs of lost productivity and the wider impacts on well‐being
(Department of Health, 2011). It therefore not only makes good therapeutic sense to improve access to
mental health treatments, it also makes good economic sense to help people recover from their
problems. Given the evidence‐based success of therapies such as CBT for common mental health
problems, many countries are now trying to find ways to increase and improve access to these therapies.
This has given rise to large‐scale initiatives commonly known as Improving Access to
Psychological Therapies (IAPT) which aim to increase significantly the availability of evidence‐
based interventions—such as CBT. The initiative aims to meet these goals by (a) training significant
numbers of practitioners in psychological therapies such as CBT—known as psychological well‐
being practitioners (PWPs) (Focus Point 4.2 provides a personal account of someone who was
trained to deliver low‐intensity CBT under the IAPT scheme), (b) improving access and reducing
waiting times for treatment, and (c) increasing client choice and satisfaction. A consequence of this will
be improved social and economic participation as those previously suffering common mental health
problems return to work and normal social and family functioning. As a result, the costs of the IAPT
programme are considered to be offset by the increased economic contribution of those who have
recovered from their mental health problems (e.g., Radhakrishnan et al., 2013).

Improving Access to Psychological Therapies (IAPT) NHS programme providing

services across England for treating people with depression and anxiety disorders.

psychological well-being practitioners (PWPs) People trained under the IAPT initiative
to deliver psychological therapies such as CBT.
 FOCUS POINT 4.2 TRAINING PRACTITIONERS UNDER THE
IAPT INITIATIVE

ASHLEY SNOWDON'S EXPERIENCE

Psychological Wellbeing Practitioner, Teeside IAPT Service
Working as a Psychological Wellbeing Practitioner (PWP) in Teesside IAPT has been
challenging and rewarding over the last few years. Since completing my training, I have seen
over 200 people, some with relatively complex problems who have never accessed mental health
treatment before, for whom brief interventions have made a huge impact on their functioning.
The range of problems clients have presented with has been surprisingly broad and has given
me excellent development opportunities as well as developing my confidence as a clinician.
Teaching people CBT‐based skills has meant that they have been able to take control of their
own problems and are more able to manage them in future. I have often found that people
integrate CBT skills into their lives and then come back and report that they have been
teaching them to their friends and family! I have also been closely involved in a pilot scheme
working with drug and alcohol users, who have responded really well to the short‐term, time‐
limited work, because they can see quicker results and seem to feel empowered by the guided
self‐help approach.

From Department of Health, 2012. Visit https://www.healthcareers.nhs.uk/explore‐roles/psychological‐

therapies/roles/psychological‐wellbeing‐practitioner for a video describing the work of Psychological
Wellbeing Practitioners.

In 2018–2019 there were 1.6 million referrals to IAPT services in the UK for assessment and treatment,
with 1.09 million people starting a course of therapy of two or more sessions. Each client had an
average of 6.9 sessions of treatment and 52.1% of referrals moved on to recovery (NHS Digital, 2019).
CBT and guided self‐help (use of a self‐help book) accounted for 61.5% of all courses of therapy
delivered.
Schemes for improving access to psychological therapies are now being rolled out in many countries,
including developing countries such as India, Pakistan, and Uganda (Patel, Chowdhary, Rahman, &
Verdeli, 2011), where lay and community health workers are being trained in evidenced‐based practices.
However, the challenges of providing access to psychological therapies for those who need them are still
immense, with the ‘treatment gap’ (a term used to describe the shortfall in mental health provision for
sufferers) exceeding 75% in most parts of the world (Kohn, Saxena, Levav, & Saraceno, 2004), with
access to mental health services even in the European Union being considered “far from satisfactory”
even for common mental health problems such as anxiety and depression (Barbato, Vallarino,
Rapisarda, Lora, & Caldas de Almeida, 2019).

Summary
With the average waiting‐time for conventional treatments provided by community mental health
services in many parts of the world often longer than 1–2 years ‐ especially for popular and specialised
treatments such as CBT—practitioners and service providers are under pressure to provide more cost‐
effective and immediate forms of interventions for people with mental health problems (London School
of Economics and Political Science, 2006). We have reviewed some of the modes of delivery that may
prove to be more immediate and cost effective, although most of these modes of delivery represent
relatively new innovations that have yet to be fully and properly evaluated.
SELF‐TEST QUESTIONS
What are the main principles of psychodynamic therapy?
Can you describe some of the basic techniques used by psychoanalysts?
Can you describe the behaviour therapy techniques that are based on classical
conditioning?
Can you describe some of the treatment techniques that have been developed based on
principles of operant reinforcement?
Can you describe at least two types of cognitive therapy?
What are ‘third‐wave’ CBT methods—can you describe at least one of these?
What are the main theoretical principles on which humanistic therapies are based?
What are the main principles used in client‐centred therapy?
What is family therapy and how is it conducted?
Can you name the main types of drug treatments for psychopathology?
Can you describe two to three types of group therapy?
What are the main characteristics of counselling?
Can you describe the main features of CCBT, e‐therapy, and VRE?
What does IAPT stand for, and what is it trying to achieve?
 SECTION SUMMARY

4.1 THE NATURE AND FUNCTION OF TREATMENTS FOR

PSYCHOPATHOLOGY
The treatment provided for a psychopathology will depend on the theoretical orientation
of the therapist and the nature of the psychopathology.
Psychodynamic approaches to therapy attempt to reveal unconscious conflicts that may be
causing psychopathology.
Behaviour therapies are mainly based on the principles of classical and operant conditioning.
Behaviour therapies based on classical conditioning include flooding, counterconditioning,
systematic desensitisation, and aversion therapy.
Therapies based on operant conditioning include functional analysis, token economy, response
shaping, and behavioural self‐control.
Important cognitive therapies include Rational Emotive Therapy (RET), Beck's cognitive therapy, and
cognitive behaviour therapy (CBT).
‘Third‐wave’ cognitive therapies include mindfulness‐based cognitive therapy (MBCT),acceptance
and commitment therapy (ACT), and behavioural activation.
Humanistic therapies attempt to consider the ‘whole’ person and not just the symptoms of
psychopathology.
Family therapy attempts to deal with psychopathology by addressing relationship dynamics
within the family.
Drug treatments have been developed to alleviate some of the symptoms of psychopathology,
particularly in disorders associated with depression, anxiety and psychosis.
Important drug treatments include antidepressant drugs, anxiolytic drugs, and antipsychotic drugs.
Recently developed modes of treatment delivery include group therapy, counselling, CCBT,
mental health apps, e‐therapy, Virtual Reality Exposure (VRE), and Improving Access to Psychological
Therapies (IAPT).

4.2 EVALUATING TREATMENT

All of the therapies and treatments we have discussed in previous sections of this chapter have at least
some degree of intuitive plausibility as treatments for psychological problems. Nevertheless, how do we
assess how effective a treatment is? This is not as simple as it sounds. First, we often have to try and
compare the efficacy of therapies that have quite different assumptions about what ‘successful therapy’
is (e.g., cognitive therapies would expect to see some significant improvement after a few weeks or
months, whereas psychoanalytic and humanistic therapies are seen as developmental, lifelong processes
promoting self‐growth). And second, we have to decide on what constitutes a therapeutic gain (i.e., on
what particular measures are we expecting to see improvement?). For example, Erwin (2000) describes
how different theoretical approaches to treatment use radically different criteria for judging outcomes.
Therapists using CBT typically use elimination of psychopathology symptoms as the main criterion of
success; behaviour therapists view the modification of maladaptive behaviours as important;
psychodynamic therapists view the elimination of unconscious conflicts as critical to therapeutic success;
and humanistic psychotherapists see enhancement of personal autonomy as their main therapeutic
objective. Erwin concludes that, at the end of the day, what constitutes a successful therapeutic
intervention is often a subjective judgement and may boil down to little more that the outcome was
beneficial in some way to the client—or at least to someone!
Despite these difficulties in deciding on a common set of criteria for gauging success across different
treatment types, there are some good reasons for wanting to try and objectively assess how successful
therapies are (a) psychological disorders are distressing to the individual, and we have a moral and
professional obligation to try to find ways of alleviating this distress rapidly and effectively; (b) some
treatments may have short‐term gains but are significantly less effective over the longer term and may
leave the individual open to relapse—we need to be sure that therapies have lasting therapeutic effects;
and (c) individuals with psychological problems are a very vulnerable group of people, and we need to
ensure that they are not exploited financially and psychologically by what is a growing industry of
essentially bogus therapies with shallow—but often beguiling—rationales and little or no medium‐term
therapeutic benefit.

4.2.1 Factors Affecting the Evaluation of Treatments

On what basis do therapists decide whether their treatments are successful? Focus Point 4.3 provides an
interesting example of this that was described by Davey (2002). The therapist in this example assumed
that her treatment was being effective because no one ever returned to complain about it! But there may
be many reasons why individuals may not complain, and the client in this example is quite happy to
return for more therapy even though her first session was not as successful as she was led to believe it
should be. The moral of this story is that a client simply saying they are satisfied with the outcome of
the therapy does not mean either (a) that any objective therapeutic gain has been achieved, or (b) if
some therapeutic gain was achieved, that it was due explicitly to the type of therapy that was used.
Therapeutic interventions are generally very complex things, and they will often contain many factors
that might help (or hinder) recovery. Some obvious factors that might help recovery include a
sympathetic therapist, a rationale for recovery that the client understands and believes will help them, a
therapeutic intervention with well thought‐out principles that have been tried and successfully tested
before. Factors that might hinder recovery include an unsympathetic therapist, an unsupportive home
environment, or the use of an intervention that is poorly structured and not soundly based on proven
psychotherapy principles. These are all factors that need to be considered when evaluating the
effectiveness of a therapy, and we will discuss these in turn below. However, one of the central issues in
evaluative research is determining whether an intervention is effective primarily because of the
therapeutic principles in the intervention (e.g., psychoanalytic principles, cognitive‐behavioural
principles, etc.), and determining whether a treatment works because of the principles it contains is
known as assessing its internal validity.
Because therapeutic interventions are usually a conglomeration of many different factors, assessing the
reasons for the efficacy of therapies is difficult, and the following sections describe some of the factors
that can confound the assessment of therapeutic effectiveness.

internal validity Determining whether a treatment works because of the principles it

contains.

Spontaneous remission
Just because someone exhibits objective improvement in symptoms after treatment does not necessarily
mean that the treatment was the cause of the improvement. The famous British psychologist, Hans
Eysenck, argued that many people who have mental health problems will simply get better anyway over
a period of time—even without therapy (Eysenck, 1961), and this can often be the result of an
individual's changing life experiences (e.g., positive life changes) (Neeleman, Oldehinkel, & Ormel,
2003). This is known as spontaneous remission, and it is estimated that 23% of cases of an
untreated common mental health problem such as depression will spontaneously remit within 3 months,
32% within 6 months, and 53% within 12 months (Whiteford et al., 2013). So, if we are assessing the
effectiveness of a therapy we would expect to see improvement rates significantly greater than 23% after 3
months, 32% after 6 months, and so on, in order to take into account the fact that many of those
undertaking the therapy would show a spontaneous improvement in symptoms anyway.

spontaneous remission The fact that many people who have psychological disorders will
simply get better anyway over a period of time, even without therapy.
 FOCUS POINT 4.3 STOP SMOKING IN ONE SESSION!

“As I was passing a local ‘holistic’ health clinic, I noticed a sign outside which—in large letters
—implored ‘STOP SMOKING IN ONE SESSION’. (which session—surely not the first one?!)
Having interests in both clinical and health psychology areas, I was intrigued to find out more.
As it turns out, a friend of mine had just recently visited the clinic and had received a single 1‐
hour session of hypnotherapy in an attempt to stop smoking—cost £50. Knowing the literature
on psychological treatments for smoking and how difficult it is to achieve abstinence, I decided
to find out a little more about these treatment claims. I emailed the hypnotherapists offering
services at the clinic asking if stopping smoking in one session of hypnotherapy was achievable,
and what their success rates were like. I did get a reply from one of the practitioners, who had
worked as a hypnotherapist for seven years. She replied: ‘I did not do follow‐up calls as I
thought this would be intrusive so therefore I did not have stats on my success rates. However, I
knew I had a high success rate as people referred others to me and came back to me for help on
other issues’. Interestingly, my friend who had attended the clinic was smoking regularly again
within three days of the hypnotherapy session, and—despite having long discussions with me
about the validity of the treatment and its lack of success—said she was thinking of attending
again (this time in relation to other aspects of her life) because the hypnotherapist had been so
caring, understanding and interested in her problems!”

From Davey (2002).

Placebo effects
If someone suffering with anxiety symptoms is given a sugar pill but they are told that it is an anxiolytic
medication, they often report significant improvements in those symptoms. This suggests that
individuals will often get better because they expect to get better—even though the actual treatment that
they have been given is effectively useless (Paul, 1966). This is known as the placebo effect (Paul,
1966). Thus, it may be the case that many psychological treatments have beneficial effects because the
client expects them to work—and not because they are treatments that are effective in tackling the factors
maintaining the psychopathology (see Ashar, Chang, & Wager, 2017, for a discussion of the potential
psychological mechanisms of the placebo effect). In some cases, placebo effects can be quite large, with
pharmacological treatments of PTSD showing that between 19% and 62% of participants taking a
placebo treatment can show benefits over the short term (Benedetti, Piedimonte, & Frisaldi, 2018).
Unfortunately, the positive gains produced by placebo effects are short lived, and comparative studies of
placebo effects with actual structured psychotherapies strongly suggest that structured psychotherapies
lead to greater improvement than placebo control conditions (Robinson, Berman, & Neimeyer, 1990;
Andrews & Harvey, 1981). This emphasises the importance of using placebo conditions as a comparison
to ensure that structured and theoretically‐based interventions are internally valid and work because of
the way they are constructed and not simply because the client ‘expects’ them to work.

Unstructured attention, understanding, and caring

We also know that people with psychological problems also show some improvement in symptoms when
they can simply talk abut their problems in an unstructured way with either a professional therapist or a
friend or relative (Lambert, Shapiro, & Bergin, 1986). This suggests that many forms of social support
may have a therapeutic effect in and of themselves (Borkovec & Costello, 1993), and this factor must be
taken into account when judging how effective a structured therapy is. One of the important things that
we want to find out about therapies is not just whether they are effective in making people better, but
whether they make people better specifically because of the principles they contain (see introduction to
this section).
Consequently, studies that attempt to evaluate the effectiveness of a therapy's principles also need to
control for other factors such as the amount of attention or empathy that the client is receiving from the
therapist. One recently developed form of control condition for attention, understanding and caring is
known as befriending (Siette, Cassidy, & Priebe, 2017). This is a control condition designed to provide
participants with approximately the same amount of therapist contact as the treatment conditions being
tested with sessions spaced at similar intervals. In the befriending condition the therapist aims to be
empathetic and nondirective and does not attempt to directly tackle symptoms, and the session is
normally focussed on discussion of neutral topics such as hobbies, sport, and current affairs (Bendall et
al., 2006; Sensky et al., 2000).

befriending A form of control condition for attention, understanding and caring used in
treatment outcome studies.

4.2.2 Methods of Assessing the Effectiveness of Treatments

We have to begin this section by acknowledging that the advocates of some therapeutic approaches do
not believe that the success or otherwise of their therapeutic approaches can be assessed using objective
or quantitative methods (e.g., Marzillier, 2004). This is because those therapists view their treatments not
as attempts to eliminate symptoms of psychopathology but as attempts to reconstruct a client's meaning
of the world (e.g., Rosen, 1996) or to move the client from one phenomenological state to another (e.g.,
humanistic approaches). In each case, these are not changes that are easy to objectively measure, and
nor are there particularly well‐defined criteria for when these goals have been reached.
Nevertheless, there are still many compelling reasons for wanting to assess in some formal way whether
a treatment is effective and successful, and at the beginning of Section 4.2 we have aired some of the
moral and compassionate reasons for wanting to do this. In addition to these reasons, mental health
service providers have a duty to ensure that the services they are offering are effective, and they will
need some benchmark by which to measure whether the treatments they offer are either successful or at
least provide satisfaction for the end users they are providing for.
Two popular methodologies for assessing the effectiveness of treatments are (a) RCTs, and (b) meta‐
analyses and systematic reviews.

Randomised controlled trials (RCT)

What are RCTs?

The current methodology of choice for assessing the effectiveness of therapies is the RCT (e.g., Jadad &
Enkin, 2007; Nezu & Nezu, 2007). This procedure compares the effectiveness of the treatment being
assessed (across a range of objective measures) with a variety of control conditions, and with other
forms of therapy and treatment (if necessary). Participants in the study are assigned randomly to each of
these conditions. Apart from the treatment being assessed, the control conditions used in RCTs are
those that will control for the kinds of effects described in Section 4.2.1. These include (a) a no
treatment or a ‘waiting list’ control group of participants who will receive no treatment (to
control for the effects of spontaneous remission); this condition is often difficult to achieve because of
the ethical issues involved in withholding treatment from clinically distressed individuals (see Section
3.4.2 in Chapter 3), (b) an expectancy and relationship control group, to control for placebo effects and
for the beneficial effects of contact with a therapist (e.g., ‘befriending’—see Section 4.2.1), and (c) a
comparative treatment group, in which the original therapy can be compared with a plausible
alternative therapy that is known to have beneficial effects. For the original therapy to be deemed
effective and possess internal validity, participants receiving that therapy must show greater
improvement than those in both the no treatment and the expectancy and relationship control
conditions, and improvement that is at least equivalent to that exhibited by the comparative treatment
group. Figure 4.1 provides a schematic example of a RCT study comparing the efficacy of cognitive
therapy and exposure plus applied relaxation treatments for social phobia. This shows how the original
116 participants in the study were assessed, the reasons why 54 were excluded from the study, how they
were randomly allocated to one of three treatment conditions, how many dropped out of the study
before completion, and when the outcome assessments were taken. The graph below this diagram
shows that the cognitive therapy condition was significantly more effective at reducing symptoms of
social phobia than both exposure and applied relaxation and those in a waiting list control condition.

Problems with RCTs

While RCTs do provide an objective way of assessing the effectiveness of therapies, they do have a
number of practical limitations: (a) participants do drop out of these studies, and may do so more from
some conditions—e.g., the no treatment conditions—more than others; (b) RCTs are costly and time
consuming to undertake; (c) because participants are assigned randomly to conditions, it does not take
account of the fact that some participants may prefer some types of therapy to others (Brewin &
Bradley, 1989); and (d) what individual practitioners would often like to know is whether a particular
intervention will work for their particular client in their particular setting, and RCTs do not provide this
kind of practical detailed information (Mulder et al., 2019).
Furthermore, to be genuinely objective, RCTs need to be free of any form of explicit or implicit bias
that might influence the results of a basic comparison between the intervention being assessed and the
control conditions. Unfortunately, this is often not the case. First, those who carry out the RCT often
have an allegiance to the psychotherapy being tested, and this may be a source of experimenter bias
that favours the effectiveness of that intervention. Meta‐analytic reviews suggest that researcher
allegiance to a particular intervention does indeed substantially bias the results of an RCT (Munder,
Brütsch, Leonhart, Gerger, & Barth, 2013). Second, there is a significant bias in scientific publication to
publishing findings when there is a significant difference between experimental interventions and
control conditions, but not when this difference is nonsignificant (the latter are known as ‘null findings’)
(Dwan et al., 2008). Thus there may well be a large number of RCTs that have shown no effect of a
treatment compared to control conditions but have never been published. This has the effect of biasing
RCTs towards providing published evidence that a treatment ‘works’ rather than ‘does not work’. In
addition, commercial interests may be associated with whether an RCT is published that reports a
positive finding or a negative finding (Killin & Della Sala, 2015). For example, Yaphe, Edman,
Knishkowy, and Hermand (2001) found that RCTs assessing the effectiveness of drug treatments were
significantly more likely to report a positive or significant effect if the study had been funded by the
pharmaceutical industry than if funds came from nonindustry sources!
Finally, we must remember that RCTs have traditionally only told us whether a particular intervention is
significantly better than a control condition or significantly better than an alternative intervention (in
terms of effect sizes, see Section 4.1.1). What they often do not tell us is what percentage of the
participants in the study exhibited recovery or clinically significant change to the point where they no
longer meet the criteria for a clinical diagnosis (Jacobson & Truax, 1991; Wise, 2004). The latter is
known as clinical significance and the former reflects recovery rates. Jacobson and Truax (1991)
pointed out that statistical significance and clinical significance do not convey the same kinds of
information about an intervention and that it is important to determine whether the intervention
‘moves the client from the dysfunctional to the functional range during the course of therapy’ (Jacobson,
Follette, & Revenstorf, 1984, p. 340). While most structured interventions are more effective than no
treatment control conditions, a look at recovery rates often suggests a less than perfect picture. Even for
well‐established psychological and pharmaceutical interventions, recovery rates for common mental
health problems (the percentage of people that are no longer diagnosable once they have finished
treatment) is normally between 50% and 70% (e.g., Baldwin, Woods, Lawson, & Taylor, 2011; Craske et
al., 2012; Hanrahan, Field, Jones, & Davey, 2013), suggesting that such interventions fail to ‘cure’
between 30% and 50% of those being treated. This probably testifies more to the complexity of many
mental health problems and the factors that maintain psychopathology than the relative ineffectiveness
of our current interventions. But clearly more needs to be done to develop interventions that will help
larger proportions of sufferers to fully recover (see https://www.papersfromsidcup.com/graham‐daveys‐
blog/the‐lost‐40 for a discussion of this).

clinical significance The percentage of participants in a study who exhibited recovery or

clinically significant change to the point where they no longer meet the criteria for a clinical
diagnosis.

recovery rates The percentage of people who are no longer diagnosable once they have
finished treatment.

Nevertheless, despite some of these limitations, RCTs have remained a popular method for assessing the
relative effectiveness of treatments and are still considered to be the main standard by which the
effectiveness of an intervention is experimentally tested.
FIGURE 4.1 A randomised controlled trial comparing the effectiveness of CBT and applied relaxation for social
phobia.
The following flow chart shows how the 116 participants in the study were allocated to experimental conditions and
assessed. The graph below shows that the CBT condition (CT) was more effective at reducing the symptoms of social
phobia than applied relaxation (Exp + AR) and a “waiting list” control (Wait).
From Clark et al., 2006.

Meta‐analyses and systematic reviews

We have already discussed meta‐analyses and systematic reviews as a research method in Chapter 3
(Section 3.3.9), and the reader is referred to this in the first instance. The benefit of meta‐analyses is that
they can be used to compare the effectiveness of studies that may have used different procedures,
different numbers of participants, different types of control procedures, and different forms of
measurement, and it does this by comparing effect sizes across studies. One important use of meta‐
analyses has been to try and answer an enduring question in psychotherapy: Are psychotherapies more
effective than no treatment at all. An early large‐scale meta‐analysis carried out by Smith, Glass, and
Miller (1980) concluded that psychotherapies were more effective than no treatment but that effect sizes
did not differ across different psychotherapies, suggesting that all different psychotherapies were equally
effective.

4.2.3 What Treatments Are Effective?

Is treatment more effective than no treatment?

We have identified a couple of objective ways of assessing whether therapies are effective, but what do
these studies using these methods tell us? Comparative studies tend to suggest that most of the accepted
therapies are all more effective than no treatment or expectancy control conditions, but that the
therapies themselves do not differ in their relative effectiveness. For example, in a study of depressed
individuals, Gibbons et al. (1993) found that cognitive therapy, interpersonal therapy, and antidepressant
medication were all as effective as each other, but all more effective than a placebo control condition
(after 16 weeks of treatment). Similarly, the early meta‐analysis conducted by Smith, Glass, and Miller
(1980) also indicated that psychotherapies were all more effective than no treatment, but none was
significantly more effective than another. This has come to be known as the Dodo Bird Verdict which
is a phrase taken from Lewis Carroll's Alice's Adventures in Wonderland implying that all psychotherapies are
winners and produce equivalent benefits for clients. This debate is considered in more detail in Focus
Point 4.4.

FOCUS POINT 4.4 THE DODO BIRD VERDICT

A number of influential comparative studies and early meta‐analyses all suggested that
although psychotherapies were more effective in treating mental health problems than placebos
and other appropriate controls, no psychotherapy was more effective than any other
psychotherapy (Gibbons et al., 1993; Luborsky, Singer, & Luborsky, 1975; Smith, Glass, &
Miller, 1980). As early as 1936 Saul Rosenzweig had labelled this effect the Dodo Bird Verdict
(Rosenzweig, 1936) after the bird in Lewis Carroll's Alice's Adventures in Wonderland. In that story, a
number of animals had become wet and in order to dry themselves ran round the lake to see
who could get dry first. No one measured how far they'd run or for how long, but when asked
who had won, the Dodo bird said ‘Everybody has won and all must have prizes’!
Those who agree with the Dodo bird verdict claim that all psychotherapies are equally effective
because they all contain some important common factors that are shared across all
psychotherapeutic interventions. This is known as the common factors theory, and one
influential common factors model is the contextual model (Wampold, 2015; Wampold &
Imel, 2015). In this view, once client and therapist have established an initial bond,
psychotherapy is assumed to work through three pathways. The first is the therapist–client
 bond, in which the relationship connects the client to a caring and empathetic person. The
second pathway is through the client's expectations and hope (e.g., the degree to which the
client is convinced by the rationale of the therapy). The third pathway is determined by the
ingredients specific to the individual therapy being used that stimulate healthy outcomes that
are beneficial to the client.
One of the most important common factors affecting outcome is the therapist‐client
relationship—known as the therapeutic alliance (Del Re, Flückiger, Horvath, Symonds, &
Wampold, 2012; Lambert, 1992), and Wampold, Minami, Baskin, and Tierney (2002) found
that 7% of the variability in treatment outcome was due to the therapeutic alliance compared
with only 1% attributable to the principles inherent in the type of psychotherapy being
deployed. Apart from the therapeutic alliance itself, specific features of the therapist have also
been identified as contributing to the success of therapy. These include positive, warm, and
caring attitudes towards the client (Najavits & Strupp, 1994), and providing good feedback,
helping the client to focus on and understand their own thoughts, attempting to promote
autonomy and self‐efficacy in their clients, and helping the client with their existing
relationships (Korchin & Sands, 1983).
However, there is evidence that can be mustered on both sides of the Dodo Bird Verdict, and
this debate is still very much alive (Siev, Huppert & Chambless, 2009; Wampold, Imel, & Miller,
2009). Some claim that improvements in statistical analyses now allow us to make fine‐grained
distinctions between the effectiveness of different therapies in a way that we could not do
previously (Chambless & Hollon, 1998; Otte, 2011); We can demonstrate that some
psychotherapies are more effective for some mental health problems than for others (Chen,
Zhang, Hu, & Liang, 2015; Siev & Chambless, 2009) and indeed, we not only have to consider
whether interventions are effective in treating psychopathology symptoms, we also have to
consider whether they might also be harmful in the sense that they may evoke negative
responses to treatment in some clients or client groups (e.g., individuals diagnosed with
substance dependency) (Dimidjian & Hollon, 2010). However, perhaps what is most damaging
to common factors theories is that very few, if any, studies have convincingly shown that those
variables championed as common factors are genuine causal factors in a client's recovery. In
order to demonstrate this, studies need to show a temporal relationship between the so‐called
‘common factor’ and the outcome, a dose–response association, and evidence that no third
variable causes changes in the ‘common factor’ and the outcome (Cuijpers, Reijners, &
Huibers, 2019).
In conclusion, while there is still lively debate about the relative efficacy of various interventions
for psychopathology, there is no doubt that hundreds of studies have clearly demonstrated that
psychotherapy is effective. The Dodo Bird Verdict has also helped to focus attention on those
aspects of psychotherapy that are common across a majority of intervention types (e.g.,
therapist characteristics, the therapeutic alliance, etc.), and clinical psychologists are working to
identify some of the important characteristics that make some psychotherapists more effective
than others.

Dodo Bird Verdict An expression from Lewis Carroll’s Alice’s Adventures in Wonderland,
implying that all psychotherapies are more effective than no treatment, but produce equivalent
benefits.

Rather than conducting objective and well‐controlled outcome studies, some others have approached
the issue of the effectiveness of treatments by viewing the client as a consumer and canvassing their
views on how satisfied they have been with the treatment ‘product’ that they received. Seligman (1995)
reported the results of a large scale survey of individuals in the US who had undergone psychotherapy
and concluded that (a) respondents claimed they benefited significantly from psychotherapy; (b)
psychotherapy alone did not differ in effectiveness from medication plus psychotherapy; (c)
psychologists, psychiatrists, social workers and counsellors did not differ in their effectiveness as
therapists; and (d) the longer the duration of their treatment, the larger the positive gains respondents
reported. While the empirical rigour of this consumer‐based study falls far short of that expected in
well‐controlled outcome studies, it does provide some information about how the recipients of
psychotherapy view their treatment and its effects. But as we have noted in Focus Point 4.3, asking a
client how satisfied they are following treatment may not be the best way to judge the effectiveness of a
treatment and may reflect the involvement of psychological factors that extend beyond the original
purpose of the treatment.

4.2.4 Summary
In this section we have described some of the methods that have been developed to try and evaluate the
effectiveness of treatments for psychopathology. Over the past 20 years a large number of studies
assessing the efficacy of therapies for psychopathologies has been carried out, and there is now good
empirical evidence to support the effectiveness and internal validity of many of these therapies. There
are too many to mention here, but the interested reader is referred to the treatment sections of
individual psychopathology chapters in this book for a review of the most effective treatments for
individual psychopathologies.

SELF‐TEST QUESTIONS
What kinds of factors can affect the evaluation of treatments and need to be controlled for
in treatment outcome studies?
What are the two most popular methodologies for assessing the effectiveness of
treatments?
Are structured treatments for psychopathology effective?
What is the ‘Dodo Bird Verdict’ in relation to the effectiveness of psychotherapies?

SECTION SUMMARY

4.2 EVALUATING TREATMENT

Factors affecting the evaluation of treatments include spontaneous remission, placebo effects, and
attentional factors provided by the therapist's relationship with the client.
Popular methods for assessing the effectiveness of treatments are randomised controlled trials
(RCTs) and meta‐analyses.
Most large‐scale studies suggest that treatment in general is significantly more effective
than no treatment, but that no psychotherapy is necessarily more effective than any other
(known as the Dodo Bird Verdict).

4.3 TREATING PSYCHOPATHOLOGY REVIEWED

Treatments for psychopathology have developed significantly over the last 50–60 years, and the main
aim of treatments are to provide relief from the distress of symptoms, equip the client with insight into
their problems, and provide the client with a means of coping with life problems and psychological
distress. Most treatments for psychopathology consist of either drug treatments or psychotherapy, and
psychotherapy can be divided into five main theoretical approaches: psychodynamic approaches,
behaviour therapy, cognitive therapy, humanistic therapies, and family or systemic therapies. Because of
the demands placed on overstretched clinicians and service providers, a number of different cost‐
effective modes of delivery have been developed in recent years, and these include group therapy,
counselling, CCBT, mental health apps, e‐therapy, virtual reality, and programmes designed to Improve
Access to Psychological Therapies (IAPT). Evaluating the effectiveness of treatments for
psychopathology is still a difficult and disputed process, with disagreements about what constitutes a
therapeutic gain, how long it may take to achieve a successful outcome, and how therapeutic gains
should be measured (if they can be measured at all). The practical need for objective methods for
assessing the relative success of treatments has given rise to the adoption of RCTs and meta‐analyses as
important methods for assessing treatments. Most large‐scale studies indicate that structured
psychotherapies generally are more effective than no treatment, and in most cases more effective than
appropriate placebo conditions, but there is much contention over whether one psychotherapy method
is necessarily more effective than another (known as the Dodo Bird Verdict). Nevertheless, the last 20
years has seen a significant increase in the number of treatment outcome studies published, and many
of these indicate that certain types of treatments may be more effective than others at treating
individual specific psychopathologies (see also the treatment sections in the chapters covering individual
psychopathologies).

This book is accompanied by Student and Instructor companion websites.

www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter References
Videos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
5
Clinical Practice

ROUTE MAP OF THE CHAPTER

This chapter starts by taking a broad perspective on clinical practice by describing the scale of
mental health problems that service providers face. We then discuss the types of mental health
professionals that work in this sector, how individuals with mental health problems access
services, and the facilities that are available across mental health services. We end the chapter by
focusing on clinical psychologists and discussing their key capabilities and competences, how
they are regulated, and how they are trained.

CHAPTER OUTLINE
5.1 THE ECONOMIC COST OF MENTAL HEALTH PROBLEMS
5.2 WHO ARE MENTAL HEALTH PROFESSIONALS?
5.3 PROVIDING MENTAL HEALTH SERVICES
5.4 THE ROLE OF THE CLINICAL PSYCHOLOGIST
5.5 CLINICAL PRACTICE REVIEWED

LEARNING OUTCOMES
When you have completed this chapter, you should be able to:
1. Describe the nature and size of mental health problems facing service providers.
2. Describe how mental health services in the UK are structured.
3. Describe the different types of mental health professionals in the UK together with some
of the skills they possess.
4. Describe and evaluate the role of clinical psychologists in the mental health services.
 My family came to England from Uganda when I was four. I found leaving our home behind quite traumatic, and
then a year after we arrived here, my father died. It was difficult, losing him on top of everything else. In some
Asian families there are rigid rules about what can and can't be talked about and intimate things aren't mentioned,
so I never spoke to anyone about how I felt or what it was like growing up. I just pushed the sadness down within
myself. I got married to an English guy but I still didn't talk about it. But, a bit like holding a ball underwater,
there's only so long you can keep your feelings hidden and by the summer of 2006 I was suffering from what I
now know was depression. In the end I went to see my GP because I felt I needed to talk through what was going
on. My GP was able to refer me to an Asian psychologist for cognitive behavioural therapy and psychodynamic
therapy, which involved talking through my problems and finding ways to tackle them. When I saw the therapist I
wasn't worried about confidentiality anymore. I live in a different area from my family now and was assured that
all our sessions would be completely confidential. There were lots of things, which she, as an Asian woman, could
relate to. I saw my therapist for 50 minutes every week or two, over 10 months, and she has helped me a lot. I've
started building my own life and learned not to get so bogged down with the pressures of having to look after
everybody else.
I've been discharged now, but I still go for follow‐up sessions to see how I'm doing. I know the service is there for
me if I need it again: all I have to do is contact them if I have a crisis or need a session. It has been great to have
support from someone I identify with. I've seen things change since I was younger and now there are services for
people when they feel ready to get help. If you want help, see your GP. They may be able to refer you for
confidential counselling, or to a psychologist with a specialist understanding of cultural issues.
Hina's Story (adapted from http://www.nhs.uk/Conditions/stress‐anxiety‐depression/Pages/therapy‐changed‐my‐
life.aspx)

Introduction
Just like Hina, we all experience life events that cause us distress in some form or another. In many cases
this distress is short lived and transient, but for others the distress stays with them for long periods and
becomes an overbearing and central feature of their life. Many people cope as best they can by keeping
their distress and their feelings to themselves. But, as Hina describes in her personal account, there's
only so long you can ‘hold a ball under water’ before it pops up on the surface. It is often only when
distress eventually becomes unbearable, affects social, occupational, and family functioning, or is
recognised by others that many people begin to seek help for their problems. So how do people begin to
seek help for mental health problems? What services are available? How are those services structured?
These are some of the questions we'll be addressing in this chapter. For Hina, her journey for help and
support began with a visit to her local GP who then forwarded her on to more specialised services such
as counselors, psychotherapists, or clinical psychologists.
Clinical psychologists are closely involved in helping people to recover from problems similar to those
described by Hina. They attempt to help people understand the causes of their distress, provide
interventions that can help to alleviate specific symptoms, and provide support and guidance through
the recovery process. However, mental health provision is characterised by the involvement of a whole
range of professionals, all with differing skills and roles, and we describe some of these people and their
individual skills later in this chapter. You are likely to meet directly with a clinical psychologist only if
your problems are relatively severe and enduring, but clinical psychologists do work within
multidisciplinary teams (MDTs) that aim to provide the basis for support and recovery from mental
health problems.
In this chapter we describe the kinds of professionals who provide mental health services, and what
services and facilities are available and how people access them. We then focus on the role of the clinical
psychologist by discussing what they do, what their skills are, and how they are trained. But first it's
probably helpful to begin by looking at the size of the problem that those who provide mental health
services are facing—what is the prevalence of mental health needs across a country such as the UK, and
why are mental health services so important?

5.1 THE ECONOMIC COST OF MENTAL HEALTH PROBLEMS

In the UK, services for mental health problems need to be accessible and robust. As in most developed
countries, in the UK mental health problems are the single largest cause of disability, contributing up to
22.8% of the total burden (compared with 15.9% for cancer and 16.2% for cardiovascular disease), and
of this, depression alone accounts for 7% of the disease burden (World Health Organization, 2008).
According to the Adult Psychiatric Morbidity Survey carried out in England by the National Health
Service (NHS) in 2014, 39% of the adult population was accessing mental health treatments with
conditions such as anxiety or depression (NHS Digital, 2014). In addition, around one in six adults met
the criteria for a common mental health problem (CMHP). The survey indicates that the number of
people accessing mental health services has risen from one in four people in 2007 to one in three in
2014. CMHPs that contribute to these figures include anxiety and anxiety disorders (see Chapter 6) and
mood disorders such as major depression (see Chapter 7). More severe mental health problems (such as
psychoses) are somewhat less prevalent at around 0.7% of adults being diagnosed with psychotic
symptoms in 2014 (NHS Digital, 2014), and around 3.7% of the population report having serious
thoughts of suicide in the prior 12 months (Substance Abuse and Mental Health Services
Administration, 2011) (Table 5.1).
As a significant cause of disability, the wider economic cost of mental health problems in the UK is
immense. This has been estimated at almost £35 billion each year in the UK alone, including the costs
of sickness absence, reduced productivity at work, and replacing staff who leave their jobs because of
their mental health (Centre for Mental Health, 2017). As a result, the cost of poor mental health to
businesses amounts to £1,300 per employee per year (Centre for Mental Health, 2017). So, apart from
the personal distress and dysfunction caused by mental health problems there is also the broader issue of
its economic cost to society, and the combination of these factors makes it essential that governments
provide suitable services and a skilled workforce trained to help those within that society who suffer
mental health problems. Ironically, in recent years it has been the need to reduce the economic burden
of mental health problems rather than aiding individual recovery from distress that has driven
restructuring and training within national service providers such as the NHS. For example, the
Improving Access to Psychological Therapies(IAPT) scheme in the UK which provides training
for large numbers of new psychological therapies practitioners (e.g., psychological well‐being
practitioners, see Chapter 4) was launched in 2006 on the premise that it would be a more cost‐effective
way of providing services. Using evidence‐based interventions such as cognitive behaviour therapy
(CBT) for CMHPs would return more people to work more quickly and reduce the costs of mental
health problems caused by loss of productivity (Layard, 2006; Radhakrishnan, Hammond, Jones,
McMillan‐Shields, & Lafortune, 2013).
TABLE 5.1 Key findings from the NHS mental health and wellbeing in England survey 2014

One adult in six had a common mental health problem (CMHP): about one woman in five and
one man in eight. Since 2000, overall rates of CMHP in England steadily increased in women
and remained largely stable in men.
Most mental health problems were more common in people living alone, in poor physical health,
and not employed. Those that do live alone were identified as having experienced higher rates of
most different mental health problems, including CMHP, post‐traumatic stress disorder, psychotic
disorder, personality disorder, and bipolar disorder
One person in three with CMHP reported current use of mental health treatment in 2014, an
increase from the one in four who reported this in 2000 and 2007. This was driven by steep
increases in reported use of psychotropic medication. Increased use of psychological therapies
was also evident among people with more severe CMHP symptoms.
There were demographic inequalities in who received treatment. After controlling for level of
need, people who were White British, female, or in midlife (especially aged 35–54) were more
likely to receive treatment. People in the Black ethnic group had particularly low treatment rates.
In 2014, one in five 16–24‐year‐old women reported having self‐harmed at some point in her life
when asked face to face and one in four reported this in the self‐completion section of the survey.
Given this background, we now move on to consider in more detail the structure of mental health
provision and the nature of clinical practice.

SELF‐TEST QUESTIONS
What percentage of people in the UK will experience a mental health problem in any 1
year?
What is the estimated annual cost of mental health problems in the UK?

SECTION SUMMARY

5.1 THE ECONOMIC COST OF MENTAL HEALTH PROBLEMS

At least one in three people in the UK will experience a mental health problem in any 1
year.
The economic cost of mental health problems in the UK has been estimated at £35 billion
each year.

5.2 WHO ARE MENTAL HEALTH PROFESSIONALS?

Mental health problems are often complex, and as a result need to be treated in many different ways by
a range of people with a variety of skills. Chapters 6–17 in this book will demonstrate how different the
various psychiatric disorders are—in the way that symptoms manifest, how sufferers are affected, and
what is required to aid recovery, and this is why mental health care professionals have many different
roles to play in the recovery process.
Your local GP or physician will usually be the first point of contact with mental health care services, and
it is estimated that around a quarter or a third of the people that GPs see on a daily basis have either
emotional or psychological problems. GPs can often make an initial assessment, prescribe medication
(such as antidepressants), and make referrals to other more specialised services, such as counselling or
child and adolescent services. Interestingly, although they are usually the first port of call for people with
mental health problems, GPs often do not receive continuing professional development (CPD) in mental
health issues as often as might be required given the percentage of their patient‐base that present with
mental health problems (Lester, 2005). Nevertheless, 91% of people with a mental health problem will
be treated within the primary care system, with only a small percentage referred on to specialist mental
health services (Airey, Boreham, Erens, & Tobin, 2003) (Photo 5.1).
Once an individual has been referred to other more specialised services, they are likely to come into
contact with one or more of a number of professional mental health care workers depending on their
individual needs and requirements. Community mental health nurses (CMHNs) or community
psychiatric nurses are registered nurses with specialist training in mental health. They have a range of
skills, from offering counselling and psychotherapy (e.g., CBT) to administering medication. They may
specialise in treating certain types of patient groups, such as children or people with substance
dependency problems, and may be attached to GP surgeries or operate from community mental health
centres.

PHOTO 5.1 GPs or physicians are usually the first point of contact for people with mental health problems, and up to
one in three patients seen by a GP on a daily basis will have either emotional or psychological problems.

Community mental health nurses Registered nurses with specialist training in mental
health
Once referred for a more detailed assessment of their mental health problems, an individual is likely to
then be seen either by a psychiatrist or a clinical psychologist. Psychiatrists are qualified medical
doctors who have received further training in mental health problems. Psychiatrists can make initial
assessments of a person's condition and needs and can also prescribe medications. Clinical
psychologists are normally psychology graduates who have completed 3 years of intensive
postgraduate training to learn the skills required for clinical practice, and they will specialise in the
assessment and treatment of mental health problems. Clinical psychologists will often specialise in
working with only one or maybe two client groups, often within a preferred psychological approach (e.g.,
cognitive, behavioural, systemic, or psychodynamic, see Chapter 4). Some may work exclusively within
child and adolescent services, known in the UK as Children & Adolescent Mental Health
Services (CAMHS), others may be involved in learning disability, with older people, or with substance
dependency. Clinical psychologists will often work within MDTs and are closely involved in providing
care and interventions for mental health problems, but—unlike psychiatrists—are not able to prescribe
medications.

Psychiatrists Medical practitioners specialising in the diagnosis and treatment of mental

illness.

Clinical psychologists Psychology graduates who have completed up to 3 years of intensive

postgraduate training to learn the skills required for clinical practice, and who specialise in the
assessment and treatment of mental health problems.

Others involved in the provision of mental health services include counsellors, psychotherapists,
occupational therapists, social workers, and approved mental health workers. Counsellors are trained
to offer talking therapies that will support people with mental health problems and help them to cope
better with their lives and their symptoms (see Chapter 4, Section 4.1.2). Psychotherapists provide a
range of psychotherapy support to individuals with mental health problems. Psychotherapists will often
specialise in a particular therapeutic approach and may provide support for more longer‐term mental
health problems. Occupational Therapists are available to help people with mental health problems
adjust to the demands of normal day‐to‐day living, including developing personal independence and
achieving levels of functioning required for employment. Social workers are trained to provide a
valuable link between mental health services and broader social service provision, and they can provide
advice and support on issues such as benefits, housing, day care, and occupational training. Finally,
approved mental health practitioners have a professional clinical qualification and have also
received special training in assessing and helping people who may need to be compulsorily detained
because of their mental health problems.

Counsellors People who are trained to offer talking therapies that will support people with
mental health problems and help them to cope better with their lives and their symptoms.

PsychotherapistsI ndividuals who are involved in the treatment of mental disorder by

psychological rather than medical means.

Occupational Therapists Clinicians who specialise in assessing and training (or retraining)
occupational and daily living skills.
 Social workers Professionals whose main focus is clients’ social care needs (e.g. housing).
Approved Social Workers are also involved in Mental Health Act assessments.

approved mental health workers Professionals who are trained to offer treatments that will
support people with mental health problems and help them to cope better with their lives and
their symptoms. They will not normally have the kinds of professional clinical qualifications
possessed by other mental health professionals, but will have received special training.

In many cases, mental health provision is characterised by professionals working in multidisciplinary

teams (MDTs, and this enables professionals to bring a range of skills from health and social care that
will provide the basis for support and recovery for individuals with mental health problems. MDTs will
provide individual clients with more holistic care and are especially helpful for dealing with complex
and challenging cases. Within this team, the clinical psychologist's role will be to offer a perspective on
each case based on their own professional skills, and this may involve providing assessments for diagnosis
or the evaluation of a client's needs, formulating aetiology or causes, or suggesting support and
conducting suitable interventions for the client's specific problems. Table 5.2 provides the descriptions of
members of a typical MDT offering community mental health services (Casares & Lake, 2015).

multidisciplinary teams (MDTs) MDTs include workers from a range of disciplines that
specialise in different aspects of health and social care, e.g., psychiatrists, clinical psychologists,
social workers and occupational therapists.

TABLE 5.2 Clinical psychologists frequently work as members of multidisciplinary teams (MDTs).
From Casares & Lake (2015)

Part of the rationale for MDTs is that they can provide clients with more holistic care, since they
include workers from a range of disciplines that specialise in different aspects of health and social care.
Managers
Psychiatrists (Doctors)
Psychologists (usually Clinical or Counselling Psychologists)
Mental health nurses
Occupational therapists
Social workers
Psychological therapists
Speech therapists (in learning disabilities teams)
Health care or nursing assistants
Support workers
Peer recovery workers (people who draw on their experiences of using mental health services to
support others)
Administrators
 SELF‐TEST QUESTIONS
How do people with mental health problems access mental health services?
Can you name at least five different types of mental health professionals in the UK?

SECTION SUMMARY

5.2 WHO ARE MENTAL HEALTH PROFESSIONALS?

Your local GP or physician will usually be the first point of contact with mental health care
services
Professional mental health care workers include CMHNs, psychiatrists, clinical psychologists,
counselors, psychotherapists, occupational therapists, social workers, and approved mental health
practitioners.
In many cases, mental health provision is characterised by professionals working in
Multidisciplinary Teams (MDTs).

5.3 PROVIDING MENTAL HEALTH SERVICES

5.3.1 What Facilities Are Available?

Mental health problems are both diverse and experienced by all members of society and so will often
require services that are flexible and geared towards managing symptoms that are often quite varied in
type and severity. Some people will need specialised short‐term help in order to recover others will need
long‐term support and care.
As a result, mental health services provide a range of facilities geared to helping with different types of
problems. Most people with a mental health problem can be treated on an outpatient basis and
treatment can take place at a dedicated community mental health centre, a day clinic, or some larger
GP or physician surgeries. Some people may need voluntary inpatient hospital care—especially if
that is agreed between the patient and their psychiatrist, psychologist, or care plan team. Some people
can even be detained in a hospital under the Mental Health Act if their mental health problems are
severe enough, and they can be compulsorily detained (a) in the interests of their own health or safety,
or (b) for the protection of other people. In England in 2017–2018, over 49,000 people were detained
under the Mental Health Act (NHS Digital, 2018), and this number has been steadily growing and has
risen by 40% between 2006 and 2016 (Care Quality Commission, 2018). This increase is likely to be
due to a number of different factors such as fewer alternatives to inpatient care, broadening legal
definitions of mental health, and growth in sections of the population likely to be detained—such as
older people who may have dementia. Detention rates are marginally higher for males than females,
and detentions for ‘Black’ or ‘Black British’ groups were over eight times the rate for White groups
(NHS Digital, 2018). However, the number of people that are compulsorily detained under the Mental
Health Act is still a small percentage of the people with diagnosable mental health problems each year
(around 0.3–0.5%) (see https://www.rcpsych.ac.uk/mental‐health/treatments‐and‐wellbeing/being‐
sectioned for further information about detention under the Mental Health Act).
 outpatient basis Most people with a mental health problem can live in the community and
be treated at a dedicated community mental health centre, a day clinic, or some larger GP or
physician surgeries.

inpatient hospital care Treatment provided to a client who has voluntarily admitted himself
or herself to hospital. Some people can be compulsorily detained in a hospital under the Mental
Health Act if their mental health problems are severe enough.

In addition to psychiatric hospitals, regional secure units and secure hospitals are available to treat
individuals who have been admitted by the courts under the Mental Health Act, transferred from prison
under the Mental Health Act, or have been transferred from an ordinary hospital ward because they
may need treatment in a more secure setting.

regional secure units Facilities available to treat individuals who have been admitted by the
courts under the Mental Health Act, transferred from prison under the Mental Health Act, or
have been transferred from an ordinary hospital ward because they may need treatment in a
more secure setting.

Finally in this section, it should be emphasised once again that while the range and type of facilities
available for treating mental health problems is quite varied, the vast majority of people with a mental
health problem are treated voluntarily on an outpatient basis usually by a care team of professionals
with a range of skills. Compulsory detention or treatment is extremely rare, and the overwhelming
majority of people with mental health problems are neither violent nor a danger to themselves or
others.

5.3.2 How Are Mental Health Services Structured?

Apart from the facilities that are available for treatment, services need to be structured so that the
different skills of health care professionals can be focused on the different sets of problems that make up
mental health problems generally. Within the UK NHS, this is currently achieved by organising services
around different client groups. Very broadly, these client groups are likely to include (a) children and
young people services (sometimes known as CAMHS—Children & Adolescent Mental Health Services)
for children and adolescents with mental health and physical health problems, (b) working age adults
who may experience a range of mental health problems, (c) older adults who often have mental health
problems combined with physical health problems, (d) children and adults with a learning disability, (e)
individuals with substance misuse problems, and (f) people with brain injuries or neurological deficits.
Most services are also likely to have a secure and forensic team to deal with mental health problems
related to criminal behaviour, and an access team devoted to ensuring that individuals seeking help with
mental health problems receive rapid access to appropriate services.

5.3.3 The Recovery Model

As well as the physical structure of mental health services, it is also important to consider the
‘philosophy’ or approach to treatment that underpins these services. When someone has a physical
illness, it is relatively easy to talk about a ‘cure’ and to define criteria by which a treatment will have
been successful or not. If someone has a broken leg an X‐ray will show that this has mended successfully
after treatment. If someone has a viral disease, drugs can be shown to have dealt with this when the
virus is no longer detected in the body. This is not so easy to do within mental health, because mental
health problems will largely be defined by the degree of distress and disability caused by the symptoms
and the individual's ability to cope with them—and distress and disability tend to be relative rather than
absolute concepts (see Chapter 2, Section 2.1.2). Instead, within the mental health sphere a number of
countries have adopted the recovery model as a basis for their provision of services. The National
Institute for Mental Health in England (NIMHE) endorsed a recovery model as a guiding principle of
mental health provision in 2005, and many NHS Trusts have now actively implemented this approach.
In this model, recovery is viewed as a personal journey rather than a set outcome, and this involves not
just individual development, but how the individual relates to their community and their society (Repper
& Perkins, 2006).
Repper and Perkins (2006) note the following as important features of recovery. Hope: developing an
ability to persevere through uncertainty and setbacks and developing a sustainable belief in oneself; A
Secure Base: ensuring appropriate housing, income, health care, and security; Self: developing a durable
sense of self, a sense of social belonging and a set of interests; Supportive Relationships: the development of
supportive relationships not just with mental health professionals, but with friends, family, and the
community; Empowerment and Inclusion: developing the confidence for independent decision‐making and
help‐seeking, and challenging stigma and prejudice about mental health problems; Coping Strategies: the
development of a range of coping strategies and problem solving skills that will enable the individual
identify and deal with stressors and crisis points; and Meaning: developing a sense of purpose that may
be related to a social or work role.
The recovery model represents a holistic approach to mental health provision, and embraces the view
that good mental health requires more than the treatment of individual symptoms but requires the
development of the person within society. For example, what is the benefit of treating an individual's
mental health problems if they are then being sent back to the original social and economic conditions
that might have given rise to those problems in the first place? The recovery model attempts to empower
people and to provide them with the hope and skills they might need to cope with and rise above these
background conditions. However, in many ways the recovery model is at odds with the diagnostic model
of mental health problems as enshrined in the Diagnostic and Statistical Manual of Mental Disorders, 5th
edition (DSM‐5; see Chapter 2). DSM‐5 rarely takes account of the causes of mental problems, it
suggests that the removal of cardinal diagnostic symptoms alone will imply recovery, and it does not
recognise the need for others to change as well as those singled out for the diagnosis (e.g., family and
friends involved in supporting the sufferer) (Compton, 2007), and this is an ongoing tension between
those who support a more eclectic recovery model of mental health and the more traditional medical
model of psychiatric symptoms.

SELF‐TEST QUESTIONS
What different types of mental health facilities are available in the UK?
What is the recovery model, and what are its main features?
 SECTION SUMMARY

5.3 PROVIDING MENTAL HEALTH SERVICES

Mental health services provide facilities on an outpatient basis, voluntary hospital care, and
regional secure units for people who have been admitted to psychiatric hospitals by the courts.
Mental health services are structured so that the skills of different health care professionals
can be focused on the different sets of problems that make up mental health problems
generally.
The recovery model represents a holistic approach to mental health provision and embraces
the view that recovery requires the development of the person within society.

5.4 THE ROLE OF THE CLINICAL PSYCHOLOGIST

We have briefly described who clinical psychologists are and offered a sketch of what they do in Section
5.2. In this section we take a more in‐depth look at the role of clinical psychologists and the skills they
deploy as mental health professionals. Before you begin to read this section take a look at Focus Point
5.1 in which a clinical psychologist describes a typical week for her working with people with psychosis
(Focus Point 5.1). This gives a flavour of the range of roles that a clinical psychologist undertakes on
almost a daily basis, including working in teams and with families, conducting assessments, and
providing treatment and support to people with distressing mental health problems.

FOCUS POINT 5.1 A WEEK IN THE LIFE OF A CLINICAL

PSYCHOLOGIST

Working with Psychosis: A Clinical Psychologist's Experience

‘I have worked with people with psychosis for the last 5 years. Most of the work that I have done
has involved either CBT or family intervention (FI) and has been provided through the NHS.
When I started this work I was anxious about trying out these therapies with people with
psychosis. I had experience of CBT working well in trauma, anxiety, and depression but was
unsure how the therapy would translate into psychosis.
A typical week would include a whole variety of very different tasks. The main focus of the
work is the therapy itself but there is a lot that goes on alongside that. Usually I attend the
Community Mental Health Team meeting where clinical cases are discussed and the team
decides on who in the team is best for an individual to see. The team is made up of nurses,
social workers, occupational therapists, psychiatrists, and psychologists and each professional
group takes a slightly different perspective on the case in hand.
In addition there are assessments to conduct. I will usually see three or four people a week for
an initial assessment and then write up this information and take it back to the team meeting
for allocation. Some more time is spent writing letters to clients or to GPs and also in speaking
 on the telephone to those people.
The bread and butter of the job is the clinical work itself. Psychosis is often confusing and
terrifying for those who experience it. This may seem like a self‐evident and simplistic
statement. However, keeping a focus on the distress that people experience helps me a great
deal in my work. It is easy to be blinded by the delusions and hallucinations and to fail to
consider the confusion, distress, and fear that so often goes with them. So, as a start point when
working in psychosis I tend to try to consider what people with psychosis have in common with
other people rather than what sets them apart. In this way I can draw on my experiences of
working in anxiety, depression and trauma when I meet, and try to help, someone with
psychosis.
In my experience CBT can help someone make sense of psychotic experiences by helping them
make links between emotional states, thoughts, beliefs, traumatic life events, and psychotic
symptoms. Helping people to make sense of psychotic and emotional experiences by discussing
psychological formulations can help them make connections between seemingly unconnected
events or beliefs and disabling and distressing psychotic symptoms. In order to succeed in this
work it is first essential to engage well with a client. Engagement in CBT for psychosis is a big
challenge to therapists. For some people having the time and space to talk through their
experiences in detail is very liberating and although it is hard work (for all parties) can be very
rewarding too.
Family interventions (FIs) make up another large part of my clinical work. They have been
designed to minimise the negative impact of a clients' symptoms on carers and to reduce the
risk of client relapse. Central importance is given to the task of defusing the large range of
difficult emotions that psychosis can often engender in families, for example, anger and fear.
The intervention is based upon a positive view of individuals with psychosis and their
caregivers; the strengths of the family unit are explicitly recognised and family members are
mobilised as supportive therapeutic allies. I conduct the FI work with my colleague (who is also
a clinical psychologist) and usually we try to see families in their own homes.
There is still a lot to learn about how psychology can help people with psychosis and that is
what makes this area of work so challenging and rewarding’.

5.4.1 Key Capabilities and Competencies

Clinical psychologists receive training in a range of different approaches, including cognitive‐
behavioural, psychodynamic, and systemic (see Chapter 4, Section 4.1.1). However, these skills are
deployed in a wider framework that would normally consist of four stages: assessment, formulation,
intervention, and evaluation.

assessment Normally, the first stage of clinical work with a client, which typically involves
understanding the problems that a client is experiencing, what may have caused these problems
and be maintaining them, and how the client would like to change.

Normally, the first stage of clinical work with a client would be to undertake an assessment. Typically
this will involve understanding the problems that a client is experiencing, what may have caused these
problems and be maintaining them, and how the client would like to change. A full assessment of these
factors may be undertaken by a team of professionals with different skills (e.g., psychiatrists, community
health workers as well as clinical psychologists), and the nature of the assessments will depend on the
theoretical orientation of the professionals involved. For example, those with a psychodynamic approach
will want to understand how the client's problems relate to underlying, intrapsychic conflicts, those with
a cognitive‐behavioural approach will want to explore the importance of cognitions and how they
influence moods and behaviour (Jones & Hartley, 2015; Lake & Whittington, 2015). Professionals with a
medical training such as psychiatrists (and also some clinical psychologists) may want to provide a
diagnosis, which will classify the client's symptoms according to current diagnostic criteria (e.g., DSM‐
5; see Chapter 2, Section 2.2.3). A variety of methods can be used to collect relevant information for an
assessment. The primary means is the clinical interview (see Chapter 2, Section 2.2.2), especially for
clients who are able to communicate their problems effectively. Validated psychological tests and tests of
cognitive ability can also be used when required (see Chapter 2). Primarily, it is important in this first
stage for the clinical psychologist to establish a good working relationship with the client, and you will
have seen in Section 4.2 that this can be an important contributor to the success of any subsequent
therapeutic interventions. Case History 5.1 provides an example of how an assessment might progress
in practice (Case History 5.1).

diagnosis A classification of the client’s symptoms according to current diagnostic criteria.

clinical interview Primary means of collecting relevant information for an assessment, in

order to understand the problems that a client is experiencing, what may have caused these
problems and be maintaining them, and how the client would like to change.

When the assessment process is complete, the process will move on to a formulation stage. This
combines psychological theory with information gained from the assessment and enables the clinical
psychologist to develop an account of how the client's problems were acquired and how they are being
maintained, and an indication of what interventions might be theoretically useful in alleviating these
problems. A formulation may acknowledge biological and genetic influences (if they are relevant) but
would normally focus on psychological and social processes. This is the stage in which the clinical
psychologist's skill in being able to link psychological theory with practice is highlighted. Formulations
can often be viewed as a series of hypotheses about what is causing a client's problems and these can be
tested out during the intervention stage. A detailed example of formulation and how it is undertaken is
provided in Chapter 2, Section 2.3.

formulation The use of clinical information to draw up a psychological explanation of the

client’s problems and to develop a plan for therapy.

Once the formulation has been completed, a psychological intervention can be implemented on the
basis of this. The intervention may be based on one specific theoretical approach (e.g., CBT), or it may
integrate a number of different approaches and ideas depending on the client's needs and strengths.
Very often the clinical psychologist will directly involve the client in the planning of the intervention to
both help the client to understand what will happen and to develop some conviction on the part of the
client about how the intervention might be successful (Hall & Llewelyn, 2006, pp. 91–92). The
intervention may also need to include the client's family members, especially if the client's difficulties
seem to be linked to family relationships and dynamics or if the client has specific disabilities, such as
learning disabilities.

intervention Psychological treatment, implemented on the basis of the formulation. May be

based on multiple theoretical approaches and may be co‐designed with the client.
 CASE HISTORY 5.1 AN INITIAL ASSESSMENT OF A CLIENT
(PETER) CARRIED OUT BY A CLINICAL PSYCHOLOGIST

The client, Peter, was reported to be suffering from an episode of clinical depression and, as a
result, was experiencing depressed mood for much of the week, was struggling to sleep properly,
and had stopped doing many of the things that he used to enjoy.
The assessment began by asking Peter to say something about why he had come along and then
focussed in detail on his current difficulties. As the clinical psychologist was taking a cognitive‐
behavioural approach, this involved being curious about the thoughts and images Peter was
experiencing (i.e., the cognitive) and the things he was doing or not doing (i.e., the behavioural),
and how these affected and were affected by his depressed mood. They went on to explore how
his problems had developed, the impact they were having on his life currently, and his goals for
the future. They also used some questionnaires to (a) establish a baseline estimate of the severity
of Peter's depression and (b) to explore whether Peter was experiencing depression related
thoughts that had not been covered in the interview. Throughout, the clinical psychologist
attempted to build a therapeutic relationship with Peter by listening carefully to what he was
saying and then summarising their understanding, and also by conveying a sense of positive
regard and kindness. Crucially, during the assessment it was also established that, while Peter
sometimes experienced suicidal thoughts, he was at low risk of acting on these. In addition, for
homework, Peter was asked to keep a record of his thoughts when he was feeling depressed,
both because doing so might identify important negative thoughts that he had forgotten in the
assessment, and because the process of recording could help him to become more aware of his
thinking and the impact it had on his mood.

(after Jones, 2011, in Davey, 2011)

Once the formulation and intervention stages have been completed it is important to evaluate them.
What has been the impact of the intervention? Is the intervention having the desired effects?
Evaluation can be achieved in a number of ways, including discussion with the client and with the use
of validated questionnaires. Therapeutic change can often be very gradual so the client may not have
good insight into the changes that may have begun to occur, and validated questionnaires can often
provide a more objective measure of change. Indeed, the use of validated means of measuring the
effectiveness of interventions is a central feature of evaluation nowadays—largely because of the need
to ensure that interventions can be identified as effective using evidence‐based criteria that will allow
services to use objective criteria by which to decide what types of interventions are effective and which
are not. However, it is still important to get the client's (and carers or family members) impressions of
whether the intervention seems to be helping and their sense of what has and has not changed as a
result of the intervention. Usually, clinical psychologists will want to collect both quantitative and
qualitative information to get a full picture of the effects of the intervention.

Evaluation Stage of treatment that seeks to ensure any intervention is having the desired
effect. Can be achieved in a number of ways, including discussion with the client and with the
use of validated questionnaires.

In summary, a clinical psychologist needs to have the competencies to assess, formulate, intervene and
evaluate, and to be able to do this in collaboration with other mental health professionals. In addition to
these core competencies, clinical psychologists will also need to be able to communicate effectively with
their clients—both verbally and in writing (Hall & Llewelyn, 2006, pp. 22–25), and these are all skills
that will be taught during the clinical psychologist's extensive period of training (see Davey, 2011,
Section 5.4.4).

5.4.2 The Reflective Practitioner Model

In Chapter 3 we discussed the widely held view that clinical psychologists should be thought of as
scientist‐practitioners, who are competent as both researchers and practitioners. Many clinical
psychologists are happy with this label—especially given the shift towards mental health professionals
being seen to provide evidence‐based interventions. However, not all clinical psychologists readily accept
this conception of themselves. For example, some prefer to adopt alternative philosophical approaches
that place less emphasis on traditional science (such as social constructionist approaches that are
described in Focus Point 3.2 in Chapter 3). Nevertheless, despite differences in agreement about the
importance of science in professional clinical psychology practice (e.g., Lilienfeld, Ritschel, Lynn,
Cautin, & Latzman, 2013), clinical psychologists are generally expected to adopt a reflective
practitioner approach to their work (Schön, 1983). This is considered to be an important key
competency in which clinical psychologists reflect on their own experience when working with clients
and on the process of interaction with their client (Hall & Llewelyn, 2006, p. 17). This reflection is
considered to have a number of benefits: (a) it facilitates the process of developing the clinical
psychologist as an autonomous, qualified, and self‐directed professional; (b) it enables clinical
psychologists to develop their practice by overcoming habituated approaches to treatment and
intervention and to consider the needs of each individual client; and (c) it encourages self‐motivation
and self‐directed learning. Most important, it is one method by which clinical psychologists can learn
from their own experiences, and practitioners may also attend regular reflective practice groups through
which individuals share experiences, or work with a supervisor who may facilitate reflective practice. A
more structured way of facilitating reflective practice is for the clinical psychologist to receive his or her
own psychotherapy. This is often the norm in many forms of psychotherapy practice, but it is an issue of
disagreement within clinical psychology practice (Macran & Shapiro, 1998).

reflective practitioner model Key competency in which clinical psychologists reflect on

their own experience when working with clients, and reflect on the process of interaction with
their client.

Finally, it must be pointed out that the reflective practitioner and scientist‐practitioner approaches are
not entirely mutually exclusive, and no matter which philosophical approach you take to your clinical
practice, it will almost certainly be beneficial to regularly reflect on that practice.

5.4.3 Regulation and Continuing Professional Development

Because clinical psychologists provide services to vulnerable groups of people their practice needs to be
properly regulated to protect the public from malpractice and exploitation from untrained individuals.
Since 2009 clinical psychologists in the UK have been regulated by an agency known as the Health &
Care Professions Council(HCPC) (www.hpc‐uk.org), and its role is to protect the public by
ensuring that clinical psychologists (amongst other groups of practicing health care professionals) meet
specified standards of training, professional skills, behaviour, and health. The HCPC maintains a
register of clinical psychologists who meet these required standards, and it has also specified that clinical
psychologist is a protected title that can only be used if the individual has received appropriate
training and is registered with the HCPC. The HCPC has the authority to take out criminal
prosecutions against anyone who uses this protected title and is not trained or registered to do so. In
addition, the HCPC can take action against any clinical psychologist who does not meet their standards
of conduct, performance, and ethics. In such circumstances, further actions taken by the HCPC may
include recommendations for further training and supervision, preventing a clinical psychologist from
practicing for a specific period of time, or striking that person off the register for life.
 protected title A job title that can only be used if the individual has received appropriate
training and is registered with the relevant regulatory body. The title of clinical psychologist is
protected and regulated by the HCPC.

The way that clinical psychologists are regulated differs from country to country. In the US and Canada
a license is required to practice as a clinical psychologist, and the terms of this license often differs
between states. But in general terms all states require (a) graduation from an accredited training
institution with an appropriate degree, (b) completion of supervised clinical experience, and (c) passing a
written exam and, in some cases, an oral exam.
Once they have qualified, clinical psychologists are expected to undertake continuing professional
development (CPD) throughout their career in order to develop their professional competencies.
This can include reading about the latest research, attending conferences, and training workshops,
carrying out new activities (e.g., supervising trainee clinical psychologists or applying for a research
grant) and undertaking further qualifications (e.g., specialist training in a particular type of
psychological therapy).

5.4.4 Training to Be a Clinical Psychologist

Training to become a clinical psychologist requires skill and dedication. This section describes some of
the pretraining qualifications and attributes required to become a clinical psychologist followed by a
brief overview of clinical psychology training.

Pretraining Qualifications and Experiences

Training to become a clinical psychologist is a challenging and competitive experience. Once a student
has decided that clinical psychology is the career for them, they need to obtain the necessary
qualifications and experience to become eligible for a place on a clinical psychology training course. In
the UK, students will need a first degree in psychology or an equivalent (e.g., a conversion course) that
will make them eligible for graduate basis for charteredmembership (GBC) of the British
Psychological Society(BPS). Once they have this qualification they can apply for a place on a
clinical training course, and these courses will be looking for evidence of experience and capability in
three areas: academic, clinical, and research. In terms of the academic experience, most training
courses will require either a first or a good upper‐second class degree, with some additional weight given
to postgraduate degrees such as relevant taught master's courses or a PhD. Candidates are also expected
to have some clinical experience in mental health areas by working as interns or volunteers in mental
health settings, or alternatively working as an assistant psychologist—the latter usually within the NHS
mental health services. Possessing good research skills is also an important quality preferred by many
clinical training courses. One of the features of clinical psychologists that differentiates them from many
other types of mental health professionals is their research skills. These research skills are important for
a number of reasons. They provide clinical psychologists with the abilities necessary for understanding,
critically appraising, and evaluating the clinical literature. Clinical psychologists can also use their
research skills to evaluate existing services and interventions and conduct research that might lead to the
development of new psychological theories and interventions. Since much of the time during clinical
training is taken up learning clinical skills, many clinical course admissions tutors prefer to take
applicants with an existing good knowledge of research methodology, and so some courses are taking an
increasing number of candidates who have successfully completed a research PhD.
Applications for clinical training courses in the UK are all managed through the Clearing House for
Postgraduate Courses in Clinical Psychology(CHPCCP) (https://www.leeds.ac.uk/chpccp).
However, applications are assessed, interviews conducted, and final decisions on acceptance made by
members of faculty at each of the relevant training institutions that a student has applied to. Apart
from evidence of academic and research ability and clinical experience, courses are usually also looking
for a good interpersonal manner, strong communication skills, and self‐awareness. Competition for
places on clinical training courses in the UK is intense, with applications increasing from 2,442 (554
places available) in 2006 to 4,054 (614 places available) in 2019 (see Figure 5.1)—a current applications
to places ratio of 6.6 : 1!

Clearing House for Postgraduate Courses in Clinical Psychology (CHPCCP) The

CHPCCP manages all applications for clinical training courses in the UK (see
http://www.leeds.ac.uk/chpccp/).

FIGURE 5.1 Number of applications and actual places for UK clinical training courses between 2013 and 2019. In
2019 the applications to places ratio was 6.6:1.

Clinical training
Clinical training courses in the UK are 3‐year programmes that lead to a doctorate in clinical
psychology. This doctorate confers eligibility to register as a chartered psychologist with the BPS and as
a practitioner psychologist with the HCPC. Training usually takes place in service with the NHS, with
the latter covering the trainee's training fees. Training can be divided into three components: (a) an
academic component that takes place in a university setting and consists of conventional teaching and
learning practices covering such topics as human development and interaction, psychological problems,
and mental well‐being and some skills learning associated with different psychological approaches to
mental health problems. Students will learn about the main approaches to alleviating mental health
problems, including cognitive‐behavioural, psychodynamic, and systemic, and a key part of training is
concerned with integrating concepts and interventions from different models to develop interventions
that best suit an individual's needs; (b) a clinical placement component, in which the trainee learns how to
apply these different approaches to different client groups, usually within the NHS. These placements
can take up 3 days a week for as long as 6 months, and a trainee will gain experience by taking
placements across a range of settings and client groups, the latter of which will normally include
working‐age adults with mental health problems, people with learning disabilities, children with mental
health problems, and older adults. During their placements, trainees receive support and guidance from
at least one supervisor who will be a practicing clinical psychologist; and (c) a research component, in which
research skills are developed through both teaching and the trainee conducting their own research
projects. The research projects usually consist of small‐scale service‐based research such as an
evaluation of an intervention, and the most substantial of these projects will form the trainee's doctoral
dissertation. Table 5.3 provides some examples of what a clinical psychology trainee will experience
during their training and covers the nature of the placements they encounter, the types of psychological
models they will learn about, and some of the key competencies they will acquire (see Mayers & Mwale,
2018, for further information on pursuing a career in clinical psychology).
TABLE 5.3 Some examples to illustrate the range of client groups, models and competencies typically covered in clinical
psychology training (for a more in depth picture see Mayers & Mwale, 2018)
Clinical placements
Working age adults with mental health problems
Children with mental health problems and their families
People with learning disabilities
Older people with mental health problems
Possible supplementary placements
Further experience in one of the ‘core’ areas
Adults with brain injury
Children with physical health problems
Adults with physical health problems
Classes of models
Cognitive‐behavioural
Psychodynamic
Systemic
Developmental
Neuropsychological
Key competencies
The ability to communicate effectively with a range of different clients.
The ability to build and maintain effective relationships with others.
The ability to conduct assessments appropriate to different settings.
The ability to develop ‘formulations’, by forming theory‐practice links.
The ability to facilitate interventions appropriate to particular clients and problems.
The ability to evaluate clinical work.
Sufficient self‐awareness to be able to reflect on and learn from clinical work.
The ability to understand, conduct, and apply the findings of psychological research.
 SELF‐TEST QUESTIONS
What are the four key capabilities and competencies of clinical psychologists?
What is the reflective practitioner approach to clinical practice?
Can you describe how clinical psychologists in the UK are regulated?
What pretraining qualifications and experiences would someone need before applying for
a clinical training place in the UK?
What are the three main components of a clinical training programme in the UK?

SECTION SUMMARY

5.4 THE ROLE OF THE CLINICAL PSYCHOLOGIST

Key capabilities and competences of clinical psychologists include their ability to conduct
assessments, create formulations of an individual's problems, prescribe and conduct
interventions, and carry out evaluations of services.
Clinical psychologists tend to adopt a reflective practitioner approach to their work, reflecting
on their own experience when working with clients.
Clinical psychologists in the UK are regulated by the HCPC
Training to become a clinical psychologist usually consists of three components: an
academic component, a clinical component, and a research component.

5.5 CLINICAL PRACTICE REVIEWED

This chapter has covered a number of important aspects of clinical practice and service provision. We
began by looking at the scale of mental health problems in terms of both personal suffering and
economic cost, and it is clearly an immense task faced by service providers to deal with the high
prevalence rates of mental health problems—especially when mental health services are relatively
underfunded compared to funding for other health problems. In 2012 mental health problems
accounted for 40% of all illness but only 13% of NHS funds were devoted to their treatment (Centre
for Economic Performance's Mental Health Policy Group, 2012). And although the UK Government
has recently introduced the notion of parity of esteem between the way in which physical and mental
health services are provided in the NHS, this has still not yet led to equality in funding for mental health
services (Full Fact, 2017).
Because of their complexity, mental health problems require a range of mental health professionals with
a variety of skills, and we have discussed who these professionals are, what skills they possess, how they
work, and where they work. Finally, we focused on the role of the clinical psychologist and covered their
role in the treatment and recovery of people with mental health problems, their key skills and
competencies, and how they are trained.
This book is accompanied by Student and Instructor companion websites.
www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter References
Videos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
Part II
Psychopathology and
Psychological Problems
6 Anxiety and Stressor-Related Problems
7 Depression and Mood Disorders
8 Experiencing Psychosis: Schizophrenia Spectrum Problems
9 Substance Use Disorders
10 Eating Disorders
11 Sexual Problems
12 Personality Disorders
13 Somatic Symptom Disorders
14 Dissociative Experiences
15 Neurocognitive Disorders
16 Childhood and Adolescent Psychological Problems
17 Neurodevelopmental Disability and Diversity
6
Anxiety and Stressor‐Related Problems

ROUTE MAP OF THE CHAPTER

This chapter describes some of the main anxiety‐based problems. It discusses contemporary
accounts of their causes (aetiology) and describes a range of relevant and effective treatments
for each. It is divided into six main sections covering specific phobias, social anxiety disorder,
panic disorder, generalised anxiety disorder, obsessive‐compulsive disorder, and trauma‐ and
stress‐related disorders such as post‐traumatic stress disorder. These topics are chosen because
they represent some of the most prevalent anxiety‐ and stress‐based problems, and they consist
of some of the most thoroughly researched psychopathologies where our understanding of
their causes has become relatively well developed.

CHAPTER OUTLINE
6.1 ANXIETY AS A COMORBID CONDITION
6.2 SPECIFIC PHOBIAS
6.3 SOCIAL ANXIETY DISORDER
6.4 PANIC DISORDER AND AGORAPHOBIA
6.5 GENERALISED ANXIETY DISORDER (GAD)
6.6 OBSESSIVE-COMPULSIVE DISORDER (OCD)
6.7 TRAUMA AND STRESS-RELATED DISORDERS
6.8 ANXIETY-BASED PROBLEMS REVIEWED
 LEARNING OUTCOMES
When you have completed this chapter, you should be able to:
1. Describe the kinds of presenting symptoms that are associated with individual anxiety‐
and stressor‐based problems.
2. Describe the characteristics and diagnostic criteria of six of the important anxiety and
stressor disorders.
3. Describe, compare, and contrast at least two contemporary theories of the aetiology of
each disorder.
4. Distinguish between biological and psychological explanations of anxiety‐based problems.
5. Describe the relevance of research methodologies that have contributed to the
understanding of the acquisition of anxiety‐ and stress‐related disorders.
6. Describe, compare, and contrast at least two therapeutic procedures used for each
individual anxiety disorder or stress‐related disorder.

I'm 26 years old and experience severe anxiety. I've had on and off panic attacks since I was 17. I've really
worked hard to manage it using breathing, daily exercise, and diet. I thought I'd beaten it…2 years pretty
symptom free. But shortly after becoming engaged, the panic attacks started and anxiety came back with a
vengeance. I can barely manage my days at work, I have little appetite and I'm terrified of negative thoughts I've
been having. My scariest thought in the past was having a heart attack. But knowing I'm in such good physical
shape I know this isn't a possibility. My scary thought for the past few weeks has been what if I kill myself…so
scary I try not to be alone. My doctor has given me some medication, but I don't know if it's working. My friends
who know about psychology say I'm fine and those thoughts are my anxiety.
Michelle's Story

Introduction
Anxiety and stress are common features of everyday living and will be experienced by us all in one form
or another, and this makes anxiety a very common mental health problem. As an adaptive emotion
anxiety can help us prepare to deal effectively with anticipated threats and challenges by increasing our
arousal and reactivity, focusing our attention, and helping us to solve problems. However, we can often
find there will be times in our lives when we have difficulty managing our anxiety, and it starts to feel
uncontrollable and distressing. Michelle's story provides an example of how anxiety can come to feel
distressing and her commentary gives us a real insight into some of the more debilitating symptoms of
an anxiety problem. These include panic attacks, lack of appetite, scary, uncontrollable thoughts,
thoughts about physical illness, even suicidal ideation—every conceivable threat seems to be amplified.
Anxiety generally has both physical and cognitive attributes. First, there are the physical symptoms of
anxiety—such as muscle tension, dry mouth, perspiring, trembling, and difficulty swallowing. In its more
chronic form, anxiety can also be accompanied by dizziness, chronic fatigue, sleeping difficulties, rapid
or irregular heartbeat, diarrhea or a persistent need to urinate, sexual problems, and nightmares. In
contrast, the cognitive features of anxiety include a feeling of apprehension or fear, usually resulting
from the anticipation of a threatening event or situation. Usually accompanying anxiety are intrusive
thoughts about the threat, catastrophic bouts of worrying about the possible negative outcomes
associated with the threat, and—in some specific types of problems—uncontrollable flashbacks about
past traumas and anxiety‐provoking experiences. Overly anxious people also find it hard to stop
thinking negative and threatening thoughts, and this is in part due to the cognitive biases that have
developed with the experience of anxiety. In the case of some anxiety‐related conditions, such as
obsessive‐compulsive disorder(OCD), the sufferer can also develop sequences of complex
ritualised behaviours designed to help them relieve their anxiety.

obsessive -compulsive disorder (OCD) A disorder characterised either by obsessions

(intrusive and recurring thoughts that the individual finds disturbing and uncontrollable) or by
compulsions (ritualiszed behaviour patterns that the individual feels driven to perform in order
to prevent some negative outcome happening).

We all experience feelings of anxiety quite naturally in many situations—such as just before an
important exam, while making a presentation at college or work, at an interview, or on a first date. Most
anxiety reactions are perfectly natural, and they have evolved as adaptive responses that are essential for
us to perform effectively in challenging circumstances. However, anxiety can often become so intense or
attached to inappropriate events or situations, that it becomes maladaptive and problematic for the
individual (Davey, 2018). This is when an anxiety disorder may develop. In a sufferer of an anxiety
disorder the anxiety response:

anxiety disorder A psychological disorder characterized by an excessive or aroused state and

feelings of apprehension, uncertainty and fear.

1. May be out of proportion to the threat posed by the situation or event (e.g., in specific phobias),
2. May be a state that the individual constantly finds themselves in and may not be easily attributable
to any specific threat (e.g., in generalised anxiety disorder[GAD], or some forms of panic
disorder[PD]),
3. May persist chronically and be so disabling that it causes constant emotional distress to the
individual, who is unable to plan and conduct their normal day‐to‐day living. This can result in an
inability to hold down a regular job, or an inability to maintain long‐term relationships with
friends, partners, and family, etc.

generalised anxiety disorder (GAD) A pervasive condition in which the sufferer

experiences continual apprehension and anxiety about future events, and this leads to chronic
and pathological worrying about those events.

panic disorder An anxiety disorder characterised by repeated panic or anxiety attacks.

Anxiety‐based problems are relatively common, and around one in five people will report high levels of
anxiety at any one time (Davey, 2018), one in three people will experience an anxiety disorder in their
lifetime (Bandelow & Michaelis, 2015), and a review of anxiety in 84 countries reported that the global
prevalence of diagnosable anxiety disorders at any one time is 7.3% (Baxter, Scott, Vos, & Whiteford,
2012). Anxiety problems may also be one mental health condition that is on the increase, with a US
study conducted by the American Psychiatric Association indicating a 5% rise in anxiety ratings
between 2017 and 2018 alone (American Psychiatric Association, 2018). Anxiety is also a mental health
problem that tends primarily to affect more people in high‐income than low‐income countries (Ruscio et
al., 2017).
As a result of its high levels of prevalence, pathological anxiety imposes a high individual and social
burden, tends to be more chronic than many other psychological problems, and can be as disabling as
physical illness. In both Europe and the US the cost of treating anxiety‐based problems runs into many
billions of pounds annually, making them more economically expensive than most other psychological
problems (Rovner, 1993; Greenberg et al., 1999). These economic costs include psychiatric,
psychological, and emergency care, hospitalisation, prescription drugs, reduced productivity,
absenteeism from work, and suicide (Lepine, 2002; Fineberg et al., 2013).
In this chapter we discuss in detail six of the main anxiety and stress‐related disorders:
Specific phobias
Social anxiety disorder (SAD)
Panic disorder
Generalised anxiety disorder (GAD)
Obsessive‐compulsive disorder (OCD)
Post‐traumatic stress disorder (PTSD)

6.1 ANXIETY AS A COMORBID CONDITION

Anxiety disorders are diagnosed when subjectively experienced anxiety is present and recurs on such a
regular and chronic basis that it is distressing and disrupts normal daily living. However, many of the
symptoms of anxiety are common to a number of different anxiety disorders, and so it is relatively
common for an individual to suffer from more than one anxiety disorder (Hofmeijer‐Sevink et al.,
2012). When anxiety disorders are comorbid with each other in this way they have an earlier age of
onset and a higher rate of chronicity and are also likely to be associated with depression, and with
greater social disability. Anxiety symptoms may be particularly prone to comorbidity because many of
the physiological and cognitive components of anxiety can be found across different disorders, and so
these vulnerability factors may trigger the development of multiple anxiety problems. Some common
cross‐disorder phenomena that may lead to anxiety‐anxiety comorbidity include:
1. Physiological symptoms of panic are found not only in panic disorder but also in the reactions to
phobic stimuli in specific phobias,
2. Cognitive biases—such as information processing biases that tend anxious people to selectively
attending to threatening stimuli (Mathews & MacLeod, 2005)—are common to almost all anxiety
disorders,
3. A number of prominent psychopathologies are characterised by the dysfunctional and
uncontrollable perseveration of certain thoughts, behaviours or activities (e.g., pathological
worrying in GAD, perseverative compulsions in OCD, and rumination during periods of
depression), and the psychological mechanism that underlies dysfunctional perseveration may be
similar across many of these disorders (e.g., Meeten & Davey, 2011),
4. Certain specific early experiences can be found in the aetiology of a number of different anxiety
disorders (e.g., physical or sexual abuse during childhood), and experiences such as these may
increase an individual's risk of developing several anxiety‐based problems.
Anxiety disorders are also commonly comorbid with other psychological disorders (Rodriguez et al.,
2004; McLean, Asnaani, Litz, & Hofmann, 2011), which means that a range of symptoms associated
with psychological problems can also cooccur with anxiety (e.g., depression, substance abuse, eating
disorders, are commonly experienced with anxiety). Table 6.1 shows prevalence rates and comorbidity
figures for a number of anxiety and stress‐related disorders from a survey by McLean et al. (2011). In
this survey, lifetime prevalence rates for developing an anxiety disorder that was comorbid with another
psychological disorder was 44% for women and 34% for men. In particular, anxiety disorders were
highly comorbid with mood disorders and with substance use disorders.
TABLE 6.1 Lifetime and 12‐month prevalence rates of comorbid disorders among individuals diagnosed with an anxiety
disorder
From McLean, Asnaani, Litz, & Hofmann (2011).

12‐Month Lifetime
Disorder Women, % Men, % Women, % Men, %
Mood disorders
Major depressive disorder 23.7 19.1 38.3 30.0
Dysfunctional beliefs 11.2 8.9 12.9 10.6
Bipolar disorder I 2.4 3.3 3.0 3.3
Bipolar disorder II 3.3 3.9 3.4 3.2
Substance use disorders
Alcohol abuse 4.3 8.2 15.0 33.2
Alcohol dependency 2.9 4.8 7.9 16.7
Drug abuse 1.4 4.5 10.0 21.8
Drug dependency 1.0 2.2 4.9 9.3
Eating disorders
Anorexia nervosa 0.0 0.0 0.6 0.2
Bulimia nervosa 1.0 0.0 2.2 0.5
Binge‐eating disorder 2.0 1.3 2.7 2.3
Other
Attention deficit/hyperactivity disorder 6.9 7.6 7.8 11.1
Intermittent explosive disorder 9.4 12.5 11.6 19.3
Anxiety disorder
Any additional 37.3 27.9 44.8 34.2
Let's look at each of the anxiety diagnostic categories in turn, starting with a closer look at specific
phobias.

6.2 SPECIFIC PHOBIAS

Specific phobias are defined as a ‘marked fear or anxiety about a specific object or situation (e.g.,
flying, heights, animals, receiving an injection, seeing blood)’, and a summary of the Diagnostic and
Statistical Manual of Mental Disorders, 5th Edition (DSM‐5) criteria for specific phobia are presented in
Table 6.2. The phobic trigger usually elicits extreme fear and often panic, which usually means that the
phobic individual develops avoidance strategies designed to minimise the possibility of contact with that
phobic trigger. Phobic individuals are normally aware that their fear to the phobic situation or event is
excessive or unreasonable (in comparison either with the actual threat it represents or with the less
fearful responses of other people), but they do acquire a strong set of phobic beliefs that appear to
control their fear (Thorpe & Salkovskis, 1997). These beliefs normally contain information about why
they think the phobia is threatening and how to react when they are in the phobic situation (e.g., avoid,
etc.) (Table 6.3). Many contemporary psychological treatments for specific phobias are designed to
challenge these dysfunctional phobic beliefs and replace them with more functional beliefs that foster
approach and contact with the phobic stimulus instead of avoidance.
 Specific phobias An excessive, unreasonable, persistent fear triggered by a specific object or
situation.

TABLE 6.2 Summary: DSM‐5 Criteria for Specific Phobia

Disproportionate and immediate fear relating to a specific object or situation

Objects or situations are avoided or are tolerated with intense fear or anxiety
Symptoms cannot be explained by other mental disorders and persist for at least six 6 months
Phobia causes significant distress and difficulty in performing social or occupational activities

phobic beliefs Beliefs about phobic stimuli that maintain the phobic’s fear and avoidance of
that stimulus or situation.

6.2.1 Prevalence
Specific phobias are extraordinarily common, with surveys suggesting that a clear majority of the
general population (60.2%) experience ‘unreasonable fears’ (Chapman, 1997)—although in most cases
these fears are rarely severe enough to result in impairment or distress. Cross‐national epidemiological
studies suggest lifetime and 12‐month prevalence rates of 7.4% and 5.5% respectively (Wardenaar et al.,
2017) indicating that severe and disruptive phobic symptoms can be relatively common and Table 6.4
shows the prevalence rates for some of the more common forms of specific phobia. There is also a clear
gender difference in the prevalence of specific phobias, with women being twice as likely as men to be
diagnosed with a specific phobia (Wardenaar et al., 2017).

6.2.2 Common Phobias

Interestingly, common phobias tend to focus on a relatively small group of objects and situations, and
the main ones are animal phobias (including fear of snakes, spiders, rats, mice, creepy‐crawlies such as
cockroaches, invertebrates, such as maggots and slugs), social phobia, dental phobia, water phobia,
height phobia, claustrophobia, and a cluster of blood‐injury‐inoculationphobias (known as BII).
Most other types of phobias are less common and can be thought of as quite unusual given the degree
of threat they might realistically pose—such phobias include fear of cotton wool, buttons, chocolate,
dolls, and vegetables (McNally, 1997) (Photo 6.1)! DSM‐5 specifies five subgroups of specific phobias
which are (a) animal phobias (e.g., spiders, insects, dogs), (b) natural environment phobias (e.g.,
heights, storms, water), (c) blood‐injection‐injury phobia (e.g., needles, invasive medical
procedures), and (d) situational phobias (e.g., airplanes, elevators, enclosed spaces), and other
phobias (e.g., situations that may lead to choking or vomiting; in children, loud sounds or costumed
characters!) There is some evidence that if you suffer from a specific phobia in one of these categories,
you are more likely to suffer a phobia of one or more of the other phobias in that category (e.g., Davey,
1992b; Fredrikson, Annas, Fischer, & Wik, 1996), and thus, phobias within each category can have a
higher incidence of comorbidity (Kendler, Myers, Prescott, & Neale, 2001). There are also important
cultural differences in the kinds of stimuli and events that can become the focus of clinical phobias. For
example, Taijin‐kyofu‐sho (TKS) is a common Japanese syndrome characterised by a fear of
embarrassing or offending other people (Prince & Tcheng‐Laroche, 1987). This is rather different to the
Western syndrome of social phobia, where the fear is based on the public embarrassment experienced
by the phobic individual himself or herself. Davey et al. (1998) also found a number of important cross‐
cultural differences in animal fears. For example, while fear of spiders is a common phobic reaction in
most Western cultures, spiders were significantly less feared in the Indian sample used in the study. This
kind of cross‐cultural variability suggests that ‘fear‐relevance’ may at least in part be determined and
developed by factors that are specific to individual cultures, and this should be contrasted with more
biologically oriented views which argue that fear responses have been universally prewired by
evolutionary selection pressures (Davey, 1995; see evolutionary accounts of phobias, in section 6.2.3).
TABLE 6.3 The Phobic Beliefs of Spider Phobics
Adapted from Arntz, Lavy, van den Berg, & van Rijsoort (1993) and Thorpe & Salkovskis (1995)
Phobics develop a set of dysfunctional beliefs about their phobic stimulus or event. These beliefs are
very rarely challenged because the phobic avoids all circumstances where such beliefs might be
disconfirmed. These beliefs maintain phobic fear and serve to motivate responses designed to avoid
contact with the phobic stimulus. Following are some examples of phobic beliefs held by spider
phobics. Such beliefs are the kinds that are challenged in both exposure therapy and cognitive therapy
procedures.
Harm Beliefs:
When a spider is in my vicinity I believe that the spider will:
a. bite me
b. crawl towards my private parts
c. do things on purpose to tease me
d. get on to parts of me that I cannot reach
Chaser and Prey Beliefs:
When I encounter a spider it will:
a. run towards me
b. stare at me
c. settle on my face
d. not be shaken off once it is on me
Unpredictability and Speed Beliefs:
When I encounter a spider:
a. its behaviour will be very unpredictable
b. it will be very quick
c. it will run in an elusive way
Invasiveness Beliefs:
When I encounter a spider it will:
a. crawl into my clothes
b. walk over me during the night
c. will hide in places I do not want, such as my bed
Response Beliefs:
When I encounter a spider I will:
a. feel faint
b. lose control of myself
c. go hysterical
d. scream
TABLE 6.4 Lifetime Prevalence Rates for Common Specific Phobias
Lifetime prevalence rates
Blood–injury–injection phobia 3.0%a
Animal phobias generally 3.8%a
Dental phobia 3–5%b
Water phobia 2.3%a
Height phobia 2.8%a
Claustrophobia/enclosed spaces 2.2%a
Flying 1.3%a
a
Wardenaar et al. (2017).
b Kent (1997).

6.2.3 The Aetiology of Specific Phobias

Attempts to explain specific phobias have a long history and date back to the early days of the
psychoanalytic approaches pioneered by Freud and the conditioning views developed by the
behaviourist J.B. Watson. Originally, there was a tendency to try to explain all types of phobias with just
one explanatory theory (e.g., classical conditioning), but this approach has now given way to the view
that different types of phobias might be acquired in quite different ways (a multifaceted approach). Over
the years, an intriguing debate has taken place about whether phobias are biologically determined
through evolutionary processes or whether they are responses learned during the lifetime of the
individual. This debate will be an important feature of what follows.

Psychoanalytic accounts
Phobias have intrigued psychologists for more than a century. This may be because they manifest as
irrational fears to things that usually pose little if any realistic threat, and their acquisition more often
than not cannot be explained by recourse to simple learning experiences such as a specific traumatic
event. This has led at least some approaches to psychopathology to view phobias as symbolic of other,
more deep‐rooted psychological difficulties. For example, psychoanalytic theory as developed by Freud
saw phobias as a defence against the anxiety produced by repressed Id impulses, and this fear became
associated with external events or situations that had a symbolic relevance to that repressed Id impulse.
Focus Point 6.1 describes the classic case of Little Hans, a 5‐year‐old boy who developed a severe
phobia of horses. Within Freud's psychoanalytic theory, the function of phobias was to avoid
confrontation with the real, underlying issues (in this case, a repressed childhood conflict). However,
because of the nature of psychoanalytical theorising, there is little in the way of objective evidence to
support such accounts of phobias. Nevertheless, there is often an element of insight that can be drawn
from the symbolic interpretations of case histories provided by psychoanalysis, and many anxiety
disorders may indeed function for the sufferer as a way of avoiding confrontation with more challenging
life issues and difficulties.

Classical conditioning and phobias

Attempts to explain phobias in terms of classical conditioning (see Chapter 1, Section 1.3.2) date
back to the famous ‘Little Albert’ study reported by Watson and Rayner in 1920. Albert was a 9‐month
old infant, and Watson and Rayner attempted to condition in him a fear to his pet white rat. They did
this by pairing the rat—the conditioned stimulus(CS)—with the frightening event of a loud noise
produced by striking an iron bar—the unconditioned stimulus(UCS), which distressed Albert (the
unconditioned response, UCR) (Figure 6.1). After several pairings of the rat with the noise Albert
began to cry (the conditioned response, CR) whenever the rat was introduced into the room. This
type of explanation has been popular over the past 50 years, and more sophisticated contemporary
conditioning models of specific phobias have been developed (e.g., Davey, 1992a, 1997). However, it is
difficult to generally explain the range of features possessed by specific phobias with conditioning
theories alone. These criticisms include the following:

FOCUS POINT 6.1 LITTLE HANS—THE PSYCHOANALYTIC

INTERPRETATION OF A SPECIFIC PHOBIA

One of the most famous cases in the history of psychoanalysis is that of ‘Little Hans’, a 5‐year‐
old who revealed many of his perceptions, fantasies, and fears to his physician father, who, in
turn, reported them to Sigmund Freud. Hans began to have a fear of horses, which eventually
grew to the point that he refused to leave the house. The immediate event that precipitated this
phobia was seeing a big, heavy horse fall down. Freud interpreted this to mean that Hans at
that moment perceived his own wish that his father would fall down. Then Hans, a little
Oedipus, could take his father's place with his beautiful mother. Another part of the fear
derived from the large size of horses, which Hans unconsciously identified with the great power
of his father. He expressed the fear that a horse would come into his room. He also became
afraid not only of horses biting him, but of carts, furniture vans, and buses. This revealed, to
the psychoanalyst, still another aspect of Hans' unconscious fantasies, namely that the falling‐
down horse stood not only for his father but also for his mother in childbirth, the box‐like carts
and vehicles representing the womb. All these complicated, repressed feelings and perceptions
were thus incorporated in a single phobia.
It is important to note that Little Hans was basically a straightforward, cheerful child who
experienced normal psychosexual development marred only by the episode of the phobia, from
which he recovered rather promptly. Fourteen years later, 19‐year‐old Hans came to see Freud.
He had continued to develop well and had survived without unusual difficulty the divorce and
remarriage of both parents. The problems of his childhood were used by Freud to illustrate the
normal process of psychosexual development—the complex, intense, erotic drama of early
childhood.
FIGURE 6.1 The ‘Little Albert’ classical conditioning study by Watson & Rayner (1920) demonstrated the
acquisition of a phobia by pairing Little Albert's pet rat (the conditioned stimulus, CS) with a loud noise (unconditioned
stimulus, UCS).
1. Traumatic experiences are essential for traditional conditioning accounts, yet many phobics appear
unable to recall any trauma or aversive conditioning experience at the time of the onset of their
phobia (Rachman, 1977; Marks, 1969; Emmelkamp, 1982). This appears to be particularly true of
some animal phobics such as snake and spider phobics (Davey, 1992b; Murray & Foote, 1979), and
also height and water phobics (Menzies & Clarke, 1993a, 1993b);
2. Not all people who have pain or trauma paired with a situation develop a phobia. For example, not
everyone who has a traumatic experience undergoing dental treatment acquires a dental phobia
(Lautch, 1971), not everyone who experiences a violent thunderstorm acquires a thunderstorm
phobia (Liddell & Lyons, 1978), and not all fliers who experience a traumatic flying accident
express a subsequent anxiety of flying (Aitken, Lister, & Main, 1981. Goorney, 1970). This suggests
that a potential conditioning experience is itself insufficient to cause a phobia.
3. Simple conditioning models treat all stimuli as equally likely to enter into association with aversive
consequences, yet fears and phobias are not evenly distributed across stimuli and experiences.
People appear to develop phobias of animals (snakes, spiders), heights, water, death, thunder, and
fire more readily than fears of hammers, electric outlets, knives, guns, etc., even though the latter
group of stimuli seem to have a high likelihood of being associated with pain or trauma
(Seligman, 1971);
4. A simple conditioning model does not appear to account for the common clinical phenomenon of
incubation. Incubation is where fear increases in magnitude over successive encounters with the
phobic stimulus—even though it is not followed by a traumatic consequence (Eysenck, 1979).
 Incubation is a phenomenon that is frequently observed clinically, but according to conditioning
theory it should lead to extinction rather than enhancement of the fear response.
Due to these features it is problematic for a classical conditioning account to explain the acquisition
of all phobias as resulting from traumatic conditioning episodes, but there is strong evidence that
traumatic conditioning experiences are responsible for the acquisition of at least some phobias.
These include dental phobia (Davey, 1988), choking phobia (Greenberg, Stern, & Weilburg, 1988),
accident phobia (Kuch, 1997), and most dog phobias (DiNardo et al., 1988; Doogan & Thomas,
1992).

Biological accounts of phobias—the role of evolution

The fact that phobias tend to be focused on a limited set of fears that seem to have a prima facie
evolutionary significance has led some researchers to suggest that we may be biologically prepared or
prewired to acquire certain phobias. For instance, clinical phobias tend to cluster around things such as
heights, water, spiders, snakes, blood, injury, etc.—all of which can be considered to have a real life‐
threatening significance that has been present for many thousands of years. In contrast, we rarely
develop clinical phobias of life‐threatening stimuli that have only appeared more recently in our
phylogenetic past—such as guns and electricity.
There are two predominant evolutionary theories of phobias. First, Seligman (1971) argued that
evolutionary selection pressures have evolved in us a biological predisposition to learn to associate fear
with stimuli that have been hazardous for our pretechnological ancestors. That is, we tend to have a
built‐in predisposition to learn to fear things such as snakes, spiders, heights, and water because these
have been life threatening to our ancestors, and those of our ancestors that evolved a biological
predisposition to fear these kinds of stimuli will have been more likely to survive and pass that fear
predisposition on to future generations. This account is known as biological preparedness and has
been supported by two lines of evidence:

biological preparedness A theory which argues that we have a built-in predisposition to

learn to fear things such as snakes, spiders, heights and water because these have been life-
threatening to our ancestors.

If participants in a classical conditioning experiment are shown pictures of ‘fear‐relevant’ stimuli such
as snakes and spiders (CSs) paired with electric shock (UCSs), they develop fear of the CSs more quickly
and show a greater resistance to extinction than if pictures of less fear irrelevant stimuli are used as CSs
(e.g., pictures of houses) (Öhman, Erixon, & Lofberg, 1975).
Cook and Mineka (1989, 1990) also found that laboratory‐reared rhesus monkeys that had never before
seen a snake rapidly acquired fear reactions to snakes after being shown a demonstration of another
monkey being frightened in the presence of a snake. They did not acquire fear reactions after watching
a demonstration of another monkey being frightened in the presence of a stimulus such as a rabbit or a
flower. Both studies suggest that humans and primates such as rhesus monkeys may have an unlearned
predisposition to rapidly acquire fear responses to some types of stimuli and not others (see Öhman &
Mineka, 2001).
Second, Poulton & Menzies (2002) have argued for the existence of a limited number of innate,
evolutionary‐relevant fears. This nonassociative fear acquisition model argues that fear to a set of
biologically relevant stimuli develops naturally after very early encounters given normal maturational
processes and normal background experiences, and no specific traumatic experiences with these stimuli
are necessary to evoke this fear. Following repeated exposure to these stimuli, the innate fear reaction
will habituate and should eventually disappear. Poulton and Menzies (2002) claim that this account
explains why most children go through a discrete developmental period when they appear to be
frightened of potential life‐threatening stimuli such as heights and water (Graham & Gaffan, 1997), and
why there is little evidence in retrospective studies for phobias such as height and water phobia being
caused by specific traumatic experiences (Menzies & Clark, 1993a, 1993b). This account then goes on to
explain adult phobias as instances where these developmental phobias have failed to habituate properly.

nonassociative fear acquisition A model that argues that fear of a set of biologically
relevant stimuli develops naturally after very early encounters given normal maturational
processes and normal background experiences, and no specific traumatic experiences with these
stimuli are necessary to evoke this fear.

While evolutionary accounts are appealing and appear to have at least some face validity, we must be
cautious about accepting them on the basis of existing evidence (Delprato, 1980). First, such accounts
depend on the fact that current phobic stimuli have actually acted as important selection pressures over
our evolutionary past. But this is very difficult to empirically verify. For example, do we tend to have
phobic reactions to spiders because they once constituted an important life‐threatening pressure on our
pretechnological ancestors? There is no convincing evidence to suggest this. Second, evolutionary
accounts can be constructed in a post hoc manner and are at risk of being either ‘adaptive stories’
(McNally, 1995) or ‘imaginative reconstructions’ (Lewontin, 1979) (cf. Merckelbach & de Jong, 1997).
This view argues that it is possible to construct, post hoc, an adaptive scenario for the fear and
avoidance of almost any stimulus or event (McNally, 1995)—see Activity Box 6.1. This does not mean
that evolutionary accounts are wrong (see Öhman & Mineka, 2001, for a recent evolutionary account of
phobias), merely that they are tantalisingly easy to propose, but very difficult to substantiate. You might
find this informal blog discussion on the ‘Mystery of the Origins of Phobias’ useful and informative
(https://www.papersfromsidcup.com/graham‐daveys‐blog/the‐mystery‐of‐the‐origins‐of‐phobias).

PHOTO 6.1 A majority of people claim to have a phobia of some kind, although most are not severe enough to cause
distress or to disrupt normal daily life. Some phobias are unusual, such as phobia of cotton wool or buttons—but they are
much more common than you think.

Biological accounts of phobias—neuroimaging studies

An alternative way of trying to understand specific phobias is by investigating the brain neurocircuitry
that underlies specific phobias, and we can do this using functional neuroimaging techniques (see
Chapter 2, Section 2.2.4). The key brain structure that mediates fearful responding to phobic stimuli is
the amygdala, an almond‐shaped group of nuclei located within the medial temporal lobes (see Figure
6.2). The amygdala plays a significant role in the formation and storage of memories associated with
emotionally relevant events and acts as a neural centre that identifies emotional input and then
coordinates this with information from higher cortical areas and subcortical nuclei, the amygdala then
provides feedback to the thalamus that results in appropriate motor action (Del Casale et al., 2012). The
importance of the amygdala in activating phobic fear is indicated by the fact that there is a linear
relationship between subjective experience of fear and amygdala activation (Goosens et al., 2007; Ahs et
al., 2009). Functional neuroimaging studies have also demonstrated that blood‐injection‐injury phobia
and dental phobia are functionally different to other phobias, in that they can lead to a biphasic
response that begins with an increase in heart rate and blood pressure but then can result in decreased
parasympathetic responding that causes fainting. Accounts of specific phobias in terms of brain
neurocircuitry are not in conflict with other types of explanations of phobias (e.g., conditioning,
evolutionary accounts) but help to specify how the conditions through which specific phobias are
acquired are stored and activated in the brain (e.g., Garcia, 2017).
FIGURE 6.2 The amygdala at the crossroads of fear‐related information processing. Phobic stimuli enter the amygdala
through the thalamus, are then processed by the amygdala, which provides connections to both higher brain function‐related
cortical areas (light gray) and subcortical nuclei (darker gray). On receiving their output, the amygdala integrates messages,
thus providing feedback to the thalamus to generate a motor output. DLPFC, dorsolateral prefrontal cortex; OFC,
orbitofrontal cortex; Ventral PFC, ventral frontopolar prefrontal cortex; VLPFC, ventrolateral prefrontal cortex; VMPFC,
ventromedial prefrontal cortex
(after Del Casale et al., 2012).

Multiple pathways to phobias

There is no reason why the acquisition of all phobias should be explained by just a single process—and
evidence has been accumulating to suggest that different types of phobias are acquired in quite different
ways (Merckelbach, de Jong, Muris, & van den Hout, 1996). We have already suggested that some
phobias, such as dog phobia, dental phobia, choking phobia, and accident phobia, can be caused by
traumatic conditioning experiences. In contrast, many other common phobias do not appear to be
characterised by a traumatic experience at their outset—in fact, sufferers often cannot recall the exact
onset of their phobia, which suggests that the onset may be gradual and precipitated by factors that are
not immediately obvious to the individual. Phobias that fit this description include most animal phobias
(including snake and spider phobia) (Murray & Foote, 1979; Merckelbach, Muris, & Schouten, 1996),
and height and water phobia (Menzies & Clarke, 1993a, 1993b).
Recent evidence suggests that at least some phobias are closely associated with the emotion of disgust.
High levels of disgust sensitivity have been found to be associated with small animal phobias in general
(Ware, Jain, Burgess, & Davey, 1994; Davey, 1994b), spider phobia specifically (Mulkens, de Jong, &
Merckelbach, 1996), and has been hypothesised to play a role in mediating blood‐injury‐injection
phobia and contamination fears (Page, 1994; Olatunji, Sawchuk, Lohr, & de Jong, 2004). Disgustis a
food‐rejection emotion whose purpose is to prevent the transmission of illness and disease through the
oral incorporation of contaminated items (Davey, 1994c; Rozin & Fallon, 1987), and elevated disgust
sensitivity implies increased avoidance of disgust‐relevant objects (such as faeces, mucus, etc.). In the
case of animal phobias, Davey (1994a) has argued that many animals that become the focus for phobic
responding do so because they have disgust relevance. Specifically, they may have acquired a disgust
relevance (a) by directly spreading disease and being a source of contamination (e.g., rats, cockroaches);
(b) by possessing features which mimic primary disgust relevant stimuli (by resembling, for example,
faeces or mucus, for example, slugs or animal that are perceived as slimy such as snakes, snails or
lizards); or (c) by having contemporary or historical significance as stimuli that signaled disease, illness,
or contamination (e.g., maggots, spiders, cf. Davey, 1994a). This disease‐avoidance model of animal
phobias (Matchett & Davey, 1991) is supported by the findings that high levels of disgust sensitivity is a
vulnerability factor for animal phobias (such as spider phobia) and can mitigate against successful
therapy if it is not directly addressed in treatment (de Jong, Andrea, & Muris, 1997; Mulkens, de Jong, &
Merckelbach, 1996). Disgust is an emotion not just relevant to the acquisition of phobias but has
becoming increasingly an emotion of study in relation to many different psychopathologies, including
contamination fears in OCD and eating disorders (see Davey, 2011, in press; Olatunji, Cisler, McKay, &
Phillips, 2010; Knowles, Jessup, & Olatunji, 2018). (Photo 6.2).

disgust A food-rejection emotion whose purpose is to prevent the transmission of illness and
disease through the oral incorporation of contaminated items.

disease‐avoidance model The view that some animal phobias are related to attempts to
avoid disease or illness that might be transmitted by these animals.

Alternatively, there is evidence that factors closely associated with panic and panic disorder (see Section
6.4) are also linked to a number of specific phobias. First, there is a fairly high comorbidity rate between
panic disorder and some specific phobias. Studies have identified comorbidity rates of between 40%
and 65% (de Ruiter, Rijken, Garssen, van Schaik, & Kraaimaat, 1989; Starcevic, Uhlenhuth, Kellner, &
Pathak, 1992) suggesting that panic is common in people suffering from many different types of specific
phobia. Second, some categories of specific phobia—especially situational phobias (e.g., fear of heights,
enclosed spaces)—share important characteristics in common with panic disorder. For example,
situational phobias appear to have a preponderance of spontaneous onsets typical of panic disorder
(Himle, Crystal, Curtis, & Fluent, 1991), have a significantly higher rate of comorbidity with panic
disorder than do other types of phobias, such as animal phobias (Starcevic & Bogojevic, 1997), and
frequently have uncontrollable panic attacks as one of the symptoms of phobic responding (e.g., height
phobia, Antony, Brown, & Barlow, 1997; flying phobia, McNally & Louro, 1992; claustrophobia,
McIsaac, 1995). Similarly, both claustrophobia and height phobia share aetiological factors in common
with panic disorder. For instance, subjective fear in claustrophobia is focussed not just on external
dangers but on anxiety expectancies and bodily sensations (Craske, Mohlman, Yi, Glover, & Valeri,
1995), and spontaneous panic attacks are found significantly more often in claustrophobics than in other
types of phobias (Rachman & Levitt, 1985; Craske & Sipsas, 1992). Height phobia is associated not only
with heightened discrimination of bodily sensations, but also with a bias towards interpreting
ambiguous bodily sensations as threatening—a characteristic which is central to the aetiology of panic
disorder (Davey, Menzies, & Gallardo, 1997) (see Section 6.4.4).
PHOTO 6.2 Small animal phobias are very common and consist of creepy‐crawlies, insects, molluscs, rodents, spiders,
snakes, and lizards, etc. Interestingly, if you are fearful of one of these types of animals you are more likely to be fearful of
others in this group. Fear of such animals may be related more to the emotion of disgust rather than anxiety.
These examples suggest that specific phobias may have a number of different causes—depending on the
nature of the phobic stimulus or event—and the aetiologies appear to involve quite different
vulnerability factors and psychological processes. This being so, specific phobias are a coherent category
only on the basis of their defining symptoms, and therapists may need to look more closely at the
different aetiologies to construct successful treatments.

6.2.4 The Treatment of Specific Phobias

Traditionally, successful treatment for specific phobias has tended to revolve around some form of
exposure to the phobic stimulus or situation, and, in the past, behavioural treatments of choice for
specific phobias have tended to include systematic desensitisation, flooding, and counterconditioning
(see Chapter 4, Section 4.1.1). One important issue in therapy for specific phobias is to address the
phobic beliefs that sufferers hold about their phobic event or situation (see Table 6.4). These beliefs are
often dysfunctional in that they do not match with the reality of the threat (or lack of it) posed by the
phobic stimulus, and they also maintain fear and avoidance responses. Because of their strong
avoidance of any contact with their phobic situation, sufferers rarely find themselves in a situation
where they encounter evidence that disconfirms their phobic beliefs (e.g., continually avoiding spiders
never helps the spider phobic to disconfirm their belief that, for example, ‘I would come to physical
harm in the presence of a spider’) (Thorpe & Salkovskis, 1995, 1997). One important feature of
exposure therapy is that it does put the phobic individual in situations where they can experience
evidence that is contrary to their dysfunctional beliefs (e.g., Norberg et al., 2017).
Two more recent developments in the treatment of specific phobias have been the elaboration of
integrated one‐session therapies and the use of virtual reality exposure. For example, specific
behavioural treatments such as exposure have been combined with cognitive therapy techniques to
produce integrated short‐term therapies that involve cognitive restructuring, intensive exposure to the
phobic event or stimulus, and modelling, and these can be effective in as little as one 3‐hour session
with both adults and children (Öst, 1997; Davis, Ollendick, & Öst, 2019) (Treatment in Practice 6.1).
The use of virtual reality environments in the treatment of phobias has also been beneficial (see
Chapter 4, Section 4.1.2). Virtual reality exposure has the advantage of simulating environments that
are difficult to find in everyday life (such as extreme heights) and can be customised to the client's own
needs and requirements (e.g., Garcia‐Palacios, Hoffman, Carlin, Furness, & Botella, 2002).

CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 6.1

ONE‐SESSION RAPID TREATMENT OF SPIDER PHOBIA

One‐session treatments for specific phobias were developed during the 1990s and are
remarkably successful as effective and long‐lasting treatments for many specific phobias (Öst,
1997: Koch, Spates, & Himle, 2004; Öst, Alm, Brandberg, & Breitholtz, 2001). One‐session
treatments usually include a combination of graduated in vivo exposure and modeling. The
following is an example of a one‐session treatment procedure for spider phobia.
STEP 1:Catching a small spider in a plastic bowl: The therapist first models how the
client should pick up the spider by putting a bowl over it and then sliding a card
underneath to trap the spider and then picking the bowl up using the card as a lid. This is
repeated three to four times and on the last occasion the client is instructed to hold the
bowl in the palm of his/her hand. At this point a brief role‐play can be carried out by
having the therapist play the part of a person born blind, and the client has to describe
what is happening (thus forcing the client to look at the spider in the bowl).
STEP 2: Touching the spider: The therapist asks the client what they think will happen if
they touch the spider. Most spider phobics say the spider will climb up their arm. This is a
prediction that can be tested by the therapist who then touches the spider. This is repeated
up to 10 times to show the client that the spider's reaction is almost always to run away.
This is followed by the client touching the spider—usually with some physical guidance
from the therapist.
STEP 3: Holding the spider in the hand: The therapist takes the spider on his/her hand,
letting it walk from one hand to another. The client is then encouraged to put their index
finger on the therapist's hand so that the spider can walk across the finger and back to the
therapist's hand. This is repeated a number of times until the spider walks across all the
client's fingers. Gradually, the therapist withdraws physical support and the client allows
the spider to walk from one hand to another.
These three steps are then repeated with spiders of increasingly larger size. Throughout the
session, the client is taught that he/she can acquire control over the spider by gradually being
able to predict what the spider will do. The goal of the therapy is to ensure that at the end of
the session the client can handle two spiders with low or no anxiety and no longer believe
his/her catastrophic cognitions about spiders.
From Öst (1997).

In conclusion, it must be remembered that many people can live with their phobias—either because
they are subclinical in intensity or their fears are so specific that they do not interfere substantially with
their daily lives. So only those with the most distressing or disabling phobias are the ones who seek
treatment. In general, recently developed therapies for specific phobias have been shown to be
extremely effective and successful, and these therapies are usually multifaceted and combine aspects of
exposure therapy with cognitive restructuring.
 SELF‐TEST QUESTIONS
What are the main diagnostic criteria for specific phobias?
What are the most common phobias, and what are the kinds of phobic beliefs that
accompany them?
How do classical conditioning and evolutionary theories attempt to explain the acquisition
of phobias? What are their similarities and differences?
What is the role of brain areas such as the amygdala in the formation of specific phobias?
Why is exposure such an important feature of treatment for specific phobias?

SECTION SUMMARY

6.2 SPECIFIC PHOBIAS

Specific phobias are defined as an excessive, unreasonable, persistent fear triggered by a
specific object or situation.
Around 7% of people will meet diagnostic criteria for a specific phobia within their
lifetime.
Common phobias include small animal phobias (insects, rodents, spiders, snakes), social
phobia, dental phobia, water phobia, height phobia, claustrophobia, and blood‐injury‐
injection phobia.
The famous ‘Little Albert’ study by Watson & Rayner (1920) is an example of how
phobias can be acquired through classical conditioning.
Evolutionary accounts of phobias suggest that we have an inbuilt biological predisposition
to fear certain stimuli and events (e.g., heights, water, snakes), because these stimuli were
life‐threatening to our pre‐technological ancestors. Evolutionary accounts of phobias
include biological preparedness theory and the nonassociative fear acquisition model.
The amygdala is a brain area that plays a significant role in the formation and storage of
memories associated with specific fears and phobias.
There is now strong evidence that different phobias may be caused by quite different
processes, some involve classical conditioning, some are caused by high disgust sensitivity,
while others appear to be caused by processes similar to those that cause panic disorder.
Successful treatment for phobias tends to depend on some kind of exposure to the phobic
stimulus or situation, and exposure therapies that are combined with cognitive behaviour
therapy can be effective in as little as one 3‐hour session.

6.3 SOCIAL ANXIETY DISORDER

Social anxiety disorder (SAD) is distinguished by a severe and persistent fear of social or
performance situations. The socially anxious individual tries to avoid any kind of social situation in
which they believe they may behave in an embarrassing way or in which they believe they may be
negatively evaluated, and these types of situations can range from something as simple as having a
conversation, eating or drinking in front of others, or performing in front of others (e.g., giving a
speech). So pervasive is anxiety of these socially based situations that it is also a predictor of several
other debilitating problems such as depression and substance abuse (Rapee & Spence, 2004).
DSM‐5 describes some of the defining features of SAD, which include situations in which the sufferer
believes he or she will show anxiety symptoms that will be negatively evaluated (e.g., they will be
humiliated, embarrassed, or rejected) or will offend others. They may fear public speaking because of
concern that others will notice their trembling hands or voice. Or they may experience extreme anxiety
when conversing with others because of fear they will appear inarticulate. They may avoid eating,
drinking, or writing in public because of fear of being embarrassed by having others see their hands
shake. Individuals with SAD almost always experience symptoms of anxiety in the feared social
situations (e.g., palpitations, tremors, sweating, gastrointestinal discomfort, diarrhea, muscle tension,
blushing, confusion), and, in severe cases, these symptoms may turn into a full‐blown panic attack. As a
result of their reluctance to engage with social situations, sufferers of SAD also tend to underperform in
education and in the workplace and have impaired social and romantic relationships and reduced
productivity (Moitra, Beard, Weisberg, & Keller, 2011; Kessler, 2003). SAD is as common in
adolescence as it is in adulthood (Chavira, Stein, Bailey, & Stein, 2005), and it is a common reason for
school refusal in young children and is the only mood or anxiety disorder that has consistently been
associated with dropping out of school early (Stein & Kean, 2000). Table 6.5 lists the DSM‐5 criteria
for the diagnosis of SAD (The Client's Persective 6.1)
TABLE 6.5 Summary: DSM‐5 Criteria for Diagnosis of Social Anxiety Disorder

Distinct fear of social interactions, typified by anxiety around receiving negative judgement or of
giving offense to others
Social interactions are avoided or are experienced with intense fear or anxiety
The avoidance, fear, or anxiety often lasts for 6 or more months and causes significant distress and
difficulty in performing social or occupational activities
Anxiety cannot be explained by the effects of other mental or medical disorders, drug abuse, or
medication

6.3.1 Prevalence
Cross‐national epidemiology studies have indicated that SAD has a lifetime prevalence of 4% and a 1‐
year prevalence rate of 2.4%, and globally is associated with specific socio‐demographic features such as
younger age, female gender, unmarried status, lower education, and lower income (Stein et al., 2017).
However, the prevalence rates of social fears and phobias generally may be relatively higher at lifetime
prevalence and 1‐year rates of 12% and 8% respectively (Ruscio et al., 2008). Age of onset is
considerably earlier than for many of the other anxiety disorders, with typical age of onset in early to
mid‐teens, and usually prior to 18 years of age (Rapee, 1995; Otto et al., 2001). It is also a particularly
persistent disorder and has the lowest overall remission rate of the main anxiety disorders (Massion et
al., 2002; Hirshfeld, Micco. Simoes, & Henin, 2008).

6.3.2 The Aetiology of Social Anxiety Disorder

Although it is a phobia in its own right, SAD is considered separately from specific phobias in DSM‐5,
and as we will see, theories of SAD suggest that factors rather specific to social anxiety are important in
the aetiology of SAD. In particular, socially phobic individuals possess a range of information
processing and interpretation biases that cause them to make excessively negative predictions about
future social events, and we discuss these various types of bias in the following sections after we have
first discussed genetic and developmental factors.

Genetic factors
There is evidence accruing that there is an underlying genetic component to SAD, although it is not
clear how specific this genetic component might be, and a systematic review of heritability studies has
revealed heritability rates that vary drastically between 13% and 76%—largely as a result of significant
differences in methodologies between studies (Moreno, Osório, Martín‐Santos, & Crippa, 2016).
Evidence consistent with a genetic component indicates that children with SAD are more likely to have
parents with the disorder than nonphobic children (Lieb et al., 2000; Mancini et al., 1996), and twin
studies also suggest that there is a significant but moderate genetic influence on the development of
SAD (Beatty, Heisel, Hall, Levine, & La France, 2002; Ollendick & Hirshfeld Becker, 2002). While
indicating the importance of genetic influences, such studies do beg the question of what aspect of SAD
is inherited. Some studies have been able to identify specific constructs related to SAD that appear to
have a genetic component, and these include submissiveness, anxiousness, social avoidance, introversion,
and behavioural inhibition (Warren, Schmitz, & Emde, 1999; Robinson, Kagan, Reznick, & Corley,
1992; Stein et al., 2017). Other studies indicate that SAD contains an inherited component that is
shared with other anxiety disorders—and this suggests that what might be inherited is a vulnerability to
anxiety disorders generally rather than social phobia specifically (Kendler et al., 1995; Nelson et al.,
2000). Several genes have been associated with socially anxious traits such as shyness and introversion,
although these studies have been far from consistent in their findings (Gelernter, Page, Stein, & Woods,
2004; Stein & Stein, 2008; Stein & Gelernter, 2014).

Familial and developmental factors

Family studies have indicated that offspring with SAD are also more likely to have parents (and
particularly mothers) with SAD (Merikangas, Lieb, Wittchen, & Avenevoli, 2003; Lieb et al., 2000), and
offspring of parents with an anxiety disorder are marginally more likely to have SAD than offspring of
parents with depression (Hirshfeld‐Becker, Micco, Simoes, & Henin, 2008), suggesting there is a specific
familial link between anxiety generally and an offspring developing SAD. Because SAD appears at a
relatively early age compared to other anxiety disorders, it has been argued that various developmental
factors and early experiences may precipitate the disorder (Neal & Edelmann, 2003). For example, there
is considerable evidence that children who exhibit a behaviourally inhibited (BI) temperament style are
at increased risk for subsequent social phobia (Neal, Edelmann, & Glachan, 2002; Kagan, Reznick,
Clark, Snidman, & Garcia Coll, 1984). However, it is also the case that a significant proportion of
children who are highly behaviourally inhibited in early life do not subsequently develop social phobia—
so childhood behavioural inhibition is not a sufficient condition for social phobia (Schwartz, Snidman &
Kagan, 1999) (see Focus Point 6.2). Early parent–child interaction styles may also play a role in the
development of social anxiety. Studies of parent–child interactions suggest that the parents of children
with SAD exert greater control over their children, show less warmth, are less sociable than the parents
of individuals without social phobia, exhibit behaviours signaling fears of social evaluation and
avoidance of social situations, and also use shame as a method of discipline (Rapee & Melville, 1997;
Siqueland, Kendall, & Steinberg, 1996; Bruch & Heimberg, 1994; Ollendick & Benoit, 2012; see
Halldorsson & Creswell, 2017, for a review of these factors). While these factors seem to be important
predictors of subsequent SAD, it is impossible to determine at present whether they represent actual
causal factors.

Cognitive factors
There appear to be a number of cognitive processes that are characteristic of SAD and which may all
act in some way to maintain fear of social situations (Stravynski, Bond, & Amando, 2004). First,
individuals diagnosed with SAD possess an information processing and interpretation bias in which they
make excessively negative predictions about future social events (Heinrichs & Hofmann, 2001; Hirsch &
Clark, 2004)—predictions that are often based on past failures, poor performance, or rejection (Sluis,
Boschen, Neumann, & Murphy, 2017). For example, individuals with SAD rate the probability of
negative social events occurring as higher than either nonclinical controls or individuals with other
anxiety disorders (Foa, Franklin, Perry, & Herbert, 1996; Gilboa‐Schechtman, Franklin, & Foa, 2000),
and this negative evaluation is likely to maintain their avoidance of social situations. Second, individuals
with SAD interpret their performance in social situations significantly more critically than nonsufferers
and independent assessors who have observed their behaviour (Stopa & Clark, 1993; Rapee & Lim,
1992) and also underestimate their own social skills (Dodd, Hudson, Lyneham, Morris, & Monier,
2011). Socially anxious individuals also find it very difficult to process positive social feedback (Alden,
Mellings, & Laposa, 2004). This focus on negative aspects of the social situation, and the relative
inability to take anything ‘good’ from a social performance are likely to maintain the socially anxious
individual's dysfunctional beliefs that social situations are threatening and that their own performance is
likely to be flawed. Third, some theories of SAD argue that sufferers show a strong tendency to shift
their attention inwards onto themselves and their own anxiety responses during social performance—
especially when they fear they will be negatively evaluated (Clark & Wells, 1995; Rapee & Heimberg,
1997) This is known as self‐focused attention (Spurr & Stopa, 2002; Bogels & Mansell, 2004) and
has the effect of leading socially anxious individuals to believe they may look as anxious as they feel
inside. This prevents objective processing of the social situation, leads them to engage in critical self‐
evaluation, and may well adversely affect their actual performance in the social situation (e.g., Kley,
Tuschen‐Caffier, & Heinrichs, 2011). Studies have shown that social phobics do indeed display higher
levels of self‐reported self‐focused attention than nonclinical populations (Bogels & Lamers, 2002) and
that they recall social memories more often from an observer perspective than a personal perspective
(suggesting that they do indeed ‘observe’ themselves while performing socially) (Wells, Clark & Ahmad,
1998) (Figure 6.3). Self‐focused attention therefore appears to have the effect of reinforcing the
individual's perception of their own anxiety in the social situation, can distract the individual from
focusing on the social task at hand and lead to unskilled performance, and result in avoidance of future
social situations (Alden, Teschuk, & Tee, 1992). Finally, individuals with SAD also indulge in excessive
post‐event processing of social events that includes critical self‐appraisal of performance and assessment
of symptom severity. Such post‐event rumination has the effect of maintaining negative appraisals of
performance over time and maintaining social anxiety (Abbott & Rapee, 2004; Gavric, Moscovitch,
Rowa, & McCabe, 2017) (Focus Point 6.3).
THE CLIENT'S PERSPECTIVE 6.1 SOCIAL ANXIETY
DISORDER

‘You have to be a sufferer of Social Anxiety to understand the pure terror that a victim of this
illness feels. It's the sort of blind panic dread and fear that one would feel facing a firing squad
or if you fell into a lions cage. You shake like a leaf, you blush, your mouth goes dry, you can't
speak, you break out in a cold sweat, your legs feel so weak you think you're going to fall. Your
thoughts become confused and disorientated. Forget butterflies in the stomach—your guts are
twisted inside out with FEAR.
Social Anxiety made me sink so low I ended up cleaning public toilets for a living. I never
married (No I'm not gay) I had no children I never owned my own house. I rent a small flat in a
very poor part of London all because of SEVERE Social Anxiety. My parents were cold
reserved people unable to show their emotions I was never abused in any way but I look back
on my childhood as a lonely unhappy time. Maybe that was the root cause of my phobia. I
mention that because we can all think of something that may have been the cause. My Social
Anxiety started in my last year at school when I became very self‐conscious and developed a
fearful dread of being asked to read in front of the class. This extreme anxiety moved on with
me into my working life. I was a smart looking young man so I got some good jobs, but because
of Social Anxiety no way could I hold them. Would you buy from a salesman who went a deep
red, stammered, couldn't look you in the eye, and shook so much that even his head trembled.
No—nor would the boss who in the end would say get lost, you're bad for business.
Over the years I slid down and down the social ladder with long spells out of work and, of
course, no money. By the time I was 30 I could only do work where I did not have to deal with
people like road sweep, night work in factories and in the end cleaning public toilets when
closed at night. Social Anxiety was now so bad I couldn't face going into a shop to buy
something. To pass a queue of people waiting for a bus was hell I was sure they were all staring
at me. I couldn't sit facing other passengers on a train unless I had a newspaper to hide behind.
If I attempted going into a restaurant or café, I'd pick a table facing the wall and if anyone sat
at my table my hands would shake so much I couldn't get the food into my mouth. I became the
ultimate night person only going out late to walk the streets’.

Clinical Commentary
This client’s perspective highlights the extreme fear experienced by many social phobics
in a range of social and performance situations, and the impact it can have on social
functioning specifically and life planning more generally. This description highlights a
number of important features of SAD, including (a) the biased interpretations that
social phobics have of the reactions of others to them (e.g., ‘To pass a queue of people
waiting for a bus was hell I was sure they were all staring at me’), (b) the belief that there
are obvious physical signs of their nervousness which observers interpret judgementally
(e.g., ‘Would you buy from a salesman who went a deep red, stammered, and couldn’t
look you in the eye’), and (c) the tendency of social phobics to focus their attention on
themselves and their own reactions to the possible detriment of their own performance
(e.g., ‘My social anxiety started in my last year at school when I became very self‐
conscious and developed a fearful dread of being asked to read in front of the class’).
FOCUS POINT 6.2 BEHAVIOURAL INHIBITION (BI) AND
SOCIAL ANXIETY DISORDER

Many children seem quiet, isolated, and anxious when confronted either with social situations
or with novelty, and this characteristic has come to be defined by the construct called
behavioural inhibition (BI) (Kagan, Reznick, Clark, Snidman, & Garcia Coll, 1984). BI
represents ‘a consistent tendency to display extreme fearfulness, withdrawal, reticence, and
restraint in the face of novelty’ (Hirschfeld‐Becker, 2010), and toddlers exhibiting BI will show
overt distress and cling to their mothers in unfamiliar or novel situations. They are also
reluctant to approach novel objects, peers, and adults. Preschoolers with BI seem quiet and are
reticent to speak or play spontaneously, and by age 7 the reluctance to socialise is found mainly
in group contexts. BI is estimated to have quite a high level of inheritability—between 50 and
70% (Smoller & Tsuang, 1998), and BI is considered to be a specific risk factor for SAD
(Hirschfeld‐Becker, 2010).
FIGURE 6.3 High and low socially anxious participants were asked to give a speech to a group of observers. After
giving the speech, the high socially anxious participants rated observers' audience's enjoyment of their speech significantly
lower than low socially anxious participants. The high socially anxious participants even do this when the observers have
been instructed to provide positive feedback—suggesting that socially phobic individuals do not attend to positive feedback
cues given by an audience.
After Perowne & Mansell, (2002).

self‐focused attention A theory of social anxiety disorder arguing that sufferers show a
strong tendency to shift their attention inwards onto themselves and their own anxiety responses
during social performance – especially when they fear they will be negatively evaluated.

6.3.3 The Treatment of Social Anxiety Disorder

Both pharmacological treatments and cognitive behaviour therapies (CBT) have been shown to be
effective in alleviating the symptoms of SAD (Rodebaugh, Holaway, & Heimberg, 2004; Davidson,
2003), and both are used widely to treat the disorder.
Successful CBT treatments include elements of the following:
Exposure therapy (where the client remains in a feared social situation despite distress)—either in
vivo, or through the therapist taking on the role of a stranger in a social situation (Heimberg &
Becker, 2002) (Treatment in Practice 6.2),
Social skills training (consisting of modelling, behavioural rehearsal, corrective feedback and
positive reinforcement)—this training addresses the social skills deficits usually characteristic of
social phobics,
Cognitive restructuring (designed to challenge and replace the negative biases in information
processing and the dysfunctional negative self‐evaluations of social performance, and to reduce
self‐focused attention) (Rodebaugh & Chambless, 2004).
Each of these elements used alone do show therapeutic gains, but an integrated CBT programme
appears to result in maintenance of gains over 6–12 month follow‐up periods (Feske & Chambless,
1995). Recent reviews of treatments for SAD in youth suggest that CBT might be more efficacious if
integrated with specific social‐skills training (Scharfstein & Beidel, 2011).
In addition to CBT, new developments in the use of virtual reality exposure have led to the successful
use of virtual environments in the treatment of SAD—especially when those with a diagnosis of SAD
are reluctant to seek treatment because of their fear of in vivo social exposure (e.g., Bouchard et al.,
2017). Attention bias modification (ABM) procedures (see Section 6.3.3) have also been shown to
successfully augment CBT for SAD by training clients' attention away from social threat (Lazarov et al.,
2017), but when used alone, current evidence suggests that ABM procedures may be less effective
(Ollendick et al., 2019).
First‐line medications for SAD are selective serotonin reuptake inhibitors (SSRIs) and selective serotonin
norepinephrine reuptake inhibitors (SNRIs) (see Chapter 4, Section 4.1.1) and these have been shown to
cause improvement in measures of social anxiety (Blanco, Bragdon, Schneier, & Liebowitz, 2013;
Bandelow, Michaelis, & Wedekind, 2017). Comparative outcome studies have suggested that both
pharmacological and CBT treatments together are more effective than nontreatment controls (Gould,
Buckminster, Pollock, Otto, & Yap, 1997), but that the two types of therapy may offer complementary
benefits—drug therapy offering a more immediate benefit than CBT, but CBT helping patients to
maintain their therapeutic gains over time (Liebowitz et al., 1999, Canton, Scott, & Glue, 2012).

FOCUS POINT 6.3 A NETWORK ANALYSIS OF FEAR AND

AVOIDANCE IN SOCIAL ANXIETY DISORDER
Social Anxiety Disorder
Numbers Situations
1. Telephoning in public
2. Participating in small groups
3. Eating in public places
4. Drinking with others in public places
5. Talking to people in authority
6. Acting, performing, or giving a talk in front of an audience
7. Going to a party
8. Working while being observed
9. Writing while being observed
10. Calling someone you don't know very well
11. Talking with people you don't know very well
12. Meeting strangers
13. Urinating in a public bathroom
14. Entering a room when others are already seated
 15. Being the centre of attention
16. Speaking up at a meeting
17. Taking a test
18. Expressing a disagreement or disapproval to people you don't know very well
19. Looking at people you don't know very well in the eyes
20. Giving a report to a group
21. Trying to pick up someone
22. Returning goods to a store
23. Giving a party
24. Resisting a high‐pressure salesperson
From Heeren & McNally (2017).

Healthy Comparison Group

A network analysis showing the connectivity between different situations that the socially
anxious individual either fears (prefix ‘f ’) or avoids (prefix ‘a’). On the left is the network derived
from the responses of individuals with SAD and on the right the network derived from a health
comparison group. The two networks differ only in the extent and strength of the connectivity
between nodes. The densely interconnected network found in SAD means that activation of
each node can easily spread to other ones, ultimately producing a cascade of fear and
avoidance to a range of social situations.
See Chapter 2, Focus Point 2.2 for a description of how network analyses are constructed.

CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 6.2

COGNITIVE THERAPY FOR SOCIAL ANXIETY DISORDER

The following provides a step‐by‐step account of the Cognitive Therapy for SAD devised by
Clark & Wells (1995). The aims of this procedure are (a) to decrease self‐focused attention, (b) to
reduce the level of negative interpretations of internal information (e.g., sweating as a sign of
poor performance), (c) eliminate the use of safety behaviours which maintain negative beliefs
(e.g., if the phobic believes they are trembling and this may be visible, they may grip objects
tightly in order to conceal this—this response merely maintains the phobic's belief that they are
anxious and trembling), and (d) reduce negative post‐event processing (see Section 4.2.1).
STEP 1: The initial phase is designed to inform the client about those factors that are
maintaining their social phobia (see above) and that these are the factors that the therapy is
specifically designed to target.
STEP 2: The second phase attempts to manipulate safety behaviours. Here the client has
to role play a social situation and observe his or her own responses and identify key safety
behaviours. The client will then attempt to drop these safety behaviours during subsequent
role playing.
STEP 3:Clients are trained to shift their attention externally and away from their own
internal responses and cognitions.
Step 4: Video feedback of performance can be used to modify distorted self‐imagery.
STEP 5: The client is provided with some behavioural experiments in which they specify
their fears of particular social situations and then test out whether they occurred during
role‐play sessions.
STEP 6: Problematic post‐event processing is identified and modified using focused
cognitive restructuring techniques.

From Stangier, Heidenreich, Peitz, Lauterbach, & Clark, 2003

 SELF‐TEST QUESTIONS
Can you describe the main symptoms of a panic attack, and the diagnostic criteria for
panic disorder?
What is the relationship between symptoms of panic disorder and agoraphobia?
How is hyperventilation supposed to cause a panic attack?
What role does the catastrophic misinterpretation of bodily sensations play in the
acquisition and maintenance of panic disorder?
Can psychological explanations of panic disorder explain more of the facts of panic
disorder than biological explanations?
What is the role of safety behaviours in maintaining panic disorder?
What are the important features of cognitive behaviour therapy for panic disorder?

SECTION SUMMARY

6.3 SOCIAL ANXIETY DISORDER

SAD is distinguished by a severe and persistent fear of social or performance situations.
SAD has a lifetime prevalence rate of around 4% in cross‐national epidemiology studies.
There is evidence for a genetic component to SAD, but this may be a predisposition to
develop anxiety disorders generally rather than social phobia specifically.
There are a number of cognitive factors that are characteristic of SAD, and these include
a tendency (a) to make excessively negative predictions about future social events, (b) to
overcritically evaluate their own social performance, (c) to shift their attention inwards on
to themselves, and (d) to indulge in post‐event critical appraisal of their own performance.
Serotonin reuptake inhibitors (SSRIs) have been shown to be a helpful pharmacological
treatment for SAD, and CBT is the psychological treatment of choice.

6.4 PANIC DISORDER AND AGORAPHOBIA

Panic disorder and agoraphobia are related—but separable—anxiety‐based problems. Panic disorder is
the more prevalent of the two, but around a third of those suffering panic disorder also suffer
agoraphobia. In those with agoraphobic symptoms, around half will experience regular panic attacks
but the remainder will not (Andrews et al., 2009). Furthermore, for a majority of those people who
develop agoraphobic symptoms, these symptoms will begin within a year of an initial panic attack and
are usually the result of fearing the consequences of having a panic attack in public. However, there is
still a substantial number of people who suffer agoraphobia symptoms without panic attacks and who
appear to fear what might happen if other anxiety symptoms develop.
6.4.1 Panic Disorder
As the name suggests, panic disorder is characterised by repeated panic or anxiety attacks. These attacks
are associated with a variety of physical symptoms, including heart palpitations, perspiring, dizziness,
hyperventilating, nausea, and trembling (Case History 6.1). In addition, the individual may experience
real feelings of terror or severe apprehension, and depersonalisation (a feeling of not being connected to
your own body or in real contact with what is happening around you). Individual panic attacks
themselves are not that rare and are probably experienced at some point in their life by up to one in
four people (Kessler et al., 2006), but panic disorder is diagnosed when recurrent, unexpected panic
attacks keep occurring, and are followed by at least 1 month of persistent concerns about having a
further attack (see Table 6.7). For some individuals panic attacks are unpredictable, but for others they
may become associated (perhaps through classical conditioning, see Chapter 1, Section 1.3.2) to specific
situations or events (e.g., riding on public transport).
CASE HISTORY 6.1 PANIC DISORDER

Marilyn is a 33‐year‐old single woman who works at a local telephone company and lives alone
in her apartment. She has panic disorder with agoraphobia and her first panic attack occurred
3 years ago when driving over a bridge on a very rainy day. She experienced dizziness,
pounding heart, trembling, and difficulty breathing. She was terrified her symptoms meant she
was about to pass out and lose control of her car. Since that time she has experienced eight
unexpected panic attacks during which she feared she was about to pass out and lose control of
herself. She frequently experiences limited symptom attacks (e.g., feels dizzy and fears she may
pass out). As a result of her intense fear of having another panic attack she is avoiding the
following situations: waiting in line, drinking alcohol, elevators, movie theatres, driving over
bridges, driving on the freeway, flying by plane, and heights (e.g., will not go out on her 10th
floor balcony). She is often late for work because of taking a route that doesn't require her to
take the freeway. She is also finding herself avoiding more and more activities. She frequently
feels tearful and on guard. Sometimes she gets very angry at herself as she does not understand
why she has become so fearful and avoidant.
Sharon is a 38‐year‐old single mother of two teenage daughters who works as a fitness
instructor at a local gym. She experienced her first panic attack during her teens when watching
a horror movie with friends at a local movie theatre. Since that time she has experienced one to
two full panic attacks per year that come out of the blue in a variety of situations (e.g., while
waiting in line at the bank, at a shopping mall, walking alone at the park). The panic attacks
reoccurred out of the blue when she was 29 while eating a hot and spicy meal at a local
restaurant. Her panic attacks always include dizziness, feeling of choking, dry mouth, unreality,
feeling detached from her body, and feeling as if she may lose bowel control. Her main fear is
that she is dying due to a stroke although medical problems have been ruled out. Sharon does
not avoid anything to prevent the panic attacks and there has not been a huge negative impact
of the panic attacks upon her work, family or social functioning.

Clinical Commentary
Both Marilyn and Sharon exhibit a number of physical symptoms typical of panic attacks, although
these examples show that not everyone experiences similar symptoms. Panic attacks often come ‘out of the
blue’ and are unpredictable, and this adds to their frightening nature. In both examples, the individual
believes that the symptoms are signs of impending physical illness or loss of control (catastrophic
misinterpretation). The pervasive fear of further attacks means that Marilyn has developed avoidance
responses in an attempt to minimise future attacks. These avoidance responses interfere with her normal
daily life (causing further stress), and inadvertently help to maintain dysfunctional catastrophic beliefs.
TABLE 6.6 Summary: DSM‐5 Criteria for a Panic Attack
A sudden feeling of extreme fear or distress, which can originate from either a calm or an anxious
state. Symptoms intensify in a short space of time and will include a range of sensations such as:
fluctuations in heart rate
shortness of breath or chest pain
nausea
dizziness
shaking

The person may fear they are dying or ‘going crazy’.

TABLE 6.7 Summary: DSM‐5 Criteria for a Diagnosis of Panic Disorder

Repeated panic attacks followed by at least 1 month of:
worrying about further panic attacks and/or the consequences of a panic attack, such as loss of
control
significant, non‐beneficial modification of behaviour(s), designed to avoid future attacks, such as
avoidance of triggering situations
DSM‐5 defines a panic attack as an abrupt surge of intense fear or discomfort in which four or more of
a list of symptoms develop suddenly (Table 6.6). The criteria for panic disorder state that the individual
must experience recurrent panic attacks, and in addition they must develop a persistent concern that
future panic attacks will occur (see Table 6.7). The frequency of panic attacks in panic disorder can vary
considerably between individuals from one attack per week to frequent daily attacks. Panic disorder is
associated with a number of fears and apprehensions that the sufferer develops. These include fears that
the attacks indicate an underlying serious medical condition (e.g., cardiac disease, seizure disorder)—
even though repeated medical tests indicate no life‐threatening illness. Others feel they are losing control
or simply ‘going crazy’. Sufferers often make significant changes to their behaviour and their life as a
result of the disorder. For example, they may ensure that there is always a ‘safe’ place available in case
they have an attack, and this may cause them to avoid social situations and even quit their job. Concerns
about future attacks often result in the development of avoidant behaviour; sufferers may find it difficult
to leave the ‘safety’ of their own home, in which case panic disorder with agoraphobia is a common
diagnosis. (Photo 6.3).
PHOTO 6.3 The Little Mix star Perrie Edwards has spoken publicly about her anxiety and in particular the panic
attacks she experienced which she says made her feel like she was ‘losing her mind’. She describes how her first panic attack
was so intense and overwhelming that she felt like she was having a heart attack, ‘I was so scared and confused and had no
idea what was happening to me … It affected me so badly that I didn't even want to leave the house. I would step foot out
of the door and feel the overwhelming need to go straight back inside. It completely took over my life’. Such reactions to
unexpected panic attacks are common and can often lead to further anxiety about symptoms and in some cases to fear of
leaving a safe place such as the home. Fortunately, contemporary treatments for panic disorder, such as CBT, are very
effective at alleviating symptoms and will usually lead to full recovery.
TABLE 6.8 Summary: DSM‐5 Criteria for a Diagnosis of Agoraphobia

Distinct fear of situations where the individual is outside, in a crowd or an open space, or in
public spaces such as shops, cinemas, or buses
Situations are avoided or are experienced with intense fear that help will be unavailable or that
panic or other resultant symptoms will occur
The individual experiences fear in at least two different situation types and symptoms of anxiety
or avoidance will last for 6 months or more
Fear causes difficulty in performing social or occupational activities and cannot be explained by
the effects of other mental or medical disorders

6.4.2 Agoraphobia
Agoraphobia is a fear or anxiety of any place where the sufferer does not feel safe or feels trapped,
and is accompanied by a strong urge to escape to a safe place (e.g., home). Very often, this urge to
escape or avoid ‘unsafe’ places is associated with the fear of having a panic attack and the
embarrassment that might cause. Agoraphobia is typically associated with fear of specific types of
places or situations, including public transport; open spaces such as car parks; bridges; being in shops,
supermarkets, theatres, or cinemas; standing in a queue or being in a crowd; or simply being alone away
from home. As a result of these fears, many individuals with a diagnosis of agoraphobia rarely venture
far from home, and when they do, they may do so only with a trusted friend or relative. Thus,
agoraphobia can be a severely disabling condition that often confines sufferers to their homes for many
years, rendering them unable to work or to socialise. Sufferers also come to rely heavily on friends and
relatives to help them with even basic activities like shopping or trips to the doctor. This will often put a
severe strain on those family members who care for individuals suffering from agoraphobia (Table 6.8).

Agoraphobia A fear or anxiety of any place where the sufferer does not feel safe or feels
trapped, and is accompanied by a strong urge to escape to a safe place (e.g. home).

6.4.3 Prevalence
Cross‐national studies indicate that, among individuals who have ever had a panic attack, 2 out of 3 of
those will probably have recurrent panic attacks, and of those who do experience recurrent panic
attacks only 1 in 8 (12%) will fulfill DSM‐5 criteria for panic disorder (de Jonge et al., 2016). The 12‐
month prevalence rate for panic disorder is around 1.5–3% and between 0.4% and 3% for agoraphobia
(e.g., Goodwin et al., 2005). Onset is common in adolescence or early adulthood and can often be
associated with a period of stress in the individual's life (de Lijster et al., 2016; Pollard, Pollard, & Corn,
1989). Prevalence rates differ considerably across different countries (de Jonge et al., 2016), possibly
because of the culturally different ways in which symptoms are expressed. For example, in some Asian
societies, prevalence is particularly low—possibly because of the stigma related to admitting and
reporting psychological disorders (e.g., in Taiwan—Weissman et al., 1997). However, in other cultures,
panic disorder may be expressed in the form of quite different symptoms. For example, Ataque de
Nervos is an anxiety‐based disorder found almost exclusively in Latinos in the Caribbean. This appears
to be a form of panic disorder brought on by stressful life events (such as economic or marital
difficulties), but whose expression is determined by the social and cultural norms within that cultural
group (see Chapter 1, Focus Point 1.3). In particular, Latino cultures place less emphasis on self‐control
and emotional restraint than other Western cultures, and so the distress of panic disorder in Latinos
tends to be externalised in the form of screaming, uncontrolled behaviour and aggression (Salman et al.,
1998). In contrast, in Western cultures the distress of panic disorder is usually coped with by adopting
avoidance and withdrawal strategies—hence the common diagnosis of panic disorder with agoraphobia
(see Davey, 2018, chapter 9, for a further discussion of how panic disorder symptoms are experienced in
other cultures).
It is important to remember that panic attacks may be a feature of the symptoms in a number of the
anxiety disorders (e.g., specific phobias and social phobia). However, panic disorder itself is
characterised by frequent uncontrollable panic attacks, and an important aspect of this anxiety‐based
problem is the individual's intense fear of experiencing panic attacks. As we shall see, it is this latter
feature of panic disorder that plays a central role in theories of the disorder.

6.4.4 The Aetiology of Panic Disorder and Agoraphobia

Agoraphobia has been recognised only recently as a specific and distinct disorder in DSM‐5, so its
aetiology has rarely received the kind of attention that has been given to panic disorder. In addition,
because agoraphobia is often preceded by panic attacks and full‐blown panic disorder, much of the
research on the aetiology of these two anxiety‐problems has been focused on panic disorder. However,
agoraphobia can occur independently of panic attacks and panic disorder so its origins cannot always
be traced to panic, and this has given rise to a view that agoraphobia might be a disorder with multiple
causes, some of which might be genetic in nature ‐ in terms of a genetic vulnerability to anxiety
(Wittchen et al., 2010), and others which are more cognitive—in which agoraphobic avoidance is
acquired through the development of negative and catastrophic thoughts about the consequences of
experiencing anxiety in public (Hoffart, 2016; Goldstein & Chambless, 1978). Because of this dearth of
research on the causes of agoraphobia, the remainder of this section focuses on the causes of panic
disorder.

The aetiology of panic disorder

Because of the intense nature of the physical symptoms of panic disorder, many researchers have
looked towards biological causes. However, it has become clear that there are also important
psychological and cognitive factors that contribute to the aetiology and maintenance of panic disorder.

Biological theories of panic disorder

Biological factors
Panic attacks represent an activation of our physiological fight/flight defensive reaction that's evolved to
provide us with the immediate means to avoid danger. So during periods of stress or danger, our
sympathetic nervous system is activated, and its major effect is to signal release of the hormones
adrenalin and noradrenalin that release energy and prepare the body for action. These chemicals have
the effect of generating an increase in heartbeat that increases blood flow and improves delivery of
oxygen to the muscles (the pounding heart experience), they increase the speed and depth of breathing
to provide more oxygen to the tissues for action (this hyperventilation can make the individual feel dizzy
or light headed), and they increase perspiration which prevents the body from overheating (and makes it
harder for a predator to grab you!). There are some other effects which give rise to panic‐type
symptoms, such as the redirecting of blood away from places where it's not needed (such as the stomach)
towards places where it is needed (the muscles), resulting in feelings of nausea as a result of reduced
activity in the digestive system. The pupils widen to let in more light, resulting in the blurred vision
often experienced during a panic attack. Finally, adrenaline and noradrenaline also cause muscle groups
to tense up in preparation for fight or flight, which can often give rise to sensations such as chest pains
which many panic attack sufferers will interpret as signs of an impending heart attack or cardiac arrest.
These biological symptoms of panic attacks help us to understand the physical experiences that define a
panic attack, but they don't immediately tell us what triggers a panic attack. However, in biological
terms, panic attacks are associated with the brain area known as the locus coeruleus which is located
in the brain stem. This is an area of the brain that is the main source of the neurotransmitter
norepinephrine, and it is the release of norepinephrine in response to stress that activates most of the
biological reactions found in a panic attack. Individuals with a diagnosis of panic disorder show a
greater sensitivity to norepinephrine and to drugs that increase activity in the locus coeruleus (Bandelow
et al., 2017), suggesting that it may be the greater reactivity of the locus coeruleus in some individuals
that bestows a vulnerability for panic attacks.

The role of hyperventilation Hyperventilation

Hyperventilation is a common feature of panic attacks, and Ley (1987) has suggested that dysfunctional
breathing patterns may trigger a series of autonomic reactions that precipitate a full‐blown panic attack.
Hyperventilation is defined as a ‘minute ventilation that exceeds metabolic demand’ and has an end
result of raising blood pH level. Oxygen is then delivered less efficiently to body cells, and this can lead
to cardiovascular changes that try to help compensate for the lack of oxygen in the cells and in turn can
produce the symptoms of panic attacks that are recognised as anxiety (Zvolensky & Eifert, 2001). This
type of explanation has been partially supported by evidence from what are called biological
challenge tests, where panic attacks have been induced by administering carbon dioxide enriched air
(CO2) or by encouraging hyperventilation (Ley & Walker, 1973). Similarly, sensitivity to increases in
CO2 have been suggested as a risk factor for panic disorder (Papp, Klein, & Gorman, 1993), and have
given rise to what are known as ‘suffocation alarm theories’ of panic disorder, where a
combination of increased CO2 intake may activate an over‐sensitive suffocation alarm system and give
rise to the intense terror and anxiety experience during a panic attack (Klein, 1993). In support of this
account, panic disorder patients do report significantly more symptoms of shortness of breath when
anxious and more frequent frightening suffocation experiences than other anxiety patients. However,
when panic disorder patients are asked to participate in periods of breath‐holding, they do not report
any greater levels of anxiety than nonanxious controls, suggesting that they do not necessarily possess a
more sensitive suffocation alarm system (Roth, Wilhelm, & Trabert, 1998). One further intriguing
feature of the hyperventilation account is that, while biological challenge tests produce physiological
changes that often provoke full‐blown panic attacks, they only tend to do so in individuals with a history
of panic attacks or panic disorder (Margraf, Ehlers, & Roth, 1986). This is the case even though the
physiological changes caused by biological challenge tests are the same in people diagnosed with panic
disorder and those that have no anxiety disorder (Gorman et al., 2001). This evidence quite strongly
suggests that an important causal factor in panic disorder is the way that the individual interprets the
physiological changes caused by the biological challenge, and this gives rise to the psychological
accounts of panic disorder that have been developed over the past 30 years.

biological challenge tests Research in which panic attacks are induced by administering
carbon dioxide-enriched air (CO2) or by encouraging hyperventilation.

suffocation alarm theories Models of panic disorder in which a combination of increased

CO2 intake may activate an oversensitive suffocation alarm system and give rise to the intense
terror and anxiety experienced during a panic attack.

Psychological theories of panic disorder

Classical conditioning
Goldstein and Chambless (1978) were the first to suggest that an important feature of panic disorder
was the sufferer's ‘fear of fear’. That is, when they detected what they thought were any internal signs of
a panic attack (e.g., mild dizziness), they would immediately become fearful of the possible
consequences. The stress of this fear would then precipitate a full‐blown attack. Goldstein and
Chambless (1978) interpreted this as a form of interoceptive classical conditioning, in which the internal
cue (such as dizziness) had become established as an internal CS predicting a panic attack (the UCS)
(see Chapter 1, Section 1.3.2 for a brief description of classical conditioning). However, while this
account has intuitive appeal, it is not clear in conditioning terms what is the CS and what is the UCS.
For example, is a skipped heartbeat a CS that precipitates a panic attack, or is it a symptom of the panic
attack itself (the UCS) (McNally, 1990)? Bouton, Mineka, & Barlow (2001) have attempted to address
these conceptual difficulties by suggesting that anxiety and panic are separable aspects of panic disorder.
They suggest that anxiety is anticipatory and prepares the system for a trauma, whereas panic deals
with a trauma that is already in progress. In this conditioning account, anxiety is the learned reaction,
called CR to the detection of cues CS that might predict a panic attack, and once conditioned anxiety
develops it will exacerbate subsequent panic attacks and lead to the development of panic disorder. As
predicted by this model, studies confirm that panic attacks are regularly preceded by anxiety in
individuals with panic disorder (Barlow, 1988; Kenardy & Taylor, 1999).
Anxiety sensitivity
What is clear about the phenomenology of panic disorder is that sufferers become extremely anxious
when they detect any cues (internal or external) that may be indicative of a panic attack. So any theory
of panic disorder needs to explain why sufferers are made anxious by the detection of these cues, and
how this subsequently leads to a full‐blown panic attack. Individuals who do not suffer panic disorder
report a number of interoceptive and affective responses in biological challenge tests, but they are only
rarely made anxious by these symptoms and hardly ever panic (Bass & Gardner, 1985; Starkman,
Zelnik, Nesse, & Cameron, 1985). So, what determines whether someone will panic in response to
unusual bodily sensations? Reiss & McNally (1985) proposed that some individuals have preexisting
beliefs that bodily sensations may predict harmful consequences. They developed the construct of
anxiety sensitivity, which refers to fears of anxiety symptoms that are based on beliefs that such
symptoms have harmful consequences (e.g., that a rapid heartbeat predicts an impending heart attack).
In order to measure this construct, Reiss, Peterson, Gursky, and McNally (1986) developed the Anxiety
Sensitivity Index (ASI) (see also the Revised Anxiety Sensitivity Index, ASI‐R, Taylor & Cox, 1998),
and this contains items such as ‘Unusual body sensations scare me’ and ‘It scares me when I feel faint’.
Studies have shown that individuals with panic disorder score significantly higher on the ASI than either
nonclinical controls or individuals diagnosed with other anxiety disorders (Taylor & Cox, 1998; Rapee,
Ancis, & Barlow, 1988). Furthermore, in a prospective study, high ASI scores predicted the occurrence
of subsequent panic attacks in army recruits undergoing a stressful period of training (Schmidt, Lerew,
& Jackson, 1997), and this suggests that elevated anxiety sensitivity may be a risk factor for panic and
also panic disorder (McNally, 2002).

anxiety sensitivity Fears of anxiety symptoms based on beliefs that such symptoms have
harmful consequences (e.g. that a rapid heartbeat predicts an impending heart attack).

Anxiety Sensitivity Index A measure, developed by Reiss, Peterson, Gursky & McNally
(1986), to measure anxiety sensitivity.

So where does anxiety sensitivity come from? Why are some people high on anxiety sensitivity and
others seemingly unbothered about whether they're anxious or not? There are still relatively few
comprehensive studies of the origins of anxiety sensitivity, but there are some possible causal candidates
in the research literature. One is genetics. Twin studies suggest that anxiety sensitivity is ‘moderately’
heritable (accounting for up to 61% of the variance in anxiety sensitivity scores) and this genetic effect is
generally stable over time (Zavos, Gregory, & Eley, 2012). Stressful life events are also associated with
subsequent increases in anxiety sensitivity in adolescents, especially stressful events related to health (e.g.,
the individual or a member of the family being hospitalised) and to family discord (e.g., parents being
divorced) (McLaughlin & Hatzenbuehler, 2009), suggesting some experiential factors might also
facilitate anxiety sensitivity.

Catastrophic misinterpretation of bodily sensations

Based on the fact that panic disorder sufferers are clearly anxious about the possible consequences of
bodily symptoms, Clark (1986, 1988) developed an influential model of panic disorder in which he
hypothesised that panic attacks are precipitated by the individual catastrophically misinterpreting their
bodily sensations as threatening. Many body sensations are ambiguous, for example, the heart skipping a
beat could mean either an imminent heart attack (negative interpretation) or someone you like has just
walked into the room (positive interpretation). However, individuals who tend to develop panic disorder
appear to catastrophically misinterpret bodily sensations, that is, they have a cognitive bias
towards accepting the more threatening interpretation of their sensations (Clark et al., 1997; see
Waddington, 2019, for a review). Clark argues that this leads to a vicious cycle where any apprehension
is interpreted threateningly and increases the perceived threat, which leads to an escalation of anxiety
symptoms that then precipitate a panic attack; this is represented schematically in Figure 6.4. There is a
good deal of evidence to support this psychological account. Individuals with panic disorder have been
shown to attend to and discriminate their bodily sensations more closely than individuals without panic
disorder (Ehlers & Breuer, 1992), and panic disorder sufferers report that thoughts of imminent danger
typically accompany their attacks (Hibbert, 1984; Ottaviani & Beck, 1987). In addition, individuals with
panic disorder will experience a panic attack when they have been told they will receive a CO2
challenge, but in fact are given only compressed air (Sanderson, Rapee, & Barlow, 1989)—suggesting that
just the expectancy of an attack is enough to trigger one (Figure 6.4).

FIGURE 6.4 Clark's (1986) model of panic disorder. Perception of a threat triggers apprehension and then bodily
sensations associated with that apprehension are interpreted catastrophically. This causes further anxiety which feeds into a
vicious cycle that triggers a full‐blown panic attack.
Despite being the explanation of choice for most clinical psychologists, the catastrophic
misinterpretation of bodily sensations model still begs the question of why some people misinterpret
bodily sensations catastrophically and others do not. One possibility is that those individuals who do
develop panic disorder may have a history of medical illness that has been distressing for them, and now
leads them to interpret all bodily sensations as distressing and threatening, and this possibility is
supported by the fact that panic disorder is frequently comorbid with a number of forms of medical
illness (Meuret, Kroll, & Ritz, 2017).

Summary
All of these accounts suggest that while the symptoms of panic attacks are very much biological
manifestations of the sympathetic nervous system, there is likely to be an important psychological
component to the development of panic disorder, and one that involves a negatively valenced bias in
how the individual interprets and reacts to their own bodily sensations. This interpretation bias appears
to trigger anxiety, which in turn triggers a panic attack. The issues that remain to be resolved in these
accounts are (a) exactly how the anxiety elicited by catastrophic misinterpretation of bodily sensations
leads to panic, and (b) why some individuals have acquired high levels of anxiety sensitivity and
catastrophic beliefs in the first place.

6.4.5 The Treatment of Panic Disorder

Because of the distressing physical symptoms experienced in panic disorder, medication is often the first
line of treatment provided for sufferers, and SSRIs and tricyclic antidepressants may be effective in
controlling symptoms (Bandelow, Michaelis, & Wedekind, 2017) (see Chapter 4, Section 4.1.1).
However, there is good evidence that structured exposure therapy or CBT is as effective, if not superior,
to drug treatments over the longer term (e.g., Craske, Brown, & Barlow, 1991), and combined
psychotherapy with medication is more effective than treatment with medication alone (Cuijpers et al.,
2014).
In exposure‐based treatments, the client is persuaded to experience the conditions that precipitate a
panic attack in the controlled environment of the therapy situation (Barlow & Craske, 1994; Craske &
Barlow, 2001). For example, someone whose attacks are preceded by bouts of dizziness may be asked to
spin around in a chair, or if hyperventilation is a trigger, the individual will be asked to breathe rapidly
for a period of time. At the first bodily signs of the symptoms associated with panic, the client is then
asked to apply cognitive and physical techniques design to manage the attack (such as applying
relaxation techniques). This enables the client to manage the attack under relatively ‘safe’ conditions
and to learn to exercise control over the cues that would normally predict panic (Craske, Maidenberg, &
Bystritsky, 1995).
Clearly, an important distinguishing feature of individuals with panic disorder is their fear of bodily
sensations, their catastrophic misinterpretation of these sensations, and the effect these cognitions have
in triggering a panic attack. The development of CBT for panic disorder has therefore focused
specifically on providing clients with challenges to these beliefs in the form of both corrective
information and experiences designed to eliminate faulty emotional responding (e.g., Clark et al., 1994;
Telch et al., 1993; Luermans, De Cort, Schruers, & Griez, 2004). A typical treatment programme would
include:
1. Education about the nature and physiology of panic attacks
2. Breathing training designed to control hyperventilation
3. Cognitive restructuring therapy to identify and challenge faulty threat perceptions
4. Interoceptive exposure to reduce fear of harmless bodily sensations
5. Prevention of ‘safety’ behaviours that may maintain attacks and avoid disconfirmation of
 maladaptive threat beliefs (Treatment in Practice 6.3).
While such programmes have been shown to produce a durable reduction in symptoms and a significant
increase in quality of life for panic disorder sufferers (Barlow, Gorman, Shear, & Woods, 2000;
Kaczkurkin & Foa, 2015; Hansen et al., 2018), it is still not entirely clear which are the active
ingredients that best promote recovery. Recent studies indicate that interoceptive exposure and cognitive
restructuring are associated with better treatment efficacy than most other elements, while breathing
training and in vivo exposure improve the acceptability of the treatment for the client but have only
small effects on efficacy (Pompoli et al., 2018).

CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 6.3

COGNITIVE THERAPY FOR PANIC DISORDER

The following transcript gives an example of how a cognitive therapist (T) would try to
challenge the catastrophic beliefs of a panic disorder sufferer (P) who believes that signs of an
impending panic attack are signals for an imminent heart attack.

P:
When I'm panicking, it's terrible I can feel my heart pounding; it's so bad I think it could
burst through my chest.

T:
What thoughts go through your mind when your heart is pounding like that?

P:
Well I'll tell you what I think; it's so bad that I think I'm going to have a heart attack. It can't
be good for your heart beating like that.

T:
So you're concerned that anxiety can damage your heart or cause a heart attack.

P:
Yes, it must do you some damage. You hear of people dropping down dead from heart
attacks caused by stress.

T:
Do you think more people have stress in their lives than die of heart attacks?

P:
Yes, I suppose so.

T:
How can that be if stress causes heart attacks?

P:
Well, I suppose it doesn't always cause problems. Maybe it does only in some people.
 T:
Yes, that's right; stress can cause some problems in some people. It tends to be people who
have something wrong with their hearts in the first place. But stress is not necessarily the
same as sudden anxiety or panic. When you panic your body releases adrenalin which
causes the heart to speed up and your body to work faster. It's a way of preparing you to deal
better with danger. If adrenalin damaged the heart or body, how would people have evolved
from dangerous primitive times? Wouldn't we all have been wiped out?

P:
Yes, I suppose so.

T:
So maybe panic itself doesn't cause heart attacks, there has to be something physically
wrong for that to happen. When people have had heart attacks they are often given an
injection of adrenalin directly into the heart in order to help start it again. Do you think they
would do that if it damaged the heart even more?

P:
No I'm sure they wouldn't.

T:
So, how much do you now believe that anxiety and panic will damage your heart?

From Wells (1997) pp. 123–124.

SELF‐TEST QUESTIONS
What are the main diagnostic criteria for social anxiety disorder and how does this
disorder manifest itself ?
Can you describe the various cognitive factors that appear to play an important role in
maintaining social anxiety disorder?
How do CBT and drug treatments complement each other in the treatment of social
anxiety disorder?
 SECTION SUMMARY

6.4 PANIC DISORDER AND AGORAPHOBIA

Panic disorder is characterised by repeated panic or anxiety attacks associated with a
variety of physical symptoms, including heart palpitations, dizziness, perspiring,
hyperventilation, nausea, trembling, and depersonalisation.
Agoraphobia is a fear or anxiety of any place where the sufferer does not feel safe or feels
trapped, and is accompanied by a strong urge to escape to a safe place (e.g., home)
The lifetime prevalence rate for panic disorder is between 1.5% and 3%, although
prevalence rates do differ between different cultures.
Individuals with a diagnosis of panic disorder show a greater sensitivity to norepinephrine
and to drugs that increase activity in the locus coeruleus area of the brain
Hyperventilation is a common feature of panic disorder, and some theorists have argued
that the effect of hyperventilation on body CO2 levels is a causal factor in the development
of a panic attack.
Individuals with panic disorder have high levels of anxiety sensitivity, which is a fear of
anxiety symptoms.
Individuals who develop panic disorder tend to catastrophically misinterpret bodily
sensations, and interpret them as signs of an imminent medical threat (e.g., an imminent
heart attack signalled by a missed heartbeat). This cognitive bias leads to a vicious cycle
that increases the anxiety symptoms that precipitate a panic attack.
Safety behaviours are activities that a panic disorder sufferer will deploy during a panic
attack in the hope of avoiding an attack and these behaviours will maintain the belief that
panic attacks might have catastrophic consequences.
SSRIs and tricyclic antidepressants are an effective first‐line treatment for panic disorder,
but structured exposure therapy or CBT is as effective, if not superior, to drug treatments
over the longer term.

6.5 GENERALISED ANXIETY DISORDER (GAD)

GAD is a pervasive condition in which the sufferer experiences continual apprehension and anxiety
about future events, and this leads to chronic and pathological worrying about those events. We all
worry about things to some degree—and, indeed, many people find it beneficial to think about how
they might deal with challenging future events. However, for the individual with GAD worrying has a
number of features that make it disabling and a source of extreme emotional discomfort. For example,
for the individual suffering GAD:
1. Worrying is a chronic and pathological activity that is not only directed at major life issues (e.g.,
health, finances, relationships, work‐related matters) but also to many minor day‐to‐day issues and
hassles that others would not perceive as threatening (Craske, Rapee, Jackel, & Barlow, 1989; Tallis,
Davey, & Capuzzo, 1994),
2. Worrying is perceived as uncontrollable—the individual with GAD feels they cannot control either
the onset or termination of a worry bout,
 3. Worrying is closely associated with the catastrophising of worries—that is, worry bouts persist
for longer in GAD, they are associated with increasing levels of anxiety and distress as the bout
continues, and worrying seems to make the problem worse rather than better (Table 6.9). While
pathological and chronic worrying is the cardinal diagnostic feature of GAD it may also be
accompanied by physical symptoms such as fatigue, trembling, muscle tension, headache, and
nausea.

catastrophising An example of magnification in which the individual takes a single fact to its
extreme, one example being catastrophic worrying.

6.5.1 Diagnosis and Prevalence

A summary of the DSM‐5 criteria for diagnosis of GAD are shown in Table 6.10 and include:
Excessive anxiety and worry about two or more domains of activities or events occur on more days
than not for 3 months or more.
Anxiety and worry are associated with physical symptoms such as restlessness or muscle tension.
Anxiety and worry are accompanied by one or more of avoidance of events with possible negative
outcomes, time and effort preparing for events with negative outcomes, procrastination, or
repeated reassurance seeking about worries.
Finally, a consequence of these symptoms will be clinically significant distress or impairment in
social, occupational, or other important areas of functioning.

6.5.2 Prevalence
Cross‐national studies indicate that DSM‐5 diagnosed GAD has a lifetime prevalence rate of 3.7% and
a 12‐month prevalence rate of 1.8%, and the disorder is significantly more prevalent and impairing in
high‐income than in low‐income countries (Ruscio et al., 2017). Subthreshold GAD is also a significant
problem worldwide, with as many as 12% of individuals suffering disabling and distressing subthreshold
symptoms in their lifetime (Haller, Cramer, Lauche, Gass, & Dobos, 2014). GAD is almost twice as
common in women as in men and can often persist from adolescence to old age (McLean, Asnaani,
Litz, & Hofman, 2011; Barlow, Blanchard, Vermilyea, Vermilyea, & DiNardo, 1986), and GAD is
associated with significant impairments in psychosocial functioning, role functioning, work productivity
and health‐related quality of life (Revicki et al., 2012). Comorbidity is also highly prevalent in sufferers
of GAD, with rates ranging from 45% to 98% (Goisman, Goldenberg, Vasile, & Keller, 1995).
Individuals diagnosed with GAD are likely to be diagnosed with other mental health problems such as
major depression (Zhou et al., 2017) and eating disorders (Brown, O'Leary, & Barlow, 2001), with
comorbidity predicting poorer treatment outcomes.

6.5.3 The Aetiology of Generalised Anxiety Disorder

The challenge in explaining GAD is to understand why some individuals worry chronically and
pathologically, while many other individuals—often with more stressful lifestyles—worry significantly
less. Theories will therefore have to explain why GAD sufferers persist with their worrying even when it
causes them significant distress.

Biological theories
There is some evidence for a genetic component in both anxiety generally and GAD specifically (Noyes
et al., 1992), which suggests that GAD has an inherited component. Twins studies estimate the heritable
component at around 30% (Dellava, Kendler, & Neale, 2011; Hettema, Neale, Myers, Prescott, &
Kendler, 2001) and recent genome‐wide association studies (GWAS) have reported a similar figure of
30% heritability (Gottschalk & Domschke, 2017). But what appears to be inherited more than anything
else is a vulnerability to anxiety disorders and neuroticism generally, and less an inherited vulnerability
to a specific disorder such as GAD (Tambs et al., 2009).
Neuropsychological perspectives on GAD are still in their infancy, with neuroimaging studies of worry
implicating prefrontal brain regions in this activity (Hoehn‐Saric, Schlund, & Wong, 2004; Paulesu et
al., 2010), but such studies have not yet provided any convincing reasons why worrying in GAD
sufferers should be so extreme and distressing. Other neuroimaging studies have focused on possible
abnormalities in emotional regulation in GAD sufferers (Mennin, Holaway, Fresco, Moore, &
Heimberg, 2007). A common finding is decreased connectivity between the amygdala (the emotional
centre that mediates fear‐related emotion) and the prefrontal cortex (PFC)(the brain area involved in
complex cognitive behaviour such as decision making and planning), and the PFC is critical for the
effective regulation of emotion, and particularly negative emotions such as anxiety, suggesting that
individuals with a diagnosis of GAD may have significant problems in regulating and inhibiting their
anxiety (Roy et al., 2013; Patriquin & Mathew, 2018).
TABLE 6.9 Catastrophising in Worriers and Nonworriers
After Vasey & Borkovec, (1992).
These catastrophising sequences generated by a chronic worrier (top) and a nonworrier (bottom) were
generated using the catastrophic interview procedure in which the individual is first asked ‘What is
your main worry at the moment?’ In this case both participants replied, ‘Getting good grades in
school’. The interviewer then passes this response back to the participant by saying ‘What is it that
worries you about getting good grades in school?’ each time the participant responds, the interviewer
passes that response back by asking what it is about the response that worries them. The interview
continues until the participant can no longer think of any reasons.

By looking at the catastrophising sequences above, we can deduce a number of things about chronic
worriers: (a) they produce significantly more catastrophising steps than nonworriers, (b) they
experience increasing emotional distress as catastrophising continues as evidenced by their ‘discomfort’
scores, and (c) the content of their catastrophising steps becomes more and more threatening and
catastrophic, as evidenced by their increasing ‘likelihood’ scores as catastrophising progresses.
Discomfort Likelihood
Chronic Worrier Topic: Getting good grades in school.
Catastrophising step
I won't live up to my expectations. 50 30
I'd be disappointed in myself. 60 100
I'd lose my self‐confidence 70 50
My loss of self‐confidence would spread to other areas of my life. 70 50
I wouldn't have as much control as I'd like. 75 80
I'd be afraid of facing the unknown. 75 100
I'd become very anxious. 75 100
Anxiety would lead to further loss of self‐confidence. 75 80
I wouldn't get my confidence back. 75 50
I'd feel like 1 wouldn't have any control over my life. 75 80
I'd be susceptible to things that normally wouldn't bother me 75
I'd become more and more anxious. 80 80
I'd have no control at all and I'd become mentally ill. 85 30
I'd become dependent on drugs and therapy. 50 30
I'd always remain dependent on drugs. 85 50
They'd deteriorate my body. 85 100
I'd be in pain. 85 100
I'd die. 90 80
I'd end up in hell. 95 80
Nonworrier Topic: Getting good grades in school.
Catastrophising step
I might do poorly on a test. 3 20
I'd get a bad grade in the class. 3 100
That would lower my grade‐point average. 2 100
I'd have less of a chance of getting a good job. 2 60
I'd end up in a bad job. 2 80
I'd get a low salary. 2 100
I'd have less money to spend on what I want. 2 100
I'd be unhappy. 2 35
It would be a strain on me. 2 10
I'd worry more. 2 5

TABLE 6.10 Summary: DSM‐5 Criteria for Diagnosing Generalised Anxiety Disorder (GAD)

Disproportionate fear or anxiety relating to areas of activity such as finances, health, family, or
work/school life
The individual experiences fear relating to at least two different areas of activity and symptoms of
intense anxiety or worry will last for 3 months or more and will be present for the majority of the
time during this period
Feelings of anxiety or worry will be accompanied by symptoms of restlessness, agitation, or
muscle tension
Anxiety or worry are also associated with behaviours such as frequently seeking reassurance,
avoidance of areas of activity that cause anxiety, or excessive procrastination or effort in
preparing for activities
Symptoms cannot be explained by other mental disorders such as panic disorder

Psychological theories

Information processing biases in GAD

A good deal of research has now indicated that anxious individuals, and especially those suffering
GAD, have a series of information processing biases which appear to maintain their
hypervigilance for threat, create further sources for worry, and maintain anxiety. For example,
experimental evidence has demonstrated that individuals with GAD preferentially allocate attention to
threatening stimuli and threatening information (Mogg & Bradley, 1998; Mathews & MacLeod, 2005),
Highly anxious individuals also exhibit a threat‐interpretation bias. That is, they resolve ambiguity by
selecting the more negative or threatening interpretation of ambiguous information (Blanchette &
Richards, 2010). Anxious individuals also have a bias towards expecting negative outcomes following
predictive cues in classical conditioning studies (Davey, 1992c), and they also exhibit reasoning biases
that maintain threatening interpretations of events (de Jong, Weertman, Horselenberg, & van den Hout,
1997; de Jong, Haenen, Schmidt, & Mayer, 1998). Many of these threat‐related information‐processing
biases cooccur in individuals with anxiety and increase the anxious individual's vulnerability to
interpreting daily events as threatening and challenging. It is easy to conceive of ways in which this
interpretational bias might maintain anxiety by maintaining the range of potential threats perceived by
the individual (Davey, 2006; Davey & Meeten, 2016). Indeed, recent studies have shown that these
biases causally contribute to worrying in anxious individuals typically diagnosed with GAD (Hirsch et
al., 2011). Furthermore, there appears to be an important reciprocal relationship between experienced
anxiety and threat‐interpretation biases. Early research indicated that anxiety gave rise to threat‐
interpretation biases (Mathews & MacLeod, 1994; Mogg & Bradley, 1998; Butler & Mathews, 1983),
but more recent research has indicated that forced learning of threat‐interpretation biases also increases
the individual's reported experience of anxiety (Mathews & MacLeod, 2002; Hertel, Mathews,
Peterson, & Kintner, 2003; Mathews & Mackintosh, 2000; Wilson, MacLeod, Mathews, & Rutherford,
2006). This has given rise to interventions for anxiety and GAD that attempt to correct the attentional
bias to threat found in anxious individuals (MacLeod & Mathews, 2012; see Mogg, Waters, & Bradley,
2017, for a review of these procedures). This is known as attention bias modification (ABM) and is
described in Treatment in Practice 6.4.
Cognitive biases have also been implicated in causing and maintaining pathological worrying in
individuals with a diagnosis of GAD, and these biases include attentional biases and negative
interpretation biases (Hayes & Hirsch, 2007; Hirsch, Hayes, & Mathews, 2009). The tendency to attend
to threatening material will heighten the perception that the world is a threatening place and initiate
worrying that will be maintained by the tendency of the individual with GAD to continue to attend to
threats and to interpret ambiguous information as threatening (Hirsch & Mathews, 2012; Davey &
Meeten, 2016).

information processing biases Biases in interpreting, attending to, storing or recalling

information which may give rise to dysfunctional thinking and behaving.

attention bias modification (ABM) Highly anxious individuals have attentional and
interpretational biases towards threat that are known to cause anxiety. ABM is a practical way
of reversing these biases and uses experimental procedures that will neutralise them.

Beliefs about worry and the function of worrying

We mentioned earlier that individuals with GAD persist chronically with their worrying even though it
causes them considerable distress and generates symptoms that disrupt normal day‐to‐day living. This
suggests that worrying may serve a particular function for such individuals, and this functionality may
outweigh the negative effects of their worrying. Some theories of GAD emphasise this functional aspect
of worrying. First, both pathological worriers and individuals diagnosed with GAD hold strong beliefs
that worrying is a necessary process that must be undertaken fully and properly in order to avoid future
catastrophes (Davey, Tallis, & Capuzzo, 1996; Wells, 1995; Borkovec, Hazlett‐Stevens, & Diaz, 1999),
and these dysfunctional beliefs about the utility of worrying appear to motivate the worrier to persist
with their worrying. A similar view is taken by metacognitive theories of GAD (e.g., Wells, 1995, 2010).
Metacognitions are overarching cognitive processes that are responsible for appraising, monitoring and
controlling thinking, and so have an important influence on what we think about and how long we will
persist in thinking about something. Metacognitive theories of worry argue that the individual with
GAD engages in worrying in response to negative thoughts (e.g., ‘What if I lose my job?’) as a means of
trying to anticipate problems, avoid them or find a solution. However, individuals with GAD have
developed metacognitive beliefs about worry that drive their worrying and also make that worry process
distressing. These include positive beliefs that worrying will help them solve or avoid problems (Davey et
al., 1996) or that being in a constant state of arousal and worry will keep them alert to future threats
and challenges and enable them to deal more effectively with these events (e.g., Newman & Llera, 2011),
as well as negative metacognitive beliefs that worrying will be uncontrollable or harmful. It is the
apparent contradiction between these two sets of beliefs that causes the worry‐related distress in GAD
according to this model, and metacognitive therapy is a specific form of intervention developed to deal
with these GAD‐causing beliefs (Wells, 2010).
Second, there is growing evidence that worrying may indeed be reinforced because it distracts the
worrier from experiencing other negative emotions and processing even more stressful phobic images.
That is, worry is an internal narrative process that prevents the individual from processing other—often
more stressful—information (Borkovec, 1994; Borkovec & Lyonfields, 1993). Evidence to support this
view comes from the fact that worry produces very little physiological or emotional arousal (Hoehn‐
Saric & McLeod, 1988) and appears to block the processing of emotional images (Borkovec, Lyonfields,
Wiser, & Diehl, 1993).

CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 6.4

ATTENTION BIAS MODIFICATION (ABM)

Because highly anxious individuals have attentional and interpretational biases towards threat
that are known to cause anxiety, a practical way of reversing these biases is to use experimental
procedures that will neutralise them. This training procedure is known as attention bias
modification (ABM) and has been used to modify both attentional and interpretation biases in
anxious individuals and to reduce anxiety vulnerability and levels of dysfunctional anxiety
(MacLeod & Mathews, 2012; Hakamata et al., 2010).
The procedure uses the classic dot probe task that has traditionally been used to measure
attentional biases (van Rooijen, Ploeger, & Kret, 2017). Stimuli are presented on a computer
screen. First, the participant sees a focus point (+), and this is followed by two words presented
simultaneously for a very short duration (usually 500 ms). One will be threatening, (e.g.,
‘Humiliated’) and the other with be nonthreatening (e.g., ‘Dishwasher’). In the ABM procedure,
immediately after the words have appeared a ‘probe’ appears (e.g., a colon) and the participant
has to respond as quickly as possible by indicating where the probe appeared. However, in the
ABM task, the probe always appears in the position where the non‐threatening word had been
presented. This process trains the individual to attend more rapidly to the nonthreatening than
the threatening word and so ameliorates any attentional bias to threat that the participant
possessed.
To date, the effect of ABM procedures in reducing clinical and nonclinical anxiety has been
mixed, with different types of methodologies reporting different rates of success (Mogg, Waters,
& Bradley, 2017). More adequately powered randomised controlled trials (RCTs) are required
with a broader range of relevant measures of anxiety and treatment satisfaction before we are
able to conclude that ABM interventions are an effective and long‐lasting means of reducing
anxiety.
Dispositional characteristics of worriers
In addition to these specific psychological models of pathological worrying, there is a good deal of
knowledge available about what other kinds of psychological features chronic worriers possess. For
example, worriers are intolerant of uncertainty (Ladouceur, Talbot, & Dugas, 1997; Birrell,
Meares, Wilkinson, & Freeston, 2011), are high on perfectionism (Pratt, Tallis, & Eysenck, 1997), and
have feelings of responsibility for negative outcomes (Startup & Davey, 2003; Wells & Papageorgiou,
1998). All of these suggest they possess characteristics that will drive them to attempt to think about
resolving problematic issues. However, worriers also have poor problem‐solving confidence (Davey,
1994a) and couch their worries in ways that reflect personal inadequacies and insecurities (Davey &
Levy, 1998), and this contrasting combination of characteristics appears to drive the individual to try to
resolve problems, but the process is thwarted by their personal doubt about their own ability to solve
them successfully (Davey, 1994b).
A further characteristic of chronic worriers is that they often experience negative mood (negatively
experienced emotional states such as anxiety, sadness, anger, pain, tiredness), and this negative mood
can facilitate their worrying in a number of ways. First, negative mood promotes a more systematic,
deliberate and effortful information‐processing style which facilitates detailed worrying (Dash, Meeten,
& Davey, 2013), and it also raises performance standards which means the worrier will be less satisfied
with the solutions their worrying generates and so want to continue with their worrying (Scott &
Cervone, 2002). Second, worriers often judge the acceptability of their worrying by using their
concurrent mood as information about whether their worrying has been successful (known as the
mood‐as‐input hypothesis). Because they are usually in a negative mood, they interpret this
negativity as though they are not satisfied with their worrying so they should therefore continue to worry
(Meeten & Davey, 2011). In these different ways the worrier's negative mood contributes to making the
worry bout longer, and this may be one factor that makes worrying seem uncontrollable in those with a
diagnosis of GAD.

mood‐as‐input hypothesis A hypothesis claiming that people use their concurrent mood as
information about whether they have successfully completed a task or not.

6.5.4 The Treatment of Generalised Anxiety Disorder

As with most of the anxiety disorders, GAD can be treated either with drugs, with structured
psychological therapy such as CBT, or with a combination of both. However, deciding what type of
treatment to use is often the most important decision for service providers and therapists—especially for
a disorder that is as prevalent as GAD. Medication might be a suitable first step if immediate
management of the problem is important (if the patient is experiencing extreme distress or has suicidal
ideation). Otherwise, longer‐term structured psychological therapy (such as CBT) or self‐help
programmes should be offered. Some self‐help options are outlined in my blog in ‘10 Tips to Manage
Your Worrying’ (http://www.psychologytoday.com/blog/why‐we‐worry/201206/10‐tips‐manage‐your‐
worrying), in chapter 12 of The Anxiety Epidemic (Davey, 2018), and in chapter 6 of our CBT self‐help
guide for managing anxiety (Davey, Cavanagh, Jones, Turner, & Whittington, 2012).

Pharmacological treatments
Because GAD involves chronic daily anxiety and emotional discomfort, we might expect that anxiolytics
—such as the benzodiazepines—would be the first line of treatment for sufferers. However, at least 50%
of GAD sufferers receive initial treatment with antidepressants such as SSRIs or SNRIs on the basis of
their proven effectiveness in treating the symptoms of GAD in clinical trials, whereas less than 35% are
treated with benzodiazepines (Berger et al., 2011). In support of the use of antidepressants in the
treatment of GAD, a recent large‐scale meta‐analysis of RCTs for drug treatments of GAD indicated
that SSRIs and SNRIs are relatively well tolerated and do reduce symptoms of GAD (Slee et al., 2019).
Treatment with antidepressants is justified in many cases because GAD is regularly comorbid with
depression and SSRIs tend to be better tolerated than benzodiazepines. However, the long‐term
effectiveness of pharmacological treatments for GAD is questionable given that at least one in four of
GAD sufferers do not respond to the most effective medications (Baldwin, Waldman, & Allgulander,
2011).

Psychological treatments
Psychological treatments for GAD have developed using both behavioural and cognitive methodologies.
For example, stimulus control treatment was original developed out of behaviour therapy principles for
dealing with worry behaviours, while acceptance and commitment therapy (ACT, see Chapter 4,
Section 4.1.1) and a number of effective variants of CBT are now available for dealing with the
pathological worrying found in GAD (e.g., cognitive restructuring and metacognitive therapy).

Stimulus control treatment

One of the earliest behavioural interventions for worry in GAD adopted the principle of stimulus
control. This is based on the conditioning principle that the environments in which behaviours are
enacted come to control their future occurrence and can act to elicit those behaviours (the principle of
stimulus control). Because worrying can occur almost anywhere, and so come under the control of a
vast range of contexts, the first aim of stimulus control treatment is to limit the contexts in which
worrying occurs. This is achieved by telling clients that they can worry—but only for a specific period in
a particular location each day (Borkovec, Wilkinson, Folensbee, & Lerman, 1983). For example, they are
instructed to worry at a specific time (e.g., between waking and the end of breakfast) or in a particular
location (the living room). (Treatment in Practice 6.5).

stimulus control treatment An early behavioural intervention for worry in GAD which
adopted the principle of stimulus control, based on the conditioning principle that the
environments in which behaviours are enacted come to control their future occurrence and can
act to elicit those behaviours.

Cognitive behaviour therapy

In the previous section we reviewed a number of psychological theories of GAD which suggest that
cognitive biases and dysfunctional beliefs about the function of worrying may be central to the
development and maintenance of the disorder. This being so, integrated cognitive behavioural therapy
seems a suitable method to tackle GAD. CBT for GAD normally consists of a number of elements, the
main ones being:
Self‐monitoring
Relaxation training
Cognitive restructuring
Behavioural rehearsal

CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 6.5

STIMULUS CONTROL TREATMENT FOR GENERALISED
ANXIETY DISORDER

Stimulus control treatment for GAD is an effective treatment for reducing the frequency of
worry by controlling the range of contexts in which the activity occurs (see Section 6.4.4).
There are four basic instructions underpinning this procedure:
1. Learn to identify worrisome thoughts and other thoughts that are unnecessary or
unpleasant. Distinguish these from necessary or pleasant thoughts related to the present
moment.
2. Establish a half‐hour worry period to take place at the same time and in the same location
each day.
3. When you catch yourself worrying, postpone the worry to the worry period and replace it
with attending to present‐moment experience.
4. Make use of the half‐hour worry period to worry about your concerns and to engage in
problem‐solving to eliminate those concerns.

From Borkovec, 2005; Borkovec, Wilkinson, Folensbee, & Lerman, 1983.

Self‐monitoring involves making the client aware of their fixed patterns of behaviour and the
triggers that may precipitate worry. These triggers are often thoughts about future events that have very
low probabilities of happening (e.g., the accidental death of a loved one while driving to work), and the
client's attention is drawn to the fact that these are cognitively constructed rather than real events.
Relaxation training is an obvious way of dealing with the chronic stress experienced by GAD
sufferers. The specific technique of progressive muscular relaxation is often used (Bernstein, Borkovec,
& Hazlett‐Stevens, 2000), and relaxation is found to be as effective as some forms of cognitive therapy
(Arntz, 2003). Cognitive restructuring methods are used to challenge the biases that GAD sufferers
hold about how frequently bad events might happen (Beck, Emery, & Greenberg, 1985) and to generate
thoughts that are more accurate (Borkovec, 2005). One way of doing this is by using an outcome diary
in which the client writes down on a daily basis their worries and how likely they think the focus of their
worries will actually happen. Clients can then compare their own inflated estimate of the likelihood of
the event with subsequent reality (Borkovec, Hazlett‐Stevens, & Diaz, 1999).

Self‐monitoring A form of clinical observation that involves asking clients to observe and
record their own behaviour, to note when certain behaviours or thoughts occur, and in what
contexts they occur.

Relaxation training A method of dealing with the chronic stress experienced by

psychopathology sufferers. A specific technique of progressive muscular relaxation is often used,
and relaxation is found to be as effective as some forms of cognitive therapy.

Cognitive restructuring Methods used to challenge the biases that a client might hold about
how frequently bad events might happen and to generate thoughts that are more accurate.

Other types of cognitive restructuring involve the challenging and replacement of dysfunctional
metacognitive beliefs about worrying—known as metacognitive therapy (Wells, 1999, 2010)—or the
belief held by pathological worriers that uncertainty has to be resolved by thinking through every
possible scenario (Dugas et al., 2003). Finally, behavioural rehearsal involves either the actual or
imagined rehearsal of adaptive coping responses that need to be deployed when a worry trigger is
encountered. These coping strategies may involve the deployment of relaxation exercises or pleasant
distracting activities designed to avoid worry (Butler, Fennell, Robson, & Gelder, 1991). CBT for GAD
has been shown to be effective with or without the use of pharmacological treatments (Lang, 2004), has
long‐term effectiveness for an important proportion of clients (Durham, Chambers, MacDonald, Power,
& Major, 2003), and can also help to alleviate comorbid depression (Cuijpers et al. (2014). However,
recent meta‐analyses suggest that while CBT treatments for GAD have improved over the past 15–20
years, there is still a significant percentage of sufferers who fail to recover fully following cognitive
treatments for GAD (Hanrahan, Jones, Field & Davey, 2013), and this is a testament to GAD as a
pervasive condition that can last for many years in a large percentage of sufferers despite treatment with
either medications or psychological therapy (see my blog ‘The Lost 40%’,
https://www.psychologytoday.com/gb/blog/why‐we‐worry/201211/the‐lost‐40).

behavioural rehearsal A coping strategy that involves either the actual or imagined
rehearsal of adaptive coping responses that need to be deployed when a worry trigger is
encountered.
 SELF‐TEST QUESTIONS
What is the cardinal diagnostic feature of GAD?
What are the features of worry in GAD that make it a distressing experience for the
sufferer?
How do information processing biases and cognitive factors contribute to the acquisition,
maintenance and experience of anxiety in GAD?
How do psychological treatments of GAD attempt to manage the activity of worrying?

SECTION SUMMARY

6.5 GENERALISED ANXIETY DISORDER

The cardinal diagnostic characteristic of GAD is chronic uncontrollable worrying, which
is accompanied by physical symptoms such as irritability, muscle tension, fatigue, poor
concentration, restlessness, and disturbed sleep.
Around 3.7% of the population will be diagnosed with GAD in their lifetime, and 12% of
those who attend anxiety disorder clinics will present with GAD.
Individuals with GAD possess an information processing bias that appears to maintain
their hypervigilance for threat and create the opportunity to catastrophically worry about
events. There is evidence that these information‐processing biases may actually cause
anxiety generally and can be manipulated therapeutically using attention bias
manipulation (ABM) techniques.
Worrying in GAD appears to be maintained by dysfunctional beliefs about the utility of
worrying which appear to motivate the individual with GAD to persist with their worrying.
A majority of GAD sufferers receive initial treatment with SSRIs, but treatments based on
controlling the process of worrying and challenging dysfunctional beliefs about worrying
appear to have more longer‐term benefits.

6.6 OBSESSIVE‐COMPULSIVE DISORDER (OCD)

We have all occasionally gone back to check whether we locked a door, and we have all experienced a
sudden, intrusive thought that we find disturbing and out of place (e.g., harming our own child).
However, for the person with OCD such thoughts and actions are repeated often and result in a
distressing and disabling way of life. OCD has two important and sometimes independent
characteristics. Obsessions are intrusive and recurring thoughts that the individual finds disturbing
and uncontrollable. These obsessive thoughts frequently take the form of causing some harm or distress
to oneself or to some important other person (such as a partner or offspring). Common obsessions also
take the form of fear of contamination (i.e., contaminating oneself or important others), thoughts about
harm, accidents, and unacceptable sex (Rowa & Purdon, 2005; Berry & Laskey, 2012). Obsessive
thoughts can also take the form of pathological doubting and indecision, and this may lead to sufferers
developing repetitive behaviour patterns such as compulsive checking or washing. Very often, obsessive
thoughts can be ‘autogenous’—that is seem uncontrollable and ‘come out of the blue’, and it this
autogenous characteristic that helps to make obsessive thoughts distressing. Compulsions represent
repetitive or ritualised behaviour patterns that the individual feels driven to perform in order to prevent
some negative outcome happening. This can take the form of ritualised and persistent checking of
doors and windows (to ensure that the house is safe), or ritualised washing activities designed to prevent
infection and contamination. Ritualised compulsions such as these also act to reduce the stress and
anxiety caused by the sufferer's obsessive fears. Whilst the main compulsions are usually related to
checking or washing, compulsions can also manifest as stereotyped sequences of behaviour, such as
flicking a light switch on and off a specific number of times before going to sleep, or ensuring that items
in the room are arranged so they seem to be ‘just right’. In most cases, compulsions are clearly
excessive, and are usually recognised as so by the sufferer. Rituals can become rigid, stereotyped
sequences of behaviours which the individual is driven to perform as a result of cognitive triggers such
as intrusive thoughts related to the individual's specific fears. For example, individuals distressed by
unwanted immoral or blasphemous thoughts can attempt to suppress the thought and reduce anxiety by
indulging in compulsive acts such as counting backwards from a number until the thought has gone.

Obsessions Intrusive and recurring thoughts that an individual finds disturbing and
uncontrollable.

Compulsions Repetitive or ritualised behaviour patterns that an individual feels driven to

perform in order to prevent some negative outcome happening

6.6.1 Diagnosis and Prevalence

In DSM‐5, the importance of OCD as a distinctive mental health problem was recognised by including
OCD and a number of related disorders in a separate chapter independent of anxiety disorders
generally, and this acknowledges some of the special features that OCD and related disorders possess.
Table 6.11 shows the main DSM‐5 diagnostic criteria for OCD. Diagnosis is dependent on the
obsessions or compulsions causing marked distress, being time consuming, or significantly interfering
with the person's normal daily living. This latter diagnostic criterion delineates OCD compulsions from
other urges, such as the uncontrollable desire to eat, drink or gamble, because the latter are often
engaged in with pleasure (see Chapters 10 and 12 for discussions of these alternative types of
compulsive behaviour) (Case History 6.2).

CASE HISTORY 6.2 OBSESSIVE‐COMPULSIVE DISORDER

Luke was 21 years old and attending university, living a considerable distance from his family
with whom he had always been close. It was 2 months before his final year exams and his alarm
went off at 8:30 a.m. Turning to switch off his alarm, Luke was immediately overwhelmed by
the feeling of dread that had been with him constantly since the beginning of term.
He quickly got out of bed and went to the bathroom. Luke washed his hands and brushed his
teeth before washing his hands twice more. Stepping into the shower Luke scrubbed himself all
over with shower gel, and washed his hands several more times in between cleaning the rest of
his body. After rinsing his hair through, Luke washed his hands again and got out of the
shower; by now it was 9:30.
Luke began to dry his hair but he felt that his hands were still dirty, though by now they were
 red raw. He washed them again, rapidly rubbing the backs of his hands and cleaning repeatedly
under his nails. They still felt dirty. Telling himself not to be stupid, Luke moved to the door of
the bathroom but felt a strong urge to go back and clean his hands once more. The feeling was
too strong to resist so he quickly rinsed his hands again, dousing them in sanitiser gel, and
rushed out of the bathroom, knowing he would be late for his lecture.
Before he could leave the house, Luke checked that the back door was locked and all his
housemates’ windows were securely closed, then he went back to the bathroom to wash his
hands twice more. Grabbing a clean towel from the wash, Luke carefully wrapped up his hand
so he could open the front door without touching the dirty handle. Once the door was open,
Luke ran back inside to check that he had remembered to secure the windows in all his friends’
rooms and to close all the doors.
Pulling the front door shut with his foot, Luke tested it was firmly shut and then ran towards the
bus stop. It was now 10:15 and he was already 15 minutes late. A bus was arriving just as he
reached the stop, hot and out of breath. Sitting on the bus, Luke felt the sweat on the palms of
his hands and wiped them clean on a tissue, repeatedly cleansing them with the sanitiser gel he
always carried with him.
Halfway through the journey, Luke began to panic that he hadn’t locked up the house and
imagined coming home to find he had been burgled and all his housemates’ belongings had
been ransacked. Luke got off at the next stop and took another bus back home, only to find that
the doors and windows were locked. Cursing himself for his irrationality, Luke turned to leave
the house once more but, looking at his watch, saw it was now 11:30 and his lecture was almost
over.
Later on, when Luke was diagnosed with obsessive compulsive disorder, 6 months after failing
his exams, he felt a huge sense of relief and was pleased that he could now give his friends and
family a logical explanation for his behaviour. Luke is now receiving treatment for his OCD
and, when he explained his condition to the university, they agreed he could return and re‐sit
his exams.

Clinical Commentary
This example shows how obsessions and compulsions in OCD are often compelling and difficult for the
sufferer to resist—even when the individual is aware that these thoughts and actions are ‘stupid’ or
irrational. Luke’s compulsions are fueled by the ‘feelings of dread’ that he experiences most mornings
when he wakes up, and this provides the highly anxious state under which compulsions (such as
compulsive washing) are performed. ‘Doubting’ is also a common feature of OCD, and Luke experiences
this on his way to university in the form of doubting whether the doors and windows are locked. The
high levels of inflated responsibility usually possessed by OCD sufferers mean that Luke is driven to
continually check that his doubts are unfounded.

OCD onset is usually gradual and frequently begins to manifest itself in early adolescence or early
adulthood following a stressful event such as pregnancy, childbirth, and relationship or work problems
(Kringlen, 1970). OCD symptoms are also a common way for anxiety to manifest itself in childhood,
and this is discussed further in Chapter 16. Lifetime prevalence of OCD is around 2.5% with a 12‐
month prevalence rate of around 1.2%, and affects women marginally more frequently than men
(Ruscio, Stein, Chiu, & Kessler, 2010; Adam, Meinlschmidt, Gloster, & Lieb, 2012).
Risk factors for OCD in adulthood include childhood isolation and poor peer relationships during
childhood, negative emotionality in adolescence (this is a measure of interpersonal alienation, irritable‐
aggressive attitudes, and reactivity to stress), a history of childhood physical and sexual abuse (those who
reported physical abuse had a specific risk for OCD), experiencing problems at birth such as
haemorrhaging or respiratory distress, poor motor skills, and lower IQ measures during childhood
(Grisham et al., 2011). However, it must be pointed out that many of these risk factors are also risk
factors for other anxiety‐based problems, so they are not necessarily specific to OCD. But there are also
some cultural and ethnic practices that seem to increase the risk of developing OCD symptoms
specifically. In particular, religiosity is a known risk factor for OCD because many religions define
taboos that explicitly prohibit certain behaviours or thoughts and they often ritualise many basic aspects
of daily life (Huppert, Siev, & Kushner, 2007). Some of the ways in which these factors can lead to
obsessions and compulsions in anxious individuals are described in Case History 6.3.
TABLE 6.11 Summary: The Main DSM‐5 Diagnostic Criteria for Obsessive‐Compulsive Disorder

Presence of obsessions such as repeated and unwanted thoughts, urges, or images that the
individual tries to ignore or suppress, and/or
Presence of compulsions where the individual feels compelled to repeat certain behaviours or
mental activities
The individual believes that the behaviours will prevent a catastrophic event but these beliefs have
no realistic connections to the imagined event or are markedly excessive
Obsessions and compulsions consume at least 1 hour per day and cause difficulty in performing
other functions
Symptoms cannot be explained by the effects of other mental or medical disorders, drug abuse, or
medication

6.6.2 OCD‐Related Disorders

DSM‐5 has divided OCD‐type problems into a number of separate diagnostic categories. The main
OCD diagnostic category is described in Table 6.11, but other OCD‐related diagnostic categories
include (a) body dysmorphic disorder(BDD): this is a preoccupation with perceived defects or flaws
in physical appearance that are not usually perceived by others, which gives rise to compulsive
grooming, mirror checking, and reassurance seeking (see Focus Point 6.4); (b) hoarding disorder: this
problem centres around a difficulty discarding or parting with possessions to the point where the
individual's living area is severely congested by clutter (see Focus Point 6.5); (c) hair‐pulling disorder
(trichotillomania): the individual compulsively pulls out their own hair resulting in significant hair
loss; and (d) skin‐picking disorder: Recurrent picking of the skin that results in skin lesions (see
Davey, Dash, & Meeten, 2014 for a fuller description of OCD‐related disorders). Since the publication
of DSM‐5 there has been much discussion about whether these OCD‐related conditions share much in
common with OCD itself other than a few overlapping features based on symptoms (e.g., compulsivity).
Reviews of these related disorders suggest that, with the exception of BBD, other related disorders have
little in common with OCD in terms of known causes and treatment response (Abramowitz & Jacoby,
2015).

hoarding disorder Difficulty discarding or parting with possessions to the point where the
individual’s living area is severely congested by clutter.

trichotillomania Hair-pulling disorder in which the individual compulsively pulls out their
own hair resulting in significant hair loss.
 skin-picking disorder Recurrent picking of the skin that results in skin lesions.

CASE HISTORY 6.3 RELIGIOSITY AND OCD — ANA'S

HISTORY OF SELF‐DOUBT

Ana's history of self‐doubt dated back to age 7, when she first recalled being uncertain about
adhering to many of the religious rituals normally associated with her community's
cultural/religious beliefs. For example, many Orthodox Jews observe a waiting period of 6 hrs
between eating meat and dairy foods. Ana would carefully count the hours between eating a
meat meal and a dairy meal, but she would later be beset with doubts about whether or not she
had waited the religiously allowed number of hours. Such self‐doubt extended into other
religiously defined regulations, but for the most part she was able to refrain from any ritualistic
behaviours. At the age of 18, Ana attended a girls' school in Israel and embarked on a course of
chronic checking rituals. Thus, if she stopped at restaurants that served nonkosher food, she
compulsively washed her hands repeatedly because she feared that she might have
unintentionally touched some forbidden food, utensils, table, or countertop. She began to skip
meals because she was afraid that she might contaminate her own food with nonkosher food
products unknowingly carried on her hands. Other symptoms included habitually rechecking
labels of food products to ensure that they were kosher.
Ana met her husband‐to‐be in an arranged meeting. Two months after the marriage, however,
her obsessions and compulsions returned and began to trouble her more than ever. She was
unable to prepare any meals because of increasing self‐doubt about contaminating utensils
meant to be used for meat dishes with those reserved for dairy foods, and vice versa.
After marriage, Orthodox Jewish men are prohibited from touching their wives during the time
of menstruation or for 7 days thereafter. According to stipulated ritual, an Orthodox Jewish wife
is responsible for ensuring that she is no longer exhibiting vaginal bleeding by swabbing herself
carefully with a linen cloth for each of the 7 days following the overt cessation of the menstrual
flow. It is only then, after a ritual bath (the Mikvah), that she and her husband are allowed to
physically touch one another. Faced with this responsibility, Ana obsessed about whether there
was a tinge of pink on her linen cloths. She checked the linen cloths repetitively and was unable
to decide definitively that the menstrual flow had ceased. Ultimately, she consulted with her
rabbi, who agreed to check the linen on a monthly basis and make the decision about whether
or not she was free of blood.

From Burt & Rudolph, 2000

6.6.3 The Aetiology of Obsessive‐Compulsive Disorder

When considering the aetiology of OCD, the reader should be aware that it represents a psychological
problem that possesses a number of quite different, and often independent, features. For example,
obsessions do not always occur with compulsions, and the two main types of compulsions (i.e., washing
and checking) rarely occur together in the same individual. This means that many theories of the
aetiology of OCD have been developed to address only some of its features (e.g., thought suppression
accounts are relevant to explaining only obsessive thoughts), and they are not meant to be universal
explanations of OCD. Bear this in mind when reading through the following sections.

Biological factors
As with other anxiety disorders, there is evidence of an inherited component to OCD. Large‐scale
community twin studies suggest that the heritability estimate for OCD is ‘moderate’ (Monzani, Rijsdijk,
Harris, & Mataix‐Cols, 2014)—and it is well known that OCD tends to run in families, which may
reflect this heritable component (Lenane et al., 1990; Hanna et al., 2002). More recent genetic linkage
studies have also begun to identify some of the candidate genes for the transmission of the inherited
component to OCD (e.g., Wang et al., 2008), and serotonin neurotransmitter genes have been an
important focus in OCD candidate gene studies (Sinopoli, Burton, Kronenberg, & Arnold, 2017)—
largely because SSRIs are often effective in alleviating OCD symptoms, suggesting that serotonin
neurotransmitter abnormalities may be influencing OCD symptoms (Nicolini, 2010).
However, OCD is a heterogeneous disorder with considerable variation in the nature of its symptoms
and severity across sufferers, suggesting that the causes of the condition may themselves be varied. For
example, there is evidence that, in some sufferers, small but significant deficits in brain functioning may
be associated with generating repetitive and compulsive responding. These cognitive deficits may not
necessarily give rise to OCD symptoms on their own, but in combination with life experiences that give
rise to anxiety (e.g., periods of stress or increased responsibility) they may help to establish compulsions
and rituals as a way of dealing with that anxiety. They may also make it difficult to inhibit or control the
obsessive aversive thoughts that often generate anxiety during OCD. Cognitive problems identified in
those with a diagnosis of OCD include difficulties in shifting attention (which will make it difficult to
shake off obsessive thoughts or to move away from ritualised trains of behaviour), difficulties in
suppressing tendencies to behave in old, no‐longer relevant ways (this deficit would help to maintain
dysfunctional, lengthy rituals once they've been established), problems with working memory updating
(meaning that more time is required to collect sufficient information to inform actions and decision‐
making, leading to uncertainty and doubting), poor working memory capacity (making it hard to keep
in mind relevant information for decision‐making resulting in doubting caused by reduced memory
confidence), and deficits in what are known as executive functioning skills, such as strategic planning,
organised searching, goal‐oriented behaviour, and ability to suppress responding when required (all of
which give rise to impaired cognitive flexibility and poor abstraction skills, and may lead to the
development of very explicit and well‐defined sequences of behaviour that the individual finds difficult
to inhibit) (Aydin, Koybasi, Sert, Mete, & Oyekcin, 2014).

FOCUS POINT 6.4 BODY DYSMORPHIC DISORDER

One OCD‐related disorder described in DSM‐5 is body dysmorphic disorder (BDD). This is a
preoccupation with assumed defects in appearance that are often imaginary, but if there is a
physical anomaly, those suffering from BDD will greatly exaggerate its importance. Common
complaints include flaws in facial features or facial asymmetry, hair thinning, acne, wrinkles,
scars, vascular markings, irregular complexions, or excessive facial hair. Other common
preoccupations include body shape generally (e.g., preoccupations with being obese or
overweight), and dissatisfaction with specific body parts, such as breasts, genitals, buttocks, etc.
Sufferers will often be so embarrassed about their supposed appearance defects that they will
often talk about them only in general terms and may simply refer to themselves as being ‘ugly’.
The way in which BDD overlaps with OCD is in the obsessive thoughts that sufferers have
about their appearance, and sufferers can also develop ritualistic compulsions around their
defects, spending many hours a day viewing themselves in mirrors or attempting to deal with
their problems with excessive grooming behaviour (e.g., skin picking, hair combing, applying
cosmetics, dieting, etc.), with such behaviours usually adding to the distress that is experienced
(see Krebs, de la Cruz, & Mataix‐Cols, 2017, for a review of recent advances in the
understanding of BDD).
Concerns about appearance in BDD are frequently accompanied by a host of repetitive and
time‐consuming behaviours, aimed at verifying, camouflaging, or enhancing the person's
appearance, and one particular repetitive behaviour is known as ‘mirror gazing’ (Windheim,
Veale, & Anson, 2011). Studies have shown that about 80% of individuals with BBD will
repetitively check their appearance in mirrors—often for considerable periods of time.
Interestingly, the remaining 20% tend to avoid mirrors altogether (Veale & Riley, 2001). Mirror
gazing can be construed as a ‘safety‐seeking behaviour’ which briefly acts to reduce distress, but
in the longer term it increases distress, maintains negative beliefs about appearance, and
reinforces repetitive appearance‐checking behaviours (Veale & Riley, 2001).
Individuals with BDD also develop dysfunctional biases and beliefs about their appearance and
are quite convinced that their own perceptions are correct and undistorted. These cognitive
distortions include selectively attending to perceived threats related to appearance,
misinterpreting ambiguous stimuli as threatening, overvaluing the importance of attractiveness,
and having inaccurate coding and recall for facial or bodily stimuli (Johnson, Williamson, &
Wade, 2018). As a consequence of these beliefs they may regularly seek cosmetic surgery in
order to correct their perceived ‘defects’. In a study of individuals seeking cosmetic surgery,
Aouizerate et al. (2003) found that 9.1% of applicants were diagnosable with BDD. In fact, in
those applicants who had no defects or only a slight physical defect, 40% were diagnosable with
BDD.
The point prevalence of BDD is around 1.7% in community samples (Veale et al., 2016), with a
mean age of onset of around 16 years of age (Bjornsson et al., 2013). This study also indicated
that those diagnosable with BDD had high rates of previous cosmetic surgery (15.6%) and
higher rates of suicidal ideation (31%). BDD is also relatively common in individuals who
already have a diagnosis of OCD, with lifetime prevalence rate for BDD of 12.1% in
individuals with OCD (Costa et al., 2012)—reinforcing the view that OCD and BBD may be
related disorders. CBT can be a helpful treatment for BBD, although its effectiveness has yet to
be fully evaluated (Harrison, de la Cruz, Enander, Radua, & Mataix‐Cols, 2016). Although the
positive effects of CBT appear to be durable up to 12 months after the end of treatment, the
majority of suffers often remain symptomatic and may require longer‐term monitoring (Krebs
et al., 2017).

FOCUS POINT 6.5 HOARDING DISORDER

Hoarding disorder is a new diagnostic category included in DSM‐5 (Frost, Steketee, & Tolin,
2012; Pertusa et al., 2010). It is a complex problem made up of three specific attributes: (a)
collecting too many items (some sufferers will actually actively collect or steal more items to
 hoard), (b) difficulty parting with or getting rid of hoarded items, and (c) general problems with
organising their possessions, probably as a result of problems with more fundamental cognitive
processes such as information processing, attention, categorisation, and decision‐making (e.g.,
Tolin & Villavicencio, 2011). The result of this hoarding is large piles of clutter that make living
spaces impassable, home utilities (such as a toilet) usable, and this can pose both health and
safety risks. Initial epidemiology studies suggest that hoarding disorder afflicts between 2 and
6% of the current population and affects men and women equally (Timpano et al., 2011;
Nordsletten et al., 2013).
Individuals with hoarding disorder may often try to organise their possessions, but their lack of
organisational skills simply makes the chaos worse. The disorder is particularly associated with
an inability to throw away even normally disposable items such as food and sweet wrappings. If
the individual has other, more classic, OCD symptoms this can compound the problem. For
example, fear of contamination and superstitious thoughts (e.g., ‘throwing something away will
result in a catastrophe of some kind’) may prevent the sufferer from touching or throwing away
items. However, the accumulation of clutter in hoarding disorder is not simply something that is
tolerated by the individual, the hoarding causes clinically significant distress and has a
significant impact on social and occupational functioning.
Hoarding appears to begin in childhood or adolescence, with a chronic and progressive course
throughout the lifespan. This means that many sufferers of hoarding disorder are elderly, and it
is often comorbid with dementia and other psychiatric diagnoses such as major depression,
social phobia, and inattentive attention deficit/hyperactivity disorder (ADHD) (Frost, Steketee
& Tolin, 2011). Hoarding disorder can also be restricted to collecting and hoarding individual
types of items. Animal hoarding is one recently identified example that can lead to considerable
animal suffering and neglect (Patronek, 1999; Frost, Patronek, & Rosenfield, 2011).

Interestingly, one group of individuals who often possess a number of these cognitive deficits are those
with a diagnosis of autism spectrum disorder (ASD) (see Chapter 17), and apart from being associated
with social and communication deficits, repetitive behaviours are also a diagnostic feature of autism
spectrum disorder. Studies suggest that around 37% of children with ASD also suffer diagnosable OCD
symptoms (de Bruin, Ferdinand, Meester, Nijs, & Verheij, 2007; Leyfer et al., 2006), and there are
moderate correlations between measures of autism and measures of OCD (Wakabayashi, Baron‐
Cohen, & Ashwin, 2012). However, there are differences between the types of symptoms exhibited by
individuals with autism and those with a single diagnosis of OCD, and individuals with ASD tend to
exhibit higher levels of touching/tapping/rubbing, repetitive self‐injury, hoarding, ordering, and
repeating compulsions (Ruta, Mugno, D'Arrigo, Vitiello, & Mazzone, 2010). This relationship between
symptoms in OCD and ASD has led some researchers to suggest that there may be a symptoms overlap
between ASD and OCD (Wakabayashi, Baron‐Cohen, & Ashwin, 2012) or that ASD may be a clinically
important feature of many people diagnosed with OCD (Bejerot, 2007). Interestingly, both individuals
with ASD and OCD tend to exhibit executive function deficits and a preference for local rather than
global information processing, with the possibility that these characteristics may represent a risk factor
for OCD symptoms in both groups (Savage, Baer, & Keuthen, 1999).
Finally, despite difficulties in interpreting many of the studies that have linked cognitive and brain
deficits with OCD, there is one brain area that has been regularly associated with OCD. This is the
basal ganglia. The basal ganglia is made up of a series of structures deep in the brain, including the
striatum, the globus pallidus, the substantia nigra, the nucleus accumbens, and the subthalamic nucleus.
When all the structures in the basal ganglia are functioning properly, they are believed to contribute to
voluntary planning of actions and habit formation. Attention was first drawn to the basal ganglia when
it was found that individuals with a condition known to affect the basal ganglia (such as Huntington's
disease and Parkinson's disease) were shown to be at significant risk for OCD. In addition, lesions to that
area of the basal ganglia called the striatum resulted in behaviours similar to those seen in OCD
sufferers, such as stereotyped activities with highly patterned compulsive and obsessive behaviour
(Laplane et al., 1989; Gunaydin & Kreitzer, 2016). However, rather than this being the result of a
localised abnormality in the basal ganglia, it is possible that it's the cortico‐basal ganglia neurocircuitry
itself that's dysfunctioning. This pathway links the basal ganglia with cortical brain regions that are
involved in decision‐making and may be responsible for developing smooth sequences of behaviour. A
problem in this pathway would therefore lead to disjointed sequences of behaviours very much like the
overcontrolled and ritualised chains of behaviour seen in many OCD sufferers.

Psychological factors

Memory deficits
‘Doubting’ is a central feature of OCD, especially the compulsions associated with the disorder. As a
result, it has been suggested that OCD may be characterised by memory deficits that give rise to the
doubting that, for example, doors have been locked or hands have been washed properly. Memory
deficit models take a number of different forms. It has been suggested that OCD sufferers may have:
A general memory deficit (Sher, Mann, & Frost, 1984)
Less confidence in the validity of their memories (Watts, 1993)
A deficit in the ability to distinguish between the memory of real and imagined actions (Brown,
Kosslyn, Breiter, Baer, & Jenike, 1994).
However, evidence supporting the role of these memory deficits in OCD is equivocal (Hermans et al.,
2008), and more recent theoretical views suggest that the deficits that give rise to OCD “doubting” may
not be problems with memory or working memory per se, but are the result of a deficit in executive
functioning in general (Harkin & Kessler, 2011). For example, if OCD sufferers spend a lot of time
checking both relevant and irrelevant things on a daily basis, this will overload executive processes and
result in poor encoding of information and poor attention to relevant information, which in turn will
cause memory deficits. This is consistent with another body of evidence which suggests that lack of
confidence in recall may be a consequence of compulsive checking or washing rather than a cause of it
(van den Hout & Kindt, 2003; Harkin & Kessler, 2011; Radomsky & Alcolado, 2010). In effect, the
more someone checks, the less confident they will be about what they have checked (see Hezel &
McNally, 2016, for a brief review of memory biases in OCD).

Clinical constructs and OCD

Clinical psychology researchers regularly use their clinical experience as a starting point for
understanding the causes of a disorder, from this experience they develop what are known as clinical
constructs, and the purpose of these constructs is to link thoughts, beliefs, and cognitive processes to
subsequent symptoms. These constructs can be developed in such a way that they can be objectively
measured (e.g., with questionnaires) and in many cases manipulated experimentally. This then provides
an insight into how symptoms are affected by the cognitive factors that clinicians observe in their
everyday practice. In this section we briefly look at the role of three clinical constructs that have helped
us to understand OCD. These are inflated responsibility, thought‐action fusion(TAF), and
mental contamination.

clinical constructs Clinical psychology researchers develop constructs in order to describe

the combination of thoughts, beliefs, cognitive processes and symptoms observed in individual
psychopathologies

inflated responsibility The belief that one has power to bring about or prevent subjectively
crucial negative outcomes. These outcomes are perceived as essential to prevent. They may be
actual: that is, having consequences in the real world, and/or at a moral level.
 mental contamination Feelings of dirtiness can be provoked without any physical contact
with a contaminant. Mental contamination can be caused by images, thoughts, and memories
and may be associated with compulsive washing and even betrayal experiences.

thought‐action fusion A defence mechanism used by individuals with obsessive thoughts to

actively suppress them (using either thought suppression or distraction techniques).

Inflated responsibility
Everyone experiences uncontrollable intrusive thoughts on almost a daily basis (Rachman & DeSilva,
1978). However, what differentiates these normal intrusive thoughts from the distressing and obsessive
thoughts experienced in OCD is the meaning attached to them by OCD sufferers. Individuals
diagnosed with OCD appear to have developed a series of dysfunctional beliefs about their obsessional
thoughts. For example:
1. Because they had the thought, they feel responsible for its content—so, if a sufferer thinks of
murdering their child, they believe they may be going crazy and will murder their child (Salkovskis,
1985),
2. Sufferers appraise obsessional thoughts as having potentially harmful consequences and this causes
intense anxiety and triggers compulsive actions designed to eradicate the thought or to make sure
the perceived harm does not occur (e.g., compulsive thought suppression strategies such as
counting backwards or checking and re‐checking locks and windows to ensure that the home is
safe),
3. Individuals with OCD tend to have inflated conceptions of their own responsibility for preventing
harm, and this inflated responsibility appears to be an important vulnerability factor in developing
OCD (Salkovskis, 1985; Rachman, 1998).
Salkovskis et al. (1996) have defined inflated responsibility as ‘the belief that one has power which is
pivotal to bring about or prevent subjectively crucial negative outcomes. These outcomes are perceived
as essential to prevent. They may be actual, that is having consequences in the real world, and/or at a
moral level’. There is considerable evidence that inflated responsibility is a characteristic that is a central
causal feature of OCD generally (Salkovskis, Shafran, Rachman, & Freeston, 1999; Salkovskis et al.,
2000) and compulsive checking specifically (Rachman, 2002; Bouchard, Rheaume, & Ladouceur, 1999).
Experimental studies that have manipulated inflated responsibility have shown that it causes increases in
perseverative activities such as compulsive checking (Lopatka & Rachman, 1995; Bouchard, Rheaume,
& Ladouceur, 1999).

Thought‐action fusion
It is a common clinical experience that many individuals with OCD believe that their unpleasant,
unacceptable thoughts can influence events in the world. For example, if they have an intrusive thought
about an airplane crashing, they believe this may cause an airplane to crash. If they have a thought
about becoming ill, they believe this makes it more likely that they will become ill. This is known as
thought‐action fusion (TAF) (Shafran & Rachman, 2004), and it is a belief that simply having thoughts
can in some way directly affect what happens in the world. If the supposed consequences of thoughts
are aversive or negative, then this will cause the sufferer to try to suppress these thoughts (see section on
thought suppression), and it will generate considerable distress and anxiety. Interestingly, TAF will be
related to the degree to which an individual assigns importance to thoughts, and this is something that
has been identified as making religiosity a risk factor for OCD (see Section on Diagnosis and
Prevalence). It is not clear why some individuals hold these significant views about thoughts, but they
may have developed more general metacognitive beliefs that ‘thoughts are dangerous’ or ‘thoughts must
be controlled’ which give rise to obsessive thoughts and to the development of compulsions (Hezel,
Stewart, Riemann, & McNally, 2019), and these negative beliefs about thoughts may even be precursors
to more complex beliefs related to inflated responsibility for preventing harm (Amir, Freshman, Ramsey,
Neary, & Brigidi, 2001).

Mental contamination
While there are a significant number of OCD sufferers who fear actual contamination (e.g., by contact
with dirt, germs, etc.), there is also another group for whom comparable feelings of dirtiness can be
provoked without any physical contact with a contaminant, and this has come to be called mental
contamination (Rachman, 2004, 2006). Mental contamination can be caused by images, thoughts, and
memories, and tends to be caused by a violation of some kind by another person, e.g., degradation,
betrayal, emotional abuse, physical abuse, or humiliation which give rise to feelings of dirtiness or
pollution and in many cases may be associated with compulsive washing or cleansing (Zysk, Shafran, &
Williams, 2018; Rachman, 2010). In addition to these feelings of contamination, individuals also
experience anxiety, disgust, shame, anger, guilt, and sadness (Rachman, Radomsky, Elliot, & Zysk,
2012). While mental contamination seems to represent a very specific form of OCD contamination fear
that is caused by quite specific experiences, it is possible to ameliorate the symptoms using adaptations
of standard CBT interventions (Warnock‐Parkes, Salkovskis, & Rachman, 2012) (Focus Point 6.6).

Thought suppression
Because individuals with obsessive thoughts find these intrusions aversive and distressing, they may try
to actively suppress them (using either thought suppression or distraction techniques). However, there is
good evidence that actively suppressing an unwanted thought will actually cause it to occur more
frequently once the period of suppression or inhibition is over (known as a ‘rebound’ effect) (Figure 6.5),
and this may account to some degree for the fact that OCD sufferers experience significantly more
intrusions than nonclinical populations (Wenzlaff & Wegner, 2000). Wenzlaff, Wegner, and Klein (1991)
have also argued that suppressing an unpleasant thought induces a strong negative emotional state that
results in the suppressed thought becoming associated with that negative mood state. Whenever that
negative mood state occurs in the future, it is therefore more likely to elicit the unwanted and aversive
thought, and this may also contribute to the OCD sufferer experiencing regular, uncontrollable
intrusions (see Abbott & Norton, 2019, for a recent review of the thought suppression paradigm and its
relevance to mental health problems).

FOCUS POINT 6.6 DISGUST AND CONTAMINATION FEARS

IN OCD
Around half of all individuals diagnosed with OCD have significant contamination fears,
including obsessions related to dirt and disease, and have developed compulsions and rituals
around cleanliness (Rachman, 2004). However, while anxiety is an obvious emotion that drives
these obsessions and compulsions, one other central feature of these contamination‐based fears
is the disease‐avoidance emotion of disgust.
The disgust emotion is described as a specially evolved natural defensive emotion whose
primary biological function is to protect the individual specifically against pathogens, illness,
disease, and contamination (Davey, 2011; Tybur, Lieberman, Kurzban, & DeScioli, 2013), and
studies have demonstrated a significant positive correlation between obsessive‐compulsive
contamination fears and disgust proneness (Olatunji, Ebesutani, David, Fan, & McGrath,
2011). The main features of the disgust emotion are (a) a distinctive, universal facial expression
involving a wrinkling of the nose and down‐turning of the corners of the mouth that would
facilitate the ejection of bitter substances or poisons from the mouth; (b) feelings of revulsion
and nausea; (c) fear of contagion; and (d) physical avoidance of ‘disgusting’ objects. These are
all reactions that can potentially serve to prevent contact with pathogens or sources of illness,
disease, and contamination and—in more specific cases—to prevent the oral incorporation of
items that might potentially be causes of illness and disease.
Being oversensitive to the emotion of disgust (and so being oversensitive to disgusting stimuli
such as faeces, mucus, vomit, and other vehicles of disease and illness) may be a significant risk
factor for developing OCD contamination fears, and measures of disgust sensitivity have been
shown to predict subsequent OCD symptoms (Olatunji & Sawchuk, 2005), and facilitate
avoidance behaviour (Goetz, Lee, Cougle, & Turkel, 2013). Because of this apparent causal role
of disgust proneness in the development of OCD contamination fears, it has become important
to consider decreasing disgust proneness during treatment for contamination fears. For
example, decreasing disgust proneness predicts decreases in obsessive‐compulsive washing
symptoms (Athey et al., 2015), and individuals with high levels of disgust sensitivity exhibit the
worst treatment outcomes (Andersson et al., 2015). Taken together, this evidence suggests that
targeting disgust during exposure‐based treatment for OC contamination fears is likely to be a
key component of successful treatment.
FIGURE 6.5 After listening to a tape of a recorded story, participants were then asked to verbalise their stream of
conscious. However, participants in one group (Group A) were asked to suppress their thoughts of the tape during this
period, while other participants were not (Groups B and C). In the final period, all participants were asked to think about
anything. The figure shows that participants in the suppression condition subsequently reported more thoughts about the tape
than participants in the other groups (a ‘rebound’ effect).
After Clark, Ball, & Pape, (1991).

Family accommodation and excessive reassurance seeking

Family functioning is often compromised when one or more individual in the family has a diagnosis of
OCD, mainly because families of individuals with OCD are often more involved with the condition
than relatives of individuals with other forms of mental health problem, and this adds a significant
burden to the lives of those carers and family members associated with an OCD sufferer (Stewart et al.,
2017). Family accommodation refers to those family responses that are specifically related to OCD
symptoms, and encompasses behaviours such as directly participating in compulsions and rituals,
helping the sufferer to avoid triggers that may precipitate obsessions and compulsions, and assisting a
relative with OCD‐related behaviours while they are performing these behaviours (e.g., ensuring that
the individual with OCD is ‘correctly’ taking a shower without touching anything ‘dirty’ or potentially
‘contaminating’; having to pass towels to the patient, taking particular care that they do not touch
‘contaminated’ surfaces, etc.) (Albert, Baffa, & Maina, 2017). Family accommodation is very common in
OCD and is associated with the maintenance of more severe OCD symptoms in the sufferer and with
poorer treatment outcomes to the point where recent studies have identified the reduction of family
accommodation as a key component to include in therapy (Lebowitz & Omer, 2013).
A phenomenon closely associated with family accommodation is excessive reassurance seeking.
Excessive reassurance seeking is the repeated solicitation of safety‐related information from carers or
family members despite having already received it (Kobori, Salkovskis, Read, Lounes, & Wong, 2012),
and it can be considered as compulsive checking by proxy that transfers responsibility from the OCD
sufferer to others. It can take an overt form (‘Do you think these dishes are clean enough?’) or a more
covert form through the use of subtle statements (‘Surely its fine for us to leave the house and go on our
trip now without checking for our passports again’). It is a form of checking by proxy that becomes
particularly ritualised and is reinforced by the anxiety relief that it affords. However, such behaviour can
impair recovery from OCD because the sufferer begins to feel dependent on others for anxiety relief, it
diffuses responsibility away from the sufferer, and it is an additional form of checking that may need to
be directly addressed during treatment (Parrish & Radomsky, 2010).

Perseveration and the role of mood

OCD is one example of a number of perseverative psychopathologies, each of which is characterised by
the dysfunctional perseveration of certain thoughts, behaviours, or activities (others include pathological
worrying and chronic rumination in depression). In almost all examples of these psychopathologies the
perseveration (e.g., compulsive checking, washing) is viewed as excessive, out of proportion to the
functional purpose that it serves, and a source of emotional discomfort for the individual concerned. In
this context, some theories have attempted to explain why OCD sufferers persevere at an activity for
significantly longer than nonsufferers. One such account is the mood‐as‐input hypothesis (Meeten
& Davey, 2011; Davey, 2006; MacDonald & Davey, 2005). This model states that OCD sufferers
persevere with their compulsive activities because they use an implicit goal‐directed ‘stop rule’ for the
compulsive activity which says they must only stop when they are sure they have completed the task fully
and properly (known as an ‘as many as can’ stop rule); and they undertake the task in a strong negative
mood (usually an anxious mood). The mood‐as‐input account claims that OCD sufferers use their
concurrent mood as ‘information’ to assess whether they have met their strict stop rule criteria.
However, their endemic negative mood is interpreted as providing information that they have not
completed the task properly—so they persevere (i.e., a negative mood implies all is not well and the
criteria have not been met). This model is supported by the fact that the inflated responsibility that
OCD sufferers possess is likely to give rise to deployed ‘as many as can’ stop rules (to ensure that, for
example, checking or washing is done properly so that no harm will ensue). Interestingly, and consistent
with the mood‐as‐input account, inflated responsibility is not a sufficient condition for an individual to
persevere at a compulsive activity—it has to be accompanied by negative mood (MacDonald & Davey,
2005). This is because a negative mood is continually being interpreted as providing feedback that the
important goals of the compulsive activity have not been met, so the activity needs to be continued.

Summary
As we mentioned at the outset of this section on aetiology, many of these theories are designed to
address only specific features of OCD rather than represent universal explanations of the disorder. For
example, some theories try to explain why ‘doubting’ is a central feature of OCD (these include both
neurophysiological and memory deficit models), others address why intrusive thoughts become so
aversive and uncontrollable (e.g., inflated responsibility and thought suppression accounts), and yet
others try to explain why individuals with OCD show dysfunctional perseveration at activities such as
checking or washing (e.g., the mood‐as‐input model). Undoubtedly, a full account of OCD will contain
at least some, if not all, of these different elements of explanation. (Clinical psychologists Amita Jassi
and Gazal Jones talk to freelance journalist Jo Carlowe about OCD and its treatment in a podcast at
https://soundcloud.com/user‐664361280/in‐conversation‐ocd‐with‐dr‐amita‐jassi‐dr‐gazal‐jones).
6.6.4 The Treatment of Obsessive‐Compulsive Disorder

Problems in treating OCD

OCD is a slow‐onset disorder where symptoms increase only gradually over a number of years, and
having lived with subclinical symptoms for many years many sufferers fail to seek help when the
symptoms become well established. There is typically an astonishing average interval of 11 years
between a sufferer meeting the diagnostic criteria for OCD and receiving treatment (Pinto, Mancebo,
Eisen, Pagano, & Rasmussen, 2006). This can be attributed to the slow onset and also to the stigma
associated with unusual and excessive compulsive behaviour preventing people seeking professional
help. However, OCD sufferers can find it difficult to contemplate the loss of their compulsions and
many view their symptoms as a way of life. As a consequence they either resist seeking help, or
frequently fail to complete the therapies they've entered. OCD is undoubtedly a very resilient disorder.
Without treatment, remission rates are low, and only 20% of those with diagnosable OCD symptoms
have fully recovered from the disorder up to 20 years later (Bloch et al., 2013). Even when those with a
diagnosis of OCD do seek help, at the end of treatments such as CBT only around half have recovered
to a point where they no longer meet diagnostic criteria (Öst, Havnen, Hansen, & Kvale, 2015). The
reasons for this seemingly high failure rate are complex. Around 15% refuse therapy, another 15% of
treatment starters drop out before they have completed the therapy (Leeuwerik, Cavanagh, & Strauss,
2019), and many others fail to complete the behavioural tasks their treatment requires of them.

Exposure and ritual prevention treatments (ERP)

The most common, and arguably the most successful, treatment for OCD is exposure and ritual
prevention (ERP, also known as exposure and response prevention) (Kyrios, 2003; Hezel & Simpson,
2019). This therapy consists of two components. The first is graded exposure to the situations and
thoughts that trigger distress—e.g., for someone with compulsive washing this may involve touching a
dirty dish or imagining touching a dirty dish (the latter is called imaginal exposure) (see Treatment in
Practice 6.6). Clients will encounter their triggers in a graded and planned way until distress levels have
significantly decreased. The second component is ritual or response prevention, which involves
strategies such as practicing competing behaviours, habit reversal, or modification of compulsive rituals
(see Treatment in Practice 6.6). Preventing the client from engaging in their rituals:
1. allows anxiety to extinguish by habituating the links between obsessions and their associated
distress,
2. eliminates ritualistic behaviours that may negatively reinforce anxiety (Steketee, 1993),
3. contributes to the disconfirmation of dysfunctional beliefs (e.g., ‘I will catch an infectious disease if
I touch a dirty cup’) by forcing the client to encounter feared situations and experiencing the reality
of the outcomes associated with that action.

TREATMENT IN PRACTICE 6.6 EXPOSURE HIERARCHIES

AND RESPONSE PREVENTION IN ERP TREATMENTS OF
OCD

Arguably the most effective therapies for OCD are Exposure & Ritual Prevention
Therapies (ERP) (see Section 6.6.4). The first table gives examples of a graded exposure
regime for fear of contamination from germs and distressing thoughts about sexual abuse. The
second provides some examples of response prevention techniques.
 Exposure & Ritual Prevention Therapies A means of treatment for
obsessivecompulsive disorder (OCD) which involves graded exposure to the thoughts
that trigger distress, followed by the development of behaviours designed to prevent the
individual’s compulsive rituals

Example 1: Fear of Example 2. Teacher's distressing intrusive thoughts about

contamination sexually abusing students (distress level/100)
(distress level/100)
1. Touch rim of own 1. Watch video or listen to audio tape of expert discussing sexual
unwashed coffee cup abuse of children (40)
(30)
2. Touch rim of 2. Listen to tape of expert while looking at class photo (50)
partner's unwashed
coffee cup (40)
3. Eat snack from dish 3. Listen to loop tape of own distressing thoughts about sexually
in cupboard after abusing students in general (60)
touching partner's
unwashed coffee cup
(45)
4. Drink water from 4. Listen to loop tape about students in general looking at class photo
partner's glass (55) (65)
5. Eat snack straight 5. Listen to loop tape of distressing thought about sexually abusing
from unwashed specific student (70)
tabletop (65)
6. Have coffee at a café 6. Listen to loop tape about specific student looking at class photo (75)
(70)
7. Have meal at a 7. Listen to loop tape holding specific student's homework (80)
restaurant (80)
8. Touch toilet seat at 8. Stand in front of class repeating statement on loop tape to self (90)
home without washing
hands for 15 mins. (85)
9. Touch toilet seat at 9. Stand close to specific student repeating statement on loop tape to
home without washing self (95)
hands for 30 mins. (90)
10. Using public toilet 10. Stand next to specific student repeating statement on loop tape to
(100) self (100)
OCD symptom Response prevention strategy
Hand‐washing or Response delay (i.e., extending period between ‘contamination’ and
cleaning rituals cleaning or washing); use of ritual restrictions (e.g., decreasing
cleaning or washing time); clenching fists; extension strategies to
undermine avoidance (e.g., touch self, clothes, etc.)
Checking lights, Response delay; use of ritual restrictions (e.g., restrict number of
switches, oven, checks); turning and walking away; extension strategies (whistle a
appliances, etc. happy tune)
Counting (e.g., bricks, Refocusing techniques; singing a song; going ‘blank’; meditation
words, etc.)
 From Kyrios, (2003).

ERP is a highly flexible therapy that can be adapted to group, self‐help, inpatient, outpatient, family
therapy, mindfulness (Strauss et al., 2018), cognitive therapy (Rector, Richter, Katz, & Leybman, 2018),
Acceptance and Commitment Therapy (ACT) (Twohig et al., 2018), and computer‐guided interventions
(Fischer, Himle, & Hanna, 1998; Grayson, 1999; Wetzel, Bents, & Florin, 1999; Hand, 1998; Grunes,
1999; Nakagawa et al., 2000).

Cognitive behaviour therapy (CBT)

Although ERP has been the treatment of choice for OCD for over 20 years, it is often a difficult
treatment for many sufferers to enter. This is because sufferers may feel unable to expose themselves to
their fear triggers and find it very challenging when trying to prevent themselves acting out their rituals.
An alternative form of therapy for such individuals is CBT based on targeting and modifying the
dysfunctional beliefs that OCD sufferers hold about their fears, thoughts, and the significance of their
rituals (Abramowitz, Brigidi, & Roche, 2001; Salkovskis, 1999; Wilhelm, 2000; Marks, 2003; see Section
6.3.3—Inflated Responsibility). Dysfunctional beliefs that are usually challenged in cognitive therapy for
OCD include:
Responsibility appraisals, where the sufferer believes they are solely responsible for preventing any
harmful outcomes,
Overimportance of thoughts, where sufferers believe that having a thought about an action is like
performing the action (thought‐action fusion) (see Treatment in Practice 6.6),
Exaggerated perception of threat, where the sufferer has highly inflated estimates of the likelihood of
harmful outcomes (Van Oppen & Arntz, 1994).
An integrated cognitive therapy for OCD would thus consist of:
Educating clients that intrusive thoughts are quite normal, and that having a thought about an
action is not the same as performing it (Salkovskis, 1999),
Focusing on changing the client's abnormal risk assessment—perhaps by working through the
probabilities associated with feared outcomes (Van Oppen & Arntz, 1994),
Providing the client with behavioural exercises that will disconfirm their dysfunctional beliefs (e.g.,
a client who fears shouting out blasphemous thoughts in church would be asked to go to church
and see if this happens) (Salkovskis, 1999).
Cognitive therapy of this kind is often used in conjunction with exposure‐based therapy (ERP) and this
can improve tolerance of distress, ameliorate symptom‐related dysfunctional beliefs, aid adherence to
treatment, and reduce dropout (McKay et al., 2015).

Pharmacological and neurosurgical treatments

Pharmacological treatments can be a beneficial and cost‐effective way of treating OCD for many
sufferers, although relapse tends to be common on discontinuation of the drug treatment (McDonough,
2003; Pato, Zohar‐Kadouch, Zohar, & Murphy, 1998). The tricyclic antidepressant clomipramine and
serotonin reuptake inhibitors (SSRIs) are the most commonly prescribed drugs for OCD (see Chapter 4,
Section 4.1.1) and have greater effects on symptoms than drug placebo controls (Skapinakis et al., 2016).
However, there is still no consensus view on a model of serotonin dysfunction in OCD (e.g., Delgado &
Moreno, 1998), and this issue is confounded by the fact that increases in serotonin neurotransmitter
synthesis is a consequence of symptom improvement regardless of whether this was a result of SSRI
administration or psychological therapy (CBT) (Lissemore et al., 2018)—one interpretation of this is
that increased serotonin synthesis may simply be an indicator of recovery regardless of the type of
intervention used. Tricyclic antidepressants can have beneficial effects across some specific symptoms of
OCD (such as reducing the persistence and frequency of compulsive rituals), but may have their effect
only when OCD is comorbid with depression (Hohagen et al., 1998). Comparative studies have
suggested that both SSRIs and tricyclic drugs are less effective than standard psychological therapies
such as ERP (Rauch & Jenike, 1998; Greist, 1998), but that a combination of psychological and
pharmacological interventions is likely to be most effective, particularly where OCD symptoms are
severe (Skapinakis et al., 2016).
When pharmacological and psychological treatments have failed, neurosurgery has become an
intervention of last resort in OCD. The most common procedure is cingulatomy, which involves
destroying cells in the cingulum, close to the corpus callosum (Brown et al., 2016). These treatments do
report some improvement in OCD symptoms in 45–70% of clients who undergo this procedure
(Dougherty et al., 2002; Bourne et al., 2013), but there is a lack of evidence on the longer‐term gains of
neurosurgical treatments and their possible side‐effects (McDonough, 2003).

SELF‐TEST QUESTIONS
Can you describe what obsessions and compulsions are, and provide some examples of each?
How have biological theories attempted to explain the obsessions and compulsions found
in OCD?
How does the construct of ‘inflated responsibility’ help to explain how OCD is acquired
and maintained?
What are the similarities and differences between exposure & ritual prevention treatment
(ERP) and cognitive behaviour therapy (CBT) for OCD?
 SECTION SUMMARY

6.6 OBSESSIVE‐COMPULSIVE DISORDER

OCD is characterised by either obsessions—which are intrusive and recurring thoughts
that the individual finds disturbing and uncontrollable, or compulsions—which are
ritualised behaviour patterns that the individual feels driven to perform in order to reduce
their anxiety and prevent some negative outcome happening.
Common compulsions include washing, checking, and the systematic arrangement of
objects. Related compulsions include hoarding, hair pulling (trichotillomania) and skin
picking.
OCD onset is usually gradual and has a lifetime prevalence rate of around 2.5%.
Biological theories of OCD argue that there is both a genetic component to OCD and
some cognitive deficits that may make it difficult for the individual to inhibit habitual
behaviour patterns.
Psychological theories of OCD argue that cognitive factors such as inflated responsibility,
thought‐action fusion, and mental contamination may generate and mediate the important
symptoms of the disorder.
Factors such as family accommodation and excessive reassurance seeking can also act to
maintain symptoms and lead to poorer treatment outcomes
ERP treatments are the most common, and arguably the most successful, means of
treatment for OCD. These involve graded exposure to the thoughts that trigger distress,
followed by the development of behaviours designed to prevent the individual's compulsive
rituals.
The tricyclic antidepressant clomipramine and serotonin reuptake inhibitors (SSRIs) are
the most commonly prescribed drugs for OCD and have greater effects on symptoms than
drug placebo controls.

6.7 TRAUMA AND STRESS‐RELATED DISORDERS

In this section we explore trauma‐ and stress‐related disorders. In DSM‐5 these forms of disorder are
now listed separately from anxiety disorders, but the major diagnostic category in this section remains
post‐traumatic stress disorder (PTSD). There is still considerable debate about whether PTSD
should be considered an anxiety disorder, a stress‐induced fear response, a dissociative disorder (see
Chapter 14, Section 14.1.4 for a discussion of PTSD, dissociative disorders, and ‘complex PTSD’), or a
trauma and stressor related disorder, but acknowledgement that its primary precipitating cause is a
traumatic experience has led to PTSD being placed in its own broader diagnostic category (Friedman et
al., 2011) (The Client's Perspective 6.2).

post‐traumatic stress disorder(PTSD) A set of persistent anxiety-based symptoms that

occurs after experiencing or witnessing an extremely fear-evoking or life-threatening traumatic
event.
6.7.1 Diagnosis and Prevalence of Trauma and Stress‐Related Disorders
The DSM‐5 diagnostic criteria for PTSD and acute stress disorder are provided in Tables 6.12 and
6.13. PTSD is one of the few disorders in DSM‐5 in which the cause of the disorder is a defining factor.
In this case, diagnosis of PTSD is considered only if the individual has experienced an extreme trauma
prior to symptoms. They may have (a) directly experienced the trauma (e.g., been involved in a natural
disaster such as an earthquake or fire, or been subjected to life‐threatening physical abuse such as rape),
(b) witnessed a traumatic event in which others may have suffered (e.g., witnessing a terrorist attack), (c)
learnt that a severe traumatic event has happened to a close family member or friend, or (d) been
subjected repeatedly to distressing details of trauma (e.g., the kind of regular exposure to details of
trauma that might be experienced by police officers or emergency workers). The symptoms typical of
PTSD are grouped into four categories. These are (a) intrusive symptoms such as flashbacks,
intrusive thoughts, or physiological reactions; (b) avoidance responding such as active avoidance of
thoughts, memories or reminders of the trauma; (c) negative changes in cognition and mood such as
persistent fear, horror, anger, guilt or shame, persistent negative beliefs about themselves, others or the
world (e.g., ‘no one can be trusted’, ‘I've lost my soul forever’), or dissociative feelings of detachment or
estrangement from others; and (d) increased arousal and reactivity such as hypervigilance and
exaggerated startle responses.

THE CLIENT'S PERSPECTIVE 6.2 POST‐TRAUMATIC

STRESS DISORDER

‘It's been 8 months since my experience and I still deal with these feelings. I'm doing a lot better
but throughout the week, I can feel myself getting worse and worse until I breakdown. The
worst part is the irritability and rage I have inside of me. I don't know why I'm so mad at life
but the littlest things will set me off. I don't have the “flashbacks” anymore…just the feelings I
had when I was going through the ordeal. It's a very dark and depressing place and it's getting
harder to come out of it each time it happens. I almost feel blinded and out of control when I
get these attacks. It scares me to think of what I'm capable of doing. The worst part about this
is that I don't know what triggers these feelings. I can be fine all day and then my mood will
change for the worst. I generally feel very depressed and it's hard to deal with at times. Just
when I think I don't have to worry about it anymore, it hits ten times harder. I've tried just
about every remedy there is. I've seen four therapists and have been on three SSRIs…all of
which made me worse. I feel very discouraged with life. I don't know if this even has to do with
PTSD because I thought I was over it.’
From http://www.healthboards.com

Clinical Commentary:
This description is typical of many PTSD sufferers and highlights feelings of depression, lack of control
and anger. Some theories of PTSD (such as ‘Mental Defeat’) emphasise that those who develop PTSD
after a severe trauma tend to view themselves as a victim, process all information about the trauma
negatively, and view themselves as unable to act effectively. Such individuals believe they are unable to
influence their own fate and do not have the necessary skills to protect themselves from future trauma.
Ehlers and Clark (2000) suggest that such individuals only partially process their memory of the
trauma because of their perceived lack of control over it, and so they do not integrate that event fully into
their own autobiographical knowledge.
Once symptoms develop, PTSD is often a chronic condition that can last for years (Perkonigg et al.,
2005). It can also have significant social consequences such as marital problems, physical illness, sexual
dysfunction, substance abuse, suicidal thoughts, and stress‐related violence, as well as suicidal thoughts
and self‐harm. The kinds of traumatic events that precipitate PTSD are usually life threatening in their
severity. Studies suggest that PTSD symptoms are reported by up to 90% of rape victims (Chivers‐
Wilson, 2006), between 70 and 90% of torture victims (Moisander & Edston, 2003), over 50% of
prisoners of war (POWs) (Engdahl, Dikel, Eberly, & Blank, 1997), between 20 and 28% of earthquake
and flood survivors (Basoglu, Kilic, Salcioglu, & Livanou, 2004; Dai et al., 2016), and around 15% of
motor vehicle accident victims (Bryant & Harvey, 1998). DSM‐5 also emphasises that PTSD symptoms
can be acquired in cases where the stressor has not been life threatening to the sufferer (e.g., suffering
PTSD after the loss of a loved one—Breslau, Holmes, Carlson, & Pelton, 1998) or has involved simply
viewing stressful images of life‐threatening traumas (e.g., watching images of the 9/11 terrorist attacks
on TV—Piotrowski & Brannen, 2002), and this extension of the diagnostic criteria for PTSD has
generated controversy, either because it makes the symptoms of PTSD easier to fake in those who might
benefit financially from a diagnosis (Rosen, 2004) or because it confuses PTSD with merely
experiencing stress (McNally, 2003).
TABLE 6.12 Summary: DSM‐5 Criteria for the Diagnosis of PTSD

The individual has been exposed to or threatened with death, serious injury, or sexual violation:
by direct experience or by witnessing a traumatic event; upon learning about a violent or
accidental death of a close friend or family member; or by extreme or repeated exposure to the
effects of a traumatic event, such as emergency workers encountering human remains
Intrusive symptoms associated with the traumatic event will be experienced, such as disturbing
dreams or feeling that the event is recurring while awake; uncontrolled memories of the event;
extreme physical reactions or mental distress upon being reminded of the trauma
Individuals will avoid internal and/or external reminders of the trauma
At least two changes to mood or thought processes will occur, such as feelings of disconnection,
continual negative emotions and ongoing difficulty in experiencing positive emotions, extreme
and disproportionate negative expectations; reduced interest in activities, being unable to
remember certain aspects of the traumatic event
Changes to reactive behaviour will occur, and individuals will display two or more of the
following symptoms: recklessness, aggression, hypervigilance, inability to concentrate, difficulty
sleeping, an exaggerated startle response
Symptoms began or worsened after the traumatic event(s) and continued for at least 1 month,
causing significant difficulty in functioning
Symptoms cannot be explained by the effects of other mental or medical disorders, drug abuse, or
medication
Prevalence rates for PTSD vary considerably between countries, with prevalence in European countries
ranging between 0.56% and 6.6% in the general population (Wittchen et al., 2011)—findings which at
least in part may be explained by the different probabilities of experiencing trauma as a result of factors
such as the social or political conditions existing in different countries (Burri & Maercker, 2014).
Prevalence rates also differ for groups who are at risk of experiencing severe trauma. These include a
12–33% prevalence rate for civilians living in war zones (Farhood & Dimassi, 2012; Charlson et al.,
2012), 10% for rescue workers (Berger et al., 2012), and 13.2% for members of operational infantry in
the recent Iraq and Afghanistan conflicts (Kok, Herrell, Thomas, & Hoge, 2012). Around 50% of adults
experience at least one event in their lifetime that might qualify as a PTSD‐causing trauma (Ozer &
Weiss, 2004). Following such events, women are significantly more likely than men to develop PTSD (by
a factor of 2.4 : 1), and this is not explained simply by differences in the perceived threat to life from the
experience (Holbrook, Hoyt, Stein, & Sieber, 2002). Apart from gender differences in prevalence rates,
there is also some emerging evidence on the role that cultural variables play in PTSD. Ethnic groups
can differ quite significantly in the prevalence of PTSD ‐ Caucasian disaster victims show lower
prevalence rates than Latinos or African Americans—and these differences cannot be entirely explained
simply by differences in the frequency of exposure to traumatic experiences (Perilla, Norris, & Lavizzo,
2002; Norris, Perilla, Ibanez, & Murphy, 2001). The fact that around 50% of the population will
experience at least one event in their life that could be classified as a PTSD‐relevant trauma means that
many people experience trauma but do not develop PTSD. It is understanding these individual
differences in susceptibility to PTSD that will give us some insight into the mechanisms that give rise to
PTSD.
TABLE 6.13 Summary: DSM‐5 Criteria for the Diagnosis of Acute Stress Disorder
The individual has been exposed to or threatened with death, serious injury, or sexual violation: by
direct experience or by witnessing a traumatic event; upon learning about a violent or accidental death
of a close friend or family member; or by extreme or repeated exposure to the effects of a traumatic
event. At least nine of the following symptoms will be displayed:
Recurrent, intrusive, and involuntary memories of the traumatic event
Repeated distressing dreams related to the traumatic event or feeling that the event is recurring
while awake
Extreme physical reactions or mental distress upon being reminded of the trauma
Numbness or detachment from others
Changes in the individual's sense of reality and an altered perspective of oneself or one's
surroundings
Difficulty in remembering aspects of the traumatic event
Avoidance of internal and/or external reminders of the trauma
Difficulties in sleeping
Hypervigilance
Irritability or aggression
Difficulty in concentrating
Exaggerated startle response

Symptoms may begin within 3 days to 1 month of the trauma taking place and will persist for at least
3 days or up to 1 month
Symptoms cannot be explained by the effects of other mental or medical disorders, drug abuse, or
medication
Symptoms cause difficulties in performing important functions and cause clinically significant distress
The symptoms of acute stress disorder are very similar to those of PTSD, but the duration is much
shorter (3 days to 1 month after trauma exposure). DSM‐5 criteria have been explicitly modified to
make ASD symptoms much more compatible with PTSD, and so ASD may well be a diagnostic
category that predicts subsequent PTSD—but that remains to be determined. There has been some
prior debate about whether ASD actually represents a psychological disorder as such, or whether it is a
normal short‐term psychological and physical reaction to severe trauma (Harvey & Bryant, 2002).
However, with the diagnostic criteria for ASD in DSM‐5 shifting significantly towards that of PTSD, it
remains to be seen whether fewer post‐trauma survivors are diagnosed with ASD as were with DSM‐
IV‐TR criteria.
 acute stress disorder A short-term psychological and physical reaction to severe trauma.
Symptoms are very similar to those of PTSD, but the duration is much shorter (3 days to 1
month after trauma exposure).

6.7.2 The Aetiology of Post‐Traumatic Stress Disorder

The diagnostic criteria for PTSD specify either a life‐threatening trauma or severe stress as a causal
factor in the disorder. However, not everyone who has these kinds of experiences develops PTSD. This
is the main challenge for any theory of the aetiology of PTSD—why do some people develop PTSD
symptoms after these experiences, but not others? The answer must lie either in psychological or
biological vulnerability factors, or in the psychological strategies that individuals have developed to deal
with events like trauma and stress (e.g., differences in learnt coping strategies). Also, because PTSD has
many different symptom features, some theories address specific features of the symptomatology (e.g.,
the flashbacks), and others address the time course of the disorder and how it is emotionally
experienced (Brewin & Holmes, 2003). We explore these various possibilities when we look at some of
the main models of the aetiology of PTSD.

Biological factors
Family and twin studies suggest that PTSD has a genetic element to it, and a heritability component in
the range of 30–50% has been estimated (Smoller, 2016). More recent molecular genetic research has
examined the ways in which traumatic experiences may impact gene expression through the process of
epigenetics (see Chapter 1, Section 1.3.1). Thus, certain inherited genes may only be expressed
following trauma, and this makes those who have inherited these genes and have experienced trauma
vulnerable to PTSD symptoms (Sheerin, Lind, Bountress, Nugent, & Amstraster, 2017).
One inherited factor that may make some individuals vulnerable to PTSD symptoms is the level of
corticosteroid hormones normally secreted from the adrenal glands following a stressful experience.
Those who go on to develop PTSD symptoms—especially intrusive vivid memories—have been found
to have significantly lower cortisol levels immediately after the traumatic experience than individuals
who do not develop PTSD (Delahanty, Raimonde, & Spoonster, 2000). This is important because high
levels of cortisol can interfere with the laying down of memories of trauma, so low levels of cortisol will
do the opposite and result in the overconsolidation of traumatic memories (Chou, La Marca, Steptoe, &
Brewin, 2014)—an over‐consolidation that retains the vivid detail of the experience and retains this
detail over a long period of time. Even more intriguing is the finding that low levels of cortisol in
pregnant mothers who experience trauma and develop PTSD can also be passed on to their unborn
children through the process of epigenetics (Yehuda, Teicher, Secki, Grossman, & Morris, 2007). That is,
the trauma experience doesn't affect DNA sequences as such but does affect gene activity by switching
specific genes ‘on’ or ‘off ’, and some of this chemically altered activity is inherited from one generation
to another.
Other studies have identified the hippocampus as a brain area linked to PTSD. For example, the
hippocampus is that region of the brain that plays a critical role in memories related to emotion and
also plays a central role in regulating stress hormones such as cortisol. Studies have indicated that this
region is significantly smaller in individuals who develop PTSD (Logue et al., 2018) and a smaller
hippocampus represents a real risk factor for the development of PTSD following a traumatic
experience (Gilbertson et al., 2002). The implications of this are that a smaller hippocampus may make
the regulation of stress hormones less efficient and may also make it more difficult to coordinate
emotional memories such that it can become difficult for the individual to locate emotional memories in
space, time, and context. As a result, the soldier who witnessed friends and comrades die on a hill in
Afghanistan may feel the same extreme emotions experienced during that event when seeing any hill—
even after returning home.

Vulnerability factors
As not everyone who experiences a life‐threatening trauma develops PTSD, there must be factors that
make some people more vulnerable than others. A number of factors have been identified that
characterise those individuals likely to develop PTSD after trauma, which include:
A tendency to take personal responsibility for the traumatic event and the misfortunes of others
involved in the event (Mikhliner & Solomon, 1988),
Developmental factors such as early separation from parents or an unstable family life during early
childhood (King et al., 1996)
Personality factors such as neuroticism, hypochondriasis, and paranoia (DiGangi et al., 2013)
An emotion‐focussed, avoidant or negative coping style (Constans et al., 2012)
A family history of PTSD (Foy et al., 1987),
Existing high levels of anxiety or a preexisting psychological disorder (Breslau et al., 1997).
Interestingly, lower IQ and lower cognitive ability generally increased risk of PTSD (Vasterling et al.,
2002; Betts, Williams. Najman, Bor, & Alati, 2012), and high IQ is the best predictor of resistance to the
development of PTSD (Silva et al., 2000). This may be because there is a link between IQ level and the
development of coping strategies to deal with experienced trauma or stress. Other important predictors
of PTSD development are the experiences reported by trauma victims at the time of the trauma. These
include the reporting of dissociative symptoms at the time of the trauma (see below) and a belief that
one is about to die (McNally, 2003). These types of experiences may be important in that they may
relate to how the individual processes and stores information about the trauma at the time, and this is
important in some specific theories of PTSD symptoms.

Avoidance and dissociation

After any distressing and traumatic experience, how the individual copes with that experience will be
critical to their subsequent psychological health. One coping style that is not conducive to a beneficial
outcome is avoidance coping, and individuals who avoid thinking about their trauma are more likely to
develop PTSD following a traumatic experience (Sharkansky et al., 2000). One psychological process
that seems to be used to enable individuals to detach and distance themselves from trauma is
dissociation (see Chapter 14). Dissociation is the feeling that one is detached from both mind and
body and is associated with an inability to recall important personal information of a stressful nature,
and in the context of PTSD, dissociation may represent an avoidant strategy for coping or confronting
painful or stressful memories. In particular, dissociation seems to be an important risk factor for PTSD.
Individuals who experience dissociation either just before or during the trauma are more likely to
develop PTSD (Ehlers, Mayou, & Bryant, 1998), those who use dissociation as a coping strategy after
the trauma are at risk of chronic long‐term PTSD symptoms (Briere, Scott, & Weathers, 2005), and
those with a history of trauma such as childhood abuse are more likely to develop PTSD, possibly
because they have already developed dissociation as an avoidant coping strategy for traumatic
experiences (Wolf et al., 2012)(see Section 14.1.4 in Chapter 14 for a discussion of the relationship
between PTSD and dissociative experiences).

Conditioning theory
Because there is always an identifiable traumatic experience in the history of PTSD, it is quite
reasonable to suppose that many of the symptoms of PTSD may be due to classical conditioning (see
Chapter 1, Section 1.3.2). That is, trauma (the UCS) becomes associated at the time of the trauma with
situational cues associated with the place and time of the trauma (the CS) (Keane, Zimering, & Caddell,
1985). When these cues (or similar cues) are encountered in the future, they elicit the arousal and fear
that was experienced during the trauma. For example, seeing a pile of bricks on the ground may elicit
strong arousal, fear, and startle responses for an earthquake survivor, because such cues had become
associated with the fear experienced during the traumatic earthquake experience. The conditioning
model would further argue that such conditioned fear responses do not extinguish because the sufferer
develops both cognitive and physical avoidance responses which distract them from fully processing such
cues and therefore does not allow the associations between cues and trauma to extinguish. The
reduction in fear resulting from these avoidance responses reinforces those responses and maintains
PTSD symptoms. There is probably an element of classical conditioning in the development of PTSD,
largely because formally neutral cues do come to elicit PTSD symptoms. There is also evidence that
individuals suffering PTSD will more readily develop CRs in laboratory‐based experiments than
nonsufferers (Orr et al., 2000). However, classical conditioning does not provide a full explanation of
PTSD. It does not explain why some individuals who experience trauma develop PTSD and others do
not, and it cannot easily explain the range of symptoms that are peculiar to PTSD and rarely found in
other anxiety disorders, such as reexperiencing symptoms, dissociative experiences, etc.

Emotional processing theory

Foa et al. (1989) have suggested that the intense nature of the trauma in PTSD creates a representation
of the trauma in memory that becomes strongly associated with other contextual details of the event
(e.g., if a person has been badly injured in a serious traffic accident, cues to do with roads, cars,
hospitals, and even traveling generally will come to selectively activate the fear network in memory).
The avoidance of any contexts that might activate this fear network means that there is little
opportunity for the PTSD sufferer to weaken these associations between fear and the everyday cues that
will activate that fear. This account has elements in common with classical conditioning models of
PTSD, but it differs in some significant ways. First, emotional processing theory claims that severe
traumatic experiences are of such major significance to the individual that they lead to the formation of
representations and associations in memory that are quite different to those formed as a result of
everyday experience. For example, if severe trauma has become associated with certain cues (e.g., after
being assaulted in an alleyway) this experience will now override any other positive associations formed
as a result of previous experience with that cue (the alleyway). Second, severe trauma not only results in
cues eliciting very strong fear responses, it also changes the individual's previous assumptions about how
safe the world is, so many more cues than previously will come to elicit responses related to fear, startle,
and hypervigilance (Foa & Rothbaum, 1998).
The emotional processing theory is an example of those theories of PTSD that have attempted to
include explanations about how fear responses are learned, stored, and triggered and about how the
traumatic event changes the individuals assumptions and beliefs about themselves and the world. These
types of theories have come to be known as information‐processing models because they specify how
fear memories are laid down and activated in fear networks. They have also given rise to some successful
therapeutic procedures for PTSD which address how the fear network resulting from traumatic
experience can be modified (Foa & Rothbaum, 1998).

‘Mental defeat’
Ehlers and Clark (2000) have suggested that there is a specific psychological factor that is important in
making an individual vulnerable to PTSD. This is a specific frame of mind called ‘mental defeat’, in
which the individual sees themselves as a victim: they process all information about the trauma
negatively, and view themselves as unable to act effectively. This negative approach to the traumatic
event and its consequences simply adds to the distress, influences the way the individual recalls the
trauma, and may give rise to maladaptive behavioural and cognitive strategies that maintain the
disorder. In effect, these individuals believe they are unable to influence their own fate and do not have
the necessary skills to protect themselves from future trauma. Ehlers and Clark suggest that such
individuals only partially process their memory of the trauma because of their perceived lack of control
over it, and so they do not integrate that event fully into their own autobiographical knowledge. This
leads to symptoms such as reexperiencing the trauma in the present (outside of a temporal context),
difficulty in recalling events from the trauma, and dissociation between the experience of fear responses
and their meaning. The ‘mental defeat’ model is supported by evidence suggesting that PTSD sufferers
do indeed have negative views of the self and the world, including negative interpretations of the
trauma (Dunmore, Clark, & Ehlers, 1999), negative interpretations of PTSD symptoms (Clohessy &
Ehlers, 1999; Mayou, Bryant, & Ehlers, 2001), negative interpretations of the responses of others
(Dunmore, Clark, & Ehlers, 1999), and a belief that the trauma has permanently changed their life
(Dunmore, Clark, & Ehlers, 1999; Ehlers, Maercker, & Boos, 2000). Importantly, mental defeat has been
identified as a critical risk factor for PTSD after just a single traumatic experience or even after multiple
traumatisations (as experienced by Ugandan rebel war survivors) (Wilker et al., 2017), suggesting that it
is still a significant factor in the development of PTSD even after an individual has experienced multiple
traumas.

mental defeat A specific frame of mind in which the individual sees themselves as a victim.
This is a psychological factor that is important in making an individual vulnerable to PTSD.

Dual representation theory

A rather different approach to explaining PTSD, called dual representation theory, is that it may be a
hybrid disorder consisting of the involvement of two separate memory systems (Brewin, 2001; Brewin,
Dalgleish, & Joseph, 1996). The ‘verbally accessible memory’ (VAM) system registers memories of
the trauma that are consciously processed at the time. These memories are narrative in nature and
contain information about the event, its context, and personal evaluations of the experience. They are
integrated with other autobiographical memories and can be readily retrieved. The “situationally
accessible memory’ (SAM) system, however, records information from the trauma that may have
been too brief to apprehend or take in consciously, and this includes information about sights and
sounds and extreme bodily reactions to trauma. The SAM system is thus responsible for the vivid,
uncontrollable flashbacks experienced by PTSD sufferers that are difficult to communicate to others
(because these memories are not stored in a narrative form). There is good neuropsychological evidence
for the existence of these two separate memory systems and their links with the brain centre associated
with fear (the amygdala) (Brewin, 2001). There is also evidence that is consistent with predictions from
the dual representation theory. For example, Hellawell & Brewin (2004) found that, when describing
their memories, PTSD sufferers characterised flashback periods with greater use of detail, particularly
perceptual detail, by more mentions of death, more use of the present tense, and more mention of fear,
helplessness, and horror. In contrast, ordinary memories were characterised by more mention of
secondary emotions such as guilt and anger. These findings are consistent with the view that flashbacks
are the result of sensory and response information stored in the SAM system. However, while dual
representation theory provides useful insights into the development of PTSD flashbacks in
particular, it is still a work in progress, with the theory having to be adjusted to take account of new
findings from cognitive neuroscience studies of these different forms of memory systems (Pearson, Ross,
& Webster, 2012; Brewin & Burgess, 2014).

dual representation theory An approach to explaining post-traumatic stress disorder

(PTSD) suggesting that it may be a hybrid disorder involving two separate memory systems.
Summary
Once again, it is clear that PTSD has a number of different features, each of which requires
explanation. Some theories have tried to explain some of the specific features of PTSD (such as Dual
Representation Theory's attempt to explain specific features such as flashbacks), while others have tried
to identify the dispositional features that make some individuals vulnerable to developing PTSD while
others do not (e.g., ‘Mental Defeat’). Others attempt to describe why severe trauma causes the symptoms
that it does, and why these anxiety‐based symptoms persist for such long periods (e.g., conditioning
theory and emotional processing theory).

emotional processing theory Theory that claims that severe traumatic experiences are of
such major significance to an individual that they lead to the formation of representations and
associations in memory that are quite different to those formed as a result of everyday
experience.

6.7.3 The Treatment of Post‐Traumatic Stress Disorder

The treatment of PTSD has two main aims. The first is to try to prevent the development of PTSD
after an individual has experienced a severe trauma. The second is to treat the symptoms of PTSD once
these symptoms have developed.
Rapid psychological debriefing has usually been the accepted way of trying to intervene
immediately after trauma in order to try to prevent the development of PTSD, although there is now
some doubt about whether this kind of rapid intervention provides any therapeutic gains.

psychological debriefing A structured way of trying to intervene immediately after trauma

in order to try to prevent the development of PTSD.

Once symptoms have developed, most psychological therapies either rely on some form of exposure
therapy (usually involving the client imagining events during their traumatic experience) in an attempt
to extinguish fear symptoms, or adopt other treatments that focus on the client's trauma memories or
their meanings, and international treatment guidelines have recommended trauma‐focused
psychological treatments as the first‐line treatment for PTSD (Ehlers et al., 2010). Therapies that possess
this exposure element include imaginal flooding, eye movement desensitisation and reprocessing
(EMDR), and cognitive restructuring, but there is an ever‐expanding set of emerging treatments for
PTSD (see Cukor, Spitalnick, Difede, Rizzo, & Rothbaum, 2009), which meta‐analyses suggest may all
be equally effective in treating PTSD symptoms (Benish, Imel, & Wampold, 2008), and which contain
additional elements helping to address factors such as self‐blame, to reduce guilt, bolster effective
problem‐solving coping, and improve emotional regulation (e.g., Kulkani, Barrard, & Cloitre, 2014;
Tran et al., 2016).

Psychological debriefing
Over the past 30 years or so there has been a growing belief amongst mental health professionals that
PTSD can be prevented by immediate and rapid debriefing of trauma victims within 24–72 hr after the
traumatic event (Caplan, 1964; Bisson, 2003). The exact form of the intervention can vary, with the
most widely used techniques referred to as crisis intervention or critical incident stress
management(CISM) (Everly, Flannery, & Mitchell, 2000). The purpose of these interventions is to
ensure the participants that they are normal people who have experienced an abnormal event, to
encourage them to review what has happened to them, to express their feelings about the event, and to
discuss and review support and coping strategies in the immediate post‐trauma period. Psychological
debriefing has been used with survivors, victims, relatives, emergency care workers, and providers of
mental health care (Bisson, 2003). The scale of this type of intervention can be gauged by reactions to
the terrorist attacks on the World Trade Centre on 9/11, when more than 9,000 counsellors went to
New York to offer immediate aid to victims and families of the attack (McNally, Bryant, & Ehlers, 2003).
Critical incident stress debriefing includes a number of components, including:

PHOTO 6.4 The psychological impact of the devastating Asian tsunami of December 2004 is difficult to calculate.
Over the past 20 years it was felt that immediate counseling of victims was the best way to prevent the development of
PTSD. However, more recent research has suggested that such immediate interventions may not be helpful, and in many
cases may impede natural recovery.
Explanation of the purpose of the intervention
Asking participants to describe their experiences
Discussion of the participants feelings about the event
Discussion of any trauma‐related symptoms the participant may be experiencing
Encouraging the participant to view their symptoms as normal reactions to trauma
Discussing the participant's needs for the future
As laudable as immediate professional help may seem in these circumstances, there is much criticism of
psychological debriefing and its value as an intervention for PTSD. First, it is not clear whether victims
will gain any benefit from being counselled by strangers and possibly ‘coerced’ into revealing thoughts
and memories that in the immediate wake of the trauma may be difficult to reveal. Second, many of
the survivors of severe trauma do not display symptoms of psychological disorders, nor will they
develop PTSD. Psychological debriefing techniques make little attempt to differentiate these survivors
from those who may genuinely need longer‐term guidance and treatment. Third, controlled
comparative studies that have attempted to evaluate the effects of psychological debriefing techniques
suggest there is little convincing evidence that debriefing reduces the incidence of PTSD—and indeed it
may in some cases impede natural recovery following trauma (Bisson, 2003; McNally, Bryant, & Ehlers,
2003). Most recent reviews of early psychological interventions for the prevention of PTSD suggest that
no psychological intervention can be recommended for routine use following traumatic events with
adults (Roberts, Kitchiner, Kenardy, & Bisson, 2009), or with children (National Institute for Health and
Care Excellence, 2018) (Photo 6.4).
Exposure therapies
Arguably the most effective form of treatment for PTSD is exposure therapy, in which the sufferer is
helped by the therapist to confront and experience events and stimuli relevant to their trauma and their
symptoms. Exposure‐based treatments are more effective than medications (Powers et al., 2010), and
have been found to result in therapeutic benefits that can persist over a minimum of 5‐years post‐
therapy (Foa & McLean, 2016). In vivo exposure involves the direct confrontation of feared objects,
activities, or situations by a person under the guidance of the therapist. For example, a woman with
PTSD who fears the location where she was assaulted may be assisted by her therapist in going to that
location and directly confronting those fears (as long as it is safe to do so).
Exposure therapy typically requires between 8 to 15 90‐minute sessions occurring either once or twice a
week (Foa & McLean, 2016), and the rationale behind exposure therapy is that (a) it will help to
extinguish associations between trauma cues and fear responses (Foa & Rothbaum, 1998), and (b) it will
help the individual to disconfirm any symptom‐maintaining dysfunctional beliefs that have developed
as a result of the trauma (e.g., ‘I can't handle any stress’) (Foa & Rauch, 2004). For the individual
suffering PTSD, exposure to their fear triggers is often a difficult step to take and exposure may even
make symptoms worse in the early stages of treatment (Keane, Gerardi, Quinn, & Litz, 1992). As a
result, up to a third of clients may drop out of treatment because of the need for them to re‐live their
experiences (Imel, Laska, Jakupcak, & Simpson, 2013). This being the case, exposure can be tackled in a
number of different forms—especially in various imaginal forms. This can be achieved (a) by asking the
client to provide a detailed written narrative of their traumatic experiences (Resick & Schnicke, 1992),
(b) with the assistance of virtual reality technology using computer‐generated imagery (Peskin et al.,
2019), or (c) by simply asking the client to visualise feared, trauma‐related scenes for extended periods of
time (known as imaginal flooding) (Keane, Fairbank, Caddell, & Zimering, 1989). Such imaginal
treatments are usually then supplemented with subsequent in vivo exposure that would require graded
exposure to real trauma‐related cues.

imaginal flooding A technique whereby a client is asked to visualise feared, traumarelated

scenes for extended periods of time.

A somewhat controversial form of exposure therapy for PTSD is known as Eye movement
desensitisation & reprocessing therapy (EMDR) (Shapiro, 1989, 1995). In this form of
treatment, the client is required to focus their attention on a traumatic image or memory while
simultaneously visually following the therapist's finger that is moving backwards and forwards in front of
their eyes. This continues until the client reports a significant decrease in anxiety to the image or
memory. The therapist then encourages the client to restructure the memory positively, by thinking
positive thoughts in relation to that image (e.g., ‘I can deal with this’). The rationale for this procedure is
that combining eye movements with attention to fearful images encourages rapid deconditioning and
restructuring of the feared image (Shapiro, 1995, 1999). There is evidence that EMDR is more effective
than no treatment, supportive listening and relaxation (McNally, 1999), but some studies have shown
that it has a higher relapse rate than CBT (Devilly & Spence, 1999). Nevertheless, recent reviews suggest
that EMDR is one of the most effective treatments for PTSD, despite its controversial status (Bradley,
Greene, Russ, Dutra, & Westen, 2005). Critics of EMDR argue that, although it does have some success
in treating the symptoms of PTSD, it is little more than just another form of exposure therapy.
However, experimental studies have demonstrated that the eye movement component of EMDR is
essential for successful treatment no matter how this might be achieved (e.g., up and down eye
movements are as effective as side to side movements) (Lee & Cuijpers, 2013). What does appear to be
important is that the eye movement task—however achieved—should tax working memory and so
weaken traumatic memories (van den Hout & Engelhard, 2012).
 Eye movement desensitisation & reprocessing therapy (EMDR) A form of exposure
therapy for PTSD in which clients are required to focus their attention on a traumatic image or
memory while simultaneously visually following the therapist’s finger moving backwards and
forwards before their eyes.

Cognitive restructuring
There are various forms of cognitive restructuring therapy for PTSD, but most attempt to help clients
do two things: evaluate and replace intrusive or negative automatic thoughts; and evaluate and change
dysfunctional beliefs about the world, themselves and their future that have developed as a result of the
trauma (Marks, Lovell, Noshirvani, Livanou, & Thrasher, 1998; Foa & Rothbaum, 1998). For example,
Foa & Rothbaum (1998) suggested that two basic dysfunctional beliefs mediate the development and
maintenance of PTSD. These are (a) ‘the world is a dangerous place’, and (b) ‘I am totally
incompetent’. Foa & Cahill (2001) argued that immediately after a severe trauma, all victims develop a
negative view of the world and themselves, but for most individuals these beliefs become disconfirmed
through daily experience. However, those who avoid trauma‐related thoughts will also avoid
disconfirming these extreme views and this will foster the development of chronic PTSD. While
exposure therapy alone may encourage experiences that disconfirm these dysfunctional beliefs, cognitive
therapists have proposed that procedures that directly attempt to alter PTSD‐related cognitions should
also be included in the treatment (Resick & Schnicke, 1992), and meta‐analyses that have compared
cognitive restructuring therapies and exposure therapies do not find that one approach necessarily
outperforms the other (Watkins, Sprang & Rothbaum, 2018).

SELF‐TEST QUESTIONS
Can you describe the main symptoms of PTSD and how they may differ from the
symptoms found in other anxiety disorders?
What are the diagnostic differences between PTSD and acute stress disorder?
Can you list some of the important risk factors for PTSD, and describe how they might
contribute to the development of PTSD?
We discussed four main theories of the aetiology of PTSD (conditioning theory, emotional
processing theory, ‘mental defeat’, and dual representation theory), can you describe the
main features of at least two of these and discuss their similarities and differences?
What are the main treatments for PTSD, and how have these been derived from theories
of the aetiology of PTSD?
 SECTION SUMMARY

6.7 TRAUMA AND STRESS‐RELATED DISORDERS

The diagnosis of PTSD is based on identifying exposure to a specific fear evoking, and
usually life‐threatening, event (e.g., being involved in a natural disaster, serious physical
assault, etc.).
Acute stress disorder is a short‐term psychological and physical reaction to severe trauma.
The main symptoms of PTSD include increased arousal, numbing of emotions, flashbacks
and the reexperiencing of the trauma.
The lifetime prevalence rates for PTSD vary between 0.5 and 6.6% in European
countries, but depend significantly on the social and political conditions in individual
countries (e.g., whether there is conflict or civil strife).
Vulnerability factors for PTSD include a tendency to take personal responsibility for the
event, developmental factors such as an unstable early family life, negative personality
factors, an avoidant or negative coping style, a family history of PTSD, and existing high
levels of anxiety or a pre‐existing psychological disorder.
There is no consensus on a specific psychological model of PTSD, and current
explanations include (a) classical conditioning, (b) emotional processing theory, (c) ‘mental
defeat’, and (d) dual representation theory.
Attempting to prevent the development of PTSD through the rapid and immediate
debriefing of trauma victims (Critical Incident Stress Debriefing) is now generally
acknowledged to be largely ineffective.
The most effective forms of treatment for PTSD are exposure therapies, where the sufferer
is helped by the therapist to confront and experience events and stimuli relevant to their
trauma. These may include imaginal flooding or EMDR, and graduated exposure
treatment can be supplemented with cognitive restructuring designed to evaluate and
change dysfunctional beliefs about the world.

6.8 ANXIETY‐BASED PROBLEMS REVIEWED

In this chapter we have reviewed six of the main anxiety‐based problems—specific phobia, SAD, panic
disorder, GAD, OCD, and trauma and stressed related problems such as post‐traumatic stress disorder
(PTSD). Common to all of these disorders is the intense experience of anxiety that the individual finds
distressing and which causes significant impairment in social, occupational, or other important areas of
functioning. However, anxiety manifests itself in many different ways in these different disorders—as
pathological worrying in GAD, as compulsive ritualised thoughts and actions in OCD, as physical panic
attacks in panic disorder, and the reexperiencing of trauma in PTSD. Many of these anxiety problems
are precipitated by periods of stress in a person's life (e.g., panic disorder, GAD, OCD), yet we do not
yet know why an individual who has experienced a period of life stress will develop one particular
disorder (e.g., OCD) rather than another (e.g., panic disorder). This will be an important issue for future
clinical research.
Just as the symptoms of these anxiety‐based problems are often quite different, so are the theories that
try to explain them, and there is certainly no single, unified theory that can convincingly explain the
development of anxiety‐based problems generally. However, there are some features that are common
to these different problems and these may provide some insight into how different anxiety‐based
problems develop. These features include the information‐processing and interpretational biases that
accompany most anxiety disorders, and also the dysfunctional beliefs that anxiety sufferers seem to form
which maintain their symptoms (e.g., the spider phobic's beliefs that spiders are threatening and
harmful, and the GAD sufferer's belief that worrying is an important and necessary activity to engage
in). These phenomena may eventually form the basis of a unified theory of anxiety‐based problems.

This book is accompanied by Student and Instructor companion websites.

www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter References
Videos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
7
Depression and Mood Disorders

ROUTE MAP OF THE CHAPTER

This chapter describes depression and mood disorders, their symptoms, theories of their
aetiology, and the main forms of treatment for these problems. The two main mood disorders
covered are major depression and bipolar disorder (characterised by periods of mania
alternating with periods of depression). The chapter covers a range of theories of depression
and mood disorders including biological theories and psychological theories. The section on
treatment looks at the way in which antidepressant drugs attempt to alleviate the symptoms of
depression, and how a number of psychological therapies have been developed to address the
cognitive and behavioural biases that characterise major depression. The chapter ends by
discussing two phenomena associated with mood disorders and depression in particular, namely
deliberate nonsuicidal self‐injury (NSSI) and suicide.

CHAPTER OUTLINE
7.1 MAJOR DEPRESSION
7.2 BIPOLAR DISORDER
7.3 THE TREATMENT OF DEPRESSION
7.4 NONSUICIDAL SELF-INJURY (NSSI)
7.5 SUICIDE
7.6 DEPRESSION AND MOOD DISORDERS REVIEWED
 LEARNING OUTCOMES
When you have completed this chapter, you should be able to:
1. Describe the characteristics and main diagnostic criteria of major depression and bipolar
disorder.
2. Compare and contrast at least two biological theories of the aetiology of depression and
mood disorders.
3. Compare and contrast at least two psychological theories of the aetiology of depression
and mood disorders.
4. Distinguish between biological and psychological theories of depression.
5. Describe and evaluate the role of cognitive factors in explaining the development of
depression.
6. Compare and contrast biological, behavioural, and cognitive therapies for depression and
mood disorders.
7. Summarise the main psychological characteristics of suicide and nonsuicidal self‐injury
(NSSI).

My name is Sally; I'm 36 and live with my partner and two young children in a small village. But about 6
months after my daughter Georgia was born I started to feel really low and was crying all the time. I stopped
eating and stopped going to the local parent and baby group or meeting up with my friends. I thought I wasn't a
good enough mum and would sit at home and dwell on all the reasons why I wasn't doing a good enough job.
Although my mood improved after a few months, it has recently become much worse and I am finding it difficult to
cope. Everyone else is coping well and I feel that I am completely useless.
Sally's Story

Introduction
In Sally's Story, her account of the experience of depression gives considerable insight into the various
disabling features of this psychological problem. These include the overwhelming feelings of sadness
and lethargy. Each day is as miserable as the next in an unrelenting cycle of emptiness, and Sally ends
up hardly ever experiencing pleasure or any positive emotion. Those suffering depression lack initiative
and often move and speak more slowly than nonsufferers (Sobin & Sackeim, 1997). They spend more
time alone and may spend long periods ruminating about their low mood and its causes. Episodes of
depression and low mood sometimes follow significant life events such as the birth of a child or may
follow a series of more day‐to‐day difficulties, but depression can also emerge for what appears to be no
good reason at all. Some people experience just a single episode of depression and recover relatively
quickly; others may endure chronic or recurrent depression that may cause problems for much of their
life. Beck (1967) described depression as a ‘paralysis of will’ in which individuals experience only
pessimism and hopelessness about their lives. This can often lead to suicidal thinking, and suicide often
feels like the only solution for many individuals suffering depression.
We all experience periods of depression in our lives, and we can often attribute these periods of
depression to specific events. Two types of events are particularly important in triggering periods of
depression: losses and failures. Experiences such as losing a job or the death of a loved one are likely to
trigger periods of sadness, lethargy, and rumination. Similarly, failures—such as failing an exam or
failing to persuade someone you like to date you—can also lead to periods of hopelessness and the
fostering of negative cognitions associated with pessimism and self‐doubt. Nevertheless, most of us can
shake off these feelings within a few days or weeks and get on productively with life. For others, however,
the symptoms of depression may linger and spread to all aspects of their lives—emotional, behavioural,
cognitive, and physical—and this can result in diagnosable bouts of depression that are debilitating
enough to prevent an individual from living normal day‐to‐day lives. In extreme cases, the symptoms of
depression can develop even without the occurrence of a precipitating life event, such as a loss or a
failure, and will often persist for much longer than would be expected following a loss such as a
bereavement.

Depression A mood disorder involving emotional, motivational, behavioural, physical and

cognitive symptoms.

Mania An emotion characterised by boundless, frenzied energy and feelings of euphoria.

bipolar disorder A psychological disorder characterised by periods of mania that alternate

with periods of depression.

Depression is the prominent emotion in mood disorders, but it can often be associated with its
opposite—namely mania. Mania is an emotion characterised by boundless, frenzied energy and
feelings of euphoria. As we shall see later, individuals who have a bipolar disorder frequently
oscillate between deep depression and frenetic mania.
Depression involves emotional, motivational, behavioural, physical, and cognitive symptoms. The
emotional experiences of depressed individuals are usually restricted to negative ones and these are often
described as ‘sad, hopeless, miserable, dejected, and discouraged’. Such individuals are often close to
tears and have frequent crying episodes. Only very rarely do depressed individuals report experiencing
pleasant or positive emotions, they often exhibit a loss of sense of humour and rarely display positive
facial expressions (Sloan, Strauss, & Wisner, 2001). Anxiety is also commonly experienced with
depression, which suggests that many sufferers may experience simultaneously a range of negative
emotions (Bakish, 1999) that may be reflective of a single underlying symptomatology. Depressed
individuals exhibit a range of motivational deficits, and these include a loss of interest in normal daily
activities or hobbies. They exhibit a lack of initiative and spontaneity, and frequently report ‘not caring
anymore’ and not getting pleasure from activities that they previously enjoyed. This lack of initiative
may manifest itself initially in social withdrawal (depressed individuals regularly report wanting to stay
where they are and to be left alone), and appetite and sexual desire can also be significantly reduced.
Depressed individuals exhibit a number of behavioural symptoms, including a slowness of speech and
behaviour generally (Joiner, 2002). They become physically inactive, stay in bed for long periods, and
reports of decreased energy, tiredness, and fatigue are common. Even the smallest of tasks seem to
require substantial physical exertion. Depression also has an embodied element to it. People who
experience depression also exhibit characteristic postures and movements that are an integral feature of
their depression experience, and the role of these embodiments is discussed more fully in Focus Point
7.1. Physical symptoms also include sleep disturbance such as middle insomnia (waking up during the
night and having difficulty getting back to sleep) and terminal insomnia (waking early and being unable
to return to sleep). In some cases, depression can be associated with oversleeping (hypersomnia), where
the individual indulges in increased daytime sleeping. Depressed individuals also report regular
headaches, indigestion, constipation, dizzy spells, and general pain (Fishbain, 2000).
Arguably the most disabling of the symptoms of depression are its cognitive features, and, as we shall see
later, many theories of depression view these cognitive symptoms as central and as factors that need to
be addressed in order to complete effective treatment. In particular, depressed individuals tend to have
developed extremely negative views of themselves, the world around them, and their own future (Beck,
1987; Strauss, 2019), and this generates pessimistic thinking where sufferers believe nothing can improve
their own lot. This in turn leads to a lack of initiative, with individuals reporting impaired ability to
think, concentrate or make decisions. This inability to affect the future also generates other problematic
beliefs, such as a sense of worthlessness, shame, and guilt. Because of this, many depressed individuals
develop the dysfunctional belief that others would be better off if they were dead, and this can often
lead to transient but recurrent suicidal thoughts (see Section 7.5)
There are two main types of clinical depression. The most common is major depression, and the
second is bipolar disorder. Major depression (sometimes known as unipolar depression) is one of
the most common of all the psychological problems and is characterised by relatively extended periods
of clinical depression that cause significant distress to the individual and impairment in social or
occupational functioning. Bipolar disorder is characterised by periods of mania that alternate with
periods of depression, and this leads individuals with bipolar disorder to describe their lives as an
‘emotional roller‐coaster’. Sufferers experience the extremes of these emotions in ways that cause
emotional discomfort and distress.

major depression A psychological problem characterised by relatively extended periods of

clinical depression which cause significant distress to the individual and impairment in social or
occupational functioning.

unipolar depression A psychological disorder characterised by relatively extended periods of

clinical depression that cause significant distress to the individual and impairment in social or
occupational functioning (see also major depression).

This chapter now discusses the diagnosis, prevalence, and aetiology of major depression, and then—in
Section 7.2—the diagnosis, prevalence, and aetiology of bipolar disorder.

FOCUS POINT 7.1 DEPRESSION, EMBODIMENT, AND THE

ROLE OF EXERCISE
 Most people will associate depression with an internal feeling that they would describe as sad,
lethargic, or empty, but recent evidence suggests that the experience of ‘depression’ also has an
embodied component. That is, there is a reciprocal relationship between bodily expression and
how an emotion is experienced and processed. For example, a report by Michalak et al. (2009)
describes how depressed patients exhibit embodied components of their experience in the form
of reduced walking speed and smaller amplitude of vertical movements of the upper body.
Similarly, hunched postures also elicit feelings of depression (Riskind & Gotay, 1982). These
embodiments are not just reflections of inner feelings; they comprise an integral part of the
depression experience because attempts to directly modify these postural features of depression
also relieve the experience of depression. In such an intervention, Michalak et al. (2010) found
that using mindfulness therapy to normalise gait patterns in depressed patients also helped to
relieve their depression experiences.
Many studies have also found that exercise can reduce depression severity in people with a
diagnosis of major depression (Rimer et al., 2012; Schuch & Stubbs, 2019)—including even
treatment‐resistant forms of depression (Mota‐Pereira et al., 2011), and exercise has also been
shown to be beneficial for older people suffering depression (Bridle, Spanjers, Patel, Atherton, &
Lamb, 2012). There are many reasons why a regular exercise programme may help alleviate
depressive symptoms. For example, exercise may help to eliminate poor postures that contribute
to the embodied depression experience; it can also decrease the incidence of cardiovascular
disease, hypertension, and type 2 diabetes (Powers, 2002)—all of which may enable better
psychosocial functioning and increase quality of life.

7.1 MAJOR DEPRESSION

7.1.1 The Diagnosis and Prevalence of Major Depression

The Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM‐5) introduced a number of
changes to the way in which major depression is categorised and diagnosed. It specifies the criteria for a
major depressive episode (which is not a codable disorder), which can be found in Table 7.1, and
then defines two main types of depressive disorder based on the criteria for a major depressive episode.
These disorders are major depressive disorder, single episode and major depressive
disorder, recurrent. A major depressive episode is defined by the presence of five or more depressive
symptoms during the same 2‐week period (Table 7.2). However, depression is often a normal reaction to
a number of life events (such as bereavement, financial problems, natural disasters, etc.), and for
depression to become clinically problematic a diagnosis of major depressive disorder requires the
presence of dysfunctional symptoms such as feelings of worthlessness, suicidal ideation, and impairment
of daily functioning. In addition, there has been much discussion about whether depression in response
to bereavement should be included as one of the criteria contributing to a diagnosis of major depressive
disorder and bereavement symptoms had been excluded prior to DSM‐5. However, recent research has
indicated that bereavement‐related depression is not significantly different from major depressive
disorder that presents in other contexts, it is most likely to occur in individuals with past histories of
major depressive disorder, and is also likely to be chronic and recurrent (Zisook et al., 2012). For these
reasons, bereavement‐related symptoms are now no longer excluded from the diagnostic criteria.

major depressive episode Episode of major depression, defined by the presence of five or
more depressive symptoms during the same 2-week period, as stated by the DSM-5.

TABLE 7.1 Summary: DSM‐5 criteria for a major depressive episode

At least five of the following are present, including either depressed mood or loss of interest:
Depressed mood most of the time
Less interest or enjoyment of most activities
Significant weight change not associated with dieting
Insomnia or excessive sleep
Excessive increase or reduction in physical movement
Substantial fatigue or lack of energy
Feelings of worthlessness or excessive or inappropriate guilt
Lack of concentration or ability to think or make decisions
Recurrent thoughts of death and suicide or suicide attempt
The symptoms are not better accounted for by schizoaffective disorder or other mental disorder
or due to the effects of a substance or other medical condition

TABLE 7.2 Summary: DSM‐5 criteria for major depressive disorder, single episode & recurrent
Major Depressive Disorder
Presence of a single major depressive episode (not attributable to normal and expected reactions
to bereavement, etc.) without previous manic or hypomanic episode where symptoms are not
better accounted for by other disorders
The symptoms must cause clinically significant distress or impairment in social, occupational, or
other forms of functioning.

Chronic mood disturbances primarily characterised by depressive symptoms can also be diagnosed,
although these conditions must have been apparent for at least 2 years, and would normally not be
severe enough to disrupt normal social and occupational functioning and warrant a diagnosis of major
depression. The most significant of these is dysthymic disorder, in which the sufferer has
experienced at least 2 years of depressed mood for more days than not. Individuals diagnosed with this
disorder experience many of the behavioural and cognitive characteristics of major depression, but
these are less severe (meeting only two or more of the symptom criteria for major depression) (Table
7.3).

dysthymic disorder A form of depression in which the sufferer has experienced at least 2
years of depressed mood for more days than not.
TABLE 7.3 Summary: DSM‐5 criteria for dysthymic disorder

Depressed mood most of the time for at least 2 years

Presence of at least two of the following:
Poor appetite or overeating
Lack of or excessive sleeping
Low levels of energy or fatigue
Low self‐esteem
Poor concentration or decision‐making abilities
Feelings of hopelessness
The symptoms are not due to the effects of a substance or other medical condition
However, diagnosing depression is a controversial issue for a number of reasons. First, DSM‐5 requires
the identification of five symptoms for a period of 2 weeks for a diagnosis of major depression. But are
such people any different in their experiences and their functioning from someone who exhibits only
three symptoms? Yet studies have suggested that individuals with three symptoms exhibit similar levels
of distress and problems with day‐to‐day living as individuals with five symptoms (Gotlib, Lewinsohn, &
Seeley, 1995).
Second, depression is one of the most prevalent of all psychological problems and is experienced in
some form or other by almost everyone at some time in their life. Indeed, experiencing depression is the
third most common reason for consulting a doctor or general practitioner (GP) in the UK (Singleton,
Bumpstead, O'Brien, Lee, & Meltzer, 2001). In order for doctors to be able to provide treatment for
such individuals, there is a tendency for them to over diagnose mild or moderate depression (Middleton,
Shaw, Hull, & Feder, 2005). This raises a number of issues, including the possible stigmatisation that
such a label might incur for the patient. In addition, lay beliefs about depression suggest that many
people already view depression as a ‘disease’ that is a consequence of everyday life stress (Lauber,
Falcato, Nordt, & Rossler, 2003). If lay people already view depression as a ‘disease’ or biological illness,
and medical doctors are more than willing to diagnose it, then we run the risk of the ‘medicalisation’ of
normal everyday negative emotions such as mild distress or even unhappiness (Shaw & Woodward,
2004).
Third, depression occurs in a variety of different guises within psychopathology and is commonly
comorbid with other important disorders (Kessler et al., 1996) (Table 7.4). This has given rise to a range
of different diagnosable disorders that have depression as a central feature within them. As a result,
major depression is a relatively ‘pure’ diagnosis where the cause of depression cannot be attributed
either to some other diagnosable disorder (such as the consequences of substance abuse) or to specific
biological, environmental factors or other life events (for example, such as postnatal depression).
Prominent examples of diagnosable problems which have depression as a significant core element
include premenstrual dysphoric disorder(PMDD), seasonal affective disorder(SAD), and
chronic fatigue syndrome (CFS or myalgic encephalomyelitis, ME), and these are discussed briefly
in Focus Point 7.2.

premenstrual dysphoric disorder (PMDD) A condition in which some women

experience severe depression symptoms between 5 and 11 days prior to the start of the
menstrual cycle. Symptoms then improve significantly within a few days after the onset of
menses.
 seasonal affective disorder (SAD) A condition of regularly occurring depressions in winter
with a remission the following spring or summer.

chronic fatigue syndrome (CFS) A disorder characterised by depression and mood

fluctuations together with physical symptoms such as extreme fatigue, muscle pain, chest pain,
headaches and noise and light sensitivity.

TABLE 7.4 Comorbidity of Major Depressive Disorder with Other DSM Disorders
After Kessler et al. (1996).

Lifetime comorbidity 12‐month comorbidity

% %
Anxiety disorders
Generalised anxiety disorder (GAD) 17.2 15.4
Agoraphobia 16.3 12.6
Specific phobia 24.3 23.7
Social phobia 27.1 20.0
Panic disorder 9.9 8.6
Post‐traumatic stress disorder (PTSD) 19.5 15.2
Any anxiety disorder 58.0 51.2
Substance use disorders
Alcohol dependence 23.5 13.0
Drug dependence 13.3 7.5
Alcohol abuse w/o dependence 4.1 1.4
Drug abuse w/o dependence 6.5 1.1
Any substance use disorder 38.6 18.5
Other disorders
Dysthymia 6.7 4.0
Conduct disorder 16.2 –
Aggregate number of disorders
One 24.7 58.9
>One 74.0 26.9
Two 17.4 15.4
>Three 31.9 16.5
Note that the lifetime comorbidity rate of major depression with another anxiety disorder is 58% and with more than
one other DSM disorder is 74%, suggesting that individuals with depression tend to experience a range of negative
emotions and comorbid disorders.
Finally, depression is highly comorbid with anxiety problems and around 60% of people with
depression will also experience an anxiety disorder (Moffitt et al., 2007). Mixed anxiety/depressive
disorder is used to describe a significant number of people who experience this mix of anxiety and
depression. It is associated with diagnosable levels of distress, impairment of daily living skills, and
reduced health‐related quality of life, but neither the depression nor the anxiety is clearly the
predominant feature (Möller et al., 2016). (around 8% of people with either depression or anxiety
symptoms meet the criteria for mixed/anxiety depressive disorder) (Zinbarg et al., 1994). This has led
some researchers to suggest that depression and anxiety are not truly independent disorders but
represent subcategories of a larger group of emotional disorders with symptoms that can often intermix
(e.g., Watson, 2005; see also Chapter 2, Section 2.1.4, Figure 2.2).
Depression is arguably the most prevalent of the psychopathologies that are covered in this book.
Estimates of lifetime prevalence rates for major depression in American community samples range from
5.2% to as high as 20.6% in recent epidemiological surveys (Hasin et al., 2018; Kessler et al., 1994;
Weissman et al., 1996), with studies showing the prevalence of diagnosable levels of depression
increasing significantly in the US between 2005 and 2015 especially for those in the youngest and oldest
age groups (Weinberger et al., 2017, see Figure 7.1). Similarly, in 2014 19.7% of people in the UK aged
16 or over showed symptoms of depression or anxiety—a 1.5% increase from 2013 (Evans, Macrory, &
Randall, 2016).
The lifetime risk for major depression may be as high as 20% for men and 30% for women (Kruijshaar
et al., 2005), and the World Health Organization (WHO) estimates that more than 264 million people
worldwide of all ages suffer from depression (WHO, 2020). However, gauging the prevalence of
depressive symptoms has been difficult because (a) prevalence rates appear to differ significantly across
different cultures (Kessler & Bromet, 2013), (b) the incidence of the diagnosis of depression has
increased steadily over the last 90 years, and (c) different studies have tended to use different diagnostic
tools when assessing prevalence. For example, studies conducted by the Crossnational Collaborative
Group reported very large cultural variations in the prevalence of major depression. These ranged
from 1.5% in Taiwan to 19.0% in Lebanon. Lifetime prevalence rates for Puerto Rico and Korea were
relatively low at 4.3% and 2.9% respectively compared to 10.2% for the US (Weissman et al., 1996).
Even in high‐income countries, prevalence rates can vary considerably, from 6.6% in Japan to 21.0% in
France (Kessler & Bromet, 2013). There appear to be a number of reasons for these large international
variations in lifetime prevalence rates. These include (a) the stigmatising of psychopathology in many
non‐Western societies, indicating that many individuals in those societies will be unwilling to report
symptoms of major depression (Compton et al., 1991), (b) higher levels of somatisation (the expression
of psychological distress in physical terms) in non‐Western countries (Simon, VonKorff, Piccinelli,
Fullerton, & Ormel, 1999), (c) the fact that—unlike many other psychopathologies (such as obesity and
hypertension)—depression cannot be observed or measured directly, so there will always be an element
of subjectivity in the way the symptoms are measured and recorded (Patten, 2003a), and (d) lifetime
prevalence rates will always be affected by recall problems, and recall failure with age appears to
account for the fact that lifetime prevalence rates often appear to decrease with increasing age cohorts
(Patten, 2003b).

FOCUS POINT 7.2 DEPRESSION‐RELATED PROBLEMS

SEASONAL AFFECTIVE DISORDER (SAD)

SAD is a condition of regularly occurring depressions in winter with a remission the following
spring or summer, and is a relatively common condition affecting 1–3% of adults in temperate
climates (Westrin & Lam, 2007). The main symptoms include depressed mood, lack of energy,
hypersomnia, craving for carbohydrates, overeating, and weight gain (Rosenthal & Blehar,
1989). There is some evidence that individuals who develop SAD do so because the longer
periods of darkness in winter increase their secretion of the hormone melatonin, which acts
to slow organisms down, making them sleepy and less energetic (Wetterberg, 1999). The answer
to this is to provide individuals suffering from SAD with light therapy or photo therapy in which
they are exposed to periods of artificial sunlight during the darker winter months (Magnusson &
Boivin, 2003; Reeves, Nijjar, et al., 2012).

melatonin A hormone that acts to slow organisms down, making them sleepy and less
energetic.

CHRONIC FATIGUE SYNDROME (CFS)

CFS is characterised by depression and mood fluctuations together with physical symptoms
such as extreme fatigue, muscle pain, chest pain, headaches, and noise and light sensitivity
(Yancey & Thomas, 2012). Its causes are unclear at present, and this may be the reason why it is
given a variety of names, including ‘yuppie flu’ because of its tendency to afflict predominantly
successful young people—especially women—struggling with stressful work and family
responsibilities (Ho‐Yen, 1990). About 75% of reported cases are adult White females
(Showalter, 1997), but this may simply reflect the reluctance of males to report such symptoms.
The causes of CFS have not been clearly identified, although theories have argued for the
involvement of viral or immunological factors (Behan, More, & Behan, 1991) and
environmental stressors such as pollution or organophosphates (Jason et al., 1995). Other
researchers have pointed out that depression can be identified as a risk factor in CFS, with a
predisposition among CFS sufferers to develop depression and to exhibit frequency of
depression prior to CFS onset at twice the level of controls (Straus et al., 1988). Interestingly,
studies that have provided cognitive behaviour therapy for adolescents with CFS have resulted
in significant decreases in fatigue severity and functional impairment, suggesting that addressing
psychological factors in CFS may play a significant role in successfully treating the syndrome
(Stulemeijer, de Jong, Fiselier, Hoogveld, & Bleijenberg, 2005).

PREMENSTRUAL DYSPHORIC DISORDER (PMDD)

PMDD is a condition in which some women will experience severe depression symptoms
between 5 and 11 days prior to the start of the menstrual cycle, but these symptoms then
improve significantly within a few days after the onset of menses. DSM‐5 notes that such
symptoms can cause significant distress and disruption to normal daily living and include
symptoms such as mood swings, irritability or anger, feelings of hopelessness, decreased interest
in usual activities, disruption of normal sleep patterns, lethargy, and food cravings. PMDD
affects between 2% and 5% of women during the years they experience menstrual periods
(Epperson et al., 2012) but can be successfully treated using healthy lifestyle management (e.g.,
adopting a balanced diet and taking regular exercise), antidepressant medication, or cognitive
behaviour therapy [CBT] (Kleinstauber, Witthoft, & Hiller, 2011).
FIGURE 7.1 The prevalence of past‐year depression between years 2005 and 2015 in the USA. (After Weinberger,
Gbedemah, Martinez, Nash, Galea & Goodwin, 2017)
The incidence of major depression has steadily increased since 1915 and median age of onset has
decreased to around 27 years in the US (Kessler, 2002). Most strikingly, women are almost twice as
vulnerable to periods of major depression as men (Nolen‐Hoeksema, 2002), and this is independent of
cultural background. Some of the factors that might contribute to this gender difference in vulnerability
to depression are discussed in Activity Box 7.1 on the book’s website.

7.1.2 The Aetiology of Depression and Mood Disorders

Risk factors for depression

We begin this section on aetiology by taking a very general look at the factors that put people at risk for
developing major depression. It is worth remembering that we experience depression because it has
probably evolved as an adaptive emotion that bestows survival benefits. For example, depression helps to
curb activity during periods of harsh weather such as winter (e.g., SAD) (Eagles, 2004) and is associated
with key immune responses to infection that are likely to enhance survival (Raison & Miller, 2013). In
this respect, the fact that periods of depression often follow experiences associated with loss (e.g.,
bereavement) and failure (resulting in loss of self‐esteem and confidence) can be viewed as a perfectly
normal and adaptive reaction to life's challenges, giving us time to regroup and recover to eventually
face the world again.
However, against this background of potential adaptive benefits of periodic depression, it can also
become a chronic distressing and disabling condition that in some cases may lead to an individual taking
their own lives. Bearing this in mind, it is important to determine whether there are significant
differences between the risk factors that lead to periods of depression (which may be part of a naturally
occurring process), and risk factors that lead to chronic, lifelong depression, and even suicide (see
Section 7.5.1). Challenging life experiences are frequently identified as risk factors for depression (see
Hammen, 2018). These include childhood maltreatment, especially in the form of emotional abuse and
neglect (Nelson, Klumparendt, Doebler, & Ehring, 2017); adverse psychosocial working conditions
characterised as job strain (Madsen et al., 2017); chronic stress occurring as a result of marital, parental,
financial, and occupational functioning (Hammen, 2016); and interpersonal difficulties such as
dysfunctional family functioning and difficulties socialising in childhood and adolescence (Conway,
Hamman, & Brennan, 2012). But some other risk factors appear to be independent of life challenges
generally, and these may represent examples of biologically, genetically, or psychologically mediated
risks, and these risk factors include being the offspring of a depressed mother (Goodman et al., 2011),
possessing negative information‐processing biases (Beck, 1967, see Negative Cognitions and Self‐
Schemas in Section 7.1.2), or being female (Kuehner, 2016). However, risk factors are important when it
comes to helping to identify people who may possibly be at risk for depression, but they tell us relatively
little about the actual causes of depression, and discovering the mechanisms that underlie the
development of depression is the purpose of more detailed research.

Biological theories

Genetic factors
There is good evidence that depressive symptoms run in families, and this suggests the possible existence
of an inherited or genetic component to major depression, and first‐degree relatives of major
depression sufferers are around two to three times more likely to develop depressive symptoms than are
individuals who are not first‐degree relatives of sufferers (Gershon et al., 1982; Maier et al., 1992).
Heritability based on twin studies can often vary considerably between studies, but meta‐analyses and
genome studies generally estimate heritability to be between 30% and 40% (Sullivan, Neale, & Kendler,
2000; Lubke et al., 2012), with adoption studies suggesting that the inherited component arises from
genetic factors with rearing experiences contributing to approximately an equal extent (Kendler,
Ohlsson, Sundquist, & Sundquist, 2017).
However, after 2 decades of genetic research the specific genes contributing to this inherited component
appear to be diverse—not least because major depression is a heterogeneous condition with a broad
range of symptoms. A recent genome‐wide meta‐analysis of depression identified 102 independent gene
variants and 269 genes associated with depression, including genes and gene pathways associated with
synaptic structure in the brain and factors associated with brain neurotransmitters (Howard et al., 2019)
Candidate genes that may be important include the serotonin transporter gene (SLC6A4) that can
enhance or terminate the action of the brain neurotransmitter serotonin (see next section on
Neurochemical Factors) (Clarke, Flint, Attwood, & Munafò, 2010; Levinson, 2006). However, there is
growing evidence that a gene such as the serotonin transporter gene may increase the risk of depression
only when it interacts with certain environmental risk factors, and risk factors that have been identified
include childhood maltreatment and serious interpersonal stressors (i.e., major events that primarily
affect the quality or quantity of one's interpersonal relationships) (Vrshek‐Schallhorn et al., 2014; Caspi
et al., 2003). So, just as with psychotic symptoms (see Chapter 8), there may be a diathesis–stress
relationship in depression between inherited genes and experienced stressors, such that severe
depression symptoms only develop when there is an interaction between a high‐risk inherited gene and
certain stressful life events.

Neurochemical factors
Depression and mood disorders have been shown to be reliably associated with abnormalities in the
levels of certain brain neurotransmitters, and three neurotransmitters are particularly significant—
namely the monoamines serotonin, norepinephrine and dopamine (Delgado & Moreno, 2000),
and major depression is often associated with low levels of these neurotransmitters. For example,
depression is associated with decreased serotonin transporter binding in the midbrain and amygdala
(Gryglewski, Lanzenberger, Kranz, & Cumming, 2014), and decreased 5‐HT1A receptor binding in
frontal, temporal, and limbic regions (Sargent et al., 2000), all suggesting that depression is associated
with some form of monoaminergic dysfunction. However, impaired monoamine pathway activity alone
is unlikely to be sufficient to cause depression, and studies that have experimentally manipulated
monoaminergic pathway activity have shown that this induces depression only in those people with
either a family history of depression or have suffered previous episodes of depression (Ruhé, Mason, &
Schene, 2007).
A number of factors led to findings about the importance of monoamines such as serotonin and
norepinephrine. First, in the 1950s it was noticed that many medications for high blood pressure also
caused depression (Ayd, 1956), and this effect was found to be the result of such medications decreasing
brain serotonin levels. The 1950s also saw the development of drugs that significantly alleviated the
symptoms of depression. The main ones were tricyclic drugs (such as imipramine) and monoamine
oxidase(MAO) inhibitors (such as trancylcypromine). Both of these drugs have their effects by
increasing levels of both serotonin and norepinephrine in the brain. These findings led to the
development of neurochemical theories of depression that argued that depression was caused by either
low norepinephrine activity (Bunney & Davis, 1965) or low serotonin activity (Golden & Gilmore, 1990).
Because these neurotransmitters are necessary for the successful transmission of impulses between
neurones, their abnormally low levels in depressed individuals may account for the cognitive,
behavioural, and motivational deficits found in major depression. In addition to abnormalities in
serotonin and norepinephrine levels, it is also believed that low levels of the neurotransmitter dopamine
might be involved in major depression (Naranjo, Tremblay, & Busto, 2001). Dopamine is significantly
involved in the reward systems in the brain, and so depleted dopamine levels may be responsible for
deficits in this system in depression giving rise to a lack of motivation, initiative, and pleasure (Treadway
& Zald, 2011).

tricyclic drugs Drugs which block the reuptake of both serotonin and norepinephrine.

The medications that are often prescribed for people suffering major depression are assumed to have
their beneficial effects by preventing the reuptake by the presynaptic neurone of neurotransmitters
serotonin and norepinephrine. This results in higher levels of these neurotransmitters in the synapse,
and this facilitates the transmission of impulses to the postsynaptic neurone—thus facilitating brain
activity. More recently, the development of selective serotonin reuptake inhibitors (SSRIs) (such
as fluoxetine) and serotonin‐noradrenaline reuptake inhibitors (such as Duloxetine) has allowed
researchers to assess the specific roles of serotonin and noradrenaline in depression, and researchers
now believe that serotonin levels in particular play a central role in major depression (Figure 7.2).
However, this picture is relatively simplistic, and more recent neurochemical theories of mood disorders
suggest that interactions between different neurotransmitters may be important. Some researchers
suggest that depression is associated more with an imbalance in neurotransmitters than with deficits in
specific neurotransmitters (Rampello, Nicoletti, & Nicoletti, 2000; Ressler & Nemeroff, 1999). Other
theorists have suggested that low levels of serotonin interact with levels of norepinephrine in rather
complex ways, such that combinations of low levels of both serotonin and norepinephrine produce
depression, but low levels of serotonin and high levels of norepinephrine result in mania (Mandell &
Knapp, 1979) (see also Chapter 4, Section 4.1.1 for a fuller discussion of how antidepressant
medications may have their effect on depression symptoms).
FIGURE 7.2 Neurones release the neurotransmitters serotonin and norepinephrine from their endings when they fire and
these help transmission between brain cells. Some of the neurotransmitter molecules are recaptured by the neurone using a re‐
uptake mechanism, and this can occur before they are received by the receptor neurone, thus weakening the transmission
between neurones. Both tricyclic drugs and SSRIs have their effect by blocking the reuptake of these neurotransmitters and so
ensure that neural transmission is more effective. Tricyclic drugs block the reuptake of both serotonin and norepinephrine,
while SSRIs selectively block the reuptake only of serotonin.

Brain abnormalities and depression

Recent developments in cognitive neuroscience together with the evolution of new technologies for
scanning and photographing the brain (e.g., magnetic resonance imaging, MRI, see Chapter 2, Section
2.2.4) have led to a greater understanding of the brain areas involved in depression and mood disorders
(Davidson, Pizzagalli, Nitschke, & Putnam, 2002). Studies have identified dysfunction or abnormalities
in a number of brain areas that appear to be associated with depression. These areas are the prefrontal
cortex, the anterior cingulate cortex(ACC), the basal ganglia, the hippocampus, and the amygdala
(e.g., Davidson et al., 2002; Disabato et al., 2016) (see Figure 7.3). This raises the question of the role
that such areas may play in relation to depression, and Davidson et al. (2002) have attempted to address
these issues. First, depression is associated with significantly lower levels of activation in the prefrontal
cortex (Drevets, 1998), and this area is important in maintaining representations of goals and the
means to achieve them. Decreased activation in this area may result in the failure to anticipate
incentives that is a common feature of depression. Second, decreased ACC activation is also reported in
major depression (Beauregard et al., 1998). Evidence suggests that ACC activation is present when
effortful emotional regulation is required in situations where behaviour is failing to achieve a desired
outcome (Ochsner & Barrett, 2001), and Davidson et al. suggest that this may reflect a deficit in the
‘will‐to‐change’ that is also characteristic of depressed individuals. Third, individuals with depression
and mood disorders also show signs of dysfunction in the hippocampus (Mervaala et al., 2000). The
hippocampus is important in adrenocorticotropic hormone secretion and is also critical in learning
about the context of affective reactions (Fanselow, 2000). Thus, deficits in hippocampal function in
depression may result in the individual dissociating affective responses from their relevant contexts. In
depression, this may manifest itself as feelings of sadness occurring independently of contexts in which
we would normally expect such emotions (i.e., sadness is experienced in all contexts, not just following
relevant life events such as a bereavement). Finally, major depression has also been found to be
associated with structural and functional abnormalities in the amygdala, and especially with increased
amygdala activation (Abercrombie et al., 1998). A role of the amygdala is in directing attention to
affectively salient stimuli and prioritising the processing of such stimuli. The effect of raised levels of
activation in the amygdala may therefore result in the depressed individual prioritising threatening
information for processing and interpreting such information negatively.

anterior cingulate cortex (ACC) The frontal part of the cingulate cortex resembling a
‘collar’ form around the corpus callosum, used for the relay of neural signals between the right
and left hemispheres of the brain.

Prefrontal Cortex An area of the brain which is important in maintaining representations of

goals and the means to achieve them.
FIGURE 7.3 Key brain regions involved in affect and mood disorders: (a) Orbital prefrontal cortex (green) and the
ventromedial prefrontal cortex (red), (b) Dorsolateral prefrontal cortex (blue), (c) Hippocampus (purple) and amygdale
(orange), (d) Anterior cingulated cortex (yellow).
After Davidson et al. (2002).
In addition, structural anatomical abnormalities in depressed individuals have been found for grey
matter and white matter in the brain. Decreased grey matter levels are found in the prefrontal cortex,
the orbitofrontal cortex, the ACC, and the basal ganglia (Kaltenboeck & Harmer, 2018). White matter
lesions are frequently found in late‐life depression and may cause symptoms by affecting the limbic
projections to the prefrontal cortex that are important in mood regulation (Disabato et al., 2016).

Neuroendocrine factors
Depression is regularly associated with problems in the regulation of body cortisol levels—a hormone
that is secreted in times of stress. We mentioned earlier that the hippocampus is important in
adrenocorticotropic hormone secretion, and that depressed individuals frequently exhibit hippocampal
abnormalities (Mervaala et al., 2000). These hippocampal abnormalities are regularly linked with high
levels of cortisol (an adrenocortical hormone)—especially high cortisol levels at the time of wakening
(Vrshek‐Schallhorn et al., 2013)—and patients receiving chronic corticosteroid therapy for endocrine
problems have smaller hippocampal volumes and higher depression ratings than non‐patient controls
(Brown et al., 2004). The hypothalamic‐pituitary‐adrenocortical (HPA) network is the biological system
that manages and reacts to stress, and triggers the secretion of cortisol in response to stress. It is the lack
of inhibitory control over cortisol secretion that is linked with depression, and around 80% of
individuals who are hospitalised because of their depressive symptoms show poor regulation of the HPA
network (Heuser, Yassourides, & Holsboer, 1994) and are more likely to be prone to future bouts of
depression (Aubry et al., 2007). Furthermore, increased early life stress (a known risk factor for
depression) has been shown to cause hyperactivity of the HPA network that persists into adulthood
(Pariante & Lightman, 2008).
Depression has also been associated with abnormalities in the immune system and in particular with
increases in inflammation, and this may lead to symptoms of depression by inducing a tryptophan‐
metabolising enzyme that decreases the availability of serotonin in the brain (Cowen, 2015). The
relationship between inflammation and depression is of current interest to researchers and is discussed
more fully in Focus Point 7.3.

Summary of biological theories

The preceding evidence suggests that biological factors may play an important role in the development
and maintenance of mood disorders such as major depression. There is clearly an inherited component
(which accounts for around a third of the variance in measures of depression), and imbalances in
specific brain neurotransmitters such as serotonin, norepinephrine, and dopamine have been linked to
symptoms of depression. Recent developments in brain scanning technology have also allowed
researchers to identify abnormalities in specific areas of the human brain that are associated with
depression. These are all impressive and important findings, but we must remember that depression and
mood disorders almost certainly do not stem solely from biological dysfunction. As we shall see in the
next section, psychological and cognitive factors are equally important in the aetiology and maintenance
of mood disorders and supplement our knowledge of biological factors. Biological and psychological
explanations are not mutually exclusive and they attempt to explain phenomena at different levels of
description. Indeed, it is still not clear whether many of the biological factors we have described in
Section 7.1.2 are truly causal factors in depression, or whether they simply represent biological changes
that reflect the experience of depression. That is, biological factors may give rise to many of the symptoms
of depression, but psychological processes may in turn trigger these biological factors.

Psychological theories

Psychodynamic explanations
There are a number of different psychodynamic views of depression (see Blatt & Homann, 1992), but
the most well established is the psychoanalytic account pioneered by Freud (1917/1963) and Abraham
(1916/1960). This view argues that depression is a response to loss, and, in particular, a response to the
loss of a loved one such as a parent. Because, according to psychoanalytic theory, such losses return the
individual to the oral stage of development, psychoanalysis argues that depression has a functional role
to play, in that it returns the person to a period in their life when they were dependent on others (their
parents). During their depressed state, this regression to the oral stage allows the individual to become
dependent on their relationships with others in order to utilise the support that this will offer.
FOCUS POINT 7.3 DEPRESSION AND INFLAMMATION

As we mentioned at the beginning of this chapter, depression is a widely experienced mental

health problem. It has significantly high prevalence rates, is highly comorbid with other
psychopathologies, it is also commonly experienced during many physical illnesses (such as
cardiac illnesses, cancer, diabetes, rheumatoid arthritis, and multiple sclerosis) and also
experienced during degenerative brain disorders such as Parkinson's disease and Alzheimer's
disease (see Chapter 15). However, depression is not just a consequence of physical illness, it is
also in many cases a predictor of future illness. For example, depression is known to be a risk
factor for coronary artery disease (Stewart, Rand, Muldoon, & Kamarck, 2009; Suls & Bunde,
2005) and for strokes (May et al., 2002).
This link between depression and physical illnesses has led to the development of theories
arguing that inflammation may contribute to the experience of depression. Central to this view
are cytokines—proteins made by immune cells that control responses to foreign antigens and
germs, generating inflammation and fever. Consistent with this is the fact that depression also
seems to be associated with changes in the immune system, especially those changes that involve
cytokines. Studies have also shown that both medically ill and medically healthy individuals
with major depression exhibit all the cardinal features of inflammation, including elevations in
inflammatory cytokines and symptoms such as fatigue, cognitive dysfunction, and impaired
sleep (Miller, Maletic, & Raison, 2009; Meyers, Albitar, & Estey, 2005).
So how might inflammation and symptoms of depression be causally linked? Animal studies
suggest administration of cytokines can profoundly affect the metabolism of the
 neurotransmitters implicated in depression, including serotonin, norepinephrine, and dopamine
(Anisman, Merali, & Hayley, 2008; Felger et al., 2007). Cytokines also generate behaviours
strikingly similar to symptoms found in depression, such as listlessness, loss of appetite, lack of
interest in socialising and sex, and increased sensitivity to pain (Smith, Au, Ollis, & Schmitz,
2017). From an adaptive viewpoint, it makes sense for an organism that is fighting disease and
infection to restrict activity generally and eat less to allow available resources to be focussed on
the area that is under physical attack from illness.
There is still much more research required before we can be confident that inflammation is a
process that contributes significantly to the experience of depression, but the current arguments
seem compelling and logical. It remains to be seen whether inflammation is an explanation for
all depression experience (e.g., Amodeo, Trusso, & Fagiolini, 2017), or whether some other
causes of depression and depression experience are independent of inflammation—research
has already shown that not everyone with increased inflammation develops depression (Du
Preez, Leveson, Zunszain, & Pariante, 2016). However, if inflammation and depression are
inseparably bound together, then one implication of this is that treatment for depression will
also need to take account of those medical processes that can alleviate inflammation and relieve
physical illness.

One problem with this psychoanalytic interpretation is that not everyone who experiences depression
has lost a loved one, and this led Freud to propose the concept of symbolic loss in which other kinds
of losses within one's life (e.g., losing a job) are viewed as equivalent to losing a loved one. These losses
then cause the individual to regress to the oral stage of development and may trigger memories of
inadequate parental support during childhood. In addition, parental loss is no longer seen as a necessary
condition for the development of depression, and poor parenting is a more significant risk factor (Lara
& Klein, 1999). Support for this view comes from studies that have shown a relationship between risk for
depression in adulthood and having experienced a particular kind of parenting style known as
affectionless control (Garber & Flynn, 2001). This type of parenting is characterised by high levels
of overprotection combined with a lack of warmth and care.

symbolic loss A Freudian concept whereby other kinds of losses within one’s life (e.g. losing a
job) are viewed as equivalent to losing a loved one.

affectionless control A type of parenting characterised by high levels of overprotection

combined with a lack of warmth and care.

There is some empirical support for this psychoanalytic view of depression. For example, individuals
who report that their childhood needs were not adequately met by their parents are more likely to
become depressed after experiencing a loss (Goodman, 2002). Nevertheless, there are a number of
difficulties with the psychoanalytic view. First, much of the empirical evidence that is consistent with this
view is also consistent with many other theories of depression, so the evidence does not help to
differentiate between theoretical approaches. Second, many individuals who do experience parental loss
or poor parenting do not go on to develop depression. Psychoanalytic approaches do not clearly explain
why this is the case. Finally, because of the way that psychodynamic theories are formulated, many of
the key aspects of the theory are difficult to test. Psychodynamic concepts used to explain depression,
such as introjection, fixation at the oral stage of development, and symbolic loss are all difficult to
operationalise and measure, and so verify empirically. This difficulty is compounded by the Freudian
belief that such processes are thought to operate at the unconscious level.
Behavioural theories
The most obvious characteristics of depressed individuals include a lack of motivation and initiative, a
considerably diminished behavioural repertoire, and a view of the future that lacks positive and fulfilling
experiences. Some theorists have suggested that these characteristics provide evidence that depression
results from a lack of appropriate reinforcement for positive and constructive behaviours (Lewinsohn,
1974). This leads to the extinction of existing behaviours, and to a ‘behavioural vacuum’ in which the
person becomes inactive and withdrawn. It is certainly the case that periods of depression follow life
‘losses’ such as bereavement, retirement, or redundancy, and each of these events represent the loss of
important sources of reward and reinforcement for social and occupational behaviours (see also Figure
7.7 showing how suicide rates increase during a financial recession). In support of this account, it has
been shown that depressed individuals report fewer rewards in their life than nondepressed individuals,
and introducing rewards into the lives of depressed individuals helps to elevate their mood and forms
the central feature of behavioural activation(BA) therapy which encourages depressed individuals
to approach activities they may have been avoiding (Lewinsohn, Youngren, & Grosscup, 1979; Jacobson
et al., 1996; see Chapter 4, Section 4.1.1).

behavioural activation therapy (BA) A therapy for depression that attempts to increase
clients’ access to pleasant events and rewards and decrease their experience of aversive events
and consequences.

The fact that life ‘losses’ are likely to result in the reduction of reinforcing events for the depressed
individual also leads to a vicious cycle that can establish depression as a chronic condition. For example,
once a person becomes depressed, then their lack of initiative and withdrawal is unlikely to lead to the
development of other alternative sources of reinforcement. Unfortunately, the negative disposition of
the depressed individual is likely to be an active contributor to a lack of reinforcement—especially social
reinforcement. For example, depressed individuals are less skilled at interacting with others than
nondepressed individuals (Joiner, 2000; Segrin, 2000), and a chronically depressed individual will often
communicate negative attitudes, appear withdrawn and unresponsive, and tend to seek excessive
reassurances about themselves and their future. As a consequence, studies suggest that when interacting
with depressed individuals, nondepressed control participants exhibit less positive social behaviour, are
less verbal, and are less positive than when interacting with a nondepressed individual (Gotlib &
Robinson, 1982).
The frequent failure of depressed individuals to elicit reinforcing reactions from individuals with whom
they are communicating has led to interpersonal theories of depression. These theories argue that depression is
maintained by a cycle of excessive reassurance seeking from depressed individuals that is
subsequently rejected by family and friends because of the negative and repetitive way in which
depression leads the individual to talk about their problems (Joiner, 1995). Excessive reassurance seeking
is defined as ‘the relatively stable tendency to excessively and persistently seek reassurances from others
that one is lovable and worthy, regardless of whether such assurance has already been provided’ (Joiner,
Metalsky, Katz, & Beach, 1999, p. 270), and the negative beliefs about themselves, their world and their
future leads depressed individuals to doubt any reassurances they are given by friends and family, and
this continual doubting can have a negative impact on relationships with partners (Fowler & Gasiorek,
2016). Excessive reassurance seeking in depressed individuals predicts future depressive symptoms
(Haeffel, Voelz, & Joiner, 2007; Joiner et al., 1999) and can be associated with motivation to obtain self‐
confirming negative feedback, which is another risk factor for depressive symptoms and interpersonal
rejection that creates a vicious cycle of rejection and depression (Davila et al., 2009), and in turn can
exacerbate the symptoms of depression (Evraire & Dozois, 2011).
However, we must be cautious about how we interpret this evidence as a causal factor in depression.
First, much of the research on the link between lack of reinforcement and depression has been
retrospective in nature, and it is quite reasonable to suppose that depressed individuals may
underestimate the extent of the actual rewards in their life. Second, we need to understand whether
excessive reassurance seeking and seeking negative feedback are dispositional factors that create a risk
for depressive symptoms or whether depressive symptoms themselves elicit these characteristics (Evraire
& Dozois, 2011).

Negative cognitions and self‐schema

One of the most influential of all the theories of depression is Beck's Cognitive Theory (1967, 1987, see
Strauss, 2019, for a review of Beck's theory of depression and its influence on modern‐day clinical
psychology). This theory introduced the idea that depression could be caused by biases in ways of
thinking and processing information. We know that depressed individuals indulge in a good deal of
‘negative thinking’, and that they experience more negative intrusive thoughts than non‐depressed
individuals (Reynolds & Salkovskis, 1992). Facts such as this have led Beck (1987) to claim that depressed
individuals have developed a broad‐ranging negative schema that tends them towards viewing the
world and themselves in a negative way. In turn, these negative schema influence the selection,
encoding, categorisation, and evaluation of stimuli and events in the world in a way that leads to a
vicious cycle of depressive affect and symptomatology. Beck argued that these negative schema are
relatively stable characteristic of the depressed individual's personality and develop as a result of early
adverse childhood experiences—especially concerning loss (such as the loss of a parent figure). In later
life, a stressful experience will reactivate this negative schema and give rise to the biased thinking that
generates depressive symptoms such as deficits in motivational, affective, cognitive, and behavioural
functioning.

negative schema A set of beliefs that tends individuals towards viewing the world and
themselves in a negative way.

Beck argued that the depressed individual's negative schema maintained some interrelated aspects of
negative thinking that Beck called the negative triad. In particular, depressed people hold negative
views of themselves (e.g., ‘I am unattractive’), negative views of their future (e.g., ‘I will never achieve
anything’), and of the world (e.g., ‘the world is a dangerous and unsupportive place’). This set of negative
beliefs eventually generates self‐fulfilling prophecies. That is, the depressed individual interprets events
negatively, fails to take the initiative, and then inevitably experiences failure (Figure 7.4). The negative
triad of beliefs leads to a number of systematic biases in thinking, including arbitrary inference,
selective abstraction, overgeneralisation, magnification and minimisation, personalisation, and all‐or‐
none thinking (Table 7.5).

negative triad A theory of depression in which depressed people hold negative views of
themselves (e.g. ‘I am unattractive’), of their future (e.g. ‘I will never achieve anything’) and of
the world (e.g. ‘The world is a dangerous and unsupportive place’).
FIGURE 7.4 Beck's negative schema in depression.
This figure shows how the negative biases in the thinking of depressed individuals leads to a vicious cycle in which depression becomes a
self‐fulfilling prophecy.
TABLE 7.5 Thinking biases in Beck's model of depression
Arbitrary Jumping to a conclusion when evidence is lacking or is actually contrary to the
inference conclusion
Selective Abstracting a detail out of context and missing the significance of the total
abstraction situation
Overgeneralisation Unjustified generalisation on the basis of a single incident (e.g., making a single
mistake and concluding “I never do anything right”)
Magnification and Perceiving events as either totally bad or neutral or irrelevant. Catastrophising is
minimisation an example of magnification, in which the individual takes a single fact to its
extreme (e.g., a scratch on a new car means the car is wrecked and needs
replacing)
Personalisation The propensity to interpret events in terms of their personal meaning to the
individual rather than their objective characteristics (e.g., believing that a frown on
another person's face means they are annoyed specifically with you)
All‐or‐none Events are labelled as black or white, good or bad, wonderful or horrible (e.g.,
thinking assuming that everyone will either accept you or reject you)
There is considerable evidence that depressed individuals do show the negative cognitive biases that
Beck's theory predicts. First, some studies have shown attentional biases to negative information in
depressed individuals that results in them prioritising that negative information. In the emotional Stroop
procedure, depressed individuals are slower at naming the colour of negative words than positive words,
suggesting that their attention is drawn towards the meaning of such words (Gotlib & Cane, 1987; Epp,
Dobson, Dozois, & Frewen, 2012). Also, in a dichotic listening procedure, depressed individuals have
greater difficulty ignoring negative words that are presented as distractors than do nondepressed
participants (Ingram, Burnett, & McLaughlin, 1994). The exact nature of this attentional bias is
unclear, and some studies have failed to replicate these experimental effects (e.g., Mogg, Bradley,
Williams, & Mathews, 1993). Nevertheless, there is sufficient evidence to suggest that there is a bias
towards processing negative information in depression—especially if it is information that is specifically
relevant to depression (rather than more general negative information) (Gotlib, Gilboa, & Sommerfeld,
2000). Most recently, there is emerging evidence that depressed individuals may explicitly have problems
disengaging attention from negative information that has captured their attention, and this lack of
cognitive control may also cause difficulties when it comes to emotion regulation (Joorman & Stanton,
2016; LeMoult & Gotlib, 2019, see Figure 7.5).
FIGURE 7.5 Depression is associated with (a) cognitive biases in self‐referential processing, attention, interpretation,
and memory, (b) the use of maladaptive versus adaptive cognitive emotion regulation strategies, and (c) deficits in cognitive
control over mood‐congruent material, which in turn, can contribute to cognitive biases and the use of maladaptive emotion
regulation strategies (e.g., rumination, distraction), all of which exacerbate and sustain symptoms of depression.
From LeMoult and Gotlib (2019).
Second, important memory biases are also apparent in depression, with depressed individuals able to
recall more negative words than positive words in explicit memory tests (Mathews & MacLeod, 1994),
but this again seems to apply predominantly to depression‐relevant material rather than threat‐relevant
material generally (Watkins, Mathews, Williamson, & Fuller, 1992). Furthermore, studies have indicated
that depressed individuals will remember more negative than positive information about themselves
(Alloy, Abramson, Murray, Whitehouse, & Hogan, 1997), and of particular interest is the biased recall
of autobiographical memories by depressed individuals. Depressed individuals tend to favour
recalling negative autobiographical events, recall fewer positive autobiographical experiences than
nondepressed individuals, recall overgeneral and less detailed autobiographical memories than
nondepressed individuals, and are more likely to either avoid or ruminate about events from their past
(Kohler et al., 2015; Raes, Hermans, Williams, & Eelen, 2005; Williams & Scott, 1988). Subsequent
studies have suggested that there may be an association between experiencing early life trauma (such as
childhood abuse) and reduced autobiographical memory specificity (Raes, Hermans, Williams, & Eelen,
2005),and that poorly detailed autobiographical memories may be linked to the deficits in problem‐
solving ability that are characteristic of depressed individuals (Pollock & Williams, 2001).
RESEARCH METHODS IN CLINICAL PSYCHOLOGY 7.1
USING EXPERIMENTAL PSYCHOPATHOLOGY METHODS TO
UNDERSTAND DEPRESSION

Theories of depression that allude to biases in thinking and dysfunctional beliefs (such as Beck's
cognitive theory of depression) need to be empirically tested to find out whether such biases do
mediate depression. One important way of doing this is to use experimental psychopathology to study
the psychological processes that underlie basic mental health problems such as depression
(Vervliet & Raes, 2013).

experimental psychopathology Experimental field of psychological science aimed

at understanding the processes underlying psychopathology.

One aim of experimental psychopathology is to mimic in healthy individuals those processes

thought to underlie the cognitive or neurological mechanisms that give rise to psychopathology,
and so either increase our understanding of those mechanisms, or to confirm that such
mechanisms do indeed lead to increases in symptoms. There are many ways in which this can
be achieved. One is by recreating in the experimental lab the conditions thought to give rise to
symptoms and testing these out on healthy individuals (e.g., by using negative mood inductions
to generate sad mood in healthy participants, and see if this affects attentional and memory
biases in ways predicted by Beck's theory—see Section 7.1.2); an alternative is to create animal
models of individual psychopathologies that can be tested in experimental studies on animals
such as rats or mice (e.g., testing the inflammation model of depression on laboratory rats by
experimentally investigating the effects of administered cytokines on the metabolism of
neurotransmitters implicated in depression, see Focus Point 7.3).
Vervliet and Raes (2013) point out that when conducting experimental psychopathology
methods on healthy participants, we need to be sure that such methods have external validity and
are able to bridge what is called the ‘translational gap’ from healthy individuals to clinical cases.
Up to four criteria need to be met for external validity: (a) face validity—where there is at least a
degree of phenomenological similarity between the behaviour of the model and the symptoms
in the disorder, (b) predictive validity—where performance in the model predicts performance in
the disorder, (c) construct validity—where the experimental psychopathology procedure accurately
recreates the aetiological processes or mechanisms known to operate in the disorder, and (d)
diagnostic validity—where the procedure shows that any experimental manipulations produce
behavioural or cognitive outcomes that can be properly extrapolated to those found in
diagnosed patients (e.g., in intensity or frequency).
One example of the use of experimental psychopathology methods in the study of depression is
a study by Hepburn, Barnhofer, and Williams (2006). They studied the effect of experimentally
induced positive and negative mood in healthy participants on the cognitive processes
underlying future thinking. They found that participants induced into a negative mood
(equivalent to depression) rated positive future events as more negative than those in a positive
mood and became less fluent at generating future positive events. They conclude that increased
negative or depressed mood may significantly reduce the accessibility of positive future events
and also lead to the assessment of those events when retrieved as less positive than when in a
neutral or positive mood. This may have significant relevance to the processes underlying
hopelessness (see Section 7.1.2) and may be a risk factor for suicidality.
Third, there is experimental evidence that depressed individuals exhibit the interpretational bias that
would lead them to interpreting ambiguous events negatively or to judge events more negatively
(Everaert, Podina, & Koster, 2017). There is considerable evidence, for example, that depressed affect is
associated with more critical self‐judgement and a raising of personal performance standards (Forgas,
Bower, & Krantz, 1984; Scott & Cervone, 2002). Cognitive bias modification (CBM) studies designed to
alter negative interpretation biases have demonstrated that this can be achieved in depressed individuals
(LeMoult et al., 2017), although to date, evidence that the effects of this training can be sustained has
been inconsistent (Joormann, Waugh, & Gotlib, 2015).
More recent theories suggest that the combination of biases in attention, interpretation, memory and
cognitive control and their interaction may be a better predictor of depressive symptoms than any of
these biases alone (Everaert, Koster, & Derakshan, 2012; Hirsch, Clark, & Mathews, 2006), and this is a
potentially fruitful direction for future research in this area (Research Methods in Clinical Psychology
7.1).
Finally, we tend to associate depression, and Beck's cognitive theory of depression in particular, with
pessimistic thinking caused by negative self‐schemas. However, evidence suggests that what
depressed individuals may actually lack is the positive interpretation bias possessed by nondepressed
individuals. It turns out that depressed individuals are much more accurate in experimental studies at
evaluating (a) how much control they may have over a situation (Alloy & Abrahamson, 1979), and (b)
the impression they made on others in a social situation (Lewinsohn, Sullivan, & Grosscup, 1980). In
contrast, nondepressed individuals are unduly optimistic in their estimates. This suggests that depressed
individuals may be much more objective about the judgements they make, and it is nondepressed
individuals who possess a positive bias that may act to ‘make them feel good about themselves’
(Lewinsohn et al., 1980).

pessimistic thinking A form of dysfunctional thinking where sufferers believe nothing can
improve their lot.

In summary, Beck's cognitive theory of depression has been significantly influential in determining the
way we conceptualise, research, and treat depression. It has generated a range of research on cognitive
biases in depression and has contributed substantially to cognitive‐based treatments of depression (see
Section 7.3). However, it is still unclear whether the negative cognitive biases defined by Beck's theory
actually cause depression, or whether these biases are simply a consequence of experienced depression.
Further research will be needed to clarify issues such as this.

Learned helplessness and attribution

During a person's lifetime they may experience a number of unavoidable and uncontrollable negative
life events. These may include the sudden death of a close friend or relative, or being made redundant
from a job. Seligman (1975) proposed that depression could be linked specifically to these kinds of
experiences, and that they give rise to a ‘cognitive set’ that makes the individual learn to become
‘helpless’, lethargic, and depressed. It is the perceived uncontrollability of these negative life events that
is important and leads the individual to the pessimistic belief that negative life events will happen
whatever they do. Seligman (1974) first derived this hypothesis from animal learning experiments in
which dogs were first given unavoidable electric shocks and subsequently taught to learn a simple
avoidance response that would avoid the shocks. He found that dogs that were given prior unavoidable
electric shocks were subsequently unable to learn the avoidance response and simply lay down in the
apparatus and ‘quietly whined’. One example of how learned helplessness theory has been applied to
depression is in the case of women who have suffered domestic abuse. Walker (2000) has suggested that
a pattern of repeated partner abuse leads women to believe that they are powerless to change their
situation. As a result, such women come to exhibit all the symptoms of depression and display the
‘passivity’ often found in what is known as battered woman syndrome.
However, while animal experiments on learned helplessness do appear to have a formalistic
similarity to human depression, there are a number of reasons for believing that it is not a full or
comprehensive account of depression. First, some studies with humans have suggested that prior
experience with uncontrollable negative events may actually facilitate subsequent performance
(Wortman & Brehm, 1975). Second, many depressed individuals see themselves as being responsible for
their failures and losses—yet someone who perceives himself or herself as helpless should not blame
themselves for these events. Third, in the specific case of battered women syndrome, passivity may not
be the result of the woman learning that she is helpless, but it may be a learned adaptive response to
abuse. This may take the form of the woman thinking, ‘If I do not make requests and acquiesce to his
demands, he is less likely to hit me’ (Peterson, Maier, & Seligman, 1993).

battered woman syndrome The view that a pattern of repeated partner abuse leads
battered women to believe that they are powerless to change their situation.

learned helplessness A theory of depression that argues that people become depressed
following unavoidable negative life events because these events give rise to a cognitive set that
makes individuals learn to become ‘helpless’, lethargic and depressed.

These difficulties and inconsistencies in the original learned helplessness theory led to the development
of a revised theory that included the important concept of attribution (Abramson, Seligman, &
Teasdale, 1978; see Watkins, 2019, for a discussion of the original Abramson et al., 1978, study and a
critique of the attributional style approach to understanding depression). Attributional theories of
depression argue that people learn to become helpless, or more specifically ‘hopeless’, because they
possess certain attributional styles that generate pessimistic thinking. Attributions are the explanations
that individuals have for their behaviour and the events that happen to them. In particular, Abramson et
al. (1978) argue that people become depressed when they attribute negative life events primarily to
factors that either cannot easily be manipulated or are unlikely to change. In particular, people who are
likely to become depressed attribute negative life events to (a) internal rather than external factors (e.g., to
personal traits rather than outside events), (b) stable rather than unstable factors (e.g., things that are
unlikely to change in the near future), and (c) global rather than specific factors (e.g., causes that have an
effect over many areas of their life rather than being specific to one area of functioning). Table 7.6
provides an example of the range of attributions that someone might make in relation to failing a maths
exam. In this case, the global, stable, and internal attribution is ‘I lack intelligence’, and this attribution
is likely to have a number of negative consequences. First, it is the kind of cause that is not easily
changed so that future failures might be avoided. Second, it reflects negatively on the individual's self‐
concept, and so is likely to reduce self‐esteem. Third, it is a global attribution, and so the individual is
likely to believe that they will fail at many other things, and not just a maths exam, and this is likely to
lead to the kinds of pessimistic thinking typical of depression. In contrast, if the student had attributed
their failure to specific, unstable factors, such as ‘I am fed up with maths’ or ‘my maths test was
numbered 13’, they would have been less likely to experience helplessness or reduced self esteem
(because these are factors that could change quite easily)

attribution theories Theories of depression which suggest that people who are likely to
become depressed attribute negative life events to internal, stable and global factors.
TABLE 7.6 Why I failed my GCSE maths exam

People who become depressed tend to attribute negative life events to internal, stable global causes (in this example ‘I
lack intelligence’ is an example of this). In contrast, had the individual attributed their failure to specific, unstable
factors (such as ‘I am fed up with maths’ or ‘My maths test was numbered 13’), they are less likely to experience
helplessness. GCSE = General Certificate of Secondary Education.
In order to test the attributional account of depression, Peterson et al. (1982) developed the
Attributional Style Questionnaire (ASQ) which measures tendencies to make the particular kinds of
causal inference that are hypothesised to play a causal role in depression. A number of studies have
subsequently found that use of the global‐stable attributional style is a vulnerability factor for future
depression (Butters, McClure, Siegert, & Ward, 1997; Chaney et al., 2004)—especially following
negative life events (Hankin & Abramson, 2002). A study by Metalsky, Joiner, Hardin, and Abramson
(1993) gave students the ASQ prior to a midterm exam and then measured depressive symptoms over
the subsequent 5 days. They found that the students' enduring depressive reactions during this period
were predicted by a global‐stable attributional style together with low self‐esteem and exam failure. This
suggests that the global‐stable attributional style in the context of a negative life event (e.g., exam failure)
is a good predictor of subsequent depression. Finally, a computer‐based attention bias modification task
(see Focus Point 6.4, Chapter 6) can be used to create either negative or positive attributional styles, and
individuals in whom the positive attributional style is induced subsequently report less depressed mood
in response to a stressor than individuals in whom a negative attributional style is induced (Peters,
Constans, & Mathews, 2011). Experimental studies such as this suggest a direct causal link between
attributional style and depressed mood.

Hopelessness theory
The attributional/helplessness account of depression has been further refined to account for the fact
that attributional style appears to interact with a number of other factors to cause depression.
Abramson, Metalsky, and Alloy (1989) suggested that the tendency to attribute negative events to
global/stable causes represents a diathesis which, in the presence of negative life events, increases
vulnerability to a group of depressive symptoms, including retarded initiation of voluntary responses,
apathy, lack of energy, and psychomotor retardation. This cluster of symptoms is known as
hopelessness, which is an expectation that positive outcomes will not occur, negative outcomes will
occur, and the individual has no responses available that will change this state of affairs. Hopelessness
theory is very similar to attributional/helplessness accounts in that negative life events are viewed as
interacting with a global/stable attributional style to generate depressed symptomatology. However,
hopelessness theory also predicts that other factors, such as low self‐esteem, may also be involved as
vulnerability factors (Metalsky et al., 1993). Many studies have supported the hopelessness theory by
confirming that depression can be predicted by a combination of negative attributional style, negative
life events, and low self‐esteem (Alloy, Lipman, & Abrahamson, 1992; Bohon, Stice, Burton, Fudell, &
Nolen‐Hoeksema, 2008; Metalsky et al., 1993; Metalsky & Joiner, 1992), and that the negative
attributional style is significantly more related to hopelessness depression symptoms (e.g., lethargy,
hopelessness, difficulty making decisions) than endogenous depression symptoms (e.g., loss of interest in
sex, loss of appetite, loss of weight) (Joiner, 2001). In addition to predicting many symptoms of
depression, hopelessness is also a construct that has been shown to predict suicidal tendencies and, in
particular, suicidal ideation and completed suicide (Conner, Duberstein, Conwell, Seidlitz, & Caine,
2001; Wolfe et al., 2019).

Hopelessness theory A theory of depression in which individuals exhibit an expectation that

positive outcomes will not occur, negative outcomes will occur, and that the individual has no
responses available that will change this state of affairs.

Nevertheless, despite the enhanced ability of the evolved model to predict depressive episodes, there are
still a number of limitations to hopelessness theory: (a) many of the studies claiming to support
hopelessness theory have been carried out on healthy or only mildly depressed participants who are not
representative of individuals who are clinically depressed (Coyne, 1994), (b) a majority of studies testing
the model are correlational in nature, and so cannot provide any evidence on the possible causal role of
hopelessness cognitions in generating depression (Henkel, Bussfield, Moller, & Hegerl, 2002), (c) the
model does not explain all of the depressive symptoms required for a DSM‐5 diagnosis, only those
related to hopelessness, and (d) there is some evidence that the negative attributional style disappears
during remission or recovery from depression (Hamilton & Abramson, 1983), and this suggests that it
may not be a universal or enduring feature of individuals who experience depression. This latter fact
raises the question of what comes first, the negative attributional style or symptoms of depression (but
see Research Methods in Clinical Psychology 7.2).

RESEARCH METHODS IN CLINICAL PSYCHOLOGY 7.2

PROSPECTIVE STUDIES

Questionnaire studies are usually designed to see whether there are any relationships (i.e.,
correlations) between different measures. This is very useful first step in researching a topic
because it tells us what measures or constructs appear to be strongly associated. For example,
measures of negative attributional style (attributing negative events to global/stable causes) are
found to be highly correlated with measures of depression (Alloy et al., 1992).
Theorists who support the hopelessness theory of depression would say that these kinds of
correlations provide support for that theory, that is, support for the view that a negative
attributional style is a causal factor in developing depression. However, when two measures are
highly correlated we must be cautious for at least two reasons:
1. We cannot infer that there is a causal relationship between these measures, because their
association might be mediated by some third variable that has not been measured. For
example, negative attributional style and depression might be highly correlated because
they are both related to the number of negative life events the people have experienced

2. Similarly, if there is a causal relationship between two variables that are highly correlated,
we do not know the direction of that causal relationship. While hopelessness theory
predicts that negative attributional style should cause depression, a correlation between
these two variables is just as likely to imply that depression causes a negative attributional
style.
 One way to overcome some of these difficulties in interpreting results from correlational studies
is to conduct what are known as prospective studies.
Prospective studies take measures of the relevant variables at a particular point in time (usually
called Time 1) and then go back to the same participants at some future time or times and take
the same measures again (usually called Time 2). Using this method a researcher can see if
measures of a variable at Time 1 (e.g., negative attributional style) predict, or are correlated
with, measures of variables taken at Time 2 (e.g., depression). In addition, because the
researchers will have taken measures of depression at both Times 1 and 2, they can also see if
levels of negative attributional style predict changes in depression scores between Times 1 and 2.
This procedure allows the researcher to make much stronger statements about the possible
causal direction of a relationship between two variables, and whether one variable is a risk factor
for the other (i.e., whether negative attributional style is a risk factor for increased depression
over time).
Such a prospective study was undertaken by Robinson and Alloy (2003). Using undergraduate
students as participants, they took measures of negative attributional style (using the Cognitive
Style Questionnaire) and depression (using the Beck Depression Inventory) at Time 1. Regular
prospective assessments then took place every 6 months for 2.5 years (Time 2, Time 3 …etc.).
Even when the level of depressive symptoms at Time 1 was taken into account, they found that
measures of variables such as negative attributional style predicted the incidence and number
of future depressive episodes. They concluded that negative cognitive style (including negative
attributional style) was a risk factor for future depression.

Rumination theory
Depressed individuals spend a good deal of time indulging in ruminative activities which may either
increase the risk of depression or increase the probability of relapse following recovery from depression.
Rumination is a tendency to repetitively dwell on the experience of depression or its possible causes,
either in a repetitive or ‘brooding’ fashion (Crane, Barnhofer, & Williams, 2007) or in an analytical way
which attempts to seek explanations for the experience (Watkins, 2008), and is a maladaptive form of
emotion regulation that has been linked to periods of stress and an inability to deploy more adaptive
forms of emotion regulation (such as reappraising emotional events) (Vanderhasselt, Brose, Koster, & De
Raedt, 2016). Tendency to ruminate has been shown to predict the onset of depressive episodes
(Morrow & Nolen‐Hoeksema, 1990; Nolen‐Hoeksema, 2000), and relapse back into bouts of depression
(Michalak, Holz, & Teismann, 2011). Rumination in depressed individuals appears to be driven by
meta‐cognitive beliefs that rumination is a necessary process to undertake in order to resolve depression
(Papageorgiou & Wells, 2001), and these beliefs appear to contribute to the repetitive or perseverative
nature of depressive rumination (Chan, Davey, & Brewin, 2013; Hawksley & Davey, 2010). Other
studies have indicated that rumination is associated with overgeneral autobiographical memory
(Sumner, 2012)—which is a common characteristic of depressed individuals. Rumination is also a
vulnerability factor for depression during the transition from early to middle adolescence (Abela &
Hankin, 2011), and is higher in women than men—possibly contributing to the significantly higher
depression rates in women than men (Nolen‐Hoeksema, 2000).

Rumination The tendency to repetitively dwell on the experience of depression or its possible
causes.

SELF‐TEST QUESTIONS
What are the two main mood disorders?
Name at least five of the symptoms that must be present during a 2‐week period for a
diagnosis of major depression.
Why has it been difficult to gauge the prevalence of depressive disorders?
Can you describe some of the problems involved in diagnosing major depression?
Describe the evidence that suggests there is a genetic component to major depression
What role do the neurotransmitters serotonin, dopamine, and norepinephrine play in
depression?
How have abnormalities in certain brain areas been linked to the experience of
depression?
How are cortisol levels supposed to be involved in the development of depression?
Why is the individual's response to loss so important in psychodynamic theories of
depression?
Can you describe how behavioural theories and interpersonal theories explain the
development of depression?
What is Beck's ‘negative triad’?
What is the evidence that depressed individuals hold negative beliefs about themselves and
the world?
What are the benefits and the limitations of learned helplessness as an explanation of
depression?
What kinds of attributions are likely to lead to depressed thinking?
What are the important features of hopelessness theory of depression?
What effect does rumination have on depressive symptoms?
SECTION SUMMARY

7.1 MAJOR DEPRESSION

Major depression (or unipolar depression) and bipolar depression are the two main types
of clinical depression.
The lifetime comorbidity rate of major depression with another anxiety disorder is 58%
and with more than one other DSM disorder is 74% suggesting that individuals with
depression experience a range of negative emotions.
Premenstrual dysphoric disorder, Seasonal Affective Disorder (SAD), and Chronic Fatigue
Syndrome (CFS) are three prominent disorders with depression as a significant element.
Estimates of lifetime prevalence rates for major depression range from 5.2% to 20.6%.
Major depression is almost twice as common in women as in men.
The incidence of major depression has increased since 1915 with a median onset age of
around 27 years.
There is good evidence for a genetic component to major depression
Abnormalities in the levels of the brain neurotransmitters serotonin, dopamine, and
norepinephrine are associated with depressed mood.
Depressed mood has been shown to be associated with abnormal activity in a number of
brain areas, including the prefrontal cortex, the Anterior Cingulate Cortex (ACC), the
basal ganglia, the hippocampus, and the amygdala.
High levels of cortisol are associated with depression and may lead to a lowering of
serotonin levels in the brain.
Psychoanalytic theory argues that depression is a response to loss, and the loss of a loved
one such as a parent.
Behavioural theories claim that depression results from a lack of appropriate
reinforcement for positive and constructive behaviours, and this is especially the case
following a ‘loss’ such as bereavement or losing a job.
Interpersonal theories of depression claim that depressed individuals alienate family and
friends because of their perpetual negative thinking, and this alienation in turn
exacerbates the symptoms of depression.
Beck's Cognitive Theory of depression argues that depression is maintained by a ‘negative
schema’ that leads depressed individuals to hold negative views about themselves, their
future and the world (the ‘negative triad’).
Learned Helplessness theory argues that people become depressed following unavoidable
negative life events because these events give rise to a cognitive set that makes individuals
learn to become ‘helpless’, lethargic, and depressed.
Attributional accounts of depression suggest that people who are likely to become
depressed attribute negative life events to internal, stable, and global factors.
Hopelessness is a cluster of depression symptoms that are characterised by an expectation
that positive outcomes will not occur, negative outcomes will occur, and the individual has
no responses available that will change this state of affairs.
Depressive rumination can increase the risk of depression or increase the risk of relapse.
7.2 BIPOLAR DISORDER
Bipolar disorder is a mood disorder characterised by alternating periods of depression and mania.
Often the swings between these two states can be very rapid, taking the individual from an extreme
‘high’ to an extreme ‘low’ very quickly. The personal accounts of experiences of bipolar disorder
described in Client's Perspective 7.1 provide some insight into the desperation generated by periods of
depression and the frightening confusion that can be experienced during periods of sustained mania.
Someone who suffers bipolar disorder and is in a manic phase can be recognised by many
characteristics, including the expression of a constant, sometimes unconnected stream of thoughts and
ideas; attention span may be limited and the person shifts rapidly from topic to topic. They will be loud
and often interrupt ongoing conversations to talk about something that has just caught their attention.
Individuals in a manic phase may spontaneously start conversations with strangers, and indulge in
inappropriate or imprudent interactions. These behaviours are usually recognised as excessive by those
who know the sufferer, but any attempt to quell these excesses is usually met with anger and annoyance.
As a result, irritability and lability of mood are often significant features of the individual in a manic
phase. Periods of mania can last for days or even weeks, and onset can occur rapidly over the course of
a single day. Table 7.7 provides the criteria for a manic episode (although this is not a codable disorder).
Because of these symptoms, bipolar disorder is a severely debilitating condition that can limit
functioning and workplace productivity. It is associated with increased mortality and relatively high rates
of relapse (Newberg, Catapano, Zarate, & Manji, 2008), and is highly comorbid with alcohol use
disorder and other substance use disorders (Hunt, Malhi, Cleary, Lai, & Sitharthan, 2016) (Focus Point
7.4). Bipolar disorder is also one of the mental health disorders with especially high suicide rates, with
one in four people diagnosed with bipolar disorder reporting at least one suicide attempt (Nordentoft,
Mortensen, & Pedersen, 2011).
CLIENT'S PERSPECTIVE 7.1 THE EXPERIENCE OF BIPOLAR
DISORDER

Descriptions offered by people with bipolar disorder give valuable insights into the various
mood states associated with the disorder:
DEPRESSION
I doubt completely my ability to do anything well. It seems as though my mind has slowed
down and burned out to the point of being virtually useless…[I am] haunt[ed]…with the total,
the desperate hopelessness of it all…Others say, “It's only temporary, it will pass, you can get
over it”, but of course they haven't any idea of how I feel, although they are certain they do. If
I can't feel, move, think, or care, then what on earth is the point?’
HYPOMANIA
At first when I'm high, it's tremendous…ideas are fast…like shooting stars you follow until
brighter ones appear…All shyness disappears, the right words and gestures are suddenly
there…uninteresting people, things become intensely interesting. Sensuality is pervasive; the
desire to seduce and be seduced is irresistible. Your marrow is infused with unbelievable feelings
of ease, power, well‐being, omnipotence, euphoria…you can do anything…but, somewhere this
changes’.
MANIA
The fast ideas become too fast and there are far too many…overwhelming confusion replaces
clarity…you stop keeping up with it—memory goes. Infectious humour ceases to amuse. Your
friends become frightened…everything is now against the grain…you are irritable, angry,
frightened, uncontrollable, and trapped’.

Clinical Commentary
This provides an insight into how the different mood states in bipolar disorder are
experienced, and how the transition from a depressive episode moves through the mild
manic episode called hypomania to full blown mania. Typical of the transition from
depression to full‐blown mania are (a) the overwhelming flow of thoughts and ideas that
lead to the sufferer seeming incoherent and interrupting on‐going conversations, (b) the
temptation to indulge in inappropriate sexual interactions as everyone around becomes
a focus of interest and shyness is lost, and (c) the inevitable drift by the sufferer into
irritability, frustration and anger as friends and acquaintances try to quell the excesses
of thought and behaviour.
TABLE 7.7 Summary: DSM‐5 criteria for a manic episode

Unusual and continual elevated, unreserved, or irritable mood and unusual and continual
increase in energy levels lasting at least a week
Presence of at least three of the following:
Inflated self‐esteem or grandiosity
Less need for sleep
Increased talkativeness
Racing thoughts
Easily distractible
Increase in goal‐directed activity or unintentional and purposeless motions
Unnecessary participation in activities with a high potential for painful consequences

FOCUS POINT 7.4 MOOD DISORDERS AND CREATIVITY

These artists are a few of many that have all suffered from symptoms of bipolar disorder, and
there is an enduring belief that creativity in the arts is associated with psychological disturbance
and even ‘madness’. Is this just a myth or is there some truth in this belief ? Kay Jamison (1992),
a psychiatrist, spent some years studying the lives of famous contributors to the arts, including
poets, artists, and musicians. She concluded that there did seem to be a link between mood
disorders such as bipolar disorder and creativity and artistic achievement. She found that
British poets during the eighteenth century were significantly more likely than members of the
general population to have suffered symptoms of bipolar disorder, have been committed to a
lunatic asylum, or have committed suicide. this view has been reinforced by a recent large‐scale
study showing that bipolar disorder is more prevalent in groups of people with artistic or
scientific professions, such as dancers, researchers, photographers, and authors (Kyaga et al.,
 2013). But what exactly might this link between bipolar disorder and creativity be?
The first question to ask is ‘what comes first—the creativity or the psychological disturbance?’
There is some evidence that creative individuals do have a family history of psychological
problems suggesting that their psychological difficulties may precede their creativity. For
example, creative individuals often had parents who suffered from psychological disorders and
may have suffered the kind of childhood abuse that may give rise to psychological problems
later in life. For instance, the author Virginia Woolf was known to have suffered childhood
sexual abuse. In addition to this evidence that psychological problems may precede creativity,
some studies have found that individuals with bipolar disorder score higher on measures of
creativity than do nonclinical control participants (Richards, Kinney, Lunde, Benet, & Merzel,
1988).
In contrast to this evidence, it could be argued that artistic communities, where emotional
expression is a valued commodity, are welcoming places for individuals with psychological or
mood disorders (Ludwig, 1995). We must also remember that psychological disorder is not a
prerequisite for creative achievement, and (a) many people make significant artistic and creative
contributions without exhibiting any signs of mental health problems, and (b) those artists
suffering psychological problems often continue to make impressive contributions to their art
even after successful treatment of their disorders (Jamison, 1995; Ludwig, 1995).
Even so, it is worth considering how psychological problems such as bipolar disorder might
contribute to creativity. First, mania gives individuals the energy and sharpened thinking that
may be required for creative achievement, and it also gives the individual confidence and
feelings of inspiration that may not be otherwise experienced. Second, there is evidence that
depressed mood can also make a contribution to creativity by raising performance standards. For
example, Martin and Stoner (1996) found that negative moods lead to lower confidence in the
adequacy of creative effort, and this spurs individuals in negative moods on to greater efforts.

7.2.1 The Diagnosis and Prevalence of Bipolar Disorder

DSM‐5 defines two main types of bipolar disorder, namely bipolar I disorder and bipolar II disorder.
Table 7.8 illustrates the main diagnostic features of these two definitions. the most common of these
two diagnoses is bipolar I disorder where individuals exhibit full manic and major depressive episodes in
alternating sequences. In bipolar II disorder, major depressive episodes alternate with periods of
hypomania (mild manic episodes—see Table 7.9 for a definition of hypomania). while the symptoms
of bipolar ii disorder must be sufficiently severe to cause distress or impairment, individuals with this
disorder can often be relatively productive during their periods of hypomania (Jamison, 1995).

hypomania Mild episodes of mania.

TABLE 7.8 Summary: DSM‐5 Criteria for bipolar disorders I and II
Bipolar Disorder I
Presence or history of at least one manic episode(s)
The manic episode may have been preceded by and may be followed by hypomanic or major
depressive episodes
Symptoms are not better accounted for by schizoaffective disorder or other disorders

Bipolar Disorder II
Presence or history of at least one major depressive episode(s)
Presence or history of at least one hypomanic episode(s)
No history of manic episode(s)
Symptoms are not better accounted for by schizoaffective disorder or other disorders

TABLE 7.9 Summary: DSM‐5 definition of hypomania

Unusual and continual elevated, unreserved, or irritable mood and unusual and continual
increase in energy levels lasting at least a week
Presence of at least three of the following:
Inflated self‐esteem or grandiosity
Less need for sleep
Increased talkativeness
Racing thoughts
Easily distractible
Increase in goal‐directed activity or unintentional and purposeless motions
Unnecessary participation in activities with a high potential for painful consequences
A noted change in functionality which is not usually seen in the individual and changes in
functionality and mood are noticeable by others
The episode is not due to the use of medication, drug abuse, or other treatment

TABLE 7.10 Summary: DSM‐5 criteria for cyclothymic disorder

For at least 2 years there have been many periods with hypomanic symptoms that do not meet the
criteria for a hypomanic episode and many periods with depressive symptoms that do not meet
the criteria for a major depressive episode. These symptoms have not been absent for more than
2 months at a time
No major depressive episode, manic episode, or hypomanic episode has been present during the
first 2 years of the disorder
The episode is not due to the use of medication, drug abuse, or other treatment
Cyclothymic disorder is a mild form of bipolar disorder in which the sufferer has mood swings over
a period of years that range from mild depression to euphoria and excitement. It is characterised by at
least 2‐years of hypomania symptoms that do not meet the criteria for a manic episode, and the sufferer
will experience alternating periods of withdrawal then exuberance, inadequacy and then high self‐
esteem, and so on (Table 7.10).
 Cyclothymic disorder A form of depression characterized by at least 2 years of hypomania
symptoms that do not meet the criteria for a manic episode and in which the sufferer
experiences alternating periods of withdrawal then exuberance, inadequacy and then high self-
esteem.

Bipolar disorder is much less common than major depression, and epidemiological studies suggest a
lifetime prevalence rate of around 1% for bipolar I disorder (Pini et al., 2005). A systematic review of
global prevalence data from all bipolar spectrum disorders showed a 12‐month prevalence rate of 0.8%
when data were compared across 20 geographic regions of the world (Ferrari, Baxter, & Whiteford,
2011).

7.2.2 The Aetiology of Bipolar Disorder

Biological theories

Genetic factors
There is good evidence that bipolar disorder has an inherited component. For example, family studies
have indicated that 10–25% of first‐degree relatives of bipolar disorder sufferers have also reported
significant symptoms of mood disorder (Gershon, 2000), and it has been estimated that approximately
7% of the first‐degree relatives of sufferers also have bipolar disorder (Kelsoe, 2003)—this is compared
to a lifetime prevalence rate in the general population of between 0.4% and 1.6%. Twin studies also
suggest a significant inherited component to bipolar disorder. For example, Table 7.11 shows the
concordance rates for bipolar disorder in sets of monozygotic (MZ) twins and dizygotic (DZ) twins
(Kelsoe, 2003). Concordance rates average 69% and 29% for MZ and DZ twins respectively, suggesting
that sharing all genes as opposed to half of genes more than doubles the risk for developing bipolar
disorder. More recent twin studies have reported heritability estimates as high as 0.93 for bipolar I
disorder (Kieseppä, Partonen, Haukka, Kaprio, & Lönnqvist, 2014).
TABLE 7.11 Concordance rates in selected twin studies of bipolar disorder
After Kelsoe (2003).

Study Monozygotic twins (MZ), % Dizygotic twins (DZ), %

Rosanoff et al. (1935) 69.6 16.4
Kallman (1954) 92.6 23.6
Bertelsen (1979) 58.3 17.3
Kendler et al. (1993) 60.7 34.9
Total 69.6 29.3

Neurochemical factors
Bipolar disorder has also been shown to be reliably associated with abnormalities in levels of brain
neurotransmitters. Like major depression, bipolar disorder seems to be associated with dopamine and
norepinephrine irregularities. Converging findings from pharmacological and imaging studies support
the view that overactive dopamine receptor availability and a hyperactive reward processing network in
the brain underlies mania (Ashok et al., 2017), but serotonin does not appear to play such a central role
in bipolar symptoms, and this is evidenced by the fact that serotonin reuptake is not a sufficient
condition for antidepressant efficacy in bipolar depression (Fountoulakis, Kelsoe, & Akiskal, 2012). In
addition, the manic episodes in bipolar disorder are also found to be associated with high levels of
norepinephrine (Altshuller et al., 1995; Bunney, Goodwin, & Murphy, 1972). These findings linking
bipolar disorder to both overactivity and deficits in a range of neurotransmitters testifies to the
complexity of the pathophysiology of this particular mental health problem, and the interactions
between these various effects is still not clearly understood (Sigitova, Fišar, Hroudová, Cikánková, &
Rabouch, 2016).

Cognitive deficits in bipolar disorder

Bipolar disorder has been found to be associated with a variety of deficits in cognitive functioning, and
these are deficits that could be linked to difficulties in emotion regulation, which is one of the main
characteristics of bipolar disorder. In particular, individuals with a diagnosis of bipolar disorder show
deficits in a number of cognitive abilities required for effective executive functioning (this is a set of
cognitive processes that are necessary for the cognitive control of behaviour). These include deficits in
verbal and nonverbal memory, attention, and working memory (Bourne et al., 2013). In addition, these
types of cognitive deficit are detected before the onset of bipolar symptoms and are also detected during
periods of remission, suggesting that they are deficits that are not simply caused by the bipolar disorder
itself (Kurtz & Gerraty, 2009; Meyer et al., 2004). Cognitive processes indicative of executive
functioning are critical for successful emotion regulation, and these processes include the ability to
inhibit negative thoughts and deploy adaptive emotion regulation strategies (such as reappraisal) rather
than maladaptive ones (such as rumination), and it is relevant that individuals with a diagnosis of
bipolar disorder report emotion‐related impulsivity (such as uncontrollable anger), the use of
maladaptive forms of emotion regulation such as rumination, and a difficulty regulating their own
negative emotions (Muhtadie, Johnson, Carver, Gotlib, & Ketter, 2014; Rowland et al., 2013). The
implication here is that these cognitive deficits may directly affect the controllability of mania and
depression affective states experienced in bipolar disorder. This raises the possibility that there is a
bidirectional relationship between cognitive deficits and emotionality in which cognitive deficits prevent
the adaptive control of emotionality, and in turn, high levels of emotionality interfere with effective
executive functioning (Lima, Peckham, & Johnson, 2018).

Triggers for depression and mania in bipolar disorder

Bipolar disorder consists of two quite different symptom types in depression and mania, and what
interests clinical researchers is the triggers for these two different types of symptoms. The triggers for a
depressive episode in bipolar disorder appear to be very similar to the factors that instigate depression
generally, namely experiences such as losses, failures, and negative life events generally (Johnson,
Cuellar, & Miller, 2010). The triggers for bouts of mania also appear to be varied and include an
increased responsiveness to rewards (e.g., mania can be a reaction to a positive life event such as passing
an exam) (Meyer, Johnson, & Winters, 2001), reactions to antidepressant medication, disrupted sleep
patterns and circadian rhythms, seasonality (bouts of mania increase in either spring or summer),
stressful life events generally, and exposure to high emotional expression in family members or
caregivers (Proudfoot, Doran, Manicavasagar, & Parker, 2011).
Study of some of these triggers has resulted in a number of models of mania. First, the study of how
mania is triggered by goal attainment (e.g., passing an exam) suggests that mania may be associated with
dysregulation in the behavioural activation system (BAS) that regulates sensitivity to rewards, and the
goal‐directed behaviours that are facilitated by the BAS are very similar to those behaviours exhibited
by bipolar sufferers during a manic phase (e.g., physiological arousal, increased sociability, and
incentive‐reward motivation) (Depue & Iacono, 1989). Second, the fact that mania is associated with
disruption to sleep and circadian rhythms suggests that this may be an important cause of mania. Not
only does sleep duration predict hypomanic symptoms the following morning (Leibenluft, Albert,
Rosenthal, & Wehr, 1996), but disruption to normal circadian rhythms (e.g., driving through the night,
long airplane journeys, working night shifts) also results in a shift to hypomania within 24 hr. Sleep
deprivation has been found to trigger mania in females more than males, is predominantly an effect
found in those with a bipolar I disorder diagnosis, and does not significantly influence periods of
depression (Lewis et al., 2017). The close relationship between sleep/circadian rhythm disruption and
manic episodes has led some theorists to suggest that sleep deprivation may be the final common
pathway through which a variety of other factors precipitate episodes of bipolar mania (Wehr, Sack, &
Rosenthal, 1987).

SELF‐TEST QUESTIONS
What are dysthymic disorder and cyclothymic disorder?
What is the distinction between bipolar disorder I and bipolar disorder II?
Describe the evidence that suggests there is a genetic component to bipolar disorder.
What are the main types of pharmacological treatments for bipolar disorder?
What factors trigger either periods of depression or periods of mania in bipolar disorder?

SECTION SUMMARY

7.2 BIPOLAR DISORDER

Bipolar disorder is characterised by periods of mania that alternate with periods of
depression.
Hypomania is the term for mild manic episodes
Cyclothymic disorder is a mild form of bipolar disorder which ranges from mild
depression to mania
The lifetime risk for bipolar disorder is 0.4–1.6%.
There is good evidence for a genetic component to bipolar disorder. 10–25% of first‐
degree relatives of bipolar disorder sufferers also report symptoms of mood disorder, as do
5–10% of first‐degree relatives of major depression sufferers.
Two significant triggers for mania in bipolar disorder include goal attainment and sleep
disruption

7.3 THE TREATMENT OF DEPRESSION

The previous sections illustrate the broad range of theories addressing the aetiology of mood disorders,
and these theories have each given rise to a variety of different treatments for these disorders. These
include a number of biological‐based treatments such as antidepressant drug therapy and
electroconvulsive therapy(ECT) which are based on addressing neurotransmitter imbalances
known to be a correlate of depression. In addition, there are a wide range of psychological therapies
including psychodynamic, behavioural, and cognitive behavioural therapies. Stepped‐care models
for the treatment of depression are often adopted (see Table 7.12), and these models advise that the type
of treatment provided for depression should be tailored to the severity of the symptoms and the
personal and social circumstances of the sufferer. An example of a stepped‐care model would be one
where (a) GPs and physicians—who are normally the first port of call for many people experiencing
depression—are advised to ensure that proper assessment is made of individuals who might present
with symptoms of depression, and they should not simply respond by providing medication; (b)
medication would not normally be recommended for the initial treatment of depression but should
mainly be reserved for the treatment of moderate to severe depression; and (c) mild depression should
be treated primarily with low intensity brief behavioural and cognitive interventions, and these include
structured exercise (e.g., three sessions per week of moderate duration for 10–12 weeks), guided self‐
help, and computerised CBT programmes (see Chapter 4, Section 4.1.2 for discussion of Improving
Access to Psychological Therapies low intensity interventions and computerised CBT).

electroconvulsive therapy (ECT) A method of treatment for depression or psychosis, first

devised in the 1930s, which involves passing an electric current of around 70–130 volts
through the head of the patient for around half a second.

Stepped-care models A treatment for psychopathology that emphasises that the type of
treatment provided for those individuals should be tailored to the severity of their symptoms
and their personal and social circumstances.

TABLE 7.12 The stepped care model of treatment for depression

From NICE (2009), https://www.nice.org.uk/guidance/cg90/chapter/1‐Guidance#stepped‐care.

The stepped‐care model provides a framework in which to organise the provision of services, and
supports patients, carers and practitioners in identifying and accessing the most effective interventions.
In stepped care the least intrusive, most effective intervention is provided first; if a person does not
benefit from the intervention initially offered, or declines an intervention, they should be offered an
appropriate intervention from the next step.
Focus of the intervention Nature of the intervention
Step 4: Severe and complex depression; risk to life; Medication, high‐intensity psychological
severe self‐neglect interventions, electroconvulsive therapy, crisis
service, combined treatments, multiprofessional
and inpatient care
Step 3: Persistent subthreshold depressive symptoms Medication, high‐intensity psychological
or mild to moderate depression with inadequate interventions, combined treatments,
response to initial interventions; moderate and severe collaborative care and referral for further
depression assessment and interventions
Step 2: Persistent subthreshold depressive Low‐intensity psychosocial interventions,
symptoms; mild to moderate depression psychological interventions, medication and
referral for further assessment and interventions
Step 1: All known and suspected presentations of Assessment, support, psychoeducation, active
depression monitoring and referral for further assessment
and interventions
7.3.1 Biological Treatments

Antidepressant medications
The three main types of medication for depression are (a) trycyclic drugs (such as imipramine), (b) MAO
inhibitors (such as tranylcypromine), and (c) SSRIs (such as Prozac) and serotonin and norepinephrine
reuptake inhibitors (SNRIs). The first two types of drug increase levels of both serotonin and
norepinephrine in the brain, while SSRIs and SNRIs act selectively on serotonin and prevent its
reuptake by the presynaptic neurone (see Figure 7.2). Treatment outcome studies have generally
indicated that depressed individuals given these forms of medication benefit when compared with
individuals taking placebos (Cipriani et al., 2018), and around 50–65% of individuals taking trycyclic
drugs show improvement (Gitlin, 2002) along with around 50% taking MAO inhibitors (Thase, Trivedi,
& Rush, 1995). Although these forms of drug treatment can be effective for some people, they often
have significant physical and psychological side effects (see Chapter 4, Table 4.1), and the most recently
developed of these drugs, SSRIs and SNRIs, do have some benefits over trycyclic drugs and MAO
inhibitors in that they produce fewer side effects (Enserink, 1999) and it is harder to overdose on them
(Isbister, Bowe, Dawson, & Whyte, 2004). However, SSRIs such as fluoxetine (Prozac) take around 2
weeks to begin to have an effect on symptoms (which is roughly the same as trycyclics) and also have
their own side effects such as headache, gastric disorders, and sexual dysfunction (Rosen, Lane, &
Menza, 1999) (see Chapter 4, Section 4.1.1 for a fuller discussion of antidepressant drugs, their
effectiveness, and how they might work when they are effective).
There is also controversy about whether SSRIs such as Prozac increase the risk of suicide. Recent meta‐
analyses suggest that increased risk of suicide with the use of SSRIs cannot be ruled out, but these risks
should be balanced against the relative effectiveness of SSRIs in treating depression (Gunnell, Saperia,
& Ashby, 2005). Nevertheless, despite these cautions, the drugs that have been developed to treat
depression do help to alleviate symptoms in a majority of cases, they provide relatively rapid relief from
symptoms in around half of those treated, and they are effective not only with bouts of major
depression but also with chronic depressive disorders such as dysthymic disorder (Hellerstein, Kocsis,
Chapman, Stewart, & Harrison, 2000). However, relapse is a common occurrence after drug treatment
for depression has been withdrawn (Reimherr et al., 2001), and a more effective treatment may be to
combine drug therapy with psychological therapies such as CBT (Kupfer & Frank, 2001).
In contrast to those drugs prescribed for major depression, the drug therapies of choice for bipolar
disorder are rather different. The traditional treatment for bipolar disorder has been lithium
carbonate. Around 80% of bipolar disorder sufferers who take lithium benefit from it, and the drug
can provide relief from symptoms of both manic and depressive episodes (Curran & Ravindran, 2014;
Won & Kim, 2017). There is some debate about how lithium actually moderates the symptoms of
bipolar disorder. Early views suggested that lithium stabilises the activity of sodium and potassium ions
in the membranes of neurones, and it is the instability of these ions that gives rise to the symptoms of
bipolar disorder (Swonger & Constantine, 1983). Other accounts argue that it changes synaptic activity
in neurons in such a way as to help neurotransmitters bind to a receiving neuron, thus helping to
increase neuronal plasticity (Ghaemi, Boiman, & Goodwin, 1999; Won & Kim, 2017). However,
treatment of bipolar symptoms with lithium carbonate does have some disadvantages. First,
discontinuation often increases the risk of relapse (Suppes, Baldessarini, Faedda, & Tohen, 1991), and
second, an added disadvantage of lithium treatment is the difficulty in prescribing a suitable dosage on
an individual basis. Lithium is a toxic substance, and the effective dose for alleviating symptoms is often
close to the toxic level. As a consequence, an overdose can cause delirium, convulsions and, in rare
cases, can be fatal. More recently, combinations of antipsychotic drugs and SSRIs have been used
successfully to address symptoms of bipolar disorder (e.g., a combination of the antipsychotic drug
olanzapine and the antidepressant SSRI drug fluoxetine), and this combination has been shown to
have significant effects on both mania and depression symptoms (Deeks & Keating, 2008).
 lithium carbonate A drug used in the treatment of bipolar disorder.

olanzapine An antipsychotic drug commonly prescribed in combination with the

antidepressant SSRI drug fluoxetine as a treatment for bipolar disorder.

fluoxetine (Prozac) A selective serotonin reuptake inhibitor (SSRI) which reduces the uptake
of serotonin in the brain and is taken to treat depression.

One drug that has received a good deal of recent publicity for its potential as an antidepressant
medication is the anaesthetic ketamine. The few randomised controlled trials that have tested the
effectiveness of ketamine to date suggest that it may have significant antidepressant effects when taken
either orally or intravenously (Rosenblat et al., 2019) and may do so by increasing neural plasticity
(Moda‐Sava et al., 2019). But a fuller judgement on the suitability of ketamine as an antidepressant
awaits the outcome of more robust randomised controlled trials and further research on the
mechanisms by which it may reduce depressive symptoms.

Transcranial magnetic stimulation (rTMS)

In 2015 the National Institute for Health and Care Excellence (NICE) published guidelines for the use
of repetitive transcranial magnetic stimulation for depression (NICE, 2015). In this procedure, an
electromagnetic coil is placed on the scalp and pulses of magnetic energy are used to increase activity in
the left dorsolateral prefrontal cortex. A treatment session would normally last for 30–60 minutes, with
daily doses lasting for between 2 and 6 weeks. Randomised controlled trials have indicated that rTMS
can be more effective than sham control treatments in relieving depression symptoms in clients who
have failed to respond to antidepressant medications (Berlim, van den Eynde, Tovar‐Perdomo, &
Daskalakis, 2014)

Electroconvulsive therapy (ECT)

This method of treatment was first discovered in the 1930s (Cerletti & Bini, 1938) and involves passing
an electric current of around 70–130 V through the head of the patient for around half a second. It was
first used as an experimental means of inducing brain seizures but was subsequently found to have
beneficial effects on symptoms of severe depression. Today, ECT is used primarily with individuals
suffering severe depression who have not responded well to other forms of treatment (Cohen et al.,
2000). While it can provide effective short‐term relief from symptoms of severe depression, it also has a
number of controversial features. First, it has a number of side effects, the most common of which is
memory loss that affects the ability to learn new material (anterograde amnesia) and the ability to recall
material learned before the treatment (retrograde amnesia). These effects can last for up to 7 months
following ECT (Lisanby, Maddox, Prudic, Devanand, & Sackeim, 2000; Sackeim et al., 2007). Second,
many people find the idea of having a strong electric current passed through their brain frightening and
will be resistant to the use of this kind of therapy. Indeed, many view the physical nature of ECT as a
form of ‘assault’ on the patient, and a means of managing unruly in‐patients rather than a form of
therapy. This was a view that was strikingly portrayed in the 1975 film One Flew over the Cuckoo's Nest
starring Jack Nicholson (Photo 7.1). Third, no one is clear how ECT does work in alleviating the
symptoms of severe depression, but it has been suggested that shock affects the levels of serotonin and
norepinephrine in the brain (Mann & Kapur, 1994). However, this beneficial effect may be short term
and limited to as little as 4 weeks (Breggin, 1997), and the relapse rate is around 50% by 12‐months after
successful initial ECT treatment (Jelovac, Kolshus, & McLoughlin, 2013). Other researchers have
argued that the short‐term beneficial effects of ECT are nothing more than would be expected
following any trauma to the brain—with immediate symptoms being confusion, headache, and nausea
followed by a period of emotional shallowness, denial, and artificial euphoria that may last for a few
weeks (Breggin, 1997).

PHOTO 7.1 Jack Nicholson's character in the famous 1975 film One Flew over the Cuckoo's Nest was subjected to
ECT treatment, and this unsympathetic portrayal led many to view ECT as a form of patient management rather than
treatment.
Nevertheless, despite these criticisms, ECT may still have a role to play in the treatment of severe
depression in both major and bipolar depression when symptoms are resistant to pharmacological
treatment (Medda, Perugi, Zanello, Ciuffa, & Cassano, 2009), and the almost immediate beneficial
effects of ECT may be helpful in alleviating depression when suicide is a real possibility.

7.3.2 Psychological Treatments

Psychoanalysis
In Section 7.1.2 we discussed some of the psychodynamic explanations of depression. Central to these
accounts is the view that depression is a response to loss (perhaps of a loved one) and may manifest as
symbolic loss, in which other kinds of losses (such as losing a job) are seen as equivalent to losing a loved
one. Psychodynamic theories (such as those developed by Freud and Abraham) argue that the
individual's response to loss is to turn their anger at the loss inwards, and this in turn can develop into
self‐hate resulting in low self‐esteem (Frosh, 2012, chapter 13). The aim of psychodynamic therapy,
therefore, is to help the depressed individual achieve insight into this repressed conflict and to help
release the inwardly directed anger. Psychodynamic therapy will do this by using various techniques to
help people explore the long‐term sources of their depression (see Chapter 4, Section 4.1.1), and this
will involve exploring conflicts and problematic relationships with attachment figures—such as parents
—and discussing long‐standing defensive patterns. For example, the psychodynamic therapist may use
free association or dream interpretation to help the individual recall early experiences of loss
that may have contributed to repressed conflicts and symptoms of depression. In this way,
psychodynamic therapies attempt to bring meaning to the symptoms of depression and help the
individual understand how early experiences may have contributed to their symptoms and affected their
current interpersonal relationships.

dream interpretation The process of assigning meaning to dreams.

Evidence for the therapeutic efficacy of psychodynamic therapies in the treatment of depression is
meagre. This is in part because processes within psychodynamic therapies are difficult to objectify and
study in a controlled way. Psychodynamic therapists also differ significantly in the way they interpret
psychodynamic principles in practice. A controlled study by the American Psychiatric Association (APA,
1993) reported that there was no evidence for the long‐term efficacy of psychodynamic treatment of
depression, although some more recent studies have indicated that short‐term psychodynamic
interventions may be effective in significantly reducing some symptoms of depression (Leichsenring,
2001; Lemma, Target, & Fonagy, 2011).

Social skills training

It was Lewinsohn and his colleagues (e.g., Lewinsohn & Shaw, 1969) who first drew attention to the fact
that depressed individuals (a) have deficits in the general social skills that are required for efficient and
effective interactions, and (b) possess a demeanour that others (e.g., other family members) may find
negative and off‐putting. These two features of the depressed individual will act to accentuate
depression by reducing the frequency of social interactions and reducing the rewards that the individual
might obtain from these interactions. The kinds of interpersonal social skills deficits possessed by
depressed individuals range from negative self‐evaluation of their own skills to deficits in behavioural
indicators of social skills such as eye contact, relevant facial expressions, and speed of response in
conversations (Segrin, 2000).
In response to these deficits, social skills training therapy for depression was developed (Becker,
Heimberg, & Bellack, 1987). Social skills training assumes that depression in part results from the
individual's inability to communicate and socialise appropriately, and that addressing these skill deficits
should help to alleviate many of the symptoms of depression. This may involve training assertion skills,
conversational interaction skills, dating skills, and job‐interview skills, and can involve procedures such
as modelling, rehearsal, role‐playing, and homework assignments out of the therapeutic setting (Becker
et al., 1987; Jackson, Moss, & Solinski, 1985).
An example of one particular social skills training programme for depression is that designed by
Herson, Bellack, and colleagues (Hersen, Bellack, & Himmelhoch, 1980; Thase, 2012). This involved 1‐
hour sessions for 12 weeks and began by focussing on skills appropriate for interactions with family,
friends, work colleagues, and strangers, respectively. Particular features of this programme included (a)
role‐playing tasks, feedback, modelling, and positive reinforcement for appropriate behaviours, and (b)
attention to the specific details of social interactions such as smiles, gestures, use of eye contact, etc.
Clients were subsequently given homework tasks requiring them to practice their skills outside of the
therapy situation. As a result of this programme, clients showed not only improvements in their social
skills but also a decrease in symptoms of depression that were still apparent 6 months after the end of
the programme. Studies evaluating the efficacy of social skills training for depression have shown that
such programmes result in an improvement in a range of social skills and a decrease in reported
symptoms of depression (Zeiss, Lewsinsohn, & Munoz, 1979). They also suggest that social skills
training is equally as effective as many other psychological therapies commonly employed for depression
(Fine, Forth, Gilbert, & Haley, 1991; Miller, Norman, Keitner, Bishop, & Dow, 1989).

Behavioural activation
Behavioural theories of depression emphasis that depression may be triggered by a life‐event loss (such
as a bereavement), and this event may represent the loss of important sources of reward and
reinforcement for the individual. This leads the depressed individual into a vicious cycle where this lack
of reward generates depressive symptoms, and in turn, the individual's depressive behaviour may
ultimately lead to aversive social consequences in the form of negative social reactions from friends and
family (Coyne, 1976). This view has led to the development of behavioural activation (BA) therapies for
depression that attempt to increase the client's access to pleasant events and rewards and decrease their
experience of aversive events and consequences (Lewinsohn et al., 1980; Turner & Leach, 2012). Early
BA programmes attempted to achieve these goals through daily monitoring of pleasant/unpleasant
events and the use of behavioural interventions that developed activity scheduling (e.g., scheduling
reinforcing activities so that they will reinforce less attractive activities). They also include social skills
and time management training (Lewinsohn & Shaffer, 1971; Zeiss et al., 1979). The use of BA was
given a further boost by the fact that a number of studies demonstrated that cognitive change is just as
likely to occur following purely behavioural interventions as after cognitive interventions (Jacobson &
Gortner, 2000; Simons, Garfield, & Murphy, 1984). That is, reductions in negative thinking and
negative self‐statements in depression can be decreased by behavioural interventions that contain no
explicit cognitive change components. Recent developments of BA include the self‐monitoring of
pleasant/unpleasant experiences and the identification of behavioural goals within major life areas (e.g.,
relationships, education, etc.) that can be targeted for development and reinforcement, and BA has also
been shown to be beneficial for individuals suffering chronic depression (Erickson & Hellerstein, 2011).
Treatment in Practice 7.1 gives an example of how a brief BA programme for depression is structured
and executed (Lejuez, Hopko, LePage, Hopko, & McNeil, 2001).
 CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 7.1
BRIEF BEHAVIOURAL ACTIVATION TREATMENT FOR
DEPRESSION (BATD)

Behavioural activation treatment for depression (BATD) is conducted over 8–15 sessions, and
sessions progress through the following stages:
1. Assessing the function of depressed behaviour; weakening access to positive reinforcement
(e.g., sympathy) and negative reinforcement (e.g., escape from responsibilities); establishing
rapport with the client and introducing the treatment rationale.
2. Increasing the frequency and subsequent reinforcement of healthy behaviour; clients begin
a weekly self‐monitoring exercise that serves as a baseline assessment of daily activities and
orients clients to the quantity and quality of their activities, and generates ideas about
activities to target during treatment.
3. Emphasis is shifted to identifying behavioural goals within major life areas, such as
relationships, education, employment, hobbies and recreational activities, physical/health
issues, and spirituality.
4. Following goal setting, an activity hierarchy is constructed in which 15 activities are rated
ranging from ‘easiest’ to ‘most difficult’ to accomplish. With progress being monitored by
the therapist, over a period of weeks the client progressively moves through the hierarchy
from easiest to most difficult. Patients are urged to identify weekly rewards that can be
administered if activity goals are met.

(from Hopko, Lejuez, Ruggiero, & Eifert, 2003)

Meta‐analyses of random controlled trials have generally reported significantly better effects of BA in
treating depression than appropriate control conditions (Ekers et al., 2014), but there is less consensus
on whether BA is superior to other treatments such as CBT or antidepressant medication (Dimijian et
al., 2016).

Cognitive therapy
As we saw in Section 7.1.2, dysfunctional cognitions appear to play an important part in the
maintenance of depressive symptoms. Beck's Cognitive Theory of depression (Beck, 1967, 1987) argues
that depression is maintained by a systematic set of dysfunctional negative beliefs that form a negative
schema though which the depressed individual views themselves, their world, and their future. From this
theory Beck developed one of the most successful and widely adopted therapeutic approaches for
depression, and this has come to be known by various names including cognitive therapy, cognitive
retraining, or cognitive restructuring. The thrust of this approach is (a) to help the depressed
individual identify their negative beliefs and negative thoughts, (b) to challenge these thoughts as
dysfunctional and irrational, and (c) to replace these negative beliefs with more adaptive or rational
beliefs (see Strauss, 2019). For example, depressed individuals tend to hold beliefs and attributional styles
that are overgeneralised. They will respond to a specific failure (such as failing their driving test) with
statements such as ‘Everything I do ends in failure’ or ‘The world is against me’. The cognitive therapist
will attempt to identify these overgeneralised beliefs and challenge them as irrational—using, if at all
possible, relevant examples from the client's own experiences. In addition to this, the client will be asked
to monitor the negative automatic thoughts that give rise to negative beliefs and depressive
symptoms, often using a form which allows them to link the automatic thoughts to particular situations
and outcomes, and to think through possible rational alternatives to the negative automatic thought
(Table 7.13). The overall philosophy of cognitive therapy for depression is to correct the negative
thinking bias possessed by depressed individuals, and in some cases this aim can be supplemented with
the use of reattribution training (Beck, Rush, Shaw, & Emery, 1979). Reattribution training
attempts to get the client to interpret their difficulties in more hopeful and constructive ways rather than
in the negative, global, stable ways typical of depressed individuals (see Table 7.6).

cognitive therapy A form of psychotherapy based on the belief that psychological problems
are the products of faulty ways of thinking about the world.

negative automatic thoughts Negatively valenced thoughts that the individual finds difficult
to control or dismiss.

reattribution training A technique used in the treatment of depression which attempts to

get clients to interpret their difficulties in more hopeful and constructive ways rather than in the
negative, global, stable ways typical of depressed individuals.

CBT is significantly more effective at reducing depression symptoms than treatment‐as‐usual (López‐
López et al., 2019), and works more quickly than interpersonal psychotherapy (Mulder, Boden, Carter,
Luty, & Joyce, 2017), Outcome studies have shown that cognitive therapy is usually at least as effective as
drug therapy in treating the symptoms of depression (Rush, Beck, Kovacs, & Hollon, 1977), and some
have shown that it is superior to drug therapy at 1‐year follow‐up (Blackburn & Moorhead, 2000;
Hollon, Shelton, & Davis, 1993). DeRubeis et al. (2005) compared cognitive therapy with drug therapy
(paroxetine) and a placebo‐control condition. After 8 weeks they found improvement in 43% of the
cognitive therapy group, 50% of the drug treatment group, against only 25% in the placebo group, and
these levels of improvement were maintained at 16 weeks. Cognitive therapy also appears to have
longer‐term beneficial effects by preventing relapse compared to medication (Dobson et al., 2008;
Hensley, Nadiga, & Uhlenhuth, 2004), but a combination of cognitive therapy with drug treatment
appears to be superior to either treatment alone (Kupfer & Frank, 2001).
Cognitive therapy has also been successfully adapted to treat individuals with bipolar disorder in
conjunction with appropriate medication (Newman et al., 2002) in both individual (da Costa et al.,
2010) and group (Gomes et al., 2011) settings. These interventions help the sufferer with medication
compliance, mood monitoring, anticipating stressors, interpersonal functioning, and problem solving
(Danielson, Feeny, Findling, & Youngstrom, 2004; Scott, Garland, & Moorhead, 2001).
While there is no doubt that cognitive therapy is successful in helping to treat depression, there is still
some debate about how it achieves these effects. We have seen earlier that cognitive change is just as
likely to occur following purely behavioural treatments as they are after cognitive treatments. Cognitive
therapy contains both elements of cognitive restructuring which aims to change cognitions directly, and
behavioural exercises designed to establish new cognitions—so is the cognitive restructuring element
entirely necessary? In addition, there is evidence that cognitive therapy not only changes negative
cognitions, but also results in improvements in abnormal biological processes (Blackburn & Moorhead,
2000). This raises the question of whether cognitive therapy has its effects by changing cognitions or
biological processes. Nevertheless, regardless of how it works, cognitive therapy certainly does work, and
recent evidence suggests that it not only reduces the occurrence of negative cognitions in depression,
but it also helps to dissociate negative cognitions from the symptoms of depression better than other
treatments (Beevers & Miller, 2005).
Mindfulness‐based cognitive therapy (MBCT)
A critical issue in the treatment of depression is how to predict and eliminate possible relapse after
remission or successful treatment. In the case of major depression, it appears that the risk of relapse
increases with every consecutive bout of depression, and this increased risk also means that depression
can reoccur with less and less external provocation (such as a stressful life event) (Kendler, Thornton, &
Gardner, 2000). This increased risk of relapse in recovered depressed individuals appears to be caused
by periods of negative mood (dysphoria) activating patterns of negative or depressogenic thinking such
as self‐devaluation and hopelessness (Ingram, Miranda, & Segal, 1998; Segal, Gemar, & Williams,
1999). That is, as soon as the recovered depressed individual begins to feel depressed again, this
reactivates negative thinking that leads to a downward spiral to relapse. Mindfulness‐based
cognitive therapy(MBCT) was developed in order to try to combat this linkage between periods of
dysphoria and the onset of negative thinking, and it aims to get individuals to take a ‘decentred’
perspective by being aware of negative thinking patterns and viewing them purely as mental events
rather than accurate reflections of reality (Teasdale, 1988; Teasdale, Segal, & Williams, 1995). MBCT
is based on an integration of aspects of CBT and components of the mindfulness‐based stress reduction
programme that contains elements of meditation and provides training in the deployment of attention
(Kabat‐Zinn, 1990). Clients are taught to become more aware of, and relate differently to, their
thoughts, feelings, and bodily sensations, and treat thoughts and feelings as passing events in the mind
rather than identifying with them. It also teaches skills that allow individuals to disengage from habitual
dysfunctional cognitive routines and depression‐related patterns of ruminative thought. Studies suggest
that MBCT can (a) significantly reduce the probability of future relapse. Ma and Teasdale (2004) found
that MBCT reduced relapse from 78% to 36%, and in participants who had experienced four or more
bouts of depression only 38% of those receiving MBCT relapsed compared with 100% in the
treatment‐as‐usual control group, and (b) significantly reduce symptoms of mood disorders generally
(Hofmann, Sawyer, Witt, & Oh, 2010). More recently, some of the mechanisms of change that make
MBCT effective have been identified, and these include reducing repetitive negative thinking (e.g.,
rumination), and facilitating self‐compassion and positive affect (Mackenzie, Abbott, & Kocovski, 2018).
These findings suggest that teaching previously depressed individuals to adopt a detached, decentred
relationship to their depression‐related thoughts and feelings can have significant therapeutic gains. A
Science Oxford Live lecture on the science of mindfulness by Professor Mark Williams can be found at
https://www.youtube.com/watch?v=wAy_3Ssyqqg.
TABLE 7.13 Example of a thought record form used to record the negative automatic thoughts (“hot thoughts”)
experienced by depressed individuals
Situation Moods Automatic Evidence Evidence Alternative/balanced Rate
thoughts that that does thoughts moods
(images) supports not now
the hot support
thought the hot
thought
Who? What do you What was Write an alternative or Re‐rate
What? feel? going balanced thought. moods
When? through Rate how much you listed in
Where? your mind believe in each column
just before alternative or balanced 2 as
you started thought (0–100%) well as
to feel this any
way? new
Any other moods
thoughts? (0–
Images? 100%)
In hotel Depressed I need The hurt When I'm
room— 100% something to inside is with other
alone— Lonely make me unbearable people,
Sunday 100% feel numb Killing talking
10 p.m. Empty and take myself will about
100% away the solve all this myself,
Confused pain People have things begin
100% Nothing is tried to help to feel better
Unmotivated going right me and I've I've felt like
100% for me been given this before
Stressed I'm many drugs, and have
worthless—I none of managed to
can never which work get myself
achieve through it
anything Some
At the mornings I
moment I wake up
simply feel feeling and
like ending it thinking
all differently,
What is so there may
there to look be hope
forward to in My friends
life? tell me that
I feel like an I have
empty shell something
to offer
I do laugh
when I'm
with others
This form relates these thoughts to possible situational triggers and attempts to get the depressed individual to think up
evidence that might be contrary to that “hot thought .” (After Greenberger & Padesky, 1995)
SELF‐TEST QUESTIONS
What is a stepped‐care model for the treatment of depression?
What drugs are important in treating depression, and how do they have their effect?
What are the important components of social skills training for depression?
What is the rationale behind behavioural activation therapy for depression?
How does cognitive therapy attempt to eradicate negative thinking?
What is reattribution training?
What is MBCT and what role does it play in the control of depression?
What are the main types of pharmacological treatments for bipolar disorder?
What is transcranial magnetic stimulation?
 SECTION SUMMARY

7.3 THE TREATMENT OF DEPRESSION

Stepped‐care models for the treatment of depression advise that the treatment should be
tailored to the severity of symptoms
Drug treatments have been developed that attempt to address imbalances in
neurotransmitters such as serotonin, dopamine, and norepinephrine.
Three main types of medication for depression are trycyclic drugs, MAO inhibitors, and
SSRIs and serotonin and norepinephrine reuptake inhibitors (SNRIs).
Transcranial magnetic stimulation (rTMS) is used to treat depression with the use of pulses
of magnetic energy to increase activity in the left dorsolateral prefrontal cortex.
Lithium carbonate is the main drug prescribed for Bipolar disorder.
Electroconvulsive therapy (ECT) is sometimes used with individuals suffering severe
depression who have not responded well to other forms of treatment.
Psychodynamic therapy uses a range of techniques (e.g., free association, dream analysis)
to help the individual to explore the long‐term sources of their depression.
Social skills training assumes that depression results from the depressed individual's
inability to communicate and socialise appropriately, and addresses this deficit using social
skills training programmes.
Behavioural activation therapies attempt to increase the individual's access to pleasant
events and rewards and decrease their experience of aversive events.
Cognitive therapy for depression attempts to help the depressed individual identify
negative beliefs and thoughts, challenge these beliefs as irrational, and replace them with
positive rational beliefs.
Outcome studies suggest that cognitive therapy is at least as effective as drug therapy.
Mindfulness‐based cognitive therapy (MBCT) has been developed to prevent relapse in
recovered depressed individuals by making them aware of negative thinking patterns that
may be triggered by subsequent bouts of depression.
Computerised CBT is also an effective treatment for milder forms of depression.

7.4 NONSUICIDAL SELF‐INJURY (NSSI)

Nonsuicidal self‐injury (NSSI), sometimes known as deliberate self‐harm, is defined as direct
and deliberate bodily harm in the absence of suicidal intent (Nock, 2010) and most frequently takes the
form of cutting and carving the skin with a knife or similar sharp instrument (usually on arms, legs, and
stomach). Other forms of NSSI include burning, taking overdoses, pulling hair, or picking skin.
Deliberate self‐harm is included under the DSM‐5 diagnostic category called NSSI that covers
‘intentional self‐inflicted damage to the surface of the body that is likely to induce bleeding or bruising’.
(Table 7.14). This phenomenon has previously been labelled in many ways, including ‘self‐mutilation’,
‘self‐harm’, ‘cutting’, and parasuicide, but it is important to distinguish deliberate self‐harm from both
suicide and parasuicide. The large majority of people who indulge in deliberate self‐harm do not have
suicidal intentions and nor are they at risk for suicide (Greydanus & Shek, 2009).

nonsuicidal self-injury (NSSI) The act of deliberately causing injury to one’s body
without conscious suicidal intent.

deliberate self-harm A parasuicidal phenomenon that commonly includes cutting or

burning oneself, taking overdoses, hitting oneself, pulling hair or picking skin, or self-
strangulation.

Deliberate self‐harm is predominantly an adolescent activity with surveys suggesting that between 7.5%
and 45% of adolescents may have deliberately self‐harmed at some time (e.g., Cipriano, Cella, &
Cotrufo, 2017; Plener, Libal, Keller, Fegert, & Muehlenkamp, 2009), rising to 38.9% among university
students, and 4–23% among adults (Andover, 2014; Whitlock et al., 2011). People typically engage in
self‐harm when they are alone and experiencing negative thoughts and feelings (e.g., having a bad
memory, feeling angry, experiencing self‐hatred, or numbness) (Nock, Prinstein, & Sterba, 2009). This
suggests that self‐injury is performed as either a means of self‐soothing or of help‐seeking (e.g., with the
end goal of enlisting others to help the individual cope with their negative feelings or negative self‐
image) (Muehlenkamp et al., 2009). Many adolescents who self‐harm do not usually suffer any long‐
term psychological effects from doing so, but there are groups of individuals who are more at risk of
developing self‐harm activities, and these include depressed adolescents (Hawton & James, 2005)—
especially those going through inter‐personal crises, or individuals with existing mental health problems
such as eating disorders (Wedig & Nock, 2010), excessive alcohol intake (Hussong, 2003), substance
abuse (Greydanus & Shek, 2009; Koob & Kreek, 2007), and psychosis (Gerard, de Moore, Nielssen, &
Large, 2012). In particular, adolescents at risk of deliberate self‐harm show intrapersonal vulnerabilities
such as higher physiological arousal in response to frustrating tasks and stressful events (Nock & Mendes,
2008; Nock, Wedig, Holmberg, & Hooley, 2008), and poor verbal communication and social problem‐
solving skills (Nock & Mendes, 2008; Nock & Photos, 2006) (Client's Perspective 7.2).
TABLE 7.14 DSM‐5 diagnostic criteria for nonsuicidal self injury

Over the previous year on at least five occasions the individual has intentionally self‐inflicted
damage to the surface of their body to induce bleeding, bruising, or pain with the anticipation
that the injury will lead to only minor or moderate physical injury
Presence of at least two of the following:
Negative feelings or thoughts such as depression, anxiety, and suchlike immediately prior to
the self‐injury
Before the self‐injury a period of fixation with the intended self‐injury which is hard to resist
Preoccupation with self‐injury occurs frequently even when not acted upon
The self‐injury is carried out with the expectation that it will relieve a negative feeling or
induce a positive feeling during or directly after the self‐injury
The self‐injury does not occur only during states of psychosis, delirium, or intoxication
There is no suicidal intent

CLIENT'S PERSPECTIVE 7.2 DELIBERATE SELF‐HARM

 Comments from an adolescent self‐harmer posted on an Internet message board:
“Hello. . . Um where to start. The thing is self‐harm is the only way I can deal with things.
Ive tried everything in the book and yeah, none of it even comes close to cutting. I tried the
rubber‐band thing and ended up with huge welts that actually bruised and thats just another
form of self‐harm. I tried writing, doing other things… None of it helps. My scars are
another thing about self‐harm that I cant draw myself away from. I like them in some odd
way… I know. Your probably thinking im insane or an attention‐getter or something… But
is there ANYONE who feels the same? I mean likes the way it feels and honestly doesnt want
to stop even though its bad and all . . . ?”
Deliberate self‐harm is primarily an adolescent phenomenon, and estimates suggest that
between 13% and 45% of adolescents have deliberately self‐harmed at some time (e.g., Plener
et al., 2009). Self‐harm usually occurs when the person is alone and experiencing negative
thoughts or feelings, and appears to serve a self‐soothing or help‐seeking function (Nock, 2010).
The most common forms of deliberate self‐harm are cutting or carving the skin with a sharp
instrument, usually on the arms, legs, and stomach, but can also include burning, taking
overdoses, pulling hair, and picking skin. Many adolescents who self‐harm do not suffer any
long‐lasting psychological effects from doing so, but there are vulnerable groups of adolescents
for whom self‐harm may be a more enduring problem. These include depressed adolescents,
those with interpersonal crises, or individuals with some existing mental health problems such
as psychosis, substance abuse problems, or eating disorders (Greydanus & Shek, 2009; Hawton
& James, 2005).

Preventing self‐harm can be difficult because acts of self‐harm are often impulsive and carried out in
secret, and denial is a common feature of those who self‐harm—especially when the self‐harm may
have a positive effect by providing temporary relief from their difficulties. Similarly, most self‐injurers
also report feeling little or no pain during self‐harming, and this also makes the activity difficult to detect
(Favazza, 1996; Nock & Prinstein, 2004). However, it may be possible to target vulnerable groups and to
ensure that they have access to mental health services and support services. As we have noted,
vulnerable groups that have been identified include (a) depressed adolescents; (b) those with
interpersonal crises, such as those who have lost a partner or have run away from home; and (c) those
who have previously self‐harmed (especially in conjunction with substance misuse and conduct disorder)
(Hawton & James, 2005).
Effective treatments for NSSI are still being developed, but psychological interventions such as
dialectical behaviour therapy, CBT, and mentalisation‐based therapy (MBT) have all been shown to
reduce levels of self‐harming (Ougrin, Tranah, Stahl, Moran, & Asarnow, 2015). The evidence on the
effectiveness of medications for NSSI is less convincing, but some antidepressant and antipsychotic
drugs have been shown to reduce the level of self‐harming during treatment with these medications
(Turner, Austin, & Chapman, 2014).

SELF‐TEST QUESTIONS
How is nonsuicidal self‐injury defined and what kinds of problems lead adolescents in
particular to self‐harm?
What are the most common forms of nonsuicidal self‐injury?
What psychological functions is nonsuicidal self‐injury thought to serve?

SECTION SUMMARY

7.4 NONSUICIDAL SELF‐INJURY

Nonsuicidal self‐injury is common in adolescence and frequently includes cutting and
carving the skin, burning, taking overdoses, pulling hair, or picking skin.
Nonsuicidal self‐injury can be performed as a form of self‐soothing or as help‐seeking.
Treatments for nonsuicidal self‐injury include CBT and dialectical behaviour therapy, and
antidepressant or antipsychotic medications.

7.5 SUICIDE
The World Health Organization estimates that 800,000 people commit suicide each year (WHO,
2019), but the number of people who attempt suicide can be up to 20 times higher. The WHO report
also described other sobering facts about suicide. Suicide is the third highest cause of death worldwide
amongst 15–19 year‐olds and does not occur in just high‐income countries but is a global phenomenon
with over 79% of global suicides occurring in low‐ and middle‐income countries in 2016 (Figure 7.6).
 suicide The action of killing oneself intentionally.

FIGURE 7.6 Suicide rates worldwide. From WHO (2019).

Source: Retrieved from: http://www.who.int/news‐room/fact‐sheets/detail/suicide
Suicide attempts often occur in the context of mental health problems (especially depression), and it has
been estimated that between 60% and 98% of all suicides involve a mental health problem as a risk
factor (Ferrari et al., 2014). More than one in four people with a diagnosis of depression are likely to
attempt suicide at least once in their lifetime (Bernal et al., 2007), and the cognitive construct of
‘hopelessness’ is one of the best single predictors of suicide, especially in those with a diagnosed
psychotic disorder (Klonsky, Kotov, Bakst, Rabinowitz, & Bromet, 2012) (see Section 7.1.2). Estimates of
suicide rates indicate that the 12‐month prevalence rate for suicide attempts for developed countries is
0.4% and for suicidal ideation is 2% (Borges et al., 2010). Studies that have investigated the lifetime
prevalence rates for suicide suggest that 18.4% of people report lifetime suicidal ideation (Lee et al.,
2010), 3.9% have planned a suicide, and 4.6% have attempted suicide in their lifetime (Kessler, Borges,
& Walters, 1999). The likelihood of an individual committing suicide tends to increase with age (Nock
et al., 2008), and women are around three times more likely to attempt suicide than men, but the rate for
successful suicide is around four times higher in men than women (Peters & Murphy, 1998), and this is in
part because men will tend to adopt more lethal methods than women (such as guns and jumping, see
Table 7.15).
TABLE 7.15 Characteristics that define suicide attempters and completers
From Fremouw et al. (1993).
Characteristics Attempters Completers
Gender Mainly female Mainly male
Age Mainly young Increased risk with age
Method Pills, cutting More violent (guns,
jumping)
Common Mild depression, borderline personality disorder, Major depression,
diagnoses schizophrenia alcoholism
Dominant affect Depression with anger Depression with
hopelessness
Motivation Change in situation, cry for help Death, self‐annihilation

Suicidal phenomena have become more common in teenagers and adolescents. In the UK there were
177 suicides among 15–19 year olds in 2017, compared with 110 in 2010. However, the UK male
suicide rate in 2017 was 15.5 deaths per 10,000 which was the lowest since the time series began in
1981. The suicide rate for females in the UK in 2017 was 4.9 deaths per 100,000, which has remained
at roughly the same rate since 2007 (Office for National Statistics, 2018). The reasons for the increase in
adolescent suicide rates is unclear, but a number of factors may be relevant: (a) modern teenagers are
probably exposed to many of the life stressors experienced by adults, yet may lack the coping resources
to deal with them effectively (Reynolds & Mazza, 1994); (b) suicide is also a sociological as well as a
psychological phenomenon, and media reports of suicide often trigger a significant increase in suicides
(Gould, Jamieson, & Romer, 2003). This is especially true in the case of adolescents and teenagers,
where news of celebrity suicides are often associated with increases in the rate of teenage suicide
attempts (Focus Point 7.5); and (c) there has been a recognised increase in stress‐ and anxiety‐related
problems amongst children and adolescents over the past decade, and this is discussed in Focus Point 1.1
in Chapter 1.

7.5.1 Risk Factors for Suicide

One of the best predictors of future suicide attempts is a history of at least one previous suicide attempt
(Leon, Friedman, Sweeney, Brown, & Mann, 1990). However, since only 20–30% of those who attempt
suicide have made a previous attempt, it is important to look at other risk factors. Suicide is a complex
phenomenon, and risk factors encompass a broad range of domains such as psychiatric, psychological,
physical, personal, familial, and social factors (Evans, Hawton, & Rodham, 2004; see O'Connor &
Portzky, 2018, for an overview of new developments in suicide research). For example, (a) suicide is
related to diagnoses of depression, schizophrenia, borderline personality disorder, panic disorder,
alcoholism, and substance abuse (e.g., Isometsa et al., 1995). Absolute risk of suicide is highest for those
with a diagnosis of bipolar disorder (6–10%) and major depression (5–7%), but all psychiatric disorders
studied resulted in an increase in suicide risk of between 2% and 8% compared to the rate of less than
1% found in the control group of individuals without a psychiatric diagnosis (Nordentoft et al., 2011);
(b) psychological predictors of suicide include the cognitive construct of ‘hopelessness’ (Abramson et al.,
2000) and also low self‐esteem (Fergusson & Lynskey, 1995), (c) both poor physical health and physical
disability are also predictors of suicide (Dubow et al., 1989; Wagman Borowsky, Resnick, Ireland, &
Blum, 1999); and (d) low socio‐economic status is also a significant risk factor (Li, Page, Martin, &
Taylor, 2011; Lorant et al., 2018), and the impact of the recent world‐wide economic recession has
resulted in a significant 3.8% increase in the suicide rate since the onset of the recession (Reeves,
Stuckler, et al., 2012) (see Figure 7.7).
FOCUS POINT 7.5 MEDIA CONTAGION AND SUICIDE AMONG
THE YOUNG

When Nirvana lead singer Kurt Cobain committed suicide in April 1994 it had a significant
impact on young people who saw Cobain as the spokesman for their troubled generation. The
sudden deaths of celebrities in this way have given prominence to social factors that may
influence suicide—especially amongst the young. That is, reporting of suicide in the media may
trigger ‘contagion’ effects in which young people imitate their idols. However, the evidence for
media contagion effects on suicide rates is equivocal. Some studies have found evidence for
increased rates of adolescent suicide after high‐profile media stories about suicide (Littman,
1985; Motto, 1970; Phillips & Carstensen, 1986), while others have failed to find any effect. In
particular, Martin and Koo (1997) investigated the effect of the suicide of Kurt Cobain on
Australian adolescent suicide rates for the 30‐day period after his suicide. They found no
evidence for a ‘suicide contagion’ effect, with suicide rates for the 30‐day period after Cobain's
death being lower than rates for the same period in some previous years. Nevertheless, a recent
systematic review of the effects of media reporting on suicide rates concludes that media
reporting and suicidality are probably related, suggesting that the media need to be responsible
 about the way they report celebrity suicides in order to minimize imitation by vulnerable groups
(Sisask & Varnik, 2012).

FIGURE 7.7 Suicide and the economic recession. Time trend analysis of suicide rates in 50 US states between 1999
and 2010. Vertical line shows onset of the economic recession.
After Reeves et al. (2012).

In a large‐scale study of risk factors carried out for the World Health Organization, Borges et al. (2010)
found that risk factors for suicidal behaviours in both developed and developing countries included
being female, being young, lower education and income, unmarried status, unemployment, parent
psychopathology, childhood adversities, and a current DSM psychiatric diagnosis. A combination of
these risk factors was able to predict suicide attempts with some accuracy. Perhaps not surprisingly, life
stress is one of the most significant predictors of suicide, and suicide attempts are often preceded by a
significant negative life event. The types of life events that may trigger suicide can differ across age
groups. For adolescents and teenagers these are more likely to be relationship issues, separations, and
interpersonal conflicts, in middle age they are more likely to be financial issues, and in later life they
tend to be related to disability and physical health (Rich, Warstadt, Nemiroff, Fowler, & Young, 1991).
Finally, there is also a genetic element to suicidal behaviour. Both twin studies and adoption studies
support the view that suicidality has an inherited component that may be as high as 48% (Joiner, Brown,
& Wingate, 2005) and which is independent of the heritability of other psychiatric disorders (Rujescu,
Zill, Rietschel, & Maier, 2009). In addition, recent twin studies have also indicated that suicidal ideation
has a substantial inherited component of 57% (Dutta et al., 2017). This genetic component may be
related to factors controlling low levels of serotonin metabolites in the brain which have been found to
be associated with suicidal behaviour in individuals suffering major depression (e.g., Lutz, Mechawar, &
Turecki, 2017).
This diversity of risk factors has led researchers to argue that suicide probably results from a complex
interplay between sociocultural factors, traumatic events, psychiatric history, personality traits and
genetic vulnerability (e.g., Balazic & Marusic, 2005; Rujescu et al., 2009), all of which will need to be
included in a comprehensive model of suicide aetiology (O'Connor & Portzky, 2018).

7.5.2 Identifying and Preventing Suicide

It is notoriously difficult to pick up the signs that an individual is seriously contemplating a suicide
attempt. Prior to an attempt, suicidal individuals will often seem calm, rational, and even show signs of
improvement in their psychological condition. This calm and rationality may simply reflect the period
of thought and planning that many who decide to attempt suicide go through. Individuals planning
suicide will often meticulously dispose of their possessions, plan how their family will be cared for, and
take time to plan the act itself—often choosing a time and place where they cannot be disturbed.
According to Kessler et al. (1999), a national survey of suicide in the US suggested that about 39% of
those who attempt suicide are determined to die, while 47% do not wish to die but are communicating a
‘cry for help’ to friends and relatives in an attempt to convey their pain and hopelessness. Their survey
also suggested that around 72% of those who had constructed a suicide plan went on to make a suicide
attempt, and they suggest that prevention is best focussed on those who plan suicide attempts and
identifying those factors that indicate that a suicidal individual is drawing up a plan (Client's Perspective
7.3).
The fact that around half of those attempting suicide do not want to die, but need to convey their pain
and despair, means that intercepting these individuals before they make a successful suicide attempt is
important. The main forms of intervention include 24‐hour helplines and telephone support lines such
as those provided by The Samaritans in the UK (www.samaritans.org). School‐based educational
programmes are also being developed, and these are aimed at warning teenagers about the early signs
of suicidal tendencies in their peers and providing them with appropriate support information.
However, while these prevention schemes have some success with some groups of users (e.g., young
females), they are less effective in preventing suicide in other groups (e.g., adolescent boys) (Gould &
Kramer, 2001). Multilevel interventions for suicide preventions are also being developed, and best
practices that have been identified as effective are (a) training general practitioners (GPs) or family
physicians to recognize and treat depression and suicidality, (b) improving accessibility of care for at‐risk
individuals, and (c) restricting access to means of suicide (van der Feltz‐Cornelis et al., 2011). Related to
this last point, awareness of methods used to commit suicide and attempts to reduce the lethality of
those methods is also important in reducing the number of successful suicides. For example, an
Australian study found that lethality rates for suicide attempts involving motor vehicle exhaust fumes
and hanging had decreased sharply over the previous 10 years (Spittal, Pirkis, Miller, & Studdert, 2012).
This appeared to be a consequence of the introduction of catalytic converters on car engines that
significantly reduced lethal carbon monoxide emissions and systematic removal of ligature points from
institutional settings in which those at risk of suicide might be living.
Finally, both psychological and pharmacological treatments can be helpful for individuals who are at
high risk for repeated suicide attempts. Medications for mood disorders (see Section 7.3.1) can reduce
the risk of suicide significantly, and these may include antidepressants (Näslund, Hieronymus, Lisinski,
Nilsson, & Eriksson, 2018) and antipsychotics (Meltzer et al., 2003). CBT and dialectical behavioural
therapy (DBT) interventions can also be used successfully to reduce suicide risk and suicide behaviours
in particular client groups, such as adolescents (Hawton et al., 2016; Méndez‐Bustos et al., 2019) and
individuals suffering psychosis (Tarrier, Haddock, Lewis, Drake, & Gregg, 2006). In addition, the WHO
brief intervention and contact(BIC) procedure has also been shown to be effective in facilitating
suicide prevention (Riblet, Shiner, Young‐Xu, & Watts, 2017). BIC is a 1‐hour individual information
session as close to the time of discharge from hospital as possible, followed by periodic follow‐up
contacts (phone calls or visits) over the ensuing 18‐month period by experienced clinical professionals.
CLIENT'S PERSPECTIVE 7.3 SUICIDE NOTES
 Around one in three people who commit suicide leave a suicide note, and analysis of such
notes can provide an insight into the feelings and motives of individuals who are no longer
around to explain why they took their own life.
This suicide note was written by an individual who committed suicide by jumping under a
moving train in the UK, and it is typical in that it is short, expresses guilt at the action, but
also emphasizes the extreme pain and hopelessness that the victim experiences.
Most suicide notes are addressed to specific individuals, usually in an attempt by the victim
to justify their actions to family and friends. However, they can often be as confusing as
they are enlightening—especially since those taking their own lives may be in such a
confused and desperate state that they do not fully understand their own reasons for
committing suicide (Shneidman, 1973).
Research on the content of suicide notes has not particularly enlightened us to why some
people commit suicide, but there are age differences in the content of such notes. Young
people usually point to interpersonal relations as the reason for their suicide, middle‐aged
people tend to report simply being unable to cope with life stressors, and older individuals
are more likely to report being driven to suicide by health problems and physical
disabilities (Lester, 1998).

SELF‐TEST QUESTIONS
Can you name the main risk factors for suicide?
What are the best ways of identifying and preventing suicide?
 SECTION SUMMARY

7.5 SUICIDE
The World Health Organization estimates that 800,000 people worldwide commit suicide
each year.
One in four people with a diagnosis of depression are likely to attempt suicide at least once
in their lifetime.
The prevalence rate for suicide attempts for developed countries is between 0.4% and 2%
in any 1 year.
Women are three times more likely to attempt suicide than men, but the rate for successful
suicide is four times higher in men than women.
Risk factors for suicide include an existing psychiatric diagnosis, low self‐esteem, poor
physical health and physical disability, and experiencing a significant negative life event.
There is an inherited component to suicide which may be as high as 48%
The main forms of intervening to prevent suicide include 24‐hour helplines and telephone
support lines (e.g., the Samaritans), school‐based educational programmes warning about
the early signs of suicidal tendencies, and the WHO BIC procedure.
Both medications for mood disorders and CBT can be helpful in reducing suicide risk in
vulnerable people.

7.6 DEPRESSION AND MOOD DISORDERS REVIEWED

Depression is arguably the most prevalent of all the main psychopathology symptoms we will cover in
this text (lifetime prevalence rates between 5.2% and 20.6%); it afflicts women twice as frequently as
men, and is ranked by the World Health Organization as the single largest contributor to global
disability (7.5% of all years lived with disability, WHO, 2017).
It is an emotion that all of us experience at some point—especially in relation to losses and failures in
our lives. However, for some it is a sustained, crippling, and distressing problem (see the personal
description given at the beginning of this chapter), and may even lead to suicidal ideation, and suicide
attempts (Section 7.5). Bipolar disorder is the other main mood disorder covered in this chapter, and this
is characterised by alternating periods of depression and mania (see Client's Perspective 7.1). This is a
significantly less prevalent disorder (lifetime prevalence rate between 0.4% and 1.6%) that appears to
have a basis in neurotransmitter imbalances in the brain (Section 7.2.2). Theories of depression range
from biological theories covering inherited factors, brain neurochemical imbalances and brain
abnormalities, to a full spectrum of psychological theories attempting to explain both the behavioural
and cognitive features of depression. Drug treatments, such as trycyclic drugs, monamine oxidase
inhibitors, and, more recently, SSRIs and SNRIs, have been shown to alleviate symptoms of severe
depression for many sufferers (Section 7.3.1). However, both behavioural and cognitive therapies appear
to have promise as long‐term effective treatments for depression, and therapies such as CBT help the
sufferer by enabling them to identify and challenge ingrained negative views of themselves and the
world. Finally, two important clinical phenomena related to mood disorders and depression are NSSI
and suicide. NSSI is an increasingly recognised problem that mainly afflicts adolescents, while mental
health problems generally—and mood disorders specifically—are a significant risk factor for suicide.

This book is accompanied by Student and Instructor companion

websites.
www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter References
Videos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
8
Experiencing Psychosis: Schizophrenia Spectrum
Problems

ROUTE MAP OF THE CHAPTER

This chapter describes the symptoms of psychosis and examines the heterogeneous diagnostic
categories within the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM‐5). We
begin by describing the main symptoms of psychosis and then cover the main diagnostic
categories within schizophrenia spectrum disorder. We also consider the stages through which
psychotic symptoms develop. We then describe and evaluate a range of explanations of
psychosis, and these theories often attempt to explain symptoms at a number of different levels,
such as biological, psychological, and social levels. We finish by describing a variety of
biological and psychological treatments for psychotic symptoms and discussing the role of
community care as a means of long‐term supervision and management for those suffering from
psychosis.

CHAPTER OUTLINE
8.1 THE NATURE OF PSYCHOTIC SYMPTOMS
8.2 THE DIAGNOSIS OF SCHIZOPHRENIA SPECTRUM DISORDERS
8.3 THE PREVALENCE OF SCHIZOPHRENIA SPECTRUM DISORDERS
8.4 THE COURSE OF PSYCHOTIC SYMPTOMS
8.5 THE AETIOLOGY OF PSYCHOTIC SYMPTOMS
8.6 THE TREATMENT OF PSYCHOSIS
8.7 EXPERIENCING PSYCHOSIS REVIEWED

LEARNING OUTCOMES
When you have completed this chapter, you should be able to:
1. Describe the main clinical symptoms of psychosis, and the key features of the main
diagnostic categories defining schizophrenia spectrum disorders in DSM‐5.
2. Describe and evaluate the main biological theories of the aetiology of psychosis—
especially the role of genetics, brain neurotransmitters, and brain abnormalities.
3. Describe, evaluate, and compare the main psychological and sociocultural theories of the
aetiology of psychosis.
4. Describe a range of treatments for psychotic symptoms, including biological,
psychological, familial, and community care interventions.
 Looking back I had a lot of factors that contributed to my psychosis. I was a quiet child, lacking in confidence.
My parents divorced when I was 8 years old and my father was treated for depression so it seems to run in the
family. My father was a disinterested one, reinforcing my feelings of worthlessness.
I found it hard at secondary school to make friends and not having a lot of money meant I was singled out. While
it wasn't physical, mainly name calling and being spat at, it reinforced the feeling that I didn't deserve to be here.
By now I was hearing ‘inside’ voices in my head telling me I was useless, shouting words like ‘Bitch!’ and ‘Die!’.
I was having severe mood swings. I thought about self‐harming and became controlling about my food intake. At
age 14 I started taking drugs and drinking alcohol. Between 14 and 21 I had a cannabis and cocaine addiction
which I overcame. At age 24 I was planning my suicide when my father died. Within 3 days I was having
extreme audio and visual hallucinations such as whispering and people calling my name and seeing deceased
people, dead bodies and shadows as well as everyday objects. People also transformed into other people in front of
me leading me to believe they were possessed by the dead. I also heard menacing voices issuing commands. I
experienced strange smells, tasting poison in my food and on one occasion felt someone stroking my hair. I thought
that my mind was being controlled, that I could communicate with the dead and that, because of this, the
government was spying on me and plotting to kill me.
Jo's Story (from Hayward, Meddings, & Harris, 2015)

Introduction
Psychotic symptoms can be crippling and are often characterised by disturbances in thought and
language, sensory perception, emotion regulation, and behaviour. Sufferers may experience sensory
hallucinations and also develop thinking biases which may lead to pervasive false beliefs or delusions
about themselves and the world around them. Individuals with psychotic symptoms may often withdraw
from normal social interaction because of these disturbances of perception and thought, and this can
result in poor educational performance, increasing unproductivity, difficulties in interpersonal
relationships, neglect of day‐to‐day activities and a preoccupation with a personal world to the exclusion
of others. As a result, many individuals exhibiting psychotic symptoms fall to the bottom of the social
ladder or even become homeless because they cannot hold down a job or sustain a relationship—a
phenomenon known as downward drift (Hollingshead & Redlich, 1958) (see Section 8.5.3).

delusions Firmly held but erroneous beliefs that usually involve a misinterpretation of
perceptions or experiences.

downward drift A phenomenon in which individuals exhibiting psychotic symptoms fall to

the bottom of the social ladder or even become homeless because they cannot hold down a job
or sustain a relationship.

Jo's Story is a common example of how psychotic symptoms can manifest themselves. She hears voices
criticizing her and calling her names, believes other people are controlling her, finds it hard to develop
friendships, and uses alcohol and street drugs to help control her emotions and feelings. Eventually Jo
begins to experience sensory hallucinations in which she sees dead bodies and everyday objects
transform into menacing and frightening figures, she hears threatening voices and begins to develop
paranoid thoughts. In time she feels so hopeless about the future that she just wants to die.
Psychosis is a collective name given to an extensive range of disparate symptoms that can often leave
an individual feeling frightened and confused, and the presence of different combinations of these
symptoms may lead to a diagnosis of any one of a number of schizophrenia spectrum disorders.
DSM‐5 has moved away from a single overriding diagnostic category (schizophrenia) split into a series
of subtypes (paranoid, disorganised, catatonic, undifferentiated) and now lists a number of separate
psychotic disorders that range across a spectrum depending on severity, duration and complexity of
symptoms. The main diagnostic categories in DSM‐5 are schizophrenia, schizotypal personality
disorder, delusional disorder, brief psychotic disorder, and schizoaffective disorder, and we discuss these
individually later in this chapter. But first we will discuss the key cognitive and behavioural features that
define psychosis—combinations of which give rise to the different diagnoses. These key features include
delusions, hallucinations, disorganised thinking, abnormal motor behaviour, and negative symptoms
(indicative of diminished emotional expression) (Focus Point 8.1).

schizophrenia spectrum disorders The name for separate psychotic disorders that range
across a spectrum depending on severity, duration and complexity of symptoms.

FOCUS POINT 8.1 HISTORY OF SCHIZOPHRENIA AS A

DIAGNOSTIC CATEGORY

The symptoms of psychosis have been reported throughout history, but because the symptoms
can be so varied and wide ranging ‘schizophrenia’ has only gradually been isolated as a single
diagnostic category to cover these heterogeneous characteristics.
The European psychiatrist, Emil Kraepelin (1896), was the first to distinguish schizophrenia
from a range of other psychiatric symptoms (such as manic depressive illness). He did this by
bringing together a number of contemporary diagnostic concepts including paranoia, catatonia
and hebephrenia (symptoms indicative of incoherence and fragmentation of personality) under
the general term dementia praecox. He assumed that dementia praecox was a single disease
that manifested itself in late adolescence or early adulthood and had a deteriorating prognosis
from which there was no recovery. In contrast to Kraepelin, the Swiss psychiatrist Eugen
Bleuler (1911) believed that the onset of dementia praecox was not simply restricted to
 adolescence and early adulthood and also believed that it did not inevitably lead to dementia.
He preferred to use the term schizophrenia (from the Greek schiz, to spilt, and phren, the mind),
because he felt that it properly described the splitting of different psychological functions within
a single personality. Unfortunately, this term has also had its problems, with the popular belief
that the term schizophrenia refers to a split or double personality. In order to try and unify the
various symptoms under a single diagnostic category, Bleuler used the concept of the ‘breaking
of associative threads’ as being central to all of the symptoms of schizophrenia. That is,
effective thinking, communication, and action were not possible if the ability to associate things
together was disrupted. In this respect, it is interesting to note that in later sections in this
chapter we will see that there is evidence that at least some of the clinical symptoms of
schizophrenia may be determined by dysfunctions in associative and attentional processes (see
Section 8.5.2).

dementia praecox An early, general term for a number of diagnostic concepts

including paranoia, catatonia and hebephrenia (symptoms indicative of incoherence
and fragmentation of personality).

Recent diagnostic criteria recognize the complexity of schizophrenia as a diagnostic category,

and up until publication of DSM‐5, diagnosis was not dependent on one essential symptom but
on the basis of the presence of at least 2 or 3 of five basic symptoms. This inevitably meant that
people could receive a diagnosis of schizophrenia but exhibit quite different symptoms. The
latest diagnostic manual, DSM‐5, has moved away from defining a single overriding diagnostic
category with a series of subtypes towards considering schizophrenia as a spectrum disorder.
The important diagnostic categories in this spectrum are schizophrenia, schizotypal personality
disorder, delusional disorder, brief psychotic disorder, and schizoaffective disorder, and these are
discussed later in this chapter.

8.1 THE NATURE OF PSYCHOTIC SYMPTOMS

DSM‐5 lists five important characteristics for diagnosing schizophrenia spectrum disorders. The first
four of these characteristics are traditionally known as positive symptoms, because they tend to
reflect an excess or distortion of normal functions (e.g., developing inappropriate beliefs or perceiving
things that are not there), and the final category represents what are known as negative symptoms,
and these reflect symptoms characteristic of a diminution or loss of normal functions, such as lack of
initiative and poor emotional expression.

positive symptoms Characteristics of psychotic symptoms which tend to reflect an excess or

distortion of normal functions.

negative symptoms Symptoms characteristic of a diminution or loss of normal functions.

8.1.1 Delusions
These are firmly held but erroneous beliefs that (a) usually involve a misinterpretation of perceptions or
experiences and (b) become fixed beliefs that are resistant to change even in light of conflicting or
contradictory evidence. Such delusions are the most common symptom of psychosis in individuals with
a diagnosis of schizophrenia (Baker, Konova, Daw, & Horga, 2019), are experienced by over 75% of
those individuals hospitalised because of their psychotic symptoms (Maher, 2001) and may be the result
of abnormalities in inference or the process of shaping beliefs through experience (Hemsley & Garety,
1986). While some delusions may be clearly bizarre (e.g., the individual may believe that their entire
internal organs have been taken out and replaced by those of someone else), others may not (e.g., a
paranoid belief that the individual is constantly under surveillance by the police). Regardless of how
bizarre a delusion is, the sufferer is often able to bring reason and logic to support their delusion—even
though the underlying belief itself is clearly absurd (Maher, 2001). This ability to support absurd beliefs
with logical thought has led some clinicians to suggest that delusions may be the result of an inability to
integrate perceptual input with prior knowledge even though rational thought processes are still intact
(Frith, 1996; Frith & Dolan, 2000). For other clinicians it is suggestive of the development of biased
information processing and the development of dysfunctional beliefs about the world (e.g., Freeman,
Garety, Kuipers, Fowler, & Bebbington, 2002; Morrison, 2001a), or decision‐making processes that lead
the individual to ‘jump to conclusions’ on the basis of minimal evidence (e.g., Moritz & Woodward,
2005; Dudley, Taylor, Wickham, & Hutton, 2016).
The main types of delusion found in those experiencing psychosis are (a) persecutory delusions
(paranoia), in which the individual believes they are being persecuted, spied upon, or are in danger
(usually as the result of a conspiracy of some kind); (b) grandiose delusions, in which the individual
believes they are someone with fame or power or have exceptional abilities, wealth, or fame (e.g., Jesus
Christ, or a famous music star); (c) delusions of control, where the person believes that their
thoughts, feelings, or actions are being controlled by external forces (e.g., extraterrestrial or supernatural
beings), and this is often associated with the belief that control is being exerted through devices (such as
the radio) which are sending messages directly to the person's brain; (d) delusions of reference,
where the individual believes that independent external events are making specific reference to them
(e.g., in Jo's Story at the beginning of this chapter); (e) nihilistic delusions, where the individual
believes that some aspect of either the world or themselves has ceased to exist (e.g., the person may
believe that they are in fact dead) or a major catastrophe will occur; and (f) erotomanic delusions
when an individual falsely believes that another person is in love with him or her (see Focus Point 8.2).

persecutory delusions Delusions in which the individual believes they are being persecuted,
spied upon, or are in danger (usually as the result of a conspiracy of some kind).

grandiose delusions Delusions in which the individual believes they are someone with fame
or power or have exceptional abilities, wealth or fame.

delusions of control Delusions where the person believes that his or her thoughts, feelings or
actions are being controlled by external forces (e.g. extraterrestrial or supernatural beings).

delusions of reference Delusions where the individual believes that independent external
events are making specific reference to him or her.

nihilistic delusions Delusions where individuals believe that some aspect of either the world
or themselves has ceased to exist (e.g. the person may believe that they are in fact dead).
 erotomanic delusions A relatively rare psychotic delusion where an individual has a
delusional belief that a person of higher social status falls in love and makes amorous advances
towards them.

One common feature of psychotic thought is that sufferers frequently believe that their thoughts are
being interfered with or controlled in some way, either by being openly broadcast to others or by having
thoughts planted into their mind by external forces. This type of delusion (sometimes known as ‘hearing
voices’, see Section 8.5.2 on interpretational biases) is so common that it may offer some insight into the
cognitive deficits underlying a majority of psychotic thought. For example, in an experimental study,
Blakemore, Oakley, and Firth (2003) used hypnosis to generate beliefs in nonclinical participants that
their self‐generated actions could be attributed to an external source. They found that such erroneous
beliefs generated higher than normal levels of activation in the parietal cortex and cerebellum and they
suggest that these areas of the brain may be altered during psychotic episodes so that self‐produced
actions and thoughts are experienced as external.

FOCUS POINT 8.2 EROTOMANIA AND STALKING

BBC NEWS—4 April 2000—‘Swedish police have arrested a 34‐year‐old man accused of stalking Agnetha
Faltskog of the 70s Swedish pop phenomenon Abba. According to reports in the Swedish daily Expressen, Ms
Faltskog filed an official complaint against the man last week, saying she feared for her life after being stalked for
3 years.
The man was detained 2 days later. The man had reportedly become smitten by the singer when he was 8 years
old and had left his native Netherlands to buy a house near Ms Faltskog's country estate at Ekero near Stockholm.
According to Expressen, she told police that the stalker had sent her some 300 letters between 1997 and 1999,
telephoned her up to three times a day and followed her wherever she went’.
One form of psychotic delusion is called erotomania. This is a relatively rare disorder where an
individual has a delusional belief that a person of higher social status falls in love and makes
amorous advances towards them. As a result of these delusions, the individual suffering
erotomanic delusions may often end up stalking their target by regularly visiting their homes in
an attempt to meet and talk with them or by following them as they go about their daily
business. There are two types of erotomanic delusion. The first is where the individual believes
their victim loves them. In this case the individual believes they are having a relationship with
their victim, and they will make regular attempts to try and contact and meet their victim in
order to substantiate the relationship. The American actress Rebecca Schaeffer was tragically
shot in 1989 by a stalker who was rebuffed by her when attempting to talk to her about their
 ‘relationship’. The second form of erotomanic delusion is when the individual believes that they
are destined to be with their victim, even though they are aware they may never have met them.
So if they pursue them long enough, they will eventually come to have a relationship with their
victim. An example of this is the case of Agnetha from the Swedish pop group ABBA, who was
stalked for some years by a Dutch man who believed he was destined to be with her.
Stalking appears to be on the increase in many Western countries (Pathe, 2002), causes
substantial distress to its victims, and can be caused by a range of psychopathologies (e.g.,
erotomanic delusions, severe personality disorder, obsessive‐compulsive disorders). Studies of
individuals with erotomanic delusions indicate that they are usually isolated loners without a
partner or full‐time occupation and around half have a first‐degree relative with a delusional
disorder (Kennedy, McDonough, Kelly, & Berrios, 2002). Many also develop fantasies in which
they are driven to protect, help or even harm their victims (Menzies, Federoff, Green, &
Isaacson, 1995). One example is the German stalker who was obsessed with tennis star Steffi
Graf, and this drove him to attack and stab her tennis rival, Monica Seles, during a tournament
in Hamburg in 1993 in a deluded attempt to try and further Graf's career.

8.1.2 Hallucinations
People suffering psychotic symptoms regularly report sensory abnormalities across a broad range of
sensory modalities, and this is usually manifested as perceiving things that are not there.
Hallucinations can occur in any modality (e.g., auditory, olfactory, gustatory, and tactile), but the most
common are auditory hallucinations that are reported by around 80% of sufferers (Laroi et al., 2012).
Auditory hallucinations are usually manifested as voices, and these can be experienced as external voices
commanding the individual to act in certain ways, two or more voices conversing with each other, or a
voice commentating on the individual's own thoughts. In all cases these voices are perceived as being
distinct from the individual's own thoughts. Research of brain areas involved in speech generation and
the perception of sounds suggests that when sufferers claim to hear ‘voices’ this is associated with neural
activation in these areas of the brain associated with language (Keefe, Arnold, Bayen, McEvoy, &
Wilson, 2002; Dollfus et al., 2018), and the sufferer attributes them to external sources.

hallucinations A sensory experience in which a person can see, hear, smell, taste or feel
something that isn’t there.

Visual hallucinations are the second most common type of hallucination and can take either a diffuse
form as in the perception of colours and shapes that are not present, or they can be very specific such as
perceiving that a particular person (e.g., a partner or parent) is present when they are not (see Jo's Story
at the beginning of this chapter). Other hallucinations can be tactile and somatic (e.g., feeling that one's
skin is tingling or burning) or olfactory and gustatory (e.g., experiencing smells that are not present or
foods that taste unusual).
For those who believe that their hallucinations are real, such experiences can be extremely frightening.
However, while some individuals suffering psychosis are convinced their hallucinations are real, many
others are aware that their hallucinations may not be real. This suggests that psychotic episodes may be
associated with a reality‐monitoring deficit. That is, individuals suffering psychotic symptoms may have
difficulty identifying the source of a perception and difficulty distinguishing whether it is real or
imagined. In support of this possibility, Brebion et al. (2000) found that when individuals diagnosed with
schizophrenia and nonclinical controls were asked to remember words that had either been generated
by themselves or been generated by the experimenter, individuals with a diagnosis of schizophrenia
differed in three important ways from nonclinical controls. First, they were more likely to identify items
as having been in the generated list of words when they were not (false positives); second, they were
more likely to report that words they had generated themselves were generated by the experimenter;
and third, they were more likely to report that spoken items had been presented as pictures. These
results suggest that individuals diagnosed with schizophrenia have a reality‐monitoring deficit (i.e.,
a problem distinguishing between what actually occurred and what did not occur), and a self‐
monitoring deficit (i.e., they cannot distinguish between thoughts and ideas they generated
themselves and thoughts or ideas that other people generated).

reality-monitoring deficit Where an individual has a problem distinguishing between what

actually occurred and what did not occur.

self-monitoring deficit Where individuals cannot distinguish between thoughts and ideas
they generated themselves and thoughts or ideas that other people generated.

8.1.3 Disorganised Thinking (Speech)

Disorganised thinking will normally be inferred from the individual's speech, and there are a
number of common features displayed by individuals experiencing psychotic symptoms. The most
common are derailment or loose associations, where the individual may drift quickly from one
topic to another during a conversation. Their answers to questions may be tangential rather than
relevant (tangentiality), and in some cases their speech may be so disorganised that it is neither
structured nor comprehensible. Instances of the latter are ‘clanging’, the use of neologisms, and
‘word salads’; examples of these are given in Focus Point 8.3, and examples of the confused speech
generated by some individuals exhibiting psychotic symptoms are provided in Focus Point 8.3. These
loose associations that appear to govern psychotic speech suggest that sufferers (a) have difficulty
inhibiting associations between thoughts (Titone, Holzman, & Levy, 2002) and so tend to follow the
track of the first association that comes to mind, and (b) have difficulties understanding the full context
of a conversation (Cohen, Barch, Carter, & Servan‐Schraiber, 1999) and so cannot distinguish the full
meaning of a conversation or sentence from its detail. The result of these loose associations is that
psychotic speech can be very detailed in terms of number of words, breadth of ideas, and grammatical
correctness but it will usually convey very little.

derailment A disorder of speech where the individual may drift quickly from one topic to
another during a conversation.

loose associations Disorganised thinking in which the individual may drift quickly from one
topic to another during a conversation.

tangentiality A disorder of speech in which answers to questions may be tangential rather

than relevant.

clanging A form of speech pattern in schizophrenia where thinking is driven by word sounds.
For example, rhyming or alliteration may lead to the appearance of logical connections where
none in fact exists.
neologisms Made up words, frequently constructed by condensing or combining several
words.

word salads When the language of the person experiencing a psychotic episode appears so
disorganised that there seems to be no link between one phrase and the next.

FOCUS POINT 8.3 DISORGANIZED SPEECH INDICATIVE OF

DISORGANIZED THINKING

Psychotic symptoms frequently exhibit a range of attributes that indicate disordered thinking.
The following are examples of some of the more common of these disorganized speech
symptoms.

Word Salad
In many cases, the language of the person experiencing a psychotic episode appears so
disorganised that there seems to be no link between one phrase and the next, and this is known
as a ‘word salad’. Some word salads simply do not seem to be attempts to communicate
anything structured and appear to drift without substance from one unconnected sentence to
the next:
‘Everything is going around in slow motion. The boxes are clanging and chattering to be let out. Behind my
forehead the past is surfacing mixing a bottle of acid solution. A stake jams a door that leads to a mirage of
broken appearances. Inside a box, pounding fists try to pull down my imagination. The ground work is split
into hundreds of pieces; each fragment is separate as if it had some kind of individual purpose. The truth is
locked up in a unit’.
In other cases, word salads appear to be sets of phrases or words linked by association to the
previous phrase. For example, in answer to the question ‘What colour is your dress?’, a sufferer
answered ‘red…Santa Claus…flying through the sky….God’. This is known as loose
association or derailment and makes it very difficult to follow the conversation of an individual
when a single, often unimportant word from the previous sentence becomes the focus of the
next sentence.

Neologisms
In order to try and communicate, many individuals suffering psychotic symptoms often make
up words and use them in their attempts to communicate. These are called neologisms, and are
frequently constructed by condensing or combining several words. Some examples given by
individual sufferers are the following:

Spectroautorotation Circling in everywhere, as with checkers or a bat in baseball

Sniggeration A giggle or sniggering. I do it sometimes

Relaudation
 Praising over and over

Circlingology Study of a rolling circle; a fruit can in the form of a cylinder rolling

Clanging
People exhibiting psychotic symptoms often try to communicate using words that rhyme, and
this is known as ‘clanging’. In other cases, sufferers only appear able to construct sentences if
the words in them rhyme—and this communication may begin with a sensible response but
then degenerate into nonsense because of the urge to ‘clang’ as the following transcript shows:

TH:
‘What colour is your dress?’

CL:
‘Red. . . . Like a bed’.

TH:
‘Why is it like a bed?’

CL:
‘Because it's dead’.

TH:
‘Why is a bed like being dead?’

CL:
‘I dunno. . . maybe it's a med’.

TH:
‘What's a med?’

CL:
‘A bled’.

8.1.4 Grossly Disorganised or Abnormal Motor Behaviour

Grossly disorganised or abnormal motor behaviour may manifest itself in a variety of ways. Behaviour
may be childlike and silly (and inappropriate for the person's chronological age) or inappropriate to the
context (e.g., masturbating in public). It may be unpredictable and agitated (e.g., shouting and swearing
in the street) and the individual may have difficulty completing any goal‐directed activity (e.g., an
inability to focus on or complete basic day‐to‐day tasks such as cooking or maintaining personal
hygiene). The person's appearance may be dishevelled and they may well dress in an inappropriate
manner (e.g., wearing heavy, thick clothing in hot weather or walking around in public in only their
underwear). Catatonic motor behaviours are characterised by a significant decrease in reactivity to
the environment (catatonic stupor), maintaining rigid, immobile postures (catatonic rigidity), resisting
attempts to be moved (catatonic negativism), or purposeless and excessive motor activity that often
consists of simple, stereotyped movements (catatonic excitement or stereotypy, see Photo 8.1).

catatonic motor behaviours Characterised by a decrease in reactivity and maintaining

rigid, immobile postures.
PHOTO 8.1 In some very severe cases of psychosis, the individual may lapse into a catatonic stupor. Those who lapse
into this state become withdrawn and inactive for long periods. In extreme cases this may take the form of catatonic rigidity,
in which the individual will adopt a rigid, often awkward posture for many hours. Others exhibit what is known as waxy
flexibility, and will maintain a posture into which they have been placed by someone else.

8.1.5 Negative Symptoms

Negative symptoms are common within a diagnosis of schizophrenia but less so in the other
schizophrenia spectrum disorders. Negative symptoms include diminished emotional expression,
avolition, alogia, anhedonia, and asociality. Diminished emotional expression includes reductions
in facial expressions of emotion, lack of eye contact, poor voice intonation, and lack of head and hand
movements that would normally give rise to emotional expression. Avolition represents an inability to
carry out or complete normal day‐to‐day goal‐oriented activities, and this results in the individual
showing little interest in social or work activities. Alogia is characterised by a lack of verbal fluency in
which the individual gives very brief, empty replies to questions. Anhedonia is the decreased ability to
experience pleasure from positive stimuli or an inability to recall pleasurable events (Kring & Neale,
1996). Finally, asociality refers to a lack of interest in social interactions, perhaps brought about by a
gradual withdrawal from social interactions generally.

diminished emotional expression A reduction in facial expressions of emotion, lack of

eye contact, poor voice intonation, and lack of head and hand movements that would normally
give rise to emotional expression.

avolition An inability to carry out or complete normal day-to-day goal-oriented activities, and
this results in the individual showing little interest in social or work activities

alogia A lack of verbal fluency in which the individual gives very brief, empty replies to
questions

anhedonia Inability to react to enjoyable or pleasurable events.

asociality A lack of interest in social interactions, perhaps brought about by a gradual

withdrawal from social interactions generally.
 SELF‐TEST QUESTIONS
What is the difference between the positive and negative symptoms of schizophrenia?
Can you name some of the different types of delusional states found in delusional
disorder?
What are the most common forms of hallucination experienced in schizophrenia and
approximately what percentage of sufferers report hallucinations?
Can you name the different forms of disordered speech and communication exhibited by
individuals diagnosed with schizophrenia and provide some examples of each?
What are the characteristics of catatonic motor behaviours?
Can you describe some of the specific symptoms that are collectively known as negative
symptoms?

SECTION SUMMARY

8.1 THE NATURE OF PSYCHOTIC SYMPTOMS

The first four characteristics for diagnosing schizophrenia spectrum disorders are known as
positive symptoms, and the fifth category represents negative symptoms.
75% of people hospitalised with a diagnosis of schizophrenia experience delusions.
The main types of delusions are (a) persecutory delusions, (b) grandiose delusions, (c)
delusions of control, (d) delusions of reference, and (e) nihilistic delusions.
Around 80% of individuals diagnosed with schizophrenia report auditory hallucinations.
Individuals suffering hallucinations may have a reality‐monitoring deficit (distinguishing
between what actually occurs and what does not).
The most common forms of disorganised speech are derailment, loose associations, clanging,
neologisms, and word salads.
Grossly disorganised or abnormal motor behaviour is usually behaviour inappropriate to a context
(e.g., masturbating in public). Catatonic motor behaviours are characterised by a decrease
in reactivity and maintaining rigid, immobile postures.
Negative symptoms are characterised by flat affect, lack of interest in social or work
activities, poverty of speech (alogia), and apathy (avolition).

8.2 THE DIAGNOSIS OF SCHIZOPHRENIA SPECTRUM

DISORDERS
DSM‐5 has organised schizophrenia spectrum disorders along a gradient of psychopathology and
impairment—from less severe to more severe and disabling. Clinicians are asked to consider diagnosis
along this continuum, taking into account the number of diagnosable symptoms, the severity of those
symptoms, and the time period over which symptoms have been manifested. We describe the diagnostic
criteria for four of these spectrum disorders, namely delusional disorder, brief psychotic disorder,
schizophrenia, and schizoaffective disorder. Although DSM‐5 considers schizotypal personality disorder
to be within the schizophrenia spectrum, it is normally considered as a personality disorder, and so its
diagnostic criteria and description can be found in Chapter 12 under personality disorders.

8.2.1 Delusional Disorder

The DSM‐5 diagnostic criteria for delusional disorder are given in Table 8.1. Subtypes of
delusional disorder include the most common which is the persecutory or paranoid type, where the
individual believes they are being conspired against, cheated, spied on, followed, poisoned, maliciously
maligned, harassed, or obstructed in the pursuit of long‐term goals. Other common subtypes are
erotomanic type (see Focus Point 8.2) and the grandiose type (where the individual has a strong
conviction that they have some great talent or insight). Grandiose delusions may often have a religious
content or consist of beliefs that the individual has a special relationship with a prominent person.
Apart from the direct impact of the delusions, psychosocial functioning in such individuals may seem
quite normal. However, depending on the type of delusional belief held by the individual, this may
often give rise to social, marital, or work problems. Many also exhibit mood problems associated with
their delusional beliefs, especially anger outbursts or antagonistic behaviour when their beliefs are not
taken seriously.
TABLE 8.1 Summary: main DSM‐5 diagnostic criteria for delusional disorder

One or more delusions lasting at least 1 month

Apart from the impact of the delusions, normal functioning is not markedly impaired and is not
bizarre
Any manic or major depressive episodes which have occurred have been brief in relation to the
delusional episode
The disorder is not directly attributable to the use of a substance or medication and is not better
explained by other mental disorder

8.2.2 Brief Psychotic Disorder

The core feature of brief psychotic disorder is the sudden onset of at least one of the main
psychotic symptoms–namely, delusions, hallucinations, disorganised speech, or grossly abnormal
psychomotor behaviour (see Section 8.1), with this change from a nonpsychotic state to the appearance
of symptoms occurring within 2 weeks and being associated with emotional turmoil or overwhelming
confusion. A summary of the full diagnostic criteria is provided in Table 8.2.

brief psychotic disorder The sudden onset of at least one of the main psychotic symptoms,
with this change from a nonpsychotic state to the appearance of symptoms occurring within 2
weeks and being associated with emotional turmoil or overwhelming confusion.
8.2.3 Schizophrenia
A diagnosis of schizophrenia is given when there is a range of symptoms covering cognitive,
behavioural, and emotional dysfunction and also impaired occupational or social functioning—but no
single symptom is characteristic of this diagnosis. Table 8.3 shows the DSM‐5 diagnostic criteria for
schizophrenia, and two or more of the five symptoms must be present for a significant proportion of
time during a 1‐month period or longer. It is also important, and these recognise that symptoms must be
associated with impaired functioning across areas such as work, interpersonal relations, or self‐care.
Prodromal symptoms often precede the active phase, and residual symptoms may follow it (see below).
Similarly, negative symptoms or social isolation are common during the prodromal phase and can be a
significant indicator of later full‐blown symptoms of psychosis (Lencz, Smith, Auther, Correll, &
Cornblatt, 2004). Additional symptoms displayed by individuals with a diagnosis of schizophrenia may
include inappropriate affect (e.g., laughing inappropriately), depressed mood, anxiety or anger, disturbed
sleep patterns, and lack of interest in eating. Individuals with a diagnosis of schizophrenia may often
show a lack of insight into their symptoms and may be hostile and aggressive. However, aggression is
more common in younger males and for individuals with a past history of violence, nonadherence to
treatment, substance abuse, and impulsivity (DSM‐5, American Psychiatric Association, 2013, p. 101;
Johnson et al., 2016; Buchanan, Sint, Swanson, & Rosenheck, 2019). It must, however, be emphasised
that the vast majority of people with a diagnosis of schizophrenia are not aggressive and are more likely
to be the victims of violence and aggression than be perpetrators.
TABLE 8.2 Summary: the main DSM‐5 diagnostic criteria for brief psychotic disorder

Presence of at least one of the following:

Delusions
Hallucinations
Disorganised speech
Highly disorganised or catatonic behaviour
The disturbance lasts between 1 day and 1 month with eventual return to normal behaviour
The disorder is not directly attributable to the use of a substance or medication and is not better
explained by other mental disorder

TABLE 8.3 Summary: main DSM‐5 diagnostic criteria for schizophrenia

At least two of the following must be present for a significant period of time during a 1‐month
period:
Delusions
Hallucinations
Disorganised speech
Highly disorganised or catatonic behaviour
Negative symptoms such as diminished emotional expression
The ability to function in one or more major areas such as work, self‐care, or interpersonal
relationships is markedly diminished
Continuous signs of the disturbance last for at least 6 months
The disorder is not directly attributable to the use of a substance or medication and is not better
explained by other mental disorder
8.2.4 Schizoaffective Disorder
Schizoaffective disorder is diagnosed when an individual displays symptoms that meet the criteria
for schizophrenia (discussed previously) but where there is also a significant mood episode reflecting
either depression or mania that are present for the majority of the duration of the illness.
Schizoaffective disorder will frequently impair occupational functioning and may be associated with
restricted social functioning, difficulties with self‐care, and an increased risk for suicide (see Table 8.4).

Schizoaffective disorder Characterised by schizophrenia symptoms plus a period reflecting

either depression or mania.

TABLE 8.4 Summary: main DSM‐5 diagnostic criteria for schizoaffective disorder

A continuous period of illness during which there is a major mood episode (major depressive or
manic)
Delusions or hallucinations for 2 or more weeks without the occurrence of a major mood episode
Symptoms for a major mood episode are present for the majority of the duration of the illness
The disorder is not directly attributable to the use of a substance or medication and is not better
explained by other mental disorder

SELF‐TEST QUESTIONS
What are the four main schizophrenia spectrum disorder diagnostic categories in DSM‐5?

SECTION SUMMARY

8.2 THE DIAGNOSIS OF SCHIZOPHRENIA SPECTRUM DISORDERS

DSM‐5 has organised schizophrenia spectrum disorders along a gradient of
psychopathology and impairment—from less severe to more severe and disabling.
The most common forms of delusional disorder are persecutory type and grandiose type.
Brief psychotic disorder is typified by the sudden onset of one of the main psychotic
symptoms.
Schizophrenia is the main diagnostic category in schizophrenia spectrum disorders, and
occurs when there is a range of symptoms covering cognitive, behavioural, and emotional
dysfunction and also impaired occupational or social functioning.
Schizoaffective disorder is characterised by schizophrenia symptoms plus a period reflecting
either depression or mania.
8.3 THE PREVALENCE OF SCHIZOPHRENIA SPECTRUM
DISORDERS
When precise methods for its diagnosis are applied, the lifetime prevalence rate for a diagnosis of
schizophrenia is around 0.75% worldwide (Moreno‐Küstner, Martin, & Pastor, 2018). The World
Health Organization has recognised that schizophrenia is one of the top 10 medical disorders causing
disability, and currently around 20 million people worldwide have a diagnosis of schizophrenia (World
Health Organization, 2019). The mortality rate among people with a diagnosis of schizophrenia is
around 2–3 times higher than for the general population and sufferers tend to die around 10 years
earlier than individuals who have never been diagnosed with schizophrenia (Jeste et al., 1996). This high
mortality rate is often due to preventable physical diseases such as cardiovascular disease, metabolic
diseases and infections (World Health Organization, 2019), but around 10% die by suicide (National
Institute for Health and Care Excellence [NICE], 2014). The first symptoms of psychosis are usually
experienced between the ages of 15 and 30 years, with males experiencing the onset of symptoms
slightly earlier than females, and the first appearance of symptoms is relatively rare after the age of 40
years (see Figure 8.1). While treatments and interventions for psychosis are continually improving, a
significant number of people with a diagnosis of schizophrenia continue to suffer life‐long impairment,
with over 80% continuing to have problems with social functioning and between 80 and 90% of
sufferers unemployed—even in high‐income welfare societies (Thornicroft et al., 2004; Evensen et al.,
2016).
FIGURE 8.1 Males tend to experience the first symptoms of schizophrenia between the ages of 15 and 25 years
(average age of onset 18 years), whereas females tend to develop symptoms slightly later, between the ages of 18 and 30
years (average age of onset 25 years).
From Sham, McLean, & Kendler, 1994.

Some studies have identified some consistent cultural differences in the prevalence of schizophrenia
within individual countries. For example, in a UK‐based study, King et al. (2005) found that the
reporting of psychotic symptoms was higher in ethnic minority groups than in ethnic White individuals.
This increase in the reporting of symptoms was twice as high in people of African‐Caribbean origin as
in Whites. There have been a number of hypotheses that have attempted to explain this apparent
cultural difference, and there is at least some evidence that the higher symptom levels in Black American
men than White American men may be the result of racial disparities in mental health treatment
between Blacks and Whites in the US (Whaley, 2004). However, higher levels of stress experienced by
ethnic minorities may also be a reason why ethnicity is a risk factor for psychosis, and some studies have
shown that this differential effect of ethnicity disappears once psychological stress levels are controlled
for (Cohen & Marino, 2013; Tortelli et al., 2018). In other within‐country studies, immigrants have been
shown to have significantly higher rates of schizophrenia diagnosis than members of the endogenous
population. A personal or family history of migration is an important risk factor, and immigrants from
developing countries are at greater risk than those from developed countries (Cantor‐Graae & Selten,
2005). At least part of the explanation for the higher incidence in immigrants can be traced to the stress
caused by many of the initial consequences of immigration, such as language difficulties,
unemployment, poor housing, and low socio‐economic status (Hjern, Wicks, & Dalman, 2004). Finally,
the incidence of schizophrenia is similar for males and females, although females tend to have a later
age of onset and fewer hospital admissions, and this may be the result of females attaining higher levels
of social role functioning before illness, which confers a better outcome (Hafner, 2000; Murray & Van
Os, 1998; Angermeyer, Kuhn, & Goldstein, 1990).
Finally, delusional disorder and brief psychotic disorder are new diagnostic categories within
schizophrenia spectrum disorders, but DSM‐5 estimates that the lifetime prevalence rate for delusional
disorder is around 0.2% and that brief psychotic disorder may account for 9% of cases of first‐onset
psychosis (DSM‐5, American Psychiatric Association, 2013).

SELF‐TEST QUESTIONS
What is the estimated lifetime prevalence rate for a diagnosis of schizophrenia worldwide?
Some ethnic and cultural differences in the prevalence rates of schizophrenia have been
found. Can you describe some of these differences?

SECTION SUMMARY

8.3 THE PREVALENCE OF SCHIZOPHRENIA SPECTRUM DISORDERS

The lifetime prevalence rate for a diagnosis of schizophrenia is around 0.75% and is
similar across different countries and cultures.
Rates of diagnosis of schizophrenia do tend to be higher in ethnic minority groups and in
immigrant populations generally.
Estimates for the lifetime prevalence rate for delusional disorder is around 0.2%.

8.4 THE COURSE OF PSYCHOTIC SYMPTOMS

Psychotic symptoms usually develop through a well‐defined succession of stages. The three predominant
phases are (a) the prodromal stage, (b) the active stage, and (c) the residual stage.

8.4.1 The Prodromal Stage

The large majority of those who develop psychotic symptoms show the first signs of these symptoms
during late adolescence or early adulthood (see Figure 8.1). A study of nine countries by the World
Health Organization found that 51% of individuals diagnosed with schizophrenia were aged between
15 and 25 years of age (Sartorius et al., 1986), and over 80% are between 15 and 35 years of age. For
some individuals, the onset of psychotic symptoms can be rapid and dramatic, but for most it represents
a slow deterioration from normal functioning over an average period of around 5 years (Hafner et al.,
2003). This slow deterioration is known as the prodromal stage and is first exhibited as slow
withdrawal from normal life and social interaction, shallow and inappropriate emotions, and
deterioration in personal care and work or school performance (George, Maheshwari, Chandran,
Manohar, & Rao, 2017), with some evidence that gray matter loss may occur in those brain areas
mediating social cognition (Bhojrai et al., 2011) (Case History 8.1). That psychosis initially develops
during late adolescence is one of the basic facts of this psychopathology, but why should onset occur
during this rather specific point in an individual's lifespan? The course of psychosis is best understood in
terms of a diathesis–stress model, in which psychotic symptoms are caused by an underlying
inherited biological vulnerability, but this vulnerability frequently manifests as specific symptoms if the
individual has certain critical and stressful life experiences. There is a good deal of evidence that a
majority of individuals who first show symptoms of psychosis have experienced stressful life events
immediately prior to their first psychotic episode (Brown & Birley, 1968), and exposure to trauma up to
the age of 17 years is associated with significantly increased odds of psychotic experiences at age 18
years (Croft et al., 2019). The transition from adolescence to adulthood is arguably one of the most
stressful periods of an individual's life, and Harrop & Trower (2001) have argued that prodromal‐like
signs in normal adolescents may emerge from a troubled teenage state that has failed to cope with
normal maturation. This leaves the adolescent unable to cope with a majority of the life challenges that
they will have to deal with at this stage of development, and the resulting response is a withdrawal from
social interaction and a fall in educational performance. Eventually such tendencies will become noted
by family and friends, and the development of cognitive dysfunctions giving rise to disordered thoughts,
delusions and erratic and bizarre behaviour mark the onset of the active stage.

prodromal stage The slow deterioration from normal functioning to the delusional and
dysfunctional thinking characteristic of many forms of schizophrenia, normally taking place
over an average of 5 years.

diathesis-stress The perspective that psychopathology is caused by a combination of a

genetically inherited biological diathesis (a biological predisposition) and environmental stress.

During the development of DSM‐5, a case was made for including what was to be called attenuated
psychotic symptoms syndrome (also known as ‘psychosis risk syndrome’) (Woods, Walsh, &
McGlashan, 2010). This would have been characterised by mild psychotic symptoms that don’t meet the
diagnostic criteria for full‐blown schizophrenia, but would enable clinicians to identify at least some
individuals who were in the prodromal state for subsequent schizophrenia spectrum disorders. However,
the final decision was to omit this category from DSM‐5 because of the poor diagnostic reliability
revealed in an earlier clinical trial (Carpenter & van Os, 2011) and the fact that only a proportion of
those who exhibit prodromal symptoms go on to warrant a full diagnosis of schizophrenia (studies
suggest a conversion rate of between 20 and 50%, Corcoran, First, & Cornblatt, 2010).

8.4.2 The Active Stage

In the active stage, the individual begins to show unambiguous symptoms of psychosis, which may
manifest as delusions, hallucinations, disordered speech and communication, and a range of full‐blown
symptoms that are outlined in Section 8.1 of this chapter. First episode psychosis is the term used
to describe the first time a person experiences a full‐blown psychotic episode, and this can be a very
frightening, confusing, and distressing experience for the sufferer. Many individuals who experience first
episode psychosis do improve, and remission rates following first episode psychosis have been estimated
at between 40 and 58% (Lally et al., 2017), although many fewer actually meet the criteria for full
recovery (estimates between 13 and 38%) (e.g., Jääskeläinen et al., 2013).

active stage The stage in which an individual begins to show unambiguous symptoms of
psychosis, including delusions, hallucinations, disordered speech and communication, and a
range of fullblown symptoms.

8.4.3 The Residual Stage

Recovery from the symptoms of psychosis is usually gradual, but many sufferers may still retain some
symptomatology over the longer term. The residual stage is reached when the individual ceases to
show prominent signs of positive symptoms (such as delusions, hallucinations, disordered speech, etc.).
However, during the residual stage they may well still exhibit negative symptoms, such as blunted affect,
withdrawal from social interaction, and find it difficult to cope with normal day‐to‐day activities such as
holding down a job. Studies suggest that as many as 50% of sufferers will remit after one or more active
stages (Lally et al., 2017), and around 50% will alternate between active and residual stages (Wiersma,
Nienhuis, Slooff, & Giel, 1998). These statistics indicate that relapse is relatively common, and relapse
can often be traced to either (a) stressful life events or return to a stressful family environment after a
period of hospitalisation or care (see Section 8.5.3), or (b) nonadherence to medication. Discontinuation
rates for medication are startlingly high, with studies reporting discontinuation rates of between 75 and
90% within 12–24 months of discharge from hospital (Mullins, Obeidat, Cuffel, Naradzay, & Loebel,
2008), and partial compliance is likely to result in significantly higher levels of relapse and
rehospitalisation (Eaddy, Grogg, & Locklear, 2005). The factors most associated with nonadherence or
noncompliance with medication include poor insight, negative attitudes to medication, a history of
nonadherence, difficult side effects, substance abuse, inadequate discharge or aftercare planning, and
poorer therapeutic relationships between patient and service providers (Lacro et al., 2002; Wade, Tai,
Awenat, & Haddock, 2017).

residual stage The stage of psychosis when the individual ceases to show prominent signs of
positive symptoms (such as delusions, hallucinations or disordered speech).
CASE HISTORY 8.1 THE PRODROMAL STAGE—IDENTIFYING
THE EARLY SIGNS

‘Fifteen‐year‐old Caitlin was an excellent student with many friends when she entered the
ninth grade. One year later, she suddenly became restless in school, stopped paying attention
to her teachers, and eventually failed all of her subjects. At home she appeared increasingly
withdrawn and isolated, spending hours sleeping or watching television. The previously
even‐tempered adolescent became angry, anxious, and suspicious of those around her, and
was occasionally seen talking to herself while making repetitive, odd hand motions. Several
years later, hearing voices and insisting that the CIA was hatching an elaborate plot to
murder her and her family, she was diagnosed with schizophrenia’.
(https://www.disorders.org/personality‐disorders/schizophrenia/can‐we‐prevent‐or‐delay‐
schizophrenia/)

Clinical Commentary
This description of the development of Caitlin’s symptoms is typical of the prodromal
stage of schizophrenia. She became withdrawn, ill‐tempered, anxious, and suspicious
and showed a marked decline in academic performance. Unfortunately, these signs are
often difficult to differentiate from many of the behavioural changes exhibited by
normal individuals as they progress through adolescence, so diagnosis at an early stage is
often difficult. These difficulties with early diagnosis are unfortunate, because evidence
suggests that the earlier treatment begins after the development of actual psychosis, the
more rapid the immediate recovery and the better the overall outcome.
Some more specific prodromal features associated with schizophrenia include:
Peculiar behaviours
Impairment in personal hygiene and grooming
Inappropriate affect (e.g., laughing when talking about something sad)
Vague, overly elaborate, or circumstantial speech
Poverty of speech
Odd beliefs or magical thinking
Unusual perceptual experiences

SELF‐TEST QUESTIONS
What are the main stages through which psychotic symptoms normally develop?
What are the factors that may contribute to relapse following recovery from an acute
psychotic episode?
 SECTION SUMMARY

8.4 THE COURSE OF PSYCHOTIC SYMPTOMS

The large majority of those who develop psychotic symptoms show the first signs of
symptoms during late adolescence or early adulthood. This is known as the prodromal stage.
Around 70% of those who show first signs of psychotic symptoms have experienced
stressful life events in the previous 3 weeks.
Around 50% of those diagnosed with schizophrenia will remit after one or more active
stages, and 50% will alternate between active and residual stages.
Remission rates following first episode psychosis has been estimated at between 40 and 58%.

8.5 THE AETIOLOGY OF PSYCHOTIC SYMPTOMS

The evidence we have reviewed so far portrays psychosis as a broad range of loosely associated
symptoms. It can manifest as disordered thinking and communication, disordered perceptions,
hallucinations and delusions, and behavioural deficits. In addition, no single clinical symptom is the
cardinal feature by which the main DSM‐5 diagnostic category of schizophrenia is characterised. This
being the case, theories of the aetiology of psychosis are also diverse and include biological,
psychological, and sociological approaches to understanding this psychopathology. The overarching
approach to understanding psychosis is a diathesis–stress perspective. That is, psychosis is thought to be
caused by a combination of a genetically inherited biological diathesis (a biological predisposition to
psychotic symptoms) and environmental stress. This means that even if you have a genetically pre‐
programmed disposition to psychosis, you may well not develop any symptoms unless you experience
certain forms of life stressors. Such stressors might involve early rearing factors (Schiffman et al., 2001),
dysfunctional relationships within the family such as insecure attachment (Carr, Hardy, & Fornells‐
Ambrojo, 2018), an inability to cope with the stresses of normal adolescent development (Harrop &
Trower, 2001), childhood adversities, and in particular childhood sexual abuse (McGrath et al., 2017)
(see Radua et al., 2018, for a fuller description of risk factors for psychosis). In addition, recent research
on the diathesis–‐stress approach to schizophrenia suggests that stress may worsen symptoms in those
with a genetic vulnerability to psychosis through its effect on cortisol production in the body (Jones &
Fernyhough, 2007; Karanikas & Garyfallos, 2015).
Because of the heterogenous nature of schizophrenia as a diagnostic category and the range of diverse
symptoms that accompany psychosis, the study of the causes of these symptoms has focused on
explaining specific features of psychosis rather than attempting to elaborate an all‐inclusive explanation.
This is sometimes known as a ‘complaint‐oriented approach’ (Bentall, 2006) which not only argues that
there is a need to study individual symptoms, but also that individual symptoms may have their origin in
psychological mechanisms that underlie normal experience (Bentall, 2004). For example, some theories
have attempted to identify the inherited component of individual symptoms, others the abnormalities in
brain biochemistry or brain functions that accompany psychotic symptoms. Still others have tried to
understand the cognitive processes that underlie delusions and disordered thought and communication
—many of which do have their origins in normal psychological processes. Others have attempted to
identify the nature of the stressors that might trigger psychotic symptoms in vulnerable individuals.
Finally, sociocultural views of psychosis take an entirely different perspective and argue that the course
of psychotic symptoms may be determined by the simple act of diagnosing someone with schizophrenia
or by the fact that they are born into a disadvantaged socio‐economic group, and factors such as these
may be enough to promote the development of psychotic symptoms. We explore all of these different
approaches in the following sections.

8.5.1 Biological Theories

Genetic factors
It has always been known that psychotic symptoms appear to run in families, and this suggests that there
may well be some form of inherited predisposition. That psychosis has an inherited component has
been supported by the results of concordance studies. If an individual is diagnosed with
schizophrenia, Table 8.5 shows the probability with which a family member or relative will also develop
the disorder. This shows that the probability with which the family member or relative will develop
schizophrenia is dependent on how closely they are related—or more specifically, how much genetic
material the two share in common (Gottesman et al., 1987; Cardno et al., 1999). Studies have suggested
that an individual who has a first‐degree relative diagnosed with schizophrenia is 6–10 times more likely
to develop psychotic symptoms than someone who has no first‐degree relatives diagnosed with
schizophrenia (Schneider & Deldin, 2001; Chou et al., 2017).
TABLE 8.5 Concordance rates for individuals with a diagnosis of schizophrenia (after Gottesman, McGuffin, &
Farmer, 1987)
Relation to Proband % Diagnosed with Schizophrenia
Spouse 1.00
Grandchildren 2.84
Nieces/Nephews 2.65
Children 9.35
Siblings 7.30
Dizygotic (Fraternal) Twins 12.08
Monozygotic (Identical) Twins 44.30
However, simply because psychotic symptoms tend to run in families does not establish a genetic basis
for this psychopathology. For example, some family environments may have dysfunctional elements (e.g.,
difficulties in communication between family members) that may give rise to the development of
psychosis. In order to examine the genetic basis more carefully, many researchers have undertaken twin
studies, in which they have compared the probability with which monozygotic (MZ) and dizygotic
(DZ) twins both develop symptoms indicative of schizophrenia. MZ twins share 100% of their genetic
material, whereas DZ twins share only 50% of their genes, so a genetic explanation of psychotic
symptoms would predict that there would be greater concordance in the diagnosis of schizophrenia in
MZ than in DZ twins. This can clearly be seen in Table 8.5 where the concordance rate for MZ twins is
44% but falls to only 12% in DZ twins. Twin studies have indicated that the heritability estimate for
schizophrenia is high at between 64 and 81% (Sullivan, Kendler, & Neale, 2003; Lichtenstein et al.,
2009), which makes schizophrenia one of the most heritable of psychiatric disorders (Gejman, Sanders,
& Kendler, 2011).
As convincing as these data may seem, there are still problems in interpreting twin studies. For example,
(a) MZ twins will always be the same sex whereas DZ twins may not be; (b) MZ twins are usually
physically identical, unlike DZ twins, and this may lead to family and friends treating MZ twins more
similarly than they would DZ twins (i.e., MZ twins could experience more similar environmental factors
than DZ twins); and (c) MZ twins are likely to have shared the same placenta prior to birth whereas DZ
twins do not, and this would mean that any interuterine abnormalities would be more likely to affect
both MZ twins through the shared placenta (Davis & Phelps, 1995) (see also Chapter 1, Figure 1.2 for a
discussion of how twin studies may overestimate the heritability of a psychopathology when compared
with molecular genetics research).
However, many of these difficulties of interpretation can be overcome by studying the offspring of MZ
and DZ twins rather than the twins themselves (Gottesman & Bertelsen, 1989). If one MZ twin develops
psychotic symptoms and the other does not, any genetic element in psychosis should still show up in the
children of either of the two MZ twins. That is, the children of the MZ twins should still exhibit similar
rates of risk for schizophrenia (because they have inherited the same predisposition)—even though one
of their parents developed schizophrenia and the other did not. This is exactly what Gottesman &
Bertelson (1989) found: 16.8% of the offspring of the MZ twins who were diagnosed with schizophrenia
were likely to develop psychotic symptoms themselves, and 17.4% of the offspring of the MZ twins who
were not diagnosed with schizophrenia were also likely to develop psychotic symptoms. This suggests
that a genetic risk factor has been passed on to offspring, even though one set of parents did not develop
schizophrenia themselves. A similar kind of family‐based study of the genetics of schizophrenia is
known as a familial high‐risk study, which begins with biological parents with schizophrenia and
then studies their offspring in a longitudinal study to identify the frequency with which these offspring
develop psychotic symptoms. One such study has found that children of a parent with schizophrenia are
six times more likely to develop a schizophrenia spectrum disorder than offspring of parents without a
diagnosis of schizophrenia (Goldstein, Buka, Seidman, & Tsuang, 2010).
Another way of tackling the problems of separating out the influence of genetic inheritance and
environmental experience is to look at the incidence of schizophrenia in children who are biologically
similar but have been reared apart (adoption studies). If there is an important genetic element to
psychosis, then we would expect the children of a mother diagnosed with schizophrenia to have similar
probabilities of developing schizophrenia regardless of whether they had been reared with their mother
or not. A seminal study by Heston (1966) compared 47 adopted children who were reared apart from
their schizophrenic biological mothers with 50 control adopted children whose mothers were not
diagnosed with schizophrenia. He found symptoms of psychosis in 16.6% of the adopted children of
the schizophrenic mothers and no symptoms in the adopted children of mothers without schizophrenia.
Studies of adopted children conducted in Denmark have shown similar results. Kety (1988) and Kety et
al. (1994) found that adopted children who develop psychotic symptoms are significantly more likely to
have had biological relatives with a diagnosis of schizophrenia (21.4%) than adoptive relatives with a
diagnosis of schizophrenia (5.4%). These types of studies provide strong evidence for a genetic
component to schizophrenia and psychosis.

adoption studies Research conducted on children who have been reared by individuals other
than their biological parents.

However, some more recent adoption studies suggest that genetic liability still interacts with
environmental factors to predict the development of psychotic symptoms. Wahlberg et al. (2004) found
that in adopted children, inherited genetic factors were an important predictor of a diagnosis of
schizophrenia but only in combination with certain environmental factors found in the adopted home
environment. In this particular study, an adopted child was more likely to be diagnosed with
schizophrenia if they had a biologically inherited predisposition and they were also brought up in an
adopted home environment where there were dysfunctional communication patterns (see Section 8.5.3).
While genetic inheritance is an important predictor of psychotic symptoms, this is further evidence that
genetic factors interact with environmental factors in a way predicted by diathesis–stress models.
Not only are these kinds of genetic studies important in determining whether a diagnosis of
schizophrenia has a significant inherited component, they are also beginning to show that individual
symptoms associated with a diagnosis of schizophrenia may also have an important inherited
component, and these include factors such as experiencing hallucinations (Hur, Cherny, & Sham, 2012),
volume of gray matter in specific brain regions (van Haren et al., 2012), and catatonia (Beckmann &
Franzek, 2000). However, for some other psychotic symptoms there is less evidence for overriding
genetic determination, and these include some negative symptoms such as anhedonia (Craver & Pogue‐
Geile, 1999) and delusions (Cardno & McGuffin, 2006; Varghese et al., 2013).
Finally, recent genetic studies of schizophrenia and its related disorders have begun to show that there
are genetic overlaps between schizophrenia and some other psychiatric disorders, such as bipolar
disorder and autism, suggesting that variation in a specific gene or set of genes may simultaneously
affect the development of these different diagnoses (Gejman, Sanders, & Kendler, 2011; Fromer et al.,
2013).

Molecular genetics
If, as seems likely, there is a genetic component to psychosis, how is it transmitted between related
individuals, and how does this inherited component influence the development of psychotic symptoms?
In recent years, much effort has been directed at attempting to identify the specific genes through which
the risk for psychosis may be transmitted (Henriksen, Nordgaard, & Jansson, 2017), the chromosomes
on which these genes are located (see Owen & Doherty, 2016), and how these genes, their possible
defects, and their interaction with environmental factors may give rise to psychotic symptoms
(Andreasen, 2001; Zwicker, Denovan‐Wright, & Uher, 2018).
These endeavors have often involved genetic linkage analyses, in which blood samples are collected
in order to study the inheritance patterns within families that have members diagnosed with
schizophrenia. Linkage analyses work by comparing the inheritance of characteristics for which gene
location is well known (e.g., eye colour) with the inheritance of psychotic symptoms. If the inheritance
of, for example, eye colour follows the same pattern within the family as psychotic symptoms, then it can
reasonably be concluded that the gene controlling psychotic symptoms is probably found on the same
chromosome as the gene controlling eye colour, and is probably genetically linked to that ‘marker’
characteristic in some way. Research Methods in Clinical Psychology 8.1 illustrates an example of how a
particular trait of those diagnosed with schizophrenia, in this case poor eye‐tracking of a moving object,
can be used as a genetic marker to track other psychotic symptoms that may be linked genetically to this
characteristic (Research Methods in Clinical Psychology 8.1).
Using analyses such as these, genes associated with the development of psychotic symptoms have been
identified on a number of chromosomes including 8 and 22 (Kendler et al., 2000), 2, 3, 5, 6, 11, 13, and
20 (Badner & Gershon, 2002; Levinson et al., 2002), and 1 and 15 (Gejman, Sanders, & Kendler, 2011).
Also, other techniques, such as genome‐wide association studies (GWAS) allow researchers to
identify genetic loci that are associated with schizophrenia. In 2014 the Psychiatric Genomics
Consortium, an international consortium of scientists conducting analyses of genetic data in relation to
mental health problems, identified 108 different genetic loci that were associated with schizophrenia
(Schizophrenia Working Group of the Psychiatric Genomics Consortium, 2014), confirming that
schizophrenia is a condition underpinned by very many genes that in various combinations can create a
large variety of symptoms with a range of symptom severities. GWAS can also identify rare mutations
in genes that might give rise to psychotic symptoms—especially those mutations that give rise to ‘copy
number variations’ (CNVs) which refers to an abnormal copy of DNA in a gene (either a deletion or a
duplication). Mutations resulting in DNA deletions (International Schizophrenia Consortium, 2008) as
well as mutations causing DNA duplications (Levinson et al., 2011; Kirov et al., 2009) have been found
to be associated with schizophrenia, and one candidate gene called DRD2 encodes information specific
to dopamine receptors in the brain (Lawford et al., 2005)—a neurotransmitter that has frequently been
implicated in psychotic symptoms (see following section on brain neurotransmitters). Other studies have
regularly identified 22q11.2 deletion syndrome, which is a deletion found on the long arm of
chromosome 22, as one of the strongest known genetic risk factors for schizophrenia (Owen & Doherty,
2016), and a high proportion of adults with this deletion have a diagnosis of schizophrenia (25% in
22q11.2 deletion syndrome compared with 0.75% in the general population) (Murphy, Jones, & Owen,
1999). The physical phenotype of this deletion is very variable, but cognitive impairment—which is a
significant feature of schizophrenia—is a common characteristic.

genome-wide association studies (GWAS) Technique which allows researchers to identify

rare mutations in genes that might give rise to psychopathology symptoms.

RESEARCH METHODS IN CLINICAL PSYCHOLOGY 8.1

SMOOTH‐PURSUIT EYE‐TRACKING AS A MARKER FOR THE
INHERITANCE OF PSYCHOSIS

Smooth‐pursuit eye‐tracking is the ability to follow a moving object in a smooth continuous

movement with your eyes while keeping your head still. However, many individuals with a
diagnosis of schizophrenia are unable to do this, and can only follow a moving object with jerky
movements of the eyes (known as saccadic movements) (Schneider & Deldin, 2001). This may
seem like a relatively innocuous symptom, but it has importance because it is a characteristic
that can be used as a genetic marker for schizophrenia. That is, unlike the broader symptoms
of schizophrenia (such as thought disorder, delusions, and hallucinations), abnormalities in
smooth‐pursuit eye‐tracking are probably related to a rather specific neurological abnormality
which may be directly linked to abnormalities in individual genes. If this is so, then the gene
responsible for specific eye‐tracking deficits may also be associated with many of the more
disabling symptoms of schizophrenia. So, by tracing the gene responsible for eye‐tracking
deficits we may also locate the gene or genes responsible for other psychotic symptoms.
There is now a large body of evidence indicating that around 30–45% of first‐degree relatives
of individuals diagnosed with schizophrenia exhibit poor performance in smooth pursuit eye‐
tracking tasks—even when those first degree relatives have not been diagnosed with
schizophrenia (Karoumi et al., 2001; Louchart‐de la Chapelle et al., 2005), and this suggests
that deficits in eye‐tracking performance are likely to be an indicator of an inherited
predisposition to schizophrenia. In addition, studies of twins in which only one of the pair have
developed psychotic symptoms (discordant twins) show that concordance of eye‐tracking
abnormalities are twice as high in monozygotic twins than dizygotic twins (Levy & Holzman,
1997) (see Section 8.5.1 for an explanation of concordance studies in twins), providing more
evidence for the involvement of inherited genetic factors. Studies have still been unable to track
down the specific gene associated with this eye‐tracking abnormality, although there is some
evidence that it may be linked with a number of genes that are also responsible for interfering
with dopamine metabolism (Trillenberg, Lencer, & Heide, 2004), and this may be the important
connection between eye‐tracking deficits and the broader symptoms of schizophrenia.

However, while many studies have shown associations between individual genes and schizophrenia
symptoms, there have also often been failures to replicate many of these findings (Kim, Zerwas, Trace,
& Sullivan, 2011). This probably testifies to the heterogeneity of schizophrenia as a diagnostic category
and the fact that different people with a diagnosis of schizophrenia may not have the same underlying
genetic factors contributing to their symptoms. For example, many of the mutations causing the CNVs
mentioned above are very rare, and so schizophrenia symptoms may be caused by many different and
very rare gene mutations. Second, some of the gene factors associated with schizophrenia may have
their impact on quite specific aspects of psychological functioning. For example, deficits in executive
functioning (planning, working memory, problem solving) are known to be characteristic of
schizophrenia, and some genes have been identified that are associated specifically with executive
functioning deficits in schizophrenia (Harrison & Weinberger, 2004; Owen, Williams, & O'Donovan,
2004). But executive functioning deficits are also associated with many other psychiatric disorders, such
as autistic spectrum disorder, intellectual disabilities, and bipolar disorder, and so this particular gene
mutation may not be purely a risk factor for schizophrenia and we might predict it to be present
without an individual necessarily developing psychotic symptoms.

Brain neurotransmitters
Cognition and behaviour are very much dependent on the efficient working of brain neurotransmitters
which enable effective communication between brain cells and functionally different parts of the brain
itself. It is not surprising, therefore, that many researchers have suspected that the thought disorders,
hallucinations, and behaviour problems characteristic in the diagnosis of schizophrenia may be caused
by malfunctions in these brain neurotransmitters. The biochemical theory of schizophrenia that has
been most prominent over the past 50 years is known as the dopamine hypothesis, and this account
argues that the symptoms of schizophrenia are importantly related to excess activity of the
neurotransmitter dopamine. There are a number of factors that have led to the implication of excess
dopamine activity.

dopamine hypothesis A theory which argues that the symptoms of schizophrenia are related
to excess activity of the neurotransmitter dopamine.

First, the discovery of antipsychotic drugs that helped to alleviate the symptoms of psychosis (such as
the phenothiazines) led to the discovery that such drugs acted by blocking the brain's dopamine
receptor sites and so reduced dopamine activity (Schneider & Deldin, 2001). Interestingly, while the
administration of antipsychotic drugs alleviated many of the positive symptoms of schizophrenia, such
as thought disorder and social withdrawal, they also had the side effect of producing muscle tremors
very similar to those seen in Parkinson's disease, and it was already known that Parkinson's disease was
caused by low levels of dopamine. In contrast, when people suffering Parkinson's disease were given the
drug L‐dopa to raise brain dopamine levels, they often began to exhibit psychotic symptoms (Grilly,
2002). This evidence implies that either high levels of brain dopamine or excess dopamine activity is
responsible for many of the symptoms of psychosis. Subsequent research has suggested that many
antipsychotic drugs have their effect by binding specifically to dopamine receptors and reducing brain
dopamine activity (Burt, Creese, & Snyder, 1977).

phenothiazines A group of antipsychotic drugs that help to alleviate the symptoms of

psychosis by blocking the brain’s dopamine receptor sites and so reduce dopamine activity.

Second, during the 1970s it was noticed that there was a strong link between excessive use of
amphetamines and a syndrome known as amphetamine psychosis. When taken in high doses for
long periods of time, amphetamines produce behavioural symptoms in humans and animals that closely
resemble symptoms of psychosis. These include paranoia and repetitive, stereotyped behaviour patterns
(Angrist, Lee, & Gershon, 1974). Subsequently we have learned that amphetamines produce these
disturbed behaviour patterns by increasing brain dopamine activity, and giving amphetamines to those
diagnosed with schizophrenia actually increases the severity of their symptoms (Faustman, 1995).

amphetamine psychosis A syndrome in which high doses of amphetamines taken for long
periods of time produce behavioural symptoms in humans and animals that closely resemble
symptoms of psychosis.

Third, brain imaging studies have indicated that individuals diagnosed with schizophrenia show
excessive levels of dopamine released from areas of the brain such as the basal ganglia—especially when
biochemical precursors to dopamine, such as dopa, are administered to the individual (Carlsson, 2001;
Goldsmith, Shapiro, & Joyce, 1997).
Finally, post‐mortem studies have found increased levels of dopamine and significantly more dopamine
receptors in the brains of deceased schizophrenia sufferers—especially in the limbic area of the brain
(Seeman & Kapur, 2001).
So, how might dopamine activity be involved in the production of psychotic symptoms? Figure 8.1
illustrates two important dopamine pathways in the brain, the mesolimbic pathway and the
mesocortical pathway. These two pathways begin in the ventral tegmental area of the brain but
may have quite different effects on the appearance of psychotic symptoms. First, an excess of dopamine
receptors only seems to be related to the positive symptoms associated with schizophrenia
(hallucinations, delusions, disordered speech). This is consistent with the fact that antipsychotic drugs
only appear to attenuate positive symptoms and have little or no effect on negative symptoms (the
behavioural symptoms associated with flattened affect), and this effect of excess dopamine appears to be
localised in the mesolimbic dopamine pathway (Davis, Kahn, Ko, & Davidson, 1991). However, the
mesocortical pathway begins in the ventral tegmental area but projects to the prefrontal cortex, and the
dopamine neurons in prefrontal cortex may be underactive. This has important implications for
cognitive activity because the prefrontal cortex is the substrate for important cognitive processes such as
working memory, and these cognitive processes contribute to motivated and planned behaviour
(Winterer & Weinberger, 2004). In this way, dopamine activity might account for both the positive and
the negative symptoms observed in schizophrenia, but because antipsychotic drugs block dopamine
receptors only in the mesolimbic pathway, this accounts for why such drugs only affect positive
symptoms.

mesolimbic pathway One of two important dopamine pathways in the brain, which may be
impaired during schizophrenia. The other pathway is the mesocortical pathway.

mesocortical pathway One of two important dopamine pathways in the brain, which may
be impaired during schizophrenia. The other pathway is the mesolimbic pathway.

While the dopamine hypothesis has been an influential biochemical theory of schizophrenia for more
than 30 years, there is still some evidence that does not fit comfortably within this hypothesis. First, while
antipsychotic drugs are usually effective in dealing with many of the symptoms of schizophrenia, they
do not start having an effect on symptoms until about 6 weeks after treatment has commenced. This is
unusual, because antipsychotic drugs are known to start blocking dopamine receptors in the brain
within hours of administration, so we would expect improvement to be immediate (Sanislow & Carson,
2001; Davis, 1978). Second, many new antipsychotic drugs are effective despite having only a minimal
effect on brain dopamine levels (e.g., clozapine) or appear to be effective because they not only block
dopamine receptors but also block other neurotransmitters such as serotonin (Nordstrom et al., 1995).
Other neurotransmitters that have been implicated in psychotic symptoms include serotonin,
acetylcholine, glutamate, and gamma‐aminobutyric acid (GABA) neurons (Stone, Morrison, & Pilowsky,
2007; Brisch et al., 2014), and this is perhaps not so surprising given that serotonin neurons regulate
dopamine neurons in the mesolimbic pathway, and glutamate and dopamine dysregulation may interact
with each other. A full understanding of the role of neurotransmitters in psychotic symptomatology will
only result from a full understanding of how these brain neurotransmitters affect each other, and how
this interaction influences brain processes that give rise to both positive and negative symptoms.

The neuroscience of schizophrenia

The brains of individuals with a diagnosis of schizophrenia show a number of structural differences to
those of nonsufferers, and these differences can often be linked to the nature of the symptoms displayed
by sufferers. These differences appear to continue to develop throughout the lifetime of the individual
displaying psychotic symptoms, and are usually apparent at the time of the first psychotic episode—
suggesting that they may play a causal role in symptoms rather than simply being a consequence of
psychotic symptoms (Cecil, Lenkinski, Gur, & Gur, 1999; Olabi et al., 2011). The most important of
these structural differences are (a) enlarged ventricles (the spaces in the brain filled with cerebrospinal
fluid), (b) reduced gray matter in the prefrontal cortex, and (c) structural and functional abnormalities in
the temporal cortex and its surrounding areas, including reduced volume in the basal ganglia,
hippocampus, and limbic structures.
First, the brains of individuals with schizophrenia tend to be smaller than those of nondiagnosed
controls, and this is also the case in first‐degree relatives of sufferers who have not developed psychotic
symptoms (Ward, Friedman, Wise, &Schulz, 1996; Baare et al., 2001). This suggests that smaller brain
size may be determined by genetic rather than environmental factors. This is consistent with the most
frequently confirmed finding that schizophrenia is associated with enlarged ventricles (the areas in
the brain containing cerebrospinal fluid) and this is associated with overall reduction in cortical gray
matter (Andreason et al., 1994). In cases of chronic schizophrenia, the enlargement of the ventricles is a
continuous process (Mathalon, Sullivan, Lim, & Pfefferbaum, 2001) and contributes to faster aging in
the brains of individuals with a diagnosis of schizophrenia (Schnack et al., 2016). However, enlarged
ventricles are found even in individuals who have just experienced their first psychotic episode, implying
it may be a feature that is present prior to the first symptoms developing (Cecil et al., 1999).

enlarged ventricles Enlargement of the areas in the brain containing cerebrospinal fluid,
associated with schizophrenia.

Second, schizophrenia is associated with reduced volume of gray matter in the prefrontal cortex
(Buchanan, Vladar, Barta, & Pearlson, 1998). This area plays an important role in a number of
cognitive processes, the most important being executive functioning, which enables planning, goal‐
directed behaviour, and decision‐making; it also mediates speech and coordinates working memory.
Deficits in executive functioning would encompass poor performance on cognitive tasks associated with
speed and accuracy, abstraction/categorisation, memory, and sustained attention, and they are also
associated with negative symptoms of schizophrenia such as blunted affect and social withdrawal
(Antonova, Sharma, Morris, & Kumari, 2004; Artiges et al., 2000; Pinkham, Penn, Perkins, &
Lieberman, 2003). In particular, individuals with a diagnosis of schizophrenia who exhibit negative
symptoms show significantly lower prefrontal cortex metabolic rates than nonsufferers (Potkin et al.,
2002), and they have reduced prefrontal cortex blood flow when undertaking decision‐making card
sorting tasks such as the Wisconsin card sort test (WCST) (Weinberger, Berman, & Illowsky, 1988). All
of this is consistent with the fact that the mesocortical dopamine pathway extends to the prefrontal
cortex, and that dopamine neurons in the prefrontal cortex are relatively less active in individuals with
schizophrenia. Most recent evidence suggests that these deficits in prefrontal cortex functioning in
schizophrenia are not necessarily due to a reduction in the number of neurons in this area, but to
disrupted synaptic connections between neurons in the glutamatergic, GABAergic, and dopaminergic
pathways (Seshadri, Zeledon & Sawa, 2013) and to a reduction in the dendritic spines of neurons
which reduces the connectivity between these cells (Paspalas, Wang, & Arnsten, 2013; McGlashan &
Hoffman, 2000). This reduced connectivity between neurons in an area of the brain responsible for
executive functioning may well give rise to the disordered speech and behavioural disorganisation often
found in schizophrenia. Figure 8.2 shows how a positron emission tomography (PET) scan reveals
decreased frontal lobe activity in a schizophrenia sufferer compared with a healthy control participant,
as well as the enlarged ventricles in the brain of the schizophrenia sufferer.

dendritic spines Small protrusion from a neuron’s dendrite that receives input from a single
synapse of an axon.
FIGURE 8.2 Abnormalities in dopamine activity may be linked to the brain's mesocortical pathway and the mesolimbic
pathway. Both begin in the ventral tegmental area, but the former projects to the prefrontal cortex and the latter to the
hypothalamus, amygdala, hippocampus and nuclear accumbens. The dopamine neurons in the prefrontal cortex may be
underactive (leading to the negative symptoms of schizophrenia), and this underactivity may then fail to inhibit dopamine
neurons in the mesolimbic pathway causing an excess of dopamine activity in this pathway (resulting in positive symptoms)
(e.g., Davis, Kahn, Ko, & Davidson, 1991).
Third, brain imaging studies have also shown abnormalities in the temporal cortex, including
limbic structures, the basal ganglia, and the cerebellum (Shenton, Dickey, Frumin, &
McCarley, 2001; Gur, Cowell, et al., 2000; Gur, Turetsky, et al., 2000). Abnormalities in neural activity
in the temporal lobe‐limbic system are more associated with the positive symptoms of schizophrenia
such as hallucinations and symptoms of thought disorder (McCarley et al., 2002), and auditory
hallucinations have been shown to be associated with neural activation in the temporal lobes‐limbic
system (Shergill, Brammer, Williams, Murray, & McGuire, 2000). These deficits are also associated with
reduced volume in the temporal cortex and hippocampus in individuals with a diagnosis of
schizophrenia (Steen et al., 2006; Fischer et al., 2012). Furthermore, impaired hippocampal function in
schizophrenia could underlie a range of symptoms because of the role of the hippocampus in memory
for events and facts and in pattern completion, all of which are disrupted in schizophrenia and could
give rise to spurious associations, chaotic speech, and hallucinations (Tamminga, Stan, & Wagner, 2010;
Lieberman et al., 2018).

temporal cortex Abnormalities in this brain area are associated with symptoms of
schizophrenia.

basal ganglia A series of structures located deep in the brain responsible for motor
movements.
 cerebellum The part of the brain at the back of the skull that coordinates muscular activity.

These findings tend to suggest that abnormalities in different areas of the brain may each be associated
with different symptoms of psychosis. Some individuals with a diagnosis of schizophrenia show
abnormalities in some of these brain areas, but many others show abnormalities in all of them—which
explains why many exhibit both positive and negative symptoms (Kubicki et al., 2002).
One final issue, of course, is what causes these structural and functional differences in the brains of
individuals with a diagnosis of schizophrenia? One factor we have already mentioned is genetic
mutation in genes that control the development of the brain and its associated cognitive processes.
Many of the neurological defects found in schizophrenia research are ones that could have occurred
only during early brain development when the complex structure of the brain is developing, and this
suggests that prenatal factors may be important in causing subsequent brain abnormalities (Allin &
Murray, 2002). In particular, individuals diagnosed with schizophrenia do not show the normal
hemispheric asymmetry in brain development that occurs during the second trimester of pregnancy (4–
6 months), and this may give rise to deficits in those areas of the brain concerned with language and
associative learning (Sommer, Aleman, Ramsey, Bouma, & Kahn, 2001). In addition, brain damage or
abnormalities that occur after the third trimester of pregnancy are normally self‐repairing through a
process known as glial reactions. That such repair is not found in post‐mortem studies of the brains of
individuals diagnosed with schizophrenia suggests that brain areas must have been damaged or suffered
abnormal development prior to the third trimester (Brennan & Walker, 2001).
Another important consideration is that environmental factors may influence the early development of
the brain either during gestation or at birth. Risk factors that have been postulated include birth
complications, maternal nicotine consumption during pregnancy, and maternal infections. Birth
complications—such as reduced supply of oxygen to the brain—appear to occur at a higher rate in
individuals who eventually display symptoms of psychosis (Brown, 2011; Walker, Kessler, Bollini, &
Hochman, 2004), but, of course, not everyone who suffers birth complications then develops psychosis,
so other factors must be involved. Cigarette smoking during pregnancy has been associated with
significantly higher risk of schizophrenia symptoms in the offspring—possible as a result of maternal
nicotine consumption on offspring brain development (Niemelä et al., 2016). And the probability of an
offspring developing schizophrenia is also significantly higher in mothers who have suffered an infection
during pregnancy (Brown & Derkits, 2010), and one particular infection that has been widely studied in
this respect is influenza. For example, one study suggested that a mother's exposure to influenza during
the first trimester of pregnancy resulted in a sevenfold increase in the probability of their offspring
developing psychotic symptoms (Brown et al., 2004). However, the effect sizes in studies such as these
are small, and there have been many failed attempts to demonstrate that maternal influenza is a risk
factor for offspring psychosis, so the jury is still out on this issue. Some of the evidence for a role of
maternal influenza on offspring psychosis is discussed in Focus Point 8.4.

FOCUS POINT 8.4 VIRAL INFECTIONS AND PSYCHOTIC

SYMPTOMS
One interesting hypothesis is that psychotic symptoms may be triggered by viral infections
experienced either prenatally or postnatally (Torrey, 1991; Mednick, Machon, Huttunen, &
Bonnett, 1988). There is a range of converging, but largely circumstantial, evidence for the
involvement of viral infections in the aetiology of some cases of psychosis. First,
epidemiological studies have shown that people diagnosed with schizophrenia are significantly
more likely than others to have been born in the winter, and so were more likely to have been
exposed to viruses prenatally or during the first 6 months of their lives (Torrey, Miller, Rawlings,
& Yolken, 1997). Second, there also appears to be a relationship between the outbreak of
epidemics, such as influenza epidemics, and the development of psychotic symptoms.
Individuals who were exposed prenatally to influenza are significantly more likely to develop
psychotic symptoms in later life (Mednick et al., 1988), and a study of nearly 2 million
individuals in a Swedish cohort found that infections generally during pregnancy increased the
risk of psychosis in their offspring (Blomström et al., 2015). Third, mothers of individuals
diagnosed with schizophrenia are more likely to have been exposed to influenza during
pregnancy than the mothers of individuals who are not diagnosed with schizophrenia, and
recent systematic reviews strongly suggest that prenatal exposure to a number of infections and
inflammatory responses may be associated with increased risk of adult schizophrenia
(Khandaker, Zimbron, Lewis, & Jones, 2013). In particular, exposure to the influenza virus
appears to be important during the first trimester (Brown et al., 2004) and the third trimester
(de Messias, Cordeiro, Sampaio, Bartko, & Kirkpatrick, 2001)—and the latter is a prenatal
period which is known to be connected to the possible development of brain abnormalities
associated with schizophrenia (but see Selten & Termorshuizen, 2017, for a critique of this
evidence).
 Most viral infections have their effects relatively immediately, so how might viral infections
prenatally or in early childhood lead to the development of psychotic symptoms in later
adolescence? One possibility is that viral infections—especially prenatally—might disrupt brain
development and lead to the kinds of brain abnormalities that are typical in individuals
diagnosed with schizophrenia. To this extent, animal research provides some useful information
suggesting that rats or mice prenatally infected with viruses such as influenza experience
developmental abnormalities that result in permanent changes in brain structure and function
(Pearce, 2001; Fatemi, Pearce, Brooks, & Sidwell, 2005; Kneeland & Fatemi, 2013). However,
we must remember that not everyone who is exposed to viruses at a critical age develops
psychotic symptoms and we need to be able to explain this fact. For example, it may be that if
viruses do cause developmental abnormalities leading to psychotic symptoms, this may only
happen in those who already have an inherited vulnerability to these symptoms.

Finally, if the causes of schizophrenia can be traced to early brain development, then why don't at‐risk
individuals develop psychotic symptoms until they are usually well into adolescence? There may be at
least two reasons for this. First, we have argued that many of the symptoms of schizophrenia—and
especially the negative symptoms can be traced to abnormalities in the prefrontal cortex—the area that
controls many complex cognitive activities. However, the prefrontal cortex is a brain structure that only
fully matures in adolescence and early adulthood, so any developing deficits in that brain region are
only likely to manifest in an obvious way at maturation (Giedd, 2004), and this is consistent with
adolescents at risk for psychosis showing prodromal symptoms such as social withdrawal, shallow
emotion, and deterioration in school work during their early teens. Second, late adolescence is also a
period associated with increased stress, and especially exposure to stressors that the individual will not
have experienced before (e.g., sexual relationships, and social and educational responsibilities). Stress
increases cortisol levels which in turn activates brain dopamine activity, and any factor that stimulates
brain dopamine activity in at risk individuals is likely to trigger the onset of psychotic symptoms
(Walker, Mittal, & Tessner, 2008; Schifani et al., 2018).
FIGURE 8.3 This PET scan shows sections of brains from a patient diagnosed with schizophrenia (right) and a
healthy control (left). In the top pictures, higher activation is indicated by red areas, and these are more widespread in the
brain of the healthy control. The bottom pictures show ventricular enlargement in the brain of the individual diagnosed
with schizophrenia (indicated by dark blue areas), and this is a common feature of the brains of individuals diagnosed with
schizophrenia.
Reproduced by permission of Monte S Buchsbaum, Mount Sinai School of Medicine.
In summary, there is now good evidence that psychotic symptoms are associated with deficits in
important brain areas. These deficits manifest as lower brain volume, neurotransmitter imbalances—
especially in dopamine, serotonin, glutamate, and GABA pathways—and poorer performance on
cognitive neuropsychological tasks. Particularly important brain areas exhibiting deficits are the
prefrontal cortex, the temporal cortex, and the hippocampus, and deficits in functioning in the
prefrontal cortex and temporal cortex can be clearly associated with both negative and positive
symptoms respectively. The causes of these structural and functional brain deficits in schizophrenia are
unclear, although gene mutations, environmental factors influencing prenatal development, and
maternal infections are all possibilities that are being currently researched.
8.5.2 Psychological Theories
Over the past 40 years or so most research has been focused on genetic and biological theories of
schizophrenia, and psychological models have generally received less attention. However, the past 10
years has seen a resurgence of interest in psychological models of psychosis—especially cognitive
models that view psychotic symptoms as the result of cognitive biases in attention, reasoning and
interpretation (Savulich, Shergill, & Yiend, 2012; Ramos & Torres, 2016). We begin this section by
discussing some traditional psychological interpretations of psychosis—especially psychodynamic and
behavioural accounts. We then move on to consider cognitive accounts of psychosis, including both
cognitive deficits (impairments in cognitive functioning) and cognitive biases (the tendency to attend to a
certain type of stimulus or interpret ambiguity in just one particular direction).

Psychodynamic theories
Freud (1915, 1924) hypothesised that psychosis is caused by regression to a previous ego state which
gives rise to a preoccupation with the self—this is known in psychoanalytic terminology as regression to
a state of primary narcissism characteristic of the oral stage of development. This regression is
thought to be caused by cold and unnurturing parents, and the regression to a state of primary
narcissism gives rise to a loss of contact with reality. Freud described the symptoms of thought disorder,
communication disorder, and withdrawal typical of psychosis as evidence of a self‐centred focus, and he
argued that any attempts to re‐establish contact with reality gave rise to the hallucinations and delusions
characteristic of psychosis.

primary narcissism Regression to a previous ego state which gives rise to a preoccupation
with the self.

In the 1950s and 1960s, many psychodynamic explanations of psychosis were related to dysfunctional
family dynamics, and championed by such contemporary psychodynamic theorists as Gregory Bateson
and R.D. Laing. Prior to this, Fromm‐Reichmann (1948) had developed the concept of the
‘schizophrenogenic mother’—literally a mother who causes schizophrenia! According to Fromm‐
Reichmann, schizophrenogenic mothers were cold, rejecting, distant, and dominating. Such mothers
demanded dependency and emotional expressions from their children but simultaneously rejected
displays of affection and even criticised the dependency that they implicitly attempted to foster in their
children. This account suggests that when subjected to such conflicting messages and demands from a
dominant close relative, the child withdraws and begins to lose touch with reality—at least in part as a
way of avoiding the stresses and conflicts created by the mother.

schizophrenogenic mother A cold, rejecting, distant and dominating mother who causes
schizophrenia according to Fromm-Reichmann.

The empirical evidence supporting these psychodynamic theories of psychosis is meagre (Harrington,
2012). First, genetic accounts of psychosis are now largely accepted as important contributors to
psychosis—even by psychodynamic theorists and have been incorporated in some way into
psychodynamic theories. In some cases it is argued that inherited biological predispositions may
facilitate regression to earlier psychological states (Willick, Milrod, & Karush, 1998), whereas others
suggest biological predispositions may prevent the individual from developing an ‘integrated self ’, and
this gives rise to the disrupted behaviour patterns exhibited in individuals diagnosed with schizophrenia
(Pollack, 1989). Second, there is very little evidence that mothers of individuals displaying psychotic
symptoms actually possess the characteristics of the schizophrenogenic mother described by Fromm‐
Reichmann (Waring & Ricks, 1965).
Behavioural theories
There are a number of views that suggest a role for learning and conditioning in the development of
psychotic symptoms—if not as a full theory of psychosis, then as an explanation of why unusual
behaviour patterns are typical of many forms of psychosis. Ullman & Krasner (1975) argued that the
bizarre behaviours of individuals diagnosed with schizophrenia developed because they are rewarded by
a process of operant reinforcement. That is, because of the disturbed family life often experienced by
individuals diagnosed with schizophrenia and the attentional difficulties that are a central feature of the
psychopathology, such individuals tend to find it difficult to attend to normal social cues and involve
themselves in normal social interactions. Instead, their attention becomes attracted to irrelevant cues,
such as an insect on the floor, an unimportant word in a conversation, a background noise, etc.
Attention to irrelevant cues such as these makes their behaviour look increasingly bizarre, and as a result
it gets more and more attention, which acts as a reinforcer to strengthen such behaviours.
There is some limited evidence to support the view that inappropriate reinforcement may generate
some bizarre behaviours, and it may account for the frequency of inappropriate behaviour emitted by an
individual diagnosed with schizophrenia. For example, Focus Point 8.5 describes a study conducted
some years ago by Ayllon, Haughton & Hughes (1965). They reinforced a female resident in a
psychiatric hospital for carrying a broom. Whenever she was observed holding the broom nurses were
asked to approach her, offer her a cigarette, or give her a token which could be exchanged for a cigarette
(Focus Point 8.5). This study suggests that what look like quite bizarre and inappropriate behaviours can
be developed by simple contingencies of reinforcement. Further support for a learning view comes from
evidence that extinction procedures can be used to eliminate or to significantly reduce the frequency of
inappropriate behaviours simply by withdrawing attention or withholding rewards when these
inappropriate behaviours are emitted. Ayllon (1963) describes the behaviour of a 47‐year‐old female
diagnosed with schizophrenia who insisted on wearing around 25 pounds of excess clothing, even in hot
weather. This individual's bizarre clothing habits were, however, soon returned to normal when a
weight limit was set each time she tried to enter the hospital dining room. On each day she was allowed
into the dining room only if she weighed 2 pounds less than the previous day. This could be achieved
only by discarding some of the excess clothing and within 14 weeks she was down to wearing quite
normal clothing. The fact that inappropriate behaviours can be eliminated and acceptable social and
self‐care behaviours developed using operant reinforcement procedures does suggest that at least some
of the unusual behaviours emitted by individuals diagnosed with schizophrenia may be under the
control of contingencies of reinforcement.
 FOCUS POINT 8.5 CAN PERFECTLY NORMAL
PSYCHOLOGICAL PROCESSES CAUSE BIZARRE
BEHAVIOUR?

A revealing study by Ayllon, Haughton, and Hughes in 1965 provides insight into some of the
processes that might generate the kinds of bizarre and apparently irrational behaviour that
make up some forms of psychopathology.
They used operant reinforcement methods (see Chapter 1, Section 1.1.3) to reward a female
patient diagnosed with schizophrenia for carrying a broom.
Whenever she was observed holding the broom a nurse would approach her, offer her a
cigarette, or give her a token which could be exchanged for a cigarette. After a period of this
reinforcement, the patient was carrying the broom around for most of the day, and even taking
it to bed with her when she slept.
At this point, the researchers called in two psychiatrists (who were unaware of the
reinforcement schedule) to give their opinions on the nature of the behaviour. One of them
gave the following reply:
‘Her constant and compulsive pacing, holding a broom in the manner she does, could be seen
as a ritualistic procedure, a magical action. . .Her broom would be then: (1) a child that gives
her love and she gives him in return her devotion, (2) a phallic symbol, (3) the scepter of an
omnipotent queen. . . .this is a magical procedure in which the patient carries out her wishes,
expressed in a way that is far beyond our solid, rational and conventional way of thinking and
acting’. (Ayllon et al., 1965, p. 3)
First, this psychodynamic explanation given by one of the psychiatrists is a good example of
how easy it is to over‐speculate about the causes and meaning of a behaviour when the real
causes are unknown.
Second, it shows how behaviour that is viewed as representative of psychopathology can be
acquired through a perfectly normal learning mechanism (in this case operant reinforcement).

Cognitive theories

Cognitive deficits
Cognitive deficits are one of the core features of schizophrenia that evolve during the development of
the disorder. These deficits include dysfunctions in working memory, attention, processing speed, visual
and verbal learning, and consequential deficits in reasoning, planning, abstract thinking, and problem
solving (Heinrichs & Zakzanis, 1998; Fioravanti, Bianchi, & Cinti, 2012). A decline in these cognitive
processes is one of the earliest signs of psychosis and occurs in the prodromal phase as well as
throughout the development of explicit symptoms. The deterioration in working memory efficiency is
also an identifiable precursor of relapse (Hui et al., 2016). Working memory impairment is particularly
important because of its role in many complex forms of cognition, including maintaining
representations in an activated easily accessible state required during activities involving reasoning and
language (Baddeley, 2012), and studies show that working memory deficits are highly correlated
with poor cognitive performance in individuals with a diagnosis of schizophrenia (Johnson et al., 2013;
Gold et al., 2019). Research in Clinical Psychology 8.2 describes how working memory capacity can be
tested and compared across healthy controls, individuals with a diagnosis of schizophrenia, and
individuals with an alternative mental health diagnosis (Research Methods In Clinical Psychology 8.2).
These cognitive deficits almost certainly have their origins in the biological and neurological factors
discussed in Section 8.5.1, including abnormalities in brain neurotransmitter activity and abnormalities
in brain structure and function, and this decline in cognitive function probably underlies many of the
cognitive biases discussed later in this section that contribute to psychotic thinking and give rise to
disorganised thought, hallucinations, delusional beliefs, paranoia, hearing voices, and deficits in social
cognition and emotion regulation.

Cognitive biases
Of specific interest to cognitive theorists are the hallucinations and delusional beliefs that are regularly
developed during psychotic episodes, with over 50% of individuals diagnosed with schizophrenia
exhibiting paranoid beliefs (Guggenheim & Babigian, 1974). This raises the issue of why so many
sufferers should develop these particular kinds of delusions. Amongst individuals diagnosed with
schizophrenia who are living in the community, Harris (1987) found that they were 20 times more likely
than nonsufferers to report intrusive or confrontational experiences, such as threats from landlords,
police enquiries, burglaries, and unwanted sexual propositions, so there may be some basis in experience
to the development of persecutory beliefs. However, researchers have pointed out that paranoid
delusions may also be the result of cognitive biases that have been developed by the sufferer (in much
the same way that cognitive biases may underlie the experience of anxiety and its related disorders, see
Chapter 6, Section 6.4.1). In the following section, we consider the evidence for four types of biased
cognition: attentional biases, attributional biases, reasoning biases, and interpretational biases,
as well as the potential role of theory of mind (TOM) impairments. In particular, these types of
accounts have led to a greater understanding of how individuals develop paranoid ideation in delusional
disorder, and why “hearing voices” is such a prominent and distressing feature of psychosis.
 RESEARCH METHODS IN CLINICAL PSYCHOLOGY 8.2
TESTS OF WORKING MEMORY IN SCHIZOPHRENIA

Working memory is a limited capacity system used for temporarily holding information
available in awareness so it can be manipulated, transformed into a more useful form, or used
in other more complex cognitive tasks such as reasoning or decision‐making.
Working memory capacity differs from individual to individual, and there are a number of
cognitive tests that can be used to determine this capacity.
One is the digit‐span task. In this task participants are presented with a series of digits and
must repeat them back. If they do this successfully, they are given a longer series of digits.
Working memory capacity is judged by the number of digits that the individual can successfully
remember and repeat back.
In an alternative task (sometimes called the AX‐CPT, continuous performance task) the
participant is instructed to make a response which distinguishes between stimuli. For example,
in a typical study, the target letter is X. However, there is an added constraint: X is only a target
when it is preceded by the letter A. Thus, if a participant sees A‐X‐A‐X, both Xs are targets. If
a participant sees B‐X‐B‐X, neither of those Xs are targets. Researchers can manipulate how
likely it is that a target appears. Thus, the AX‐CPT measures a person's ability to maintain a
goal state (e.g., that X must follow A to be a target).
Such tests can be used to test the working memory capacity of individuals with a diagnosis of
schizophrenia and compared with healthy controls or individuals with a different mental health
diagnosis.

This figure shows that individuals with a diagnosis of schizophrenia (SZ) perform significantly
worse on an AX‐CPT continuous performance task (left panel) and a digit span task (right
panel) than healthy controls (HC) and individuals with a diagnosis of bipolar disorder but
without psychotic symptoms (BPD‐). But the bipolar group that does exhibit psychotic
symptoms (BPD+) performs as badly as the schizophrenia group (Frydecka et al., 2014),
suggesting that both groups SZ and BPD+ have working memory deficits when compared with
healthy controls.

Attentional biases
Anxiety disorders are typically associated with attentional biases towards threatening stimuli
(Chapter 6, Section 6.4.1) and individuals suffering psychotic symptoms also show some similar
attentional biases. There is evidence that individuals with delusional disorder selectively attend to
pathology congruent information. For example, individuals with persecutory delusions exhibit
attentional biases towards stimuli that have emotional meaning or are paranoia relevant (Fear, Sharp, &
Healy, 1996; Bentall & Kaney, 1989; Moritz & Laudan, 2007). Interestingly, individuals prone to
persecutory delusions may have a bias towards avoiding attending to some forms of threatening stimuli.
For example, they are slower to locate angry faces than control participants (Green, Williams, &
Davidson, 2001) and make fewer fixations and show reduced attention to the salient information of
facial features than controls (Loughland, Williams, & Gordon, 2002; Philllips & David, 1998). This is
particularly interesting given that potentially angry facial expressions would have added significance for
someone with a persecutory delusion and suggests that although they may be initially attentive to threat,
they then adopt an avoidance strategy that involves avoiding fixating on threatening stimuli (Green,
Williams, & Davidson, 2003). However, what is not yet clear is whether attentional biases to threat in
paranoia are specifically linked to psychotic symptoms, or whether they may alternatively be developed
by a history of stress or trauma (Gibson, Cooper, Reeves, Olino, & Ellman, 2019), and it is relevant that
individuals with persecutory beliefs often report stressful experiences in the period immediately prior to
the onset of full persecutory delusions (Freemanet al., 2019).

Attributional biases
Early research indicated that individuals with delusional beliefs (particularly persecutory beliefs) have a
bias towards attributing negative life events to external causes (Bentall, 1994; Bentall & Kinderman,
1998; Bentall, Corcoran, Howard, Blackwood, & Kinderman, 2001). For example, using the
Attributional Style Questionnaire (see Chapter 7, Section 7.1.2), Kaney & Bentall (1989) found that
patients with paranoid delusions made excessively stable and global attributions for negative events (just
like depressed individuals) but also attributed positive events to internal causes and negative events to
external causes. A subsequent study by Bentall, Kaney, & Dewey (1991) found that this tendency of
individuals with paranoid delusions to attribute negative events to external causes was only evidenced
when there was a perceived threat to the self—they did not necessarily attribute negative events to
external sources when describing the experiences of others. These studies all suggest that individuals
exhibiting paranoid delusions have had significantly more negative, threatening life events than control
individuals without a diagnosis, and have also developed a bias towards attributing negative events to
external causes. At the very least, such an attributional bias will almost certainly act to maintain
paranoid beliefs and maintain their delusions that someone or something external is threatening them.
However, more recent studies have called into question the generality of a specific externalizing bias to
negative events and indicated that paranoia may instead be associated with a decreased sense of self‐
causation generally, and the significance of this psychological process in creating paranoid beliefs still
requires further research (Langdon, Still, Connors, Ward, & Catts, 2013a,b; Randjbar, Veckenstedt,
Vitzthum, Hottenrott, & Moritz, 2010).
 PHOTO 8.2 Suspicious Minds. People vulnerable to paranoid thinking try to make sense of unusual internal experiences
by using those feelings as a source of evidence that there is a threat, and they then incorporate other evidence around them to
substantiate that belief (e.g., interpreting the facial expressions of strangers in the street as additional evidence that they are
threatened). Freeman (2007) argues that these paranoid interpretations often occur in the context of emotional distress, are
often preceded by stressful events (e.g., difficult interpersonal relationships, bullying, isolation), and happen against a
background of previous experiences that have led the person to have beliefs about the self as vulnerable, others as potentially
dangerous, and the world as bad. In addition, living in difficult urban areas is likely to increase the accessibility of such
negative views about others.

Reasoning biases
Over the past 20 years or so, considerable evidence has accrued to suggest that individuals with
delusional disorders exhibit reasoning biases. One form of this is known as ‘jumping to
conclusions’. That is, such individuals make a decision about the meaning or importance of an event
on the basis of significantly less evidence than someone without a delusional disorder. This has been
demonstrated using the classic Jumping to Conclusions task (Huq, Garety, & Hemsley, 1988;
Westermann, Salzmann, Fuchs, & Lincoln, 2012). In this task, participants view two jars each
containing 100 beads: Jar A with 85 red beads and 15 yellow beads and Jar B with 85 yellow beads and
15 red beads. The experimenter hides the jars from view and then, one by one, draws a series of beads
from one of the jars and asks the participant to say which jar the beads are being drawn from. The
fewer the number of beads drawn before the participant reaches a decision indicates a greater jumping
to conclusions bias. Typically, individuals with a delusional disorder draw three beads or fewer before
making a decision (Fine, Gardner, Craigie, & Gold, 2007; Peters & Garety, 2006), and this jumping to
conclusions bias has been shown in individuals that are delusion‐prone (Colbert & Peters, 2002), at high
risk for psychosis (Broome et al., 2007), and are suffering a first episode of psychosis (Falcone et al.,
2010). These studies collectively suggest that jumping to conclusions may create a biased reasoning
process that leads to the formation and acceptance of delusional beliefs and eventually to delusional
symptoms (Savulich, Shergill, & Yiend, 2012). However, it's not clear whether jumping to conclusions is
symptomatic of all delusional beliefs (e.g., delusions of grandeur or reference), or whether it is restricted
to persecutory delusions (Startup, Freeman, & Garety, 2008).

jumping to conclusions The process of making a decision about the meaning or importance
of an event on the basis of insufficient evidence.

The reason why individuals with psychotic symptoms jump to conclusions is also not clear. Jumping to
conclusions is correlated with cognitive impairments—particularly working memory impairments
(Ormrod et al., 2012; Garety et al., 2013), implying that sufferers cannot hold information in working
memory long enough to make fully informed judgments. Alternatively, individuals with a diagnosis of
schizophrenia may simply make decisions based on less evidence or may have a tendency to ‘overvalue’
each individual piece of evidence (Evans, Averbeck, & Furl, 2015).
One final issue is how reasoning biases might interact with the experiences of psychosis‐prone
individuals to cause persecutory symptoms? One particular model that attempts to deal with these issues
is the threat‐anticipation model of persecutory delusions (Freeman, Garety, Kuipers, Fowler, &
Bebbington, 2002). This model argues that four factors are important in contributing to the
development of cognitive biases involved in persecutory ideation: (a) anomalous experiences (such as
hallucinations) that do not appear to have a simple and obvious explanation (and are therefore open to
biased interpretations); (b) anxiety, depression, and worry, that would normally cause a bias towards
negative thinking and threatening interpretations of events (see Chapter 6, Section 6.4.1); (c) reasoning
biases on the part of the individual which lead them to seek confirmatory evidence for their persecutory
interpretations rather than question them (Eisenacher & Zink, 2017); and (d) social factors, such as
isolation and trauma, which add to feelings of threat, anxiety, and suspicion. Of particular importance
is the relationship between anxiety and jumping to conclusions, where anxiety is known to increase the
tendency to jump to conclusions even in a healthy population, and so to generate and reinforce
paranoid ideation (Lincoln, Peters, Schafer, & Moritz, 2009). In addition, there is now a growing body
of evidence showing that there is a significant association between state anxiety and jumping to
conclusions in individuals with a diagnosis of schizophrenia (Ellet, Freeman, & Garety, 2008; Lincoln,
Lange, Burau, Exner, & Moritz, 2009).

FOCUS POINT 8.6 CANNABIS USE AND PSYCHOTIC

SYMPTOMS

‘Brian, my brother, started smoking at a very young age, in his teens. He was a daily smoker and he used to smoke
the equivalent of a pack of cigarettes a day. I had a phone call once from the police in High Wycombe saying they
had found him. He was talking like a Rastafarian and he believed he was John the Baptist. I had to get him
sectioned which absolutely broke the family up. My father and mother had very old‐fashioned ideas about mental
illness—you didn’t speak about it—and they practically disowned him. He came to live with me. He would be
awake all night and sleep all day. One doctor asked me if he was smoking cannabis and I said he was—she
believed that was what triggered his downfall. They put him on medication because they believed he was
schizophrenic—he was hearing voices, saw messages in the paper and was having delusions of grandeur. I believe
the last time anyone saw him was around High Wycombe in 1996 and he was basically living the life of a
down‐and out. I believe his problems were brought on by the smoking. He had to live 28 days off it while in
hospital and he improved. He seemed in better shape to me’.
This BBC news interview describes how one woman believed that smoking cannabis had
caused her brother to develop psychotic symptoms. There has long been a view that regular
psychotropic drug use may be related to the development of psychotic symptoms, and this has
focussed on the relationship between cannabis use and subsequent diagnosis of schizophrenia
(Arsencault, Cannon, Witton, & Murray, 2004). Apart from legal substances such as alcohol
and tobacco, cannabis is the most widely used illicit drug used by schizophrenia sufferers, and
substance use disorder generally is estimated to be 4.6 times higher in schizophrenia sufferers
than the general population (Regier et al., 1990).
Cross‐sectional studies have shown that individuals diagnosed with schizophrenia use cannabis
significantly more often than other individuals in the general population (Degenhardt & Hall,
2001). Some have argued that this relationship between cannabis use and schizophrenia reflects
a form of ‘self‐medication’, in which individuals may start using cannabis because of a
predisposition for schizophrenia (Khantzian, 1985). However, others have argued for a direct
causal link between cannabis use and schizophrenia, and case history studies frequently
describe psychotic episodes being preceded by the heavy use of cannabis (Wylie & Burnett,
1995), and cannabis use being associated with earlier onset of symptoms (Buhler, Hambrecht,
Löffler, An der Heiden, & Hafner, 2002).
Prospective studies that have monitored cannabis use and psychotic symptoms in individuals
over a lengthy period of time appear to indicate that there is indeed a causal link between
cannabis and the development of psychotic symptoms. First, Andreasson, Allebeck, Engstrom,
and Rydberg (1987) found a dose‐response relationship between cannabis use at 18 years and
later increased risk of psychotic symptoms. Subsequent prospective studies found that 18‐year‐
olds meeting the criteria for cannabis dependence had rates of subsequent psychotic symptoms
that were twice the rate of young people not meeting these criteria (Fergusson, Horwood, &
Swain‐Campbell, 2003). Also, this relationship could not be explained by high cannabis use
being associated with any pre‐existing psychiatric symptoms (Fergusson, Horwood, & Ridder,
2005). Statistical modelling of these longitudinal data show that the direction of causality
appears to be from cannabis use to psychotic symptoms and not vice versa (Fergusson et al.,
2005), and this causal link has recently been supported using a genetic approach to estimating
the risk of psychotic symptoms following cannabis use (Vaucher et al., 2017). In addition,
further studies have demonstrated that cannabis use increases the risk of psychotic symptoms
but has a greater impact on those that already have a vulnerability to schizophrenia (Verdoux,
Gindre, Sorbara, Tournier, & Swendsen, 2003; Henquet et al., 2005). Finally, meta‐analyses
suggest that the mean age of onset of psychotic symptoms among cannabis users is almost 3
years earlier than that of non‐cannabis users—even when other factors such as tobacco use are
controlled for (Myles, Newall, Nielssen, & Large, 2012), and patients with schizophrenia using
cannabis are more regularly hospitalised than non‐cannabis users, and have higher relapse rates
(van Dijk, Koeter, Hijman, Kahn, & van den Brink, 2012; Schoeler et al., 2016).
So if there is a causal link between cannabis use and schizophrenia, what is the mechanism that
mediates this link? First, there may be a neurological explanation. Research suggests that
cannabis has an important effect on brain chemistry, and the compound tetrahydrocannabinol
(THC) that is found in cannabis can release the neurotransmitter dopamine (Tanda, Pontieri, &
Di Chiara, 1997; Arnold, Boucher, & Karl, 2012). Excess dopamine activity has been identified
 in the aetiology of schizophrenia, and heavy cannabis use may therefore raise brain dopamine
activity to levels triggering psychotic episodes (but see contrary evidence reported by Bloomfield
et al., 2014). In addition, regular cannabis use may also affect the course of brain maturational
processes associated with schizophrenia, and has been shown to result in smaller cerebellar
white‐matter volume in schizophrenia patients who use cannabis regularly (Solowij et al., 2011).
Alternatively, Freeman, Garety, Kuipers, Fowler& Bebbington (2002) have argued that
anomalous experiences (that do not have a simple and obvious explanation) are one of the
fundamental factors contributing to the development of delusional thinking, and psychoactive
street drugs such as cannabis are likely to increase the frequency of such anomalous
experiences. If the individual is in an anxious state and already feeling isolated, then these
anomalous experiences are likely to be interpreted threateningly and give rise to the persecutory
and paranoid ideation often found in schizophrenia.
In conclusion, despite over 30 years of research highly suggestive of a link between cannabis
use and psychosis, that tantalizing piece of evidence confirming a direct causal link is still
elusive, as is a clear indication of the mechanism by which any causal link might operate.

Interpretational biases
In addition to attentional, attributional and reasoning biases, accounts of psychotic delusions have been
supplemented by findings that a number of other information processing biases may be involved
in the development of delusions. For example, an enhanced tendency to interpret ambiguous
information as threatening is likely to increase perception of risk of personal harm and negative
interpretations of hallucinations that may facilitate stress and paranoia. Such negative interpretation
biases have been observed in individuals with psychosis (Savulich, Shergill, & Yiend, 2012) and these
biases appear to be present before the onset of psychotic symptoms, suggesting that such negative biases
could contribute to the development of psychosis (Yiend et al., 2019).

information processing biases Biases in interpreting, attending to, storing or recalling

information which may give rise to dysfunctional thinking and behaving.

In addition, Morrison (2001) has argued that many individuals diagnosed with schizophrenia have a
bias towards interpreting cognitive intrusions such as ‘hearing voices’ in a negative or threatening
way. In this case, a perfectly normal auditory hallucination may then be interpreted as threatening (e.g.,
‘I must be mad’, ‘the Devil is talking to me’, ‘if I do not obey the voices they will hurt me’), and this
misinterpretation causes anxiety, negative mood, and physiological arousal which produces more
auditory hallucinations, which are in turn interpreted negatively, and so on (Baker & Morrison, 1998).
Interestingly, hearing voices is not restricted to individuals suffering psychosis, and around 13% of
healthy individuals report hearing voices (Bevan, Read, & Cartwright, 2011). However, what
characterises hearing voices in individuals suffering psychosis is the distress that these voices induce.
Individuals with a diagnosis of schizophrenia report the voices they hear as more unacceptable,
uncontrollable, and distressing than healthy individuals (Morrison, Nothard, Bowe, & Wells, 2004), and
interpreting voices as dominating or insulting is associated with distress (Vaughan & Fowler, 2004). In
addition, Peters, Williams, Cooke, & Kuipers (2012) found a link between beliefs about voices and both
emotional and behavioural responses to voices. Beliefs about the omnipotence of voices was significantly
associated with measures of distress, and beliefs about the intent of voices (e.g., malevolence vs.
benevolence) was associated with resistance to or engagement with voices respectively.

hearing voices Auditory hallucinations, generally associated with psychotic delusions.

However, what is not yet fully clear is why individuals suffering psychosis develop the negative
interpretations of voices that they do—such as them being uncontrollable, external, dominating, and
distressing. Waters et al. (2012) argue that the aberrant voices heard by both healthy and psychosis‐
suffering individuals are generated by hyperactivation of auditory neural networks that may be
triggered by environmental or internal factors, and it is failures in signal detection that lead the
individual to accept these voices as real and meaningful but not self‐generated. In addition to this, the
deficits in working memory and executive functioning exhibited by individuals suffering psychosis means
that they in particular may be unable to suppress these voices using deliberative, top‐down processing,
nor are they able to easily distract from them. The distress this uncontrollability will cause is likely to be
one source of interpretational bias, which will lead the individual increasingly to interpret the voices as
threatening, and the voice content as malevolent. In addition to voices being potentially uncontrollable
in this way, hearing voices is often a consequence of traumatic experiences such as physical assault,
sexual trauma, and victimisation (Mueser et al., 1998), and the voices may become distressing because
they reflect elements of the original traumatic experiences (Garety, Kuipers, Fowler, Freeman, &
Bebbington, 2001; Luhrmann et al., 2019)
Finally, as individuals suffering psychosis increasingly come to interpret the voices they hear as external
and uncontrollable, they will develop a ‘relationship’ with these voices, and the nature of this
relationship may determine the level of distress and disability and control that the voices elicit in the
individual. Hayward, Berry, & Ashton (2011) have identified a number of different types of
relationships that individuals with a diagnosis of schizophrenia have with their voices. Often this is a
‘power’ struggle, in which the sufferer is constantly engaged in trying to regain power over their voices.
It can lead some individuals to become socially isolated as they withdraw into the world of their voices.
But for others who are already socially withdrawn, it may lead to the generation of hallucinations and
delusions to make sense of the world of their voices (Hoffman, 2007).

Theory of mind (TOM)

Another cognitive account of psychotic delusions alludes to the possible inability of individuals
diagnosed with schizophrenia to understand the mental state and intentions of others. Individuals who
cannot infer the beliefs, attitudes and intentions of others are said to lack a ‘theory of mind’ (TOM),
and this is a deficit that is known to be prominent in autistic individuals (see Chapter 17, Section 17.4.4).
Frith (1992) has argued that TOM deficits may also be an important factor in the development and
maintenance of psychotic delusional beliefs. If individuals diagnosed with schizophrenia are unable to
infer the intentions or mental states of others, then they may begin to believe that others are either
hiding their intentions or their intentions are hostile. In one study, Corcoran, Cahill, and Frith (1997)
tested the ability of individuals diagnosed with schizophrenia to understand different types of jokes. In
one set of jokes, the participant needed to infer the mental state of one of the characters in order to
understand the joke; in the other set of jokes, only interpretation of the physical events in the cartoon
was needed (see Figure 8.3). They found that individuals with persecutory delusions found the first type
of joke more difficult to understand. However, individuals without persecutory delusions found both
types of jokes equally easy to understand. Furthermore, in tasks designed to test the ability of
individuals to understand situations in which individuals hold false beliefs or intend to deceive,
individuals with persecutory delusions performed significantly worse than nonclinical control
participants. However, TOM deficits are not specific to paranoid delusions, and have subsequently been
described in individuals with a diagnosis of schizophrenia (Bora et al., 2009), to be a stable marker for
the condition across time (Lysaker et al., 2011), and TOM deficits have also been identified in the
prodromal stages of psychosis (Bora & Pantelis, 2013). The fact that TOM deficits appear to be a
feature of a number of schizophrenia spectrum disorders and can be detected at various stages of their
development suggests that TOM deficits may be indicative of more global cognitive dysfunction,
including deficits in executive functioning and working memory, and may contribute to the impairment
in social cognition often found in individuals with a diagnosis of schizophrenia (Yang et al., 2017).

theory of mind (TOM) The ability to understand one’s own and other people’s mental
states.
 FIGURE 8.4 Two typical cartoons taken from the study by Corcoran, Cahill, & Frith (1997). In type (a) jokes the
participant needs to infer the mental state of one of the characters to understand the joke, and if individuals with
persecutory delusions lack a ‘theory of mind’ they will find these jokes difficult to understand. The type (b) joke is an
example from their physical/behavioural joke, where only interpretation of the physical events in the cartoon is needed to
understand the joke. Corcoran et al. found that individuals with persecutory delusions found type (a) jokes more difficult to
understand, whereas people without persecutory delusions were equally able to understand both types (a) and (b).

Metacognitive deficits
Metacognition is the ability to think about thinking or to consciously monitor ongoing thoughts in order
to make judgements based in information from our senses and combine this with prior knowledge. Such
abilities are necessary for planning complex tasks, awareness of the cognitive requirements necessary for
complex tasks, and exerting cognitive control over the different cognitive requirements for a task (Cella,
Reeder, & Wykes, 2015). Metacognition has been found to be impaired in individuals with
schizophrenia spectrum disorders, and this has been linked to a range of symptoms and disabilities
including negative symptoms, lack of insight, poor self‐awareness and self‐knowledge (such as an
inability to know what one knows) (e.g., Pinkham, 2017). Metacognitive deficits also have a
significant impact on important aspects of social cognition, including understanding speech nuances,
facial expressions, and hence the intentions of others and also means the individual with a diagnosis of
schizophrenia has poorer insight into their own mental states (Lysaker, Dimaggio, & Brüne, 2014). In
effect, the inability to ‘oversee’ and manage the different cognitive processes involved in activities such as
social cognition and decision planning means that the psychosis sufferer's experience of these activities is
fragmented, resulting in an inability to integrate information required for successful completion of tasks
and also to form an integrated sense of self (Gagen, Zalzala, Hochheiser, Schnakenberg, & Lysaker,
2019). A number of treatments are being developed to help improve metacognition in individuals with a
diagnosis of schizophrenia, including cognitive remediation approaches (see also Section 8.6.2 this
chapter), metacognitive training, and metacognitive interpersonal therapy for psychosis, and these
interventions have been shown to result in modest improvements in measures of metacognition and
cognitive functioning generally (Reeder et al., 2017; Lysaker, Gagen, & Schweitzer, 2018).

8.5.3 Sociocultural Theories

The overarching diathesis–stress model of schizophrenia emphasises that a biological predisposition
interacts with environmental or life stressors to trigger psychotic symptoms. Sociocultural views of
schizophrenia attempt to supplement this view by identifying social, cultural or familial factors that
generate stressors that could precipitate psychotic symptoms. First, we look at general social factors that
have been implicated in the aetiology of psychosis and then look more closely at how the family
environment can influence the development of psychotic symptoms.

Social factors
The highest rates of diagnosis of schizophrenia are usually found in poorer inner‐city areas and in those
of low socio‐economic status, and this has given rise to two rather different sociocultural accounts of
schizophrenia. The first is known as the sociogenic hypothesis. This claims that individuals in low
socio‐economic classes experience significantly more life stressors than individuals in higher socio‐
economic classes, and these stressors are associated with unemployment, poor educational levels, crime,
and poverty generally. Having to endure these stressors may trigger psychotic symptoms in vulnerable
people. A study conducted in Denmark indicated that factors associated with low socio‐economic status
may be risk factors for psychosis, and these include unemployment, urbanicity, low educational
attainment, lower wealth status, low income, parental unemployment, and lower parental income
(Byrne, Agerbo, Eaton, & Mortensen, 2004; Lee et al., 2018). Studies conducted on immigrants have
also indicated that such groups have a higher incidence of the diagnosis of schizophrenia, and this has
been attributed to the stress caused by many of the initial consequences of immigration, such as
language difficulties, unemployment, poor housing, and low socio‐economic status (Hjern, Wicks, &
Dalman, 2004). However, while this evidence provides some support for the sociogenic hypothesis, there
is little evidence that socio‐economic class per se increases the risk of psychotic symptoms. In particular,
parental socio‐economic class is not a significant risk factor for a diagnosis of schizophrenia (Byrne,
Agerbo, Eaton, & Mortensen, 2004), and studies of individuals with a diagnosis of schizophrenia have
indicated that, although they may be of low socio‐economic status, they are as likely to have parents
from a higher socio‐economic class as a low one (Turner & Wagonfeld, 1967).

sociogenic hypothesis The theory that individuals in low socio-economic classes experience
significantly more life stressors than individuals in higher socio-economic classes, and these
stressors are associated with unemployment, poor educational levels, crime and poverty
generally.

An alternative explanation for the fact that individuals diagnosed with schizophrenia appear to have low
socioeconomic status is that the intellectual, behavioural, and motivational problems afflicting
individuals with psychotic symptoms mean they will suffer a downward drift into unemployment,
poverty, and the lower socio‐economic classes as a result of their disorder. This is known as the social‐
selection theory and claims that individuals displaying psychotic symptoms will drift into lifestyles
where there is less social pressure to achieve and no need to hold down a regular job, and they can cope
with their difficulties on a simple day‐to‐day basis. This hypothesis is supported by the fact that many
individuals diagnosed with schizophrenia may have parents with high socio‐economic status, even
though they themselves are living in poverty‐ridden areas of towns and cities (Turner & Wagonfeld,
1967). In addition, longitudinal studies have suggested there may be a reciprocal relationship between
socio‐economic status and mental health where each factor influences the other (Mossakowski, 2014).

social-selection theory Argues that there are more individuals diagnosed with schizophrenia
in low socio-economic groups because after they have developed psychotic symptoms they will
drift downwards into unemployment and low-achieving lifestyles

One final sociocultural view of schizophrenia is known as social labelling, in which it is argued that
the development and maintenance of psychotic symptoms is influenced by the diagnosis itself (Modrow,
1992). In particular, if someone is diagnosed as ‘schizophrenic’ then it is quite possible (a) that others
will begin to behave differently towards them, and define any deviant behaviour as a symptom of
schizophrenia, and (b) that the person who is diagnosed may themselves assume a ‘role’ as someone who
has a disorder, and play that role to the detriment of other—perhaps more adaptive—roles. At the very
least this is likely to generate a self‐fulfilling prophecy, in which a diagnosis leads to the individual, their
family, and friends behaving in ways which are likely to maintain pathological symptoms. Evidence for
such an effect can be found in the classic study by Rosenhan (1973) in which eight individuals without
any symptoms of psychopathology presented themselves at psychiatric hospitals complaining of various
psychotic symptoms. Not only were these ‘normal’ individuals immediately diagnosed with
schizophrenia, they were subsequently treated in an authoritarian and uncaring manner by hospital
staff; began to feel powerless, bored, and uninterested; and even had great difficulty being viewed and
treated as ‘normal’ once they had left the hospital! (see Bentall, 2019, for a fuller discussion of this
study).

social labelling The theory that the development and maintenance of psychotic symptoms
are influenced by the diagnosis itself.
Familial factors
There is a general belief across most theoretical perspectives on schizophrenia that the characteristics of
the family are in some way important in making an individual vulnerable to acquiring psychotic
symptoms. As we have already seen, some psychodynamic views believed it was certain characteristics
possessed by the mother that was important in precipitating psychosis (the schizophrenogenic mother,
Section 8.5.2). However, more recently, attention has turned from the characteristics of individual
family members to the patterns of interactions and communications within the family.
Some approaches suggest that the risk factor within families for the development of psychotic symptoms
lies in the nature of the way that parents and children communicate. In the 1950s, Bateson, Jackson,
Haley, & Weakland (1956) argued that psychosis may develop in families where communication is
ambiguous and acts to double‐bind the child. This double‐bind hypothesis claims that the
individual is subjected within the family to contradictory messages from loved ones (e.g., a mother may
both request displays of affection, such as a hug, and then reject them as being a sign of weakness). This
leaves the individual in a conflict situation, in which they may then eventually withdraw from all social
interaction. Focus Point 8.7 offers some examples of double‐bind situations and conversations, and it is
clear from these examples that, whichever of the themes the child reads into the ambiguous message,
they are in a no win situation (Focus Point 8.7).

double-bind hypothesis Theory advocating that psychotic symptoms are the result of an
individual being subjected within the family to contradictory messages from loved ones.

The double‐bind hypothesis has subsequently been superseded by more empirical research which has
identified a construct called communication deviance(CD) in families and which is related to the
development of psychotic symptoms. CD is a general term used to describe communications that would
be difficult for an ordinary listener to follow and leave them puzzled and unable to share a focus of
attention with the speaker. Such communications would include (a) abandoned or abruptly ceased
remarks or sentences, (b) inconsistent references to events or situations, (c) using words or phrases oddly
or wrongly, or (d) use of peculiar logic. Studies have demonstrated that CD is a stable characteristic of
families with offspring who develop psychotic symptoms (Wahlberg et al., 2001). When children with a
biological predisposition to schizophrenia have been adopted and brought up in homes with adopted
parents who do not have a biological predisposition for schizophrenia, CD has been found to be an
independent predictor of the adopted child developing psychotic symptoms (Wahlberg et al., 2004;
Roisko, Wahlberg, Hakko, Wynne, & Tienari, 2011). This suggests that CD is a risk factor for a
diagnosis of schizophrenia that is independent of any biological or inherited predisposition, and that
CD is not simply the product of a shared genetic defect between parents and offspring.

communication deviance (CD) A general term used to describe communications that

would be difficult for ordinary listeners to follow and leave them puzzled and unable to share a
focus of attention with the speaker.

Another construct that has been closely linked to the appearance and reappearance of psychotic
symptoms is known as expressed emotion(EE). The importance of the family environment in
contributing to psychotic symptoms was first recognised when it was found that individuals who left
hospital following treatment for psychosis were more likely to relapse if they returned to live with
parents or spouses than if they went to live in lodgings or to live with siblings (Brown, Carstairs, &
Topping, 1958). From this it was discovered that many of the discharged patients were returning to
environments where communications were often hostile and critical. This led to the development of the
construct of EE which refers to high levels of criticism, hostility and emotional involvement between key
members of a family, and some examples of high EE are shown in Activity Box 8.1. Since its
development, EE has been shown to be a robust predictor of relapse (Kavanagh, 1992) and, in
particular, relapse involving positive psychotic symptoms. Families high in EE tend to be intolerant of
the sufferer's problems and have inflexible strategies for dealing with their difficulties and symptoms.
High EE families also have an attributional style that tends to blame the sufferer themselves for their
condition and the consequences of their symptoms (Weisman, Nuechterlein, Goldstein, & Snyder, 2000;
Barrowclough, Johnston, & Tarrier, 1994). It is not clear how high EE within a family might influence
tendency to relapse—but a recent 20‐year prospective study suggests that EE is a valid predictor of
relapses and rehospitalisations (Cechnicki, Bielanska, Hanuszkiewicz, & Daren, 2013). One mechanism
by which EE may trigger relapses is through a high sensitivity to stress in psychosis sufferers. The stress
caused by EE may trigger cortisol release in the hypothalamic‐pituitary‐adrenal system, and this is
known to increase dopamine activity and so reactivate symptoms in vulnerable individuals (Walker,
Mittal, & Tessner, 2008). The link between EE and psychotic symptoms is further supported by the fact
that some studies have shown that interventions to moderate the high EE levels in a family may actually
have a beneficial effect on relapse, suggesting a possible causal link between high EE and relapse
(Hogarty et al., 1986; Tarrier et al., 1988). Finally, cultural factors also appear to moderate the effect of
EE on symptoms and relapse. Aguilera, Lopez, Breitborde, Kopelowicz, & Zarate (2010) found that EE
was less likely to cause relapse in Mexican immigrants to the US than in the indigenous population.
However, as immigrants became more familiar with American culture (language and media) EE became
increasingly related to relapse, which suggests that the EE‐schizophrenia relapse link may be mediated
by cultural differences in warmth, mutual interdependence, and kin relationships (Singh, Harley, &
Suhail, 2013).

expressed emotion (EE) A qualitative measure of the ‘amount’ of emotion displayed,

typically in the family setting, usually by a family member or caretakers.
 FOCUS POINT 8.7 DOUBLE BIND AND PARADOXICAL
COMMUNICATION

The following are some visualisations inspired by double‐bind theory where the verbal message
may contradict the implied message therefore invalidating both.

8.5.4 Summary of Theories of Psychotic Symptoms

The overarching explanation of psychosis is one of diathesis–stress. That is, individuals who develop
psychotic symptoms have an inherited vulnerability to develop these symptoms (diathesis) that are likely
to be triggered by experiencing environmental stressors. We have discussed a mixture of biological,
psychological (cognitive), and sociocultural theories of psychosis, and these rather different types of
explanation are by no means mutually exclusive. They all aim to explain different features of psychosis
often at different levels of description. For example, it is pretty much established that psychosis has an
inherited component and that the development of psychotic symptoms is associated with abnormalities
in brain neurotransmitter activity (e.g., excess dopamine activity) and abnormalities in specific brain
areas (particularly the frontal lobes and the mesolimbic system). These biological abnormalities in turn
appear to give rise to deficits in cognitive functioning, such as problems in attention, executive
functioning, and working memory, and to metacognitive functioning which may affect a person's sense
of identity and their grasp of social cognition. Psychological explanations of delusional thinking have
received considerable attention in recent years, and these have identified biases in attention,
attributional processing, reasoning, and ambiguity interpretation, in ways that are likely to give rise to
delusional thinking and delusional beliefs about the world. Finally, sociocultural theories of psychosis try
to explain the uneven distribution of schizophrenia diagnosis across socio‐economic and ethnic groups
and have sought to identify sources of life stressors that may trigger psychotic symptoms. These may
include dysfunctional family structures and deviant forms of family communication. All of these views
are relevant to a full picture of psychosis.

SELF‐TEST QUESTIONS
What is the diathesis–stress perspective that is used to explain the aetiology of psychotic
symptoms?
Concordance studies, twin studies and adoption studies are used to determine the extent
of genetic factors in psychosis. Can you give examples of these types of methods?
What are genetic linkage analyses and how are they used to identify the specific genes
through which the risk for psychosis may be transmitted?
What is the dopamine hypothesis and how did the role of dopamine in psychosis come to
be discovered?
What abnormalities can be found in the brains of individuals diagnosed with
schizophrenia, and which brain areas are most affected by these abnormalities?
Can you describe the evidence supporting the view that brain abnormalities in individuals
diagnosed with schizophrenia may result from abnormal prenatal development?
What are the main features of psychodynamic explanations of psychosis?
What are the main cognitive deficits found in individuals with a diagnosis of
schizophrenia, and how do these deficits affect thinking and behaviour?
Can you describe some of the attentional deficits that are characteristic of psychosis and
explain how they might contribute to the clinical symptoms?
A number of cognitive biases have been implicated in the development of some psychotic
symptoms. What are these biases and how might they contribute to factors such as
delusional thinking?
What is metacognition and how do deficits in metacognition affect social cognition and
self‐identity in psychosis sufferers?
What is a sociocultural theory of psychosis? Can you describe and evaluate the significance
of at least two sociocultural accounts of psychosis?
What is double‐bind hypothesis and how does it try to explain the development of
psychotic symptoms?
What are expressed emotion and communication deviance, and what is the evidence that
they constitute a risk factor for the development of psychotic symptoms?

SECTION SUMMARY
8.5 THE AETIOLOGY OF PSYCHOTIC SYMPTOMS
The overarching approach to understanding psychosis is a diathesis–stress perspective in which
a combination of genetically‐inherited predisposition (diathesis) and environmental stress
are thought to cause psychotic symptoms.
Concordance studies suggest that an individual who has a first‐degree relative diagnosed with
schizophrenia is 10 times more likely to develop psychotic symptoms than someone who
has no first‐degree relatives diagnosed with schizophrenia.
The concordance rate for schizophrenia in MZ twins is 44% but falls to 12% in DZ twins.
Heritability estimates for schizophrenia are high at between 64 and 81%.
Adoption studies show that the probability of an adopted child developing schizophrenia is
linked to the probability of the biological mother developing schizophrenia and not to the
probability of the adopted mother developing schizophrenia.
Genetic linkage analyses have helped to identify some of the specific genes through which the
risk for psychosis might be transmitted.
Genome‐wide association studies (GWAS) allow researchers to identify rare mutations in genes
that might give rise to psychotic symptoms.
108 different genetic loci have been identified that are associated with schizophrenia
symptoms.
The main biochemical theory of schizophrenia is the dopamine hypothesis, which argues that
psychotic symptoms are related to excess activity of the neurotransmitter dopamine.
Two important dopamine pathways in the brain, the mesolimbic pathway and the mesocortical
pathway, may be impaired during schizophrenia.
Psychotic symptoms are associated with brain abnormalities, including smaller brain size
and enlarged ventricles (the areas in the brain containing cerebrospinal fluid).
Schizophrenia is specifically associated with reduced volume of gray matter in the prefrontal
cortex which affects executive functioning, decision‐making and working memory.
Brain imaging studies have also shown abnormalities in the temporal cortex, including limbic
structures, the basal ganglia, and the cerebellum.
Evidence suggests that schizophrenia may also be associated with birth complications,
maternal nicotine consumption during pregnancy, and maternal infections during
pregnancy.
Psychodynamic theories of psychosis have claimed that it is (a) due to regression to a state
of primary narcissism, or (b) develops because of a ‘schizophrenogenic mother’ who fosters
psychotic symptoms in her offspring (psychodynamic theories).
At least some inappropriate behaviour patterns exhibited by individuals diagnosed with
schizophrenia may be developed and maintained through processes of operant
reinforcement (behavioural theories)
Cognitive deficits in working memory, attention, processing speed, and visual and verbal
learning are core features of schizophrenia.
Individuals with persecutory delusions exhibit attentional biases towards stimuli that have
emotional meaning or are paranoia relevant.
Delusional disorder is often associated with cognitive biases in attention, attribution,
reasoning, and interpretation.
Delusional disorders are associated with a reasoning bias called ‘jumping to conclusions’ where
the individual infers meaning on the basis of very little evidence.
 There is evidence that individuals diagnosed with schizophrenia may not be able to
understand the mental states of others (a ‘TOM’ deficit), and this may be a factor in the
development of delusions—especially delusions of persecution.
Metacognition has been found to be impaired in individuals with schizophrenia spectrum
disorders, and this has been linked to a range of symptoms and disabilities including
negative symptoms, lack of insight, poor self‐awareness, and self‐knowledge.
The sociogenic hypothesis claims that individuals in low socio‐economic classes experience
significantly more life stressors than those in higher socio‐economic classes, and this is
more likely to contribute to the increased prevalence of the diagnosis of schizophrenia in
low socio‐economic groups.
Social‐selection theory argues that there are more individuals diagnosed with schizophrenia in
low socio‐economic groups because after they have developed psychotic symptoms they
will drift downwards into unemployment and low‐achieving lifestyles.
Social labelling theory claims that once an individual has been diagnosed with schizophrenia,
such labelling is likely to give rise to circumstances which will tend to maintain psychotic
symptoms.
High levels of expressed emotion (high levels of criticism, hostility and emotional involvement
between members) and communication deviance (poorly structured means of communication
between family members) within the families of individuals diagnosed with schizophrenia
have been shown to be associated with relapse and the development of positive symptoms.

8.6 THE TREATMENT OF PSYCHOSIS

With appropriate medication, care, and supervision, many people who have suffered psychotic
symptoms can eventually cope with the basics of day‐to‐day living, but most may still find it difficult to
hold down a job or make lasting relationships (Evenson et al., 2016). Supervision and care is often
necessary because relapse is a common feature of psychosis. A systematic review of remission rates in
schizophrenia suggests that remission rates vary between 17 and 78% in first‐episode schizophrenia, and
16 to 62% in multiple‐episode schizophrenia, with remission rates highest in those taking second‐
generation antipsychotics and receiving early treatment intervention (AlAqeel & Margolese, 2012).
However, after recovery from a first episode, studies have shown that around 81% will relapse within the
following 5 years, and 78% will also have a second relapse within that time. Even 10 years after the first
episode, around 50% of sufferers will have relapsed at least once and been hospitaliszed as a result
(Moilanen et al., 2013). Discontinuing antipsychotic drug therapy increases the risk of relapse by almost
5 times (Robinsonr et al., 1999), and illegal drug dependence is another risk factor (San, Bernardo,
Gomez, & Pena, 2013). These are important problems for the management and treatment of psychosis,
and in addition, individuals diagnosed with schizophrenia often lack insight into their disorder, deny
they are ill, or are too distracted and disabled to respond either to reflective therapies or to the
requirements of care programmes. In part as a consequence of this, reviews of medication
nonadherence among sufferers diagnosed with schizophrenia have been found to be as high as 75–90%
within 12–24 months of discharge from hospital (Mullins, Obeidat, Cuffel, Naradzay, & Loebel, 2008),
and predictors of nonadherence include use of illegal substances, alcohol and poor insight (Jonsdottir et
al., 2013) ‐ factors that can often impose intolerable burdens on the families and carers of those
diagnosed with schizophrenia.
Traditionally, custodial care and hospitalisation was the main form of intervention for psychosis, and
some characteristics of early custodial care can be found in Section 1.1.3 in Chapter 1. But the advent
of antipsychotic medications in the 1950s significantly reduced the need for hospitalisation, and we
begin our discussion of the treatment of psychotic symptoms by discussing various forms of biological
intervention (e.g., psychosurgery and drug therapy), followed by psychological interventions (social skills
training, cognitive behaviour therapy, cognitive remediation therapy, and family therapy interventions),
and finally we will discuss the role of early intervention programmes and then the role of community
care (e.g., assertive community treatment and assertive outreach programmes) in addressing the longer‐
term needs of those with a diagnosis of schizophrenia.

8.6.1 Biological Treatments

Electroconvulsive therapy (ECT) and psychosurgery

Early forms of intervention for psychosis seem particularly barbaric in retrospect. Between the 1930s
and 1950s, invasive interventions such as ECT (Bini, 1938) and prefrontal lobotomy (Moniz, 1936) were
used on thousands of individuals suffering psychotic symptoms. ECT involves inducing brain seizures by
passing an electric current through the head of the patient for around half a second (see Chapter 7,
Section 7.3.1), and tends to be used today to treat psychotic symptoms when they are comorbid with
depression that has failed to respond to other forms of treatment. Prefrontal lobotomy is a surgical
procedure that involves severing the pathways between the frontal lobes and lower brain areas.
Lobotomy was used frequently for patients who were disruptive or violent, and the procedure did
appear to have the effect of making such individuals more passive and many were able to be discharged
from hospital. However, during the 1950s the wisdom of the procedure came to be questioned. Fatality
rates from the procedure were unacceptably high (between 1.5–6%) and lobotomies significantly
affected the patient's intellectual capacities and emotional responsiveness (Tierney, 2000). While
lobotomies had seemed to be a good way of reducing overcrowding in hospitals in the 1930s, the
development of effective antipsychotic drugs in the 1950s provided a more acceptable and less invasive
means of managing psychotic symptoms.

prefrontal lobotomy A surgical procedure that involves severing the pathways between the
frontal lobes and lower brain areas.

Antipsychotic drugs
Specially developed antipsychotic drugs and medications are the first line of intervention for psychotic
symptoms, and arguably the most effective treatment for the positive clinical symptoms. The main
classes of drugs used for the treatment of psychotic symptoms are known as antipsychotics or
neuroleptics (because some of these drugs produce undesired motor behaviour effects similar to the
symptoms of neurological diseases such as Parkinson's disease). Nowadays, antipsychotic drugs can be
divided into two broad groups usually labelled first‐ and second‐generation drugs (see Table 4.2 in
Chapter 4), and see also Chapter 4, Section 4.1.1 for a further discussion of antipsychotic medications).
First generation antipsychotics (sometimes also called typical antipsychotics) consist of the traditional
drugs that have been developed over the past 50 years (such as chlorpromazine and haloperidol), and
second‐generation antipsychotics (sometimes called atypical antipsychotics) refer to those that have been
developed in recent years. In the years after their development, it was originally thought that second‐
generation drugs were more effective over a broader range of symptoms than first‐generation drugs
(Citrome, Bilder, & Volavka, 2002), were associated with less risk of relapse (Leucht et al., 2003) and
with less risk of involuntary motor behaviour side effects (Csernansky & Schuchart, 2002).
 neuroleptics One of the main classes of drugs used for the treatment of psychotic symptoms.

The development of new drug treatments for psychosis is an important on‐going process, and it still
unclear what biochemical mechanisms many of these drugs influence to have their successful
therapeutic effects (see Chapter 4, Section 4.1.1). However, antipsychotic drugs have become a central
feature of treatment for psychotic symptoms and significantly more independent research is needed to
improve their effectiveness, reduce their unpleasant side‐effects, and improve patient adherence to
medication regimes.

8.6.2 Psychological Therapies

Social skills training

So far in this chapter we have seen ample evidence that there are deficits in the behavioural, cognitive,
and emotional responses of individuals diagnosed with schizophrenia. This may lead their friends and
family to view their behaviour as inappropriate, their thoughts as confused, and their emotional
responses as erratic. An obvious consequence of these characteristics is that it will make it difficult for
sufferers to interact socially with others, to live normal lives in which they can readily negotiate normal
day‐to‐day activities, and to develop close relationships with others. In fact, the inappropriate responses
of individuals displaying psychotic symptoms may generate a vicious cycle in which inappropriate
behaviour causes others to back off from contact with the sufferer, and this in turn is likely to exacerbate
symptoms and generate feelings of alienation and worthlessness.
One obvious way to intervene in this cycle is to provide the sufferer with training in the appropriate
social skills they will need to deal with basic everyday interactions. Social skills training consists of a
combination of role‐playing, modelling, and positive reinforcement, and the individual is taught how to
react appropriately in a range of useful social situations. Such training will provide the client with a
range of transferable social skills, such as conversational skills, appropriate physical gestures, eye contact,
and positive and appropriate facial expressions (Smith, Bellack, & Liberman, 1996). In addition, the
client will be asked to role play in certain specific scenarios (e.g., how to respond to someone who has
just done them a favour). They are also positively rewarded for appropriate reactions. Such training may
have other tangential benefits in helping the client to maintain contact with outreach or community
supervisors and help them to find work (e.g., how to behave in job interviews) and find accommodation
(Pratt & Mueser, 2002). Randomised controlled trials have provided good evidence for the effectiveness
of social skills training on skills acquisition, assertiveness, social functioning, and a reduction in general
psychopathology (Pfammatter, Junghan, & Brenner, 2006), and providing coping skills and social
support can reduce the effects of stress on relapse and help individuals achieve their social goals
(Addington, Piskulic, & Marshall, 2010).
A more recent focus has been on interventions to facilitate social cognition in individuals with a
diagnosis of schizophrenia rather than address the behavioural skills required in social interaction.
Social cognition domains for which effective interventions have been developed include affect
recognition, theory of mind, and metacognitive processes (Grant, Lawrence, Preti, Wykes, & Cella,
2017), but further research is needed in these areas as gains are often modest, methodologies diverse,
and follow‐up periods short.
Another form of social skills training is supported employment. This was developed as an
alternative to other vocational rehabilitation schemes such as sheltered workshops, which had generally
been viewed as unsuccessful (Bond, 1992). One example of supported employment is the Individual
Placement and Support (IPS) model, which focuses on the search for jobs in integrated community
settings with the provision of follow‐along to help the individual optimise work performance support.
Supported employment has been found to lead to significantly higher rates of work and more wages
earned than comparative programmes (Bond, Drake, & Becker, 2012).

Supported employment A special programme designed with a built-in support mechanism

to help people with physical, mental or developmental disabilities reach and maintain their
customised vocational goals and objectives.

Cognitive behaviour therapy for psychosis (CBTp)

Because of their confused thinking, their frequent lack of insight into their condition, and the potential
difficulties in communicating with individuals exhibiting psychotic symptoms, cognitive therapies were
previously thought to be inappropriate and ineffective for the treatment of psychotic symptoms. This
view was strengthened by the belief that most of the disordered thinking in schizophrenia was the result
of dysfunctional brain neurotransmitter mechanisms rather than psychological factors. However, as we
have seen in the section on aetiology, there is a developing body of evidence to suggest that a number of
psychological processes may be involved in generating and maintaining psychotic thought, particularly
hearing voices, delusions and paranoid views of the world (Langdon, Still, Connors, Ward, & Catts,
2013a,b; Morrison, 2001b), and it may be possible to successfully adapt CBT to target and challenge
some of these symptoms of psychosis (and this form of CBT is currently labelled as CBTp) (Kingdon &
Turkington, 2004; Haddock & Slade, 1995; Morrison, Renton, Dunn, Williams, & Bentall, 2003;
Fowler, Garety, & Kuipers, 1995). For example, Morrison (2001b) has argued that many individuals
diagnosed with schizophrenia have a bias towards interpreting cognitive intrusions as threatening in
some way (e.g., ‘if I do not obey the voices they will hurt me’), and this misinterpretation causes a
vicious cycle which produces more hallucinations, which are in turn interpreted negatively, and so on.
Having interpreted an hallucination as threatening, many individuals may then indulge in what are
known as ‘safety behaviours’ which effectively prevent the individual from disconfirming their belief that
the hallucination is threatening. Safety behaviours include things like lying down, drinking alcohol, or
shouting at the voices to go away (Frederick & Cotanch, 1995), and they may actually have the effect of
increasing the frequency of their hallucinations (Nayani & David, 1996). Clinicians can use CBTp
methods in a variety of ways: (a) to help the sufferer challenge their delusional beliefs (O'Connor et al.,
2007), (b) to develop nonpsychotic meaning for symptoms such as hearing voices (Trower et al., 2004),
and (c) to reduce negative symptoms by challenging low expectations (Rector, Beck, & Stolar, 2005). In
addition, cognitive therapy methods generally have also been found to be effective in other areas of
treatment, and these include (a) helping the sufferer to adjust to the realities of the outside world after
dehospitalisation (known as personal therapy), and (b) helping with medication compliance. CBT can
also be extended to psychotic symptoms in the form of reattribution therapy. We have already
noted that paranoid individuals appear to make more attributions for negative events that are of an
external rather than internal nature, and this appears to maintain their delusions that someone or
something external is threatening them (Lee, Randall, Beattie, & Bentall, 2004). Reattribution therapy
can be used to challenge these dysfunctional attributions, and the client is encouraged to consider more
normal causes for their hallucinations than the dysfunctional or delusional ones that they may hold.
Treatment will usually involve monitoring the frequency of delusional beliefs, attempting to generate
alternative explanations for delusional beliefs, and then providing behavioural experiments that will
enable the client to test out the reality of their beliefs (Alford & Beck, 1994; Chadwick & Lowe, 1990).
Frequently, a verbal challenge will be enough to get the client to reject their dysfunctional belief (e.g.,
the therapist may simply ask whether it makes sense for things to be the way the client says they are, and
a logical discussion of evidence may be sufficient), in other cases a ‘reality test’ in the form of a
behavioural experiment may be necessary. For example, in the case of a client who maintained they
could tell what was going to be said on television before it was actually said, a video recording was put
on ‘pause’ at prearranged times, and the client was asked to say what was coming up (Chadwick &
Lowe, 1990).
 cognitive behaviour therapy for psychosis (CBTp) Form of CBT which helps to address
any abnormal attributional processes and information processing and reasoning biases that may
give rise to delusional thinking.

reattribution therapy A treatment used in helping individuals with paranoid symptoms to

reattribute their paranoid delusions to normal daily events rather than the threatening,
confrontational causes they believe underlie them.

FOCUS POINT 8.8 EARLY INTERVENTION SERVICES

It has been known for some time that the sooner psychotic symptoms are detected and treated,
the better the long‐term prognosis (Marshall et al., 2005). In the UK, this has led to the
establishment of multiple discipline clinical teams whose purpose is to provide an intensive case
management of at risk individuals and to educate GPs and physicians in recognition and
response to subclinical symptoms. The aims of this team are to reduce the duration of
untreated psychosis to less than 3 months, and the team will then provide intensive case
management for the patient over the next 3–5 years. Early intervention has been shown to
produce better clinical outcomes than standard service treatment (Garety et al., 2006), is cost
effective (Singh, 2010), and significantly reduces the risk of second relapse (Alvarez‐Jimenez,
Parker, Hetrick, McGorry, & Gleeson, 2011). However, it is still unclear whether these services
might merely be delaying psychosis without necessarily reducing long‐term risk (Preti & Cella,
2010; Fusar‐Poli, McGorry, & Kane, 2017). Even so, early intervention services have been
established in a number of countries world‐wide, including the UK, Australia and New
Zealand, Norway and Denmark, and Canada and the United States.

Finally, there is still vigorous debate about the success of CBTp in alleviating psychotic symptoms and
enabling recovery. Early randomised controlled trials indicated that CBTp was effective in helping to
reduce hallucinations and delusions, and decreased both positive and negative symptoms while lifting
mood and improving life functioning (Bustillo, Lauriello, Horan, & Keith, 2001; Wykes, Steel, Everitt, &
Tarrier, 2008). However, effect sizes were often modest (Hazell, Hayward, Cavanagh, & Strauss, 2016),
and while CBTp is more effective than either usual treatment or attentional control conditions, it does
not appear to perform significantly better than other forms of therapy for treating psychosis (Jones et al.,
2018; Newton‐Howes & Wood, 2013, but see Hutton, 2013 for a critical commentary on this meta‐
analysis). However, it is clear that CBTp does provide a useful adjunct to treatment for psychotic
symptoms, is well tolerated by sufferers, and can be used in conjunction with medication or other forms
of psychosocial intervention (e.g., Sommer et al., 2012).

Personal therapy
When individuals diagnosed with schizophrenia are discharged from hospital after an acute episode,
they usually find themselves in a challenging environment in which their cognitive skills and their ability
to cope leave a lot to be desired. As a consequence, relapse rates are usually high. Personal therapy is
a broad‐based cognitive‐behaviour programme that is designed to help such individuals with the skills
needed to adapt to day‐to‐day living after discharge. Clients are taught a range of skills in either a group
setting or on an individual basis, and these include (a) learning to identify signs of relapse (e.g., social
withdrawal) and what to do in such circumstances, (b) acquiring relaxation techniques designed to help
the client deal with the anxiety and stress caused by challenging events (e.g., to reduce levels of anger
that might give rise to unnecessary aggression), (c) identifying inappropriate emotional and behavioural
responses to events, and learning new and adaptive responses (e.g., to help with gaining and maintaining
employment and accommodation), (d) identifying inappropriate cognitions and dysfunctional thinking
biases that might foster catastrophic and deluded thinking (and so help the client to prevent intrusive
catastrophic thinking), (e) learning to deal with negative feedback from others and to resolve
interpersonal conflicts (known as ‘criticism management and conflict resolution’), and (f) learning how to
comply with medication regimes (Hogarty et al., 1997b; Hogarty et al., 1997a).

personal therapy A broad-based cognitive behaviour programme that is designed to help

individuals with the skills needed to adapt to day-to-day living after discharge from hospital.

Cognitive remediation training (CRT)

In earlier sections of this chapter we have described how schizophrenia is associated with a number of
important cognitive deficits, especially those relating to attention, memory, and executive functioning
(see Section 8.5.2). These cognitive deficits negatively affect psychosocial functioning (Heaton et al.,
1994) and impair the impact of psychiatric rehabilitation programmes such as social skills training and
vocational rehabilitation (Mueser & McGurk, 2004). Because of this, it makes sense to try to find ways
to improve the basic cognitive functioning of individuals with a diagnosis of schizophrenia, because this
will inevitably have positive knock on effects on other rehabilitation programmes. This has given rise to
what are called cognitive remediation programmes or cognitive enhancement therapies
(CETs), most of which employ computer‐based or pencil and paper tasks to improve attention, memory
and problem‐solving (Krabbendam & Aleman, 2003), and an example exercise is described in
Treatment in Practice Box 8.1. CRT varies in length and intensity, with most programmes providing
two training sessions per week that can last for up to 6 months or 80 hours of training (Hogarty et al.,
2004). Meta‐analyses report significant effects of CRT on attention, verbal memory, problem‐solving,
verbal working memory, processing speed, and social cognition but rather modest effects on symptom
reduction (McGurk, Twamley, Sitzer, McHugo, & Mueser, 2007; Wykes, Huddy, Cellard, McGurk, &
Czobor, 2011; Best & Bowie, 2017). However, cognitive remediation is particularly effective when
combined with social skills training and supported employment (McGurk, Mueser, & Pascaris, 2005;
Silverstein et al., 2008), and can result in improvement in social and cognitive skills up to 24 months
after entering such training programmes (Hogarty et al., 2004).

cognitive remediation training (CRT) A treatment programme for clients designed to

develop and improve basic cognitive skills and social functioning generally.

cognitive enhancement therapy (CET) A form of intervention which addresses deficits in

both social cognition (the ability to act wisely in social situations) and neurocognition (basic
abilities in cognitive functioning, such as memory and attention).
 CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 8.1
COGNITIVE ENHANCEMENT THERAPY

Cognitive enhancement therapy is a developmental approach that attempts to provide

individuals diagnosed with schizophrenia with cognitive exercises that will help the individual
develop cognitive functions that have been impaired by their disorder. These include such skills
as attention, memory, and problem solving
The following categorisation exercise is designed to help develop working memory and
abstraction skills.
Patients are asked to group the following words into four coherent categories:
love iron air home
nylon human spider sand
stone food clay wood
steel water pig paper
virus flower ink glass
The categories of ‘living things’ and ‘things one needs to live’ are fairly obvious but the last two
are sufficiently ambiguous to require abstraction. Many clients will initially group items such as
iron, wood, glass, and steel into a category of ‘building materials’, and ink, paper, clay, sand,
and nylon into ‘art supplies’. However, with some subtle coaching, clients are encouraged to
seek a more abstract basis for sorting (e.g., ‘Does nylon really have anything in common with
sand?’) Success can then be achieved when patients reason that ink, paper, glass, steel, and
nylon are all ‘fabricated materials’ The skills that clients require to complete this task
successfully include remembering previous failed attempts, remembering the words that require
further categorisation, and remembering individual words within the context of categories that
have already been established. As such, the task provides the client with training in memory and
abstraction skills that they can take to other problem‐solving situations.

(after Hogarty & Flesher, 1999)

8.6.3 Family Interventions

In Section 8.5.3 of this chapter we discovered that the family environment for someone diagnosed with
schizophrenia may contribute to both the development of symptoms and to the risk of relapse. In
particular, expressed emotion (EE) and communication deviance (CD) within families are factors that
have been shown to be associated with relapse and the development of positive symptoms. Families with
high levels of CD and EE have difficulty with effective communication between family members, high
levels of criticism, a tendency to blame the sufferer for their symptoms and the family consequences of
those symptoms, and possess inflexible strategies for dealing with difficulties. Clearly, if these
characteristics can be addressed and modified, then this should be reflected in lower risk for positive
symptoms and relapse.
Family interventions can take many forms, but the main features of a majority of these types of
intervention are that they are designed to educate the family about the nature and symptoms of
psychosis and how to cope with the difficulties that arise from living with someone with a diagnosis of
schizophrenia (sometimes known as family psychoeducation) (Harvey, 2018). More specifically, (a)
families learn about the diagnosis, prevalence, and aetiology of psychotic symptoms; (b) they learn
about the nature of antipsychotic medication and how to help the sufferer to comply with their
medication regime; (c) they are taught how to recognise the signs of relapse and to identify and deal
with stressors that could cause relapse; (d) through social skills training, they will learn how to identify
problems, to solve them and to achieve family goals; and (e) families will also learn how to share
experiences and avoid blaming either themselves or the sufferer for their symptoms and the
consequences of their symptoms. These educational targets are achieved in a variety of ways. For
example, high EE families may be asked to watch videos of how low EE families interact (modeling)
(Penn & Mueser, 1996). Counseling can be provided to help family members interact in less emotional
ways, and group discussions where families share their experiences can help to provide reassurance and
a network of social support (known as supportive family management). A more intensive form of
family intervention is known as applied family management, and this goes beyond education and
support to include active behavioural training elements. Communication and coping skills can be taught
with the active involvement of members of the family by using modelling, role‐playing, providing
positive and corrective feedback, and using homework assignments. For example, families may be taught
to have one member chair a problem‐solving meeting (leading the family through the steps) and another
as secretary (recording information on a problem‐solving form). As homework, families may be asked to
meet weekly to practice problem solving without the presence of a therapist or facilitator (Mueser et al.,
2001).

family psychoeducation Family intervention designed to educate the family about the
nature and symptoms of psychosis and how to cope with the difficulties that arise from living
with someone with a diagnosis.

supportive family management A method of counselling in which group discussions are

held where families share their experiences and which can help to provide reassurance and a
network of social support.

applied family management An intensive form of family intervention which goes beyond
education and support to include active behavioural training elements.

Outcome studies have indicated that family interventions significantly reduce the risk of relapse by
around 50–60% (MacFarlane, 2016), improve outcomes in early psychosis (Claxton, Onwumere, &
Fornells‐Ambrojo, 2017), reduce symptoms, and improve the sufferer's social and vocational functioning
for periods up to 2 years (Huxley, Rendall, & Sederer, 2000; Pharoah, Mari, Rathbone, & Wong, 2010),
and family interventions that are conducted for longer than 9 months appear to be particularly effective
(Kopelowicz & Liberman, 1998). Studies suggest that no one form of family intervention is necessarily
more effective than others (Huxley, Rendall, & Sederer, 2000), but family psychoeducation interventions
without accompanying behavioural training components may be less effective at achieving some goals,
such as medication adherence (Zygmunt, Olfson, Boyer, & Mechanic, 2002).

8.6.4 Community Care

With the development of the first antipsychotic drugs in the 1950s and 1960s, it became clear that most
people diagnosed with schizophrenia could be treated to a point where they were capable of living at
least some kind of life back in the community. This helped to relieve the economic burden of lifelong
hospitalisation and custodial care. However, even when living back in their communities, it was clear
that individuals diagnosed with schizophrenia would often need support and supervision. They would
need help maintaining their necessary medication regime, finding and keeping a job or applying for and
securing welfare benefits. They may also need help with many aspects of normal daily living that others
would take for granted, such as personal hygiene, shopping, feeding themselves, managing their money,
and coping with social interactions and life stressors.
In 1963, the US Congress passed a Community Mental Health Act which specified that, rather than be
detained and treated in hospitals, people with mental health problems had the right to receive a broad
range of services in their communities. These services included outpatient therapy, emergency care,
preventative care, and aftercare. Growing concerns about the rights of mental health patients and a
change in social attitudes away from the stigma associated with mental health problems meant that
other countries around the world swiftly followed suit in making mental health treatment and aftercare
available in the community (Hafner & Heiden, 1988). These events led to the development of a
combination of services usually termed assertive community treatment or assertive outreach, and, in the
US alone, this has led to around a 10‐fold decrease in the number of people being treated in hospital for
mental health problems (Torrey, 2001). Assertive community treatment programmes help people
recovering from psychotic episodes with their medication regimes, psychotherapy, assistance in dealing
with everyday life and its stressors, guidance on making decisions, residential supervision, and vocational
training (Bebbington, Johnson, & Thornicroft, 2002). In the UK, assertive outreach is a way of
working with groups of individuals with severe mental health problems who do not effectively engage
with mental health services. Assertive outreach staff would expect to meet their clients in their own
environments, whether that is a home, café, park, or street, and the aim is to build a long‐term
relationship between the client and mental health services. Table 8.6 provides a list of some of the main
aims and characteristics of assertive outreach programmes in the UK, and these emphasise teaching
basic living skills, providing support and guidance, and preventing relapse and there is evidence that the
introduction of assertive outreach treatment in the UK significantly reduced hospital admissions for
individuals with psychosis (Hamilton, Lloyd, Bland, & Grainge, 2015).
There is good evidence that community care programmes help to stabilise the condition of
individuals diagnosed with schizophrenia, ensure that they integrate more effectively into their local
communities, comply with their medication regimes, and stay out of hospital longer than sufferers who
are not part of a community care programme (Madianos & Madianou, 1992; Hansson et al., 2002;
Bebbington, Johnson, & Thornicroft, 2002). However, community care services are often difficult to
resource and to co‐ordinate, and it has been estimated that in any 1 year in the US, between 40 and
60% of all people experiencing symptoms of psychosis receive no treatment at all (Wang, Demler, &
Kessler, 2002). In addition, long‐term studies of community care in the UK suggest that it helps to
maintain clinical and social functioning at a stable level, but does not necessarily help to improve these
aspects of the sufferer's life (Reid et al., 2001).
The community care approach has also given rise to concerns for the physical safety of individuals with
mental health problems who are exposed to the stresses and rigours of everyday life, and for the safety
of others in the communities in which they live. For example, studies in the UK have suggested that
41% of people with mental health problems living in the community suffer physical and verbal
harassment, compared with 15% in the general population, and this abuse is usually carried out by
teenagers and neighbours (Berzins, Petch, & Atkinson, 2003). There is also concern about the role of
individuals diagnosed with schizophrenia as victims or perpetrators of violent crime such as homicide.
A Danish study discovered that the risk of being a victim of homicide was increased sixfold for people
diagnosed with a mental illness such as schizophrenia compared with individuals without a psychiatric
diagnosis (Hiroeh, Appleby, Mortensen, & Dunn, 2001). They argued that individuals diagnosed with
schizophrenia may be at such increased risk of a violent death because of a number of factors,
including (a) they are likely to live in places such as inner cities where crime is more prevalent, (b) they
may have behavioural characteristics such as alcohol or drug abuse that increases the risk, (c) they might
provoke the hostility of others because of their psychotic symptoms (such as paranoia), (d) because of
their symptoms they may be less aware of their own safety needs, (e) they may be killed by others with
mental health problems that they are in contact with, and (f) they may be more likely to be victims of
motiveless killings because of their appearance, which may be unkempt and dirty. In contrast, tragic
and high‐profile murders carried out by people with mental health problems have often been used to
imply that the community care approach to mental health care is dangerous and has failed. However,
the evidence to support this view is mixed and more complex than it looks at first sight (Bo, Abu‐Akel,
Kongerslev Haahr, & Simonsen, 2011). First, one body of evidence reaching back to the 1980s implied
that having a major mental health problem, such as schizophrenia, was not a risk factor for violence
(Elbogen & Johnson, 2009) and did not predict increased levels of violence in those exhibiting psychotic
symptoms (Quinsey, Harris, Rice, & Cormier, 2006). However, other evidence has suggested a link
between schizophrenia and violent behaviour, including increased aggressive behaviour and an
increased risk for violent and non‐violent crimes (Hodgins, 2008; Soyka, Graz, Bottlender, Dirschedl, &
Schoech, 2007). Volavka et al. (1997) found that approximately 20% of individuals with a diagnosis of
schizophrenia were involved in some kind of violent behaviour prior to contact with the health system—
suggesting that any increase in risk for violence after the onset of psychotic symptoms may be due to a
prior history of violence, or—perhaps more importantly—to the poorer socio‐economic living
conditions which many schizophrenia sufferers experience. A recent study by Johnson et al. (2016) found
that violent behaviour in individuals with a diagnosis of schizophrenia was predicted by current alcohol
use, recent violence, and recent victimisation. Bo, Abu‐Akel, Kongerslev Haahr, & Simonsen (2011)
proposed a two trajectory model for violence in patients with schizophrenia, and this is shown
schematically in Figure 8.5. One trajectory describes violence in schizophrenia sufferers with a prior
history of violence and argues that violence in this group may be due to preexisting personality
disorders such as psychopathic traits and antisocial personality disorder. The other trajectory describes
violence in sufferers who had not previously shown antisocial tendencies and ascribes the onset of
violence in this group to positive symptoms such as ‘hearing voices’ and persecutory delusions.
Nevertheless, while many epidemiological studies would lead us to believe that there is a link between
schizophrenia and violence, only a very small proportion of violence in society is accounted for by
individuals with a diagnosis of schizophrenia, and studies indicate that 99.97% of those with
schizophrenia would not commit serious violence in any one given year (Walsh, Buchanan, & Fahy,
2002).
TABLE 8.6 The aims and characteristics of assertive outreach programmes
AIMS: Assertive Outreach services aim to help clients to:

Reduce their number of hospital admissions, in terms of both frequency and duration
Find and keep suitable accommodation
Sustain family relationships
Increase social networks and relationships
Improve their money management
Increase medication adherence
Improve their daily living skills
Undertake satisfying daily activities (including employment)
Improve their general health
Improve their general quality of life
Stabilise symptoms
Prevent relapse
Receive Help at an early stage
CORE CHARACTERISTICS: Assertive Outreach involves targeting clients with severe
and enduring mental health problems who have difficulty engaging with services:

It is multidisciplinary, comprising a range of professional disciplines (nurses, psychiatrists, and

social workers at a minimum; also, depending on user needs, support workers, workers who have
also been service users, psychologists, occupational therapists, housing workers, substance misuse
specialists, and vocational specialists)
There is a low ratio of service users to workers, usually 10 clients per caseload
There is intensive frequency of client contact compared to that of standard community mental
health teams (ideally an average of four or more contacts per week with each client)
An emphasis on engaging with clients and developing a therapeutic relationship
Offers or links to specific evidence‐based interventions
Time unlimited services with a no dropout policy
Work with people in their own environment, often their own home; engages with the users
support system of family, friends, and others
A team approach that provides flexible and creative support to the individual case coordinators

What is of some concern, however, is the apparent prevalence of substance and chemical abuse by
individuals suffering psychosis and living in the community. The lifetime prevalence rate for substance
abuse among people diagnosed with schizophrenia is around 50%, and may be significantly higher in
those who are homeless (Kosten & Ziedonis, 1997). In an Australian study, Wallace, Mullen, & Burgess
(2004) found that between 1975 and 1995, substance abuse problems for individuals diagnosed with
schizophrenia increased from 8.3 to 26.1%, and significantly higher rates of criminal conviction were
found for those with substance abuse problems (68.1% compared to 11.7%). We know that regular use
of some substances (such as cannabis—see Focus Point 8.6) can directly increase the risk of developing
positive symptoms, and that the use of others (such as cocaine and amphetamines) can exacerbate these
symptoms (Laruelle & Abi‐Dargham, 1999). The challenge for community care programmes is to tackle
what appears to be increasing levels of substance abuse in individuals with psychotic symptoms living in
the community, and, in so doing, to decrease the risk of relapse and hospitalisation.
8.6.5 Summary of Treatment for Psychosis
Treating psychotic symptoms is a relatively long‐term process. This will often begin with subclinical
symptoms being picked up by an early intervention team, and may require immediate and urgent
treatment with antipsychotic drugs to deal with the positive symptoms found during early psychotic
episodes. Psychological therapies may be required to deal with the longer‐term cognitive and
behavioural deficits that may restrict full social and occupational functioning, and family‐based
interventions will help to maintain a stable, stress‐free environment in which the risk of relapse is
minimised. Long term community care is often overseen by a case manager who will help the sufferer with
their medication regimes, residential supervision, vocational training, and regular access to mental
health services. NICE recommends that a number of different interventions are considered in planning
for recovery from a first episode of schizophrenia—and these can include both medications and
psychotherapy (NICE, 2016). However, there are a range of differing views across the medical,
psychological, and social spectrum about what is the best approach to take for the long‐term treatment
of individuals with schizophrenia.
FIGURE 8.5 The occurrence of violence in schizophrenia as a consequence of two developmental trajectories stemming
from antisocial or violent behaviour prior to onset of the disorder, and no violent behaviour prior to disorder onset. Note the
different types of primary explanations for these two different trajectories
(after Bo, Abu‐Akel, Kongerslev, Haahr, & Simonsen, 2011).
SELF‐TEST QUESTIONS
What are antipsychotic drugs, how are they thought to deal with the psychotic symptoms,
and how are they categorised?
What problematic side effects do antipsychotic drugs have?
What are the important features of social skills training for individuals diagnosed with
schizophrenia?
What is CBTp and how is it used to treat individuals diagnosed with schizophrenia? With
what particular types of symptoms is it most effective?
What is cognitive remediation training (CRT)?
Can you describe a typical family‐based intervention for psychosis and the factors that
such interventions are designed to address?
What are the different types of community care programmes provided for individuals
diagnosed with schizophrenia, and is there any evidence for their effectiveness in
controlling psychotic symptoms?
 SECTION SUMMARY

8.6 THE TREATMENT OF PSYCHOSIS

Remission rates vary between 17% and 78% in first‐episode schizophrenia, and 16 to 62%
in multiple‐episode schizophrenia.
Electroconvulsive therapy (ECT) and psychosurgery were common forms of treatment for
psychosis prior to the development of antipsychotic drugs.
Antipsychotic drugs are frequently prescribed for treating the positive symptoms of
schizophrenia, and are thought to be effective because they influence neurotransmitter
activity in the brain.
Social skills training can be used to help psychosis sufferers to react appropriately in a range
of useful social situations.
Personal therapy is a broad‐based cognitive‐behaviour programme designed to help
individuals diagnosed with schizophrenia with the skills required to adapt to day‐to‐day
living after discharge from hospital.
Cognitive Behaviour Therapy for Psychosis (CBTp) helps to address any abnormal attributional
processes and information processing and reasoning biases that may give rise to delusional
thinking.
Cognitive remediation training (CRT) is designed to help the individual diagnosed with
schizophrenia to address deficits in social cognition (the ability to act wisely in social
situations) and neurocognition (memory and attention).
Family interventions are designed to educate the family about the nature of psychotic
symptoms and how to cope with difficulties that arise from living with someone with a
diagnosis of schizophrenia
Assertive community treatment and assertive outreach are forms of community care that help the
individual recovering from psychotic symptoms with their medication regimes,
psychotherapy, decision‐making, residential supervision and vocational training

8.7 EXPERIENCING PSYCHOSIS REVIEWED

Psychosis is a name given to a collection of disparate symptoms, and has led DSM‐5 to redefine its
diagnostic categories into what are known as schizophrenia spectrum disorders. The main categories
include schizophrenia, schizotypal personality disorder, delusional disorder, brief psychotic disorder and
schizoaffective disorder. Symptoms are classified as either positive symptoms (because they reflect an
excess or distortion of normal functions, e.g., hallucinations, delusions, disordered speech, and
disorganised motor behaviours) or negative symptoms (which reflect the loss or diminution of normal
functions, e.g., diminished emotional experience). These combinations of symptoms also frequently
result in a marked inability to undertake normal social and occupational functioning. The prominent
approach to explaining the development of psychotic symptoms is a diathesis–stress one. That is, there
is clear evidence for a genetic predisposition to psychotic symptoms, but the symptoms appear to be
triggered by experiencing environmental stress. The genetic predisposition does not appear to be a
specific one, and is not transmitted through a single gene (Schizophrenia Working Group of the
Psychiatric Genomics Consortium, 2014). Nor is the nature of the environmental stressors that may
trigger psychotic symptoms fully understood. These may range from stressful life experiences (such as
unemployment) (Brown & Birley, 1968), to dysfunctional family environments (where intra‐family
communication may be problematic) (Goldstein, 1988), to the hassles and challenges encountered in
normal adolescent development (Harrop & Trower, 2001). There is, however, good evidence that many
of the symptoms of psychosis are associated with imbalances in brain neurotransmitters such as
dopamine, serotonin, glutamate, and GABA (Stone, Morrison, & Pilowsky, 2007; Brisch et al., 2014),
and this occurs mainly in the mesolimbic and mesocortical pathways of the brain. This leads to
cognitive deficits in important brain areas such as the prefrontal cortex, where attention, working
memory, and executive functioning are all impaired. In addition, recent years have seen a resurgence in
interest in cognitive theories of psychotic symptoms, and especially the development of cognitive biases
in attention, attributional processes, reasoning, and ambiguity interpretation (Savulich, Shergill, &
Yiend, 2012). These processes have been shown to contribute to the development of delusional beliefs
as well as the way in which many people with psychotic symptoms hear and react to auditory
hallucinations or ‘voices’.
The development of antipsychotic drugs over the past 50 years has meant than many sufferers can lead
relatively normal lives without regularly experiencing the disabling positive symptoms that are typical of
the disorder (e.g., disordered speech and thought, hallucinations, etc.). However, after an initial
psychotic episode, relapse is the norm rather than the exception and around 50% of sufferers will rarely
fully recover from the effects of their symptoms (Wiersma, Nienhuis, Slooff, & Giel, 1998). Because of
this, long‐term care and supervision is required, and this means that individuals diagnosed with
schizophrenia will often require (a) lifelong medication; (b) individual therapies to deal with their specific
cognitive and behavioural deficits (e.g., social skills training, CBTp); (c) family interventions designed to
ensure a family environment that minimises stressors, maintains a medication regime, and can recognise
early signs of relapse; and (d) longer‐term community care to provide guidance on decision‐making,
residential supervision, vocational training, and to ensure a long‐term relationship between the
individual and mental health services is maintained.

This book is accompanied by Student and Instructor companion

websites.
www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter References
Videos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
9
Substance Use Disorders

ROUTE MAP OF THE CHAPTER

This chapter begins by discussing substance use disorders generally, including general diagnostic
criteria and prevalence rates. We then look at the specific characteristics of a number of drugs
whose use regularly gives rise to addiction and dependency. We look in detail at alcohol,
nicotine, and cannabis use and then continue by looking at a range of stimulant, sedative, and
hallucinogenic drugs. In particular, we review the physical and psychological effects of these
drugs, their prevalence of use, the nature of abuse and dependency on these substances, and
the costs of dependency in psychological, physical health, and economic terms. The chapter
then continues by reviewing a developmental model of substance use disorders in which we
consider the risk factors that contribute to experimentation, regular use and, in some cases,
eventual abuse and dependency. Finally, we cover the various types of treatment for substance
use disorders and evaluate their success.

CHAPTER OUTLINE
9.1 DEFINING AND DIAGNOSING SUBSTANCE USE DISORDERS
9.2 THE PREVALENCE AND COMORBIDITY OF SUBSTANCE USE
DISORDERS
9.3 CHARACTERISTICS OF SPECIFIC SUBSTANCE ABUSE DISORDERS
9.4 THE AETIOLOGY OF SUBSTANCE USE DISORDERS
9.5 THE TREATMENT OF SUBSTANCE USE DISORDERS
9.6 SUBSTANCE USE DISORDERS REVIEWED
LEARNING OUTCOMES
When you have completed this chapter, you should be able to:
1. Describe the main diagnostic criteria for substance use disorders and be able to define key
terms such as craving, tolerance, and withdrawal.
2. Describe the specific characteristics of a range of substances that give rise to dependency
and abuse, including specific stimulants, sedatives, and hallucinogenic drugs.
3. Describe and evaluate the psychological, physical health, and economic costs of specific
substance use disorders.
4. Describe a developmental model of substance dependency and evaluate the risk factors
that contribute to the different stages in this model.
5. Describe and evaluate the efficacy of a range of psychological and biological treatment
methods for treating substance use disorders.

My name is Tim and I am from Yorkshire. I had a normal life until I was 12 years old, and then my mother and
father started to fight. The fights were very violent and quite frightening; I have since learnt that this was mostly
my mother's fault. It became apparent that we were left outside Pubs a lot but it seemed normal. My two Brothers
and I suffered a terrible few years the scars are still with us.
Our house was sold and we ended up on a bad Council estate in Sheffield which has since been knocked down.
The violent drinking bouts got worse and I left home although I was 15. I still found a job but suffered terribly
over leaving my younger Brothers. I found a bedsit and a job and the peace was heavenly. I then moved to Derby to
live with my Uncle's family and eventually got married to a lovely lady and had two daughters.
My drinking started in Derby. No one thing made me drink but I gradually drank more and more over the years. I
started my own catering business and was extremely successful. I employed 65 staff and enjoyed all the benefits of
being my own boss. I had money, cars, and plenty of time to drink!! I did not know then what would happen
because of my drinking. My wife told me about my behaviour but I ignored her and her advice. I would not listen
to anyone. Worst of all I was out on the road driving to my catering sites and drinking all day. I still functioned
but I do not know how to this day nor do I know how I kept my licence.
I sold my Company and borrowed £100,000 from the Bank to buy—yes, you guessed—a Pub/Restaurant.
What a nightmare—my own “Booze” on tap!! Needless to say the venture was doomed from the start. I drank
morning noon and night and had plenty of friends or so I thought. Eventually my Wife left me and went back to
her Parents, and I do not blame her.
I went Bankrupt and moved to a bedsit once again. I then went on cider and anything else I could get. I had
defrauded the Customs and Excise while I was drinking so I ended up in Prison for 12 months which was a
disaster. They put me in charge of the Officers mess and bar!!!! Needless to say I was in seventh heaven and came
out a complete wreck and moved from City to City for 10 years. I was sacked from numerous chefs' jobs and was
in and out of several mental hospitals all over the Country. I did stay dry for a while but when my father died I
started to drink again and went back to Prison as I wanted the peace and friendship I found the first time, however
this was not meant to be and I found it very hard to cope without the booze second time around.
I was begging in Soho when I decided to try and turn my life around. I moved to Leicester where—through
Alcoholics Anonymous—I stopped drinking. I did have re‐lapses but following hepatitis, jaundice, and a bleeding
throat I stopped four and a half years ago. I could not suffer those terrible withdrawals again and I still have the
scars of drinking—epilepsy and digestive problems. But I am dry.
Tim's Story
Introduction
A drug can be very loosely defined as any substance, other than food, that affects either our bodies or
our minds in some way. Such substances may give us energy, relax us when nervous, change our ways of
thinking, distort our perceptions, or change our moods. They can, of course, have these effects either for
better or for worse, and the short‐term benefit of a substance may lead to longer term physical and
mental costs (as the experience of Tim, above, clearly demonstrates). Nevertheless, in most Westernised
cultures, drugs are almost a normal part of daily life. We use drugs to wake up in the morning (caffeine
in tea and coffee), to stay alert during the day (nicotine in cigarettes), to reduce pain (aspirin and
paracetamol), to control our physical shape (dieting pills), and to relax (alcohol, sleeping pills). While the
use of drugs in this way may seem to provide benefits to daily living, there are a number of problems
that arise out of this culture: (a) while many of these substances have short‐term benefits they may have
longer term negative physical and psychological effects with persistent use (e.g., alcohol), (b) many
people either become psychologically or physically addicted to a drug, and continue to use the drug
when it no longer has the original benefits (e.g., sleeping pills and dieting pills), and (c) many people
move on from taking legal drugs to taking illegal substances, many of which are physically damaging,
highly addictive, and frequently blight social, educational, and occupational performance (e.g., cocaine,
heroin, solvents, and hallucinogens such as lysergic acid diethylamide(LSD)). Furthermore, in addition
to traditional illicit drugs such as cocaine and ecstasy, recent years have been characterised by a
dramatic rise in the number of newer classes of psychostimulants—usually known as synthetic cathinones,
but more frequently referred to as ‘legal highs’, or alternatively as ‘bath salts’ or ‘PlantFood’ on the
basis of how their packaging is used to disguise the contents (Baumeister, Tojo, & Tracy, 2015) (see
Focus Point 9.5).

drug A substance that has a physiological effect when ingested or otherwise introduced into the
body.

bath salts ‘Bath salts’ is the name for an emerging group of drugs containing synthetic
chemicals related to cathinone, which is an amphetamine-like stimulant found in the khat plant.

The abuse and misuse of drugs has become one of society's biggest problems. Substance abusers often
pay a high personal cost for their dependency in terms of failed relationships, ruined careers, poor
health, and premature death (Photo 9.1). Society also pays a high cost in terms of lost productivity and
the strain such abuse puts on national health resources. In 2019, the World Drug Report (WDR; United
Nations Office on Drugs and Crime 2019a) estimated that (a) in 2017 over 271 million people
worldwide aged 15–64 had used an illicit drug at least once in the previous year, representing 1 in every
18 people in the world; (b) there were an estimated 165,000 deaths worldwide from illicit drug use in
2017, and added to this there were an additional 184,000 direct deaths from alcohol use (Ritchie &
Roser, 2019); (c) with an estimated 188 million people using cannabis in 2017, it remains the world's
most widely used illicit substance; and (d) in terms of prevalence, amphetamine‐type stimulants (ATS)
(including ‘ecstasy’) remain second only to cannabis, with an estimated 40 million users worldwide in
2017 (Figure 9.1).
PHOTO 9.1 Paul Gascoigne was well known as a talented footballer throughout Europe, having played for teams such
as Newcastle United, Tottenham Hotspur, Lazio, and Rangers. But since retiring from professional football, his life had
become dominated by his dependency on alcohol and its associated mental health problems. Like most people with a
substance use disorder, his health suffered, his problems curtailed a promising coaching career, and he has had numerous
run‐ins with the law. Despite a willingness to enter rehabilitation, his many relapses are well known, and such relapses are
a common feature of treatment for severe substance use disorder.
Even legal drugs such as tobacco and alcohol are problematic and usage regularly leads to death, illness,
and impoverishment. There are more than one billion tobacco smokers worldwide, of whom around
80% live in low‐ and middle‐income countries, and tobacco kills more than eight million people each
year, of whom seven million die as a direct result of tobacco use (World Health Organization, 2020b).
The world's population consumes an average of 6.4 L of alcohol a year per person (an equivalent of 53
bottles of wine per person older than 15 years), and the harmful use of alcohol results in 2.8 million
premature deaths a year (Ritchie & Roser, 2019). In the UK, the percentage of the population that
reports smoking cigarettes has declined to 15.1% in 2017 (down from 39% in 1980, and 21% in 2008)
(Office for National Statistics, 2018), and alcohol consumption in the UK has been slightly decreasing
over the past 20 years. This is exemplified by a steady decrease in the percentage of both men and
women drinking over 8 units a day between 2006 and 2017 (see Figure 9.2), and a decline in the
numbers in treatment for alcohol problems since 2014 (NHS, 2019a).
Although drug use in adolescents and school children in the UK is still a recognised problem and may
well lead to lifelong dependency and health problems, the numbers of young people in specialist
substance misuse services has shown a decrease of almost 35% since its peak in 2008–2009 (Public
Health England, 2018). However, despite these encouraging figures, 15% of young people in 2016 said
they had taken drugs in the previous year, up from 10% in 2014 (NHS Digital, 2017), and Department
for Education data for 2016–2017 show that school exclusions for alcohol and drug use have increase
substantially in recent years, with fixed term exclusions up 34% since 2012–2013 (Department for
Education, 2018). While these figures suggest that there may be a reduction in young people accessing
specialist substance abuse services in the UK in recent years, other factors indicate that the number of
young people using drugs may have started to increase again in most recent times (Public Health
England, 2018). Unfortunately, the evidence indicates that once an individual has used one illegal drug,
a majority will go on to abuse more than one (e.g., cocaine, cannabis, crack cocaine) (Tsuang et al.,
1998), and multiple drug abuse significantly increases other risks to well‐being such as being in a car
crash, mental health problems, violent behaviour, and promiscuous sexual behaviour (Greenwood et al.,
2001).
FIGURE 9.1 Global trends in drug use 2006–2017. The global prevalence of illicit drug use worldwide has grown
only slightly between 2006 and 2017 (at between 4% and 6%) while the prevalence of people with illicit drug use
disorders has remained relatively stable over this time (prevalence rate <1%) (United Nations Office on Drugs and Crime,
2019a).
FIGURE 9.2 Percentage of men and women in England who drank more than 8 units in a day. The percentage of men
and women drinking more than 8 units of alcohol a day has fallen significantly between 2006 and 2017 (NHS,
2019a,b,c).
The significant risk to physical health, mental health, social integration, and productivity posed by
substance abuse and dependence makes it quite a suitable subject for prevention and treatment. If we
look at Tim's story at the beginning of this chapter, we can see that his alcohol abuse and dependence
resulted in failed relationships; a ruined career and business; criminality; physical health problems such
as hepatitis, jaundice, and epilepsy; and mental health problems requiring hospitalisation. The
remainder of this chapter looks at some of the physical and psychological factors that lead to
dependence on, and abuse of, a range of substances, and how these problematic behaviour patterns can
be treated. But first, it is necessary to describe some of the terminology commonly used in this area of
psychopathology, and to look at the more general criteria for diagnosing and describing substance abuse
and dependence.

9.1 DEFINING AND DIAGNOSING SUBSTANCE USE DISORDERS

Traditionally, pathology associated with substance and drug use had fallen into two categories:
substance abuse and substance dependence. Substance abuse was defined as ‘a maladaptive pattern
of substance use manifested by recurrent and significant adverse consequences related to repeated use
of the substance’, and substance dependency as ‘a cluster of cognitive, behavioural and
physiological symptoms indicating that the individual continues use of the substance despite significant
substance‐related problems’. However, these two categories have been combined into a single substance
use disorder category in Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM‐5). The
reason for this is twofold. First, most individuals who exhibited the criteria for substance abuse rarely go
on to develop substance dependence (Schuckit et al., 2001), and second, detailed analysis of the
diagnostic criteria for substance dependency and substance abuse indicated that they represented one
and not two disorder categories. As a result DSM‐5 has defined the general criteria for just a single
substance use disorder category, and the broad criteria for this category fit within four overall groups
covering impaired control, social impairment, risky use, and pharmacological criteria. These groupings
and their associated criteria are listed in Table 9.1. In DSM‐5, these broad criteria for substance use
disorder are then applied to individual substances to produce specific diagnostic criteria for the use of
different substances (e.g., alcohol, amphetamines, cannabis, cocaine, hallucinogens, opioids, and
stimulant‐ and tobacco‐related disorders), and some of these specific diagnostic criteria are discussed
later in this chapter.

substance abuse A pattern of drug or substance use that occurs despite knowledge of the
negative effects of the drug, but where use has not progressed to full-blown dependency.

substance dependence A cluster of cognitive, behavioural and physiological symptoms

indicating that the individual continues use of the substance despite significant substance-
related problems.

TABLE 9.1 DSM‐5 general criteria for substance use disorders

Impaired Substance taken for longer than originally intended

control Reports desire to cut down, but with multiple unsuccessful efforts to quit
Individual spends a significant amount of time obtaining the substance and
recovering from its effects
In severe cases, virtually all the individuals daily activities revolve around the
substance
Craving is manifested by an intense desire or urge for the substance that may
occur at any time

Social Substance use results in failure to fulfill major role obligations at work, school,
impairment or home
Individual persists with substance use despite recurrent social and interpersonal
problems caused by the substance
The individual may withdraw from family activities and hobbies in order to use
the substance

Risky use Recurrent substance use in situations in which it is physically hazardous

The individual continues to take the substance despite knowledge of persistent
or recurrent physical or psychological problems caused by the substance

Pharmacological Tolerance is signaled by requiring increasing doses of the substance to achieve

criteria the desired effects
The individual experiences withdrawal symptoms, and continues to take the
substance in order to relieve these withdrawal symptoms
Some other terms used in the diagnosis and treatment of substance use disorders are listed in Table 9.2.
For example, when the person's ‘normal’ body state is the drugged state (so that the body requires the
substance to feel normal), this is known as addiction, and craving is the term used for the strong
subjective drive that addicts have to use the substance. The term psychological dependence is used
when it is clear that the individual has changed their life to ensure continued use of the drug, that all
their activities are centred on the drug and its use, and this leads to neglect of other important activities
such as work, social, and family commitments. While the physical consequences of substance use
disorders can be devastating (in terms of their negative effects on physical health and longevity), the
challenges for psychopathology are arguably to prevent substance abuse, to develop interventions to help
alleviate abuse and dependence, and to understand the conditions under which some individuals
develop substance use disorders. This understanding will result not only from a knowledge of the
physical effects of individual substances but also from a knowledge of how the individual uses the drug
and the negative effect it has on their daily lives. Tolerance refers to the need for increased amounts of
the substance in order to achieve similar effects across time, and withdrawal indicates that the body
requires the drug in order to maintain physical stability, and lack of the drug causes a range of negative
and aversive physical consequences (e.g., anxiety, tremors, and in extreme cases, death). As outlined in
the DSM‐5 criteria for substance use disorder, behavioural features of dependence include (a)
unsuccessful attempts to cut down on use of the drug; (b) a preoccupation with attempts to obtain the
drug (e.g., theft of money to buy illegal drugs, driving long distances late at night to buy alcohol,
multiple visits to doctors to obtain prescription drugs); (c) unintentional overuse, where people find they
have consumed more of the substance than they originally intended (e.g., ending up regularly drunk
after only going out for a quick drink after work); and (d) abandoning or neglecting important life
activities because of the drug (e.g., failing to go to work because of persistent hangovers, neglecting
friendships, relationships, childcare, and educational activities). It is also important to emphasise at this
early stage that substance use disorder is a chronic relapsing condition, in which substance users find their
habits hard to eliminate, and it is almost normal following treatment for substance dependence to be
associated with multiple relapses. We discuss the conditions that lead to this syndrome in more detail in
Section 9.5 (Focus Point 9.1).

addiction When a person’s ‘normal’ body state is the drugged state (so that the body requires
the substance to feel normal).

craving The strong subjective drive that addicts have to use a particular substance.

psychological dependence When individuals have changed their life to ensure continued
use of a particular drug such that all their activities are centred on the drug and its use.

Tolerance The need for increased amounts of a substance in order to achieve similar effects
across time.

withdrawal Where the body requires the drug in order to maintain physical stability, and lack
of the drug causes a range of negative and aversive physical consequences (e.g. anxiety, tremors
and, in extreme cases, death).
TABLE 9.2 Basic terminology in the study and treatment of substance use disorders
Terminology Definition
Addiction Drug use to the point where the body's ‘normal’ state is the drugged state (so the body
requires the drug to feel normal).
Psychological The user's tendency to alter their life because of the drug and to centre their activities
dependence around the drug
Craving A strong subjective drive to use the substance
Tolerance The need for greater amounts of the drug or substance to achieve intoxification (or the
desired effect) or a markedly diminished effect with continued use of the same amount
of the drug or substance (DSM‐IV‐TR, p. 192)

Withdrawal A maladaptive behavioural change, with physiological and cognitive concomitants,

that occurs when blood or tissue concentrations of a substance or drug decline in an
individual who has previously maintained prolonged heavy use of the substance or
drug
Substance A drug of abuse, a medication, or a toxin
Addiction is a term that is rarely used nowadays because it implies that drug dependence is primarily a physical one,
whereas in reality it is a complex mix of physical and psychological dependence.

FOCUS POINT 9.1 GAMBLING DISORDER

One interesting new inclusion in the DSM‐5 chapter on substance‐related and addictive
disorders is gambling disorder (DSM‐5, American Psychiatric Association, 2013, pp. 585–
589). It is interesting because previously DSM had considered disorders of gambling to be more
of an impulse problem rather than an addiction, and since 1980 ‘pathological gambling’ as it
was then called was included in the chapter devoted to impulse disorders.
So why have things changed? First, let's look at the diagnostic criteria for the new category of
gambling disorder. To be given a diagnosis of gambling disorder an individual must meet at
least four of the problems listed below within a 12‐month period:
Needing to gamble with more money to get the same excitement from gambling as before
Feels restless or irritable when trying to reduce or stop gambling
Keeps trying to reduce or stop gambling without success
Gambling is frequently on the person's mind—both reliving past gambling experiences
and planning future gambling events
Gambles when feeling depressed, guilty, or anxious
Tries to win back gambling losses
Lies to cover up how much they are gambling
Loses not only money but also relationships, their job, or a significant career opportunity
as a result of gambling
Becomes dependent on other people to give them money to deal with financial problems
that have been caused by gambling
Many of these problematic behaviours would fit quite well within the DSM‐5 general criteria
for substance dependence found in Table 9.1, including impaired control (such as many
unsuccessful attempts to quit), social impairment (pathological gambling can severely affect
major role obligations, such as family responsibilities, and affect work and social commitments),
and risky use (continuing to gamble knowing that it has adverse effects on financial
commitments and relationships). Although gambling does not involve putting some kind of
substance or drug into the body, it can be considered as a psychological addiction even if it is
not a physical addiction. For example, problem gamblers are known to need to gamble with
increasing amounts of money in order to achieve the desired level of excitement—an effect
which is very similar to the tolerance effects found in substance abuse. In addition, problem
gamblers are described as being restless or irritable when attempting to cut down or quit
gambling—a phenomenon very similar to substance withdrawal (Jazaeri & Hussain bin Habil,
2012). In this sense, gambling disorder also fits the fourth and final general criterion for
substance use disorder in Table 9.1, and this is supported by the fact that individuals who are
unable to stop gambling have similar patterns of brain activation to people with substance use
disorders, suggesting similar types of brain mechanisms that mediate these problem behaviours
(Holden, 2001).
Gambling disorder has a lifetime prevalence rate in the US of 0.4–4.0%, and is characterised
by high psychiatric comorbidity with a range of psychopathologies, including substance use
disorder, attention deficit/hyperactivity disorder (ADHD), personality disorders such as
borderline personality disorder, and disorders of impulse control (Black & Shaw, 2019). A direct
relationship between gambling and suicidality has been found by studies in many countries—
with suicidal thoughts being triggered by the effects of problem gambling, including economic
losses, and interpersonal and/or work challenges (Martinotti et al., 2016).
However, there is still a thin line between addictive behaviour and impulsive behaviour, and
many people diagnosed with a substance use disorder also have impulsive personality traits (e.g.,
Mitchell & Potenza, 2014). Further research will be required to understand the cognitive and
biological mechanisms that contribute respectively to addictive behaviours and impulsive
 behaviours, and this will help clinical psychologists to better categorise and diagnose these
various forms of problem behaviour.

SELF‐TEST QUESTIONS
Can you define the terms craving, tolerance, and withdrawal?
What are the main diagnostic criteria for substance use disorder?
What is craving?

SECTION SUMMARY

9.1 DEFINING AND DIAGNOSING SUBSTANCE USE DISORDERS

Substance dependence is characterised by both tolerance and withdrawal effects.
Substance abuse is a pattern of substance use that occurs despite knowledge of the negative
effects of the substance, but where it has not yet progressed to full‐blown dependence.
The DSM‐5 criteria for substance use disorders has four general criteria covering Impaired
Control, Social Impairment, Risky Use, and Pharmacological Criteria.
Craving is the term used for the strong subjective drive that addicts have to use a substance.
Tolerance refers to the need for increased amounts of a drug to achieve the same effects
across time.
Withdrawal indicates that the body requires the drug in order to maintain physical stability.

9.2 THE PREVALENCE AND COMORBIDITY OF SUBSTANCE USE

DISORDERS
Drug use and dependence are common in the general populations of many countries, although rates of
substance use disorders will vary markedly across countries depending on the legal, moral, and religious
attitudes to drugs in those countries. The global lifetime prevalence rate for substance dependence has
been calculated at just over 2% (Ritchie & Roser, 2019), although in some countries—such as the US
and several Eastern European countries, this figure rises to over 5%. In the US, the predominant
diagnosis is illicit drug dependence, and alcohol dependence is more common in Russia and Eastern
Europe. In the UK, around 3.1% of adults are diagnosable with substance use disorder, with men
(4.3%) showing higher prevalence rates than women (1.9%) (Roberts, Lepps, Strang, & Singleton, 2016).
A majority of those with substance abuse and dependency problems face a number of obstacles to
seeking help, including awareness of a perceived treatment need, accessing treatment once a need is
recognised, and compliance (on the part of both provider and client) to obtain adequate treatment. As a
result, as few as 7.1% of those with past‐year substance use disorders receive minimally adequate
treatment (Degenhardt et al., 2017).
A particularly important aspect of substance use disorders is that they are highly comorbid with a range
of other psychological disorders, and community epidemiological studies suggest that amongst
individuals with substance use disorders between 41% and 76% have at least one other co‐occurring
psychopathology (Torrens et al., 2011; Zilberman, Cao, & Jacobsen, 2003), and there is an especially
strong association of lifetime mood and anxiety disorders with substance use disorders (Conway,
Compton, Stinson, & Grant, 2006) (see Figure 9.3). Other studies have indicated significantly higher
levels of substance use disorders in individuals with bipolar disorder, ADHD, schizophrenia spectrum
disorders, antisocial personality disorder, major depression, anxiety disorders such as obsessive‐
compulsive disorder (OCD) and panic disorder, schizophrenia, bulimia nervosa, and personality
disorders than in the general population (National Institute on Drug Abuse, 2018, see Table 9.3). The
high level of comorbidity between substance use disorders and other mood and anxiety disorders has
generated a number of hypotheses about why substance use disorders occur so regularly in the context
of other psychological disorders. One view is that substance abuse and dependence may be a risk factor
for the later development of a psychopathology (e.g., Wylie, Scott, & Burnett, 1995). For example, panic
attacks may result from cocaine use and persist even after cocaine abstinence has been achieved (Rosen
& Kosten, 1992), with the latter possibly increasing the likelihood of relapse back to cocaine or another
drug to cope with these panic attacks. However, the majority of current evidence is consistent with the
view that psychiatric and psychological disorders usually predate substance abuse and dependence
(Abraham & Fava, 1999; Merikangas et al., 1998; O'Neil, Conner, & Kendall, 2011), and a UK study
indicated that the risk for substance abuse attributable to prior psychiatric illness was 14.2%, compared
to a risk for psychiatric illness attributable to substance abuse of only 0.2% (Frisher, Crome, MacLeod,
Millson, & Croft, 2005). This suggests a ‘self‐medication’ effect, in which individuals with an established
psychopathology start using substances to alleviate the negative emotional and behavioural effects of the
disorder (Turner, Mota, Bolton, & Sareen, 2018; but see Chapter 8, Focus Point 8.6 for an account of a
potential causal relationship between cannabis use and psychotic symptoms).
FIGURE 9.3 Lifetime prevalence of drug disorders among persons with mood and anxiety disorders. After Conway et al.
(2006).
TABLE 9.3 Comorbidity of substance use disorders with other psychiatric disorders (rate of substance use disorders in
the general population is around 5%)
Psychiatric disorder % of individuals also diagnosed with a substance use
disorder (SUD)
Bipolar disorder 60.7
Major depression 18
Obsessive‐compulsive disorder 32.8
(OCD)
Panic disorder 35.8
Schizophrenia 47
Bulimia nervosa 28
Personality disorders 42
Data taken from Brooner et al. (1997), Cuffel (1996), Regier et al. (1990), Zanarini et al. (1998), and Lacey (1993).
 SELF‐TEST QUESTIONS
How are substance use disorders and other psychiatric disorders related? Is one a risk
factor for the other?

SECTION SUMMARY

9.2 THE PREVALENCE AND COMORBIDITY OF SUBSTANCE USE

DISORDERS
The global lifetime prevalence rate for substance dependence is 2%
Substance use disorders are highly comorbid with a range of other DSM‐5 mental health
problems

9.3 CHARACTERISTICS OF SPECIFIC SUBSTANCE ABUSE

DISORDERS
In this chapter we need to look closely at the nature of different substance dependencies. These include
alcohol and nicotine—because of the close links that use of these substances have with normal everyday
life—then three specific groups of substances: stimulants (e.g., cocaine, amphetamines, and caffeine),
sedatives (e.g., opiates, such as heroin, and barbiturates), and hallucinogenic drugs (e.g., LSD and
other hallucinogenics, cannabis, and MDMA, better known as Ecstasy). It is important to be aware that
relatively few of the drugs we will discuss fit simply and easily into any one of these drug categories, and
many have multiple effects and some overlap between categories. That is why each textbook you read on
this topic appears to have a different form of categorisation! However, Figure 9.4 provides you with a
drug chart that maps how the different substances described in this chapter overlap across categories.
This shows that nicotine can act as both a stimulant and a depressant, hallucinogenic drugs such as
LSD and MDMA have both hallucinogenic and stimulant properties, and cannabis is probably the most
difficult to categorise because it can have a variety of psychological and physical effects.

stimulants Substances that increase central nervous system activity and increase blood
pressure and heart rate.

sedatives Central nervous system depressants which slow the activity of the body, reduce its
responsiveness, and reduce pain tension and anxiety. This group of substances includes alcohol,
the opiates and their derivatives (heroin, morphine, methadone and codeine), and synthesised
tranquillizers such as barbiturates.
FIGURE 9.4 A drug chart showing how the different substances described in this chapter overlap across categories.

9.3.1 Alcohol Use Disorder

Alcohol is one of the most commonly used drugs in a very large number of countries worldwide. In
many countries it is also legal and can be easily purchased and consumed. In the US over 86% of
people report they will at some time in their life consume a drink that contains alcohol, and 70.1%
reported they drank in the past year (Substance Abuse and Mental Health Services Administration,
2015). In 2018 in the UK 82% of adults over the age of 16 years reported drinking alcohol in the
previous year (NHS Digital, 2019b). However, in recent years in the UK there has been a steady
decrease in the percentage of men and women drinking over 8 units a day and a decline in the numbers
in treatment for alcohol problems since 2014 (NHS, 2019,b), but one in six people in the UK is still
drinking alcohol at levels that pose some risk to their physical and mental health (Public Health
England, 2016). What is known as ‘heavy episodic’ drinking or ‘binge drinking’ has also reached
epidemic levels in many European countries. Binge drinking refers to a high intake of alcohol in a single
drinking occasion. There is no single definition of binge drinking, but in the UK, it is normally defined
as taking at least 8 units (males) or 6 units (females) of alcohol in a single day. In 2016 around one in six
adults reported ‘bingeing’ on their heaviest drinking day prior to being interviewed (Office for National
Statistics, 2017a).
 binge drinking A high intake of alcohol in a single drinking occasion.

Alcohol has its physical and psychological effects when its main constituent, ethyl alcohol, is absorbed
into the bloodstream through the lining of the stomach and intestine. Alcohol then reaches the brain
and central nervous system via the bloodstream. At first, alcohol acts to relax the individual, and it does
this by influencing the receptors associated with the neurotransmitter gamma‐aminobutyric acid
(GABA). This facilitates this neurotransmitter's inhibitory function by preventing neurons firing and
making the drinker feel more relaxed (Harvey et al., 2002). Initially, this makes the drinker more
talkative, friendly, confident, and happy. As more alcohol is absorbed into the central nervous system,
the second stage of intoxication makes the drinker become less able to make judgements and talk less
coherently, memory is affected, and they may switch from being relaxed and happy to emotional and
aggressive. Finally, the physical effects of alcohol intoxication include motor coordination difficulties (in
balance and walking), slowed reaction times, and blurred vision. This course of the effect of alcohol is
known as biphasic, because the initial effects act as a stimulant (making the drinker reactive and happy),
but the later effects act as a depressant (making the drinker sluggish and experience negative emotions).
We can see how drinking alcohol can be appealing to many people because of its initial effects (i.e., it
helps alleviate stress after a busy day at work, increases sociability, reduces inhibitions, etc.). However,
many of the so‐called effects of alcohol are actually mythical, and result from a drinker's expectations
about the effects of alcohol rather than its real effects. For example, in a couple of classic studies, Lang,
Goeckner, Adessor, and Marlatt (1975) and Wilson and Lawson (1976) gave participants a disguised
nonalcoholic beverage when they were expecting alcohol. They subsequently reported increases in
sexual arousal and aggression, even though they had become less physiologically aroused. Expectations
about the effects of alcohol appear to play an important role in drinking behaviour, with positive
expectancies about the effects of alcohol being a significant predictor of its use (Sher, Wood, Wood, &
Raskin, 1996).

ethyl alcohol The intoxicating constituent of alcoholic drinks.

Alcohol abuse and dependence

Because of its short‐term positive psychological and physical effects, and probably equally as much
because of the positive cognitive expectations that have built up around the consumption of alcohol in
many societies, it has come to be seen by many as a way of enduring life's problems and relieving
tension. However, because of its availability, many come to use alcohol to the point where it begins to
have significant negative effects on both physical and psychological health. With increased use, the body
begins to show tolerance to alcohol and the drinker has to consume ever larger amounts to achieve the
same effects. The long‐term physical effects of heavy alcohol consumption include withdrawal
symptoms when the body is deprived of alcohol, and these include restlessness, inability to sleep, anxiety
and depression, muscle tremors, and rises in blood pressure and temperature. Following withdrawal
after extended heavy drinking over a number of years, the drinker may experience delirium tremens
(DTs), where the drinker becomes delirious, experiences unpleasant hallucinations, and exhibits
shaking and muscle tremors. Longer‐term negative physical effects of heavy alcohol consumption
include hypertension, heart failure, stomach ulcers, cancer, cirrhosis of the liver, brain damage
(including shrinkage of the frontal lobes), and early dementia. Furthermore, many of the effects of long‐
term alcohol dependence are similar to malnutrition. This is because alcohol contains calories, but is
entirely devoid of any required nutrients. This leads drinkers to feel full but take in little or no nutrition.
The consequence is vitamin and mineral deficiencies which can lead to dementia and memory
disorders, such as Korsakoff's syndrome. One indirect physiological risk associated with heavy
drinking in women is fetal alcohol syndrome, in which heavy drinking by a mother during
pregnancy can cause a whole range of physical and psychological abnormalities in the child, including
physical deformities, heart problems, stunted growth, hyperactivity, and learning difficulties (Hankin,
2002; Lange, Rovet, Rehm, & Popova, 2017). Prevalence studies estimate that 9.8% of women consume
alcohol during pregnancy and 1 in 67 women who consume alcohol during pregnancy will deliver a
child with fetal alcohol syndrome (Popova, Lange, Probst, Gmel, & Rehm, 2017). Finally, the important
physical effects of alcohol abuse and dependence discussed in this section substantially reduce longevity
in drinkers, and the number of alcohol‐related deaths in the UK has increased by 16% between 2007
and 2016 (NHS Digital, 2019b), suggesting that long‐term drink related disorders are still a significant
cause for concern.

delirium tremens (DTs) A severe form of alcohol withdrawal that involves sudden and
severe mental or nervous system changes.

Korsakoff’s syndrome A syndrome involving dementia and memory disorders which is

caused by long-term alcohol abuse and dependency.

fetal alcohol syndrome Physiological risk associated with heavy drinking in women, in
which heavy drinking by a mother during pregnancy can cause physical and psychological
abnormalities in the child.

The DSM‐5 diagnostic criteria for alcohol use disorder is provided in Table 9.4 and is defined by a
cluster of behavioural and physical symptoms such as evidence of tolerance effects and withdrawal
symptoms that develop within 4–12 hr of restricted consumption. However, many individuals with
alcohol dependence may never experience withdrawal once a pattern of compulsive drinking develops
in which their whole life centres around obtaining and consuming alcohol. Work performance and
childcare or household responsibilities may be significantly affected either by the aftereffects of drinking
(e.g., hangovers) or by being intoxicated while trying to perform these functions. Interestingly, a US
national survey indicated that workplace alcohol use and impairment directly affected an estimated 15%
of the US workforce, with 1.6% working under the influence of alcohol, and 9.2% working with a
hangover (Frone, 2006), and lost productivity features as the dominant economic cost of alcohol
consumption in many countries around the world (Rehm et al., 2009). Alcohol abuse is also
characterised by the drinker putting themselves at physical risk while intoxicated, including drink
driving and becoming engaged in violent arguments (see The Costs of Alcohol Use Disorders section).
Such individuals will also continue to drink when they know that their drinking is a cause of significant
social or interpersonal problems (such as their physical abuse of family members, or by causing
problems in their relationship with a partner) (Focus Point 9.2).

alcohol use disorder A problematic pattern of alcohol use leading to clinically significant
impairment or distress.
TABLE 9.4 Summary: DSM‐5 diagnostic criteria for alcohol use disorder

A pattern of alcohol use causing impairment or distress leading to at least two of the following
within a 12‐month period:
Alcohol is taken in greater amounts or for longer than was intended
A continuing desire or unsuccessful efforts to control alcohol use
A lot of time is spent in acquiring, using and recovering from the effects of alcohol
Craving, or a strong desire to use alcohol
Alcohol use results in a failure to fulfil major life roles at work, home and so forth
Persistent alcohol use despite the effect on interpersonal, recreational, or social interactions or
despite having an ongoing physical or psychological problem that is likely to have been caused or
made worse by alcohol
Tolerance symptoms associated with high alcohol use
Withdrawal symptoms associated with high alcohol use

Prevalence of use
The 12‐month and lifetime prevalence rates for alcohol use disorder are an alarming 13.9–29.1%
respectively (Grant et al., 2015). Dependence is more prevalent among men than women, in younger
and unmarried adults, and those in lower socio‐economic groups (Hasin, Stinson, Ogburn, & Grant,
2007). There are some ethnic differences in prevalence rates, with White Americans being more likely to
be diagnosed than Black Americans, and rates of diagnosis are also inversely related to educational
level. Alcohol dependence and abuse is frequently associated with abuse of other drugs, and is highly
comorbid with other psychiatric disorders. For example, heavy alcohol use is often part of polydrug
abuse or abuse of more than one drug at a time, and over 80% of alcohol abusers are smokers (e.g.,
Shiffman et al., 1994). This strong relationship between alcohol and tobacco abuse may be a result of
nicotine acting to suppress the aversive, sleep‐promoting effects of alcohol (Sharma, Lodhi, Sahota, &
Thakkar, 2015). Alcohol use disorder is also associated with other mental health diagnoses such as major
depressive disorder, bipolar I disorder, and antisocial personality disorder (Grant et al., 2015).

polydrug abuse Abuse of more than one drug at a time.

The course of alcohol use disorders

Alcohol use disorders often pass through stages of heavy and regular drinking, then on to alcohol abuse,
and finally ending up in many cases as alcohol use disorder (Jellinek, 1952), and these stages can be
fairly clearly defined in Tim's Story given at the beginning of this chapter. There are also a number of
risk factors for alcohol use disorders, and these might give us some insight into why some individuals
develop such problematic dependencies. Alcohol use disorders are predicted by a number of factors,
including: (a) a family history of alcoholism, suggesting that there may be a genetic component to the
disorder (see Section 9.4.3), or that the offspring model their drinking behaviour on those of their
parents, or that parental drinking gives rise to stressful childhood experiences that precipitate drinking in
the offspring (Sher, 1991; Mattick et al., 2017); (b) long‐term negative affect, including neuroticism and
depression (Sher, Trull, Bartholomew, & Vieth, 1999); (c) a diagnosis of childhood conduct disorder
(Johnson et al., 1995; Rohde, Lewinsohn, & Seeley, 1995); (d) experiencing life stress and particularly
childhood life stressors (Brady & Black, 2012); and (e) holding beliefs that drinking alcohol will have a
favourable outcome (e.g., that it reduces tension or makes social interactions easier) (Greenbaum,
Brown, & Friedman, 1995).

FOCUS POINT 9.2 TREATING ALCOHOL DEPENDENCE

Like most of the substance use disorders, alcohol dependence is difficult to treat successfully.
This is because of a number of factors: (a) many people dependent on alcohol use it as a way of
coping with life stresses and difficulties, and this can easily lead to relapse when stress is
experienced during or after treatment; (b) alcohol dependence is often comorbid with other
psychological disorders, which make treatment of the dependency more problematic; and (c)
alcohol is often part of polydrug abuse, where those dependent on alcohol also abuse other
drugs as well, and the use of one drug (e.g., nicotine) is likely to trigger the use of another (e.g.,
drinking alcohol).
Treatments for alcohol dependence take a variety of different forms, and we will describe some
of them here. The most successful forms of treatment, however, are usually multifaceted
approaches that combine a number of individual therapies into a single coherent programme
for the client.

SELF‐HELP GROUPS
The most commonly sought source of help for alcohol‐related problems are community self‐
help groups such as Alcoholics Anonymous (AA) (http://www.alcoholics‐anonymous.org.uk).
AA describes what it calls 12 steps that alcoholics should achieve during the recovery process
(https://www.alcoholics‐anonymous.org.uk/About‐AA/The‐12‐Steps‐of‐AA), and the 12‐step
programme has been shown to achieve long‐term abstinence in around 25% of participants
and a significant decrease in alcohol consumption in 78% (Ouimette, Finney, & Moos, 1997).
Many of the beneficial effects of self‐help groups such as AA may be attributable to the client
replacing social networks of drinking friends with other AA members.

MOTIVATIONAL ENHANCEMENT THERAPY (MET)

This form of cognitive behaviour therapy places the responsibility for change on the client and
attempts to provide them with a range of skills to deal with their drinking (Miller & Rollnick,
2002). The therapist provides individual feedback to the client on the effects of their drinking
(such as the effects on other family members), explores the benefits of abstinence, and then
designs a treatment programme specifically tailored to the individuals own needs. Motivational
enhancement therapy (MET) is a cost‐effective therapeutic approach for alcohol dependency,
and studies suggest around 50% of clients report that both levels of drinking and alcohol‐
related problems decreased significantly in the 12‐months following treatment (UKATT
Research Team, 2006). Meta‐analyses indicate that MET is significantly better than no
treatment, and has a marginally better success rate than a number of other interventions (Lenz,
Rosenbaum, & Sherpis, 2016).

SOCIAL BEHAVIOUR AND NETWORK THERAPY (SBNT)

This is a treatment aimed at mobilising and developing a positive social network for the client
that will facilitate a change in drinking behaviour (Copello, Orford, Hodgson, Tober, & Barrett,
2002). The therapist works with both the client and with those in the client's social network who
are willing to support the client's efforts to change (such as family, friends, work colleagues), and
the aim is to create a supportive social network that will sustain abstinence beyond the therapy
period. Controlled outcome studies suggest that social behaviour and network therapy (SBNT)
also has similar success rates to MET (UKATT Research Team, 2006).

PHARMACOTHERAPY
Drugs have been developed that attempt to block alcohol‐brain interactions that might promote
alcohol dependency. One of these is the drug naltrexone, which helps prevent relapse in those
recovering from alcohol dependency. Acamprosate has also been shown to be successful as a
treatment, with outcome studies suggesting that acamprosate enabled twice as many clients to
 remain abstinent 1‐year later than did psychosocial therapy alone (Swift, 1999). In addition,
some drugs, such as ondansetron, have been shown to be effective with early‐onset alcoholics
who began drinking heavily before 25 years of age (Johnson et al., 2000).

naltrexone An opioid receptor antagonist which has been found to be beneficial in the
control of hyperactivity and selfinjurious behaviour

BRIEF INTERVENTIONS
Many people with alcohol‐related problems frequently receive brief periods of treatment, such
as counselling (five or fewer sessions). Such treatments are usually conducted by GPs, nursing
staff, or trained counsellors and consist mainly of communicating alcohol‐relevant health
advice, providing information on the negative consequences of drinking, and offering practical
advice on community resources that might help achieve moderation or abstinence. Controlled
trials in the US and Canada have demonstrated that this approach significantly reduced
alcohol‐related problems and increased use of health care services (Fleming, Barry, Manwell,
Johnson, & London, 1997; Israel et al., 1996). Brief interventions are particularly valuable for
helping those in the early stages of alcohol use who are at risk of developing full‐blown alcohol
use disorders.

The costs of alcohol use disorders

In economic terms, alcohol‐related problems cost the US economy around $249 billion in 2010 in terms
of lost productivity, healthcare, and other costs (Centers for Disease Control & Prevention, 2018). Put
into perspective this amounts to costs of $2.05 per drink consumed! Costs to the UK National Health
Service alone are £2.7 billion per annum, including 1 in 26 NHS bed days for alcohol‐related health
problems and up to 35% of all accident and emergency attendance costs (World Health Organization,
2004; Department of Health, 2008). Accidents and crime are two of the biggest social problems
associated with alcohol misuse. Annual alcohol‐related costs of crime and public disorder in the UK in
2010–2011 were £11 billion with alcohol‐related crime making up 47% of violent offences in the UK
in 2014–2015 (Institute of Alcohol Studies, 2017). Drink driving accounts for 20% of all driver road
deaths in the UK and a significantly higher percentage in the US (Kennedy, Isaac, & Graham, 1996),
and level of alcohol use is one of the best predictors of an individual being involved in recurrent motor
vehicle crashes (Fabbri et al., 2005). Alcohol also increases the risk of death from boating accidents
(Smith et al., 2001) and drownings (Bell et al., 2001). In a review of the relationship between drinking
and health in a range of countries worldwide, Norstrom and Ramstedt (2005) found that per capita
alcohol consumption in a country significantly predicted (a) mortality from liver cirrhosis and other
alcohol‐related diseases, (b) mortality from accidents and homicide, and (c) death from suicide.

Summary
Alcohol use disorders are alarmingly prevalent in most societies and cause significant short‐term and
long‐term impairment, including impairment to occupational, educational and social functioning, and
they have important detrimental long‐term effects on health. Alcohol use disorders are also closely
associated with a range of social problems, such as drink driving, violent crime, and criminal activities
generally. It is still unclear why some people acquire an alcohol dependency, although alcohol use
disorders are highly comorbid with other psychiatric disorders—including other substance abuse
disorders. This suggests that, for many people, alcohol use may become a means of coping with adverse
or challenging life experiences because most alcohol users have an expectancy that drinking alcohol will
have beneficial effects (e.g., reduce tension, make social interactions easier).

9.3.2 Tobacco Use Disorder

Nicotine is the addictive agent found in tobacco, and is normally taken as cigarettes, chewing tobacco,
snuff, and in pipes and cigars. Smoking tobacco actually delivers nicotine to the brain faster than if it
were intravenously injected, and so is a highly efficient and effective way of experiencing the drug.
Nicotine has a number of physical effects. First, it acts as a stimulant by increasing blood pressure and
heart rate. But, paradoxically, it also has a calming effect by reducing self‐reported stress levels and
reducing the smoker's feelings of anxiety and anger (Warburton, 1992). In survey studies, smokers
usually endorse statements such as ‘smoking relaxes me when I am upset or nervous’ and ‘smoking
calms me down’ (Ikard, Green, & Horn, 1969). However, nicotine does have a number of important
negative effects, and smokers regularly report adverse moods when they have not smoked recently, and
periods of stress, irritability, and increased pain sensitivity are commonly experienced in the periods
between cigarettes or when attempting to quit smoking (Hughes, Higgins, & Hatsukami, 1990;
Nakajima & Al'Absi, 2014). These characteristics suggest that nicotine is an addictive drug that develops
physical and psychological dependence. First, there is growing evidence to suggest that nicotine has
rewarding sensory effects caused by releasing dopamine in the mesolimbic system of the brain
(Herman, DeVito, & Sofuoglu, 2014), and which acts through nicotinic receptors to increase the firing
rate of midbrain dopamine neurons (Dani & De Biasi, 2013). The effects of dopamine release in this
brain region are to elevate mood, decrease appetite, and enhance cognitive functioning generally, and
these are consequences that are similar to the effects of other addictive drugs such as cocaine (Stein et
al., 1998). Second, the reported calming effect of nicotine may be mediated by more basic psychological
processes representing the reversal of the unpleasant abstinence or withdrawal effects experienced if the
smoker has not taken nicotine in the recent past (known as the nicotine deprivation model, Parrott,
1999). Interestingly, when asked to report their moods over a normal day, smokers report significant
fluctuations in moods, with reports of normal moods during smoking and increased stressful and
irritable periods between cigarettes (Parrott, 1994). Smokers stress levels appear to be similar to
nonsmokers only just after having smoked, and become worse than nonsmokers during periods of
abstinence or between cigarettes (Parrott, 2006). This suggests that smokers need to smoke simply to
experience positive mood levels similar to nonsmokers, and that the stress and irritability they
experience between cigarettes are withdrawal symptoms caused by their dependence on nicotine
(Parrott & Murphy, 2012; Schachter, 1978).

Prevalence of use
After alcohol, nicotine is the second most widely used drug worldwide, and kills up to half of its users
(World Health Organization, 2013). About one‐third of the adult global population smokes and, among
teenagers aged 13–15 years, about one in five smokes worldwide. While the rate of smoking is gradually
falling in developed nations, it is rising by 3.4% per year in the developing world (World Health
Organization, 2015), and nearly 80% of the world's 1.1 billion smokers live in low‐ and middle‐income
countries (World Health Organization, 2020b). Evidence suggests that around 50% of those who start
smoking in their adolescent years will go on to smoke for at least a further 15–20 years. In the UK, the
percentage of the population that reports smoking cigarettes has declined to 15.1% in 2017 (down from
39% in 1980, and 21% in 2008) (Office for National Statistics, 2018), but the level of use in those people
who do smoke is also still unacceptably high, with smokers reporting an average 11.3 cigarettes a day
(Office for National Statistics, 2017a)—and these figures are worrying when we come to look at the
adverse long‐term health consequences of smoking (discussed later). The overall decrease in smoking
prevalence since 1980 seems to be mainly due to the increase in people who have never smoked or only
occasionally smoked, with the proportion of adults who have never smoked rising from 43% in 1982 to
55% in 2010 (UK Government Statistics, 2010). A quarter of children in the UK aged 11–15 have tried
smoking at least once, and in 2011 5% of children were regular smokers. It is worth noting that almost
two thirds of smokers in the UK said they wanted to give up, but over half said it would be difficult to
go without a cigarette for a day, and one of the main DSM‐5 criteria for substance use disorder is
repeated unsuccessful attempts to control use of the substance. However, use of e‐cigarettes has
offered the opportunity for many smokers to quit smoking traditional cigarettes, and the number of
‘vapers’ in the UK has risen to approximately 3.2 million in the UK in 2018, and more than half of
people using e‐cigarettes give their reason for vaping as an aid to stopping cigarette smoking (Office for
National Statistics, 2019a).
Finally, legislation prohibiting smoking in workplaces and enclosed public areas is being introduced in
many countries across the world, and was introduced in England in 2007. The effect of this legislation
has been to significantly reduce exposure to secondhand smoke (SHS exposure among children declined
by nearly 70%), decrease the number of hospital admissions for cardiac problems, and is associated with
a statistically significant increase in the number of smokers making a quit attempt (Bauld, 2011).

The course of tobacco use disorder

The DSM‐5 diagnostic criteria for tobacco use disorder are given in Table 9.5, and associated
features supporting diagnosis include smoking within 30 minutes of waking, smoking daily, smoking
more cigarettes per day, and waking at night to smoke. When taken for the first time, nicotine may cause
nausea and dizziness, and it may have a more intense effect when taken first thing in the morning.
However, with repeated use, these effects become significantly weaker as a tolerance to the drug builds
up. Abstinence or restricted access to nicotine produces a well‐defined withdrawal syndrome. This
consists of dysphoric or depressed mood, insomnia, irritability, frustration, anger, anxiety, difficulty
concentrating, restlessness and impatience, decreased heart rate, and increased appetite or weight gain.
A heavy smoker can exhibit these symptoms after only a few hours voluntary or enforced abstinence
(such as on an airplane journey).

tobacco use disorder A problematic pattern of tobacco use leading to clinically significant
impairment or distress.

TABLE 9.5 Summary: DSM‐5 diagnostic criteria for tobacco use disorder

A pattern of tobacco use causing impairment or distress leading to at least two of the following
within a 12‐month period:
Tobacco is taken in greater amounts or for longer than was intended
A continuing desire or unsuccessful efforts to control tobacco use
A lot of time is spent in acquiring and using tobacco
Craving, or a strong desire to use tobacco
Tobacco use results in a failure to fulfil major life roles at work, home, and so on
Persistent tobacco use despite the effect on interpersonal, recreational, or social interactions or
despite having an ongoing physical or psychological problem that is likely to have been caused or
made worse by tobacco
Tolerance symptoms associated with high tobacco use
Withdrawal symptoms associated with high tobacco use
Twelve‐month and lifetime prevalence rates for DSM‐5 nicotine use disorder in a US population are
estimated at 20.0–27.0% respectively (Chou et al., 2016) and is found to be as high as 92% in
individuals with lung cancer (Paik et al., 2019). Tobacco use disorder is also found to be comorbid with
a range of other psychiatric disorders, with the most common being alcohol/substance use disorder,
depressive, bipolar, anxiety, personality disorders, and ADHD (DSM‐5, American Psychiatric
Association, 2013) with comorbidity ranging from 22% to 32% in these cases (Focus Point 9.3).

FOCUS POINT 9.3 QUITTING SMOKING

As we have already noted, smokers find it extremely hard to quit the habit—even though they
may be fully aware of the health implications of their habit, and even when they themselves are
already suffering from smoking‐related diseases. Since around 80–90% of all smokers would
meet DSM‐5 criteria for substance dependence, successfully treating nicotine dependence is
likely to need a range of approaches, including psychological and pharmaceutical.
Smoking is difficult to treat because (a) smokers are constantly suffering nicotine withdrawal
symptoms when not smoking, and this drives the craving for further cigarettes, and (b) smokers
come to use cigarettes as a way of dealing with any negative mood (not just those associated
with withdrawal), so any life problems that cause negative affect and stress are likely to trigger
the desire to smoke.
For these reasons, treatment programmes for smokers tend to have poor success rates and high
relapse rates. Around 40% of smokers report attempts to quit in a given year and make an
average of 2.1 attempts to do so (Borland, Partos, Yong, Cummings, & Hyland, 2012) and it's
estimated that it may take regular smokers up to 30 attempts before they successfully quit the
habit (Chaiton et al., 2016).
There are some important predictors of whether an attempt to quit will fail, and these include
(a) a diagnosis of major depression (Glassman, 1993)—50% of smokers who make repeated
unsuccessful attempts to quit can be diagnosed with major depression, (b) regular bouts of
negative mood which increase cigarette cravings, and (c) whether the person has to spend
periods of time in environments where smoking is common and cigarettes are readily available
(e.g., pubs and bars).
Some of the main forms of intervention for smoking are the following:

E‐CIGARETTES
Since being introduced to the market in 2003 global use of e‐cigarettes has increased
exponentially and is frequently used as a means of quitting smoking tobacco cigarettes. An e‐
cigarette is a handheld battery‐powered vaporiser that simulates many of the behavioural
features of smoking such as the hand‐to‐mouth action but without burning the tobacco that can
create the tar that is considered responsible for many forms of smoking‐related disease. This
activity is known as ‘vaping’ and in the UK the number of users has increased from 700,000 in
2012 to 3.6 million in 2019 of whom 54% are smokers and the majority of the remainder are
ex‐smokers, only 0.8% of users are never‐smokers (Action on Smoking and Health UK, 2019).
There is evidence from randomised controlled trials that using e‐cigarettes can help people quit
smoking long‐term compared with placebos (McRobbie, Bullen, Hartmann‐Boyce, & Hajek,
2014), and may be more successful in helping smokers quit than nicotine replacement therapy
(NRT) (see next item) (Hajek et al., 2019). However, while these results are encouraging, there
are still some uncertainties about the health status of e‐cigarettes, and as of 2019 e‐cigarettes
were still banned in some countries such as Japan, Brazil, and Singapore, and their sale
regulated in many other countries (e.g., sale is prohibited to children under 18 years in the UK).
In addition, there is worrying evidence that young people who use e‐cigarettes are more likely
to go on to smoke cigarettes (US Public Health Service, 2014).

NICOTINE REPLACEMENT THERAPY (NRT)

This aims to replace the nicotine from cigarettes by means of skin patches, chewing gum,
lozenges, inhalators, or nasal sprays. Preliminary studies suggest that NRT is significantly more
effective than a placebo, and around 17% of people using NRT have fully abstained for 12
months following the treatment (National Institute for Clinical Excellence, 2002).

BUPROPION
This is a mild antidepressant drug that acts as a selective inhibitor of dopamine and
noradrenalin reuptake and is thought to act directly on the brain pathways involved in
dependence and withdrawal. Bupropion is significantly more effective than a placebo control,
and 19% of those taking the drug had not smoked in the 12 months following the treatment.
The UK National Institute for Clinical Excellence recommends using bupropion if NRTs are
inappropriate (National Institute for Health and Care Excellence, 2018).
 AVERSION THERAPY
This treatment attempts to replace the pleasant feelings associated with smoking a cigarette
with negative consequences such as feeling ill or nauseous. One form of aversion therapy is
known as rapid smoking, where the smoker puffs on a cigarette roughly every 4–5 s until
they feel ill and cannot take anther puff (Spiegler & Guevremont, 2003). This type of treatment
is known to reduce craving but has had limited success at controlling actual smoking behaviour
(Houtsmuller & Stitzer, 1999).

COGNITIVE BEHAVIOUR THERAPY (CBT)

Because depression and negative mood appear to be factors that are regularly associated with
failure to quit smoking, recent treatments have adapted CBT of depression for use in smoking
cessation programmes. In this case, CBT is used to help smokers develop alternative strategies
for dealing with depression and negative mood that do not involve a return to smoking. Such
interventions have been shown to produce higher rates of abstinence than standard health
education interventions (Hall et al., 1998) and a better treatment response for smokers with a
history of depression (Killen et al., 2008).

COMPLIMENTARY THERAPIES
Two forms of complimentary therapy frequently used by smokers in order to try and quit are
hypnotherapy and acupuncture. There is some evidence that hypnotic and suggestion‐
based approaches do yield higher rates of abstinence relative to waiting list and no treatment
controls, but there is little systematic evidence to suggest that hypnotherapy is more effective
than equivalent placebos (Green & Lynn, 2000; Villano & White, 2004)—so those ‘stop
smoking in one session’ signs outside your local holistic health centre might be somewhat
misleading! There is some evidence that compared with control participants, acupuncture can
help smokers to reduce their levels of smoking over a number of years (He, Medbo, &
Hostmark, 2001). However, there is little more than anecdotal evidence that acupuncture is an
effective means of quitting smoking (Villano & White, 2004).

hypnotherapy A form of therapy undertaken while the client is hypnotised.

The costs of nicotine use

Like many addictive drugs, arguably the main costs of nicotine dependence are those to physical health.
Smoking is the single largest preventable cause of disease and premature death in the world, kills more
than eight million people worldwide each year (World Health Organization, 2020b), and it is a
significant factor in heart disease, stroke and chronic lung cancer, cancer of the larynx, oesophagus,
mouth, bladder, cervix, pancreas, and kidneys. In the UK, around 489,000 people were admitted to
NHS hospitals in 2017–2018 as a result of smoking‐related illness (NHS Digital, 2019c), and in the UK
around 80,000 deaths are attributable to smoking‐related diseases each year (NHS, 2018). It is also
estimated that around half of all teenagers who are currently smoking will die from diseases caused by
tobacco if they continue to smoke. One quarter will die before they reach 70 years of age and will lose,
on average, 21 years of life (Peto, 1994). The economic cost of tobacco‐related health problems is
staggering. In the UK, the treatment of smoking‐related disorders in both primary and secondary care
settings is estimated at a total of £2.6 billion per year (Public Health England, 2017).
Finally, the health hazards associated with smoking extend beyond those who smoke. Cigarettes give off
smoke that contains a complex mix of thousands of chemicals—many of which can have toxic effects if
inhaled. This, of course, represents a health risk to those nonsmokers who share environments with
smokers, and is known as passive smoking from secondhand smoke. Just 30 min of exposure to SHS
is enough to reduce blood flow to the heart, and nonsmokers who are exposed to SHS in the home have
a 25% increased risk of heart disease. In particular, passive smoking is a substantial danger to health in
the case of babies and young children, causing increases in respiratory infections and asthma attacks
(Cowley, 1992; Skorge, Eagan, Eide, Gulsvik, & Bakke, 2005). Even though many countries are
introducing legislation to restrict the environments in which smoking can take place, it is estimated that
1.2 billion premature deaths a year worldwide still occur as a result of passive smoking (World Health
Organization, 2020b), although in the UK the introduction of legislation in 2007 banning smoking in
workplaces and enclosed spaces has significantly reduced exposure to SHS (Bauld, 2011).

passive smoking The breathing in of air that contains other people’s smoke.

secondhand smoke A person’s exhaled smoke, inhaled by another person.

Summary
A significant number of regular smokers meet the diagnostic criteria for nicotine dependency, which
makes it an activity of concern for both clinical psychologists and medical doctors. In part, smoking
appears to be acquired as a result of the effect of nicotine on brain dopamine reward pathways and
maintained by the smoker's need to reverse the unpleasant nicotine withdrawal effects that are
experienced between cigarettes or during abstinence. Tobacco use disorder does not have many of the
short‐term costs associated with alcohol dependency (such as impairment of occupational and social
functioning), but it does have significant medium‐ to long‐term health costs, and is the single largest
cause of premature death worldwide.

9.3.3 Cannabis Use Disorder

The drug cannabis is derived from the hemp plant, Cannabis sativa. The most powerful of the cannabis
group of drugs is hashish, and a weaker derivative—known as marijuana—consists of dried and
crushed cannabis leaves. Cannabis is normally smoked after being rolled into a cigarette known as a
‘joint’. However, it can also be eaten. The effects of cannabis are to produce feelings of relaxation (at
low doses), euphoria, sociability, and sharpened perceptions that sometimes result in mild sensory
hallucinations (known as being ‘spaced out’), but it can also cause difficulties in concentration and
impairment of memory. Although it is primarily classified as a sedative/depressant because of its
relaxing effects, it can sometimes also have stimulant effects, and make some individuals agitated and
paranoid. For example, when larger doses are taken, cannabis may exacerbate an already frightened,
stressed, or paranoid state, causing anxiety and distress. Sensory distortions may also give the user
feelings of depersonalisation similar to those experienced during panic attacks, and some cannabis users
become gripped by feelings of panic and anxiety.

hashish The most powerful of the cannabis group of drugs.

 marijuana A derivative of cannabis consisting of dried and crushed cannabis leaves.

The main active ingredient in cannabis is THC (Δ9‐tetrahydrocannabinol), and the amount of THC in
cannabis will determine the strength of its psychoactive effects. THC is generally believed to have low
addictive properties, although it is still possible for regular cannabis users to become dependent on the
drug (see below). THC has a mild stimulant effect by increasing heart rate, and has its psychoactive
effects by influencing cannabinoid brain receptors CB1 and CB2 found in the hippocampus,
cerebellum, and striatum (Zou & Kumar, 2018). These receptors appear to influence levels of dopamine
in those brain areas known to play a role in mediating reward and pleasure experiences, and this seems
to be the route by which cannabis has its most important positive psychoactive effects.
Cannabis was used in the mid‐twentieth century for its supposed medicinal properties, which included
its analgesic effects (see Focus Point 9.4), but it was smoked mainly for pleasure. It is now an illegal drug
in most countries even though its effects on behaviour and health are less severe than many other illicit
drugs.

Prevalence of use
Cannabis remains the most widely used illicit substance globally, and in contrast to many other common
drugs, its use has increased significantly worldwide in the past 25 years. There were an estimated 188
million people using cannabis in 2017 with an estimated annual prevalence of 3.3–4.4% of the adult
population aged between 15 and 64 years, and cannabis use has been estimated to have increased by
over 30% between 1998 and 2017 (United Nations Office on Drugs and Crime, 2019b). In the UK
cannabis has around two to five million regular users, with around one in five adolescents reporting
occasional or regular use of cannabis (Taylor et al., 2016).
 FOCUS POINT 9.4 THE MEDICAL APPLICATIONS OF
CANNABIS

Long before it became an illegal drug, cannabis was used primarily for medicinal purposes. It
was known to have relaxing and analgesic effects, and was used in the 1970s to reduce the
nausea and lack of appetite caused by chemotherapy in cancer patients (Sallan, Zinberg, & Frei,
1975). Neurophysiological studies have shown that cannabis has moderate analgesic effects, and
these are caused by the active ingredient in cannabis, THC, helping to block pain signals
reaching the brain (Richardson, Kilo, & Hargreaves, 1998). These analgesic effects are more
powerful than codeine and of longer duration.
Because of the potential medical applications of cannabis as a powerful analgesic, there have
been significant lobbies in many countries to legalise cannabis for medical use. In a UK survey,
individuals reported the medicinal use of cannabis with chronic pain, multiple sclerosis,
depression, arthritis, and neuropathy (Ware, Adams, & Guy, 2005). Cannabis has also been
involved in the treatment of patients with seizures, glaucoma, asthma, and anxiety (Mather,
2001). Outcome studies that have employed double‐blind randomised controlled trials and
placebo controls in patients with neuropathic pain or multiple sclerosis have demonstrated that
cannabis reduced the severity of reported pain significantly more in the cannabis treated than
in the placebo group (Berman, Symonds, & Birch, 2004; Zajicek et al., 2003). However, there
may be insufficient evidence that cannabis alleviates other forms of pain (Nugent et al., 2017).
Problems with the medical application of cannabis are (a) that it is still an illegal drug in most
developed countries, and (b) smoking cannabis may not be the healthiest way to take the drug
given the potential health risks associated with smoking (Mather, 2001). However, many
governments are now licensing the use of cannabis‐based drugs for use with specific patient
groups. For example, in 2005, the UK Home Office licensed the drug Sativex for individual
patient use (such as those with multiple sclerosis where cannabis has been shown to ease
stiffness, muscle spasms and pain). Sativex avoids the problems of smoking by providing the
active ingredients THC and cannabidol in a mouth spray. Also, in 2019, the NHS in England
approved a further cannabis‐based medicine, Epidyolex, to be used in the treatment of epilepsy.

The course of cannabis use disorder

Over the past few decades, the cannabis available on the street has become stronger and in many cases
THC content has risen from 1–5% to 10–15%. As a result, there is increasing evidence for a cannabis
abuse and dependency syndrome in many users. For example, tolerance and withdrawal effects have
been reported in some individuals who use cannabis regularly. Empirical studies have indicated that
cannabis can cause tolerance effects, and individuals who use cannabis daily over months or years may
develop a need for more potent forms of cannabis that would be toxic to most nonusers (Nowlan &
Cohen, 1977). In heavy users, dependence is indicated by withdrawal during periods of abstention, and
these include flulike symptoms, restlessness, and irritability (Kouri & Pope, 2000). Symptoms usually
begin within 1–3 days after cessation of use and peak between days 2 and 6, and usually last a
maximum of 14 days (Budney, Moore, Vandrey, & Hughes, 2003).
Individuals who regularly use cannabis can develop all the general diagnostic features of a substance use
disorder, and DSM‐5 provides a specific set of diagnostic criteria for cannabis use disorder (see
Table 9.6). Cannabis use disorder is often the only substance use disorder experienced by an individual,
and they will often report that it is being used to cope with mood, sleep, pain, or other physiological and
psychological problems. In the US, the 12‐month prevalence rate of cannabis use disorder is
approximately 3.4% among 12–17‐year‐olds, and 1.5% amongst adults according to DSM‐5 (American
Psychiatric Association, 2013). However, recent prospective studies in Australasia, Europe, and the USA
have indicated that 10–21% of adolescents are at risk of developing cannabis use disorder by early
adulthood (Farmer et al., 2015; Perkonigg et al., 2008), and between 30% and 50% of cannabis users
meet the diagnostic criteria for cannabis use disorder (Hasin et al., 2015). An individual diagnosed with
cannabis use disorder can spend much of their time daily acquiring and smoking the drug and this may
severely interfere with family, school, work, or recreational activities. Signs of cannabis intoxication
are often reported and the symptoms of intoxication after recent use of cannabis begin with a ‘high’
feeling followed by symptoms that include euphoria with inappropriate laughter and grandiosity,
sedation, lethargy, impairment in short‐term memory, difficulty carrying out complex mental processes,
impaired judgment, distorted sensory perceptions, impaired motor performance, and the feeling that
time is passing slowly (DSM‐5, American Psychiatric Association, 2013, p. 516). Occasionally, cannabis
intoxication can be associated with severe anxiety, dysphoria, and social withdrawal. Cannabis use
disorder usually develops over a period of time that is characterised by continuing increased use and
reduction in pleasurable effects.

cannabis use disorder Disorder usually develops over a period of time that is characterised
by continuing increased use of cannabis and reduction in pleasurable effects.

cannabis intoxication Symptoms of intoxication after recent use of cannabis begin with a
‘high’ feeling followed by symptoms that include euphoria with inappropriate laughter and
grandiosity, sedation, lethargy, impairment in short-term memory, impaired judgment, distorted
sensory perception and impaired motor performance.

TABLE 9.6 Summary: DSM‐5 diagnostic criteria for cannabis use disorder

A pattern of cannabis use causing impairment or distress leading to at least two of the following
within a 12‐month period:
Cannabis is taken in greater amounts or for longer than was intended
A continuing desire or unsuccessful efforts to control cannabis use
A lot of time is spent in acquiring, using, and recovering from the effects of cannabis
Craving or a strong desire to use cannabis
Cannabis use results in a failure to fulfil major life roles at work, home, and so on
Persistent cannabis use despite the effect on interpersonal, recreational, or social interactions or
despite having an ongoing physical or psychological problem that is likely to have been caused or
made worse by cannabis
Tolerance symptoms associated with high cannabis use
Withdrawal symptoms associated with high cannabis use
Studies have identified a number of risk factors for developing cannabis dependency, and these include
(a) age of onset—the earlier that first use is recorded the higher the likelihood of cannabis dependency
(Taylor, Malone, Iacono, & McGue, 2002), (b) tobacco smoking and regularity of cannabis use are both
independent predictors of cannabis dependency (Coffey, Carlin, Lynskey, Li, & Patton, 2003), (c)
impulsiveness and unpredictability of moods (Simons & Carey, 2002), (d) a diagnosis of conduct
disorder and emotional disorders during childhood (Meltzer, Gatward, Goodman, & Ford, 2003), and
(e) dependence on alcohol and other drugs (Degenhardt, Hall, & Lynskey, 2001).
Like many substance use disorders, cannabis use disorder is associated with a number of other
psychiatric diagnoses, and these include anxiety and panic disorder (Thomas, 1996), major depression
(Chen, Wagner, & Anthony, 2002), increased tendency for suicide (Serafini et al., 2012), and
schizophrenia (see Focus Point 8.6 in Chapter 8). This once more begs the question of whether
individuals suffering psychological problems are likely to resort to cannabis use as a form of self‐
medication, or whether cannabis use is linked to a future increase in psychiatric diagnoses (Forti,
Morrison, Alexander, & Murray, 2007). The evidence on this is far from clear, although prospective
studies indicate that (a) there is a causal link between regular cannabis use and the development of
psychotic symptoms typical of schizophrenia (Fergusson, Horwood, & Ridder, 2005; see also Chapter 8,
Focus Point 8.6), and (b) daily cannabis users may double their risk of subsequently developing
symptoms of anxiety and depression (Patton et al., 2002). Also, in a longitudinal New Zealand study,
McGee, Williams, Poulton, and Moffitt (2000) found that mental health problems at age 15 years were a
predictor of cannabis use at age 18 years, but that cannabis use at age 18 predicted increased risk of
mental health problems at age 21 years. While these studies tend to suggest that regular cannabis use
indeed predicts increased risk for subsequent mental health problems, the causal relationship may not
be direct. For example, both heavy cannabis use and mental health problems are also associated with
factors like low socio‐economic status, childhood behavioural problems, parental neglect, etc., and it
may be these factors that act as causes of both cannabis use and subsequent mental health problems.

The costs of cannabis use disorder

We have just discussed the possibility that regular heavy cannabis use may be associated with increased
risk for a number of mental health problems such as anxiety, depression, and schizophrenia. Such use is
also associated with a range of cognitive and health problems.
Regular cannabis use is associated with a range of cognitive deficits while individuals are under the
influence of the drug, and these include deficits in reaction time, decreased attention span, deficits in
verbal ability and working memory, slower problem‐solving, and loss of short‐term memory (Kalant,
2004; Lundqvist, 2005). This has important implications for cannabis users when complex psychomotor
skills are required while engaging in potentially dangerous activities. One such activity is driving, and
there is evidence that cannabis use does affect both driving skills and driving safety (Solowij, 1999).
Laboratory studies have demonstrated that perceptual and motor speed and accuracy are significantly
affected after smoking cannabis (Kurzthaler et al., 1999). Other studies have looked at the role of
cannabis use in drivers involved in accidents. For example, the active ingredient in cannabis, THC, is
found in the blood of impaired or accident‐involved drivers with a frequency that significantly exceeds
that in the general population (Kalant, 2004), and Scandinavian studies have indicated that 1 in 10 of
drivers arrested for impaired driving tested positive for cannabis (Christophersen, Ceder, Kristinsson,
Lillsunde, & Steentoft, 1999; Steentoft, Muller, Worm, & Toft, 2000). However, we must still be
cautious about what we conclude from these findings, because many of those involved in car accidents
are young risk‐taking males who are more likely to be using cannabis and other substances (such as
alcohol), so cannabis use may not necessarily be the main cause of accidents in these groups.
We know that cannabis causes cognitive deficits while the individual is under the influence of the drug,
but does regular cannabis use cause long‐term, permanent damage to cognitive skills and achievement
generally? First, cannabis use is associated with a syndrome of underachievement, in which regular
users exhibit lower IQ (Fried, Watkinson, James, & Gray, 2002), lower educational achievement (Gruber,
Pope, Hudson, & Yurgelun‐Todd, 2003), and motivational deficits (Lane, Cherek, Pietras, & Steinberg,
2005). However, there is very little evidence for permanent neuropsychological deficits in cannabis users
(Gonzalez, Carey, & Grant, 2002). Any cognitive deficits found during cannabis use do not appear to
persist longer than 72 hours after the drug has been used (Scott et al., 2018), and deficits are rarely
found in individuals who have quit using the drug (Iversen, 2005). However, regular heavy users are
likely to have lower educational achievement and lower income than nonusers, but this may be due to a
number of factors, including (a) use of cannabis during school and college years impairing educational
performance and subsequent career prospects, (b) heavy cannabis use being associated with deprivation
and poor educational opportunities, or (c) an amotivational syndrome in cannabis users, in which
those who take up regular cannabis use are more likely to be those who exhibit apathy, loss of ambition
and difficulty concentrating (Maugh, 1982).

amotivational syndrome A syndrome in which those who take up regular cannabis use are
more likely to be those who exhibit apathy, loss of ambition and difficulty concentrating.

There is also some debate about whether regular cannabis use has long‐term physical health
consequences. First, cannabis generally contains more tar than normal cigarettes and so presents a
significant risk for smoking‐related diseases such as cancer. Studies have suggested that cannabis smoke
can cause mutations and cancerous changes (Marselos & Karamanakos, 1999), but there is only modest
epidemiological evidence suggesting that cannabis users are more prone to cancer than nonusers
(Ghasemiesfe et al., 2019; Zhang et al., 1999). Second, regular cannabis use does appear to be
associated with a reduction in the male hormone testosterone (Grinspoon, Bakalar, Zimmer, & Morgan,
1997), and there is a possibility that this could cause impaired sexual functioning in the young males
who are cannabis' main users. Third, chronic cannabis use does appear to impair the efficiency of the
body's immune system (Nahas, Paton, & Harvey, 1999), although as yet there has been no obvious effect
of this found on the rate of physical illnesses in cannabis users (Meier et al., 2016). Overall, the most
probable adverse effects of cannabis on health generally include a dependence syndrome, increased risk
of psychotic episodes for those individuals with a prior vulnerability to such episodes, and accidental
injury as a result of cognitive deficits that can be experienced within 72 hours of using cannabis.

9.3.4 Stimulant Use Disorders

Stimulants are substances that increase central nervous system activity and increase blood pressure and
heart rate. As a result, they facilitate alertness, provide feelings of energy and confidence, and speed up
thinking and behaviour. One of the drugs we have already discussed has stimulant effects, and that is
nicotine. In this section, we discuss three more stimulant drugs, namely cocaine, amphetamine, and
caffeine. The popular recreational drug MDMA (3, 4‐methylenedioxymethamphetamine)—better
known as ecstasy—is also a stimulant similar to amphetamine, but it also has hallucinogenic effects
and is discussed later in this chapter.

cocaine A natural stimulant derived from the coca plant of South America which, after
processing, is an odourless, white powder that can be injected, snorted or, in some forms (e.g.
crack cocaine), smoked.

amphetamine A group of synthetic drugs used primarily as a central nervous system

stimulant. Common forms are amphetamine itself (Benzedrine), dextroamphetamine
(Dexedrine) and methamphetamine (Methedrine).

caffeine A central nervous system stimulant that increases alertness and motor activity and
combats fatigue; found in a number of different products, including coffee, tea, chocolate and
some over-thecounter cold remedies and weight-loss aids.

MDMA MDMA (3,4-methylenedioxymethamphetamine), the drug Ecstasy.

 ecstasy An illegal amphetaminebased synthetic drug with euphoric effects. Also known as
MDMA (3,4-methylenedioxymethamphetamine).

Stimulant use is most common among individuals aged 12–25 years, and first regular use occurs on
average at age 23 years (DSM‐5, American Psychiatric Association, 2013). Stimulants are often first used
for purposes such as controlling weight or to improve work or school performance and can be used daily
or in ‘binges’ in which high doses are used every hour or so. Addiction can occur very rapidly, and
individuals using amphetamines or cocaine can develop a stimulant use disorder as rapidly as 1
week, and sufferers can often develop conditioned responses to drug‐related stimuli (e.g., craving when
seeing white powder) which contributes to relapse and treatment difficulties (Volkow et al., 2006).
Approximately 16 million adults in the US used prescription stimulants in 2015 (that is 6.6% of the
adult population), most without use disorder (Compton, Han, Blanco, Johnson, & Jones, 2018). The
estimated 12‐month prevalence of Amphetamine‐type stimulants (ATS) disorders in the US is 0.2%
among 12–17 year‐olds and 0.2% among adults (DSM‐5, American Psychiatric Association, 2013, p.
564). Risk factors for developing stimulant use disorder include comorbid bipolar disorder,
schizophrenia, and antisocial personality disorder. Childhood conduct disorder is also associated with
later development of stimulant‐related disorders.

Cocaine
Cocaine is a natural stimulant derived from the coca plant of South America. After it has been
processed, cocaine is an odourless, white powder that can be injected, snorted, or in some forms (e.g.,
crack cocaine), smoked. When used for recreational purposes it is usually snorted and absorbed into the
bloodstream through the mucus membrane of the nose. The ‘rush’ caused by a standard dose of
cocaine takes approximately 8 minutes to take effect, and lasts for about 20 minutes. The ‘rush’ often
brings feelings of euphoria, and has its initial effects on the brain to make users feel excited and
energised. After these initial effects, the drug then affects other parts of the central nervous system to
produce increased alertness, arousal, and wakefulness. The main effects of cocaine are caused by the
drug blocking the reuptake of dopamine in the brain. This facilitates neural activity and results in
feelings of pleasure and confidence (Volkow et al., 1997) (see Focus Point 9.8).

Prevalence of use
The lifetime prevalence rate of cocaine use in developed countries is between 1% and 3% (World
Health Organization, 2020a). In European countries this varies between 0.1% and 2.7%, with the UK,
The Netherlands and Spain being at the upper end of this range (Statista, 2018). Use is reported at
around 1.8% in the US (John & Wu, 2017).

Cocaine use disorder

Because the effects of cocaine last only for around 30 minutes, there is a need for frequent doses to
maintain the “rush” caused by the drug. This means the user may spend large sums of money on the
drug in relatively short periods of time, and may even resort to theft and fraud to obtain funds to buy
the drug. Cocaine dependence occurs when the individual finds it difficult to resist using the drug
whenever it is available (the diagnostic criteria for cocaine use disorder are based on those in the general
substance use disorder shown in Table 9.1), and this in turn leads to neglect of important responsibilities
such as those associated with work or childcare. There is some evidence from animal studies that a
prolonged exposure to cocaine induces long‐term changes in dopamine neurons in the brain, leaving
the user vulnerable to longer‐term drug dependence (Ungless, Whistler, Malenka, & Bonci, 2001).
Tolerance occurs with repeated use, requiring larger doses and greater expense for similar effects. When
not taking cocaine, severe withdrawal symptoms can occur, particularly hypersomnia, increased
appetite, negative and depressed mood, and these increase the craving for further use or relapse during
abstinence. Erratic behaviour, social isolation, and sexual dysfunction are regular characteristics of long‐
term cocaine dependence, and the long‐term user may well develop symptoms of other psychological
disorders, such as major depression, social phobia, panic disorder, generalised anxiety disorder, and
eating disorders (Client's Perspective 9.1).

Cocaine dependence Occurs when the individual finds it difficult to resist using the drug
whenever it is available and leads to neglect of important responsibilities.
CLIENT'S PERSPECTIVE 9.1 COCAINE DEPENDENCY

It all began in 1983 when I first starting doing Cocaine. At first it was something that I did
about once a week. Usually on a Friday night and into Saturday. I would use it to go out to the
bars and go drinking. I would buy a gram, and usually there would be a little left over for
Saturday morning. This went on for several months and as I came in contact with more people
who liked Coke, I would start to split grams with people during the week. This increased till I
was doing that everyday, this took about a year to develop. I was fixing business machines and
would collect a little money everyday, by the second year I would buy Coke at least once a day. I
thought that I would try selling it, to help with the costs that were starting to add up. But, the
Coke I would buy would always end up being snorted by myself and a couple of close friends.
By the third year nearly all of my money was going for Coke. Food became secondary to me
and I would skip days eating to be able to afford Coke. I started to hang out with a guy who
shot his Coke up with needles. We became best friends, I would fix a machine and he would be
waiting for me in my car, we would instantly go and buy Coke with the money that I had just
made, occasionally stopping somewhere for a sandwich, which was all that I would eat any
more.
This went on till I was made homeless but we managed to get a cheap flat to share. I started to
get concerned that I had a habit that I could not kick. I saw many people wreck their lives
during this period. In fact my business was in serious trouble as I never paid my bills. Part of the
problem was that Coke was really ‘the’ thing to do in this town at the time. Seemed everyone I
knew was into it. It was a real social drug. I stopped doing it at bars, and would go back to the
flat and just lay around doing Coke all the time. My friend shot his, I snorted mine. In
desperation to make more money I expanded the territory that I was working and would drive
80 miles to do service calls. I was doing about a gram a day, my friend doing the same in his
veins. My attitude in life became one of giving up and thinking that I would die eventually, but
that was OK, as long as I could do Coke till I did.
Alan's Story

Clinical Commentary
Like many people, Alan began using cocaine as a recreational drug, taking it mainly at weekends and
when socialising in bars. Because the drug has a relatively brief ‘high’ (around 30 minutes), users
require more and more regular doses in order to maintain the euphoria generated by cocaine, and the cost
of this leads to significant financial problems. As is typical of individuals with cocaine dependency, Alan
began to neglect his responsibilities, including failing to pay bills and losing his home. Eventually,
psychological dependency was complete when his life revolved entirely around acquiring and taking the
drug.

FOCUS POINT 9.5 COCAINE STOPPED ENTWISTLE'S HEART

 On December 11, 2002, The BBC News website reported: The Who bassist John
Entwistle died after taking cocaine that caused his already diseased heart to fail, a coroner has
ruled. The 57‐year‐old was found dead in a hotel room in Las Vegas in June as the band were
about to embark on a US tour. A report from consultant Dr Jeremy Uff of Gloucestershire
Royal Hospital said there was evidence of high blood pressure and high cholesterol, which had
been compounded by smoking.
Coroner Lester Maddrell said he could not reduce the verdict to a simple phrase, but added
that the cocaine in his body had compounded heart disease that was already present. ‘He died
from the effects of a single moderate usage of cocaine superimposed upon ischaemic heart
disease caused by naturally occurring coronary’, he said. An inquest held in the US had already
ruled that Entwistle died after using a ‘significant amount of cocaine’ which brought on heart
failure.

Clinical Commentary
There are few deaths that are directly attributable to cocaine use, but cocaine is known to exacerbate
already existing cardiovascular problems because of its effect on blood‐pressure levels and heart rate.

The costs of cocaine use disorder

Apart from the negative effects of regular use on occupational, social, and educational functioning,
cocaine also has a number of adverse cognitive and health effects. For example, regular cocaine users
show evidence of deficits in decision making, judgment, and working memory (Simon et al., 2002; Pace‐
Schott et al., 2005). There is evidence from animal studies that regular cocaine use may also disrupt
learning—although there is some evidence that cocaine users who cease taking cocaine may recover
completely from some of these cognitive deficits that occur while taking the drug (Vonmoos et al., 2014).
There is also accumulating evidence that cocaine use by pregnant mothers can also cause significant
developmental deficits in their new‐born offspring, and this is manifested as retarded development in the
first 2 years of life (Singer et al., 2002), a higher incidence of ADHD at age 6 (Linares et al., 2006), and
deficits in visual motor development (Arendt et al., 2004). At least a partial cause of these effects may
be the role of cocaine in causing irregularities in placental blood‐flow during pregnancy.
Finally, because of its effects on blood pressure and cardiovascular functioning, high doses of cocaine
can cause heart problems and brain seizures, although it is unusual for death to be solely attributed to
cocaine abuse. However, cocaine may be an important contributor to death by aggravating existing
cardiovascular problems (e.g., arrhythmias, heart attacks, cerebral hemorrhages). In a UK study, 30.4%
of 112 regular male cocaine users with an average age of 44 years showed evidence of coronary artery
aneurysms, compared with only 7.6% of non‐cocaine users (Satran et al., 2005), indicating an
important and significant increase in cardiovascular disease in regular cocaine users (Focus Point 9.5).

Amphetamines
Amphetamines are a group of synthetic drugs used primarily as a central nervous system stimulant.
Common forms are amphetamine itself (Benzedrine), dextroamphetamine (Dexedrine), and
methamphetamine (Methedrine). These are highly addictive drugs that are used primarily to generate
feelings of energy and confidence, and to reduce feelings of weariness and boredom. They were
originally synthesised in the 1920s as an inhalant to aid breathing but came to be used later as a means
of appetite control and to combat feelings of lethargy and depression. When used in small doses,
amphetamines enable individuals to feel alert, confident, and energised. They also help motor
coordination but, contrary to popular belief, do not help intellectual skills (Tinklenberg, 1971). They
also have a number of physical effects, such as increasing blood pressure and heart rate, but can cause
headaches, fevers, tremors, and nausea.
Amphetamines have their effects by causing the release of neurotransmitters norepinephrine and
dopamine, and simultaneously blocking their reuptake. They are normally taken in a pill or capsule
form, but in the case of methamphetamine it can be taken intravenously or by ‘snorting’. In its clear,
crystal form, the latter is known as ‘ice’, ‘crank’, or ‘crystal meth’, and dependence on
methamphetamine can be particularly rapid. With the use of higher doses, and during withdrawal,
users experience a range of negative symptoms, including anxiety, paranoia, irritability, confusion, and
restlessness (Kaplan & Sadock, 1991) (Focus Point 9.6).

FOCUS POINT 9.6 ‘LEGAL HIGHS’

‘Legal Highs’ is the name for an emerging group of drugs containing synthetic chemicals
related to cathinone—which is an amphetamine‐like stimulant found in the Khat plant. These
synthetic cathinones can produce euphoria and increased sociability and sex drive (Prosser &
Nelson, 2012). Typically they are in the form of a white or brown crystalline powder and are
taken orally, inhaled or injected, and they are alternatively known as ‘bath salts’ or ‘PlantFood’
on the basis of how their packaging is used to disguise the contents (Baumeister et al., 2015).
The stimulant effects of ‘legal highs’ are thought to occur by raising dopamine levels in the
brain circuits that regulate reward and movement. Until recently, so‐called ‘legal highs’ were
cheap and legal in many countries, but they were placed under an emergency ban by the US
Drug Enforcement Administration in 2011. In the UK all cathinone substitutes were made
illegal in the UK in 2010, and the Psychoactive Substances Act 2016 was introduced to restrict
the production, sale, and supply of new classes of psychoactive substances. ‘Legal highs’ have
been linked to a surge in visits to Accident & Emergency Units with common complaints being
cardiac symptoms (chest pains, high blood pressure) and psychiatric symptoms such as
paranoia, hallucinations, and panic attacks. Being such a new group of drugs, it is difficult to
estimate the prevalence of “legal highs” use, but retrospective hair sample studies of individuals
who had tested positive for amphetamines or MDMA in 2009–2010 found psychoactive
substances similar to cathinone synthetics in 37% of these samples (Rust, Baumgartner, Dally, &
Kraemer, 2012). Even though this class of psychoactive substance has now been banned in
many countries, this has had only a small and limited effect on the availability of ‘legal highs’
(Haden, Wood, & Dargan, 2017; Robinson, 2018).
Prevalence of use
ATS (excluding ecstacy) have an estimated global prevalence of 0.77%, and are the second most widely
used group of drugs (Peacock et al., 2018; United Nations Office on Drugs and Crime, 2012). The
lifetime prevalence of amphetamine use disorders is around 1.5% (DSM‐IV‐TR). The World Health
Organization estimates that there are between 14 million and 52.5 million estimated global users, and
ATS account for around 16% of worldwide illicit drug abuse.

Amphetamine use disorder

Although the effects of amphetamine are longer lasting than other stimulants, such as cocaine, tolerance
to amphetamine occurs rapidly and higher and higher doses are needed to achieve similar stimulant
effects (Comer et al., 2001). Once high dose usage is achieved, the stimulant effects of amphetamine
also become associated with intense, but temporary, psychological symptoms such as anxiety, paranoia,
and psychotic episodes resembling schizophrenia (see below). Those who are dependent on
methamphetamine (so‐called ‘speed freaks’) will often use the drug continuously for a number of
days, experiencing a continuous ‘high’ without eating or sleeping. This will then be followed by a few
days feeling depressed and exhausted, but then the cycle starts again. Speed freaks who behave in this
way often become unpredictable, anxious, paranoid, and aggressive, and may be a danger to themselves
and others. Dependence is indicated by regular use of the drug whenever it is available, neglect of
normal responsibilities associated with work or family, and continuing use when the individual is aware
that using the drug is causing family or employment problems. Amphetamine intoxication normally
begins with a ‘high’ followed by feelings of euphoria, energy, talkativeness, and alertness—but is equally
likely to be followed by stereotyped, repetitive behaviour, anger, physically aggressive behaviour, and
impaired judgment. Physical symptoms of intoxication include pupillary dilation, perspiration or chills,
nausea or vomiting, chest pains, and in extreme cases, seizures or coma. Withdrawal symptoms can
appear within a few hours or a few days of ceasing use of amphetamine, and is associated with
depression, fatigue, vivid and unpleasant dreams, insomnia, and increased feelings of agitation.

methamphetamine Methedrine, a common form of amphetamine.

Amphetamine intoxication Amphetamine use, which normally begins with a ‘high’ but is
equally likely to be followed by stereotyped, repetitive behaviour, anger, physically aggressive
behaviour, and impaired judgement.

The costs of amphetamine use disorder

A number of studies using both human and nonhuman participants have suggested that regular use of
amphetamines (especially methamphetamine) may cause long‐term central nervous system damage
(Frost & Cadet, 2000; Volkow et al., 2001). Volkow et al. (2001) found that chronic methamphetamine
use inhibited the production of the neurotransmitter dopamine in the orbitofrontal cortex, and this may
play a significant role in maintaining addictive behaviours. For example, the orbitofrontal cortex is
associated with compulsive behaviour and with resistance to extinction of a behaviour even when
rewards are withdrawn. These effects are very similar to those reported by drug addicts who claim that
once they start using a drug such as methamphetamine they cannot stop—even when the drug is no
longer pleasurable. There is also evidence from animal studies showing that chronic use of
methamphetamine damages both dopamine and serotonin neurotransmitter systems in the brain (Frost
& Cadet, 2000; Yu, Zhu, Shen, Bai, & Di, 2015), and this effect appears to be reflected in slow or poor
decision‐making in individuals with methamphetamine use disorder (Paulus, Tapert, & Schuckit, 2005).

Caffeine
We are probably all familiar with taking caffeine in one form or another—as are around 85% of the
population of the world. Caffeine can be found in a number of different products, including coffee, tea,
chocolate, and some over‐the‐counter cold remedies and weight‐loss aids. Caffeine is a central nervous
system stimulant that increases alertness and motor activity and combats fatigue. However, it can also
reduce fine motor coordination and cause insomnia, headaches, anxiety, and dizziness (Paton & Beer,
2001). Caffeine enters the bloodstream through the stomach and increases brain dopamine levels in a
similar way to amphetamine and cocaine. Caffeine in the body reaches its peak concentration within an
hour, and has a half‐life of 6 hours, which implies that if you have a cup of coffee at 4 p.m. that contains
200 mg of caffeine, you will still have around 100 mg of caffeine in your body 6 hours later at 10 p.m.
So while caffeine may have beneficial short‐term effects on alertness, it may have detrimental longer‐
term effects which may prevent you from sleeping. The average caffeine intake per day in most of the
developing world is less than 50 mg, compared with highs of 400 mg in the UK and other European
countries. It is taken more by men than women, and caffeine intake usually decreases with age, with
older people showing more intense reactions and reporting greater interference with sleep.
Although caffeine consumption is almost a daily occurrence for most people, it can have both positive
and detrimental effects. On the positive side, the benefits of moderate caffeine intake are increased task
focus through alertness, attention, and cognitive function, and also elevated mood and fewer depressive
symptoms and lower risk of suicide. However, high doses of caffeine can induce psychotic and manic
symptoms, and most commonly, anxiety (Broderick & Benjamin, 2004). These anxiety‐generating effects
of high doses of caffeine make individuals with panic disorder and social anxiety disorder particularly
vulnerable to their effects (Davey, 2018; Lara, 2010). Research on the effects of regular caffeine intake
has increased significantly in recent years, and has led to the inclusion of caffeine use disorder as a
research diagnosis in DSM‐5 (American Psychiatric Association, 2013, pp. 792–793). Research that has
investigated these diagnostic criteria has found that around 8% of individuals would meet the diagnostic
criteria for caffeine use disorder which is defined as (a) unsuccessful attempts to cut down use, (b)
continued caffeine use despite having physical or psychological problems that would be exacerbated by
caffeine, and (c) aversive withdrawal symptoms (Sweeney, Weaver, Vincent, Arria, & Griffiths, 2019).

9.3.5 Sedative Use Disorders

Sedatives are a central nervous system depressant and slow the activity of the body, reduce its
responsiveness, and reduce pain tension and anxiety. This group of substances includes alcohol (see
Section 9.3.1), the opiates and their derivatives (heroin, morphine, methadone, and codeine), and
synthesised tranquilisers such as barbiturates. This group of drugs has a number of detrimental effects
on regular users, including rapid tolerance effects, severe withdrawal symptoms, and high doses can
cause disruption to vital bodily functions.

opiates Opium, taken from the sap of the opium poppy. Its derivatives include morphine,
heroin, codeine and methadone.

Opioids
The opioids consist of opium—taken from the sap of the opium poppy—and its derivatives, which
include morphine, heroin, codeine, and methadone. In the 1800s, opium was used mainly to treat
medical disorders, because of its ability to relax the patient and reduce both physical and emotional
pain. Both morphine and heroin were new drugs derived from opium during the late 1800s and early
1900s. Both were used as analgesics, but over time it became apparent that both were highly addictive,
and even after having been successfully treated with morphine or heroin, patients were unable to give
up using them. Finally, a synthetic form of opium, called methadone, was developed in Germany
during World War II. Unlike the other opioids, methadone can be taken orally (rather than injected)
and is longer lasting. Heroin is currently the most widely abused of the opioids. It is purchased in a
powder form and is normally taken by injection usually directly into a vein (known as ‘mainlining’). In
contrast, methadone is frequently used as a replacement drug for heroin abusers because of its slow
onset and weaker effects.

methadone A synthetic form of opium

Heroin A highly addictive drug derived from morphine, often used illicitly as a narcotic.

In the 1990s, heroin became the recreational drug of choice for many in Europe and the US. Most
opioids and their derivatives cause drowsiness and euphoria. In addition, heroin gives a feeling of
ecstasy immediately after injection (known as a ‘rush’, which lasts for 5–15 minutes). For about 5–6
hours after this rush, the user forgets all worries and stresses, experiences feelings of euphoria and well‐
being, and loses all negative feelings. However, as with many other drugs, individuals who regularly use
heroin rapidly develop tolerance effects and experience severe withdrawal symptoms that begin about 6
hours after they have injected the dose.
Opioids have their effects by depressing the central nervous system, and the drug attaches to brain
receptor sites that normally receive endorphins and stimulates these receptors to produce more
endorphins (Gerrits, Wiegant, & Van Ree, 1999). Endorphins are the body's natural opioids, and release
of these neurotransmitters acts to relieve pain, reduce stress, and create pleasurable sensations.

endorphins The body’s natural opioids. The release of these neurotransmitters acts to
relieve pain, reduce stress and create pleasurable sensations.

Prevalence of use
The estimated annual prevalence of opiate use (drugs extracted from the opium poppy such as
morphine and heroin) in 2016 was 0.3–0.4% of the global population aged between 15 and 64 (around
19 million people) (World Health Organization, 2018), and prescription opioid use in 2014 was around
0.7% (32.4 million adult users) (Vasilev, Milcheva, & Vassileva, 2016). While the majority of the world's
opiate users are in Asia, most prescription opioid users are in North America, followed by Asia and
Europe. In the UK there has been a steady decrease in the number of problem opiate users (mainly
heroin users) from 281,000 in 2004 to 257,000 in 2015.

Opioid use disorder

The World Health Organization estimates that there were around 27 million people worldwide suffering
from opioid use disorders in 2016 (mainly using illicitly cultivated and manufactured heroin, but an
increasing proportion using prescription opioids) (World Health Organization, 2018). Most opioid users
build up a tolerance to the drug quickly, and have to use larger and larger doses to experience
equivalent physical and psychological effects. Also associated with repeated use are severe withdrawal
effects. In the case of heroin, withdrawal symptoms will begin around 6 hours after injection, and
without further doses the user will experience a range of aversive withdrawal symptoms. These will
begin with feelings of anxiety, restlessness, muscle aches, increased sensitivity to pain, and a renewed
craving for the drug. More severe withdrawal is associated with muscle aches, insomnia, and fever. Acute
withdrawal symptoms for heroin usually peak within 1–3 days and will subside over a period of 5–7
days. Opioid use disorder is often difficult to treat because of the severe withdrawal symptoms
experienced by sufferers. It is also frequently associated with a history of drug‐related crimes (e.g.,
possession or distribution of drugs, forgery, burglary, etc.) Marital difficulties, unemployment, are often
associated with opioid use disorder at all socio‐economic levels (DSM‐5, American Psychiatric
Association, 2013). However, many users seem able to use opiates such as heroin as a periodic
recreational drug and continue to lead reasonably functioning lives in the interim. For example, a
Scottish study of long‐term heroin users who had never been in specialised treatment revealed that they
had levels of occupational status and educational achievement similar to the general UK population
(Shewan & Dalgarno, 2005). Shewan and Dalgarno found that use of heroin in this subgroup had
relatively few health risks, and suggested the terms controlled drug user or unobtrusive heroin
user to describe them. There is other evidence that opioid drug use need not necessarily lead to long‐
term dependency. Some theorists believe that opioid drug use is linked to life stressors, and if these
stressors are temporary, then so will be the drug use (Alexander & Hadaway, 1982). In support of this
view, many US soldiers became regular heroin abusers during the Vietnam War, but relatively few
continued to use the drug once they had returned home (Bourne, 1974). While heroin is undoubtedly a
dangerous drug, it does appear that some people, in some circumstances, can effectively manage and
regulate their use of the drug without problems (Warburton, Turnbull, & Hough, 2005).

opioid use disorders The development of tolerance to opiates, in which the user has to use
larger and larger doses to experience equivalent physical and psychological effects. Also
associated with severe withdrawal effects.

controlled drug user A long-term drug user who has never been in specialized treatment
and who displays levels of occupational status and educational achievement similar to the
general population.

unobtrusive heroin user A long-term heroin user who has never been in specialised
treatment and who displays levels of occupational status and educational achievement similar to
the general population.

The costs of opioid use disorder

Apart from the severe withdrawal symptoms experienced after drug use, there are a number of risks
that regular opioid users face. These include (a) the risk of accidental overdose if inexperienced users
fail to properly dilute pure forms of heroin for use; (b) being sold street heroin that contains potentially
lethal additives, such as cyanide or battery acid; and (c) the risk of contracting human
immunodeficiency virus (HIV) or hepatitis from sharing unsterilised needles. Over half of all drug
poisoning deaths in the UK involve an opiate, and in 2018 there were 1,336 deaths involving an opiate,
which is the highest ever rate since detailed record keeping began (Office for National Statistics, 2019,b).
In 2018 in the US there were 67,367 drug overdose deaths, of which two out of every three involved
opioids of some description (Centers for Disease Control and Prevention, 2020). In a long‐term US
study of heroin addicts, 28% had died before the age of 40. Interestingly, only one third of these deaths
were from overdose, and over half were from homicide, suicide, or accident (Hser, Anglin, & Powers,
1993). The high cost of opiate drugs such as heroin also leads regular users into illegal activities to raise
money for their dependence, and the most common of these are theft, fraud, and prostitution. Heroin
use is also highly associated with crime generally with regular drug users three to four times more likely
to commit a criminal offence than nonusers (Bennett, Holloway, & Farrington, 2008), and it is estimated
that in the mid‐1990s around 20% of all people arrested in the UK were taking heroin (Morgan, 2014).
So while we reported earlier that it is possible for some heroin users to live reasonable normal lives,
there are still significant risks to the life and health of many opioid users.

9.3.6 Hallucinogenic‐Related Disorders

Psychoactive drugs, or hallucinogens, have their effects by changing the user's perceptions. They may
either sharpen the individual's sensory abilities or create sensory illusions or hallucinations. Unlike
stimulants and sedatives, they have less significant effects on arousal levels, and are less addictive than
these other two classes of substances. In this section we will discuss in detail two hallucinogenic drugs—
namely LSD and the combined hallucinogen and stimulant MDMA, or Ecstasy as it is better known—a
substance that has become an important recreational drug over the past 3 decades. Other common
hallucinogenic drugs include the phencyclidines, which includes PCP, “angel dust”, and less potent
compounds such as ketamine, cyclohexamine, and dizocilpine. The phencyclidines produce feelings of
separation from mind and body in low doses, and stupor and coma at high doses, and the rising use of
some phencyclidines, such as ketamine, has led to the inclusion of phencyclidine use disorder as a
diagnostic category in DSM‐5.

hallucinogens Psychoactive drugs which affect the user’s perceptions. They may either
sharpen the individual’s sensory abilities or create sensory illusions or hallucinations.

phencyclidines Group of common hallucinogenic drugs, which includes PCP, ‘angel dust’,
and less potent compounds such as ketamine, cyclohexamine and dizocilpine.

Lysergic acid diethylamide (LSD)

LSD is an hallucinogenic drug that was first synthesised by the Swiss chemist Albert Hoffman in 1938.
LSD was probably the first of the widely used ‘psychodelic’ drugs, and came to be fashionable as a
‘mind‐expanding’ drug associated with the social changes and experimentation during the 1960s and
1970s. LSD, commonly referred to as ‘acid’, is sold on the street in tablets, capsules, and, occasionally,
liquid form. It is odourless, colourless, and has a slightly bitter taste and is usually taken by mouth.
Often LSD is added to absorbent paper, such as blotting paper or to sugar cubes. The drug starts to take
effect around 30–90 minutes after taking it, and physical effects include dilated pupils, raised body
temperature, increased heart rate and blood pressure, sweating, sleeplessness, dry mouth, and tremors.
LSD produces sharpened perceptions across a variety of senses. Colours can be enhanced and users
come to focus their attention on very small details in their environment. Advocates of the drug claim
that this heightened perception can open up new states of awareness and allow the user to become
more enlightened about the world and themselves. However, because of its sensory enhancing
properties, LSD can also cause hallucinations, including distorted perceptions of space and time
(Kaplan & Sadock, 1991), perceiving people and objects that are not present, and enabling the user to
believe they have attributes that they in fact do not possess. On a number of occasions, this latter effect
can have dangerous consequences when users who believe they have the power of flight have thrown
themselves out of upper storey windows.
The awareness enhancing properties of LSD can also have negative consequences. If the user is feeling
anxious or stressed after having taken LSD, these feelings can be exaggerated to the point where the
individual can experience extreme terror or panic. Such experiences are known as ‘bad trips’, and
feelings subside as the dose wears off. However, regular users can come to experience what are known as
‘flashbacks’. These are a vivid reexperiencing of a ‘trip’ that can occur days, months, or even years after
the actual LSD trip (Abraham & Wolf, 1988).
LSD appears to have its affects by influencing neurons in the brain that normally control visual
information and emotion, and it does this by affecting the levels of the neurotransmitter serotonin in
these brain areas and in particular the serotonin 5‐HT2A receptor (Goodman, 2002; López‐Giménez &
González‐Maeso, 2018).

Prevalence of use
In the US and Europe, use of LSD peaked during the 1960s and 1970s and has been gradually
declining ever since as stimulant drugs such as cocaine and amphetamines became the recreational drug
of choice. In the UK, the use of LSD has declined from 4% in 1996 to 0.5% in 2011–2012 (Home
Office, 2012). In the US, the 12‐month prevalence rate for LSD use in adults was 0.3% in 2011, a figure
that has also been declining significantly over the past 20 years (National Institute on Drug Abuse,
2012).

LSD abuse and dependency

While LSD is not generally considered to be a physically addictive drug, its regular use can still foster
dependency. Hallucinogen use (such as LSD or MDMA) is normally restricted to just two to three times
per week in regular users, but cravings for the drug have been reported after individuals have stopped
using them. Because most hallucinogens have an extended duration of action and a long half‐life,
individuals with hallucinogen use disorder can spend many hours and even days recovering from
the effects of the drug, and some hallucinogens—such as MDMA—are often associated with physical
‘hangover’ symptoms that occur the day after use.

The costs of LSD use

The effects of LSD are generally unpredictable, and prior to use the individual will not be sure whether
they will experience a ‘bad trip’ or not. If a large dose is taken, this can cause hallucinations and sensory
changes that can make the user frightened, can cause panic, and can make the individual think they are
going crazy. Although LSD is not considered an addictive drug, it can have tolerance effects, where
regular users have to take larger and larger doses to achieve similar effects. In a small number of
individuals, regular use can be associated with psychiatric disorders such as psychotic symptoms or
chronic depression. However, it is unclear whether such individuals already had underlying psychiatric
problems prior to their regular use of the drug, and those few empirical studies that are available have
failed to find psychedelic drugs generally to be an independent risk factor for mental health problems
(Krebs & Johansen, 2013). Finally, in the UK, between 1993 and 2014 only five deaths have been
recorded as a result of LSD use, and none have occurred since 2003 (Office for National Statistics,
2016).

Ecstasy
Most readers will by now be aware of the drug MDMA (3,4‐methylenedioxymethamphetaime)—better
known as the ‘clubbing drug’ ecstasy. Over the past 2 decades, ecstasy has often been the drug of choice
for those regularly attending techno‐dance parties, raves, or nightclubs. It is usually taken in pill form
and acts as both a stimulant and hallucinogen. It gives the user added energy to continue partying, and
elevates mood. Ecstasy has its effects by releasing the neurotransmitters serotonin and dopamine
(Malberg & Bronson, 2001; Vegting, Reneman, & Booij, 2016). Elevated levels of serotonin generate
feelings of euphoria, well‐being and sociability, and sounds and colours are experienced more intensely
(high levels of brain serotonin are also found in individuals with bipolar disorder experiencing a manic
phase). Effects can be experienced within around 20 minutes of taking the dose and will last for around
6 hours. However, high levels of brain dopamine can cause psychotic symptoms, such as paranoid
thinking and confusion, and these are symptoms often experienced by regular Ecstasy users (Photo 9.2).

PHOTO 9.2 Ecstasy—the clubbing drug.

Prevalence of use
Global use of ecstasy‐group substances is estimated at 0.2–0.6% of the adult population (between 10.5
and 28 million users) and is comparable to levels of cocaine use (United Nations Office on Drugs and
Crime, 2012). There was some evidence that usage was declining, but most recent evidence suggests a
possible resurgence of ecstasy use in Europe and the US. In the UK, there were estimated to be around
0.2 million ecstasy users in 2011–2012, although the number of users had fallen from 1.8% of the
population in 2000 to 1.4% in 2011–2012 but may have risen again in recent years to 1.7% of the
population in 2018 (Statista, 2019).

Ecstasy regular use

Regular users of ecstasy can spend many hours and even days recovering from the effects of the drug,
and hallucinogens such as MDMA are often associated with physical ‘hangover’ symptoms that occur
the day after use. Symptoms of MDMA hangovers include insomnia, fatigue, drowsiness, headaches,
and sore jaw muscles from teeth clenching. Such symptoms will inevitably interfere with normal
occupational and social functioning for some time after drug use. There are no recent figures for
ecstasy‐related substance abuse disorders, but ecstasy users do appear to be at high risk of substance use
disorders—if not with MDMA, then with other substances such as cannabis, opioids, and sedatives (Wu
et al., 2009).

The costs of Ecstasy use

There are also a number of dangers associated with regular Ecstasy use, and these include (a) the drug
causes severe dehydration by significantly reducing sweat production, which can cause heat stroke in hot
environments such as raves or nightclubs—even trying to counteract these effects by increasing fluid
intake can cause hyponatremia or water intoxication (Braback & Humble, 2001); (b) as a stimulant,
ecstasy increases heart rate and blood pressure, and this can be potentially dangerous for users with
existing cardiovascular problems; and (c) ecstasy is known to be a selective neurotoxin that destroys the
axons to which serotonin would normally bind (Ricaurte, Yuan, & McCann, 2000). Because of this,
ecstasy is thought to cause a range of longer‐term problems including memory deficits, verbal‐learning
deficits, sleep problems, lack of concentration, and increased depression and anxiety (Jansen, 2001;
Reneman, Booij, Schmand, Brink, & Gunning, 2000), and some studies and reviews have provided
evidence that ecstasy users score lower than non‐users on a number of cognitive measures of executive
functioning and working memory, particularly updating, attention shifting and access to long term
memory (Verbaten, 2010; Wagner et al., 2015). However, this is still a matter of debate. Studies do
indicate that MDMA may have a long‐term effect by reducing the availability of serotonin transporters
in the brain (Roberts, Jones, & Montgomery, 2016), but this may not necessarily be a neurotoxic effect
that has a direct adverse effect on cognitive functioning (Roberts, Quednow, Montgomery, & Parrott,
2018).

SELF‐TEST QUESTIONS

9.3 Characteristics of Specific Substance Abuse Disorders

Can you name the main groupings into which drugs of abuse are categorised?

9.3.1 Alcohol Use Disorder

How is binge drinking defined, and how prevalent is it amongst young people?
How does alcohol make the drinker feel relaxed and less stressed?
What are the main symptoms of withdrawal from alcohol in heavy drinkers?
Can you name the main criteria for alcohol use disorder?
What are the main risk factors for alcohol use disorder, and can any of them be identified
as causal factors?
Can you name three physiological risks associated with heavy alcohol drinking?
Can you list the economic and health costs of alcohol use disorders?

9.3.2 Tobacco Use Disorder

What are the main physical effects of nicotine?
Can you describe the main features of the nicotine withdrawal syndrome?
 Can you explain why people start and continue to smoke even though smoking has
important negative health consequences?
What are the main risks of smoking to physical health?

9.3.3 Cannabis Use Disorder

What are the physical and cognitive effects of cannabis?
What is the main active ingredient in cannabis?
What are the main features of cannabis dependence, cannabis abuse, and cannabis
intoxication?
What are the main risk factors for cannabis dependency?
What are the cognitive deficits that some clinicians argue are associated with regular
cannabis use?

9.3.4 Stimulant Use Disorders

What are the main stimulant drugs of abuse?
Can you describe the main effects of a standard dose of cocaine?
What are the different forms of cocaine, how are they administered and what different
effects do they have?
How does cocaine cause feelings of euphoria and ecstasy?
What are the main cognitive and health effects of regular cocaine use?
What are ‘legal highs’?
What are the main symptoms of amphetamine intoxication?
Can you describe the main features of caffeine intoxication and caffeine withdrawal?

9.3.5 Sedative Use Disorders

Can you name the different types of opioids that are the main drugs of abuse?
To which receptor sites do opioids normally attach to create their pleasurable effects?
What are the health risks faced by individuals with opioid dependency?

9.3.6 Hallucinogenic‐Related Disorders

What are the main cognitive and behavioural effects of LSD, and how does it have these
effects?
What are some of the negative psychological and physiological effects of ecstasy
(MDMA)?
SECTION SUMMARY

9.3 CHARACTERISTICS OF SPECIFIC SUBSTANCE ABUSE

DISORDERS
Substances of abuse can be categorised in three broad groups, namely stimulants (e.g.,
cocaine), sedatives (e.g., heroin), and hallucinogenic drugs (e.g., LSD)

9.3.1 Alcohol Use Disorder

Alcohol has its effects by binding to the neurotransmitter GABA, preventing neurones
firing and making the drinker feel more relaxed.
Many of the so‐called “positive” effects of alcohol are mythical, and result from the
drinker's expectations about the effects of alcohol.
Longer‐term negative physical effects of alcohol include hypertension, heart failure,
stomach ulcers, cancer, cirrhosis of the liver, brain damage, and early dementia.
Delirium tremens (DTs), Korsakoff's syndrome, and fetal alcohol syndrome are physiological risks
associated with heavy drinking.
The 12‐month and lifetime prevalence rates for alcohol use disorder are an alarming
13.9% and 29.1% respectively
Costs of alcohol‐related problems to the UK National Health Service are £2.7 billion per
annum, including 1 in 26 NHS bed days for alcohol‐related health problems and up to
35% of all accident and emergency attendance costs

9.3.2 Tobacco Use Disorder

Nicotine has its effects by releasing dopamine in the brain that acts to elevate mood.
Regular smokers need to smoke simply to experience positive mood levels similar to
nonsmokers.
The number of smokers in the UK has declined steadily in the last 15–20 years to around
15.1% of adults in 2017.
Mood manipulation is an important part of nicotine dependence, and smoking a cigarette
may eventually become a conditioned response to any form of stress.
There are substantial health risks to smoking, and passive smoking or secondhand smoke is
also an important health risk for nonsmokers.

9.3.3 Cannabis Use Disorder

The drug cannabis is derived from the hemp plant Cannabis sativa and is also known as
hashish and marijuana.
The main active ingredient in cannabis is THC (Δ9‐tetrahydrocannabinol), the amount of
which determines the strength of it psychoactive effects.
It is estimated that 3.3–4.4% of the world's adult population use cannabis at least once a
year.
 Risk factors for developing cannabis dependency include early age of first use, tobacco
smoking, impulsiveness and unpredictability of moods, diagnosis of childhood conduct
disorder, and dependence on alcohol and other drugs.
Cannabis dependency is a risk factor for a number of psychiatric diagnoses including
anxiety, panic disorder, major depression, and schizophrenia.
Regular cannabis use predicts lower educational achievement and lower income than non‐
use.

9.3.4 Stimulant Use Disorders

Stimulant drugs include cocaine, amphetamine, and caffeine.
Cocaine causes feelings of euphoria by blocking the reuptake of dopamine in the
mesolimbic areas of the brain.
Cocaine is usually snorted but can also be inhaled by smoking, which is known as free‐
basing.
The lifetime prevalence rate of cocaine use in developed countries is between 1% and 3%
Cocaine can be an important contributor to death by aggravating existing cardiovascular
problems.
Amphetamines are a group of synthetic drugs used primarily as a central nervous system
stimulant.
Amphetamines have their effects by causing the release of the neurotransmitters
norepinephrine and dopamine, and simultaneously blocking their reuptake.
The lifetime prevalence of amphetamine use disorders is around 1.5%
Caffeine enters the bloodstream through the stomach and increases brain dopamine levels
in a similar way to amphetamine and cocaine.
Caffeine use disorder has been included in DSM‐5 as a new research diagnosis

9.3.5 Sedative Use Disorders

Sedatives are a central nervous system depressant, and slow the activity of the body, and
reduce pain, tension and anxiety, and include opioids and barbiturates.
Opiates (such as heroin) attach to brain receptor sites that normally receive endorphins,
encourage the receptors to produce more endorphins that relieve pain, reduce stress, and
create pleasurable sensations.
The estimated annual prevalence rate for opiate use worldwide in 2016 was 0.3–0.4% of
adults.
Some heroin users, known as controlled drug users or unobtrusive heroin users, seem able
to use the drug without it affecting their social and occupational functioning.

9.3.6 Hallucinogenic‐Related Drugs

Hallucinogenic drugs have their effects by changing the user's perceptions, and include
cannabis, LSD, phencyclidines (e.g., PCP), and MDMA (better known as Ecstasy).
LSD is an hallucinogenic drug first synthesised in 1938.
 LSD has both awareness enhancing properties and occasional negative consequences
known as ‘bad trips’.
LSD appears to have its effects by influencing neurons in the brain that normally control
emotion and visual information, and it does this by affecting levels of the neurotransmitter
serotonin.
In the UK, the use of LSD has declined from 4% in 1996 to 0.5% in 2011/2012
MDMA is better known as the ‘clubbing drug’ Ecstasy.
Global use of ecstasy drugs is estimated at 0.2–0.6% of the adult population.
Ecstasy is known to be a selective neurotoxin that destroys the axons to which serotonin
would normally bind.

9.4 THE AETIOLOGY OF SUBSTANCE USE DISORDERS

We have so far described the characteristics of some of the main substances of abuse, and in some cases
discussed factors that may lead to abuse of and dependency on that substance. In this section we look in
more general terms at processes that lead some individuals to become substance dependent and why it is
that these individuals differ from those that may simply experiment with drugs without it significantly
interfering with their daily lives (e.g., Shewan & Dalgarno, 2005) (Focus Point 9.7).
The aetiology of substance use disorders has to be viewed in developmental terms because most
individuals who become dependent will go through a series of stages that leads to their disorder. At each
stage there may be quite different risk factors that influence transition to the next stage. Figure 9.5 shows
a representation of three important stages that individuals go through towards substance use disorder,
together with the risk factors that can influence this transition at each stage. Individuals do not
necessarily progress to the next stage unless the factors that mediate that transition are present. For
example, many substance users experience only stages 1 and 2 (experimentation and regular use), and
do not necessarily go on to become dependent on the drug in a way that significantly affects their
occupational, social, and family functioning. There may be some overlap between mediating factors and
stages (e.g., believing that smoking won't harm you may not only lead to regular use but can also be a
factor leading to nicotine use disorder), but Figure 9.7 gives you a reasonable overview of how risk
factors may influence substance use at different stages of development.

FOCUS POINT 9.7 DOES TAKING ‘SOFT’ DRUGS LEAD TO

USING ‘HARDER’ DRUGS?
Because cannabis use is prevalent amongst teenagers and young adults, there has long been
some concern that early cannabis use may be a ‘gateway drug’ that is the first step that leads
young people to experiment with ‘harder’, more addictive drugs, such as cocaine and heroin
(National Institute on Drug Abuse, 2019). This supposed progression from less addictive drugs,
such as cannabis, to more addictive drugs may then trap the individual into a cycle of substance
dependency.
So is there any truth to this theory? Certainly there is evidence that regular users of addictive
drugs such as cocaine and heroin did start out by using cannabis, and cocaine use, for example,
is significantly predicted by earlier cannabis use (Kandel, Murphy, & Karus, 1985). Another
relevant fact is that cannabis users are more likely than nonusers to go on and try cocaine or
heroin (Miller & Volk, 1996). However, these findings do not imply in any way that cannabis
users will always go on to use more addictive drugs, and 40% of regular cannabis users do not
go on to experiment with cocaine or heroin (Stephens, Roffman, & Simpson, 1993).
We tend to assume that because much drug use is associated with dependency, that individual
users will automatically be dragged along a path of ever worsening abuse and dependency, and
that cannabis use will inevitably lead down a slippery slope to dependency. However, we must
 remember that many regular substance users—even those who use potentially highly addictive
drugs such as cocaine, heroin, and amphetamines—manage to successfully confine their use for
recreational purposes only, and use the drug only when socialising or at weekends. This
controlled use does not appear to interfere substantially with occupational, social, or
educational functioning (e.g., Shewan & Dalgarno, 2005).
So why do some people appear to progress from softer drugs during adolescence to substance
dependency during adulthood? One theory is that progression to long‐term dependency is
found primarily in those who have either psychological problems at the outset of their drug use
or are suffering life stress (Alexander & Hadaway, 1982). Indirect support for this theory comes
from studies showing that drug abuse often stops when life stressors disappear (Bourne, 1974)
and that many users of addictive drugs such as cocaine and heroin are capable of kicking their
habit and turning to softer drugs, such as cannabis, as a safer option. Also, in a more recent
study, Smith, Jones, Bullmore, Robbins, and Ersche (2014) found that there is a select subset of
cocaine users who are able to use the substance recreationally without developing dependence,
and that this was due to their lack of attentional preference for cocaine‐related stimuli
compared to dependent users. This lack of attentional preference significantly reduces attention
to cues that elicit ‘craving’ (see Focus Point 9.9).

In addition to this developmental view, we also need to look at some of the neurological and
behavioural processes that underlie substance use disorders. These include the neurocircuitry of
addiction (i.e., the reward pathways in the brain that make substance use pleasurable), and the
psychology of ‘craving’ (i.e., the way in which liking and wanting a drug becomes conditioned to
external cues which trigger the desire for that drug). These two processes are highlighted and described
in Focus Points 9.8 and 9.9.

FOCUS POINT 9.8 REWARD PATHWAYS IN THE BRAIN AND

DRUG ADDICTION

With most of the drugs of abuse that we've discussed earlier in this chapter, you'll notice that
they all either have pleasurable effects on mood or they help people to feel less bad (e.g., by
alleviating negative moods or withdrawal symptoms) (Koob & Le Moal, 2008). Research on
both humans and animals suggests that a broad range of drugs have their pleasurable effects by
activating the natural reward pathways in the brain by converging on a common circuitry in the
brain's limbic system (Feltenstein & See, 2008), and many of these drugs also cause permanent
adaptive effects on this common pathway that contribute to the progression and maintenance
of addiction (Taylor, Lewis, & Olive, 2013). Drugs achieve their pleasurable effects by
influencing the dopamine system, and in particular, the dopaminergic neurons in the ventral
tegmental area(VTA) of the midbrain and subsequent areas in the limbic forebrain—
especially the nucleus accumbens(NAc). This VTA‐NAc pathway is arguably the most
important reward pathway in the brain and gives rise to the pleasurable effects caused not only
by drug use but also by food, sex, and social interactions (Kelley & Berridge, 2002; Tobler,
Fiorillo, & Schultz, 2005), and it has also been implicated in other addictive behaviours such as
pathological overeating, gambling, and sex addictions (Nestler, 2005). Several additional brain
areas have been shown to interact with this VTA‐NAc pathway and are implicated in drug
addiction. These include regions in the amygdala, hippocampus, hypothalamus, and several
regions of the frontal cortex (Koob & Le Moal, 2008; Nestler, 2001).
 ventral tegmental area (VTA) Part of the midbrain associated with the dopamine
system.

nucleus accumbens (NAc) Part of the limbic forebrain and dopamine system.

The figure shows the converging actions that a number of different drugs of abuse have by
affecting different components in the VTA‐NAc reward pathway (after Nestler, 2005).
Stimulants directly increase dopaminergic transmission (DA) in the NAc. Opiates do the same
indirectly by inhibiting GABAergic interneurons in the VTA which disinhibits dopamine
neurons in the VTA. Opiates also directly act on opiate receptors in the NAc. Nicotine seems to
activate VTA dopamine neurons directly. Alcohol appears to have a number of different effects
at different points in the pathway, and the effects of cannabis are also complex but may act
directly on NAc neurons themselves. Finally, phencyclidine (PCP) may act directly on neurons
in the NAc.

We continue by describing some of the risk factors that influence substance use at different
developmental stages (Figure 9.5).

9.4.1 Experimentation

Availability
Whether an individual can readily get access to the substance is an important factor in the early stages
of substance use, and factors such as whether the drug is legally available (e.g., alcohol and cigarettes)
and its cost are important determinants of initially experimenting with the drug. For example, there is
evidence for an inverse relationship between the use of a drug and its cost—especially amongst young
adolescents. This is true for alcohol and for cigarettes (Room, Babor, & Rehm, 2005; Stead & Lancaster,
2005), which suggests that strategies such as enforcing the minimum age for purchase of tobacco and
alcohol and increasing the price of these commodities may be effective means of controlling early use
(Ogilvie, Gruer, & Haw, 2006). Availability and cost are also significant factors influencing the use of
illicit drugs. For example, when Mexican heroin production increased from 8 to 50 metric tons a year
between 2005 and 2009, availability became one of the main factors identified in the decision by an
individual to start using heroin in the US (Cicero, Ellis, Surratt, & Kurtz, 2014).

Familial factors
Two important factors that can influence early substance use are (a) whether the substances are
regularly used by other family members, and (b) whether the family environment is problematic. For
example, if a child's parents both smoke then the offspring is significantly more likely to smoke at an
early age, and if both parents regularly drink alcohol, then the child is also more likely to drink at an
early age (Hawkins et al., 1998; Mattick et al., 2017). Similarly, having older siblings and spouses that
abuse drugs, significantly increases the risk of drug abuse (Kendler, Ohlsson, Sundquist, & Sundquist,
2013). Neglectful parenting also increases the use of alcohol, cigarettes, and cannabis by the child
(Cadoret, Yates, Troughton, Woodworth, & Stewart, 1995), and the negative background factors that
predict longer‐term substance use include (a) substance use in the childhood home, (b) extreme poverty
in the childhood home, (c) marital or legal problems in the household, (d) childhood neglect and abuse
—especially childhood sexual abuse (Sartor et al., 2013), and (e) serious psychiatric illness in the
household (Alverson, Alverson, & Drake, 2000; Wills, DuHamel, & Vaccaro, 1995).

FIGURE 9.5 The developmental model of substance abuse and dependency.

Peer group influences

Adolescents often begin drug use because of peer group influences. These influences are not necessarily
direct pressure to use the substance but take the form of conforming to group norms, so an adolescent
will start using a substance in order to self‐categorise as a member of a particular group (Schofield,
Pattison, Hill, & Borland, 2001). There is clear evidence that young people are socially motivated to
become drug users (Allbutt, Amos, & Cunningham‐Burley, 1995), but this only rarely takes the form of
deliberate ‘pressure’ or ‘persuasion’ by others (Lucas & Lloyd, 1999; Schofield et al., 2001). In most
cases, young people appear to take up activities like smoking in order to conform with group norms—
that is, they can make themselves appear more like others in the group by conforming to behaviours
that are typical in the group, such as smoking (Schmitt, Branscombe, & Kappen, 2003). Schofield et al.
(2001) found that particular group labels (such as ‘rebels’, ‘illegal drug users’, ‘motor bike riders’) were
associated with extensive smoking, and the degree of smoking determined how strongly an individual
identified with that group. In such groups, in‐group favouritism is also expressed by the sharing of
cigarettes, and smoking is used to cement friendships and to indicate commitment to the group
(Stewart‐Knox et al., 2005). This suggests that social networks can have a strong influence on an
individual's initial substance use, and identifying as part of a group that uses legal drugs, such as
cigarettes and alcohol, also predicts increased use of other drugs in late adolescence (Chassin, Curran,
Hussong, & Colder, 1996). Apart from the importance of social groups in determining substance use, it
is also the case that substance use will determine the kinds of social groups that an individual will mix
in. For example, once an individual becomes a regular drinker, they begin to choose social groups with
similar drinking patterns, and drinking in a social group environment that supports alcohol
consumption can act to consolidate regular use (Bullers, Cooper, & Russell, 2001). So, it seems that the
nature of an individual's social groups can influence drug use, but then drug users may eventually
choose to join social groups that support and maintain their drug use. The former is called a social
influence model and the latter a social selection model, and both processes may operate during
the experimental period of drug use.

Media influences
Substance use in young adolescents is significantly influenced by advertising and exposure to the
product in media contexts such as television programmes and magazines. Exposure to advertising has
been shown to be an important factor in encouraging children to take up smoking (While, Kelly, Huang,
& Charlton, 1996), and a US study found that exposure to in‐store beer displays, magazines with
alcohol advertisements, and television beer advertising predicted drinking in school‐age children
(Ellickson, Collins, Hambarsoomians, & McCaffrey, 2005) (Photo 9.3). While banning direct advertising
of a product has been shown to produce a significant fall in adolescent use of that product (Saffer,
1991), substance use (such as smoking) is still linked to indirect exposure to images found in fashion,
entertainment and gossip magazines, and TV and films—especially when alcohol and tobacco products
are regularly associated with attractive people enjoying themselves (Carson, Rodriguez, & Audrain‐
McGovern, 2005). In addition, while advertisements for smoking‐related products such as e‐cigarettes
might seem to be a good way of diverting young people away from tobacco to safer options, studies
suggest that exposure even to e‐cigarette advertisements may inadvertently decrease the perceived risks
of smoking among non‐smokers (Kim, Popova, Halpern‐Felsher, & Ling, 2017). It may not just be
explicit advertising that influences first drug use, but any exposure to a drug regardless of the context.
PHOTO 9.3 Exposure to in‐store beer and alcohol displays have been shown to be one factor that encourages children to
begin drinking alcohol.

9.4.2 Regular Use

Mood regulation
One of the main reasons for using drugs is that they have important mood altering effects. Alcohol
makes the drinker friendly, confident and relaxed (Harvey et al., 2002), smokers claim that smoking
cigarettes has a relaxing and calming effect (Ikard et al., 1969), stimulants—such as cocaine and
amphetamines—affect reward pathways in the brain causing feelings of euphoria, energy, and
confidence (Taylor, Lewis, & Olive, 2013; Volkow et al., 1997), opiates—such as heroin—generate
immediate feelings of ecstasy and feelings of well‐being and loss of negative emotions, and
hallucinogens—such as cannabis—produce feelings of relaxation, euphoria, sociability, and sharpened
perceptions. Interestingly, most of the drugs that we've discussed in this chapter have their pleasurable
effects by activating a common brain circuitry that governs reward and pleasure, and a full discussion of
this circuitry is provided in Focus Point 9.8. Given these rewarding effects of drug use, it makes sense to
assume that regular use can be achieved as a result of drug use being reinforced by these pleasurable
consequences. Furthermore, if taken regularly enough, many drugs can cause permanent changes to the
brain reward system in such a way as to facilitate addiction (Taylor et al., 2013).

reward pathways The brain neurocircuitry that make substance use pleasurable.
In addition to the intrinsic pleasurable effects of some substances, a good deal of research has been
carried out on the putative tension or stress‐reducing effects of drugs such as nicotine and alcohol.
There is some evidence that alcohol may reduce tension, even in individuals who are not alcohol
dependent (Sher & Levenson, 1982), and this is consistent with the drinker's everyday belief that
drinking is a good way to unwind, such as after a demanding day at work. However, the picture is not
quite that simple. Alcohol appears to reduce responding in the presence of both negative and positive
affect, and so may simply have an arousal‐dampening effect regardless of the valency of the drinker's
emotional state (Strikze, Patrick, & Lang, 1995). Subsequent studies have indicated that alcohol has its
apparent arousal‐dampening effects by altering perception and attention. The alcohol‐intoxicated
individual has less cognitive capacity available to process all ongoing information, and so alcohol acts to
narrow attention and means that the drinker processes fewer cues less well. This is known as alcohol
myopia (Steele & Josephs, 1990), and means that the drinker's behaviour is likely to be under the
influence of the most salient cues in the situation. In lively, friendly environments this will result in the
drinker processing only these types of cues, and as a consequence will feel happy and sociable and will
not have the capacity to simultaneously process worries or negative emotions. However, in drinking
situations where there are no happy, lively cues (such as in the case of the unhappy, lone drinker), the
reduced cognitive processing can result in attentional‐focusing on negative thoughts, experiences, and
emotions and means that the drinker experiences more negative affect than if they had abstained.

alcohol myopia The situation where an alcohol-intoxicated individual has less cognitive
capacity available to process all ongoing information, and so alcohol acts to narrow attention
and means that the drinker processes fewer cues less well.
 FOCUS POINT 9.9 CRAVING

The pleasurable effects of drug use can also act as potent stimuli that will generate “craving”
responses to cues associated with the drug. This occurs through a process of conditioning in
which the drug acts as a powerful unconditioned stimulus (UCS) that reinforces conditioned
responses to drug cues (see Chapter 1, Section 1.3.2, for a discussion of classical and operant
conditioning) (Robinson & Berridge, 2003). This means that cues such as the sensory features of
the drug (e.g., a white powder), the environment in which it is taken (e.g., a pub), or the people
the user socialises with when taking the drug can all become cues which elicit craving for the
drug. Cues for a particular drug can actually trigger responses in the user that are very similar
to those associated with actual use of the drug, and these include pleasurable feelings,
physiological arousal, and activation of brain reward centres (Filbey & DeWitt, 2012). In
addition, craving can induce attentional biases that enhance processing of drug cues, as well as
drug anticipatory responses that exacerbate the craving (Field, Mogg, Mann, Bennett, &
Bradley, 2013). Although generated by nonconscious classical conditioning process, craving is
often characterised as a conscious state that intervenes between the unconscious cues and
consumption (Andrade, May, & Kavanagh, 2012). Craving has significant effects on those
suffering substance abuse disorders. People who crave a substance do use that substance more
than people who don't crave it (Berkman, Falk, & Lieberman, 2011), and as you can imagine,
craving is a significant obstacle to successful treatment and frequently leads to relapse (Evren,
Durkaya, Evren, Dalbudak, & Cetin, 2012; Paliwal, Hyman, & Sinha, 2007).

In the case of nicotine, we saw in Section 9.3.2 that there is evidence that regular smokers use nicotine
as a means of coping with stress (Parrott & Garnham, 1998, 1999; Schachter, 1982). This begins when
the smoker lights a cigarette in order to alleviate nicotine withdrawal symptoms, but after regular use,
many smokers come to associate smoking with tension relief generally, and so become conditioned to
having a cigarette during or after any stressful experience (Kassel, 2000). This gives feelings of relaxation
and improved concentration as nicotine levels increase, and functions to reinforce the act of smoking.
Consistent with this view is the longitudinal finding that increases in negative affect and stressful life
events are associated with increases in smoking (Wills, Sandy, & Yaeger, 2002). However, while smoking
may have an immediate apparent stress‐reducing effect for the smoker, long‐term smoking actually
increases the smoker's responses to stress by creating a hyper‐responsiveness in the body's stress system
—especially in adolescents when they are at the start of their smoking career (Holliday & Gould, 2016).
This developed hyperresponsiveness to stress as a result of nicotine consumption may cause an addictive
vicious cycle in which smoking becomes the stress‐reducing response to increased stress sensitivity.
Finally, many drugs are powerful reinforcers that can condition the effects of drugs to stimuli and cues
associated with the drug (e.g., seeing a cigarette packet, or a white powder), and this gives rise to the
concept of ‘craving’ (Robinson & Berridge, 2003). Individuals who acquire learnt cravings for a drug
are more likely to consume more of that drug and to have a significantly higher rate of relapse following
abstention. The role of craving is discussed more fully in Focus Point 9.9.
In summary, there is clear evidence that many substances appear to have mood regulating effects—often
caused by their effects on a common brain reward circuitry in the limbic system, and so substance use
may be maintained by these effects. However, in many cases, these effects are more complicated than
they appear to the user. For example, alcohol appears not to have a simple mood enhancing effect, but
has an attentional‐focusing effect which makes drinkers feel relaxed and happy only when there are
happy cues for them to focus on. In the longer term nicotine use increases stress hypersensitivity even
though the smoker perceives smoking as a stress‐reducing activity. In addition, drugs can often have
important conditioned effects that will generate craving for the drug when drug‐related cues are
encountered.

Self‐medication
Rather than simply being used as a means of reducing the effects of everyday tensions and stressors,
substance use can become regular as a means of self‐medication when the individual is suffering
more severe adjustment difficulties such as those caused by diagnosable psychiatric disorders. This view
is supported by the fact that substance use disorders are highly comorbid with a range of other
psychiatric disorders including bipolar disorder, depression, eating disorders, schizophrenia, personality
disorders, and anxiety disorders such as OCD, post‐traumatic stress disorder, and panic disorder
(Brooner, King, Kidorf, Schmidt, & Bigelow, 1997; Regier et al., 1990) (see Table 9.3), and self‐
medication is frequently reported by substance users as a motive for using the substance (Sbrana et al.,
2005). There is evidence that anxiety disorders and mood disorders predate the onset of substance use
disorders such as alcohol dependency (Lazareck, Robinson, & Bolton, 2012; Liraud & Verdoux, 2000),
which is again consistent with the view that drugs are used for medication purposes after a psychiatric
disorder has already developed. However, if individuals who use drugs for self‐medication purposes are
aware of the longer‐term negative effects of these drugs, why do they continue to use them? Drake,
Wallach, Alverson, and Mueser (2002) suggest a number of reasons for continued use: (a) the drug has
intrinsic rewarding effects and leads to physical dependence, (b) the lives of individuals with psychiatric
disorders are so miserable that the medicinal effects of the drug offset its negative effects, and (c) the
drug may not only reduce tension and negative affect, it may have other positive consequences such as
helping the individual to cope in social situations. Finally, if substance abusers do genuinely use drugs to
self‐medicate, then their choice of drug should be consistent with their psychiatric symptoms. For
example, we would expect someone with ADHD to prefer amphetamines to alcohol due to its
stimulating properties, but individuals with anxiety would prefer alcohol to amphetamines because of
the anxiolytic effects of alcohol. However, there is relatively little evidence in support of these more
detailed predictions from the self‐medication account (Lembke, 2012).
 self-medication Self-administration of often illicit drugs by an individual to alleviate
perceived or real problems, usually of a psychological nature.

Long‐term expectations and beliefs

Substance users can also become regular users because they develop expectations that the substance will
have positive effects. For example, young adolescents who believe that alcohol affects behaviour in
positive ways (e.g., by increasing physical pleasure, enhancing sexual performance, facilitating socially
assertive behaviour), are significantly more likely to begin drinking than adolescents who do not hold
these beliefs, and are also more likely to become problem drinkers (Christiansen, Roehling, Smith, &
Goldman, 1989; Goldman, Brown, & Christiansen, 1987). In many cases these beliefs appear to be
culturally generated, because empirical studies suggest that alcohol does not increase levels of sexual
arousal or aggression, but in fact reduces physiological arousal (Lang et al., 1975; Wilson & Lawson,
1976). Many regular substance users also develop erroneous beliefs that the substance they use is
harmless, and these beliefs help to maintain regular use. For example, the increase in cannabis use
during the 1990s was mainly confined to those individuals who considered cannabis to be harmless (US
Department of Health and Human Services, 1994) and cannabis is more likely to be used by high
school students if they believe it to be harmless (Miech et al., 2017). In addition, many regular smokers
believe that smoking may cause cancer and illness in other smokers but not in themselves (Ayanian &
Cleary, 1999).

Cultural variables
There are some cultural factors that will influence the transition from first use to regular use. For
example, alcohol consumption differs significantly across different countries, and is most prevalent in
wine‐drinking societies (such as France, Italy, and Spain) where drinking alcohol is widely accepted as a
social and recreational activity (deLint, 1978). Increased use in these countries may be caused by the
regular availability of alcohol in a range of situations, such as drinking wine with meals and the
availability of wine and alcohol in a broad range of social settings. There are also some culturally
determined differences in beliefs about the effects of drugs which appear to affect the frequency of use,
and Ma and Shive (2000) found that white Americans reported significantly less risk associated with a
range of drugs (alcohol, cigarettes, cocaine, and cannabis) than African or Hispanic Americans. The
former group was found to use all of these drugs significantly more than the latter groups.

9.4.3 Abuse and Dependence

Regular use of a substance is not sufficient to give rise to a substance use disorder, this latter stage will be
subject to the diagnostic criteria provided in Table 9.1 and to the regular use causing significant
disruption to daily living in the form of inability to fulfill major obligations at work, school, or home and
a failure to deal with family and occupational responsibilities. In this section, we look at some of the
factors that might cause a shift from regular use to abuse and dependence.

Genetic predisposition
Based on twin, adoption and family studies, the heritability component for substance use disorders
generally has been estimated anywhere between 30% and 80% (Agrawal & Lynskey, 2008; Li &
Burmeister, 2009), around 40–60% for alcohol use disorders (Schuckit, 2009; van der Zwaluw & Engels,
2009), and around 40–48% for cannabis use (Verweij et al., 2010). Twin studies have indicated that the
concordance rates for alcohol abuse in MZ and DZ twins respectively are 54% and 28% (Kaji, 1960),
indicating a strong genetic component in alcohol abuse, and a similar concordance‐based genetic
predisposition has been found in twin studies of cannabis abuse (Kendler & Prescott, 1998), nicotine
dependency (True et al., 1999), and drug abuse generally (Tsuang et al., 1998). Adoption studies also
support a role for genetic inheritance in alcohol use disorders and drug abuse generally (Cadoret,
Troughton, O'Gorman, & Heywood, 1986; Kendler et al., 2012). In addition to family, twin, and
adoption studies, molecular genetic studies have begun to identify some of the genes that may be
involved in substance use disorders. For example, research has studied the link between smoking and
SLC6A3 (DAT1), a gene that regulates the reuptake of dopamine (e.g., Pomerleau, Collins, Shiffman, &
Pomerleau, 1993), and variability in this gene can make individuals more or less sensitive to the effects
of nicotine. In addition, the gene P450 2A6 (abbreviated as CYP2A6) may contribute to nicotine
dependence by coding for enzymes that regulate nicotine (Murphy, 2017), and greater metabolism of
nicotine is associated with smoking faster and smoking more (Park et al., 2017). Nevertheless, while the
role of some genes has been identified in the aetiology of some substance use disorders, identification of
genetic risk variants has been challenging because genome‐wide associations studies (GWAS) require
large sample sizes to obtain significant findings (Tawa, Hall, & Lohoff, 2016; Stringer et al., 2016).
However, while there are important genetic considerations in understanding substance use disorders,
there is a strong effect of interactions between genetics and environment risk factors. For instance, in a
large‐scale study in Finland, Dick et al. (2007), found that heritability was an important factor in
determining alcohol use, but this was facilitated even more in those that had many peers who drank
alcohol compared with those who had fewer peers who drank alcohol. Cloninger (1987) has also argued
that a genetic predisposition for alcohol dependency will be activated only by experiencing
environmental stress (e.g., low socio‐economic status). However, other studies have indicated that there
may be a more general genes–environment interaction, where a genetic predisposition for alcohol
dependency will only cause alcohol abuse if other environmental factors are present. These
environmental factors are not necessarily stressors, but include factors which might facilitate alcohol use,
such as living in places where there are large numbers of young people (Dick, Rose, Viken, Kaprio, &
Koskenvuo, 2001) or peer pressure or parental modelling (Rose, 1998). These environmental factors
seem to be important because they are likely to initiate drinking. Once drinking has started, genetic
factors then appear to play a significant role in determining regular use, abuse and dependency (Heath,
1995), and this process is illustrated in Figure 9.6.
FIGURE 9.6 Gene‐environment interactions in substance use disorders. The initiation of substance use is influenced
largely by environmental factors; the use of the addictive substance is affected largely by genetic factors
From Wang, Kapoor, & Goate (2012).
Genetic factors may have their effect by influencing regular use and tolerance levels to drugs such as
alcohol or affecting central nervous system responses to the drug (Schuckit, 1983). For example, alcohol
dependency requires that the user has to drink a lot and to do this regularly, and many individuals who
develop alcohol use disorders appear to have inherited a strong tolerance for alcohol. That is, they
report low levels of intoxication after a drinking bout and they show fewer signs of physical intoxication
(such as body sway) (Schuckit, 1994; Schuckit & Smith, 1996), and these higher thresholds for
intoxication may permit heavier and heavier bouts of drinking that are typical of alcohol use disorders.
There is considerable evidence that certain genes influence sensitivity to alcohol, and it is the
inheritance of these genes that determines whether a drinker will become dependent. The main
candidate is a gene known as ALDH2 (Luczak et al., 2014; Wall, Shea, Chan, & Carr, 2001). Alcohol
metabolism in the liver goes through two main stages, and these are the conversion of alcohol into a
toxic substance called acetaldehyde followed by conversion of acetaldehyde into nontoxic acetic acids.
ALDH2 is thought to affect the rate at which acetaldehyde is metabolised—if it is metabolised more
slowly, then the individual will begin to feel the negative effects of its toxicity, such as nausea, headaches,
stomach pains, and physical signs of intoxication. Interestingly, many Asians are known to have a
mutant allele for ALDH2 which slows acetaldehyde metabolism and allows it to build up after a
drinking bout, and makes drinking large amounts of alcohol aversive. This appears to be an important
factor in explaining why Asians develop alcohol use disorders at only about half the rate of non‐Asians
(Tu & Israel, 1995). Other mutant forms of this gene which allow rapid metabolism of acetaldehyde
may be the inherited factor that causes tolerance effects in some individuals and leads to regular alcohol
use and dependence. That such a tolerance is inherited is supported by the fact that sons of heavy
alcohol users report being less intoxicated than others after a standard amount of alcohol and show
fewer physical signs of intoxication (Schuckit et al., 1996). Recent studies have identified a form of the
ALDH2 allele in White American college students that is associated with lower rates of alcohol use
disorder, lower levels of drinking, and with alcohol‐induced headaches (Wall, Shea, Luczak, Cook, &
Carr, 2005), and suggests that variations in the form of this gene can have an important influence on
alcohol consumption and alcohol use disorders.

Long‐term substance‐induced cognitive deficits

As you will have read earlier in this chapter, there is much speculation about whether regular substance
use causes long‐term brain damage and permanent deficits in cognitive processes. Evidence for most of
these claims is still fairly equivocal—especially in the case of substances such as cannabis or MDMA
(Cole, Sumnall, & Grob, 2002; Iversen, 2005; Scott et al., 2018). However, most substance use disorders
tend to be associated with a syndrome of underachievement, with abusers often exhibiting lower IQ ,
lower educational achievement, and motivational deficits compared with nonusers. This may be a
consequence of individuals who have these intellectual and motivational deficits prior to drug use
lacking the necessary coping skills to pull themselves out of the vicious downward spiral of abuse and
dependency. However, an alternative explanation is that regular substance use may cause these
intellectual and motivational deficits, resulting in poorer judgement and decision‐making skills, and
making such individuals more prone to fall into a pattern of long‐term abuse. For example, there is
growing evidence that regular substance abuse can have long‐term effects on the balance and
availability of important brain neurotransmitters such as dopamine and serotonin (Heinz, Mann,
Weinberger, & Goldman, 2001; Nestler, 2001) and that methamphetamine abuse causes at least mild
cognitive decline observed in early to middle adulthood (Dean, Groman, Morales, & London, 2013). In
post‐mortem studies of the brains of regular cocaine users, Little, Krolewski, Zhang, and Cassin (2003)
found damage to striatal dopamine fibres resulting in neuronal changes causing disordered mood and
disruption to motivational processes. So this illustrates one possible route through which regular use
could develop into long‐term dependency as changes in brain structures caused by the drug affect mood
and motivation to such an extent that the user has significantly fewer cognitive resources available to
fight dependence.

Concurrent psychiatric diagnoses

We have already discussed the role that comorbid psychiatric disorders can play in turning first time
users into regular users because of the medicating properties the drug has on the psychiatric symptoms.
However, comorbid psychiatric problems appear to play an important role throughout the
developmental process to regular use and dependency. For instance, once a user has entered treatment
for their dependency, treatment outcomes are significantly poorer for users with comorbid psychiatric
disorders, and this is usually due to increased tendency to relapse after treatment (Grella, Hser, Joshi, &
Rounds‐Bryant, 2001; National Institute on Drug Abuse, 2018). There are at least two factors that
contribute to this poor treatment outcome: (a) individuals with comorbid psychiatric disorders are likely
to face more life stressors after treatment (e.g., negative emotional states) and are less likely to have the
coping resources required to deal with these stressors than those without psychiatric comorbidity (Ramo,
Anderson, Tate, & Brown, 2005)—this returns them to drug self‐medication as a way of coping, and (b)
users with a psychiatric comorbidity are less likely to consider that drugs are problematic compared to
their peers and tend to relapse very soon after treatment (Ramo et al., 2005)—this suggests that they
lack the motivation to abstain, even though their difficulties are compounded by the psychiatric
comorbidity. In summary, psychiatric comorbidity is a real risk factor for both transition from first use to
regular use, and from regular use to abuse and dependency, and it is an important factor in determining
relapse from treatment.

Poverty
Without doubt there are important socio‐economic factors at work in determining whether individuals
will use drugs and develop from being regular users into being drug dependent. One such factor is
poverty. There is evidence that an individual's first experience with an illicit drug increases in probability
if they live in or near an economically poor neighbourhood (Petronis & Anthony, 2003). This is perhaps
not surprising given that such individuals may well be unemployed, have no other forms of recreation
available to them, have little hope of occupational or educational fulfillment, and already live in
subcultures that revere drug dealing as a high‐status profession. Such conditions are perfect for the
downward spiral into drug abuse and dependency and are likely to represent circumstances in which the
individual will have poor access to treatment services and long‐term psychiatric support (Cook &
Alegria, 2011). Endemic drug use in poor communities fosters other problems, including infections such
as HIV and hepatitis C contracted through injecting drugs intravenously (Rosenberg, Drake, Brunette,
Wolford, & Marsh, 2005). Finally, substance dependency in poor areas fosters crime in the form of
robbery, fraud, and prostitution as the only means of securing money to buy drugs, and is a strong risk
factor for first‐time homelessness (Thomson, Wall, & Hasin, 2013).

9.4.4 Summary
Substance use disorder has to be viewed as a developmental process that progresses through a number
of well‐defined stages, and different factors are involved in establishing substance use at these different
stages. The main stages of development that we have highlighted are experimentation (what influences
first use of a substance?), regular use (what factors influence the move from experimentation to regular
use?), and abuse and dependency (what makes some people continue to use drugs even though this
activity is having significant negative effects on their lives and their health?). It is important to
understand that use may be confined to any one of these stages, and many regular users can often
function relatively successfully in their social, work and family environments. However, in terms of
understanding psychopathology, it is the development from regular use to abuse and dependency that is
of most interest to us as practitioners and clinical psychologists.
SELF‐TEST QUESTIONS
What factors lead young people to experiment with drugs?
How do peer group influences affect whether a young person will try a new drug?
What factors lead individuals to become regular users of a substance?
In what ways do different drugs such as alcohol, nicotine, cocaine, heroin, and cannabis
alter the user's mood?
Research suggests a broad range of drugs have their effects by activating the natural
reward pathway in the brain—what areas of the brain are involved in this pathway?
How does craving develop, and how does it contribute to relapse?
What is the evidence that regular drug use can become a form of self‐medication when the
user has severe adjustment difficulties?
What are the main factors that maintain substance abuse and dependency?
How have twin and adoption studies shown that there is an inherited component to
alcohol use disorder?
How does the gene ALDH2 influence whether a drinker is likely to become alcohol
dependent?
What is the evidence that regular substance use might cause long‐term cognitive deficits?
What is the link between poverty and substance use disorders?

SECTION SUMMARY

9.4 THE AETIOLOGY OF SUBSTANCE USE DISORDERS

The aetiology of substance dependency has to be viewed in developmental terms as
individuals go through stages of experimentation, regular use, and then substance abuse
and dependency.

9.4.1 Experimentation
Early use is influenced by the availability of the drug and its economic cost.
Whether substances are regularly used by family members and whether the family
environment is problematic can also hasten experimentation with drugs.
Peer groups influence first substance use as individuals start using a substance in order to
self‐categorise themselves as members of a particular group.
Substance use in young adolescents is significantly influenced by advertising and exposure
to substances (such as cigarettes and alcohol) in the media.

9.4.2 Regular Use

 Almost all substances of dependence have mood altering effects by either creating states of
euphoria or ecstasy or reducing tension or stress. These factors may contribute to regular
use.
Drugs achieve their pleasurable effects by influencing the dopamine system in the brain—
especially the dopaminergic neurons in the Ventral Tegmental Area (VTA) of the midbrain and
the nucleus accumbens (NAc).
Craving is a conditioned response to cues associated with individual drugs, and increases
consumption and risk of relapse.
Substance use can become regular as a means of self‐medication when the individual is
suffering severe adjustment difficulties such as those caused by psychiatric disorders.
Substance users can become regular users because they develop expectations that the
substance will have positive effects.

9.4.3 Abuse and Dependence

There is a significant inherited component to substance use disorders as shown by twin,
adoption, and family studies.
A gene known as ALDH2 affects the rate at which alcohol is metabolised and will influence
the individual's tolerance of alcohol.
Regular users may become drug dependent because they lack the motivation and the
coping skills to pull themselves out of a downward spiral into abuse and dependency.
Psychiatric comorbidity is a risk factor for both transition from first use to regular use, and
from regular use to abuse and dependency.
Endemic drug use is associated with poverty and poor communities, which also fosters
health problems such as HIV, and crime and prostitution.

9.5 THE TREATMENT OF SUBSTANCE USE DISORDERS

Treating individuals with substance use disorders is not a simple or easy process. At the point where a
user reaches the stage of abuse and dependency they are usually physically addicted to the drug, suffer
severe withdrawal symptoms when abstaining from the drug, and probably mix in social circles that will
provide regular temptations to use the drug. In addition, substance use disorders are often associated
with other comorbid psychiatric disorders that will need addressing in a full intervention plan. Many
younger individuals with substance use disorders also do not see their drug taking as dangerous or
problematic (Ramo et al., 2005) and so have a high risk of relapse after treatment. It is often the case
that those with most severe dependencies live miserable and unfulfilled lives. They may be homeless or
living in poverty, and the relief from these conditions provided by the drug may be the individual's only
solace. In 2010, the UK Centre for Social Justice has published a report proposing a series of reforms of
treatments for substance use disorders, most notably arguing that many treatment programmes are
doomed to failure without effectively addressing the poverty, unemployment, and poor living conditions
in which many drug addicts exist (Centre for Social Justice, 2010).
Because of these difficulties, treatment interventions with clients suffering substance use disorders are
usually multifaceted and address the client's problems at a range of different levels. As a consequence,
many national treatment programmes provide health care advice, general community support, easy‐
access drop‐in facilities for drug users, and structured treatment programmes—both community‐based
and residential, depending on the severity of the dependence. Treatment programmes are usually
multifaceted, in that they will combine a range of specific intervention procedures designed to make the
client aware of the circumstances and environmental stimuli that trigger substance use, deal with any
comorbid disorders, develop motivation to change, and teach the social and coping skills needed to deal
with life without drugs. These may also be combined with detoxification procedures designed to address
the physical dependence that drug use has developed. In the following sections, we will begin by looking
briefly at some community care practices, and then turn to specific psychological and detoxification
approaches.

9.5.1 Community‐Based Programmes

Community‐based programmes come in a number of forms. They can be self‐help groups,
such as Alcoholics Anonymous (AA) (see Focus Point 9.2), which tries to help the alcoholic replace
networks of drinking friends with other AA members. At least some studies have suggested that AA
participation can have positive outcomes, and may be an effective form of long‐term abstinence up to 8
years after joining the self‐help group (Timko, Moos, Finney, & Lesar, 2000). However, a systematic
review of the eight randomised outcome studies available at the time found that AA was no better than
any other kind of structured treatment (Ferri, Amato, & Davoli, 2008), and AA has notoriously high
dropout rates, which are often not factored into the results of controlled clinical trials.

Alcoholics Anonymous (AA) A support group for individuals who are alcohol dependent
and are trying to abstain.

Drug‐prevention schemes are now widespread and take many forms. Their purpose is to try and
prevent first use of a drug or to prevent experimentation with a drug developing into regular use—
usually through information about the effects of drugs and to develop communication and peer‐
education skills. In the UK, government‐sponsored schemes have a number of elements, which focus
respectively on young people (especially in schools), communities (targeting young people and their
parents who may be specifically at risk), treatment, and availability. 24‐hour telephone helplines and
websites also provide constant advice and information (e.g., talktofrank.com). Prevention schemes are
often local and tailored to the specific needs of the community. They aim to educate schoolteachers and
parents on how to deal with specific drug‐related incidents and how to provide drug advice to young
people. Many schemes train young people themselves to deliver drug education information to their
peers. Particular strategies that drug prevention schemes use are (a) peer‐pressure resistance
training, where students learn assertive refusal skills when confronted with drugs, (b) campaigns to
counter the known effects of the media and advertising (e.g., by combating tobacco advertising with
antismoking messages), (c) peer leadership, where young people are training to provide anti‐drugs
messages to their peers, and (d) changing erroneous beliefs about drugs (e.g., that use is more prevalent
than it is, or that a drug's effects are relatively harmless). The evidence on the effectiveness of these
types of schemes is difficult to gauge because they take place across different types of communities
characterised by different risk factors and employ a range of different strategies over different
timescales. However, systematic reviews of school‐based prevention programmes do indicate that such
programmes can be effective in reducing smoking and alcohol use, and have protective effects against
drugs and cannabis use (Das, Salam, Arshad, Finkelstein, & Bhutta, 2016). Some studies have also
indicated that at the very least such schemes do appear to delay the onset of drug use—even if longer‐
term effects are difficult to evaluate (Faggiano et al., 2008; Sussman et al., 1995).
 Drug-prevention schemes Communitybased services whose purpose is to try to prevent first
use of a drug or to prevent experimentation with a drug developing into regular use – usually
through information about the effects of drugs and through developing communication and
peer-education skills.

peer leadership A strategy used by drug prevention schemes where young people are trained
to provide anti-drugs messages to their peers.

Residential rehabilitation centres are also important in the treatment and longer‐term support of
individuals with substance use disorders. Such centres allow people to live, work, and socialise with
others undergoing treatment in an environment that offers advice, immediate support, group and
individual treatment programmes, and they enable the client to learn the social and coping skills
necessary for the transition back to a normal life. In such centres, detoxification programmes can be
monitored and supported with the help of peripatetic key workers. Residential rehabilitation
programmes usually combine a mixture of group work, psychological interventions, social skills training,
and practical and vocational activities. In the UK, clients would normally begin residential
rehabilitation after completing inpatient detoxification. Despite the support offered by residential
rehabilitation centres, the percentage of clients in such centres who do not complete their treatment
programme is often unacceptably high (Eastwood et al., 2018; Westreich, Heitner, Cooper, Galanter, &
Guedj, 1997) and, perhaps not surprisingly, noncompleters fare significantly less well than completers
(Aron & Daily, 1976; Berger & Smith, 1978). However, a number of studies have clearly indicated that
longer stays in residential rehabilitation centres are consistently associated with better outcomes, with a
minimum stay of 3‐months recommended (Simpson, 2001).

Residential rehabilitation centres Centres that allow people to live, work and socialise
with others undergoing treatment in an environment that offers advice, immediate support, and
group and individual treatment programmes enabling clients to learn the social and coping
skills necessary for the transition back to a normal life.

9.5.2 Behavioural Therapies

There is a tradition of using behavioural therapies with many substance use disorders, and these are
mainly adaptations of conditioning principles to the practical difficulties involved in controlling and
preventing substance abuse and dependency. Behavioural therapies have a number of aims: (a) to
change substance use from a positive or pleasurable experience to a negative or aversive one (e.g.,
aversion therapy) (Wiens, Montague, Manaugh, & English, 1976), (b) to help the individual identify
environmental stimuli and situations that have come to control substance use (e.g., contingency
management therapy) (Miller, Leckman, Delaney, & Tinkcom, 1992), (c) to reinforce abstinence by
rewarding the user when they provide drug‐free urine specimens (e.g., contingency management) (Petry,
2000), and (d) to teach the user alternative behaviours that are likely to compete with substance use
behaviours (e.g., relaxation, meditation, social skills, and anger management) (Azrin et al., 1996).

Aversion therapy
This treatment has been regularly used in the context of a number of substance disorders, but most
notably with alcohol dependency. Using a classical conditioning paradigm, clients are given their drug
(the conditioned stimulus) followed immediately by another drug (the aversive UCS) that causes
unpleasant physiological reactions such as nausea and sickness (Lemere & Voegtlin, 1950). The
assumption here is that pairing the favoured drug with unpleasant reactions will make that drug less
attractive. In addition, rather than physically administering these drugs in order to form an aversive
conditioned response, the whole process can be carried out covertly by asking the client to imagine
taking their drug followed by imagining some upsetting or repulsive consequence. This variant on
aversion therapy is known as covert sensitisation (Cautela, 1966). However, there is limited evidence
that aversion therapy has anything but short‐lived effects (Wilson, 1978; but see Elkins et al., 2017, for a
procedure with alcohol use disorder that reports some longer‐term benefits 12 months after aversion
therapy), and outcomes are significantly less favourable when clients with long‐standing substance
dependency are treated in this way (Howard, 2001). Nevertheless, aversion therapy can be used as part
of a broader treatment package involving community support, detoxification, and social skills training.

covert sensitisation The association of an aversive stimulus with a behaviour the client
wishes to reduce or eliminate.

Contingency management therapy

This is a treatment procedure that teaches the client how to restructure and control their behaviour and
environment in order to prevent drug use. This approach is also based on conditioning principles, and
these can include (a) stimulus control, where the client learns to identify environmental situations that
trigger drug use and avoid or minimise them (e.g., identifying a stressful day at work as a trigger for
drinking, and so avoiding pubs or bars), (b) using rewards to reinforce abstinence (e.g., being given
vouchers for not using a substance which can be exchanged for desired activities such as a trip to the
cinema or the theatre), (c) learning to be aware of when and how frequently drug taking occurs (e.g., by
keeping a diary noting all times that drinking occurs), and (d) setting attainable goals in a structured
step‐by‐step approach to treatment (e.g., by setting nonabstinence goals that are achievable) (Hester, 1995).
Contingency management therapy continues to be a valuable tool for therapists in this area, with
a number of new variations on this methodology being developed over the years such as teaching job‐
seeking, assertiveness, and social interaction skills (Petry, 2011).

Contingency management therapy Behavioural therapy which aims to help the individual
identify environmental stimuli and situations that have come to control symptoms such as
substance use.

controlled drinking A variant of BSCT in which emphasis is put on controlled use rather
than complete abstinence.

A particular important variant of behavioural self‐control training (BSCT) is known as controlled

drinking. Traditionally, it has been assumed that a ‘cure’ for a substance use disorder entails complete
abstinence, but programmes have been developed more recently that put the emphasis on controlled use
rather than complete abstinence. This has been a particularly useful approach to treating alcohol
dependency, and has been pioneered by Sobell and Sobell (1993). The assumptions here are that (a) in
modern western societies it is difficult to avoid alcohol altogether, and so it is better to have the aim of
controlling drinking rather than avoiding alcohol completely, and (b) teaching clients to have control
over their drinking behaviour has other benefits, such as improved self‐esteem, a sense of responsibility,
and feelings of control over particular domains in their life. Absence of these latter characteristics often
drives the individual to alcohol dependency in the first place. Clients undergo social skills training in
order to negotiate situations in which they would otherwise drink excessively, relaxation training to
prevent stressors that might trigger drinking, and are encouraged to think positively about other
domains in their life (e.g., to eat healthily). Clients are also taught to believe that they have real control
over their drinking, and the BSCT methods outlined above are regularly used to provide the client with
adaptive strategies for control. Finally, controlled drinking also teaches the client to be aware that a lapse
is not catastrophic but is often inevitable and natural, and that they can use the self‐control and social
skills they have learnt to overcome lapses. Outcome studies suggest that controlled drinking is
achievable, can be as effective over the longer‐term as treatments that require total abstinence (Foy,
Nunn, & Rychtarik, 1984; Mann, Aubin, & Witkiewitz, 2017), and can help individuals to moderate
their intake and to live more fulfilled and healthier lives (Sobell & Sobell, 1995). Controlled drinking is
also an accepted treatment strategy for a majority of substance abuse services in the UK (Rosenberg &
Melville, 2005).

FOCUS POINT 9.10 STIGMA AND CONTROVERSIAL

TREATMENT PROGRAMMES FOR SUBSTANCE USE
DISORDERS

There is stigma associated with drug abuse and substance use disorders—to the point where
there is often a public outcry if treatment programmes propose controversial interventions that
seem counterintuitive to the nondrug user. Recent examples include (a) treating heroin addicts
by giving them supervised heroin injections, and (b) giving drug addicts financial rewards for
staying ‘clean’.
In the first example, addicts are given daily injections of heroin in supervised clinics in an
attempt to wean them off the drug (known colloquially as ‘shooting galleries’). A study of this
intervention based in London, Darlington, and Brighton in the UK divided heroin addicts into
three groups, giving one group heroin and giving the other two intravenous methadone and
oral methadone. All three groups showed improvement, but the heroin‐using group fared much
better than the other two, with 75% having stopped using street heroin and also having
 significantly reduced their involvement in crime (Strang et al., 2010).
Giving drug addicts monetary rewards for staying clean also has a significant effect on the
success of treatment. In the ‘Harbour Steps’ trial run in Lambeth in London, addicts earn a
small credit each time they give a crack‐free urine sample, and can be tested up to three times a
week. Such programmes are significantly more effective at establishing abstinence than control
treatments (Lussier, Heil, Mongeon, Badger, & Higgins, 2006).
Despite the success of these types of programmes, and despite the fact that people will rarely
criticise rewarding people for losing weight or giving up smoking, there is often a public
reluctance to endorse programmes that appear to ‘reward’ individuals who have an illegal
substance use disorder, and there have been problems establishing clinics that use these types of
programmes in countries such as Germany, The Netherlands, Canada, and the UK because of
public criticism. It's clear that many people still believe that drug addiction is solely the ‘fault’ of
the addict and as such is self‐inflicted (Crisp, Gelder, Rix, Meltzer, & Rowlands, 2000). Until we
can change this unhelpful and discriminating view of those with substance use disorders, it may
continue to be difficult to propose, develop, and finance these types of interventions.

9.5.3 Cognitive Behaviour Therapies (CBT)

Cognitive behaviour therapies (CBT) have been used in the treatment of substance use disorders in at
least two different ways. The first is to use CBT to correct dysfunctional beliefs about relapse, and the
second is to deal with substance use disorder when it is comorbid with other psychiatric symptoms such
as depression and psychosis.
First, as we mentioned earlier, substance abuse disorders are notoriously difficult to treat over the
longer‐term. Individuals can usually quit the substance in the short‐term, but relapse is common in
those receiving treatment for substance dependency (Brownell, Marlatt, Lichtenstein, & Wilson, 1986)
and one in three individuals receiving inpatient treatment for illicit drug use disorders will have relapsed
within 3 months (Andersson, Wenaas, & Nordfjærn, 2019). As a result, a successful treatment
programme has to deal as effectively with relapses as it does in getting the client to quit in the first place.
Two factors appear to be important in determining whether a relapse will lead to regular use again: (a)
the client's beliefs about relapse, and (b) experiencing stressful emotional states, such as anxiety,
depression, anger, and frustration, and these states are responsible for around 30% of all relapses after
treatment (Cummings, Gordon, & Marlatt, 1980). In order to counter these relapse factors, therapists
have developed variants of CBT that address dysfunctional beliefs about relapse, and can also provide
help in coping with stressful emotions. In the first case, individuals will often hold dysfunctional beliefs
about relapse that facilitate further regular use. These may include beliefs such as “If I lapse, then my
treatment has failed,” “If I lapse, then I am a worthless individual who doesn't deserve to get better,” or
‘I've had one drink, so I may as well get drunk’ (Marlatt & Gordon, 1985). These are what are known as
abstinence violation beliefs that contribute to the transition from relapse ‘slips’ to full relapse. CBT
attempts to identify such dysfunctional beliefs, to challenge them (e.g., relapse doesn't inevitably mean
total loss of control), and to provide the client with the skills required to negotiate a relapse successfully.
In order to deal with the second factor, CBT programmes have been developed that help the client to
deal effectively with negative emotions, stress, and the factors that might give rise to stress. This is also
known as motivational‐enhancement intervention(MET) and provides communication training,
work‐ and school‐related skills, problem‐solving skills, peer refusal skills, negative mood management,
social support, and general relapse prevention methods (Miller & Rollnick, 1991). Both forms of CBT
have been shown to be more effective in establishing long‐term abstinence and effective drug avoidance
behaviours than traditional aftercare or control conditions (Farabee, Rawson & McCann, 2002;
McAuliffe, 1990) and are particularly effective if combined with family therapy (Waldron, Slesnick,
Brody, Turner, & Peterson, 2001).
 motivational-enhancement intervention (MET) An intervention for substance abuse and
dependency involving communication training,work- and school-related skills, problem-solving
skills, peer-refusal skills, negative mood management, social support and general relapse
prevention.

RESEARCH METHODS IN CLINICAL PSYCHOLOGY 9.1 HAIR

SAMPLE ANALYSIS

Many methods of collecting data about substance abuse are relatively unreliable. Self‐report is
obviously problematic, because users will often have reason to lie about their drug use (if it
involves legal issues such as child custody), or their recall of drug use may be affected by the
changed states of consciousness caused by regular use of certain substances. Even blood and
urine samples can be very variable in the data they provide (Spiehler & Brown, 1987) and are
certainly not suitable for estimating longer‐term drug use.
However, one relatively reliable method of collecting data about drug use is through hair
sample analysis (e.g., Uhl & Sachs, 2004). Small amounts of the drug will accumulate in hair
after use and, because head hair grows at approximately 0.8–1.3 cm per month, a record of
drug use is available over a period of weeks or months after intake. A hair sample of only 3–5
cm in length is required to provide a record of drug use over the previous 3–4 months, and
high‐performance chromatography is used to identify the concentrations of any drugs taken up
into the hair sample.
Hair sample analysis is not only used as a more reliable way of collecting research data about
previous drug use, it is becoming widely used for medico‐legal purposes where the user needs to
prove long‐term abstinence (especially in cases related to rehabilitation and legal custody). It is
also used to provide a longer‐term record of drug use in the case of individuals who may have
died from overdose (Tagliaro, Battisti, Smith, & Marigo, 1998) and has been used to detect the
use of opiates, cocaine, cannabis, and amphetamines (Jurado & Sachs, 2003).
Nevertheless, hair sample analysis is not a fool‐proof way of estimating drug use, and it does
have its own drawbacks as a methodology. For instance, it is not suitable as a measure of
current drug use, but only as a method of estimating previous medium‐term use. It also cannot
be used on those who present with very short hair or no head hair!

In recent years, ‘third‐wave’ CBT methods (see Chapter 4) have also been applied to the treatment of
substance use disorders. For example, metacognitive therapy for alcohol use disorder attempts to
identify and modify dysfunctional metacognitive beliefs about drug use (e.g., ‘I cannot stop thinking
about using alcohol’, ‘I have no control over alcohol because my brain is abnormal in some way’) and
this has been found to be useful in reducing weekly alcohol use in preliminary studies (Caselli, Martino,
Spada, & Wells, 2018). Similarly, mindfulness practices have also been applied to cravings for cigarettes
and alcohol and have shown benefits in terms of both craving reduction and reducing the extent to
which craving leads to substance use (Tapper, 2018).
Some approaches recommend CBT primarily when substance abuse disorder is comorbid with another
psychiatric disorder such as anxiety or depression. However, systematic reviews and RCTs indicate only
moderate support for CBT when used alone to treat some forms of substance dependency such as
alcohol use disorder (Coates, Gullo, Feeney, Young, & Connor, 2018; Hides, Samet, & Lubman, 2010),
with the implication that more potent forms of CBT still need to be developed and may need to be used
in combination with other forms of treatment to be effective.

9.5.4 Family and Couples Therapy

Because many regular drug abusers are young people they often live with their families, and because of
this family members can often provide support during treatment on a day‐by‐day basis. However, family
therapy is important for a number of other reasons. First, many of the parents of substance abusers are
also abusers themselves, and as such may constitute part of the problem that needs to be addressed.
Second, individuals with substance abuse problems (such as problem drinkers) will often physically and
sexually abuse members of their family, and so therapy may often need to involve those who have
regular close contact with the abuser. Family therapy is an effective way of identifying and altering
dysfunctional family patterns that may contribute to adolescent substance abuse (Rowe, 2012) and can
often be an effective brief intervention for adolescent substance abuse when whole families are involved
in the programme (Szapocznik, Zarate, Duff, & Muir, 2013). Family therapists will attempt to engage
members of the family in the treatment process and to reduce blaming behaviour. Subsequently, the
therapist will use contingency management and behavioural contracting procedures, and teach
communication and problem‐solving skills in order to facilitate more adaptive patterns of interaction
within the family. This approach has been shown to be particularly successful in dealing with adolescent
substance use problems and is generally as effective in the long‐term as individual psychotherapies such
as CBT (Waldron et al., 2001). Specifically involving a client's spouse or partner in therapy also has
important beneficial effects. The partner can offer support when required, but it is also important in
identifying specific problems in a relationship that may be contributing to substance abuse. Outcome
studies have indicated that, when compared with no treatment, couples therapy produces longer periods
of abstinence, fewer substance‐related problems, and improvements in the quality of the couple's
relationship (Fals‐Stewart, Birchler, & O'Farrell, 1996; O'Farrell, Schumm, Murphy, & Muchowski,
2017).

9.5.5 Biological Treatments

Drugs are used to treat substance use disorders in a variety of ways. Collectively these are known as
detoxification and are often used in conjunction with psychological treatments or as a precursor to
psychological treatments (to wean heavy users off regular substance use and make them amenable to
other forms of therapy). Detoxification is a process of systematic and supervised withdrawal from
substance use that is either managed in a residential setting or on an outpatient basis. Drug use during
detoxification can take a number of forms: (a) to help reduce withdrawal symptoms (e.g., anxiolytic
drugs), (b) to prevent relapse by using antagonistic drugs to make subsequent substance use aversive (e.g.,
Antabuse—a drug that causes vomiting if alcohol is consumed), (c) to block the pleasurable central
nervous system (CNS) effects of a substance (e.g., naxolone—used with individuals who are opiate
dependent in order to prevent opiates having their usual effects on reward centres in the brain), and (d)
to wean a user onto a weaker substance (e.g., methadone maintenance programmes, where the
user takes a less virulent opiate in order to wean themselves off heroin).

detoxification A process of systematic and supervised withdrawal from substance use that is
either managed in a residential setting or on an outpatient basis.

methadone maintenance programmes A detoxification programme where users take a

less virulent opiate in order to wean themselves off heroin.

Those drugs that help reduce withdrawal symptoms include clonidine (that reduces noradrenergic
activity in the brain, Baumgartner & Rowan, 1987) and acamprosate, a drug that helps to reduce the
cravings associated with withdrawal (Mason, 2001). Basic anxiolytic and antidepressant drugs can also
be used to improve mood and alleviate negative emotions experienced during withdrawal (Cornelius et
al., 1995).
Antabuse (disulfiram) has been used for over 60 years in the detoxification of individuals with
alcohol dependency. It affects the metabolism of alcohol so that the normal process of converting toxic
alcohol products into nontoxic acetic acids is slowed, and this causes the individual to feel nauseous or
vomit whenever they take alcohol. However, the use of Antabuse does have some problems. It is rarely
effective when patients are given the drug to take unsupervised, and noncompliance and dropout from
such programmes are high (Fuller et al., 1986). Second, it does have a number of side effects and in
some rare cases causes liver disease and hepatitis (Mohanty, LaBrecque, Mitros, & Layden, 2004).
However, when taken in properly supervised programmes, Antabuse has been shown to be more
effective at reducing drinking behaviour than placebo controls (Chick et al., 1992; Fuller, & Gordis,
2004; Skinner, Lahmek, Pham, & Aubin, 2014), including having a benefical effect on short‐term
abstinence and days until relapse (Jorgensen, Pedersen, & Tonnesen, 2011). Indeed, some long‐term
studies of alcohol treatment have suggested that abstinence rates of 50% are achievable up to 9 years
after initial treatment with the supervised and guided use of alcohol deterrents such as Antabuse
(Krampe et al., 2006), and that Antabuse can increase treatment effectiveness when combined with
CBT and individual‐based treatment (Pettinati et al., 2010; Skinner et al., 2014).

Antabuse (disulfiram) A drug used in the detoxification of individuals with alcohol

dependency.

A further set of drugs used to treat substance use disorders are those that influence brain
neurotransmitter receptor sites and prevent the neuropsychological effects of stimulants, opiates, and
hallucinogens. For example, drugs such as naltrexone, naxolone, and the more recently developed
buprenorfine attach to endorphin receptor sites in the brain. This prevents opioids from having their
normal effect of stimulating these sites to produce more endorphins that create the feeling of euphoria
when drugs such as heroin are taken. Such drugs do appear to reduce craving for opiates and they help
the therapeutic process when combined with other forms of psychological therapy (Streeton & Whelan,
2001). However, such drugs do come with a cost. Dosage has to be properly regulated, otherwise the
client may be thrown rapidly into an aversive withdrawal (Roozen, de Kan, van den Brink, Kerkhof, &
Geerlings, 2002), and narcotic antagonists such as naltrexone and naxolone are effective only for as long
as the client is taking them. However, because these drugs affect the release of endorphins, they have
been used to help treat a number of substance use disorders, including alcohol (O'Malley, Krishnan‐
Sarin, Farren, & O'Connor, 2000), cocaine and opiate dependency (O'Brien, 2005). The reason why
such drugs may be effective over a range of substances that have their psychoactive effects across
different brain neurotransmitter pathways is because they suppress the release of endorphins, and
endorphin receptors are closely associated with the brain's reward centres (Leri & Burns, 2005).

naltrexone An opioid receptor antagonist which has been found to be beneficial in the control
of hyperactivity and selfinjurious behaviour.

naxolone One of a set of drugs used to treat substance use disorders which influence brain
neurotransmitter receptor sites and prevent the neuropsychological effects of stimulants, opiates
and hallucinogens.

buprenorfine An opioid drug used in the treatment of opioid addiction.

Finally, drug replacement treatment involves treating severe cases of substance abuse and
dependency by substituting a drug that has lesser damaging effects. For example, many heroin users put
themselves at risk from overdoses, contaminated street heroin, and using unsterilised needles. To try to
address these issues as rapidly as possible, users can be switched from heroin to the less virulent opium
derivative methadone. Methadone, has a slower onset and weaker effects, and can be taken orally rather
than injected. Initial outcome studies suggested that methadone treatment was helpful in enabling
heroin addicts to withdraw from the drug and it helps to retain addicts in treatment (Mattick, Breen,
Kimber, & Davoli, 2009). However, we must remember that methadone is still an addictive drug itself
that can be difficult to withdraw from (Kleber, 1981), and because of this methadone maintenance
therapy can last for many years—and for some, for their whole lifetime (Arora & Williams, 2013; Smyth
et al., 2005). Outcome studies suggest that methadone maintenance therapy is most effective when part
of a multifaceted structured therapy programme that includes psychotherapy, drug education, skills
training, and contingency management (O'Brien & McKay, 2002), and when the client includes non‐
drug‐using family members and friends in the treatment (Kidorf et al., 2005). As well as contributing to
the success of treatment in a multifaceted approach, methadone maintenance therapy has the added
benefits of increasing the likelihood of entering into longer‐term comprehensive treatment, reducing
heroin use and criminal behaviour, and reducing health‐risks such as number of HIV cases (Arora &
Williams, 2013; Farrell, Gowing, Marsden, Ling, & Ali, 2005; Schwartz et al., 2006). While drug
maintenance therapies have been largely confined to treating opiate dependency, there have been
attempts to develop substitute drugs for other dependencies. One such example is Sativex, an aerosol
that combines THC and nonpsychoactive cannabis ingredients for the treatment of cannabis
dependency. Savitex has the benefit of having weaker effects than cannabis and is taken orally rather
than smoked (Kleber, 2005).

drug replacement treatment Involves treating severe cases of substance abuse and
dependency by substituting a drug that has lesser damaging effects.

9.5.6 Summary
The treatment of substance use disorders is inevitably a multifaceted one, with most mental health
services providing a range of treatments (detoxification, skills training, behavioural and cognitive
therapies, and family and couple therapies) in a variety of settings (e.g., individual, community‐based, or
residential). Treatments usually involve a combination of drug‐based detoxification, psychological
therapy, and skills training, and will usually attempt to involve the client's family and friends in the
therapeutic process. Substance use disorders are difficult to treat and we described some of the
difficulties at the outset of this section on treatment. Nevertheless, outcomes are often good, and total
abstinence is an achievable goal—even with severely addictive substances such as opiates and stimulants.
For example, a long‐term study of heroin dependence in a small town in the south‐east of England 33‐
years after initial treatment found that 42% of those treated had been abstinent for 10 years (Rathod,
Addenbrooke, & Rosenbach, 2005). This suggests that long‐term dependency is not inevitable after
exposure to addictive drugs, and individuals can often control their use as well as receive effective
treatment for their dependency when required.
SELF‐TEST QUESTIONS
Why are substance use disorders particularly hard to treat?
Can you describe the different kinds of community‐based programmes that help to
prevent or treat substance use disorders?
How successful is residential rehabilitation in treating substance use disorders?
How have the principles of behaviour therapy been adapted to treat substance use
disorders?
Can you name the main features of aversion therapy, contingency management therapy,
and controlled drinking?
What are some of the benefits of using controlled drinking goals rather than complete
abstinence?
What are abstinence violation beliefs and how do cognitive behaviour therapies (CBT)
attempt to treat them?
What is meant by the term detoxification, and how are drugs used in detoxification
programmes?
How have drugs such as naltrexone, naxolone, and buprenorfine proved to be useful in the
treatment of substance use disorders?
 SECTION SUMMARY

9.5 THE TREATMENT OF SUBSTANCE USE DISORDERS

Treatment of substance use disorders is difficult because of the physical effects of
dependence, the probability of comorbid psychiatric disorders, and high rates of relapse.
Treatment interventions are usually multifaceted and address the individual client's
problems at a range of different levels.
One form of community‐based service is self‐help groups such as Alcoholics Anonymous (AA).
Drug‐prevention schemes are used with young people to try and prevent first drug use.
Residential rehabilitation centres provide a controlled environment for detoxification and
longer‐term support for individuals with substance use disorders.
Behaviour therapies adapted to treat substance use disorders include aversion therapy and
contingency management therapy.
Controlled drinking can be used as a nonabstinence approach to treating alcohol abuse and
dependency.
Cognitive Behaviour Therapies (CBT) are used primarily to change individuals' beliefs about
their substance use but are best employed when a sufferer has a psychiatric disorder
comorbid with substance use disorder.
Motivational‐enhancement training (MET) provides communication training, work‐ and school‐
related skills, problem‐solving skills, peer refusal skills, relapse prevention methods, and
negative mood management.
Family and Couples Therapy is useful for ensuring that family members understand the
reasons for the substance use and can provide help and support during and after
treatment.
Detoxification is a process of systematic and supervised withdrawal from substance use that
often uses the controlled use of drugs to combat the physical problems of withdrawal and
dependence.
Antabuse (disulfiram) causes alcohol to produce toxins which make the individual feel unwell
and has been used for over 60 years as a means of controlling alcohol dependency.
Drug maintenance therapy involves treating severe cases of substance use (e.g., heroin
dependence) by normally substituting a drug that has a lesser effect (e.g., methadone).

9.6 SUBSTANCE USE DISORDERS REVIEWED

Substance use disorders are an important social and health problem, as well as also raising many mental
health issues. Substance use disorders are associated with criminal behaviour (often violent crime), short‐
and long‐term health problems, disruption to social and occupational functioning, and increased risk of
psychiatric comorbidity. The main substances of abuse can be grouped into stimulants (e.g., cocaine,
amphetamine), sedatives (e.g., opiates, barbiturates), and hallucinogenic drugs (e.g., LSD). Legal drugs
such as alcohol and nicotine can also foster dependency and can cause significant long‐term health
problems.
Most of the drugs associated with abuse and dependency have important mood altering effects that
make the user feel confident, relaxed (alcohol, cannabis), euphoric (heroin, cocaine), or energised (e.g.,
amphetamines, MDMA). More important, these effects also alleviate any negative or stressful mood the
user may be feeling prior to use. Most of these substances also have addictive properties as users quickly
develop a tolerance to the drug and experience worsening withdrawal symptoms during abstinence.
Substance use disorders can be seen as developing through a number of different stages, with different
factors affecting transition from one stage to the next (see Figure 9.5). The three stages highlighted here
are experimentation (what determines first use?), regular use, and abuse and dependency (what makes
some people use drugs regularly even though this activity has significant negative effects on their health
and social and occupational functioning?).
Some people do seem to move down a slippery slope from experimentation to abuse and dependency,
but we have to be clear that many other people do not, and people can be regular substance users
without this affecting their family, social, and occupational functioning. However, when the stage of
substance abuse and dependency is reached, this is often associated with comorbid psychiatric problems
or simply with poverty, unemployment, and even homelessness. In the former case, many who are
substance dependent use their drug to self‐medicate against the negative effects of their comorbid
psychopathy (e.g., depression, eating disorders, anxiety disorders, etc.). In the case of poverty, the mood
altering effects of the drug may provide relief from miserable and unfulfilled lives.
Treatment of substance use disorders is usually multifaceted, and many health services provide a tiered
approach by providing a range of treatments, advice, and training facilities in a variety of settings (e.g.,
individual, community‐based, or residential). Substance use disorders can be difficult to treat because of
the difficulties of dealing with withdrawal symptoms, the fact that the drug has probably been the user's
main method of coping with emotional and life stressors, frequent comorbidity of other mental health
problems, and temptation to relapse after treatment. However, outcome studies suggest that with
appropriate support and aftercare, treatment can result in long‐term abstinence in a significant
proportion of clients.
This book is accompanied by Student and Instructor companion
websites.
www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter References
Videos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
10
Eating Disorders

ROUTE MAP OF THE CHAPTER

This chapter covers the description, aetiology, and treatment of the three main eating disorders,
namely anorexia nervosa, bulimia nervosa, and binge‐eating disorder. The chapter begins by
describing the main symptoms and diagnostic features of these disorders and then explores
their cultural and demographic distribution. Eating disorders have their origins in a range of
psychological, sociological and biological processes, and all these are explored in the section on
Aetiology. Finally, eating disorders are often complex and difficult to treat, and the final section
discusses those treatments which have so far proved most effective—namely pharmacological
treatments, family therapy, and cognitive behaviour therapy (CBT).

CHAPTER OUTLINE
10.1 DIAGNOSIS AND PREVALENCE
10.2 CULTURAL AND DEMOGRAPHIC DIFFERENCES IN EATING
DISORDERS
10.3 THE AETIOLOGY OF EATING DISORDERS
10.4 THE TREATMENT OF EATING DISORDERS
10.5 EATING DISORDERS REVIEWED

LEARNING OUTCOMES
When you have completed this chapter, you should be able to:
1. Describe the characteristics and main diagnostic criteria of the three main eating
disorders.
2. Describe the cultural and demographic distribution of eating disorders, and evaluate why
this information is important in understanding eating disorders.
3. Compare and contrast a range of risk factors for eating disorders, covering risk factors at
different levels of explanation (such as genetic, developmental, cultural, and psychological).
4. Describe, compare and contrast at least two interventions commonly used in the treatment
of eating disorders.
 For as long as I can remember, I've wanted to do everything under the sun—and be the best at it. If I got a C I'd
be really hard on myself, and my parents made it pretty clear they wanted me to get a scholarship, since paying for
college would be a challenge.
Plus, things weren't so great at home. I'd always had a terrible relationship with my dad. I felt like he ignored me
most of the time. He could be pretty scary. Like screaming at me for little things ‐ like leaving crumbs on the
kitchen table after making a snack. I'd tell him when he hurt my feelings, but he'd just walk away and slam the
door. On top of it all, he and my Mum were fighting a lot, too.
It was hard to be at school and even harder to be at home. As a result, I began eating less. Starving myself wasn't
my actual goal at first—just more of a response to everything going on in my life. But I started to lose weight.
Soon, my clothes got looser. Then I became a vegetarian, also cutting out all foods with chemicals and
preservatives. I lost even more. I felt I had finally found something I could completely control—my weight. Even
though my life felt crazy, I could do this one thing very well and, initially, I got a high from this accomplishment.
Gaining or losing a single pound determined my mood for the whole day.
I remember watching a film in health class about the dangers of anorexia. I even hung warning posters around
school during Eating Disorders Awareness Week. But I never connected my own weight loss to anorexia. Denial,
of course, is a symptom of the disease. A voice in my head kept telling me the less food I let touch my lips, the
more stable and safe I would be. My friends and family kept telling me I was too skinny, but no one could force
me to eat. And, to be honest, it made me feel powerful that I could ignore pleas and starve myself. Even as my
bones poked out from under my skin, I could not admit to anyone—including myself—how incredibly sick I was.
Amy's Story

Introduction
Disorders of eating are complex and have their roots in psychological, sociological, and cultural
phenomena. In many of today's cultures, individuals are torn between advertising that implores them to
eat a range of foods high in calories and campaigns designed to promote selective and healthy eating.
(see Activity Box 10.1 on the book’s website). Eating behaviour is also influenced by media
representations of ideal body shapes. These prompt appearance‐conscious individuals to control and
restrict their eating in order to achieve these media‐portrayed ideals of a slim body—ideals which are
usually underweight. Given these pressures, and the psychological factors that accompany them, it is not
surprising that eating patterns can become pathological and result in disorders of both undereating
(anorexia nervosa) and overeating (bulimia nervosa and binge‐eating disorder).
Amy's story at the start of this chapter illustrates what a slippery slope the descent into an eating
disorder can be. The story starts with someone who is troubled in various spheres of her life, including
school life and home life. In Amy's case, this leads more by accident than design to a reduction in eating.
Eventually, controlling eating becomes a goal in itself, and a source of satisfaction when even the
smallest of dietary goals are met. The obvious physical consequences of lack of nutrition then become
exhaustion and lack of concentration, menstrual irregularities, and proneness to infections, insomnia,
dizzy spells, and sensitivity to cold. Amy's story also highlights some of the potential risk factors that
have been found to predict the development of an eating disorder such as anorexia, and these include
high levels of perfectionism and parents who exhibit coercive parental control or who are hostile and
unresponsive to the individual's needs. Also characteristic of the disorder, and featured in Amy's story,
are the need to control eating as a central feature of eating disorders generally, the development of very
durable and resistant beliefs about the need to diet and control eating, and the use of denial as a means
of avoiding confronting the disorder and challenging dysfunctional beliefs about eating. Focus Point 10.1
summarises some of the warning signs of anorexia nervosa, many of which will have been apparent as
Amy developed her own eating disorder (Focus Point 10.1).
Although men are being increasingly diagnosed with eating disorders (see Murray et al., 2017, for a
discussion of eating disorders in men), these disorders are largely conditions that are diagnosed in
women (Walters & Kendler, 1994). Many women consider themselves to be overweight despite having a
body mass index (BMI) in the normal range. Studies of college women suggest that 43% were
currently dieting despite 78% of them having a healthy BMI (Fayet, Petocz, & Samman, 2012), while
community studies indicate that between 25 and 30% of females claim to be dieting or actively
attempting to lose weight (McVey, Tweed, & Blackmore, 2004; Wardle & Johnson, 2002). Dieting is
often a significant precursor of anorexia nervosa symptoms (Patton et al., 1997) and can become an
entrenched habit that is resistant to both psychological and pharmacological treatment, and this may
contribute to the persistence of symptoms in some anorexia nervosa sufferers (Walsh, 2013).

body mass index (BMI) A way of measuring a healthy weight range, derived by using both
height and weight measurements.

FOCUS POINT 10.1 WARNING SIGNS OF ANOREXIA

NERVOSA

The main symptom of anorexia is deliberately losing a lot of weight or keeping

your body weight much lower than is healthy for your age and height.
Signs and symptoms include:
missing meals, eating very little or avoid eating any foods you see as fattening
lying about what and when you've eaten, and how much you weigh
taking medicine to reduce your hunger (appetite suppressants), such as slimming or diet
pills
exercising excessively, making yourself sick, or using medicine to help you poo (laxatives)
or to make you pee (diuretics) to try to avoid putting on weight
an overwhelming fear of gaining weight
strict rituals around eating
seeing losing a lot of weight as a positive thing
believing you are fat when you are a healthy weight or underweight
not admitting your weight loss is serious
You may also notice physical signs and symptoms such as:
if you're under 18, your weight and height being lower than expected for your age
if you're an adult, having an unusually low BMI
your periods stopping (in women who have not reached menopause) or not starting (in
younger women and girls)
bloating, constipation, and abdominal pain
headaches or problems sleeping
feeling cold, dizzy, or very tired
poor circulation in hands and feet
dry skin, hair loss from the scalp, or fine downy hair growing on the body
 reduced sex drive
People with anorexia often have other mental health problems, such as depression or anxiety.
Warning signs of anorexia in someone else
The following warning signs could indicate that someone you care about has an eating disorder:
dramatic weight loss
lying about how much and when they've eaten, or how much they weigh
avoiding eating with others
cutting their food into small pieces or eating very slowly to disguise how little they are
eating
trying to hide how thin they are by wearing loose or baggy clothes
In children with anorexia, puberty and the associated growth spurt may be delayed. Young
people with anorexia may gain less weight than expected and may be smaller than children of
the same age. (from https://www.nhs.uk/conditions/anorexia/symptoms)

Similarly, recent figures suggest that obesity is increasing significantly in Western cultures. In the UK,
obesity rates have increased significantly in the last 20 years, with 67% of men and 62% of women in
the UK considered to be overweight (a BMI >25, see Activity Box 10.1), and 29% of the population
considered to be obese (a BMI >30) (NHS Digital, 2019). This suggests that both undereating and
overeating have reached almost epidemic proportions, with surveys suggesting that 6.3% of the UK
population exhibit disordered eating patterns leading to either underweight or overweight (McBride,
McManus, Thompson, Palmer, & Brugha, 2013). Apart from the cultural pressures that can trigger
overeating and undereating, psychological factors also represent both risk factors and outcomes of
disordered eating. As we shall see later in this chapter, developmental and psychological processes
appear to act as vulnerability factors in the development of eating disorders, and eating disorders
themselves can result in psychological symptoms such as low self‐esteem, substance misuse, and suicidal
ideation (Neumark‐Sztainer & Hannan, 2000).
This chapter covers the three main eating disorders, namely anorexia nervosa, bulimia nervosa, and
binge‐eating disorder, and for each we discuss diagnosis and prevalence, the role of sociocultural factors,
aetiology, and treatment.

10.1 DIAGNOSIS AND PREVALENCE

10.1.1 Anorexia Nervosa

The main symptoms of Anorexia nervosa (AN) are self‐starvation and a refusal to maintain a
minimally normal body weight, and examples resembling anorexia have been reported throughout
history (see Focus Point 10.2). It is a disorder that afflicts mainly adolescent women and tends to have an
onset in early to middle teens following either a period of life stress or an intense period of dieting. Ten
times more females than males are afflicted by the disorder (Walters & Kendler, 1994), and in recent
years there appears to be an increasing trend towards early‐onset anorexia in girls between 8 and 13
years of age, with surveys indicating that almost 30% of 8–13 year‐olds report avoidant or restrictive
eating behaviour (van Dyck et al., 2013). Important features of anorexia nervosa include (a) a refusal to
maintain a minimal body weight, (b) a pathological fear of gaining weight, and (c) a distorted body
image in which, even when clearly emaciated, sufferers continue to insist they are overweight.
 Anorexia nervosa (AN) An eating disorder, the main features of which include a refusal to
maintain a minimal body weight, a pathological fear of gaining weight and a distorted body
image in which sufferers continue to insist they are overweight.

Weight loss is often viewed as an important achievement (see the example of Amy at the beginning of
this chapter), and weight gain as a significant loss of self‐control. Even when individuals suffering
anorexia do admit they may be underweight, they often deny the important medical implications of this
and will continue to focus on reducing fat in areas of their body that they still believe are too ‘fat’. Table
10.1 sets out the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM‐5) diagnostic
criteria for anorexia nervosa, and this stresses objective levels for judging the severity of the symptoms
based on BMI. DSM‐5 has adopted the World Health Organization lower limit for normal body weight
of a BMI of 18.5 kg/m2 as a level below which body weight should be considered as low enough to
trigger the possibility of a diagnosis of anorexia nervosa if other criteria are met. The criteria also
emphasise the pathological fear of weight ‐gain in sufferers and the distortions in self‐perception that
accompany anorexia. DSM‐5 also distinguishes two types of anorexia nervosa. These are the
restricting type in which self‐starvation is not associated with concurrent purging (e.g., self‐inducing
vomiting or use of laxatives), and the Binge‐eating/purging type anorexia nervosa, where the
sufferer regularly engages in purging activities to help control weight gain.

Binge-eating/purging type anorexia nervosa A type of eating disorder in which the

sufferer regularly engages in purging activities to help control weight gain.

Because of the severe physical effect of this disorder on the body, anorexia nervosa is usually associated
with a number of biological symptoms that are effects of the self‐imposed starvation regime. These
include (a) tiredness, cardiac arrhythmias, hypotension, low blood pressure, and slow heartbeats
resulting from altered levels of body electrolytes, such as sodium and potassium; (b) dry skin and brittle
hair; (c) kidney and gastrointestinal problems; (d) the development of lanugo (a soft, downy hair) on the
body; (e) the absence of menstrual cycles (amenorrhoea); and (f) hypothermia, often resulting in feeling
cold even in hot environments. In many cases, starvation has the effect of severely weakening the heart
muscles as the body uses these muscles as a source of protein. As a result, mortality rates (including
suicides) in anorexia nervosa and bulimia nervosa are still unacceptably high, ranging from 5 to 8%
(Herzog et al., 2000; Steinhausen, Seidel, & Metzke, 2000), with one in five of those deaths the result of
suicide (Arcelus, Mitchell, Wales, & Nielsen, 2011).
Anorexia nervosa begins to develop usually around adolescence. It rarely begins before puberty or after
40 years of age. Onset can be associated with a stressful life event, such as leaving home (Tozzi, Sullivan,
Fear, McKenzie, & Bulik, 2003), and is often preceded by a period of changed eating patterns, such as
self‐imposed dieting. Fortunately, most individuals with a diagnosis of anorexia nervosa will remit and
be symptom free within 5 years. However, for others, hospitalisation may be required to restore weight
and address other medical complications caused by self‐starvation.

FOCUS POINT 10.2 HISTORICAL EXAMPLES OF EATING

DISORDERS

There is a tendency to think of eating disorders as modern ailments driven by cultures obsessed
with projecting ideal body shapes to impressionable young people. However, examples of
disordered eating behaviour can be found throughout history, and many resemble the eating
disorders we find today (Keel & Klump, 2003). Cases of self‐starvation have been reported in
classical and medieval times, often as a means of achieving heightened spirituality amongst
religious devotees. Bell (1985) called this holy anorexia and cited the example of St.
Catherine of Siena who began self‐starvation at the age of 16 years and continued until her
death in 1380 (at the age of 32). Like modern‐day anorexics, St. Catherine portrayed herself as
being afflicted by an inability to eat, and all attempts by peers and superiors to induce eating in
such fasting saints usually failed. From the sixteenth to the eighteenth centuries, reports of self‐
starvation were relatively common (McSherry, 1985), with the case of Mary, Queen of Scots
(1542–1587) being a prominent one. During the nineteenth century, study of self‐starvation
became more systematic within the medical profession, with Marce (1860) describing a form of
hypochondria in which ‘young girls, who at the period of puberty and after a precocious
physical development, become subject to inappetency carried to the utmost limits’ (1860, p.
264). Probably the first use of the term anorexia nervosa was by Imbert (1840), who
characterised anorexie nerveuse by loss of appetite, refusal to eat, and emaciation (cited in
Vandereycken & Van Deth, 1994). However, while these historical examples bear a formalistic
similarity to modern eating disorders, the issue of the motivation behind self‐starvation in these
historical examples is important. At least some of the earliest examples of self‐starvation appear
to be motivated by religious and spiritual factors, while examples from the eighteenth and
nineteenth centuries were justified as either forms of convalescence or hysterical paralysis
(Habermas, 1996). However, Habermas (1989) quite rightly points out that individuals with
eating disorders tend to hide their goal of losing weight and give other explanations for their
refusal to eat. This may also be true of the historical examples we have reviewed here.

holy anorexia Self-starvation reported in classical and medieval times, often as a

means of achieving heightened spirituality amongst religious devotees.

Historical examples resembling bulimia nervosa are much rarer than those resembling anorexia
nervosa. Most examples taken from classical times through to the nineteenth century report
individuals exhibiting periods of fasting followed by a binge‐purge cycle, which suggests that
bingeing and purging was rarely found outside of the context of fasting or self‐starvation (Keel
& Klump, 2003). However, in the seventeenth century, Silverman (1987) reports a description
of fames canina—a disorder characterised by large food intake followed by vomiting (Stein &
Laakso, 1988). Interestingly, however, when symptoms similar to bulimia are reported in
historical writings, most cases involve adult men. This is quite unlike the current disorder of
bulimia, which is primarily an affliction of females.
This brief review suggests that disordered eating (especially self‐starvation) has been around as
long as people have been able to write about it and report it. In different periods of history, the
motivations for self‐starvation appear to be different, although the symptoms remain
remarkably similar. One implication of this is that disordered eating symptoms similar to
modern disorders have been around for a considerable period of history. However, changes in
contemporary sociocultural factors may influence the frequency and prevalence of such
disorders by providing a motivation for disordered eating (e.g., religious fasting would have
provided a suitable trigger for self‐starvation in vulnerable individuals in classical and medieval
times). In addition, sociocultural factors can also provide socially acceptable means of hiding
the psychological reasons for self‐starvation and loss of appetite. For example, when fasting
became an acceptable form of convalescence from illness in the eighteenth and nineteenth
centuries, this may have provided a suitable means of hiding the anorexic individual's simple
desire to restrict and control their eating (just as the trend to diet to achieve a media‐driven thin
ideal serves the same purpose today).
TABLE 10.1 Summary: DSM‐5 diagnostic criteria for anorexia nervosa

A significantly reduced calorie intake relative to the requirements of the body leading to a
considerably low body weight
Intense fear of gaining weight or becoming fat
A disruption in the way that the patient evaluates their body or shape, increasing undue influence
of body weight or shape on self‐evaluation
DSM‐5 cites the 12‐month prevalence rate for anorexia nervosa among young females as around 0.4%,
with a female‐to‐male ratio of around 10:1 making anorexia primarily a female disorder. Lifetime
prevalence rate for females by age 20‐years is 0.8%, with peak onset age 19–20‐years (Stice, Marti, &
Rohde, 2013), and recent data from an 8‐month surveillance study of young people aged 8–17 years in
the UK and Ireland suggest that the incidence of anorexia nervosa diagnosis for young women is 25.66
per 100 000, with a mean age of 14.6 years, and a ratio of women to men of 10:1 (Petkova et al., 2018;
see also Demmler, Brophy, Marchant, John, & Tan, 2020). In many cases anorexia can be a persistent
condition, and a 30‐year long‐term outcome study indicated that one in five individuals with a diagnosis
during adolescence had a chronic eating disorder 30 years later (6% anorexia, 2% binge eating, 11%
other eating disorders) (Dobrescu et al., 2020).
There is some evidence that cultural and societal factors can affect the frequency of anorexia, so that
prevalence rates may differ across cultures and across time (see Section 10.2) (Miller & Pumariega,
2001). However, recent analysis suggests that anorexia may represent a similar proportion of the general
psychiatric population in several Western and non‐Western nations, with numbers of cases increasing
significantly in Asian countries where industrialisation and urbanisation is occurring (Pike & Dunne,
2015). This converging evidence suggests that anorexia nervosa may not be just a disorder of affluent
Western cultures (Keel & Klump, 2003).
High rates of comorbidity exist between anorexia and other psychiatric disorders. For example, studies
suggest between 50 and 68% of anorexia sufferers also have a lifelong diagnosis of major depression
(Halmi et al., 1991), and between 15 and 69% of anorexia sufferers also meet diagnostic criteria for
OCD or Obsessive‐Compulsive Personality Disorder (OCPD) at some time during their life (Hudson,
Pope, Jonas, & Yurgelson‐Todd, 1983; Wonderlich, Swift, Slotnick, & Goodman, 1990). Surveys suggest
significant levels of comorbidity between anorexia nervosa and anxiety disorders such as OCD (21%),
panic disorder and agoraphobia (25%), social anxiety disorder (30%) and specific phobias (25%), and
with substance abuse disorders (34%) (Jordan et al., 2008). In addition, anorexia nervosa puts the
sufferer at significantly increased risk of a suicide attempt which is five to six times greater than the risk
for someone without an eating disorder (Udo, Bitley, & Grilo, 2019) (Photo 10.1).

10.1.2 Bulimia Nervosa

Like anorexia nervosa, bulimia nervosa (BN) is also a disorder that is characterised by fear of weight
gain and a distorted perception of body shape. The main feature of bulimia is recurrent episodes of
binge eating (often eating more than a normal person's full daily intake of food in one episode),
recurrent inappropriate compensatory behaviours to prevent weight gain (such as self‐induced vomiting
or the misuse of laxatives, diuretics, or enemas—vomiting is the most common form of purging and
occurs in 80–90% of those who present for treatment), and a self‐evaluation that is unduly influenced by
body shape and weight. The DSM‐5 diagnostic criteria for bulimia nervosa are provided in Table 10.2.
Most bulimia sufferers are not usually overweight compared to the norm for their height (Gordon,
2001), nor do they usually become underweight as a result of their purging—and this distinguishes them
from those suffering from the binge eating/purging anorexia nervosa subtype. Bulimia nervosa has a
typical onset in late adolescence or early adulthood with peak onset age between 16 and 20‐years (Stice,
Marti, & Rohde, 2013). Disturbed eating behaviour persists in many individuals diagnosed with bulimia
nervosa for several years, although long‐term follow‐up studies suggest that approximately 75% of
women with bulimia nervosa were in remission 20 years after being diagnosed (Keel, Gravener, Joiner, &
Haedt, 2010). About 90% of those suffering bulimia are female (Gotestam & Agras, 1995).

bulimia nervosa (BN) An eating disorder, the main features of which are recurrent episodes
of binge eating followed by periods of purging or fasting.
PHOTO 10.1 In 2020 award winning singer‐songwriter Taylor Swift revealed her struggle to overcome an eating
disorder. During her 2015 world tour, she revealed she actively restricted her food intake. Some days she would ‘starve a
little bit and just stop eating’. She also kept lists of everything she ate and exercised constantly until she was a size double‐
zero (size two in the UK). She struggled with this condition for several years and constantly denied having a problem when
she was confronted about her weight. These experiences are typical of someone with a restrictive eating disorder ‐ exercising
regularly specifically to lose weight, restricting food intake to the point of eating little or nothing for a whole day, and
denying any problem when confronted. Taylor Swift talks openly about these experiences in her Netflix film Miss
Americana.
Adapted from https://www.bbc.co.uk/news/entertainment‐arts‐51234055.
TABLE 10.2 Summary: DSM‐5 diagnostic criteria for bulimia nervosa

Repeated incidents of binge eating

Frequent inappropriate compensatory behaviours in order to avoid weight gain, such as self‐
induced vomiting, fasting, or excessive exercise
Binge eating and compensatory behaviours both occur on average at least once a week for 3
months
View of oneself is overly influenced by body shape and weight
Bulimia is frequently triggered by concerns about weight and body shape and may have its origins in a
period of dieting. What is perplexing about bulimia is that individuals with strong concerns about their
weight and body shape should indulge in such regular bouts of excessive overeating (between 2 and 12
bouts per week, Garfinkel, Kennedy, & Kaplan, 1995), and this suggests that they have lost control over
their eating patterns. Because of this lack of control over an area of their life that is important to them,
sufferers usually become ashamed of their binges and try to conceal them. Consequently, binges tend to
occur in secret, and take in foods that are normally quick and easy to consume, such as sweets, ice
cream, cakes, bread, and toast. Binge episodes are often well planned in advance and can be triggered
by periods of dysphoric or depressed mood, interpersonal stressors, or intense hunger following an
extended period of dietary restraint. Perhaps, at least in part, as a result of this perceived lack of control
over their eating behaviour, individuals with bulimia report high levels of self‐disgust, low self‐esteem,
feelings of inadequacy, and high levels of depression (Shisslak, Pazda, & Crago, 1990; Vanderlinden,
Norre, & Vandereycken, 1992; Carroll, Touyz, & Beumont, 1996). However, purging tends to confer
relief from the physical discomfort of binge eating and also reduces the fear of gaining weight. Because
of these reinforcing effects of purging, the act of purging (e.g., vomiting) may become a goal in itself
that reduces anxiety and depression.
Bulimia displays significantly fewer physical symptoms than anorexia, but the most common physical
sign of bulimia is permanent loss of dental enamel as a result of regular induced vomiting. In some
cases, swollen parotid glands can produce a typical puffy face appearance, and extreme eating patterns
caused by regular binging and purging can produce menstrual irregularity.
Bulimia is significantly more common that anorexia, and the lifetime prevalence rate among women is
between 1 and 3% (Gordon, 2001; Hoek & van Hoeken, 2003; Stice, Marti, & Rohde, 2013). In men,
the prevalence rate is approximately 10 times lower. Epidemiological studies suggest that the incidence
of bulimia nervosa might have decreased since the 1990s (Smink, van Hoeken, & Hoek, 2012), but this
is in contrast to a perceived increase in occurrence in the decades prior to 1990. Interestingly, in a study
of bulimia nervosa incidence in the UK from 1988 to 2000, Currin, Schmidt, Treasure, & Jick (2005)
found that rates of bulimia rose to a peak in 1996 but then subsequently declined (see Figure 10.1).
They relate these fluctuations in incidence to the press coverage given to Princess Diana's battle with
bulimia during the early 1990s and note that the decline in bulimia incidence in the UK appears to
coincide with her death in 1997. Much fewer cases of bulimia have been reported in women who have
not been exposed to some extent to Western ideals and influences (Keel & Klump, 2003). This suggests
that bulimia may be a disorder very closely linked to Western cultural ideals surrounding body shape
and eating behaviours, and so prevalence is likely to be influenced by changes in social conditions.
Bulimia nervosa is often found to be comorbid with other psychiatric disorders. Major depression is the
most commonly diagnosed comorbid disorder; with between 36 and 63% of bulimia sufferers being
diagnosed with depression (Brewerton et al., 1995). Increases in bulimia during winter months also
appear to be linked to symptoms of seasonal affective disorder (SAD) (Lam, Lee, Tam, Grewal, &
Yatham, 2001), suggesting that dysphoric mood disorder is a common concurrent symptom of bulimia.
There is also evidence for a strong link between bulimia and borderline personality disorder (BPD).
Studies have suggested that between 33 and 61% of women with bulimia meet the criteria for a
personality disorder (Schmidt & Telch, 1990; Carroll, Touyz, & Beumont, 1996). There is also strong
evidence for a link between the bulimic behaviours of bingeing and purging and substance abuse, and
with bipolar disorder (Jordan et al., 2008; Campos, Junior, Cordás, Angst, & Moreno, 2013). This
includes heavy alcohol use (Lacey, 1993), increased incidence of the use of soft and hard drugs when
compared with anorexia sufferers and nonclinical controls (Corbridge & Bell, 1996), and abuse of
laxatives, diet pills, diuretics, and emetics (Bulik, Sullivan, Epstein, & McKee, 1992). The frequent
comorbidity of bulimia with both personality disorders, bipolar disorder, and substance abuse has led to
the proposal that bulimia is part manifestation of a broader ‘multi‐impulsive’ syndrome in which the
individual finds it difficult to control many aspects of their behaviour, including eating and the use of
alcohol and drugs (Lacey, 1993; Brietzke, Moreira, Toniolo, & Lafer, 2011).
FIGURE 10.1 In the UK between the years 1988 to 2000, the incidence of anorexia nervosa remained relatively
stable, but incidence of bulimia nervosa increased from 1988 to 1996 and then subsequently decreased.
After Currin, Schmidt, Treasure, & Jick, 2005.
A detailed case history of the development of bulimia is described in Case History 10.1.

CASE HISTORY 10.1 BULIMIA NERVOSA

Sara was the youngest child in her family, with two brothers several years older than her who
both left home before she entered high school. Sara tried hard to please her older brothers even
though they teased her and would often call her names, telling her she was stupid and ugly.
Her father worked long hours as a salesman and was often away from home travelling or
staying late in the office. When Sara was 13 she discovered that her father had been having an
affair and that her mother had known of this for some years. Sara was very angry with her
father and also with her mother for allowing him to ‘get away with it’. She tried to be
supportive of her mother but felt hurt and confused, and their close relationship was damaged.
Sara didn't feel able to confide in her mother anymore and felt strong resentment towards her
father, who she could not forgive.
Over the next 2 years Sara felt increasingly isolated and unhappy at home and spent as little
time there as possible. When Sara was 16 she met her first boyfriend, Kyle, who was 4 years
older than her. At first Sara was very happy in the relationship and after 4 months she moved
out to live with Kyle. Soon, the relationship became difficult and they often argued about
money and household chores, as well as about Sara's belief that Kyle flirted with other women.
 Two years into their relationship Sara discovered that Kyle had been cheating on her with one
of her close friends. When Sara confronted him, Kyle confessed what he had done but blamed
Sara for being ‘boring’ and ‘a nag’. He told her that he had never found her attractive and had
always wanted to be with her friend instead. Sara was angry and upset but blamed herself for
not making more of an effort to be attractive.
Sara reluctantly moved back into her parents' house, although her relationship with them had
not improved in recent years. Feeling isolated and unhappy she began a crash diet and lost
some weight quickly. Her father often ridiculed her weight loss efforts while her mother
encouraged her to ‘make more of herself ’. Sara became increasingly unhappy after her initial
weight loss and became tired, irritable and preoccupied with food. One evening she saw a
Facebook update telling her that Kyle and her friend were now engaged and that her friend was
pregnant. She felt jealous and angry that all her efforts to lose weight and ‘improve herself ’ had
been for nothing. Sara stuffed herself with food until she couldn't eat any more. Feeling out of
control and ashamed she made herself vomit.
The next day she resolved to eat even less but a week later she binged again. Although she tried
to stop, Sara felt caught in a pattern and was soon bingeing several times a week. Her eating
became wildly erratic but her weight stayed much the same. Her parents didn't realize that
anything was wrong and regularly chastised her for not making more of her life, while Sara
began to feel increasingly desperate and alone and even thought of trying to kill herself.
Although she still saw her friends and was able to hold down a job, Sara was now locked into a
cycle of bingeing and vomiting known as bulimia nervosa.

Clinical Commentary
Sara’s case contains a number of elements that are typical of individuals who develop bulimia. She had
a difficult home environment and experienced teasing about her weight and appearance, as well as having
to adjust to significant changes in parental relationships. Her subsequent relationship was difficult and
when it came to an end she probably felt that she had little control over her life, and she had no obvious
means of escape from her situation. Arguments with her boyfriend had reinforced her belief that she had
‘let herself go’, and she resolved to diet to lose weight. Dieting then triggered feelings of extreme hunger
which led to binge eating following anger at her boyfriend’s infidelity. Following the binge, feelings of
self‐disgust and shame led to purging. This started a vicious cycle in which, after each binge, Sara
resolved to eat less but inevitably ended up bingeing again.

10.1.3 Binge‐Eating Disorder (BED)

Binge‐eating disorder is characterised by recurrent episodes of binge eating, but without the
associated purging or fasting associated with bulimia. As a consequence those suffering binge‐eating
disorder tend to be overweight and usually have a long history of failed attempts to diet and lose weight.
As a result, individuals with binge‐eating disorder feel a lack of control over their eating behaviours and
this causes them significant distress. Individuals with binge‐eating disorder are typically ashamed of
their eating problems and usually attempt to conceal their symptoms or eat in secrecy. Triggers for binge
eating can include interpersonal stress, dieting, negative body image, and boredom. Differentiating
between a diagnosis of binge‐eating disorder and bulimia nervosa is often difficult and depends on how
frequently the individual indulges in compensatory behaviours such as purging. Because of the overlap
in symptoms, some view binge‐eating disorder only as a less severe form of bulimia (Hay & Fairburn,
1998; Striegel‐Moore et al., 2001). Binge‐eating disorder can often be found in children and is
associated with excessive weight gain and is common in adolescents and college students (Napolitano &
Himes, 2011) (Table 10.3). Binge‐eating disorder is associated with high levels of major depression,
impaired work and social functioning, low self‐esteem, and dissatisfaction with body shape (Striegel‐
Moore et al., 2001). The lifetime prevalence of binge‐eating disorder in the general population is
around 3.0% and has a peak onset age of 16–20‐years (Stice, Marti & Rohde, 2013), and the disorder
can be as high as 30% among individuals seeking weight loss treatment (Dingemans, Bruna, & van
Furth, 2002). While the majority of sufferers are women, the incidence of binge‐eating disorder in
women is only one and a half times higher than in men (Striegel‐Moore, & Franko, 2003), with a survey
conducted in the US reporting that 3.5% of women and 2.0% of men reported binge‐eating disorder
during their lifetime (Hudson, Hiripe, Pope, & Kessler, 2007). A cross‐cultural study by Pike, Dohn,
Streigel‐Moore, Wifley, & Fairburn (2001) found that the incidences of the disorder in White and Black
American women were very similar, although Black American women appeared to show less concern
about the disorder than White American women. The case of Rosa is portrayed in Case History 10.2,
and this example illustrates many of the behavioural and cognitive traits exhibited by individuals
suffering from binge‐eating disorder [Case History 10.2] (Table 10.4).
TABLE 10.3 Summary: DSM‐5 diagnostic criteria for binge‐eating disorder

Repeated incidents of binge eating

Binge eating is accompanied by at least three of the following:
Eating quicker than usual
Eating until uncomfortably full
Eating sizable amounts of food when not feeling hungry
Eating alone due to being embarrassed by the amount of food eaten
Feeling disgusted, depressed or guilty after binge eating
Distress regarding binge eating
Binge eating is not accompanied by inappropriate compensatory behaviour as seen in bulimia
nervosa

TABLE 10.4 Other feeding and eating disorders in DSM‐5

In this chapter we discuss the three most clinically important eating disorders, namely anorexia
nervosa, bulimia nervosa and binge eating disorder. However, DSM‐5 also specifies a number of other
feeding and eating disorders that may cause distress. These include:
Pica
The persistent eating of nonnutritive, nonfood substances on a persistent basis. These might include
paper, soap, cloth, hair, ash, clay, starch, ice, wool, soil, talcum powder, paint, gum, pebbles, coal, etc.
Rumination Disorder
Repeated regurgitation of food
Avoidant/Restrictive Food Intake Disorder
Avoidant or restriction of food intake resulting in failure to meet requirements for nutrition or
insufficient energy intake. This eating disturbance may manifest as a lack of interest in food, avoidance
based on the sensory characteristics of food, or concerns about the aversive consequences of eating.
CASE HISTORY 10.2 BINGE‐EATING DISORDER

Rosa was a binge eater but had not had a food binge for over three‐and‐a‐half years when she
travelled to attend the wedding of her friend's daughter. Rosa was normally a confident,
professional woman, who enjoyed her work and had just successfully completed an important
project, which often left her feeling down and empty. She had spent 3 years attending
Overeaters Anonymous (OA) and knew she needed to avoid food—especially when she was
feeling low.
Rosa managed to keep herself occupied during the day of the wedding, but as nighttime came,
the bluster of the after wedding party made it easy for her to disappear—physically and
emotionally—into a binge. She started with a plate of what would have been an ‘abstinent’
meal (an OA concept for whatever is included on one's meal plan): pasta salad, green salad, cold
meats, and lots of bread. The food was plentiful, but Rosa still wanted more and spent the next
three‐and‐a‐half hours eating. Very soon she started to feel guilty and ashamed and began to
surreptitiously steal food from plates out of the gaze of the other guests.
When most of the guests had left the dining room she began helping herself to the cakes and
desserts. Then, beginning to feel desperate, Rosa began to pile the food high on her plate, so
that if other guests saw her she could always escape with a large amount of food. By now, the
food tasted of nothing to her, but she couldn't stop eating it. Eventually she realized what she
had been doing, felt that she was out of control, and ran crying back to her room.
This event was the beginning of a 6‐month relapse into binge eating for Rosa. During the
relapse, she binged on foods and refined carbohydrates, started smoking cigarettes in an attempt
to control the binging, and was driven to excessive exercise after each binge.
Throughout the relapse, Rosa went to therapy and to OA. Finally, a combination of
antidepressants and a structured food plan that excluded refined sugars, breads, crackers, and
similar carbohydrates helped her to bring her bingeing under control and manage her eating.
Rosa was eventually able to stop taking the antidepressants and continued to be active in OA.

Clinical Commentary
Rosa's case history is a good example of how a person can lose control of their own eating patterns and
eating behaviour. Features that are typical of binge‐eating disorder include (a) eating significantly more
than a normal meal portion in one session; (b) an uncontrollable urge to continue eating despite the
situation and surroundings; (c) forcing oneself to eat food that is unpalatable or contaminated; (d) a
desire to conceal her overeating from others; and (e) subsequent shame, self‐disgust, and depression when
the binge episode is over.
 SELF‐TEST QUESTIONS
What are the three main eating disorders defined by DSM‐5?
Can you describe the main diagnostic criteria for anorexia nervosa, bulimia nervosa, and
binge‐eating disorder?
What are the prevalence rates for the main eating disorders, and how do incidence rates
compare between males and females?
Both anorexia nervosa and bulimia nervosa are highly comorbid with other psychiatric
disorders—which ones?

SECTION SUMMARY

10.1 DIAGNOSIS AND PREVALENCE

There are three important eating disorders defined by DSM‐5: anorexia nervosa, bulimia
nervosa, and binge‐eating disorder.
The important features of anorexia nervosa are a refusal to maintain a minimal body
weight, a pathological fear of gaining weight, and a distorted body image in which
sufferers continue to insist they are overweight.
Lifetime prevalence rates for anorexia nervosa are around 0.4%
There are high rates of comorbidity between anorexia nervosa and other psychiatric
disorders such as major depression and OCD.
The main features of bulimia nervosa are recurrent episodes of binge eating followed by
periods of purging or fasting.
Bulimia nervosa is characterised by high levels of self‐disgust, low self‐esteem, feelings of
inadequacy, and high levels of depression.
The lifetime prevalence rate for bulimia nervosa amongst women is between 1 and 3%
Bulimia nervosa is often comorbid with major depression, borderline personality disorders,
and substance abuse.
Binge‐eating disorder is characterised by recurrent episodes of binge eating without the
purging or fasting that is associated with bulimia nervosa.
Binge‐eating disorder is associated with high levels of major depression, impaired work
and social functioning, low self‐esteem, and dissatisfaction with body shape.

10.2 CULTURAL AND DEMOGRAPHIC DIFFERENCES IN EATING

DISORDERS
10.2.1 Cultural Differences
A number of studies have suggested that cultural differences and cultural change may be associated
with differences in vulnerability to eating disorders and indeed may represent direct risk factors for
eating disorders (Miller & Pumariega, 2001). The cultural differences in eating disorders are most
striking in relation to bulimia. In an exhaustive study of the literature available at the time, Keel and
Klump (2003) found no studies reporting the presence of bulimia in individuals without exposure to
Western ideals and concluded that there does not appear to be a form of bulimia that is not related to
weight concerns which are generated by exposure to Western cultural ideals. That is, when individuals
from non‐Western countries such as Iran, Pakistan, Egypt, and Malaysia have exhibited symptoms of
bulimia, they have usually been exposed to Western standards through learning English, being of high
socio‐economic status, or being educated beyond secondary level.
The role of culture in the development of anorexia nervosa is complex. Even within individual Western
societies (such as the US) individual ethnic groups show differences in the prevalence of eating
disorders, and this can often be traced to differences in cultural ideals and practices. For example,
African American women are less likely than White women to have eating disorders (Lovejoy, 2001), but
both African American women and children have larger ideal physiques than their White counterparts
and are more satisfied with their own body shapes (Powell & Kahn, 1995; Thompson, Corwin &
Sargant, 1997; Neumark‐Sztainer & Hannan, 2000). As a result, African American women are more
likely to develop an eating disorder that does not involve a drive towards thinness and so tend to develop
bulimia rather than anorexia (Striegel‐Moore & Smolak, 1996). Interestingly, a study of White, Latina,
and Black American college women found that White and Latina women had slimmer personal body
shape ideals than Black women, and this difference predicted scores on eating disorder inventories
(Gordon, Castro, Sitnikov, & Holm‐Denoma, 2010). However, exposure of ethnic minorities to the
dominant thin ideal of American culture seems to be leading to increases in eating disorder prevalence
in minority ethnic groups. In the US, rates of eating disorders in immigrant Asian females and Hispanic
American women are significantly on the increase (Wax, 2000; Chamorro & Flores‐Ortiz, 2000), and
more recent studies have indicated more similarities than dissimilarities in body dissatisfaction between
ethnic groups in the US (Grabe & Hyde, 2006).
Despite these within‐culture ethnic differences in vulnerability to eating disorders, symptoms indicative
of anorexia nervosa have been reported in every non‐Western region of the world, and epidemiological
studies suggest that its prevalence may be very similar to that in Western nations (Keel & Klump, 2003).
This may well be because most countries in the world are nowadays subject to at least some Western
influence. An example of this is a study of eating disorders in Hong Kong, in which incidences of
anorexia and bulimia doubled between 1987 and 2007, along with 25% more women reporting body
dissatisfaction and fear of gaining weight (Lee, Ng, Kwok, & Fung, 2010). However, anorexia symptoms
have still been reported in individuals who could not have been exposed to Western cultural influence.
For instance, Abou‐Saleh, Younis, and Karim (1998) report a case of anorexia nervosa in an 18‐year‐old
nomadic woman from the Empty Quarter in the United Arab Emirates. The fact that cases of anorexia
are reliably reported in areas of the world where Western influences and ideals are almost nonexistent
has led Keel and Klump (2003) to suggest that contemporary Western ideals may determine some
aspects of anorexia (e.g., weight concern and body dissatisfaction), but are not necessary for producing
the self‐starving syndrome typical of anorexia. In effect, the presence of weight concerns or body
dissatisfaction does not appear to be a universal motivating factor for food refusal in anorexia.
This summary suggests that cultural factors do appear to influence the prevalence of eating disorders,
and the emphasis placed on weight concern and body shape in Western cultures is a potentially
important contributor to the development of an eating disorder. As both non‐Western countries and
ethnic minorities within Western countries become more and more influenced by Western ideals, rates
of eating disorder appear to rise in these communities. However, such Western ideals do not appear to
be a necessary condition for anorexia.
10.2.2 Demographic Factors Within Cultures
Females are 10 times more likely to develop an eating disorder than males (Striegel‐Moore, 1997) and
the reason for this sex‐linked effect appears to be the idealisation of female weight, size, and body shape
by the Western media (Harrison, 2001) (Photo 10.2). This results in female thinness becoming an
important social value that is associated with social acceptance and social rewards (Spitzer, Henderson
& Zivian, 1999). Interestingly, at a time when the populations of both Europe and the US are becoming
heavier, studies have suggested that 40% of men say their weight is ideal or they would like to gain some
weight (Bad Girls Bible, 2019)—and male body dissatisfaction is often associated with a perceived lack
of muscularity rather than obesity per se (Talbot, Smith, & Cass, 2019; Grogan, 2016). Moreover, in
recent times, the male muscular ideal body shape has been consolidated by the physiques of male movie
stars, male models, action figures, and even computer game characters (Murray et al., 2017; Martins,
Williams, Rattan, & Harrison, 2011). In contrast, females identify their ideal body weight as an average
of around 40 pounds (18 kgs) less than their actual weight (Irving, 2001). These differences in culturally
determined ideal body shape expectations appear to be in some part responsible for the sex‐related
difference in prevalence rates for eating disorders and may be related to the fact that sexual differences
between men and women are related to women being more likely to be defined by their bodies and men
more likely to be defined by their accomplishments (Frederickson & Roberts, 1997).
These differences in how the genders are defined seem to dissipate with age, and long‐term studies have
shown that at around age 40 women diet less, have fewer concerns about their body image, and fewer
eating disorders than when they were 20 years younger. One fact that reflects the importance of shape
ideals is that the incidence of eating disorders is significantly higher in groups of males whose body
weight and shape is of more significance and importance to them. For example, compared to the adult
male population, the prevalence rates for eating disorders is significantly higher in male body‐builders
(Holbrook & Weltzin, 1998), athletes (Byrne & McLean, 2002), and ballet dancers (Ravaldia et al.,
2003). Also, the instance of eating disorders is significantly higher amongst gay men than heterosexual
men (Strong, Williamson, Netemeyer, & Geer, 2000), perhaps reflecting the relative greater importance
placed on male physical appearance and attractiveness by gay subculture. Thus, even within cultures,
whenever an emphasis and importance is placed on body shape, size. and weight, the rate of eating
disordered behaviour is likely to rise within that subgroup. The fact that the media often create body
shape, size, and weight ideals that are rather extreme from the average or norm—even within these
subgroups—is simply more grist to this mill.
PHOTO 10.2 Western media regularly portray female role models as either naturally thin (and therefore representative of
only a minority of the female population) or unnaturally thin. Young adolescent females then strive to achieve these relatively
unattainable, or simply unhealthy, ideals.
 SELF‐TEST QUESTIONS
Can you describe some examples of eating disordered behaviour that has been reported
throughout history? How do these reports resemble the modern‐day symptoms of
anorexia and bulimia?
How do historical and cultural aspects of eating disorders help us to understand these
disorders?
How do the symptoms and incidences of eating disorders differ across cultures and ethnic
groups?
What are some of the reasons for eating disorders developing in men?

SECTION SUMMARY

10.2 CULTURAL AND DEMOGRAPHIC DIFFERENCES IN EATING

DISORDERS
Some of the origins of eating disorders lie in the values and ideals defined by cultures.
Examples of disordered eating can be found throughout history, but examples of bulimia
are much rarer than the self‐starvation typical of anorexia.
Changes in sociocultural factors may influence the frequency and prevalence of eating
disorders.
There is little evidence for examples of bulimia in individuals who have not had exposure
to Western ideals.
Eating disorders are less prevalent in ethnic minorities in the US, but their incidence is
increasing as these minorities are exposed to the dominant thin ideal espoused by
American culture.
Examples of the self‐starvation typical of anorexia nervosa can be found in cultures where
Western ideals are nonexistent and this suggests than anorexia may not simply be a
disorder caused by exposure to Western body‐image ideals.
Females are 10 times more likely to develop an eating disorder than males.
The importance of body shape ideals as a risk factor for eating disorders is reflected in the
fact that eating disorders in males are significantly higher in groups of males whose body
weight and shape is of more significance and importance to them (e.g., body‐builders,
athletes, ballet dancers).

10.3 THE AETIOLOGY OF EATING DISORDERS

Like so many other psychological disorders, eating disorders do not appear to be caused by one single
factor but have their origins in a range of psychological, sociological, and biological processes, all of
which appear to converge to generate the different eating disorder profiles. So broad is the range of
influences that has been identified in this aetiology that many researchers have limited themselves
simply to identifying the risk factors that predict eating disorders (e.g., Polivy & Herman, 2002; Jacobi,
Hayward, De Zwaan, Kraemer, & Agras, 2004; Ghaderi & Scott, 2001). Because of this complexity,
theories of the aetiology of eating disorders based on the description of either psychological or
biological processes are relatively underdeveloped, and there are still many gaps in our knowledge about
risk factors for eating disorders and how these risk factors interact (see Research in Clinical Psychology
10.1). As a result, we tend to have a good idea of what factors are involved in eating disorders (i.e., what
represent risk factors), but relatively little insight into how they are involved. For example, you may be
surprised to know that owning a microwave oven is a risk factor for an increase in BMI of average .78
BMI and an average increase of 2.1 kg in weight compared with someone who does not own a
microwave (Kanazawa & von Buttlar, 2019)! This relationship may seem odd unless you are also able to
understand how owning a microwave comes to predict a potential increase in weight. We can speculate
about the kinds of things that mediate this relationship (e.g., the convenience of preparing food,
consuming more calories from hot food than cold food, etc.), but we won't know what mediates this
relationship until further, more detailed, studies are carried out. And that to some extent is where we are
with eating disorders—we have a good understanding of risk factors but are less well informed about
what mediates the relationship between these factors and eating disorder symptomatology.

RESEARCH METHODS IN CLINICAL PSYCHOLOGY 10.1 KEY

GAPS IN THE RESEARCH LITERATURE ON RISK FACTORS
FOR EATING DISORDER ONSET

1. Few prospective studies have investigated factors that predict future onset of specific eating
disorders.
2. No prospective studies have investigated factors that predict future onset of diagnostic
levels of eating disorder symptoms (e.g., weekly binge eating for a period of 3 months).
3. Very few studies have examined the temporal sequencing of the emergence of empirically
established risk factors.
4. No study has provided a comprehensive test of potential interactions between a broad
range of risk factors.
5. No study has tested the ability of a multivariate interactive or mediational model of
aetiology to predict future onset of an eating disorder.
6. Research on the validity of scales used to assess putative risk factors is limited.

(From Stice, 2016)

Figure 10.2 illustrates a recent attempt to classify the risk factors for anorexia and bulimia across a
developmental timeframe, and this shows how important risk factors are at a number of different levels
of description. These include ‘prenatal’ risk factors such as gender and ethnicity, early developmental
influences that generate eating difficulties such as infant sleeping and eating patterns (Herle et al., 2020),
early experiences such as sexual abuse and physical neglect (Molendijk, Hoek, Brewerton, & Elzinga,
2017), dispositional factors such as low self‐esteem, perfectionism and negative self‐evaluation affect
(Bardone‐Cone, Lin & Butler, 2017), familial factors such as parental obesity and parental attitudes to
weight, adolescent attitudes to dieting and exercise, and comorbid psychological disorders such as OCD
and social phobia (see also Lindberg & Hjern, 2003). What you will also see from Figure 10.2 is that
different eating disorders such as anorexia and bulimia often share many of the same risk factors, and it
is not clear why an individual may develop one of these disorders rather than the other. As a
consequence it is often difficult to separate out theories of the aetiology of anorexia and bulimia, and
many of the following theories are addressed at understanding eating disorders generally rather than
individual eating disorders specifically.
In addition to simply identifying individual risk factors that predict future eating disorders, some
researchers have begun to investigate how risk factors may interact to predict the onset of eating
disorders, and this process is a first step in understanding their aetiology in terms of the potency of
individual variables and how different variables might interact with each other. For example, Stice and
Desjardins (2018) discovered that (a) low BMI was the most potent predictor of anorexia nervosa, and
body dissatisfaction amplified this predictive relationship; (b) overeating was the most potent predictor
of bulimia nervosa, and positive expectancies for thinness and body dissatisfaction amplified this
relationship; and (c) body dissatisfaction was the most potent predictor of binge‐eating disorder, and
overeating, low dieting, and thin‐ideal internalisation amplified this relationship. While still only being
findings that make prediction of eating disorders more precise, any future models of eating disorder
aetiology, no matter how complex, will have to take these findings into account.
FIGURE 10.2 Classification of the known risk factors for anorexia and bulimia across a developmental time frame.
This shows how important risk factors are at a number of different levels of description.
After Jacobi, Hayward, De Zwaan, Kraemer, & Agras, 2004.
In the following section, we look at risk factors in more detail and try as best we can to understand how
these risk factors might have their effects on the development of eating disorders.

10.3.1 Biological Factors

Biological approaches to the aetiology of eating disorders centre around genetic influences and
neurobiological factors.
Genetic influences
There is clear evidence that eating disorders do run in families, and this is consistent with there being a
genetic component to these disorders. First‐degree relatives of females with both anorexia and bulimia are
significantly more likely to develop these disorders than relatives of a group of females who have never
been diagnosed with an eating disorder (Strober, Freeman, Lampert, Diamond, & Kaye, 2000; Kassett,
Gershon, & Maxwell, 1989). Community‐based twin studies have also contributed to the view that there
is an inherited component, and these range from 28 to 74% for anorexia nervosa, 54–83% for bulimia
nervosa, and 41–57% for binge‐eating disorder (Thornton, Mazzeo, & Bullik, 2011; Trace, Baker,
Penas‐Lledo, & Bulik, 2013), and, while these estimates are quite broad, they are similar across
European and African‐American ethnic groups (Munn‐Chernoff et al., 2016). However, while twin
studies indicate a significant genetic influence, such studies also suggest the important impact of unique
environmental factors, such as interactions with parents, etc. (Baker, Mitchell, Neale, & Kendler, 2010),
and this implies that eating disorders are developed through a complex interaction between inherited
characteristics and individual experiences.
Molecular genetic studies have also attempted to identify the gene loci of these genetic effects, and
potential target genes have been identified that may influence appetite regulation (e.g., serotonergic
genes), feeding and food intake (e.g., dopaminergic genes), food reward sensitivity (e.g., genes that
influence opioid receptors), and weight regulation (Trace, Baker, Penas‐Lledo, & Bulik, 2013; Mayhew,
Pigeyre, Couturier, & Meyre, 2018). However, molecular genetic studies of eating disorders are largely
in their infancy and have been plagued by underpowered sample sizes and failed replications (Sullivan,
Daly & O'Donovan, 2012; Wang et al., 2011). Similarly, candidate gene studies have tended to focus on
genes related to homeostatic control and reward systems but have been unable to show a conclusive
association between a common single nucleotide polymorphism (a DNA sequence variation) and eating
disorders (Trace, Baker, Penas‐Lledo, & Bulik, 2013). Genome‐wide association studies (GWAS) have
found an association between variants in the Early B‐Cell Factor 1 (EBF1) gene (rs929626) whose
inactivation leads to a decrease in circulating leptin levels which is a feature associated with cognitive
changes in individuals suffering anorexia nervosa (Li et al., 2017).
Given that there is almost certainly an interaction between inherited and environmental factors in the
aetiology of eating disorders, there are some interesting findings from epigenetic studies (see Section
1.3.1 in Chapter 1 for an explanation of epigenetics). For example, starvation and weight loss are
central features of anorexia nervosa, and these strong environmental factors may trigger epigenetic
alterations. In particular, studies suggest that weight loss and starvation can cause alterations in DNA
methylation (a process that acts to repress gene transcription and expression), and this will affect a
variety of systems relevant to eating disorders, including behavioural/affective regulation, sensitivity to
nutritional insufficiencies, and body weight maintenance (Saffrey, Novakovic, & Wade, 2014;
Tremolizzo et al., 2014). Developmental experiences such as childhood adversity can also affect DNA
methylation that influences stress and bodily regulation, and this may represent an epigenetic route
which mediates the association between early childhood adversity and greater risk for eating disorders
(Perroud et al., 2011).
There may also be a shared familial factor across eating disorders suggesting that if an individual has
bulimia, this may raise the chances of a related individual not just developing bulimia, but also either
anorexia or bulimia (Kendler et al., 1991; Wade, Bulik, Sullivan, Neale, & Kendler, 2000). However,
Keel & Klump (2003) have argued that the genes contributing to anorexia may well differ from those
contributing to bulimia. This is because bulimia appears to be a culture‐bound syndrome whereas
anorexia is not (see Section 10.2), and the universal nature of anorexia suggests that there may be an
important genetic component to the self‐starvation which is the central feature of anorexia.
Neurobiological factors
Because eating disorders involve appetite, a number of theories of both anorexia and bulimia allude to
the role of those brain areas involved in regulating appetite (namely the hypothalamus), and to the
neurotransmitters associated with changes in appetite. Animal research has shown that lesions to the
lateral hypothalamus cause appetite loss resulting in a self‐starvation syndrome that is behaviourally
similar to that found in anorexia (Hoebel & Teitelbaum, 1966). However, there is good reason to believe
that lateral hypothalamus deficits are not a central causal factor in anorexia. First, animal studies show
that lateral hypothalamus lesions result in a lack of hunger—but anorexia sufferers usually experience
intense hunger even though they are starving themselves. Second, while there are hormonal imbalances
found in anorexia that are similar to those in animal studies of lateral hypothalamus lesions, these
imbalances appear to be the result of the disorder rather than a cause of it (Støving, Hangaard, Hansen‐
Nord, & Hagen, 1999).

lateral hypothalamus A part of the hypothalamus. Lesions to the lateral hypothalamus

cause appetite loss resulting in a self-starvation syndrome which is behaviourally similar to that
found in anorexia.

Combinations of brain mechanisms and reward pathways in the brain may also be involved in
generating eating disorders as a result in their role in triggering either satiation or food ‘craving’ or
‘liking’ (Berridge, Ho, Richard, & DiFeliceantonio, 2010), and we have already indicated that there may
be some genetic influence on the strength of these effects. For example, self‐starvation and maintaining
a low body weight may be reinforced by the endogenous opioids that the body releases during
starvation to reduce pain sensation (Hardy & Waller, 1988), and dieting and restrictive eating may itself
become rewarding and override the rewarding properties of foods (Walsh, 2013; Foerde, Steinglass,
Shohamy, & Walsh, 2015). In anorexia, starvation may directly increase the levels of opioids, thus
producing a state of euphoria; however, because bulimia sufferers are not necessarily overweight, this
disorder may be accompanied by low levels of opioids, and this is known to promote craving. In support
of this latter hypothesis, Brewerton, Lydiard, Laraia, Shook, & Ballenger (1992) did find low levels of
the opioid beta‐endorphin in bulimia sufferers. Nevertheless, it is still difficult to interpret the
significance of this finding because low opioid levels may be a consequence of the cravings that accompany
bulimia rather than a cause of them. Also, low levels of serotonin metabolites have been found in
individuals with a diagnosis of anorexia and bulimia (Kaye, Ebert, Raleigh, & Lake, 1984; Carrasco,
Dyaz‐Marsa, Hollander, Cesar, & Saiz‐Ruiz, 2000). Serotonin promotes satiety, and so people with low
levels of serotonin metabolites may be prone to binge eating; low levels of serotonin are also associated
with depression, so this might also be a reason why eating disorders are so often comorbid with mood
disorders such as depression. The problem with this as a cause of binge eating problems is that animal
studies have shown that enforced dieting tends to reduce serotonin functioning, so low levels of
serotonin metabolites in individuals with either anorexia or bulimia may have been caused by any prior
dieting behaviour (Chandler‐Laney et al., 2007). In the case of obese individuals and those who
experience regular urges to binge eat (both bulimia nervosa and binge‐eating disorder), evidence
suggests that at risk individuals show hyperresponsivity of brain reward circuitry to high‐calorie food
tastes, and overconsumption of high‐calorie food results in increased reward and attention region
responsivity to cues associated with intake of these high‐calorie foods (Stice & Burger, 2019). Finally,
dopamine is a brain neurotransmitter involved in the pleasurable and rewarding consequences of food,
and women diagnosed with anorexia and bulimia exhibit greater expression of the dopamine
transporter gene DAT suggesting that they might be more susceptible to the rewarding and
pleasurable effects of eating (Frieling et al., 2010; Thaler et al., 2012).

endogenous opioids A compound that the body releases to reduce pain sensation.

serotonin metabolites The products produced by the breakdown of serotonin.

 dopamine transporter genes A transporter gene allows drugs to enter cells or, in some
cases, acts to keep them out.Women diagnosed with anorexia and bulimia exhibit greater
expression of the dopamine transporter gene DAT suggesting that they might be more
susceptible to the rewarding and pleasurable effects of eating.

While most of the evidence seems to suggest that various brain areas and neurotransmitters are involved
in eating disorder symptoms, we still cannot be sure that these are genuine causal factors or whether
they are consequences of behaviours associated with eating disorders such as dieting or bingeing.

10.3.2 Sociocultural Influences

In Section 10.2 of this chapter we described how the incidence of eating disorders appears to be
importantly affected by factors associated with culture and ethnicity. Rates of both anorexia and
bulimia are higher in cultures that have experienced contemporary Western ideals and standards, and,
indeed, it is arguably the case that bulimia is found only in societies that have been exposed to Western
cultural influences (Keel & Klump, 2003). This suggests that Western cultural factors are a risk factor for
eating disorders, and it is important to identify specifically what these factors are and how they might
trigger an eating disorder.
Media influences, body dissatisfaction, and dieting
As we have pointed out, both anorexia and bulimia are disorders that are largely restricted to females
(Streigel‐Moore, 1997), and there is growing acknowledgement that the general increase in the
incidence of eating disorders over the past 20–30 years is associated with changes in the ideal female
body shape that is communicated to the female populations of Westernised societies. First, the media
are regularly accused of distorting reality by portraying female body images that are either naturally
thin (and therefore representative of only a minority percentage of the female population) or are
unnaturally thin (Polivy & Herman, 2002). This is supported by studies which show that the BMI (see
Activity Box 10.1) of Playboy centrefolds between 1985 and 1997 had continued to fall to a point where
almost 50% of the centrefolds had a BMI of less than 18—which is considered to be severely
underweight (Owen & Laurel‐Seller, 2000). This has resulted in young women adopting ideal body‐
shape goals that are achievable for only around 5% of the female population (Irving, 2001). There is
some evidence that exposure to these media‐portrayed extreme ideals is related to a drive for thinness in
young adolescent girls. For example, Tiggemann & Pickering (1996) found that body shape
dissatisfaction and a drive for thinness were significantly associated with watching certain types of TV
shows that portrayed idealised female images. Further studies have shown that body dissatisfaction is
directly correlated with the amount of time young female undergraduates spend reading magazines that
expose them to idealised female body shapes (Tiggemann, 2003) and also with the amount of time
young women spend watching music television channels such as MTV (Tiggemann & Slater, 2004).
More recently, evidence has emerged that the use of the Internet, and in particular appearance‐focussed
social media, is associated with heightened valuation of body image and eating concerns (Rodgers &
Melioli, 2016)—suggesting that the tendency of many social media users to post the most ‘perfect’
images of themselves increases body image awareness with a potential knock‐on effect to weight
concerns and restrictive eating practices on those viewing these images (Photo 10.3).
In addition, the more that young adolescents (between the ages of 14–16 years) indulge in ‘celebrity
worship’ of a media personality and perceive that personality as having a ‘good’ body shape, the more
that adolescent views their own body image as poor (Maltby, Giles, Barber, & McCutcheon, 2005).
Some experimental studies that have manipulated the viewing of videos with either idealised body
images or control images have suggested that the relationship between media presentations of idealised
body images and eating disorder symptoms, such as reduced body dissatisfaction, decreased self‐esteem,
dieting, and depression, is a causal one (e.g., Jett, La Perte, & Wanchism, 2010). However, the overall
effect sizes for these causal effects are small, suggesting that the influence of watching such media may
be relatively modest (Hausenblas et al., 2013).
Another socially‐relevant factor that may have contributed to the increase in eating disorder symptoms
over the last 30–40 years is food and eating fashions. The more that low‐calorie diets become
fashionable, the more they are likely to promote restricted eating, which is a risk factor for developing
eating disorder symptoms. For example, individuals with an eating disorder are considerably more likely
to have been vegetarian compared to controls (52% vs. 12%) (Bardone‐Cone et al., 2012), and the low
carbohydrate diets fashionable over the last 20–30 years will have contributed to increases in the
prevalence of restrictive eating practices.
As well as the exaltation of thinness, Western cultures disparage obesity and both implicitly and
explicitly associate it with negative characteristics—even though obesity is significantly on the increase
in most Western societies. Obese individuals are rated by others as less smart and more lazy and
worthless than nonobese individuals (DeJong & Kleck, 1986) ‐ even by health professionals who
specialise in obesity (Schwartz, Chambliss, Brownell, Blair, & Billington, 2003)! Jokes and cartoons that
ridicule obesity are commonplace, and this prejudice appears to be deep rooted and more acceptable
than jokes about race and disability. This will inevitably give rise to a fear of being fat or obese, which is
further grist to the mill of dieting and body dissatisfaction.

PHOTO 10.3 Social Media Is Not Real Life!. Many young women post glamourous photos of themselves on social
media platforms such as Instagram, Facebook, and Twitter. These postings influence millions of young women by showing
what appears to the perfect, glamourous, happy, fit lives of other people. But those photos of toned, tanned bodies of
beautiful people are hardly reflective of real life. Australian social media star Essena O'Neill decided to spill the beans.
What is supposed to be a spontaneous, candid selfie can take over 50 shots and a retouching app to perfect. Posting another
photo, this time of her in a bikini, she encouraged fans to ask themselves why someone would post a shot like that in the first
place. ‘What is the outcome for them? Make a change? Look hot? Sell something?’ she asked. ‘I thought I was helping
young girls get fit and healthy. But then I realised that placing any amount of your self‐worth on your physical form is so
limiting. I could have been writing, exploring, playing, anything beautiful and real…Not trying to validate my worth
through a bikini shot with no substance’. And, of a workout selfie, she wrote, "‘A 15‐year‐old girl that calorie restricts and
excessively exercises is not goals’. Social media platforms where people are either explicitly or implicitly encouraged to post
‘perfect’ pictures of themselves has become yet another form of media associated with heightened valuation of body image
and eating concerns and is likely to influence the weight concerns and restrictive eating practices of both women and men
who use social media on a daily basis (e.g., Rodgers & Melioli, 2016).
While the preceding evidence suggests that media images of idealised thin body shapes are relevant in
determining attitudes towards body shape—the question we need to ask is how this media‐based
pressure is converted into the eating problems that meet DSM‐5 criteria for a psychological disorder.
The most obvious route is that idealised media images generate dissatisfaction with the individual's own
body shape (especially in comparison to extreme ideals), and recent network analyses (see Focus Point
2.2 in Chapter 2 for an explanation of network analyses) of eating disorder symptoms indicate that
over‐evaluation of weight and shape and judging one's self‐worth largely by these factors is a central
causal feature of all eating disorders, including anorexia nervosa, bulimia nervosa, and binge‐eating
disorder (DuBois, Rodgers, Franko, Eddy, & Thomas, 2017; Solmi et al., 2018). Body dissatisfaction
is usually defined as the gap between one's actual and ideal weight and shape (Polivy & Herman, 2002),
and most theories of eating disorders implicate body dissatisfaction as an important component of the
aetiology, especially when the individual tends to judge their own self‐worth by body weight and shape
(e.g., Stice, 2001; Polivy & Herman, 1985; van den Berg, Thompson, Obremski, & Coovert, 2002;
Murphy, Straebler, Cooper, & Fairburn, 2010). Body dissatisfaction is likely to trigger bouts of dieting
in order to move towards the ideal body shape, and regular or excessive dieting is also a common
precursor to eating disorders (Polivy & Herman, 1987; Stice, 2001). Figure 10.3 provides a schematic
representation of one model describing how body dissatisfaction might be generated through media,
peer, and parental influences, and then this itself will affect dieting behaviour and eating disorder
symptomatology such as bulimia (e.g., Rogers, Chabrol, & Paxton, 2011). There is no doubt that body
dissatisfaction and dieting are important predictors of all eating disorders (Joiner, Heatherton, Rudd, &
Schmidt, 1997; Steiger, Stotland, Trottier, & Ghadirian, 1996; Stice, Shaw, & Nemeroff, 1998), but it is
important to note that they are not sufficient conditions for an individual to develop an eating disorder.
For example, (a) many individuals may believe that their actual body shape is quite disparate from their
ideal, yet be quite happy with that fact (Polivy & Herman, 2002), and (b) many individuals who express
real body dissatisfaction do not necessarily go on to develop an eating disorder. Similarly, while dieting is
usually an activity that precedes an eating disorder, many individuals who diet regularly do not go on to
develop an eating disorder. This suggests that additional psychological factors are necessary for body
dissatisfaction and dieting to develop into an eating disorder, and we discuss some of these factors in
Section 10.3.4. Nevertheless, body dissatisfaction and dieting are vulnerability factors, and this is
demonstrated in part by the fact that occupations that require an individual to control and monitor
their weight (usually through either exercise or dieting) have higher incidences of eating disorders.
These include fashion models (Santonastaso, Mondini, & Favaro, 2002), actors, athletes (Sudi et al.,
2004), figure skaters (Monsma & Malina, 2004), and ballet dancers (Ravaldia et al., 2003) (Figure 10.4).
Finally, because body dissatisfaction has been identified as a central node in network analyses of eating
disorder symptoms (meaning that it is likely to causally influence other symptoms), then it is a factor that
needs to be targeted early on in the treatment of an eating disorder (DuBois, Rodgers, Franko, Eddy, &
Thomas, 2017; Solmi et al., 2018).

body dissatisfaction The gap between one’s actual and ideal weight and shape.

dieting A restricted regime of eating, followed in order to lose weight or for medical reasons.
FIGURE 10.3 This is one model of how body dissatisfaction might mediate eating disorder symptoms and is known as
the tripartite model (van den Berg, Thompson, Obremski, & Coovert, 2002; Yamamiya, Shroff, & Thompson, 2008). In
this model, the effect of influences from media, parents and peers is mediated by internalization of social ideals and social
comparison, leading to body dissatisfaction, disordered eating and negative affect.
FIGURE 10.4 Research on female body shape dissatisfaction has demonstrated that females consistently overestimate
their own body size compared to (a) the body size that they thought that men would like most, and (b) the body size they
think that most women would like to have. Interestingly, women rated the body size they thought men would like most as
significantly slimmer than the body size that men themselves rated as most attractive.
Peer influences
Just like the media, peer attitudes and views can seriously influence an adolescent's view of their body,
their weight, and their eating and dieting activities, and adolescent girls tend to learn their attitudes to
slimness and dieting through their close contact with their peers (Levine, Smolak, Moodey, Shuman, &
Hessen, 1994). Peer pressure can influence attitudes to body shape and eating in a variety of ways. In
some cases, attitudes to eating and body shape within a peer group converge towards those that are
socially valued (such as dieting or restricted eating) (Meyer & Waller, 2001), and this convergence also
results in the group adopting psychological characteristics that may facilitate pathological eating
behaviours, such as perfectionism. A study of adolescent schoolgirls by Eisenberg, Neumark‐Sztainer,
Story, & Perry (2005) found that the use of unhealthy weight‐control behaviours (e.g., self‐induced
vomiting, laxatives, diet pills, or fasting) was significantly influenced by the dieting behaviour of close
friends, and this influence was effective in generating unhealthy weight‐control behaviours regardless of
whether the individual was overweight, normal weight or underweight. Despite these findings, it is
difficult to determine whether peer influence (a) determines attitudes towards eating and body shape (it
is possible that peer groups recruit members on the basis of shared concerns rather than directly
changing the attitudes of their members), or (b) has a significant role in the development of eating
disorders (while peer pressure can increase the tendency to diet or to be dissatisfied with one's body
shape, these factors do not automatically lead to the development of eating disorders).
Familial factors
We have noted earlier that eating disorders have a tendency to run in families, and while this may in
part be due to inherited characteristics, it may also be a result of the direct influence of family attitudes
and dynamics on the behaviour of those in the family. In particular, Minuchin (Minuchin et al., 1975;
Minuchin, Rosman. & Baker, 1978) has argued that eating disorders are best understood by considering
the family structure of which the sufferer is a part. This family systems theory view argues that the
sufferer may be embedded in a dysfunctional family structure that actively promotes the development of
eating disorders (see Dallos, 2019, for a review of Minuchin's seminal works on family systems theory).
The family structure may inadvertently, but actively, reinforce a child's disordered eating, and this can
function to distract from dealing with other conflicts within the family (such as a deteriorating
relationship between the child's mother and father). In Minuchin's view the families of individuals with
eating disorders tend to show one or more of the following characteristics: (a) enmeshment, in which
parents are intrusive, overinvolved in their children's affairs, and dismissive of their children's emotions
and emotional needs (Minuchin et al., 1978); (b) overprotection, where members of the family are
overly concerned with parenting and with one another's welfare, and this can often be viewed by the
child as coercive parental control (Shoebridge & Gowers, 2000; Haworth‐Hoeppner, 2000); (c) rigidity,
where there is a tendency to maintain the status quo within the family; and (d) lack of conflict
resolution, where families avoid conflict or are in a continual state of conflict. A study of 181 families
where one of the adolescent children had been diagnosed with an eating disorder revealed profiles of
problematic family functioning when compared with the profiles of balanced families (Cerniglia et al.,
2017). The families with eating‐disordered adolescent children reported interpersonal boundary
problems, avoidance of conflict resolution, and high scores on measures or enmeshment and rigidity, all
largely supporting the factors outlined by Minuchin's description of the dysfunctional family that is a
risk factor for eating disorders. How these characteristics of the sufferer's family influence the
development of an eating disorder is unclear, although the family may focus on the disorder once it has
developed in order to avoid dealing with other difficult and important problems within the family. The
disorder may serve a functional purpose for both the parents (by distracting attention away from other
family difficulties such as a problematic relationship between mother and father) and the eating
disordered child (as a tool for manipulating the family) (Minuchin et al., 1978). As we shall see later, the
issue of how a dysfunctional family environment may generate an eating disorder is still unclear, but it
may do so by generating specific psychological characteristics in the child that play an active role in the
acquisition and maintenance of the disorder (Polivy & Herman, 2002).

family systems theory A theory which argues that the sufferer may be embedded in a
dysfunctional family structure that actively promotes psychopathology.

enmeshment A characteristic of family systems theory in which parents are intrusive, over-
involved in their children’s affairs, and dismissive of their children’s emotions and emotional
needs.

overprotection A characteristic of family systems theory where members of the family are
overconcerned with parenting and with one another’s welfare, and this can often be viewed by
the child as coercive parental control.

rigidity A characteristic of family systems theory where there is a tendency to maintain the
status quo within the family.
 lack of conflict resolution A characteristic of family systems theory where families avoid
conflict or are in a continual state of conflict.

As an important part of the family, mothers may have a specific influence on the development of eating
disorders in their children. Mothers of individuals with an eating disorder are themselves more likely to
have dysfunctional eating patterns and psychiatric disorders (Hill & Franklin, 1998; Hodes, Timimi, &
Robinson, 1997) and these problematic maternal eating patterns appear to produce feeding problems in
their offspring at an early age (Whelan & Cooper, 2000) some of which may give rise to weight‐gain,
disordered eating and emotional problems in their offspring later in life (Easter et al., 2013; Micall, De
Stavola, Ploubidis, Simonoff, & Treasure, 2014). Mothers of sufferers also tend to excessively criticise
their daughters' appearance, weight, and attractiveness when compared with mothers of nonsufferers
(Hill & Franklin, 1998; Pike & Rodin, 1991), and there is a significant inverse relationship between a
mother's critical comments and her daughter's chances of successful recovery following treatment
(Vanfurth, Vanstrien, Martina, Vanson, & Hendrickx, 1996).
While this research strongly implicates the involvement of familial factors in the aetiology of eating
disorders, Polivy & Herman (2002) quite rightly point out that most of the studies are retrospective and
correlational in nature and so do not imply causation. There may indeed be some form of intrafamilial
transmission of disordered eating patterns within families, but it is quite likely that some other factor
(biological, psychological, or experiential) may be necessary to trigger the severe symptoms typical of a
clinically diagnosable disorder (Steiger, Stotland, Trottier, & Ghadirian, 1996).

10.3.3 Experiential Factors

There is some evidence that adverse life experiences may act as a vulnerability factor for eating
disorders and as a precipitating factor for the onset of an eating disorder. For example, Rastam &
Gillberg (1992) found that 14% of anorexia sufferers (compared with 0% of healthy controls) had
experienced a significant negative life experience (e.g., the loss of a first‐degree relative) within 3 months
prior to the onset of the disorder. Similarly, individuals with bulimia report significantly more adverse
life events prior to symptoms than age‐matched healthy controls (Welch, Doll, & Fairburn, 1997;
Carretero‐Garcia et al., 2012).
Individuals with eating disorders report significantly more premorbid life stresses and difficulties than do
healthy controls (Raffi, Rondini, Grandi, & Fava, 2000), and number of adverse life events has been
shown to differentiate between individuals with anorexia and healthy controls (Horesh et al., 1996). Like
the research on the role of familial factors, such studies are difficult to interpret because they are both
retrospective and correlational in nature.
However, one particular form of adverse life experience that has been implicated as a risk factor in
eating disorders is childhood sexual abuse. There is some evidence for higher levels of childhood
sexual abuse in the history of bulimia sufferers than in healthy controls (Steiger et al., 2000; Garfinkel et
al., 1995; Welch & Fairburn, 1994), and in anorexia sufferers than healthy controls (Brown, Russell,
Thornton, & Dunn, 1997). One longitudinal study of a large community‐based sample of mothers and
offspring has indicated that children who had experienced sexual abuse or physical neglect during
childhood were also at elevated risk for eating disorders (Johnson, Cohen, Kasen, & Brook, 2002). Given
that childhood sexual abuse is now largely accepted as a risk factor for eating disorders (Polivy &
Herman, 2002), it is difficult to determine how such early experiences facilitate the risk of developing an
eating disorder. This is complicated by the fact that childhood sexual abuse is a risk factor for a wide
range of psychiatric disorders (Chou, 2012), so we need to discover why some people with this history
specifically develop eating disorders. One possibility is that adverse early experiences generate other
forms of psychopathology that mediate the development of eating disorders (Casper & Lyubomirsky,
1997). For example, Molendijk, Hoek, Brewerton, & Elzinga (2017) found that individuals with an
eating disorder who reported childhood maltreatment were significantly more likely to be diagnosed
with a comorbid psychiatric disorder than eating disorder sufferers who did not report exposure to
childhood maltreatment. In addition, Steiger et al. (2000) reported that childhood sexual abuse only
facilitated bulimia in the presence of borderline personality disorder, and other researchers have argued
that eating disorders are a means of coping with the more generalised psychopathology (such as major
depression) that results from childhood sexual abuse and maltreatment (Rorty & Yager, 1996). This
latter view sees the development of an eating disorder as a way of helping the individual to cope with
emotional and identity problems (which may have been caused by earlier adverse life experiences). For
example, anorexia enables the individual to exert some control over at least one aspect of their life (i.e.,
their eating), in circumstances where they may have experienced very little control over many other
aspects of their life (Troop, 1998). Similarly, bulimia may also serve as a way of coping with the negative
affect caused by earlier life difficulties. Bulimia sufferers will gain emotional relief, which is otherwise
elusive, by bingeing (and then purging). Eating disorders also allow the individual to construct a
coherent sense of self by focussing attention on one limited aspect of their lives. This in turn provides
them with rewards that may otherwise have been missing from their lives (by attaining self‐determined
weight control goals) and also provides a very narrow life focus that may help them to avoid dealing with
more deep‐seated psychological issues (Polivy & Herman, 2002). Therefore, this rather interesting view
of eating disorders conceives them as means of coping with other, more global psychopathology. More
research is needed to verify this view.

childhood sexual abuse The sexual maltreatment of a child.

10.3.4 Psychological and Dispositional Factors

Individuals who develop eating disorders do appear to have particular personality and dispositional
characteristics that have been variously implicated in the aetiology of those disorders. We have so far
identified a number of risk factors for eating disorders, but none of these risk factors appears to be a
sufficient condition for developing anorexia, bulimia, or binge‐eating disorder. It may therefore be the
case that specific risk factors interact with personality traits to generate an eating disorder.
Various studies have identified personality traits that are characteristic of individuals with diagnosed
eating disorders. These traits include:
perfectionism
shyness
neuroticism
low self‐esteem
high introspective awareness (awareness of bodily sensations)
negative or depressed affect
dependence and nonassertiveness
(Vitousek & Manke, 1994; Leon, Fulkerson, Perry, & Early‐Zald, 1995). It is worth looking in more
detail at some of the more important of these characteristics.
 RESEARCH METHODS IN CLINICAL PSYCHOLOGY 10.2
FOOD PRELOAD TESTS

Laboratory procedures have been developed that provide an objective behavioural measure of
the tendency to ‘binge’ eat, and one of these is the food preload test (see Polivy, Heatherton,
& Herman, 1988).
This test begins by asking participants to eat a filling preload (e.g., a 15 oz. chocolate milkshake
or a large bowl of ice cream) under the pretence of rating its palatability.
After eating the preload and making their ratings, participants are then told they can eat as
much of the remaining milkshake (or ice cream) as they wish.
The real measure of interest is the amount of milkshake or ice cream that the participant eats
at the end of the study—this is a measure of how willing the individual is to continue eating
after having already had a full, filling portion of food.
This experimental procedure has shown that willingness to continue eating is a function of a
number of factors, including whether the individual (a) is a restrained eater (has a tendency to
dieting or has distorted attitudes about eating), (b) has low self‐esteem, and (c) is in a negative
mood. Restrained eaters will even eat more food than nondieters even if they rate the food as
relatively unpalatable.

Eating disorders are very much associated with negative affect (usually depressed mood), and mood
disorders are often comorbid with both anorexia and bulimia (Braun et al., 1994; Brewerton et al.,
1995). While negative mood and stress is a commonly reported antecedent of eating disorders (Ball &
Lee, 2000), there is some disagreement about whether negative affect is a cause or just a consequence of
the disorder. Nevertheless, negative affect has been proposed to play a number of discrete roles in the
aetiology of eating disorders. Experimental studies have indicated that induced negative mood does
increase body dissatisfaction and body‐size perception in bulimia sufferers (Carter, Bulik, Lawson,
Sullivan, & Wilson, 1996), and it may contribute in part to eating disorders through this route. Negative
mood states have also been shown to increase food consumption and bingeing in individuals who are
dieting or who have distorted attitudes about eating, and this may represent a role for negative mood in
generating the bingeing and purging patterns typical of bulimia sufferers (Culbert, Racine, & Klump,
2015; Herman, Polivy, Lank, & Heatherton, 1987) (Research Methods in Clinical Psychology 10.2). For
example, individuals with bulimia try to alleviate their negative mood by eating, and purging allows
them to use eating as a mood regulation process without gaining weight. However, when the bulimia
sufferer begins to realise that their eating is out of control, this activity no longer provides relief from
negative mood, and purging may take over as a means of relieving guilt, self‐disgust, and tension
(Johnson & Larson, 1982). This is consistent with laboratory‐based studies that show that bulimia
sufferers show reduced anxiety, tension, and guilt following a binge‐purge episode (Sanftner & Crowther,
1998). Studies such as these suggest that the negative mood possessed by individuals with eating
disorders may not simply be a consequence of the disorder but may play an active role in generating
symptoms by increasing body dissatisfaction and being involved in processes of mood regulation which
act to reinforce disordered eating behaviours.

negative affect Refers to the full spectrum of negative emotions.

A second prominent characteristic of individuals with eating disorders is low self‐esteem (Mora,
Rojo, & Quintero, 2017). This low self‐esteem may simply be a derivative of the specific negative views
that those with eating disorders have of themselves (such as being ‘fat’, having an unattractive body, or
in bulimia, having a lack of control over their eating behaviour). However, there is some evidence to
suggest that low self‐esteem may have a role to play in the development of eating disorders. First, it is a
significant prospective predictor of eating disorders in females (suggesting that it is not just a
consequence of eating disorders) (Button, Sonugabarke, Davies, & Thompson, 1996). Second, eating
disorders such as anorexia are viewed by some researchers as a means of combating low self‐esteem by
demonstrating control over one specific aspect of the sufferers own life—i.e., their eating (Troop, 1998).
In this sense, self‐esteem may be implicated in the development of eating disorders because controlled
eating is the individual's way of combating their feelings of low self‐esteem. In addition, low self‐esteem
may be an important factor in making a dissatisfaction with body shape into an indicator of general self‐
worth (‘I am dissatisfied with my body, therefore I am a worthless person’) and in such circumstances
self‐worth (and self‐esteem) can be raised only by dieting or purging to deal with the body dissatisfaction
problem.
Individuals diagnosed with anorexia, and, to a lesser extent, those diagnosed with bulimia both score
high on measures of perfectionism, and this personality characteristic has regularly been implicated
in the aetiology of eating disorders (Garner, Olmsted, & Polivy, 1983; Bastiani, Rao, Weltzin, & Kaye,
1995). Perfectionism is multifaceted and can be either self‐oriented (setting high standards for oneself) or
other‐oriented (trying to conform to the high standards set by others). It can also be adaptive (in the
sense of trying to achieve the best possible outcome) or maladaptive (in terms of striving to attain what
may well be unachievable goals) (Bieling, Israeli, & Antony, 2004; Bardone‐Cone, Lin, & Butler, 2017).
Perfectionism is a predictor of bulimic symptoms in women who perceived themselves as overweight
(Joiner, Heatherton, Rudd, & Schmidt, 1997), and both self‐oriented and other‐oriented perfectionism
have been found to be predict the onset of anorexia (Tyrka, Waldron, Graber, & Brooks‐Gunn, 2002).
Perfectionism is also one of the few personality traits that predicts the maintenance of eating disorders
at 10‐year follow‐up (Holland, Bodell, & Keel, 2013). Other research has suggested that the perfectionist
characteristics displayed by individuals with eating disorders may actively contribute to their disordered
eating. For example, Strober (1991) has argued that self‐doubting perfectionism predisposes individuals
to eating disorders. Perfectionism is highly associated with measures of body dissatisfaction and drive for
thinness (Ruggiero, Levi, Ciuna, & Sassaroli, 2003), and so it is not difficult to see how perfectionism
may be an indirect causal factor in the aetiology of eating disorders as it drives the dieter to achieve the
perfect body shape or the stringent dieting goals they set themselves (Keel & Forney, 2013). Interestingly,
perfectionism is a characteristic of many psychological disorders (Egan, Wade, & Shafran, 2011) and is
one of the best predictors of comorbidity across the anxiety disorders (Bieling, Summerfelt, Israeli, &
Antony, 2004). So, if perfectionism does play a causal role in eating disorders, we need to ask why it was
an eating disorder that developed and not any one of a number of other disorders that have
perfectionism as a prominent feature.

perfectionism The setting of excessively high standards for performance accompanied by

overly critical self-evaluation.

10.3.5 Cognitive Deficits

In general, eating disorders can be conceived as involving either too much control over eating behaviour
(e.g., anorexia nervosa) or too little control (e.g., binge‐eating disorder and the bingeing component of
bulimia nervosa), and this leads to the possibility that cognitive control of eating behaviour may be
impaired in some conditions. In the case of binge‐eating disorder (BED), there have been numerous
studies that have found associations between uncontrolled binge eating and deficits in the cognitive
processes that are required to control and regulate behaviour in accordance with internal goals. For
example, individuals with BED perform significantly worse that obese individuals without a BED
diagnosis on tests of executive functioning (Schag, Schonleber, Teufel, Zipfel, & Giel, 2013), they exhibit
ineffective inhibitory control of the prefrontal cortex that could cause uncontrolled consumption of
calories (Kamijo et al., 2012) and demonstrate a negative relation between working memory and body
weight, with working memory ability being predictive of weight loss during treatment (Dassen, Houben,
Van Breukelen, & Jansen, 2018). Other forms of cognitive deficit that have been reported in individuals
with a diagnosis of BED include (a) deficits in emotional regulation (Svaldi, Griepenstroh, Tuschen‐
Caffier, & Ehring, 2012) which means that an inability to cognitively regulate emotion may lead to the
use of other more physical methods of mood regulation such as comfort eating, (b) poor top‐down
regulation and inhibition of food cravings (Kober & Boswell, 2018), and (c) impairments of working
memory caused by increased levels of anxiety and depression in obese individuals that will inevitably
worsen executive function performance when control of eating is required (Restivo et al., 2017).
While most of these cognitive control deficits have been found in individuals with a diagnosis of BED,
they may also be a causal factor in the binge eating found in bulimia nervosa sufferers, but we await
further research to verify this possibility. One problem with the research described in this section is that
the vast majority of it merely indicates an association between cognitive control deficits and BED and
does not obviously imply a causal direction (Favieri, Forte, & Casagrande, 2019). For example, rather
than cognitive control deficits causing BED, some researchers believe that it may be an eating disorder
that causes cognitive control deficits, perhaps as a result of unhealthy Western diets having deleterious
effects on cognitive control processes by affecting brain development (Davidson, Jones, Roy, &
Stevenson, 2019). If this latter view were to be verified, then binge eating would become a vicious cycle
in which consuming an unhealthy Western diet would impair cognitive control mechanisms (perhaps
through the deleterious effects of an unhealthy diet on brain hippocampal function), and, in turn,
deteriorating cognitive control would promote uncontrolled eating behaviour and excessive weight gain.
Finally, research has recently indicated that eating disorders may be overrepresented in individuals with
cognitive neuropsychiatric conditions such as autism spectrum disorder (ASD) and attention deficit
hyperactivity disorder (ADHD). For example, a systematic review of available studies indicated that the
prevalence rate of ASD in eating disorder samples was as high as 22.9% (Huke, Turk, Saeidi, Kent, &
Morgan, 2013). A second study examined the prevalence of eating disorders in a sample of 228 young
adults with neurodevelopmental disorders such as ASD and ADHD, and 7.9% of the sample were
found to have a current or previous eating disorder (Karjalainen, Gilberg, Rastam, & Wentz, 2016).
These findings suggest that eating disorders may be overrepresented in individuals with specific
neuropsychiatric conditions, although it is certainly too early to speculate why. Further research is
required to ascertain whether this is a result of cognitive impairments or environmental factors.

10.3.6 Transdiagnostic Models of Eating Disorders

In this section on aetiology, we have seen that many of the factors that might give rise to eating
disorders can often be found as risk factors or causes across all of the eating disorders (e.g., anorexia,
bulimia, and binge‐eating disorder). This has led some researchers to suggest that there are some
processes or maintaining factors that are common across all eating disorder diagnostic categories, and
one such model is the transdiagnostic cognitive‐behavioural model (Fairburn, 2008; Fairburn,
Cooper, & Shafran, 2003). This model argues that a dysfunctional system of self‐evaluation is central to
the maintenance of all eating disorders and that self‐worth is defined in terms of control over eating,
weight, and shape, which in turn leads to dietary restraint. Other subsidiary mechanisms that operate to
maintain eating disorders in this model include low self‐esteem (which motivates people to pursue
achievement in the domain of weight and body shape), clinical perfectionism (which projects
achievement in dietary restraint as an important goal), interpersonal problems (which may lead people
to control their weight in order to facilitate interpersonal issues), and mood intolerance (which
encourages binge eating and purging as a way of coping with negative mood states). These four
additional maintaining factors will differ across individuals with different forms of eating disorder. For
example, mood intolerance will be important for bulimia sufferers but less so for anorexia sufferers.
Some recent studies have provided evidence supporting this model. For example, Lampard, Byrne,
McLean, & Fursland (2011) found that low self‐esteem was associated with overevaluation of weight
and shape which in turn was associated with dietary restraint, and interpersonal difficulties were also
associated with dietary restraint. As predicted by the model, Lampard, Tasca, Balfour, and Bissada
(2013) found that the processes of low self‐esteem, overevaluation of weight and shape, and mood
intolerance were transdiagnostic maintaining factors across all the main eating disorders. This cognitive‐
behavioural model of eating disorders has also provided the basis for the development of CBT
interventions for eating disorders that we discuss later (Fairburn, 2008; Murphy, Straebler, Cooper, &
Fairburn, 2010).

transdiagnostic cognitive-behavioural model A model of eating disorders that argues

that a dysfunctional system of selfevaluation is central to the maintenance of all eating
disorders, and that self-worth is defined in terms of control over eating, weight and shape, which
in turn leads to dietary restraint.

10.3.7 Summary
This section on aetiology has ended by concluding that a number of psychological and cognitive
processes may be important common factors in the acquisition and maintenance of all eating disorders,
and these psychological factors include the defining of self‐worth in terms of control over eating, low
self‐esteem, clinical perfectionism, interpersonal problems, and intolerance of negative moods such as
depression. Many of these psychological factors may be influenced by exposure to media ideals of body
shape, peer attitudes to controlled eating, and familial factors—such as intrafamily conflict or
dysfunctional mother–daughter interactions. Traumatic life events also appear to be risk factors for
eating disorders, and childhood maltreatment has been one specific form in which trauma has been
researched in relation to eating disorders. There is an inherited component to eating disorders, although
twin studies have tended to emphasise that unique environmental experiences are equally as important
as genes in the aetiology of eating disorders. Although a very small number of genes have been
identified that may contribute to eating disorders risk, the influence of epigenetic processes may be
more important. In these cases individual genes with eating disorder relevance may be switched on or
off depending on significant life experiences such as starvation, weight loss, or trauma. Finally, eating
disorder symptoms have been found to be associated with a number of brain mechanisms and reward
pathways, including opioid, serotonin, and dopamine pathways, but it is still unclear whether these
neurobiological processes are causes of eating disorder symptoms or are themselves consequences of
those symptoms. Similarly, deficits in the cognitive control of behaviours that may result in overeating
may contribute to conditions such as binge‐eating disorder and bulimia, but more research is needed to
determine the causal direction of these relationships.
SELF‐TEST QUESTIONS
Can you name some of the important risk factors for anorexia and bulimia?
Can you describe some of the biological factors that might be involved in the development
of an eating disorder?
What role might brain neurotransmitters play in the acquisition and maintenance of
eating disorder symptoms?
Can you name some of the important sociocultural factors that influence the development
of eating disorders? What evidence is there that these factors influence body dissatisfaction
and attitudes to dieting?
What are the important dispositional factors associated with eating disorders? Do they
have a causal role to play in the development of an eating disorder?
What are the main features of the tripartite model of eating disorders?
 SECTION SUMMARY

10.3 THE AETIOLOGY OF EATING DISORDERS

There is evidence of an inherited component to eating disorders but estimates of this
inherited component vary significantly between studies.
There is evidence of epigenetic processes operating in eating disorders, with weight loss
and starvation causing alterations in DNA methylation which affects systems relevant to
eating disorders, including behavioural/affective regulation, sensitivity to nutritional
insufficiencies, and body weight maintenance
Maintaining a low body weight may be reinforced by the endogenous opioids that the
body releases during starvation to reduce pain sensation.
The neurotransmitters serotonin and dopamine may be involved in eating disorders by
affecting satiety and the pleasurable consequences of eating.
Exposure to media‐portrayed extreme body shape ideals has been shown to increase body
dissatisfaction in young adolescent females and to increase their tendency to either diet or
purge after overeating.
Body dissatisfaction and dieting are important vulnerability factors for eating disorders.
Peer attitudes and views are an important factor in determining an adolescent girl's
attitudes to slimness and dieting.
Eating disorders have a tendency to run in families, and family systems views of eating
disorders suggest that a dysfunctional family structure may reinforce a child's disordered
eating.
Mothers may have a specific influence on the development of an eating disorder by
producing eating problems in their offspring and criticising their child's appearance.
Adverse early life experiences (such as childhood maltreatment) are a significant
vulnerability factor for later eating disorders
Negative affect, low self‐esteem, and perfectionism are all dispositional factors that have
been shown to exert a possible causal influence on the development of an eating disorder.
The tripartite model argues that the effect of influences from media, parents, and peers is
mediated by internalisation of social ideals and social comparison, leading to body
dissatisfaction, disordered eating, and negative affect.

10.4 THE TREATMENT OF EATING DISORDERS

Eating disorders are complex and difficult to treat, but clinical psychologists have been actively
developing a range of treatments many of which show promising results. However, before we discuss
some of these treatment methods, it is important to describe some of the challenges that face any
intervention for eating disorders. First, many individuals with eating disorders regularly deny they are ill
or have a disorder. Indeed, many individuals with bulimia see their bingeing and purging eating patterns
as a positive way of controlling weight, and there has been a recent burgeoning of websites extolling the
virtues of bingeing and purging as a way of life (Table 10.5). Similarly, individuals with anorexia
regularly deny they are pathologically underweight, and the fact that they may view their controlled
eating as a way of coping with more general psychopathology means that it is often viewed as an
activity that has benefits rather than costs (Rorty & Yager, 1996). Because of these factors between 70 to
90% of individuals with diagnosable eating disorders tend not to be in treatment (Fairburn, Welch,
Norman, O'Connor, & Doll, 1996). Second, individuals with severe eating disorders usually need
medical as well as psychological treatment, and in the case of anorexia, hospitalisation and a period of
remedial medical treatment is often necessary to increase weight, rectify body electrolyte imbalances,
and, in many cases, prevent death by self‐starvation before some of the significant psychological factors
can be addressed. Third, eating disorders are often highly comorbid with other psychological disorders
which may make treatment difficult and complex. For example, anorexia and bulimia are often
comorbid with major depression and OCD, and some psychological treatments for anorexia have
included components used to treat obsessions and compulsions (such as response prevention and
exposure methods, see Chapter 6) (e.g, Wilson, Eldredge, Smith, & Niles, 1991). Similarly, treatments for
eating disorders sometimes work better with a concurrent antidepressant drug (Marvanova & Gramith,
2018). In addition, there is growing evidence that anorexia and bulimia may be comorbid with
personality disorders such as obsessive‐compulsive personality disorder, borderline personality disorder,
and avoidant personality disorder (Carroll, Touyz, & Beaumont, 1996; O'Brien & Vincent, 2003;
Martinussen et al., 2017), and personality disorders of this kind are themselves quite resistant to
treatment (see Chapter 12).
TABLE 10.5 Treating bulimia can be difficult because many individuals with bulimia see their bingeing and purging
eating patterns as a positive way of controlling weight, and there has been a burgeoning of websites extolling the virtues of
bingeing and purging as a way of life.

ok so last night i was purging ya know and i kinda came out with more force that i was expecting
well anyway i leaned closer and actually only go half in the toilet. The other half down the side
and on my sock and the floor. i spent forever cleaning up but my mum found the leftovers and
asked if i was sick i said no i think she bought it but she'll be on the look out so how can i hide it
better? Seriously i need help!
i really don't want you to become bulimic because it makes you feel awful, you get headaches,
light‐headedness, irregular heartbeats and you can rip your throat and you burst blood vessels and
all this bad stuff. However, if you do start, to save you a lot of pain, make sure you drink lots of
water with everything, and diet coke is good too. Don't try and purge orange juice because it
hurts like hell. Make sure you chew everything thoroughly too, otherwise it can get stuck in your
throat. And if you see blood when you purge, it is not a good sign and you should stop for a while.
ok im so sure someone would have to have an answer for me … ok so i'm really good at making
myself sick … but 4 the last 2 days i cant get anything up … its nasty tho bc i definatly get dry
heaves and i gag for about 10 minutes at a time … and the last time i tried it i was choking … i
could still breath but i was gasping … i freaked myself out … and i know to chew really well and
all that, so i know thats the problem … u think its because my esophagus is irritated or something
like that?? please give me a bit of advice… thanks
Why is it that I can go without food for most of the day and then when it comes to the evening I
go totally crazy and binge, then afterwards I feel really bad and hate myself and vow never to eat
that much again, but I always do. Can somebody please give me some ideas on how to stop
binging? I'd really appreciate it.
after you eat would you go to the bathroom? I am relatively new at it but have had some luck but
just not as much coming up as I thought. How soon after and how long would you do it for?
In the table are some examples that illustrate how bulimia sufferers will actively swap experiences, information about
the best ways of purging, and how best to conceal their activities.
In the following sections, we describe and discuss the main forms of treatment that have been used for
eating disorders. These are pharmacological treatments, family therapy, and CBT. The UK National
Institute for Health and Care Excellence (NICE) recommends a number of different treatments
depending on the nature of the eating disorder (NICE, 2017). For anorexia nervosa in adults these
include individual eating‐disorder‐focussed CBT (CBT‐ED), the Maudsley Anorexia Nervosa
Treatment for Adults (MANTRA), and specialist supportive clinical management (SSCM); for bulimia
nervosa and binge‐eating disorder the recommendations are CBT‐ED and guided self‐help
programmes. Self‐help programmes are an important component of the treatment provision for both
bulimia and binge‐eating disorder, and bulimia self‐help groups that use structured manuals and
require minimum practitioner management can show significant treatment gains—especially when
these help the patient to identify triggers for bingeing and develop preventative behaviours for purging
(Cooper, Coker, & Fleming, 1994). They can be equally or more effective than CBT in establishing
remission from bingeing and purging symptoms (Bailer et al., 2004; Priemer & Talbot, 2013).
Alternative delivery systems do allow access to services for sufferers who might, for whatever reason, not
receive other forms of treatment. These include treatment and support via telephone therapy, email, the
Internet, computer‐software CD‐ROMs, and virtual reality techniques (see Chapter 4, Section 4.1.2),
and assessment of the effectiveness of these methods is encouraging (Myers, Swan‐Kremeier,
Wonderlich, Lancaster, & Mitchell, 2004; Wagner et al., 2013) (Table 10.6).
Pharmacological treatments
Because both anorexia and bulimia are frequently comorbid with major depression, eating disorders
have tended to be treated pharmacologically with antidepressants such as fluoxetine (Prozac) (Kruger &
Kennedy, 2000). There is some evidence that such treatment can be effective with bulimia when they
are compared with placebo conditions, but this evidence is still far from convincing (e.g., Grilo et al.,
2007). Some studies have indicated a modest reduction in the frequency of bingeing and purging with
such antidepressants compared to placebo controls (e.g., Wilson & Pike, 2001; Bellini & Merli, 2004),
but dropout rates can still be unacceptably high (Bacaltchuk & Hay, 2003). More significant treatment
gains are reported if antidepressant medication is combined with psychological treatments such as CBT
(Pederson, Roerig, & Mitchell, 2003). The benefits with joint drug and CBT programmes appear to be
reciprocal in that CBT helps to address the core dysfunctional beliefs in bulimia (see below), and
antidepressant drug treatment appears to reduce the tendency to relapse following cognitive behavioural
treatment (Agras et al., 1992). CBT plus antidepressants can also be effectively used in a stepped‐care
approach in which CBT comprises the initial step with the addition of fluoxetine for nonresponders
after six sessions (Mitchell et al., 2011).
TABLE 10.6 NICE guidelnes for use of CBT‐ED with anorexia nervosa
Individual CBT‐ED programmes for adults with anorexia nervosa should:

typically consist of up to 40 sessions over 40 weeks, with twice‐weekly sessions in the first 2 or 3
weeks
aim to reduce the risk to physical health and any other symptoms of the eating disorder
encourage healthy eating and reaching a healthy body weight
cover nutrition, cognitive restructuring, mood regulation, social skills, body image concern, self‐
esteem, and relapse prevention
create a personalised treatment plan based on the processes that appear to be maintaining the
eating problem
explain the risks of malnutrition and being underweight
enhance self‐efficacy
include self‐monitoring of dietary intake and associated thoughts and feelings
include homework, to help the person practice in their daily life what they have learned.
Pharmacological treatments with anorexia have tended to be significantly less successful than with
bulimia, but the studies assessing drug treatment with anorexia has been relatively limited in number
(Pederson, Roerig, & Mitchell, 2003; Claudino et al., 2006). Antidepressants would rarely be used as the
sole intervention for anorexia but might be helpful in preventing relapse and improving anxiety and
depression symptoms (Marvanova & Gramith, 2018). Nevertheless, outcome studies so far have found
very little effect of antidepressants on either weight gain in anorexia or significant changes in other core
features of the disorder, such eating attitudes, or body shape perceptions (Attia, Haiman, Wals, & Flater,
1998; Biederman et al., 1985). Pharmacological treatments of eating disorders also have the added
disadvantage of higher dropout rates from treatment than psychological therapies (Fairburn & Wilson,
1992) and also have a number of physical side effects.

Family therapy
One of the most common therapies used with eating disorder sufferers—and particularly anorexia
sufferers—is family therapy. This stems mainly from the theories of Minuchin (Minuchin et al.,
1975; Minuchin, Rosman, & Baker, 1978—see Dallos, 2019), whose family systems theory view argues
that the sufferer may be embedded in a dysfunctional family structure that actively promotes the
development of eating disorders (see Section 10.3.2). In particular, this view argues that the eating
disorder may be hiding important conflicts within the family (such as a difficult relationship between the
sufferer's parents), and the family may be implicitly reinforcing the eating disorder in order to avoid
confronting these other conflicts. As we noted in Section 10.3.2, the families of individuals with eating
disorders exhibit the characteristics of enmeshment, overprotectiveness, rigidity, and lack of conflict
resolution, and family therapy can be used to unpack and address these dysfunctional family
characteristics. Treatment in Practice Box 10.1 is an example of how family therapy is applied in the
context of an adolescent family member with anorexia. This example shows how family therapy can be
used to explore concerns about relationships and emotional expression within the family, as well as
individual feelings of failure, shame, and guilt. Exploring these issues throws up other conflicts and
difficulties within the family and how the anorexia sufferer may see themselves as trapped within these
existing relationships and conflicts (Dallos, 2004).

CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 10.1

FAMILY THERAPY FOR EATING DISORDERS

Sandy is 17 and for 2 years had been suffering with anorexia of such severity as to require two
brief stays in hospital. She was living with her parents and older brother. Two older brothers
had left home.
Though all were invited only Sandy and her parents attended for family therapy which took
place at intervals of 3–4 weeks over 18 months. The sessions, with the full permission of all of
the family were of 1‐hour length with the therapist in the room with them and a team
observing from behind a one‐way mirror. The team usually joined the family and the therapist
after 40–50 minutes and held a reflective discussion with each other in front of the family in
which they shared their ideas about the family's problems, ideas, understandings, and feelings.
The family were then invited to comment and then held a closing discussion with the therapist
when the team had left the room. The core idea of family therapy is that problems such as
anorexia are not simply, or predominantly individual but are related to wider stresses and
distress the family are experiencing. In addition it is recognised that the sense of failure and
blame associated with conditions such as anorexia can paralyse families' abilities to help each
other.
Initially each member of the family was asked to describe what they saw as the main problems
 and invited to offer their explanations of the causes of the problem. This was followed by a
focus on two broad areas: (a) the impact of the problems on each of them and their
relationships with each other, and, in turn (b) the influence that they could exert on the nature
of the problems. Initially the parents indicated that the distress caused by Sandy's anorexia was
the main problem for all of them. However, it quickly emerged that the parents had very
different ideas about what caused the problems and what to do to help. Mr. Sinclair had a
medical and practical view and Mrs. Sinclair a more relational and emotional one. Through the
use of a genogram (family tree) it was revealed that both parents had themselves had very
negative experiences of being parented that made it hard for them to know how to comfort and
help their children. It also transpired that their marriage was in serious difficulty. Sandy
commented that her parents' conflicts upset her and she felt caught in the middle in trying to
meet the emotional needs of both of her lonely parents. In effect she felt like she was a therapist
for her own family (Interestingly, she has gone on to study psychology at university).
The therapist and the reflecting team discussed the possible impacts that the parents' own
experiences may have played on how they acted towards Sandy. Along with this there were
discussions of a variety of related issues, such as the pressure on young women to confirm to
stereotypes of thinness and starving as an attempt to exert control in one's life. Some marital
work was done separately with the parents to look at their childhoods, their marriage, their own
needs and how these affected Sandy. Mrs. Sinclair in particular felt she had failed as a mother
but was relieved to hear that the team did not see it in this way. Sandy gained considerable
insight into how the family dynamics across the generations had impacted on her and her
parents. She became independent enough to go to university but initially struggled to separate,
as did her parents. Some struggle with her weight continues but she is confident that she will
cope in the long term.
Case history provided by Dr. Rudi Dallos, Consultant Clinical Psychologist (Somerset
Partnership Trust) and Director of Research, Clinical Psychology Teaching Unit, University of
Plymouth

(from Davey, 2004)

A more recent family‐based therapy for eating disorders is the Maudsley Approach, which has a
number of stages beginning with a stage which focuses on how the family can help solve the problems
they are facing, a second stage which helps the family to challenge the eating disorder symptoms, and a
third stage which develops family relations and activities once recovery from eating disorder symptoms
has occurred (Eisler, 2005; Lock et al., 2010).

Maudsley Approach Family based, staged therapy for eating disorders.

However, while there is significant support for the use of family therapy in eating disordered individuals
—especially those with a diagnosis of anorexia nervosa (e.g., Rosman, Minuchin, & Liebman, 1975),
well‐controlled treatment outcome research remains somewhat limited (Cottrell, 2003; Downs & Blow,
2013).
The Maudsley Anorexia Nervosa Treatment for Adults (MANTRA)
The MANTRA model is a treatment programme for anorexia nervosa developed at the Maudsley
Hospital in London and has been recommended as a first‐line treatment by NICE since 2017. This
model suggests that anorexia typically develops in people with anxious, perfectionist and obsessional
personality traits at times of stress or increased developmental demands, and dietary restriction becomes
a way of managing negative emotions and coping with stress (Schmidt & Treasure, 2006). In the
MANTRA model treatment targets are key anorexia nervosa maintaining factors including (a) a
thinking style characterised by rigidity, detail focus, and fear of making mistakes; (b) an inexpressive,
avoidant emotional and relational style; (c) positive beliefs about the utility of anorexia for the
individual; and (d) the response of close others (especially family members) characterised by high
expressed emotion (criticism and anger) and enabling and accommodating the eating disorder. The
treatment model is supported by recent evidence that MANTRA results in significant improvements in
BMI and reduction in eating disorder symptoms and distress levels (Schmidt et al., 2015).
Cognitive behaviour therapy (CBT)
The treatment of choice for bulimia is generally considered to be CBT. The UK NICE guidelines for
the treatment of eating disorders makes its strongest recommendation for the use of CBT with bulimia,
usually for 16–20 sessions over a 4–5 month period (Wilson & Shafran, 2005). CBT for bulimia is based
on the transdiagnostic cognitive model developed by Fairburn and colleagues (Fairburn, Shafran, &
Cooper, 1999, see Section 10.3.6). According to this model, individuals with bulimia have a long‐
standing pattern of negative self‐evaluation that interacts with concerns about weight, shape, and
attractiveness. Such individuals come to evaluate their worth solely in terms of their weight and shape—
largely because this is often the only area of their lives that they can control. They develop idealised
views of thinness that are often unachievable and as a result end up in a constant state of dissatisfaction
with their body shape and their weight. This leads them to excessive dieting, and as a result of this
dietary restriction they lapse into episodes of bingeing. This in turn invites the use of weight
compensation methods such as vomiting and laxative abuse. Each episode of bingeing and purging is
followed by a more determined effort to restrict eating which leads to an ever vicious cycle of bingeing
and purging (see Figure 10.5). Treatment in Practice Box 10.2 shows the three stages of CBT that are
required to deal with both the symptoms of bulimia and the dysfunctional cognitions that underlie these
symptoms. These cover (a) meal planning and stimulus control, (b) cognitive restructuring to address
dysfunctional beliefs about shape and weight, and (c) developing relapse prevention methods. In stage 1,
individuals are taught to identify the stimuli or events that may trigger a binge episode (such as a period
of stress or after an argument with a boyfriend or parent),and are also taught not to indulge in extremes
of eating behaviour (e.g., dieting and bingeing) and that normal body weight can be maintained simply
by planned eating. In stage 2, dysfunctional beliefs about weight, body shape, and eating are identified,
challenged, and replaced with more adaptive cognitions. For example, beliefs that relate eating and
weight to self‐worth, such as ‘no one will love me if I am a single pound heavier’ are challenged. In
stage 3 relapse prevention is often encouraged with the use of behavioural self‐control procedures that
enable the individual to structure their daily activities to prevent bingeing and purging, and rewarding
oneself for ‘good’ behaviours (e.g., sticking to a planned eating programme).
FIGURE 10.5 Wilson, Fairburn, and Agras' (1997) cognitive model of the maintenance of bulimia and on which
contemporary CBT for bulimia is based. Low self‐esteem leads to concerns about weight, followed by dietary restriction,
which—when such dieting fails—leads to binge eating and subsequent purging. Following purging, individuals become
more determined to restrict eating, and a vicious cycle is established that maintains the bingeing‐purging pattern.
 CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 10.2
THE THREE STAGES OF CBT FOR BULIMIA NERVOSA

STAGE 1 (3–9 WEEKS)

The cognitive model is explained to clients, and they learn to control eating and reduce
dietary restraint.
Clients learn to control eating by discovering what factors trigger bingeing (e.g., periods of
stress or arguments with partners or parents). This is achieved with the use of a diary that
allows the client to discover consistencies between life events and bingeing.
Clients are taught techniques such as stimulus control and meal planning.
Stimulus control is where the client is allowed to eat, but only in certain specified
environments (such as their kitchen) or at specific times (e.g., after work). Eventually eating
behaviour is controlled only by these stimuli, and is not triggered at all times in all places.
Meal planning involves ensuring that small, acceptable meals are planned are eaten every
day. Reductions in binge eating and purging usually follow the regularization of eating
patterns.
STAGE 2 (ABOUT 8 WEEKS)
Clients are taught to identify their thoughts and beliefs about eating and their weight and
to challenge dysfunctional and inappropriate beliefs and thinking patterns.
The therapist will help to foster healthy ways of thinking about eating and will also address
issues about low self‐esteem, and how dysfunctional attitudes that might link weight and
self‐worth are irrational (e.g., ‘no one will love me if I am a single pound heavier’).
STAGE 3 (ABOUT 4 WEEKS)
Clients are taught various techniques to help prevent relapse.

Outcome studies indicate that CBT of bulimia is successful in reducing bingeing, purging, and dietary
restraint, and there is usually an increase in positive attitudes towards body shape (Compas, Haaga,
Keefe, Leitenberg, & Williams, 1998; Richards et al., 2000). In addition, follow‐up studies suggest that
therapeutic gains can be maintained for up to 5 years following treatment (Fairburn et al., 1995).
Importantly, when CBT is effective it has been found to significantly reduce not only the behavioural
aspects of bulimia such as bingeing and purging (Agras, 1997; Wilson, Fairburn, & Agras, 1997) but also
has beneficial effects on core ‘cognitive’ aspects of bulimia such as beliefs about dietary restraint and
low self‐esteem (Anderson & Maloney, 2001). CBT has also been shown to be a more comprehensive
treatment of bulimia than antidepressant drugs (Whittal, Agras, & Gould, 1999), and other
psychotherapeutic interventions such as psychodynamically oriented therapy (Walsh et al., 1997) and
interpersonal psychotherapy (Wilson, Fairburn, Agras, Walsh, & Kraemer, 2002). When effective, CBT
also reports immediate improvement, including 76% of clients showing an improvement in the
frequency of binge eating and 69% showing improvement in the frequency of purging within 3 weeks
of the start of treatment (Wilson et al., 1999). Much of this rapid improvement can be ascribed to the
behavioural homework assignments that are a unique feature of CBT and which appear to help
alleviate depression and enhance self‐efficacy (Burns & Spangler, 2000; Fennell & Teasdale, 1987).
An ‘enhanced’ form of CBT has been developed for use with all forms of eating disorder (labelled
Enhanced Cognitive Behavioural Therapy for Eating Disorders or CBT‐E) and uses
strategies and procedures to address the over‐evaluation of shape and weight in eating disorder sufferers
by focussing on targeting these cognitive mechanisms (de Jong, Schoorl, & Hoek, 2018), and this can be
helpful with sufferers who are significantly underweight (e.g., anorexia nervosa sufferers) by increasing
their motivation to change and then helping them to regain weight while at the same time addressing
psychological issues relating to shape and weight (Cooper & Fairburn, 2011). Preliminary outcome
studies with anorexia sufferers suggest that a majority were able to complete this enhanced programme
with a substantial increase in weight and reduction in eating disorder symptoms (Fairburn et al., 2013),
and Table 10.6 lists the NICE guidelines for use of CBT‐ED with anorexia nervosa.
Prevention programmes
Finally, clinicians are aware of the importance of prevention programmes that put eating disorders
into a social context and try to prevent eating disorders occurring. School‐based prevention programmes
attempt to (a) educate vulnerable populations about eating disorders, their symptoms, and their causes;
(b) help individuals to reject peer and media pressure to be thin; and (c) target risk factors for eating
disorders such as dieting, dissatisfaction with body image, etc. In a review of effective prevention
programmes, Stice, Becker, and Yokum (2013) identified two contemporary prevention programmes
whose effectiveness could be empirically verified. These were the Body Project intervention (in which
young women critique the thin‐ideal in a series of exercises) (Stice, Rohde, & Shaw, 2012;
www.bodyprojectsupport.org), and the Healthy Weight intervention which attempts to improve dietary
intake and physical activity (Stice, Trost, & Chase, 2003). The most effective prevention programmes
have been found to be those that are the most interactive and selectively target individuals at high risk
for eating disorders (Stice, Shaw, & Marti, 2007). Future developments in prevention programmes will
probably need to extend the number of risk factors that they target (i.e., not just body dissatisfaction but
also dieting and negative affect), and also consider ways in which they can incorporate the prevention of
both eating disorders and obesity into individual programmes (see Khanh‐Dao Le, Barendregt, Hay, &
Mihalopoulos, 2017, for a recent review).

prevention programmes Intervention programmes that attempt to prevent the onset of a

psychopathology before the first symptoms are detected.

SELF‐TEST QUESTIONS
Can you name the three main forms of treatment for eating disorders? Which ones are
more suited to bulimia or to anorexia, and why?
What is the rationale for adopting a CBT approach to the treatment of bulimia nervosa,
and what are the important stages of this treatment?
How successful are pharmacological interventions in the treatment of eating disorders?
What are the main features of family therapy for eating disorders?
 SECTION SUMMARY

10.4 THE TREATMENT OF EATING DISORDERS

Eating disorders are often difficult to treat because of the denial by sufferers that they have
a disorder, the medical implications of the symptoms, and comorbidity with other
psychological disorders.
There is evidence that self‐help groups, alternative delivery systems, and school‐based
prevention programmes may be helpful in lowering the prevalence of eating disorders.
The major depression that is often comorbid with eating disorders can be treated
pharmacologically with antidepressants such as fluoxetine.
One of the most common treatments for eating disorders is family therapy, in which the
family's role in developing and maintaining an eating disordered individual is explored.
Enhanced Cognitive Behaviour Therapy (CBT‐E) can be an effective treatment for
anorexia and bulimia and attempts to deal with the dysfunctional cognitions associated
with disordered eating, and provide prevention against relapse.
The Maudsley Anorexia Nervosa Treatment for Adults (MANTRA) is a treatment
programme for anorexia nervosa developed at the Maudsley Hospital in London.

10.5 EATING DISORDERS REVIEWED

This chapter has reviewed the three main eating disorders—anorexia nervosa, bulimia nervosa, and
binge‐eating disorder. All of these disorders are characterised by dysfunctional eating patterns. Anorexia
represents an extreme form of self‐starvation while bulimia and binge‐eating disorder are characterised
by the individual's loss of control over their own eating patterns. In the case of bulimia, the individual
attempts to compensate for frequent binge eating by purging and fasting. The individual with binge‐
eating disorder binges without compensatory behaviour and so frequently ends up overweight or obese.
All these disorders share some common factors, including a predominance of female rather than male
sufferers, fear of weight gain, the individual's dissatisfaction with their own body shape, and other
comorbid psychopathology symptoms such as major depression. The section on aetiology shows that
these three eating disorders often share similar risk factors (see Figure 10.2), and that sociocultural
values relating to body shape ideals may play a role in initiating weight‐regulating behaviours in
vulnerable individuals. However, we still know very little about why one vulnerable individual will
become anorexic and another bulimic, but there are some theories, such as the transdiagnostic
behavioural model, which are attempting to understand these developmental processes. Treatments for
eating disorders are still at some early stages of development and refinement. Some forms of CBT have
been adapted to treating bulimia with some moderate success, and an enhanced form (CBT‐E) is
available for use with anorexia nervosa. Family therapy has been shown to be of particular help to
individuals with anorexia, but success rates are still modest. In the meantime antidepressants, such as
selective serotonin reuptake inhibitors, may provide some short‐term relief for the depression that is
often comorbid with eating disorders, and can be used in conjunction with psychological and family
therapies.
This book is accompanied by Student and Instructor companion
websites.
www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter References
Videos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
11
Sexual Problems

ROUTE MAP OF THE CHAPTER

This chapter covers the topics of sexual dysfunction and paraphilic disorders. The section on
sexual dysfunctions describes the various disorders of the sexual cycle, and considers aetiology
and a range of treatment options. Paraphilic disorders are largely disorders of male sexual
function, and are often associated with sexual offending. The various paraphilic disorders are
described and evidence for theories of aetiology is assessed. Finally, we cover some of the
aspects of treating paraphilic disorders, including the difficulties of treating those who are
sexual offenders.

CHAPTER OUTLINE
11.1 DEFINING PATHOLOGICAL SEXUAL BEHAVIOUR
11.2 SEXUAL DYSFUNCTIONS
11.3 PARAPHILIC DISORDERS
11.4 SEXUAL PROBLEMS REVIEWED

LEARNING OUTCOMES
When you have completed this chapter, you should be able to:
1. List the various types of sexual dysfunction and their place in the sexual cycle, and
describe their diagnostic criteria.
2. Compare and contrast various theories of the aetiology of sexual dysfunctions.
3. Describe and evaluate both psychological and biological treatments for sexual
dysfunctions.
4. Describe the basic characteristics of paraphilic disorders and their diagnostic criteria.
5. Describe and evaluate both psychological and biological explanations for the aetiology of
paraphilic disorders.
6. Describe and evaluate behavioural, cognitive, and biological treatments for paraphilic
disorders.
7. Discuss some of the conceptual and ethical issues involved in defining and diagnosing
sexual and gender identity problems.
 ‘So, I have kind of a weird problem here. Normally, getting an erection is no problem for me. I wake up with one
every morning, masturbate all the time, sometimes pop them up at inopportune moments, etc. I'm 21, by the way.
Also in most sexual encounters there's no problem. I'd say 90% of the time. However, the problem arises (or fails
to arise!) when I'm in bed with someone I'm extremely attracted to and very interested in. To date this has only
happened with two men, but it is happening with the second of those two people right now and it's driving me
crazy. Things will start out fine (i.e., erect) and I can be rolling around in bed with an erection for an hour, but it
seems that as soon as it's time for my penis to do its duty (that is when foreplay ends and penetration commences),
it deflates and vehemently refuses to be resuscitated. I don't know what to do! It's unendingly embarrassing, but
the worst is that it only occurs with people I really like’.
James' Story

Introduction
Sexual behaviour plays a central role in most of our lives. It is a very personal and individual topic that
we very rarely discuss openly with others. Sexual development is also an important part of our lives,
where we learn about the nature of sexual behaviour and develop our own personal likes and dislikes
about sexual activities. Furthermore, during adolescence and early adulthood, sexual performance is
often related to self‐esteem and so becomes an important contributor to psychological development.
The importance of sexual behaviour and the critical role it may play in many of our relationships
means that it can regularly affect psychological functioning and quality of life generally. There is no
definition of what is sexually ‘normal’, but clinical psychologists may become involved when an
individual becomes distressed by their sexuality or their sexual activities or when these cause interpersonal
difficulties. James story is one of problematic sexual performance, where his normally active libido fails
him just prior to intercourse with men he particularly likes. This provides a simple example case that
clinical psychologists are likely to encounter when sexual performance has an impact on psychological
well‐being, causing anxiety and distress, and feelings of guilt, shame, and depression.

11.1 DEFINING PATHOLOGICAL SEXUAL BEHAVIOUR

As you can imagine, what constitutes a sexual dysfunction is not a simple matter. Opinions about what is
morally and socially acceptable and unacceptable change within societies over time, and there are
significant differences between cultures in the implicit rules that constitute acceptable public behaviour.
For example, until 1973 the Diagnostic and Statistical Manual of Mental Disorders (DSM) listed homosexuality
as a sexual disorder, along with paedophilia, sadism etc., but it is now considered a perfectly normal
form of sexual activity in most Western societies. The actual nature of the sexual activity per se does not
constitute grounds for labelling it as pathological, and people differ significantly in the range of stimuli
that trigger sexual urges or fantasies. However, two factors are important when attempting to identify
psychopathology in sexual behaviour. First, a sexual activity may be considered a suitable case for
psychological treatment if it is frequent, chronic, causes the individual significant distress, and affects
interpersonal relationships and other areas of functioning. Such examples include the personal distress
and strain on interpersonal relationships caused by problems associated with completion of the normal
sexual cycle (see sexual dysfunctions). Second, some individuals persistently direct their sexual activity at
individuals who do not consent to the activity or who cannot legally give consent (e.g., children). Such
activities include exhibitionism (exposing of the genitalia to a stranger), paedophilia, and rape, and
DSM‐5 includes some of these activities (e.g., exhibitionistic disorder, paedophilic disorder) even though
the diagnostic criteria do not require that the individual committing these acts should experience
distress. Whether such categories of activity should be labelled as psychopathologies is a debatable
point, and in many cases they may be more suitably characterised as illegal criminal activities outlawed
by particular societies.
The disorders of sexual functioning that we cover in this chapter can be found in two separate chapters
of DSM‐5: (a) sexual dysfunctions—which represent problems with the normal sexual response
cycle (e.g., lack of sexual desire or pain during intercourse), and (b) paraphilic disorders—which
represent sexual urges or fantasies involving unusual sources of gratification (e.g., nonhuman objects or
nonconsenting individuals). DSM‐5 also contains a chapter dedicated to gender dysphoria, where
the individual has a sense of gender that is not congruent with the biological sex they were born with.
This is a controversial diagnostic category, criticised as stigmatising transgender individuals and
unreasonably associating gender identity issues directly with psychiatric disorders. These issues are
discussed in Focus Point 11.1.

sexual dysfunctions Problems with the normal sexual response cycle (e.g. lack of sexual
desire or pain during intercourse).

paraphilic disorders Represent sexual urges or fantasies involving unusual sources of

gratification (e.g. non-human objects or non-consenting individuals).

gender dysphoria A gender identity disorder in which an individual has a sense of gender
that is opposite to his or her biological sex.

gender identity The internal sense of being either male or female. Usually congruent with
biological gender, but not always, as in gender identity disorder.

FOCUS POINT 11.1 GENDER DYSPHORIA

Most of us take our sexual identity for granted. We do not question that we are the sex we were
born as, and we find that behaving as either a male or a female is natural and effortless. Our
gender identity seems to have been determined for as long as we have lived, and we think,
act, and dress accordingly. However, many individuals develop a sense of gender dysphoria
(unhappiness with their own gender) and feel that they have a sense of gender that is not
congruent with the biological sex they were born with. In such circumstances, the individual
may see themselves biologically developing as a man or a woman (e.g., growing a beard, or
developing breasts) but cannot shake off the belief that underneath the physical appearance
they are of a different gender.
In a survey of over 150,000 people in the US, around 1 in every 200 persons endorsed having a
gender identity problem or being transgender (Crissman, Berger, Graham, & Dalton, 2017).
The UK Office for National Statistics (2017) reports that estimates for the size of the
transgender community in the UK may range from 65,000 to 300,000, and in 2008 the Gender
Identity Research & Education Society reported that there were 6,200 people in the UK who
had transitioned to a new gender role via medical intervention.
Many people who experience gender identity problems opt to change their body's physical
characteristics to be consistent with their feelings of gender. This can be achieved by using
hormonal treatments to change secondary sexual characteristics or undergoing gender
reassignment surgery to alter the genitalia to be consistent with their feelings of gender. Despite
the radical nature of gender reassignment surgery, outcome studies tend to indicate that a large
majority of clients who undergo the full treatment are generally satisfied with the outcome and
express no regrets about their decision (Smith, van Goozen, Kuiper, & Cohen‐Kettenis, 2005;
Gijs & Brewaeys, 2007), and such individuals report improvements in life satisfaction, sexual
satisfaction, and mental health (Monstrey, Vercruysse, & De Cuypere, 2009).
But gender identity is not simply a binary matter where there are only two alternatives, male
and female, many people feel that they do not fit obviously into either of these categories. The
Office for National Statistics in its ‘Trans data position paper’ adopted the term Trans to
describe such individuals and defined it as ‘an umbrella term referring to individuals whose
gender identity or gender expression falls outside of the stereotypical gender norms’ (O'Neil,
McWhirter, & Cerezon, 2008).
Gender dysphoria is also the title of a diagnosable psychopathology in DSM‐5. In 2013 the
American Psychiatric Association changed the diagnostic category called ‘gender identity
disorder’ to ‘gender dysphoria’ and removed this condition from a general chapter on sexually‐
related problems and assigned it to a chapter of its own. The DSM‐5 criteria for gender
dysphoria in adolescents and adults are:
A marked discrepancy between an individual's expressed gender and assigned gender, over
a period of at least 6 months, as expressed by at least two of the following:
A discrepancy between expressed gender and sex characteristics
An intense desire to be without existing sex characteristics due to a discrepancy between
expressed and assigned gender
An intense desire for the sex characteristics of another gender or to be treated as another
gender
An intense belief that one has the typical feelings and reactions of another gender
Symptoms cause significant distress or impairment in performing major occupational,
social, or interpersonal life functions
As a psychopathology diagnostic category, this inclusion of gender dysphoria in DSM‐5 has
caused considerable controversy. Labelling these criteria as ‘gender dysphoria’ appears to imply
that anyone who has gender identity problems has a diagnosable psychiatric disorder, but it is
only the final criterion (symptoms cause distress and impairment) that makes this diagnostic
category eligible as a potential mental health problem.
However, it is clear that many articles and studies alluding to the DSM‐5 category of gender
dysphoria implicitly view the gender identity issues as mental health problems in their own right
—which, of course, they are not (Davy & Toze, 2018). Associating gender identity issues
directly with psychiatric disorders stigmatises transgender individuals, and although it is the case
that transgendered individuals as a group are particularly vulnerable to common mental health
problems such as anxiety and depression, they are no more likely to suffer major psychiatric
disorders such as schizophrenia and bipolar disorder than any member of the general
population (Dhejne, Van Vlerken, Heylens, & Arcelus, 2016).
In 2017, in an attempt to destigmatise transgender individuals, Denmark became the first
country taking official action to ensure that the country's medical code titles did not associate
terms such as ‘gender’ or ‘transgender’ with ‘dysphoria’, ‘problem’, or ‘incongruence’. This
action explicitly recognises that a mismatch between one's birth gender and adopted gender
identity is not necessarily pathological and shifts the emphasis in treating individuals from fixing
a ‘psychiatric disorder’ to resolving any distress caused by the mismatch. We wait to see how the
next edition of DSM reacts to these controversial and important matters!
 SELF‐TEST QUESTIONS
What are the sociocultural problems involved in defining pathological sexual behaviour?

SECTION SUMMARY

11.1 DEFINING PATHOLOGICAL SEXUAL BEHAVIOUR

A sexual activity or a sexual problem can be considered a suitable case for treatment if it is
frequent, chronic, causes the individual significant distress, and affects interpersonal
relationships and other areas of functioning.
Some individuals direct their sexual actives at nonconsenting others, and these can be
described as both paraphilic disorders and sexual offences (e.g., paedophilic disorders).

11.2 SEXUAL DYSFUNCTIONS

Sex is mainly a private subject, and many people rarely talk with anyone other than their partner about
intimate sexual matters. During the 1960s and 1970s a greater openness about sex and sexual activities
developed as part of the liberalising climate of the time. Changes in longevity, available leisure time,
employment, childrearing practices, and media coverage of leisure activities led to increased interest in
sexual practices. Similarly, effective oral contraceptives and treatments for venereal disease helped to
remove sexual inhibitions. Finally, changes in obscenity laws permitted sexual explicitness in the mass
media in a way never previously broadcast. All this led to increased interest in sexual activity generally
and sexual satisfaction in particular (Tiefer, 2006). At around this time, Masters and Johnson (1966)
(Photo 11.1) were beginning to publish their pioneering research on what they called the ‘human sexual
response’, and the Kinsey reports provided hitherto unavailable statistical information on the frequency
with which Americans engaged in various sexual activities (Kinsey, Pomeroy, Martin, & Gebhard, 1953).
To most people's surprise, these reports revealed that sexual activities were significantly more
widespread than most people were willing to believe at that time. They showed that 90% of males had
masturbated, and oral sex was a common sexual activity. In addition, the studies revealed that around
80% of men and 50% of women had indulged in premarital sex. More recent data from the 3rd UK
National Survey of Sexual Attitudes & Lifestyles conducted between 2010 and 2012 suggests that sexual
activity in both males and females in the UK had decreased slightly between 2000 and 2010. In 2010,
men and women between the ages of 16–44 years reported having had an average of 11.7 and 7.7
sexual partners of the opposite sex respectively in their lifetime, and 7.3% of men (down from 8.4% in
2000) and 16.0% of women (up from 9.7% in 2000) reported having had a sexual experience with a
partner of the same sex. Frequency of sexual activity was lower in 2010 than 2000, with the number of
sexual intercourse occasions for men in the past 4 weeks down from 6.2 to 4.9 in men, and down from
6.3 to 4.8 in women (Mercer et al., 2013).
PHOTO 11.1 Masters and Johnson were the first to publish statistical information on the human sexual response and to
develop integrated psychological theories of sexual dysfunction.
Since the 1950s and 1960s there has been a significant change in behaviour and attitudes towards sex in
Western societies. There has been an increase in the rate at which both men and women take sexual
partners and a drop in the age at which adolescents report having their first sexual experience. This is
accompanied by a relaxation of attitudes to same‐sex sexual partners, nonexclusive sexual relationships
and sex outside of marriage. Although sexual activity appears to have increased over the past 50 years, it
is difficult to estimate whether this increase has also given rise to increased sexual performance
problems. However, the fact that research on sexual activity can nowadays proceed openly and without
stigma has meant that significant developments have been made in how we conceptualise sexual activity
and categorise potential dysfunctions. For example, the normal sexual cycle has been divided into four
stages, and sexual dysfunctions can occur at any one of these distinct stages. Table 11.1 lists these four
stages and the specific diagnosable disorders that have been identified with each. The four stages of the
sexual response cycle are: (a) desire—relating to the desire to have sex, (b) arousal—a subjective sense
of sexual pleasure and accompanying physical changes in the genitalia (e.g., penile erection in the male,
and vaginal swelling and lubrication in the female), (c) orgasm—the peaking of sexual pleasure, and (d)
resolution—a post‐coital sense of muscular relaxation and well‐being. There are no DSM‐5 disorders
specifically associated with the resolution stage, but there is an additional set of disorders known as
sexual pain disorders that can occur at different stages during the sexual cycle and significantly
affect the normal sense of well‐being experienced during the resolution stage. We discuss the disorders
relating to each stage in more detail later, after we have considered general diagnostic issues.
TABLE 11.1 Stages of the sexual cycle and their associated DSM‐5 disorders
Stage of Description Disorders Main diagnostic
the symptom
sexual
cycle
Desire Sexual thoughts and fantasies and the desire Male hypoactive Persistent or deficient
to have sex sexual desire sexual/erotic
disorder thoughts and desire
for sexual activity
Arousal Subjective sense of sexual pleasure and Female sexual Absent/reduced
accompanying physical changes in the interest/arousal interest in sexual
genitalia (e.g., penile erection in the male, disorder activity or
and vaginal swelling and lubrication in the Erectile disorder erotic/sexual
female) thoughts
In males, marked
difficulty in obtaining
or maintaining an
erection during
sexual activity
Orgasm Peaking of sexual pleasure (including Female orgasmic In females, a marked
ejaculation in the male and vaginal disorder infrequency of
contractions in the female) orgasms or reduced
intensity of orgasms
Delayed In males, a marked
ejaculation delay in ejaculation
or marked
infrequency or
absence of
ejaculation
Early ejaculation A persistent onset of
orgasm and
ejaculation with
minimal sexual
stimulation and
before the individual
wishes it
Sexual Genito‐pelvic Persistent difficulties
pain pain/penetration with vaginal
disorders disorder penetration/vaginal
or pelvic pain/fear or
anxiety about pain
during intercourse

11.2.1 Diagnosis of Sexual Dysfunctions

In general terms, sexual dysfunctions are a heterogenous group of disorders characterised clinically by
the individual's inability to respond sexually or to experience sexual pleasure (DSM‐5, American
Psychiatric Association, 2013, p. 423). The specific dysfunction must also cause the individual subjective
distress, affect areas of functioning such as relationships, and be persistent or recurrent. In each case,
the clinician needs to exercise considerable judgement about what might and might not constitute a
diagnosable problem in this area. The age and experience of the client needs to be considered. For
example, sexual activity and performance usually decline with age, and in females may do so after the
menopause (Dennerstein, Koochaki, Barton, & Graziottin, 2006)—and this is a perfectly normal
developmental process rather than a dysfunction. The clinician also needs to take into account the
client's ethnic, cultural, religious, and social background—factors which may influence desire,
expectations, and attitudes about performance. As we mentioned earlier, diagnosis of a dysfunction is
given only when the symptoms are persistent, cause the individual significant psychological distress, and
impair general day‐to‐day functioning and cause interpersonal distress. In many cases, distress occurs in
cases of sexual dysfunction because it is associated with diagnosable mood disorders or anxiety disorders
(especially obsessive‐compulsive disorder, panic disorder, social phobia and specific phobia), and sexual
dysfunction can often be a frequent complication of these latter disorders (Figueira, Possidente,
Marques, & Hayes, 2001).

Specific sexual dysfunctions

In DSM‐5 sexual dysfunction disorders have been categorised around the stages of the sexual cycle,
namely desire, arousal, orgasm, and resolution (see Table 11.1), and also include a category relating to
pain experienced during the sexual cycle.

Disorders of desire and arousal

The first two phases of the sexual response cycle are the desire and arousal stages, which consist of the
urge and desire to have sex, to indulge in sexual thoughts and fantasies, the experience of sexual
attraction to others (all defined by desire), and a subjective sense of sexual pleasure and accompanying
physical changes in the genitalia (arousal). DSM‐5 identifies three disorders that span these two phases
of the sexual cycle and these are male hypoactive sexual desire disorder, erectile disorder,
and female sexual interest/arousal disorder.

male hypoactive sexual desire disorder Absent/reduced interest in sexual activity or

erotic/sexual thoughts.

female sexual interest/arousal disorder Characterised by combinations of: significantly

reduced sexual interest or arousal related to lack of interest in sexual activity, absence of erotic
thoughts, unreceptiveness to sexual approaches, reduced sexual excitement, and reduced sexual
sensations during sexual activity.

Male hypoactive sexual desire disorder

This disorder is characterised by a persistent and recurrent deficiency or absence of desire for sexual
activity and absence of sexual fantasies that cause the individual marked distress or interpersonal
difficulty. Low sexual desire may be general or it may be focused on sexual activity with one individual
(such as the client's partner) or on a particular sexual activity itself (such as oral sex). This disorder may
be frequently associated with erectile and/or ejaculation concerns, and it may be an inability to obtain
an erection that leads to the man's loss of interest in sexual activity. The prevalence of male hypoactive
sexual desire disorder depends very much on the individual's nationality and country of origin, although
6% of younger men (aged 18‐24 years) and 41% of older men (age 66‐74 years) have problems with
sexual desire, and overall prevalence rates vary from 12.5% in Northern European men to 28% in
Southeast Asian men (DSM‐5, American Psychiatric Association, 2013, p. 442). Mood and anxiety
symptoms appear to be strong predictors of low sexual desire in men, and alcohol may increase this risk
(Table 11.2).

Erectile disorder
The basic feature of erectile disorder is the repeated failure to obtain or maintain erection during
partnered sexual activities, on all or almost all occasions over a significant period of time (see Table
11.3). This is often associated with low self‐esteem, low self‐confidence, and a decreased sense of
masculinity. Male erectile disorder is one of the most common of the sexual dysfunctions in men, is
usually the disorder that is most commonly referred for treatment, and is likely to have a significant
impact on the sexual satisfaction of both the sufferer and his partner. Approximately 13–21% of men
aged 40–80 years experience occasional problems with erections, but only 2% of men younger than 40
years do (DSM‐5, American Psychiatric Association, 2013, p. 427). The causes of male erectile disorder
are complex, and appear to range across physical, psychological, and sociocultural factors. Hormonal
and vascular problems such as high blood pressure, diabetes, and heart disease are associated with
erectile disorders (Berman et al., 1999) as are activities such as smoking and excessive alcohol
consumption (Westheimer & Lopater, 2002; Lee, Ho, Yip, Fan & Lam, 2010). Psychological factors that
may affect the ability to achieve and maintain erection include severe depression (Seidman, 2002), and
marital, financial, and occupational stress (Morokoff & Gillilland, 1993).

erectile disorder The inability to maintain an adequate erection during sexual activity.
Around 10 per cent of males report erection problems, but this increases to 20 per cent in the
over 50s.

TABLE 11.2 Summary: DSM‐5 diagnostic criteria for male hypoactive sexual desire disorder

Incessantly or recurrently deficient sexual/erotic thoughts or desire for sexual activity for a period
of at least 6 months, causing significant distress to the patient
The sexual dysfunction is not better accounted for by a nonsexual mental disorder or as a
consequence of relationship or other significant stressors and is not attributable to the effects of a
medication/substance or other medical condition

TABLE 11.3 Summary: DSM‐5 diagnostic criteria for erectile disorder

At least one of the following occurs during at least 75% of sexual activity for a period of at least 6
months causing significant distress to the patient:
Difficulty in obtaining an erection during sexual activity
Difficulty in maintaining an erection until the completion of sexual activity
Decrease in erectile rigidity
The sexual dysfunction is not better accounted for by a nonsexual mental disorder or as a
consequence of relationship or other significant stressors and is not attributable to the effects of a
medication/substance or other medical condition

Female sexual interest/arousal disorder

This disorder is characterised by combinations of the following characteristics: significantly reduced
sexual interest or arousal related to lack of interest in sexual activity, absence of erotic thoughts,
unreceptiveness to sexual approaches, reduced sexual excitement, and reduced sexual sensations during
sexual activity (see Table 11.4). For a diagnosis to be made, clinically significant distress must also be
associated with these symptoms. This disorder is frequently associated with problems in experiencing
orgasm, and may be associated with pain during sexual activity. It is important to recognise that there
are many women who experience normal sexual desires, but who—for their own reasons—decide not to
engage in sexual activities. Such individuals should not be diagnosed with female sexual interest/arousal
disorder, and the discussion found in Focus Point 11.2 provides some insight into the issues behind the
use of the label ‘female sexual dysfunction’.
TABLE 11.4 Summary: DSM‐5 diagnostic criteria for female sexual interest/arousal disorder

Significant reduction or lack of interest in sexual arousal/receptiveness as marked by at least three

of the following for a period of at least 6 months causing significant distress to the patient:
Lack of/reduced interest in sexual activity
Lack of/reduced interest in sexual/erotic thoughts or fantasies
No/reduced initiation of sexual activity and unreceptive to partner's attempt to initiate
sexual activity
No/reduced excitement or pleasure during sexual activity in at least 75% of sexual
encounters
Lack of/reduced sexual interest in response to any internal or external sexual cues
Lack of/reduced genital or nongenital sensations during sexual activity in at least 75% of
sexual encounters
The sexual dysfunction is not better accounted for by a nonsexual mental disorder or as a
consequence of relationship or other significant stressors and is not attributable to the effects of a
medication/substance or other medical condition

Disorders of orgasm
Orgasm is the third stage of the sexual cycle when sexual stimulation has been sufficient to enable the
individual's sexual pleasure to peak. In both males and females this involves a rhythmic muscular
contraction of the genitals which results in a release of sexual tension, and in the male is accompanied
by ejaculation of semen. There are three DSM‐5 defined disorders of this stage, and these are female
orgasmic disorder, delayed ejaculation, and early ejaculation.

female orgasmic disorder Marked absence, delay or infrequency of orgasm and markedly
reduced intensity of orgasmic sensations.

delayed ejaculation Persistent or recurrent delay in ejaculation following a normal sexual

excitement phase.

Female orgasmic disorder

This is a persistent or recurrent delay in or absence of orgasm following normal sexual excitement that
causes the individual marked distress or interpersonal difficulty. Once again, the clinician has to exercise
judgement about whether a diagnosis is relevant in individual cases. Prevalence rates for female
orgasmic problems range from 10 to 42% depending on factors such as age, culture, duration, and
severity of symptoms (DSM‐5, American Psychiatric Association, 2013, p. 431). Women exhibit
significant differences in the type and intensity of stimulation that triggers orgasm, and as many as 10%
of adult women may never have experienced an orgasm (Andersen, 1983), and the proportion of
women usually experiencing orgasm during intercourse is around 50% (Komisaruk, Beyer‐Flores, &
Whipple, 2006). In addition, whether a woman achieves orgasm or not may be a significant factor in her
partner's attitude to sex. Female orgasmic disorder is one of the most frequent female sexual disorders
referred for treatment, and it is experienced by around one in four women at some point in their lives
and more significantly in the postmenopausal period (Heiman, 2002), but women who are assertive and
who experienced masturbatory orgasm before becoming sexually active are significantly less likely to be
diagnosed with female orgasmic disorder (Hite, 1976). Early sexual experiences may be important in
determining whether a woman develops female orgasmic disorder. For example, positive early sexual
encounters fostering emotional involvement are directly related to the probability of reaching orgasm in
later sexual encounters (Heiman, Gladue, Roberts, & LoPiccolo, 1986). In contrast, an upbringing that
implies the woman should deny her sexuality is more likely to lead to orgasmic dysfunction, as are the
experiences of being punished for childhood masturbation and receiving little or no advice or
information about menstruation (LoPiccolo, 1997, but see McCool‐Myers, Theurich, Zuelke, Knuettel,
& Apfelbacher, 2018, for a systematic review of risk factors for female orgasmic disorder and female
sexual dysfunction generally) (Table 11.5).

early ejaculation The onset of orgasm with minimal sexual stimulation. Treatment for this
disorder is typically sought by men under the age of 30 years.
 FOCUS POINT 11.2 CONSTRUCTING FEMALE SEXUAL
DYSFUNCTION

Sexual dysfunction is not diagnosed simply on the basis of problems in sexual desire and
performance but is dependent on the condition also causing marked distress and interpersonal
difficulty. Clearly, many people may only rarely experience sexual desire and very rarely indulge
in sexual activity—but a sizable proportion of those people are quite happy with this state of
affairs and indeed may even advocate and seek sexual abstinence. But what happens if attempts
are made to make such people feel inadequate or in some way ‘abnormal’?
In 1966, a New York gynaecologist called Robert A. Wilson published a best‐selling book called
Feminine Forever, in which he argued that the menopause robbed women of their femininity, their
sexuality and ruined the quality of their lives. He labelled postmenopausal women as ‘castrates’
and described the menopause as a ‘deficiency disease’ that should be treated pharmacologically
with hormone replacement therapy. The book and its ensuing publicity had two effects—it
made some postmenopausal women begin to believe they were inadequate and had a disorder
that needed treatment. It made many others—especially those in the feminist movement that
was developing at the time—believe that menopausal symptoms as described by Wilson were
not a medical deficiency, but the creation of a sexist society (Houck, 2003).
More recently, other writers have argued that the pharmaceutical industry has also attempted to
manipulate women's beliefs about their sexuality in order to sell their products (Moynihan,
2006). Some drug companies claim that sexual desire problems affect up to 43% of American
women (Moynihan, 2003), and can be successfully treated with, for example, hormone patches.
However, others claim that this figure is highly improbable and includes women who are quite
happy with their reduced level of sexual interest (Bancroft, Loftus, & Long, 2003).
Tiefer (2006) lists a number of processes that have been used either wittingly or unwittingly in
the past to ‘medicalise’ what many see as normal sexual functioning. These include:
1. Taking a normal function and implying that there is something wrong with it and it should
be treated.
2. Imputing suffering that is not necessarily there.
3. Defining as large a proportion of the population as possible as suffering from the disease.
4. Defining a condition as a ‘deficiency’, disease, or disease of hormonal imbalance.
5. Taking a common symptom that could mean anything and making it sound as if it is a
sign of a serious disease.
While sexual dysfunctions are sometimes caused by medical conditions (see Section 11.2.2), lack
of sexual desire and interest is itself often portrayed as a medical condition in need of
treatment. Yet a reduction in sexual interest and desire can be a healthy and adaptive response
to normal changes in body chemistry or as a normal reaction to adverse life stressors or
relationship changes.

Delayed ejaculation
This is a persistent or recurrent delay in, or absence of, ejaculation following a normal sexual
excitement phase that causes the individual marked distress and interpersonal difficulty. This is the least
common of the male sexual complaints, and less than 1% of men will complain of problems in
reaching ejaculation over a period of 6 months or longer (DSM‐5, American Psychiatric Association,
2013, p. 425). The clinician must make judgements about whether ejaculation is problematically
delayed by taking into account the client's age and the degree of sexual stimulation. The problems can
be caused by physical factors such as low testosterone levels (Stahl, 2001), alcohol consumption, and
prescription drugs such as antidepressants and anxiolytic drugs, all of which can affect the response of
the sympathetic nervous system (Seagraves, 1995; Altman, 2001). (Table 11.6).
TABLE 11.5 SummaryDSM‐5 diagnostic criteria for female orgasmic disorder

Delay, infrequency, or absence of orgasm or reduced intensity of orgasmic sensations in at least

75% of sexual activity for a period of at least 6 months causing significant distress to the patient
The sexual dysfunction is not better accounted for by a nonsexual mental disorder or as a
consequence of relationship or other significant stressors and is not attributable to the effects of a
medication/substance or other medical condition

TABLE 11.6 Summary: DSM‐5 diagnostic criteria for delayed ejaculation

Delay, infrequency or absence of ejaculation in at least 75% of partnered sexual activity for a
period of at least 6 months causing significant distress to the patient
The sexual dysfunction is not better accounted for by a nonsexual mental disorder or as a
consequence of relationship or other significant stressors and is not attributable to the effects of a
medication/substance or other medical condition

Early ejaculation
This is the persistent or recurrent onset of orgasm and ejaculation with minimal sexual stimulation
within 1 minute of penetration, and before the person wishes it to happen. Early or premature
ejaculation is not unusual when aspects of the sexual activity are novel (e.g., the person is indulging in
novel sex acts, with new partners, or has sex only rarely), and this must be taken into account by the
clinician when making a diagnosis. Most young males learn to delay orgasm with continued sexual
experience and age, but some continue to have premature ejaculation problems and so may seek
treatment for the disorder, but these are typically men under the age of 30 years (Bancroft, 1989). In
men between the ages of 18 and 70 years, 20–30% express concern about premature ejaculation, but in
practice only around 1% of men would meet the DSM‐5 diagnostic criteria for early ejaculation (DSM‐
5, American Psychiatric Association, 2013, p. 444). Early ejaculation has been linked to infrequent
climactic sex (Spiess, Geer, & O'Donohue, 1984), overresponsiveness to tactile stimulation (Rowland,
Cooper, & Slob, 1996), sexual performance anxiety (Dunn, Croft, & Hackett, 1999; McMahon, Jannini,
Serefoglu, & Hellstrom, 2016), and, in some cases, with physical or biological causes (Metz, Pryor,
Nesvacil, Abuzzhab, & Koznar, 1997) (Table 11.7).

Sexual pain disorders

Pain can become a common experience that is associated with sexual activity. It can occur before,
during, or after sexual intercourse, and significantly affect the feeling of well‐being that is an important
feature of the resolution stage of the sexual cycle. In DSM‐5, pain during sexual activity has been
included in a single new diagnostic category called genito‐pelvic pain/penetration disorder.
 genito-pelvic pain/penetration disorder Refers to four commonly occurring symptoms,
namely difficulty having intercourse, genito-pelvic pain, fear of pain or vaginal penetration, and
tension of the pelvic floor muscles.

TABLE 11.7 Summary: DSM‐5 diagnostic criteria for premature (early) ejaculation

Continual or recurring pattern of ejaculation occurring in least 75% of partnered sexual activity
with approximately 1 minute of vaginal penetration and before the patient desires it for a period
of at least 6 months causing significant distress to the patient
The sexual dysfunction is not better accounted for by a nonsexual mental disorder or as a
consequence of relationship or other significant stressors and is not attributable to the effects of a
medication/substance or other medical condition

Genito‐pelvic pain/penetration disorder

This disorder refers to four commonly co‐occurring symptoms, namely difficulty in having intercourse,
genito‐pelvic pain, fear of pain or vaginal penetration, and tension of the pelvic floor muscles (see Table
11.8). This disorder is often associated with other sexual dysfunction disorders such as reduced sexual
desire and interest, and pain is often associated with behavioural avoidance and an unwillingness to
attend gynaecological examinations despite medical advice. Factors that are relevant to aetiology in the
case of genito‐pelvic pain/penetration disorder include partner's sexual problems, relationship
problems, individual vulnerability factors (such as poor body image, history of sexual or emotional
abuse), and stress. Often the causes of sexual pain are physical and may relate to gynaecological or
urological problems in women or to allergic reactions to substances in contraceptive creams, condoms,
or diaphragms (e.g., Brown & Ceniceros, 2001). Because this is a new disorder, prevalence rates are
unknown, but up to 15% of women in North America report recurrent pain during intercourse (DSM‐
5, American Psychiatric Association, 2013, p. 438).
TABLE 11.8 Summary: DSM‐5 diagnostic criteria for genito‐pelvic pain/penetration disorder

Persistent or recurring difficulties with at least one of the following over a period of at least 6
months:
Sexual vaginal penetration
Vulvovaginal or pelvic pain during vaginal penetration
Distress about vulvovaginal or pelvic pain during or in anticipation of vaginal penetration
Tensing or tightening of the pelvic floor muscles during vaginal penetration
The sexual dysfunction is not better accounted for by a nonsexual mental disorder or as a
consequence of relationship or other significant stressors and is not attributable to the effects of a
medication/substance or other medical condition

Summary of specific sexual dysfunction disorders

The specific disorders that we have discussed can be associated with individual stages of the sexual
cycle. However, there is clearly a good deal of overlap between these different disorders, and a disorder
in one particular stage of the sexual cycle may well affect performance in other stages (e.g., disorders of
arousal and orgasm may subsequently affect sexual urges and desires). Diagnosing a sexual dysfunction
is not as simple as referring to a list of criteria symptoms because the clinician has to make judgements
about what is dysfunctional in the light of the client's sexual experience, age, religious views, cultural
norms, ethnicity, and upbringing. The clinician also has to decide whether the sexual problems that are
referred are caused primarily by physical or medical conditions, and if so, whether the client might be
better referred for medical treatment, perhaps by a pain specialist or a gynaecologist. Finally, it is
important to remember that many people may not be particularly satisfied with their own sexual
performance or that of their partner, but manage to live their daily lives quite happily. For example,
older women are less likely to be distressed by low sexual desire than younger women (Derogatis &
Burnett, 2008) (see Focus Point 11.2), and it is relatively common for many people to have sexual
symptoms for a month without this causing undue distress. As a consequence, DSM‐5 has specifically
introduced some minimum durations for symptoms before a diagnosis can be made, and a sexual
dysfunction is diagnosed only when the condition is persistent, causes the client considerable distress,
and causes significant interpersonal difficulty (see Activity Box 11.1 on the book’s website).

11.2.2 The Aetiology of Sexual Dysfunctions

In describing the various sexual disorders in the previous section we have hinted in some cases about
factors that might cause these specific disorders to develop. This section provides a more thorough
review of the aetiology of sexual dysfunction by looking first at the kinds of risk factors that are
associated with the development of specific disorders and then in more detail at theories that attempt to
explain in more general terms how people might acquire sexual dysfunctions.

Risk factors for sexual dysfunctions

Risk factors for individual sexual dysfunctions will usually be to some extent gender related, because
many of the disorders apply only to a specific gender. So, for example, experiencing the menopause is
an important risk factor for female sexual interest/arousal disorder, and surgically menopausal women
(who have undergone hysterectomy) are at significantly greater risk (Dennerstein, Koochaki, Barton, &
Graziottin, 2006). For specific male dysfunctions such as erectile disorder, risk factors include ageing, a
diagnosis of depression, cigarette smoking, alcohol drinking, and medical conditions such as diabetes
and cardiovascular and urogenital disease (Korenman, 2004; Droupy, 2005; Lee, Ho, Yip, Fan, & Lam,
2010). For early ejaculation, risk factors include being young, having experienced divorce, and being
more educated (Fasolo, Mirone, Gentile, Parazzini, & Ricci, 2005). Educational level in men has a
complex relationship to sexual dysfunction, and men who are more educated are more likely to report
early ejaculation than less educated men (Fasolo et al., 2005), but less educated men are more likely to
report erectile disorder than better educated men (Lyngdorf & Hemmingsen, 2004). Childhood sexual
abuse is also a significant risk factor for sexual dysfunction in later life. In a large‐scale Australian study,
more than one in three women and one in six men reported a history of childhood sexual abuse, and
there was a significant association between childhood abuse and symptoms of sexual dysfunction
(Najman, Dunne, Purdie, Boyle, & Coxeter, 2005). Sexual trauma and childhood sexual abuse has been
found to be a significant risk factor in specific disorders such as female sexual interest/arousal disorder
(Stuart & Greer, 1984; Pulverman, Kilimnik, & Meston, 2018) and sexual pain disorders (Binik,
Bergeron, & Khalife, 2000; Westheimer & Lopater, 2002). Finally, sexual dysfunction is more prevalent
in women than in men, 43 and 31% respectively, and is more likely amongst those experiencing poor
physical and emotional health generally (Laumann, Paik, & Rosen, 1999). However, we must remember
that this gender difference may be due at least in part to men being more embarrassed by sexual
dysfunction than women and so reporting disorders significantly less. For example, a study of male
erectile disorder found that two out of three men suffering erectile dysfunction were embarrassed when
discussing this problem with a doctor, and only 25% subsequently sought medical advice (Droupy, 2005)
(Focus Point 11.3).
 FOCUS POINT 11.3 SEXUAL DYSFUNCTIONS AND THE
DISGUST EMOTION

The disgust emotion has evolved as a means of protecting the individual from disease and
contamination, and research suggests that high levels of disgust sensitivity may play a significant
role in a number of sexual dysfunctions. For instance, the evolutionary purpose of the disgust
emotion is to prevent pathogens entering the body, and the mouth and vagina represent areas
of the body that are likely to become the focus of disgust reactions as the individual attempts to
ensure they do not allow pathogens or disease‐relevant substances into their body (Rozin,
Nemeroff, Horowitz, Gordon, & Voet, 1995). In addition, the stimuli usually involved in sexual
encounters are highly disgust relevant, and these include saliva, sweat, semen, and body odours.
As a result, if an individual has developed a strong sensitivity to disgust‐relevant stimuli, this
may well interfere with normal sexual behaviour.
It is only recently that disgust has been investigated in the female sexual dysfunctions of
vaginismus and dyspareunia. Vaginismus is the persistent and involuntary contraction of
the muscles of the vagina when vaginal penetration occurs, and dyspareunia is female genital
pain experienced during or after coitus. Studies by de Jong and colleagues have found that
women suffering vaginismus displayed a general enhanced dispositional disgust propensity (de
Jong, van Overveld, Schultz, Peters, & Buwalda, 2009), and women diagnosed with both
vaginismus and dyspareunia exhibited enhanced automatic sex‐disgust associations in an
implicit association task (IAT) (Borg, de Jong, & Schultz, 2010). Based on this growing body of
research, de Jong, van Lankveld, Elgersma, and Borg (2010) have argued that enhanced disgust
sensitivity in relation to sexual activity may be an important part of the mechanism in
disruption of sexual arousal, and this conclusion makes intuitive sense given that sexual
activities emerge as a primary disgust elicitor in factor analysis and cluster analysis studies of
disgust (Marzillier & Davey, 2004). Thus, if sexual activities are a natural disgust elicitor for
many people, then heightened disgust propensity and sensitivity will enhance anxiety by
priming avoidance goals to sexually related stimuli and activities.
Also, it may be the case that sexual arousal itself directly interacts with disgust, and in both men
and women, disgust sensitivity is reduced as sexual arousal increases (Oaten, Stevenson, Tapp,
Case, & Cousins, 2019; Borg & de Jong, 2012). If there is a bidirectional relationship between
disgust and sexual arousal, then we would also expect sexual arousal to be affected by changes
in disgust sensitivity. Given what appears to be this important relationship between disgust and
sexual behaviour, interventions that directly attempt to reduce disgust sensitivity may help to
alleviate sexual dysfunctions such as vaginismus and dyspareunia that are known to be linked to
the disgust emotion.

Theories of the aetiology of sexual dysfunction

Psychoanalytic theory
Much of the psychoanalytic approach to understanding behaviour revolves around repressed emotions
and desires, and specifically around repressed sexual desires, so it is not unusual that psychodynamic
theorists have had something to say about the factors underlying sexual dysfunction. Thus,
vaginismus (an involuntary contraction of muscles around the vagina making sexual intercourse
involving penetration painful or impossible) may be seen as a women unconsciously expressing hostility
towards men, premature ejaculation as men expressing repressed hostility towards women, and female
orgasmic disorder as a function of enduring penis envy. Because sexual activity is usually pleasurable—
yet often frowned upon by society—many psychodynamic views see sexual dysfunction as resulting from
this conflicting state of affairs. Still others view male sexual dysfunctions such as male erectile disorder
as a result of an unresolved Oedipus complex based on a continual sexual attachment of the male to his
mother (Fenichel, 1945). Regardless of the theoretical validity of these analyses, these views gave
psychoanalysis an important therapeutic function prior to the development of therapies based on more
objective and more detailed knowledge of sexual dysfunctions such as those pioneered by Masters and
Johnson in the 1970s.

vaginismus The involuntary contraction of the muscles surrounding the vagina when vaginal
penetration is attempted. Of all women who seek treatment for sexual dysfunctions, around
15–17 per cent are suffering from vaginismus

The two‐factor model of Masters and Johnson

Masters and Johnson were the first researchers to collect detailed information about sexual dysfunctions,
and to develop a model of sexual dysfunction based on this empirical evidence. Their model had two
important components, both of which contributed to sexual dysfunction. The first component consisted
of a learned or conditioned factor where adverse early sexual experiences had given rise to a learnt fear
or anxiety response whenever the individual was engaged in sexual activity. Adverse experiences include
(a) psychosexual trauma, such as rape or childhood sexual abuse;, (b) religious and social taboos that
give rise to feelings of shame and guilt about sex; (c) embarrassing or belittling early experiences with
sex (e.g., appearing unknowledgeable or inexperienced to a sexual partner); or (d) excessive alcohol use
in men, which can affect the ability to achieve and maintain erection. Once these factors have begun to
generate anxiety about sexual performance, the second component of this model is the spectator role
that individuals adopt in response to their fears and anxieties. Instead of taking a relaxed attitude to sex,
the fearful individual constantly monitors their own sexual performance and the responses of their
partner. Their focus of attention is therefore directed away from the stimuli that provide sexual arousal
and sexual pleasure and onto factors that provide feedback about how well the individual is performing.
There are some important similarities between this theory of sexual dysfunction and self‐focused
attention accounts of social anxiety disorder (see Chapter 6) where self‐focused attention prevents
objective processing of the social situation, leads the social phobic to engage in critical self‐evaluation,
and may well adversely affect their actual performance in the social situation. Because of these
similarities, many of the processes involved in self‐focused attention may also apply to sexual
dysfunction. Although Masters and Johnson's theory was the first attempt to develop an empirical model
of sexual dysfunction based on objectively collected data about sexual performance, we must still be
cautious about how the two components of their model interact. For example, while it is clear that many
people suffering sexual dysfunction experience performance anxiety, it is still not clear whether this
anxiety is a cause or a consequence of the dysfunction. We have already noted that many specific sexual
disorders can be caused by physical or medical conditions, and it may be that anxiety about sexual
performance is a consequence of sexual performance being impaired by these conditions rather than a
cause of the condition per se.

performance anxiety The fear of failing to achieve an acceptable level of sexual performance,
causing an individual to become distanced from the sexual act and fail to become aroused.
Sexual dysfunction and interpersonal problems
Sex is usually an interpersonal activity, and it may be that interpersonal problems may be a cause of at
least some of the sexual dysfunctions. Many clinicians believe that individuals with sexual dysfunctions
have both sexual and interpersonal problems, and that the latter may be an important cause of the
former (e.g., Rosen & Leiblum, 1995). For example, there is an inverse relationship between a woman's
sexual desire and their level of concern about their partner's affection (Nobre & Pinto‐Gouveia, 2006),
and individuals who are angry with their partners are less likely to desire sexual activity (Beck &
Bozman, 1995). If negative emotion is a central feature of a couple's relationship, then emotions such as
resentment, disgust, anxiety, anger, distrust, and depression are likely to significantly interfere with the
development of positive feelings required in the desire and arousal stages of the sexual cycle. If general
communication is poor within a couple, then this is likely to have an important impact on talk about
intimate activities such as sex (Brotto et al., 2016). Studies have indicated that interpersonal difficulties
are apparent in sexual dysfunctions diagnosed in both men and women, and are associated with early
ejaculation and erectile disorders in men (Patrick et al., 2005; Swindle, Cameron, Lockhart, & Rosen,
2004) and sexual dysfunctions generally in women (Clayton, 2003). Men are also significantly more
likely to seek help for their sexual dysfunction if it is associated with interpersonal difficulties
(Papaharitou et al., 2006). However, we must still be cautious about how to interpret these findings
because they indicate only that there is an association between sexual dysfunction and interpersonal
difficulties and we do not know the direction of any causal relationship.
Apart from general difficulties that may have arisen in a relationship, sexual dysfunction may result from
specific deficiencies in sexual knowledge or sexual expertise in one or both of the couple. For example,
women who suffer female orgasmic disorder often have partners who are awkward or inexperienced
lovers (LoPiccolo, 1997; Kaplan, 1974), and individuals who develop sexual dysfunctions often lack the
knowledge and skills required to fully stimulate their partner or satisfy themselves (LoPiccolo & Hogan,
1979). Sexual problems can also develop if one member of a couple is overanxious about pleasing the
other, giving rise to performance anxiety that may inhibit sexual feelings and responsiveness to sexual
stimuli (Kaplan, 1974).
Finally, untangling the role that interpersonal difficulties may play in causing sexual dysfunction is
problematic. This is because interpersonal difficulties are very often a central outcome of sexual
dysfunction anyway (Brotto et al., 2016). However, therapies for sexual dysfunction that focus on the
relationship between couples are often successful, and this suggests that at least some of the causes of
some sexual dysfunctions lie in the details of individual relationships.

The role of negative emotion and psychopathology

Satisfying sexual experiences are usually dependent on the individual being open to positive pleasurable
emotions and being attentive to those stimuli during sexual activity. Because of this, chronic negative
emotions such as depression or anxiety are likely to interfere significantly with sexual performance, and
depression and anxiety are significant risk factors for sexual dysfunction (Hayes, Dennerstein, Bennett,
& Fairley, 2008). Studies suggest that 62% of those people with depression are also likely to have a
sexual dysfunction, compared with only 26% of people without depression (Angst, 1998), and
depression appears to have a bidirectional relationship with sexual dysfunction—both causing sexual
dysfunction and being a significant outcome of sexual dysfunction (Atlantis & Sullivan, 2012). In
women, depressive symptoms have been shown to be associated with deficits in sexual desire, sexual
fantasy, sexual arousal, and orgasmic function (Cyranowski, Frank, Cherry, Houck, & Kupfer, 2004),
and men with depression are almost twice as likely to experience erectile dysfunction as nondepressed
men, and the degree of erectile dysfunction increases with increasing degree of depression (Araujo,
Drante, Feldman, Goldstein, & McKinlay, 1998).
Anxiety is another negative emotion that can potentially have a significant effect on sexual functioning.
We have already discussed the role that performance anxiety may play in causing sexual dysfunction,
and anxiety disorders themselves are associated with sexual dysfunction. These include panic disorder,
social anxiety disorder, specific phobia, generalised anxiety disorder, and obsessive–compulsive disorder
(Figueira, Possidente, Marques, & Hayes, 2001; Rajkumar & Kumaran, 2015). Anxiety disorders have
been found in 1 in 4 men suffering from erectile dysfunction or premature ejaculation (Mallis et al.,
2005), and the anxiety disorder is known to predate the onset of the sexual dysfunction (Rajkumar &
Kumaran, 2015). High levels of anxiety may lead to sexual dysfunction simply because it is a negative
emotion that may inhibit the development of pleasurable emotions associated with sexual pleasure. It
may also prevent allocation of attention to stimuli likely to provide sexual stimulation and pleasure.
Specific anxiety disorders may also influence sexual performance in quite specific ways. For example,
panic disorder is associated with a fear of bodily sensations, and so the increases in heart rate and
perspiration caused by sexual activity may be interpreted negatively by someone with panic disorder
(Sbrocco, Weisberg, Barlow & Cater, 1997). Similarly, fear of contamination associated with some forms
of OCD may make the individual fearful of bodily contact and sexual secretions (see Focus Point 11.3).
Finally, social anxiety disorder is known to be associated with a self‐critical attitude, which may well give
rise to performance anxiety during sexual activity.

Remote vs immediate causes

One view of the causes of sexual dysfunction is that chronic sexual dysfunction is caused by a
combination of immediate causes and remote causes (Kaplan, 1974). Immediate causes are factors
that may directly influence sexual performance, such as performance anxiety, communication problems
between partners, lack of sexual knowledge, clumsy technique, etc. However, many of these are factors
that may influence the sexual performance of many people at one time or another, and are not
necessarily chronic features of a person's lovemaking. However, these immediate performance problems
may arise because of longer‐term remote causes of sexual dysfunction, and these refer to more deep‐
rooted psychological and psychodynamic factors that incline someone to be anxious about their sexual
performance. Remote causes include feelings of shame and guilt about sexual activity (which may
vary with culture, e.g., Woo, Brotto, & Gorzalka, 2011), general feelings of inadequacy, feelings of
conflict brought about by long‐term life stress, childhood abuse, etc. (Kaplan, 1979; Pulverman,
Kilimnik, & Meston, 2018). In particular, while men may worry during sex about their performance,
women worry about their attractiveness and may experience intrusive thoughts about their weight
(Pujols, Seal, & Meston, 2010).

Remote causes Include feelings of shame and guilt about sexual activity, general feelings of
inadequacy, feelings of conflict brought about by long-term life stress, and suchlike.

Biological causes
There is considerable debate about whether sexual dysfunctions are the result of psychological or
organic (biological) causes. In the period following the pioneering work of Masters and Johnson,
researchers began to focus on the importance of psychological factors in the aetiology of sexual
dysfunction. However, nowadays, there is a belief that organic or biological factors may be an
underlying factor in many cases and that these may combine with psychological factors to generate a
chronic disorder.
Biological causes can be classified into three broad categories: (a) dysfunction caused by an underlying
medical condition, (b) dysfunction caused by hormonal abnormalities, and (c) changes in sexual
responsiveness caused by ageing.
A whole range of medical conditions can give rise to sexual desire and performance problems. For
example, male erectile and orgasmic disorders are associated with high blood pressure, diabetes, heart
disease, cigarette smoking, and alcoholism. Dysfunctions are also associated with a variety of
medications such as antidepressant and anxiolytic drugs, and with treatments for hypertension and renal
problems (Berman et al., 1999; Altman, 2001; Wincze & Weisberg, 2015). Medical conditions that
reduce blood flow to the penis (such as blocked arteries or heart disease) will influence the ability to
reach and maintain an erection (Stahl, 2001), and other medical conditions may cause central nervous
system damage that affects sexual performance and desire, and these include diabetes, multiple sclerosis,
and renal problems (Frohman, 2002). Female arousal and orgasm is also affected by medical conditions
in much the same way that these conditions influence erection and ejaculation in men. Female arousal
and orgasmic disorder has been linked to multiple sclerosis and diabetes, and both antidepressant (e.g.,
SSRIs such as Prozac, Kronstein et al., 2015) and anxiolytic medications can affect sexual desire in
women in much the same way that they do in men (Hensley & Nurnberg, 2002). Similarly, sexual pain
disorders may have an organic or medical origin, and these may range from painful allergic reactions to
contraceptive creams, condoms or diaphragms (e.g., in the case of female dyspareunia) to
gynaecological diseases and infections of the vagina, bladder, or uterus (which may cause symptoms of
vaginismus) (Brown & Ceniceros, 2001). Nevertheless, although these forms of organic disorder may be
an underlying cause of sexual desire and performance problems, it is quite likely that they will often
generate associated psychological problems that give rise to a diagnosable sexual dysfunction. For
example, sexual pain or disability caused by disease or medical conditions can give rise to anxiety about
sexual performance or to relationship difficulties.

dyspareunia A genital pain that can occur during, before or after sexual intercourse. Some
clinicians believe this is a pain disorder rather than a sexual dysfunction.

Sexual desire and subsequent arousal and orgasm are dependent on levels of the sex hormones
testosterone, estrogen, and prolactin, and imbalances in these hormones can cause sexual desire
problems in both men and women. In women, either high or low levels of estrogen can cause sexual
desire problems, and estrogen levels can be affected if a woman is taking the birth pill, which will
artificially raise her estrogen levels, or is being given anti‐estrogen therapy for breast cancer that will
lower estrogen levels (Amsterdam, Wheler, Hudis, & Krychman, 2005). High prolactin levels have the
effect of suppressing the hormones responsible for the normal functioning of the ovaries and testes, and
high prolactin levels can therefore lead to menstrual irregularity and/or fertility problems. In men,
erectile dysfunction is usually associated with high levels of prolactin, and erectile problems can be
eased with the use of drugs that lower prolactin levels (Spollen, Wooten, Cargile, & Bartztokis, 2004).
However, in middle‐aged and elderly men low prolactin levels are associated with reduced enjoyment of
orgasmic experiences and lower levels of physical activity generally (Corona et al., 2014).

prolactin A hormone from the pituitary gland stimulating milk production after childbirth.

Finally, one of the important variables that affect sexual functioning is age, and the prevalence of sexual
dysfunction in both males and females increases with age. For example, reports of erectile problems in
men increase significantly after 50 years of age (Laumann, Gagnon, Michael, & Michael, 1994; Gareri,
Castagna, Francomano, Cerinara, & De Fazio, 2014), and a study of Australian men over the age of 40
years indicated that 34% of those men surveyed reported one or more reproductive health disorder,
including erectile dysfunction (21%), lower urinary tract symptoms (16%), and prostrate disease (14%)
(Holden et al., 2005). Such findings may indicate that levels of male hormones generally decrease with
age, or that reproductive health disorders may significantly affect sexual functioning. Sexual desire and
performance also decreases with increased age in women, and the menopause has a significant influence
here. Menopause is associated with decreases in estrogen and testosterone levels that can exacerbate
female sexual dysfunction (Graziottin & Leiblum, 2005). Studies suggest that around one in four women
report a loss of sexual desire after the menopause, and this is associated with fluctuations in levels of
estrogen and testosterone. However, menopause is associated not only with physical changes but also
with psychological changes, and loss of sexual desire in postmenopausal women has been shown to be
associated with physical factors such as lower hormonal levels, vaginal dryness and psychological factors
such as depression and living with children (Gracia et al., 2004).
One final biological factor that has been researched in the aetiology of sexual dysfunctions is genetics,
and recent epidemiology and candidate gene studies have suggested a strong genetic influence on
female sexual functioning, with the hope that successful identification of biomarkers and novel genes
underlying female sexual dysfunction will help to improve diagnosis and treatment (Burri, Cherkas, &
Spector, 2009). Similarly, researchers have identified a genetic variant that increases the risk of erectile
dysfunction. They found that DNA variations near the SIM1 gene were associated with a 26%
increased risk of erectile dysfunction, and the SIM1 gene is part of the leptin‐melanocortin system
which has a role in sexual function (Jorgenson et al., 2018).

Sociocultural causes
The level of sexual dysfunction within a society can change depending on a range of cultural and
economic factors within that society. For example, the stress caused by poverty, financial problems, or
unemployment have all been linked to erectile dysfunctions in men (Morokoff & Gillilland, 1993) and
this effect has been identified during the recent economic downturn in European countries (Christensen
et al., 2011).

Summary
We can see from this section that theories of sexual dysfunction are quite wide ranging and encompass
both psychological and biological explanations. There is no doubt that many cases of sexual dysfunction
have an organic or biological basis, and these can range from dysfunctions caused by medical
conditions, hormone imbalances, and changes in biology with age. However, since the pioneering work
of Masters and Johnson, psychological factors have also been identified in the aetiology of sexual
dysfunction, and these include performance anxiety, underlying interpersonal problems, existing
psychopathology such as depression and anxiety, and a variety of life experiences, such as childhood
abuse, psychosexual trauma, and exposure to religious and social taboos.

11.2.3 The Treatment of Sexual Dysfunctions

Over the past 60–70 years the treatment of sexual dysfunctions has developed through a number of
distinct stages. Prior to the 1950s, psychodynamic therapy was probably the only structured form of
psychological treatment available to those courageous enough in the existing social climate to admit
sexual problems. With its emphasis on underlying conflicts and tensions tied to repressed sexual desires,
psychoanalytic theory seemed ideally suited to treat sexual dysfunctions. However, the liberating social
climate of the 1960s and 1970s allowed freer discussion of sexual problems, and with this came the
pioneering early work of Masters and Johnson published in their 1970 book Human Sexual Inadequacy.
This led to the development of what are now known as direct treatments for sexual dysfunction. These are
often behaviourally based treatments for the specific symptoms of the disorder. So, for example, rather
than consider erectile dysfunction to be a manifestation of underlying psychological problems, therapists
would provide the client with specific training on how to achieve and maintain an erection (e.g., the
‘tease’ technique). Most modern‐day treatment programmes now include some components designed to
directly address the main symptom of the disorder (such as lack of desire, erectile problems, or
premature ejaculation) as well as components designed to deal with accompanying psychological
problems (such as performance anxiety, related depression, or relationship problems). As well as these
developments in psychological treatment, there have been significant advances in biological treatments
for sexual dysfunctions. Treatments available today include drug and hormone treatments for problems
of desire, arousal, and orgasm, and mechanical devices for aiding penile erection in men. In the
following sections we cover some of these treatments in more detail, beginning in Treatment in Practice
Box 11.1 with an overview of the general structure of sex therapy. The following then covers a range of
psychological and behavioural therapies in more detail, followed by a description and evaluation of
biologically‐based treatments.

Psychological and behavioural treatments

Direct treatment of symptoms

Direct treatments are techniques targeting the specific sexual performance deficit. For example, there
are two specific techniques used to help clients with early ejaculation. These are the ‘stop‐start’
technique and the ‘squeeze’ technique. In the former, the client's partner stimulates the penis until
close to ejaculation, at which point the partner is signaled to stop by the client (Semans, 1956). This
process continues once the desire to ejaculate subsides. This acts to increase the amount of stimulation
required to achieve ejaculation. The ‘squeeze’ technique is very similar, where the client's partner will
firmly squeeze below the head of the penis just prior to ejaculation. This has the effect of reducing the
erection and can be repeated several times in order to help the client control ejaculation (St Lawrence &
Madakasira, 1992). Evidence from randomised controlled trials on the efficacy of the ‘stop‐start’ and
‘squeeze’ techniques is equivocal—some studies have shown an effect on ejaculatory latency time (e.g.,
Abdel‐Hamid, Naggar, & Gilany, 2001), whereas a number of other studies have not (Cooper et al.,
2015), but both techniques may be more effective when combined with drug treatments.

stop-start technique A technique used to help clients with premature ejaculation where the
client’s partner stimulates the penis until close to ejaculation, at which point the partner is
signalled to stop by the client.

squeeze technique A technique used to help clients with premature ejaculation where the
client’s partner firmly squeezes below the head of the penis just prior to ejaculation.

CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE BOX

11.1 WHAT IS SEX THERAPY?

Current forms of sex therapy involve a number of components, and these different components
are designed to identify specific sexual problems, to address these specific problems with direct
treatment, to deal with associated psychological and relationship issues, and to provide clients
with sexual knowledge and sexual skills. Sex therapy usually treats the couple rather than the
individual who manifests the dysfunction, and couples are urged to share the responsibility for
the sexual problem. The following are some of these separate components which form the
important core stages of sex therapy.

ASSESSMENT
Through interview, the therapist will collect information about specific sexual problems (e.g.,
 lack of desire by one partner or erectile problems in a male partner) and discuss current life
issues and past life events that may be contributing to the problem. This stage will usually be
accompanied by a medical examination to determine whether there are organic factors
contributing to the problems.
DEALING WITH ORGANIC DYSFUNCTION
If there are clearly organic or medical factors contributing to the dysfunction (such as low
hormone levels, medical conditions such as diabetes or high blood pressure, or other
medications, such as antidepressants or anxiolytics), then these may be addressed early in the
programme (e.g., by reducing levels of antidepressant drugs).
SEXUAL SKILLS TRAINING
Many types of sexual problem arise through lack of knowledge about the physiology of sex and
a lack of basic technique during lovemaking. The therapist can address these factors by
providing the clients with educational materials such as booklets and videos.
CHANGING DYSFUNCTIONAL BELIEFS:
Sex is associated with a whole range of myths and false beliefs (e.g., ‘too much masturbation is
bad for you’, ‘nice women aren't aroused by erotic books or films’, etc.) (Bach, Wincze, &
Barlow, 2001), and if a client holds these false beliefs they may be preventing full sexual arousal
and satisfaction. Using a range of methods, such as those used in CBT, the therapist will
attempt to identify any dysfunctional beliefs, challenge them, and replace them with more
functional beliefs.
DIRECT INTERVENTION AND BEHAVIOURAL TRAINING:
Depending on the specific sexual dysfunction that has been referred for treatment, the therapist
will advise the clients on the use of a range of behavioural techniques designed to help their
specific problem. These techniques, discussed more fully in Section 11.2.3, include the ‘tease
technique’ for erectile dysfunction, ‘stop‐start technique’, and ‘squeeze technique’ for premature
ejaculation (Semans, 1956; LoPiccolo, 1997), and directed masturbation training for arousal
and orgasmic disorders (Heiman, 2002). Therapists may also teach clients a technique known as
nondemand pleasuring, which involves a couple exploring and caressing each other's body
to discover sexual pleasure rather than achieving orgasm. This allows couples to learn how to
give and receive sexual pleasure without the pressure of needing to achieve orgasm.
DEALING WITH RELATIONSHIP AND LIFESTYLE ISSUES
Sexual dysfunction is often related to conflict within the relationship and to stressful lifestyles
(e.g., one partner may be dominating and controlling or the demands of factors such as family
and work may be causing unnecessary stress). The therapist will usually attempt to identify any
factors that may be contributing to the disorder and advise clients on how to improve these.

A direct treatment method designed to deal with symptoms of erectile disorder and female orgasmic
disorder is the tease technique.This involves the partner caressing the client's genitals, but stopping
when the client becomes aroused (e.g., achieves an erection) or approaches orgasm. This enables couples
to experience sexual pleasure without the need to achieve orgasm and as a result may reduce any
performance anxiety that may have been contributing to erectile problems or arousal and orgasmic
problems (LoPiccolo, 1997). For individuals with arousal or orgasmic problems, directed
masturbation training is often helpful (Heiman, 2002; Faubion & Rullo, 2015). With the use of
educational material, videos, diagrams, and—in some cases—erotic materials, a woman can be taught
step by step to achieve orgasm—even in cases where she has never previously experienced an orgasm.
This method has been shown to be highly effective, and over 90% of women treated with this method
learn how to achieve orgasm during masturbation (Heiman & LoPiccolo, 1988).

tease technique A direct treatment method designed to deal with symptoms of erectile
dysfunction or male and female orgasmic disorder. It involves the partner caressing the client’s
genitals, but stopping when the client becomes aroused (e.g. achieves an erection) or approaches
orgasm.

directed masturbation training A treatment for individuals with arousal or orgasmic

problems using educational material, videos, diagrams and – in some cases – erotic
materials.

Couples therapy
As we have mentioned several times in this chapter, sexual dysfunction may be closely associated with
relationship problems. If sexual dysfunctions are a manifestation of broader problems within a
relationship, then the latter need to be effectively addressed. For example, a lack of sexual desire in one
partner may be a way that the partner can exert some control within the relationship—especially if
there are conflicts over power and control. In such cases, underlying sexual dysfunction may entail some
implicit reward for both partners, one partner gaining reward from their ability to control sex, and the
other gaining reward by viewing their partner's lack of desire as a weakness which enables them to see
themselves as controlling. A therapist will explore these issues with a couple and try to identify if there
are any implicit payoffs within the relationship for maintaining the sexual dysfunction.

Sexual skills and communication training

For many couples, sexual dysfunction is simply another manifestation of the couple's inability to
communicate effectively with one another. They may be unable to tell each other what stimulates and
pleasures them, or they may be nervous, shy, or unknowledgeable about sexual matters. With the use of
educational materials and videos, a therapist can help clients to acquire a more knowledgeable
perspective on sexual activity, begin to communicate to each other effectively about sex, reduce any
anxiety about indulging in sexual activity, and, where appropriate, increase satisfaction with married life
(McMullen & Rosen, 1979; Farah & Shahram, 2011).

sexual skills and communication training A treatment method in which a therapist can
help clients to acquire a more knowledgeable perspective on sexual activity, communicate to
partners effectively about sex, and reduce any anxiety about indulging in sexual activity.

CBT for sexual dysfunction

Because psychological factors often play a central role in sexual dysfunction, the use of cognitive
behaviour therapy (CBT) is appropriate for managing dysfunctional beliefs about sexual performance
(such as ‘every sexual act has to be performed perfectly’) and for replacing dysfunctional thoughts and
beliefs with more practical ones (such as ‘sexual pleasure should be shared’) (e.g., Metz, Epstein, &
McCarthy, 2017). Furthermore, CBT is tailor made to deal with problems such as anxiety and
depression which are common features of sexual dysfunction, and CBT can be used to focus on and
manage these factors and as a consequence remove the anxiety and depression components that might
be maintaining sexual dysfunction (Hoyer et al., 2009). CBT has proven to be a helpful treatment for a
number of different female sexual dysfunctions (ter Kuile, Both, & van Lankveld, 2010) and male sexual
dysfunctions such as premature ejaculation (Mohammadi, Mohammadkhani, Dolatshahi, & Dadkhah,
2013).

Summary of psychological interventions for sexual dysfunction

There are very few comparative studies of the relative effectiveness of psychological therapies for sexual
dysfunction. However, a recent meta‐analysis suggests that psychological‐based treatments (e.g., sexual
skills training, CBT, couples therapy) are effective options for sexual dysfunction—with outcomes
being particularly good for female sexual interest/arousal disorder and female orgasmic disorder
(Fruhauf, Gerger, Schmidt, Munder, & Barth, 2013).

couples therapy A treatment intervention for sexual dysfunction that involves both partners
in the relationship.

Biological treatments
Many cases of sexual dysfunction may have biological or organic causes such as medical conditions,
hormone imbalances, changes in biology with age, or are a reaction to other medications being taken by
the client. This indicates that a biological or medical treatment may be appropriate for the disorder.
Biological treatments fall into three broad categories: (a) drug treatments, including medications that
directly influence the organic nature of the disorder; (b) hormone treatments designed to correct any
hormonal imbalances caused by age or illness; and (c) mechanical devices, designed to aid mechanical
functioning during sex (such as achieving erection).

Drug treatments
Perhaps the most well‐known drug treatments for sexual dysfunction are Viagra (sildenafil citrate)
and Cialis (tadafil), both phosphodiesterase type 5 (PDE‐5) inhibitors which are used primarily to
treat erectile dysfunction in men. Viagra acts directly on the tissue of the penis itself. It causes relaxation
of the smooth muscle of the penis that increases blood flow and encourages erection. Studies suggest
that 75% of men taking Viagra can achieve erection within 60 mins of administration (Goldstein et al.,
1998), and in clinical trials Viagra results in significantly more erections and successful intercourse
attempts than a placebo control (Moore, Edwards, & McQuay, 2002) (see Figure 11.1). Viagra has also
proved to be an effective treatment for male erectile disorder, with over 95% of clients treated with
Viagra over a 1–3 year period expressing satisfaction with their erections and their ability to effectively
engage in sex (Carson, Burnett, Levine, & Nehra, 2002). In addition, Viagra has been considered to be
an effective treatment for male erectile disorder in cases where this is due to a medical condition (such as
diabetes or cardiovascular disorder) or as a result of ageing (Salonia, Rigatti, & Montorsi, 2003).
However, Viagra may not be the treatment of choice for many clients because it also has a number of
side effects, such as headaches, dizziness, and facial flushing, and may interact badly with some
medications for cardiovascular disease (Bach, Wincze, & Barlow, 2001).

Viagra (sildenafil citrate) A drug treatment for sexual dysfunction which is used primarily
to treat erectile dysfunction in men.

Cialis (tadafil) A drug treatment, used primarily to treat erectile dysfunction in men.
FIGURE 11.1 Mean number of erections per week (blue) and erections resulting in successful intercourse (red) with
placebo and different doses of Viagra (sildenafil citrate).
From Moore, Edwards, & McQuay (2002).
Other drugs that have proved useful in treating sexual dysfunctions include yohimbine for erectile
dysfunctions, which facilitates norepinephrine excretion in the brain. This appears to have the effect of
correcting any brain neurotransmitter problems that are causing the erectile dysfunction (Mann et al.,
1996). Interestingly, both Viagra and yohimbine have also been shown to be effective in treating female
sexual desire problems (Hernandez‐Serrano, 2001).

yohimbine A drug treatment for sexual dysfunction which is used primarily to treat erectile
dysfunction in men by facilitating norepinephrine excretion in the brain.

Finally, antidepressant SSRIs such as Prozac are also an effective treatment for early ejaculation, and
delayed orgasm is a known side‐effect of SSRIs in depressed individuals who are taking these
medications (Assalian & Margolese, 1996).

Hormone treatments
At least some sexual dysfunctions may result from imbalances in hormone levels, and disorders can
result from either high or low levels of estrogen in women, low levels of testosterone in men, and high
levels of prolactin in men. These hormonal imbalances can be caused by medical conditions or ageing.
Hormone replacement therapy can be used to treat disorders of sexual desire—especially in older
women or women who have undergone hysterectomy, and sexual pain disorders such as genito‐pelvic
pain/penetration disorder can also be helped with estrogen treatment, which can improve vaginal
lubrication in postmenopausal women (Walling, Anderson, & Johnson, 1990).

Mechanical devices
Because an erect penis is such an important contributor to successful sexual penetration, a number of
mechanical devices have been developed that can help the male with an erectile dysfunction achieve
erection.
The first of these is known as a penile prosthesis, and use of these devices is normally reserved for
nonreversible organic‐based erectile problems. The prosthesis consists of a fluid pump located in the
scrotum and a semirigid rod that is surgically inserted in the penis. A discrete squeeze of the pump
releases fluid into the rod that causes the penis to erect. Studies suggest that the penile prosthesis is a safe
and effective means of dealing with erectile dysfunction caused by organic or medical conditions, and
over a period of 7 years since the implant, the penile prosthesis was still successfully dealing with erectile
dysfunction in 82% of patients (Zermann, Kutzenburger, Sauerwein, Schubert & Loeffler, 2006). [Case
History 11.1].

penile prosthesis A mechanical device normally reserved for non-reversible organic-based

erectile problems.

An alternative to the penile prosthesis is a vacuum erection device (VED). This is a hollow cylinder
that is placed over the penis. The client then draws air out the cylinder using a hand pump, and this has
the effect of drawing blood into the penis and causing an erection. As cumbersome as this may seem,
many clients prefer the VED to other more conventional treatments for erectile dysfunction such as
Viagra. Of those given a choice between equally effective VED or Viagra treatments, 33% preferred
the VED—largely because they disliked the adverse side effects of Viagra (Chen, Mabjeesh, &
Greenstein, 2001).

vacuum erection device (VED) A mechanical device normally reserved for non-reversible
organic-based erectile problems.

Mechanical devices to aid penile erection may seem outdated now that effective drugs have been
developed that reliably aid erection during sexual intercourse. However, while around 70% of men
respond well to drugs such as Viagra, this rate is significantly lower in men with diabetes or have been
treated for prostate cancer, and at least some will find mechanical devices preferable. Even though a
‘wonder drug’ such as Viagra may seem like it has solved the problem for most men with erectile
difficulties, new technology is already progressing the range of treatments. These new technologies
include external penis supports, penile vibrators, low intensity extracorporeal shockwave (using
ultrasound to promote the formation of new blood vessels), tissue engineering, nanotechnology, and
endovascular technology (Stein, Lin, & Wang, 2014).
 CASE HISTORY 11.1 ERECTILE DYSFUNCTION

R.K., 47, a senior corporate executive had been happily married for 20 years and had three
children but complained of declining erections. Over the preceding 6 months, his erections had
become so weak that he could not penetrate. He stopped trying 3 months ago.
He thought that this was due to his highly stressful lifestyle and pressures at the workplace. He
even took a vacation with his wife hoping that this would improve matters. It only made them
worse. His wife, at first very co‐operative, eventually began to feel rejected and there was a
palpable friction in their marriage.
When first seen at the clinic, R.K. was defensive. ‘How can this happen to someone like me? I
could do it all night, several times a night, night after night. My family doctor says that this kind
of thing is quite common these days and it's probably the stress’.
It turned out that R.K. was a diabetic of 8 years' standing. He also had high blood pressure for
which he was on beta blockers. He was obese (209 lbs.—175 cm) and smoked 40 cigarettes a
day. He partied 7 days a week and drank quite heavily. He had never exercised in his life. Sadly,
his family doctor had never connected any of these to his sexual problem.
Tests revealed that his overall rigidity levels were well below normal and that he had problems
both with his arteries and his veins. He was eventually cured with an inflatable penile prosthesis.
Adapted from www.testosterones.com

Clinical Commentary
R.K. was quick to link his erectile problems with a stressful lifestyle, and his defensive reaction is typical
of a man who values his own sexual performance as an indicator of his own worth. However, once
R.K.'s medical history was investigated, it became clear that there were a variety of organic and lifestyle
factors that were probably contributing to his erectile dysfunction, including a history of diabetes, high
blood pressure, medications that can interfere with sexual arousal, heavy smoking, and heavy drinking.
Because many of the important causes were organic (e.g., diabetes and cardiovascular problems), the
best long‐term solution in this case was to implant a mechanical device such as a penile prosthesis to aid
erection.

Summary of treatments of sexual dysfunction

This section has discussed the range of treatments available for sexual dysfunctions. Multifaceted
psychological and behavioural based treatments are now used to deal with the specific symptoms of the
disorder as well as any underlying psychological, behavioural, and relationship issues. These are
supplemented by a variety of drug and biological based treatments that help to address any
physiological, organic or hormonal deficits.

11.2.4 Summary of Sexual Dysfunction

Sexual dysfunction has an unusual history in the context of psychopathology. In the first half of the
twentieth century, sexual problems were rarely admitted and discussed, let alone treated. With the
liberating social climate of the 1960s and 1970s this attitude changed, and the pioneering research work
of a few dedicated clinicians (such as Masters and Johnson) provided a database of evidence on these
kinds of disorders, as well as the first integrated sex therapies for sexual dysfunctions. The causes of
sexual dysfunctions range across the biological and organic, psychological factors such as performance
anxiety and negative cognitions about sex, to interpersonal problems, and an equally broad range of
treatments have been developed to address this array of possible causes. Given all this, it is important to
remember that not everyone with less than adequate sexual performance is suffering a sexual
dysfunction. The DSM‐5 criteria clearly state that any performance deficits must be accompanied by
distress and interpersonal difficulties, and it is these latter two factors that define sexual dysfunction
disorders.

SELF‐TEST QUESTIONS

11.2 Sexual Dysfunctions

Can you describe the four stages of the normal sexual response cycle?

11.2.1 Diagnosis of Sexual Dysfunctions

Can you name the disorders of desire and their main diagnostic characteristics?
What are the main disorders of sexual arousal and how are they defined?
Roughly what percentage of men report erection problems, and how does this change with
age?
What are the main disorders of orgasm and how are they defined in DSM‐5?
What is the main sexual pain disorder described in DSM‐5 and how is it defined?
What kinds of decisions does a clinician have to make when diagnosing a sexual
dysfunction?

11.2.2 The Aetiology of Sexual Dysfunctions

Can you list some of the risk factors that have been associated with sexual dysfunctions?
How have repressed emotions and desires been used by psychoanalytic theorists to explain
sexual dysfunctions?
What are the two factors in Masters and Johnson's theory of sexual dysfunction?
How is performance anxiety important in explaining some forms of sexual dysfunction?
In what ways might interpersonal difficulties be associated with sexual dysfunctions?
Is there evidence to suggest that negative emotions such as depression and anxiety are
outcomes or causes of sexual dysfunctions?
What is the difference between remote and immediate causes of sexual dysfunctions? Can
you give some examples of both?
Can you name the three broad categories into which the biological causes of sexual
dysfunctions can be classified?
 In what ways does age affect sexual functioning?

11.2.3 The Treatment of Sexual Dysfunctions

What are direct treatments for sexual dysfunctions?
Can you name and describe at least three direct treatments for sexual dysfunctions?
Why is couples therapy an important form of treatment for sexual dysfunction?
What are the main drug treatments for sexual dysfunctions, and what is the evidence that
they are successful?
What are the main mechanical devices used to treat male sexual dysfunctions?

SECTION SUMMARY
11.2 SEXUAL DYSFUNCTIONS
The four stages of the sexual response cycle are desire, arousal, orgasm, and resolution,
and sexual dysfunctions can be diagnosed in any of these individual stages.
11.2.1 Diagnosis of Sexual Dysfunctions
Sexual dysfunctions are a heterogeneous group of disorders characterised clinically by the
individual’s inability to respond sexually or to experience sexual pleasure.
Male hypoactive sexual desire disorder is characterised by a persistent and recurrent deficiency
or absence of desire for sexual activity.
Erectile disorder is the inability to maintain an adequate erection during sexual activity.
Approximately 13–21% of men aged 40‐80 years experience occasional problems with
erections, but only 2% of men younger than 40 years do.
Female sexual interest/arousal disorder is characterised by significantly reduced interest or lack
of interest in sexual activity, erotic thoughts, and reduced sexual sensations during sexual
activity.
Female orgasmic disorder is characterised by a delay or absence of orgasm during sexual
activity, and around 10% of adult women may never have experienced an orgasm.
Delayed ejaculation is a persistent or recurrent delay in ejaculation following a normal sexual
excitement phase.
Early ejaculation is the onset of orgasm with minimal sexual stimulation. Treatment for this
disorder is typically sought by men under the age of 30 years.
Genito‐pelvic pain/penetration disorder refers to four commonly occurring symptoms, namely
difficulty having intercourse, genito‐pelvic pain, fear of pain or vaginal penetration, and
tension of the pelvic floor muscles.
11.2.2 The Aetiology of Sexual Dysfunctions
Sexual dysfunction is more prevalent in women than in men (43% and 31% respectively)
and is more likely amongst those experiencing poor physical and emotional health.
Psychoanalytic theory attempts to account for sexual dysfunctions in terms of repressed
sexual desires or hostility to the opposite sex.
Masters and Johnson developed a two‐factor model of sexual dysfunction where (a) early
 sexual experiences give rise to anxiety during sex, and (b) this anxiety leads the individual
to adopt a spectator role during sexual activity which directs attention away from stimuli
providing sexual arousal.
Interpersonal difficulties may be both a cause and an outcome of sexual dysfunctions.
Anxiety and depression are closely associated with sexual dysfunctions, and these negative
emotions may interfere with sexual performance.
The causes of sexual dysfunctions can sometimes be defined in terms of immediate causes
(e.g., lack of sexual knowledge) and remote causes (e.g., feelings of shame and guilt that are a
result of a specific upbringing).
Biological causes of sexual dysfunctions can be classified as (a) dysfunctions caused by an
underlying medical disorder, (b) dysfunction caused by hormonal abnormalities, and (c)
changes in sexual responsiveness with age.
11.2.3 The Treatment of Sexual Dysfunctions
Direct treatments attempt to deal with the specific symptoms of the disorder (e.g., the squeeze
technique for premature ejaculation).
The ‘stop‐start’ technique, squeeze technique, and the tease technique are all specific behavioural
treatments designed to treat premature ejaculation and orgasmic disorders.
If sexual dysfunctions are a manifestation of broader problems then couples therapy can be
adopted.
Biological treatments can be categorised into (a) drug treatments, including medications
that directly influence the organic nature of the disorder; (b) hormone treatment designed
to correct hormone imbalances caused by age or sickness; and (c) mechanical devices,
designed to aid mechanical functioning during sex.
75% of men who take Viagra can achieve erection within 60 minutes of administration,
and over 95% of clients treated with Viagra over a 1–3 year period express satisfaction
with their ability to effectively engage in sex.
Mechanical devices to aid penile erection and penetration include the penile prosthesis and
the VED.

11.3 PARAPHILIC DISORDERS

Sexual dysfunctions are one side of the sexual disorders coin, where individuals complain of deficiencies
or inadequacies in their sexual desire and performance. On the other side of the coin are those
psychopathologies that are associated with high frequencies of sexual activity or unusual sexual activities
that are often directed at inappropriate targets. Sexual experience is normally highly valued in Western
cultures, but there is now a good deal of evidence that high rates of sexual behaviour can be
problematic, interfere with personal happiness and social adjustment, and be channeled into unusual
sexual activities (Kafka, 1997, 2003). When high rates of sexual behaviour are channeled into unusual
or very specific sexual activities, these are known collectively as paraphilic disorders. In DSM‐5 the
term paraphilia denotes ‘any intense and persistent sexual interest other than sexual interest in genital
stimulation or preparatory fondling with phenotypically normal psychically mature, consenting human
partners’ (DSM‐5, American Psychiatric Association, 2013, p. 685). Some paraphilias concern the
individual's own erotic activities, and others primarily concern the individual's erotic targets, and a
paraphilic disorder is one that currently causes distress or impairment to the individual or whose
satisfaction has entailed personal harm, or risk of harm, to others. A list of the paraphilias included in
DSM‐5 is provided in Table 11.9. These paraphilias have been listed in three groups. The first group
includes fetishistic disorder and transvestic disorder, where the individual experiences sexual desire
towards inanimate objects or from cross‐dressing. However, to be diagnosed with either of these
disorders, these tendencies must cause the individual significant distress or social and/or occupational
impairment. The second group consists of exhibitionistic disorder, voyeuristic disorder, frotteuristic
disorder, and paedophilic disorder. These disorders have been grouped together because they usually
involve sexual fantasies, urges and activities directed at nonconsenting persons. The exhibitionist will
expose himself to unsuspecting victims; the voyeur will take sexual pleasure from watching unsuspecting
others either naked or in the process of undressing; the frotteurist is sexually aroused by rubbing
themselves against a nonconsenting person; and the paedophile has sexual urges towards and indulges
in sexual acts with prepubescent children, who—by their very age—are unable to legally consent to
these activities. This second group of paraphilic disorders is defined by the fact that the individual does
not have to experience distress or social or occupational impairment to be diagnosed with these disorders
but merely has to have acted on these urges with nonconsenting persons (Hilliard & Spitzer, 2002).
TABLE 11.9 Paraphilic disorders
Fetishistic Recurrent sexual arousal involving
disorder Sexual urges that are not directed at nonanimate objects
Transvestic another person Recurrent, intense sexual arousal from cross‐
disorder dressing
Exhibitionistic Sexual urges directed at nonconsenting Sexual arousal from the exposure of one's
disorder other persons (in many societies these genitals to an unsuspecting person
Voyeuristic activities represent sexual offences) Recurrent sexually arousal fantasies involving
disorder acts of observing an unsuspecting person who
is naked or in the act of undressing
Frotteuristic Recurrent sexual arousal from touching or
disorder rubbing against a nonconsenting person
Paedophilic Recurrent, intense sexually arousing fantasies
disorder or urges involving sexual activity with a
prepubescent child
Sexual Sexual arousal from inflicting or Sexual arousal from being humiliated or
masochism experiencing suffering otherwise forced to suffer
disorder
Sexual sadism Sexual arousal from the psychological or
disorder physical suffering of others
The final group consists of sexual masochism disorder and sexual sadism disorder, where individuals
experience sexual arousal from either the desire to be humiliated or made to physically suffer
(masochism) or inflict physical suffering on others (sadism). Most often sadomasochistic acts are
performed with a consenting partner, but even in such circumstances, the individual may be bothered or
distressed by these tendencies and acts, and personal distress is an important contributor to diagnosis of
these disorders.
From these categorisations it is clear that some paraphilic disorders are victimless (e.g., fetishistic disorder
and transvestic disorder), whereas others will be defined in law as sexual offences (e.g., exhibitionistic
disorder, voyeuristic disorder, frotteuristic disorder, paedophilic disorder, and those acts of sexual sadism
where harm is inflicted on others without consent). Some require these activities to cause personal
distress to be diagnosed, whereas others do not. This leads to an issue of where the line is drawn
between acceptable sexual activity and a psychopathology. Clearly, many of the urges and fantasies
defined in the diagnostic criteria for paraphilias are experienced by many people, and there is a huge
industry willing to cater for these urges in films, magazines, and Internet sites. However, (a) most people
are unwilling to act on their fantasies, and are quite happy to restrict their sexual interest in paraphilic
activities to viewing erotic or pornographic material, and (b) it is only when a person's sexual urges
become linked to just one specific type of stimulus or act, that society begins to deem that behaviour as
‘abnormal’. We must bear these issues in mind when discussing the individual paraphilias.
The following section describes the diagnostic criteria and main characteristics of each of the paraphilic
disorders. We then progress to discuss some of the theories of the aetiology of paraphilic disorders and
finally describe and evaluate forms of treatment.

11.3.1 The Diagnosis and Description of Paraphilic Disorders

Fetishistic disorder
A diagnosis of fetishistic disorder is given when a person experiences recurrent, intense sexually
arousing fantasies and urges involving nonanimate objects, and this causes them personal distress or
affects social and occupational functioning. Often fetishes are restricted to articles associated with sex,
such as women's clothing or undergarments (bras, stockings, shoes, boots, etc.) or to body parts such as
feet, toes, or hair. The individual with fetishistic disorder may experience strong desires to obtain or
touch these items (e.g., by stealing them from washing lines), may ask a sexual partner to wear them
during sex, or may masturbate while holding, rubbing or smelling these articles. A fetish will usually
have developed by adolescence and may have developed as a result of specific experiences during
childhood or early adolescence. Some individuals exhibit a phenomenon known as partialism, which
is fascination with an individual object or body part to the point where normal sexual activity no longer
occurs. Note that fetishistic disorder is not diagnosed if the object concerned is for the purpose of tactile
genital stimulation (such as a vibrator). However, Focus Point 11.4 provides some case reports from the
British Medical Journal of penile injuries and illustrates the lengths to which some individuals will go to
gain sexual excitement. While the injuries incurred were obviously not amusing for the victims, the
reader may be amused by the reasons given for these injuries! (Focus Point 11.4) (Table 11.10).

fetishistic disorder Recurrent, intense sexually arousing fantasies and urges involving non-
animate objects, and this causes them personal distress or affects social and occupational
functioning.

partialism A phenomenon in which there is a fascination with an individual object to the

point where normal sexual activity no longer occurs.

Transvestic disorder
A diagnosis of transvestic disorder is given when a heterosexual male experiences recurrent, intense
sexual arousal from cross‐dressing in women's attire, and this causes significant distress or impairment
in social or occupational functioning. A Swedish study has indicated that 2.8% of men and 0.4% of
women report at least one episode of transvestic behaviour during their life, and risk factors for this
disorder include same‐sex sexual experiences, being easily sexually aroused, pornography use, and
relatively high masturbation frequency (Langstrom & Zucker, 2005). In this particular disorder, sexual
excitement is achieved primarily because female clothes are a symbol of the individual's femininity
rather than because the garments trigger sexual arousal per se (as would be the case with a simple
fetish). The person with transvestic disorder will often keep a collection of women's clothes, and sexual
arousal is normally caused by the man having thoughts or images of himself as a female. Case History
11.2 is a typical example of transvestic behaviour. Like Chris, most individuals diagnosed with
transvestic disorder are relatively happily married men but are worried what others (including their
wives) may think of their behaviour. As a result, over half of those who admit cross‐dressing usually seek
counselling at some stage because of its effects on their intimate relationships (Doctor & Prince, 1997).
Most men with transvestic disorder have been cross‐dressing for many years, usually since childhood or
early adolescence (Doctor & Fleming, 2001), and many women are happy to tolerate their husbands'
cross‐dressing or even incorporate it into their own sexual activities (Case History 11.2) (Table 11.11).
Because of its close association with the gender dysphoria diagnosis in DSM‐5, and the controversy
surrounding that issue (see Focus Point 11.1), there is also considerable discussion about whether
transvestic fetishism should be conceived as a prima facie mental health problem (Gijs & Carroll, 2011).

transvestic disorder When a heterosexual male experiences recurrent, intense sexual arousal
from cross-dressing in women’s attire, and this causes significant distress or impairment in social
or occupational functioning.
FOCUS POINT 11.4 PENILE INJURIES RESULTING FROM A
VACUUM CLEANER

The following are four cases of penile injury incurred when using a vacuum cleaner in search
of sexual excitement. At least two of these injuries were caused by a ‘Hoover Dustette’ which
has fan blades only 15 cm from the inlet.

Case 1—A 60‐year‐old man said that he was changing the plug of his Hoover Dustette vacuum
cleaner in the nude when his wife was out shopping. It ‘turned itself on’ and caught his penis,
causing tears around the external meatus and deeply lacerating the side of the glans.
Case 2—A 65‐year‐old railway signalman was in his signal box when he bent down to pick up
his tools and ‘caught his penis in a Hoover Dustette which happened to be switched on’. He
suffered extensive lacerations to the glans, which were repaired with cat gut with a good result.
Case 3—A 49‐year‐old man was vacuuming his friend's staircase in a loose‐fitting dressing
gown when, intending to switch the machine off, he leaned across to reach the plug: ‘At that
moment his dressing gown became undone and his penis was sucked into the vacuum cleaner’.
He suffered multiple lacerations to the foreskin as well as lacerations to the distal part of the
shaft of the penis.
Case 4—This patient was aged 68, and no history is available except that the injury was caused
by a vacuum cleaner. The injury extended through the corpora cavernosa and the corpus
spongiosum and caused complete division of the urethra proximal to the corona.
From Citron & Wade, 1980
TABLE 11.10 Summary: DSM‐5 diagnostic criteria for fetishistic disorder

Over a period of 6 months, recurring and strong sexual arousal from the use of nonliving objects
or a highly specific focus on nongenital body parts as part of fantasies, urges, or behaviours,
causing significant distress or impairment in social, occupational, or other areas of life
The fetish is not limited to the clothing used in cross‐dressing or objects such as vibrators and
other genital simulators

TABLE 11.11 Summary: DSM‐5 diagnostic criteria for transvestic disorder

Continuing and powerful sexual arousal from cross‐dressing as part of fantasies, urges, or
behaviours, over a period of at least 6 months, causing significant distress or impairment in social,
occupational, or other areas of life

Exhibitionistic disorder
This paraphilic disorder involves sexual fantasies about exposing the genitals to a stranger. These
fantasies are usually strong and recurrent to the point where the individual feels a compulsion to expose
himself or herself, and this compulsion often makes the individual oblivious of the social and legal
consequences of what they are doing (Stevenson & Jones, 1972). The onset of exhibitionistic
disorder usually occurs before 18 years of age, and is often found in individuals who are immature in
their relationships with the opposite sex, and many have problems with interpersonal relationships
generally (Mohr, Turner, & Jerry, 1964). The sufferers urge to expose himself/herself will often lead
them to find a victim in a public place, often a park or a side street, where they expose themselves—
usually to a single victim. The victim's response of shock, fear, or revulsion often forms part of the
gratification that reinforces this behaviour, and the exhibitionist may sometimes masturbate while
exposing himself/herself (especially if he finds the victim's reaction to his behaviour sexually arousing)
or may return home to masturbate while fantasising about the encounter. Exhibitionists will usually
expose themselves to women or children, and while no physical harm is usually involved, the experience
for the victim is often traumatic and may have lasting psychological consequences. A significant
percentage of individuals with a diagnosis of exhibitionistic disorder are nondisclosing, deny any urges
or fantasies related to exposing themselves, and report that incidents of exposure were either accidental
or nonsexual. Men are significantly more likely to be diagnosed with exhibitionistic disorder than
women, and the prevalence rate of exhibitionist acts in men is estimated to be between 2‐4% (DSM‐5,
American Psychiatric Association, 2013, p. 690) (Table 11.12).

exhibitionistic disorder Involves sexual fantasies about exposing the genitals to a stranger.
 CASE HISTORY 11.2 TRANSVESTIC DISORDER

‘I am sure I am not the first cross‐dresser to feel this way but when I get the chance to dress at first I am excited, I
can hardly wait to put on the stockings, skirt and get all dolled up and once I am fully dressed I feel so good!
Almost like this is the way I am supposed to be but that feeling does not last……Sometimes it will last an hour
to hours but I have actually had it diminish within 15 mins before I feel guilty and then undress and go back to
my guy clothes. For some reason a light goes on in my head that tells me, I am a guy…. why am I wearing a
skirt?!? and then I quickly undress. But then when I am dressed as a guy I will admire women in skirts and
dresses and wish that could be me and all I want to do is rush home and dress (when my wife is not home). I
would love to tell my wife about my CD'ing but I need to come to terms with it first’.

Chris's Story

TABLE 11.12 Summary: DSM‐5 diagnostic criteria for exhibitionistic disorder

Continuing and powerful sexual arousal from exposing one's genitals to an unsuspecting audience,
over a period of at least 6 months, as part of fantasies, urges, or behaviours
The patient has acted on these urges with a nonconsenting person or the urges cause significant
distress or impairment in social, occupational, or other areas of life

Voyeuristic disorder
A diagnosis of voyeuristic disorder is given when an individual experiences recurrent, intense
sexually arousing fantasies or urges involving the act of observing an unsuspecting person who is naked,
in the process of undressing, or engaging in a sexual activity. Sexual arousal normally comes from the
act of looking (‘peeping’), and the individual may masturbate while in the act of observing others.
However, the individual rarely seeks sexual activity with those being observed. Voyeurism usually begins
in early adolescence, and may often constitute that individual's sole sexual activity in adulthood (Kaplan
& Kreuger, 1997). The risk of being discovered while indulging in voyeuristic behaviours may also add
to the excitement that this behaviour engenders. However, we must be clear that voyeurism can be a
perfectly acceptable sexual activity when practiced between consenting individuals, but is clearly
problematic when the voyeur begins seeking non‐consenting victims and violates their privacy.
Voyeuristic acts are the most common of the potentially illegal paraphilic behaviours, with estimates of
the possible lifetime prevalence of voyeuristic acts being as high as 12% in males and 4% in females
(DSM‐5, American Psychiatric Association, 2013, p. 688). (Table 11.13).

voyeuristic disorder When an individual experiences recurrent, intense sexually arousing

fantasies or urges involving the act of observing an unsuspecting person who is naked, in the
process of undressing, or engaging in a sexual activity.

Frotteuristic disorder
This involves intense, recurrent sexual urges to touch and rub up against nonconsenting people—
usually in crowded places such as underground trains, buses, cinema or supermarket queues, etc. This is
usually a male activity, and manifests as a sexual urge to rub the genitalia against the victim's thighs and
buttocks or to fondle the victim's genitalia or breasts with his hands. This behaviour is usually
undertaken in a surreptitious way in order to try to make it appear unintentional or as if someone else
in the crowded environment is the culprit. Like exhibitionism and voyeurism, this activity usually begins
in adolescence, but may subside in frequency by the time the individual is in their late 20s. Frotteurism is
considered by many to be a form of sexual assault, and at least part of the excitement for frotteurs is the
feeling of power it gives them over their victim—a feeling that is relatively common in those who
indulge in sexual assault generally. Around 10‐14% of adult males seen in outpatient settings for
paraphilic disorders meet the criteria for frotteuristic disorder (DSM‐5, American Psychiatric
Association, 2013, p. 693) (Table 11.14).
TABLE 11.13 Summary: DSM‐5 diagnostic criteria for voyeuristic disorder

Continuing and powerful sexual arousal from the observance of an unsuspecting person who is
naked, undressing, or engaging in sexual activity, over a period of at least 6 months, as part of
fantasies, urges, or behaviours
The patient has acted on these urges with a nonconsenting person or the urges cause significant
distress or impairment in social, occupational, or other areas of life
The individual experiencing the arousal is at least 18 years of age

Paedophilic disorder
Paedophilic disorder is defined as sexual attraction towards prepubescent children, normally of 13‐
years or younger. To be diagnosed with paedophilic disorder, the individual must be at least 16 years of
age and at least 5 years older than the victim. Recent studies suggest that up to 9% of men have
described having at least one sexual fantasy with a child, and so such fantasies are not that uncommon
in the general population (Seto, 2009). However, DSM‐5 does highlight the fact that paedophilic
disorder is only diagnosed if the individual acts on these fantasies or is distressed by them.

paedophilic disorder Sexual attraction towards prepubescent children, normally of 13 years

or younger.

The extensive use of pornography depicting children is usually an indicator of paedophilic disorder,
and the condition often becomes apparent as a sexual interest in children around puberty. Those who
report paedophilic sexual urges, usually report a preference for males or females, or sometimes for both.
Those attracted to females usually prefer 8‐ to 10‐year‐olds, whereas those attracted to males usually
prefer older children (DSM‐IV‐TR, p. 571). Paedophilia generally appears to be a lifelong condition, in
which many with a sexual interest in children will often deny attraction to children despite multiple
sexual approaches to children. Paedophilic disorder, however, is defined by other elements that may
change over time such as guilt, shame, or feelings of isolation. The highest likely prevalence for
paedophilic disorder in males is around 3‐5% (DSM‐5, American Psychiatric Association, 2013, p. 698;
Tenbergen et al., 2015).
TABLE 11.14 Summary: DSM‐5 diagnostic criteria for frotteuristic disorder

Continuing and powerful sexual arousal from touching or rubbing against a nonconsenting
person, over a period of at least 6 months, as part of fantasies, urges, or behaviours
The patient has acted on these urges with a nonconsenting person or the urges cause significant
distress or impairment in social, occupational, or other areas of life
The central feature of the psychopathology is sexual attraction to children, but this is not equivalent to
‘child sexual abuse’, ‘incest’, or ‘child molestation’ because the latter represent criminal acts. It is
important to make this distinction because not all who sexually abuse children are diagnosable with
paedophilic disorder—for example, many who sexually abuse children may opportunistically select
children simply because they are available, and such people do not necessarily have specific fantasies
about having sex with children (Fagan, Wise, Schmidt, & Berlin, 2002). Girls are 3 times more likely
than boys to be sexually abused, and children from low‐income families are 18 times more likely to be
sexually abused (Sedlak & Broadhurst, 1996a,b). The paedophile's sexual activity with children is usually
limited to acts such as undressing the child, exposing themselves, masturbating in the presence of the
child, or gently touching or fondling the child and their genitalia. However, in more severe cases, this
activity can extend to performing oral sex acts with the child, or penetrating the child's vagina, mouth
or anus with fingers, foreign objects, or their penis. In general, paedophiles rarely believe that what they
are doing is wrong and avidly deny their sexual attraction to children. They will also often use
egocentric forms of rationalisation to justify their acts (e.g., the acts had ‘educational value’ or that the
child was consenting or gained pleasure from the activity). Because of this, they often fail to experience
distress or remorse, and so experiencing distress or psychological impairment is not a necessary part of
the diagnostic criteria for paedophilic disorder (Table 11.15).
There are a number of unofficial subtypes of paedophilia. First, some paedophiles limit their activities
to their immediate family (e.g., children, stepchildren, nieces and nephews, etc.) and incest is listed as a
specifying factor in DSM‐5. Men who indulge in incest tend to differ from other paedophiles (a) by
indulging in sexual activity with children of a slightly older age (e.g. an incestuous father may show
sexual interest in a daughter only when the daughter begins to become sexually mature), and (b) by
having a relatively normal heterosexual sex life outside of the incestuous relationship. In contrast,
nonincestuous paedophiles will normally become sexually aroused only by sexually immature children
and are sometimes known as preference molesters (Marshall, Barbaree, & Christophe, 1986).
Second, most paedophiles rarely intend to physically harm their victims (even though they may threaten
their victims in order to prevent disclosure), but some may get full sexual gratification only from
harming and even murdering their victims. This latter group are probably best described as child
rapists; they appear to be fundamentally psychological different to other paedophiles and often have
comorbid diagnoses of personality disorder or sexual sadism (Groth, Hobson, & Guy, 1982).

preference molesters Non-incestuous paedophiles who normally only become sexually

aroused by sexually immature children.

child rapists A group of paedophiles who only get full sexual gratification from harming and
even murdering their victims.

TABLE 11.15 Summary: DSM‐5 diagnostic criteria for paedophilic disorder

Continuing and powerful sexual arousal from fantasies, urges, or behaviours involving sexual
activity with a prepubescent child or children (aged 13 years or younger)
The individual has acted on these urges or the urges cause significant distress or impairment in
social, occupational or other areas of life
The individual is at least 16 years old and at least 5 years older than the child or children involved
Does not include an individual in late adolescence in an ongoing sexual relationship with a 12‐ or
13‐year‐old

Because their behaviour is illegal and socially outlawed, and because they need to gain the trust of their
child victims in order to indulge in their sexual activities, most individuals diagnosable with paedophilic
disorder develop elaborate ways of gaining access to children. This can involve taking jobs in
environments where children are frequently found (e.g., schools, residential children's homes, etc.),
gaining the confidence of the parents or family of a child, or more recently by ‘grooming’ children in
Internet chat rooms by pretending to be someone of a similar age to the victim. Focus Point 11.5
provides an example of how paedophiles may ‘groom’ and lure children for sexual purposes on the
Internet (Focus Point 11.5). In a qualitative study of the modus operandi of male paedophiles, Conte,
Wolf, and Smith (1989) were able to describe a standard process through which many paedophiles
operated to attract and isolate their victims and desensitise them to their sexual advances. This process
included (a) choosing an open, vulnerable child who would be easily persuaded and would remain silent
after the abuse, (b) using nonsexual enticements such as purchases or flattery on early encounters with
the child, (c) introducing sexual topics into the conversation, and (d) progressing from non‐sexual
touching to sexual touching as a means of desensitising the child to the purpose of the touching. After
the abuse, the paedophile would use his adult authority to isolate the child and their ‘shared behaviour’
from family and peers.

FOCUS POINT 11.5 PAEDOPHILE ‘GROOMING’ OVER THE

INTERNET

HOW DO ONLINE PREDATORS WORK?

Predators establish contact with kids through conversations in chat rooms, instant messaging,
email, or discussion boards. Many teens use peer support online forums to deal with their
problems. Predators, however, often go to these online areas to look for vulnerable victims.
Online predators try to gradually seduce their targets through attention, affection, kindness,
and even gifts and often devote considerable time, money, and energy to this effort. They are
aware of the latest music and hobbies likely to interest kids. They listen to and sympathise with
kids' problems. They also try to ease young people's inhibitions by gradually introducing sexual
content into their conversations or by showing them sexually explicit material. Older predatory
paedophiles don't usually pose as teenagers but do look for signs of a kid who is attention
starved or whose parents don't seem to care much about them. He will then begin to discover
where they might live by asking questions about their school or their locality.
Some predators work faster than others, engaging in sexually explicit conversations
immediately. This more direct approach may include harassment or stalking. Predators may
also evaluate the kids they meet online for future face‐to‐face contact.

From www.bewebaware.ca

Finally, it is important to remember that by their very age, the victims of paedophilia are nonconsenting
victims, and that sexual activity with prepubescent children is illegal in most societies. Self‐report studies
indicate that 20% of adult females and 5–10% of adult males recall a childhood sexual assault or sexual
abuse incident (National Center for Victims of Crime, 2011). Furthermore, it is also important to note
that the victims of paedophilia can suffer long‐term psychological problems as a result of their
experiences, and these can manifest as eating disorders, sleep disorders, depression, anxiety disorders
such as panic attacks and phobias, self‐harm, and dissociative disorders, all persevering well into
adulthood. These psychological problems are more intense and more enduring if the abuse occurred at
an early age and the victim knew their abuser well (Kendall‐Tuckett, Williams, & Finkelhor, 1993).

Sexual masochism disorder and sexual sadism disorder

A diagnosis of sexual masochism disorder is given if the individual gains sexual arousal and
satisfaction from being humiliated, beaten, bound, or otherwise made to suffer, and these urges cause
significant distress or social and occupational impairment. In contrast, sexual sadism disorder is
when the person gains sexual arousal and satisfaction from the psychological or physical suffering of
others. A diagnosis of sexual sadism disorder is given if these symptoms cause distress or significant
social or occupational impairment to the individual, or if the individual acts on these urges with a
nonconsenting person. Sadomasochistic acts are often performed between consenting mutual partners,
one who gains satisfaction from sadistic acts and the other who enjoys being humiliated. Sadistic or
masochistic activities include acts that emphasise the dominance and control of one person over the
other. These may include restraint, blindfolding, spanking, whipping, pinching, beating, burning, rape,
cutting, stabbing, strangulation, torture, and mutilation. Acts of dominance (or submission) may include
forcing the submissive partner to crawl on the floor or keeping them restrained in a cage. Sexual
masochists can often cause their own suffering, and one prominent example is known as
hypoxyphilia, which involves the individual using a noose or plastic bag to induce oxygen deprivation
during masturbation. In contrast, when they are unable to obtain consenting partners, sexual sadists
may resort to rape, mutilation, and murder to satisfy their sexual desires (Dietz, Hazelwood, & Warren,
1990), and there is a high rate of comorbidity between sexual sadism disorder and impulse disorders.
For example, in individuals with a diagnosis of sexual sadism disorder, 31% were also diagnosed with
borderline personality disorder, and 42% with antisocial personality disorder (Berger, Berner,
Bolterauer, Guterrez, & Berger, 1999), and an association between sexual masochism and borderline
personality disorder in women has also been reported (Frías, González, Palma, & Farriols, 2017). It is
estimated that around 5–10% of the population indulge in some kind of sadomasochistic activity at
some time in their life (Baumeister & Butler, 1997), and most are heterosexual, reasonably affluent, well
educated, indulge in these activities with a consenting partner, and are not unnecessarily distressed or
disturbed by their sexual predilections (Moser & Levitt, 1987). If this is so, then most sadomasochistic
activity does not involve either psychological distress or imposition of a sexual urge on non‐consenting
persons, and so would not meet the DSM‐5 criteria for a disorder. Because sadomasochism is enjoyed by
many individuals who incorporate these activities into their normal sexual relationships, there is a
growing market for such activities catered for by sex shops, underground newspapers, and websites.
Indeed, over the years, sadomasochism (known as S & M) has also become a significantly accepted
subculture within homosexual circles (Tables 11.16 and 11.17).

sexual masochism disorder When an individual gains sexual arousal and satisfaction from
being humiliated, and this causes the individual significant distress.

sexual sadism disorder When a person gains sexual arousal and satisfaction from the
psychological or physical suffering of others, and this diagnosis is given if the symptoms cause
the individual significant distress or if the person acts on the impulses with a non-consenting
person.

hypoxyphilia An act performed by sexual masochists which involves the individual using a
noose or plastic bag to induce oxygen deprivation during masturbation.

TABLE 11.16 Summary: DSM‐5 diagnostic criteria for sexual masochism disorder

Continuing and powerful sexual arousal from the act of being humiliated, tied up, beaten, or
made to suffer, over a period of at least 6 months, as part of fantasies, urges, or behaviours
The urges cause significant distress or impairment in social, occupational, or other areas of life
TABLE 11.17 Summary: DSM‐5 diagnostic criteria for sexual sadism disorder

Continuing and powerful sexual arousal from the physical or psychological suffering of another
person, over a period of at least 6 months, as part of fantasies, urges, or behaviours
The patient has acted on these urges with a nonconsenting person or the urges cause significant
distress or impairment in social, occupational, or other areas of life

11.3.2 The Aetiology of Paraphilic Disorders

The causes of paraphilia disorders are relatively under‐researched compared to other
psychopathologies, and what research is available has mainly been confined to the study of those
paraphilic disorders that involve sexual offending (e.g., paedophilia, exhibitionism). Traditionally,
psychodynamic explanations had been popular but these have now tended to be superseded by cognitive
and, to a lesser degree, biological explanations. We begin this section by looking at some of the risk
factors associated with the development of paraphilic disorders to give you an indication of some of the
experiential and psychological factors associated with paraphilias.

Risk factors for paraphilic disorders

It may not have escaped the reader that most of the DSM‐5 diagnosable paraphilias are mainly male
activities, so being male is in itself a risk factor for paraphilic disorders. For example, surveys have
suggested that 89% of acts of child sexual abuse are perpetrated by men, and only 11% by women
(Sedlak & Broadhurst, 1996a,b), and male masochists outnumber females by 20 to 1. It is by no means
clear why paraphilias should be such a male preserve, but this may in part be due to female sexuality
being repressed more than male sexually—especially during socialisation. There is some evidence of a
link between high rates of sexual activity generally, and anxiety and depression, and paraphilias (Kafka,
1997: Raymond, Coleman, & Miner, 2003). High rates of sexual activity is known as hypersexuality,
and it was itself considered for inclusion as a disorder in DSM‐5, although it was omitted from the final
published version (Walters, Knight, & Langstrom, 2011). One implication of the link between
hypersexuality and paraphilias is that high rates of sexual activity may lead individuals to evolve specific
sexual inclinations and urges that are characteristic of paraphilia. Hypersexuality is found more often in
men who are young, have experienced separation from parents during childhood, live in major urban
areas, have had sexual experiences at an early age, frequently experience same‐sex sexual behaviour, pay
for sex, and are relatively more dissatisfied with sexual life than non‐hypersexual men (Langstrom &
Hanson, 2006). The study by Langstrom and Hanson also identified a strong association between
hypersexuality and exhibitionism, voyeurism, and sexual masochism and sexual sadism. Hypersexual
men were also characterised by their willingness to indulge in a range of risky behaviours, including
tobacco smoking, heavy drinking, using illegal drugs, and gambling. These initial studies do suggest
some kind of important link between hypersexuality and paraphilia, and further research in this area
may help to clarify the risk factors and causes of individual paraphilias. Given that we now know some
of the factors that predict hypersexuality, then these might also play a significant role in predicting the
development of paraphilias.

hypersexuality The occurrence of high rates of sexual activity.

A number of studies have also identified some of the risk factors involved in paedophilia. These can be
categorised as either remote factors (i.e., factors from the individual's developmental history) or
precipitant factors (i.e., factors that lead directly to the expression of paedophile behaviour). Remote risk
factors for paedophilia include being a victim of childhood sexual abuse (Cohen et al., 2010), or
possessing an inadequate attachment style that results from being brought up in a dysfunctional family
(Hanson & Slater, 1988). Precipitating risk factors include depression, psychosocial stress (for example,
as a result of losing a relationship or a job), alcohol abuse (Fagan, Wise, Schmidt, & Berlin, 2002), social
incompetence, emotional dysregulation, and substance abuse generally (Yakeley & Wood, 2014).
Psychiatric comorbidity is also highly associated with paedophilic disorder, with 93% of paedophiles
being diagnosed with at least one other psychopathology during their lifetime, such as major depression
or anxiety disorders. In addition, 60% of paedophiles are diagnosed with a substance abuse disorder,
and 60% meet the diagnostic criteria for a personality disorder (Raymond, Coleman, Ohlerking,
Christensen, & Miner, 1999). The statistics support the view that psychopathology may be a
precipitating factor in triggering paedophile behaviour.

The psychodynamic perspective

Psychodynamic theorists take a range of views about the causes of paraphilias. They can be viewed
either as (a) defensive reactions that are attempting to defend the ego from repressed fears, or (b) as
representing fixation at a pre‐genital stage of development (usually the Oedipal stage). For example,
fetishism and paedophilia can be viewed as the behaviour of individuals who find normal heterosexual
sex with women too threatening—perhaps because of a castration anxiety—and voyeurism is a
behaviour that protects the individual from having to deal with the relationships that are often an
inherent part of sexual life. In this respect, psychodynamic approaches view those with paraphilias as
individuals whose sexual development is immature or who are unable to deal with the complexity of
relationships that usually surround normal heterosexual behaviour. (Lanyon, 1986). Alternatively,
paraphilias may be associated with a fixation at the Oedipal stage of development, which is itself
associated with castration anxiety. For example, transvestic fetishism is seen as a denial of the mother's
castration. Dressing in a woman's clothes but still having a penis underneath the clothing is seen as
reassuring the transvestite that his mother has not been castrated and he should not therefore worry
about himself being castrated (Nielson, 1960). Castration anxiety again crops up in psychodynamic
interpretations of other paraphilias such as sexual sadism, where the sadist is seen as feeling relief from
castration anxiety by taking on the role of castrator rather than the castrated.

castration anxiety A psychoanalytic term referring to a psychological complex in males with

a fear of being castrated.

Because of the way in which psychodynamic theory is couched, it is difficult to find objective evidence
to support these explanations of paraphilias. If such factors do underlie paraphilia behaviour, then
exploring them in psychoanalysis should help to alleviate these diverse sexual activities. However, there
is only modest evidence that psychoanalysis is successful in the treatment of paraphilias (Cohen &
Seghorn, 1969), and it is usually entirely ineffective in treating sexual offenders (Knopp, 1976).

Classical conditioning
One very simple explanation for paraphilic disorders is that unusual sexual urges are the result of early
sexual experiences (such as masturbation) being associated with an unusual stimulus or behaviour
through associative learning (classical conditioning). For example, an adolescent boy's first sexual
experiences may be masturbating to pictures of women dressed in fur or leather (resulting in a fur or
leather fetish), or masturbating after accidentally seeing a neighbour undressing (resulting in voyeurism).
Such early experiences may determine the route an adolescent's sexual development will take, and this
conditioning account is consistent with the fact that many of the paraphilias first manifest in early
adolescence. Support for the classical conditioning account also comes from an early experiment that
attempted to develop a fetish for women's knee‐length leather boots in a group of male volunteers.
Rachman (1966) showed participants slides of a pair of black, knee‐length woman's leather boots (the
conditioned stimulus, CS) followed immediately by a slide of an attractive female nude (the
unconditioned stimulus, UCS). After a number of pairings of the CS with the UCS, participants
showed an increase in penis volume (as measured by a phallo‐plethysmograph) whenever the CS slide
was shown. One participant even generalised this sexual response to pictures of other forms of female
footwear! Nevertheless, while the conditioning of a sexual fetish can be experimentally demonstrated
under controlled conditions, it is unlikely that conditioning is the cause of all paraphilias. It may
account for the initial development of some fetishes, and may also account for why sexual urges initially
become associated with specific activities such as voyeurism, frotteurism, or object‐assisted sexual
behaviours in women (O'Keefe et al., 2009). However, as normal sexual activities become experienced
during adolescence and early adulthood, conditioning theory would predict sexual urges to become
associated with these normal sexual activities and links between sexual urges and early, learnt paraphilia
behaviour should extinguish. Nevertheless, paraphilias frequently persist—even when the sufferer finds
them distressing and even when they are also concurrently engaging in normal sexual behaviour.

Childhood abuse and neglect

As we have seen many times in this book, childhood abuse and neglect is an important predictor of
psychological problems later in life, and this is no less true for the development of paraphilic disorders.
However, the way in which negative early experiences may facilitate the development of paraphilic
disorders is probably complex. First, physical and sexual abuse is a feature of the history of many
individuals with paraphilias, as is a history of disturbed and neglectful parenting (Mason, 1997;
Murphy, 1997), and childhood sexual abuse is reported by between 40 to 66% of adult sexual offenders
(Jepersen, Lalumiere, & Seto, 2009; Levenson & Grady, 2016). So what is it that makes childhood
victims of sexual abuse more likely to become sexual offenders? One factor is being made familiar with
sexual acts from an early age, but other studies have suggested that anger may mediate the transition
from victim to offender. Ramirez, Jeglic, and Calkins (2015) found that sex offenders who were rated as
being highly angry were more likely to have been abused as children and were more likely to have used
violence in their crimes. This finding held for both rapists and child molesters.
However, childhood abuse and neglect is not a prerequisite for developing a paraphilic disorder or
becoming a sexual offender, and less than 30% of sexual offenders have a history of childhood sexual
abuse (Maletzky, 1993). Nevertheless, the level of childhood abuse experienced by sexual offenders is
almost double the level found in the general population (Laumann, Gagnon, Michael, & Michael,
1994), so childhood abuse may presumably contribute to paraphilia in some as yet unspecified way.
Problematic parent–child relationships may also play a significant role in the development of specific
paraphilic disorders. For example, neglectful or abusive parenting can leave the child with low self‐
esteem, poor social skills, a lack of effective coping strategies, and an inability to form lasting
relationships (Marshall & Serran, 2000). These psychological and behavioural deficits may lead the
individual to find sexual satisfaction in ways that do not require them to deal with the consensual
relationships required by normal sexual activity (e.g., transvestism, voyeurism, exhibitionism,
frotteurism) or may lead them to seek sexual satisfaction with others, such as children, with whom their
underdeveloped social and emotional skills do not put them at a disadvantage.
In conclusion, childhood abuse and neglect are certainly factors that can be found in the history of
some individuals who develop paraphilias, but the mechanisms by which these experiences are
translated into problematic sexual urges have still to be identified in detail.

Dysfunctional beliefs, attitudes, and schemata

Many problematic behaviours that are central to psychopathology are often maintained by
dysfunctional beliefs or biases in information processing that lead the individual to think and behave in
the way they do (see Chapters 6 and 7 for examples). This also appears to be true of some of the
paraphilic disorders, and especially those that are either illegal or involve behaviours towards a
nonconsenting victim (e.g., paedophilic disorder, exhibitionistic disorder, voyeuristic disorder). A
considerable body of research suggests that cognitive distortions, dysfunctional beliefs, and information
processing biases play an important role in facilitating paraphilias that involve sexual offending in males
(Abel et al., 1989; Ward, Hudson, Johnston, & Marshall, 1997; Shruti, Ward, & Gannon, 2008) and
females (Gannon & Alleyne, 2013). For example, incest offenders hold beliefs that children are both
sexually attractive and sexually motivated (Hanson et al., 1994), and many paedophiles believe that
children want sex with adults, and see contact as being socially acceptable and not harmful to the child
(Stermac & Segal, 1989). Abel et al. (1989) labelled these beliefs cognitive distortions and argued
that, for paedophiles, they serve to legitimise or justify sexual involvement with children and function to
maintain the behaviour. These beliefs not only act as reasons why the paedophile should sexually offend,
they also function as excuses for the behaviour, a means of diffusing responsibility for the behaviour
after the act, and morally disengaging from the act (Petruccelli et al., 2017). They also appear to be a
means by which the paedophile can maintain their self‐esteem after offending (Pollock & Hashmall,
1991; Ward, Hudson, Johnston, & Marshall, 1997). Table 11.18 provides examples of the cognitive
distortions found in the post‐offending statements of paedophiles and exhibitionists, together with the
putative functions that these cognitive distortions serve. However, there is still some debate about
whether sexual offenders such as paedophiles genuinely hold these beliefs or whether they are faked in
order to diffuse responsibility after the offence. Using a procedure in which child molesters believed
their responses were being monitored by a lie detector, Gannon (2006) found that participants endorsed
fewer cognitive distortions than when they believed their responses were unmonitored (Research Box
11.1). This suggests that at least some cognitive distortions may be faked in order to provide post‐offence
excuses for the paedophile's behaviour, and more experimental techniques may need to be developed to
understand the mechanisms that underlie the development and purpose of cognitive distortions in sex
offenders (Gannon, Ward, & Collie, 2007).

cognitive distortions Beliefs held by sexual offenders that enable them to justify their sexual
offending.

TABLE 11.18 Cognitive distortions found in the post‐offending statements of paedophiles and exhibitionists
Adapted from Maletzky (2002).
Function of Paedophilia Exhibitionism
statement
Misattributing ‘She would always run around half‐ ‘The way she was dressed, she was asking
blame dressed’. for it’.
Denying sexual ‘I was just teaching her about sex’. ‘I was just looking for a place to pee’.
intent
Debasing the ‘She always lies’. ‘She was just a slut anyway’.
victim
Minimising ‘She's always been really friendly to me— ‘I never touched her—so I couldn't have
consequences even afterwards’. hurt her’.
Deflecting ‘This happened years ago, why can't ‘It's not like I raped anyone’.
criticism everyone forget about it?’.
Justifying the ‘If I wasn't molested as a kid, I'd never ‘If I knew how to get dates, I wouldn't
cause have done this’. have to expose myself ’.

RESEARCH METHODS IN CLINICAL PSYCHOLOGY 11.1 THE

BOGUS PIPELINE PROCEDURE TO INCREASE HONEST
RESPONDING IN PAEDOPHILES
Sexual offenders such as paedophiles appear to possess a set of cognitive distortions that serve
to legitimise or justify sexual involvement with children and function to maintain the behaviour
(Abel et al., 1989) (see Table 11.15). These beliefs may well act as reasons why the paedophile
should sexually offend, but there is still some debate about whether sexual offenders genuinely
hold these beliefs or whether they are faked in order to diffuse responsibility after the offence.
So how might psychologists find out whether these beliefs are real or faked? A study by Gannon
(2006) used what is known as a bogus pipeline procedure with child molesters. In this
procedure, participants are wired to an apparatus that measures skin conductance through
electrodes attached to the fingers. Some participants are then told to refrain from answering
dishonestly because skin conductance may be related to dishonest responses (as if they were
wired up to a ‘lie detector’, but in fact the evidence that skin conductance can reliably indicate
lying is modest).
The study has three stages:
Stage 1: Convicted paedophiles are asked to say whether they agree or disagree with
statements related to cognitive distortions in sexual offenders. Example items are the following:
Some children know more about sex than adults AGREE/DISAGREE
An 8‐year‐old can enjoy a good sex joke AGREE/DISAGREE
Children are not as innocent as most people think AGREE/DISAGREE
Stage 2: One week later the same participants had to response to the same statements (but they
were not told it was the same questionnaire). Half were simply asked to fill out the
questionnaire for a second time. The other half were connected to the bogus pipeline and given
instructions that skin conductance could detect dishonest responses.
Results: The results show that, compared with control participants, those attached to the
bogus pipeline showed a significant reduction in agreeing with the cognitive distortion
statements between time 1 (when they were not connected to the bogus pipeline) and time 2
(when they were connected to the bogus pipeline)
 Conclusions: This imaginative empirical approach to this problem indicates that sexual
offenders may to some extent be faking the cognitive distortions they hold in order to justify
their sexual offending. However, we must also note that (a) this study does involve some
deception, so it is important to ensure that such studies comply with normally accepted ethical
guidelines (such as the BPS guidelines on ethical principles for conducting research with human
participants, www.bps.org.uk), and (b) to ensure a proper balanced design, at Time 2 both
experimental andcontrol participants should have been connected to the bogus pipeline, but
only the experimental group told that it may detect dishonesty—for instance, simply being
connected to the bogus pipeline may itself influence responding.

The cognitive distortions that many sex offenders hold are often the products of more dynamic
cognitive processes. For example, Stermac and Segal (1989) found that sexual offenders interpret sexual
information in a biased way, usually in a manner consistent with their underlying beliefs about the
acceptability of their behaviour. They found that child molesters differed from other respondent groups
by having a predisposition to interpret information as implying benefits could be gained from sexual
contact with children, there was greater complicity on the child's part, and less responsibility on the
adult's part. Finally, research has suggested that sex offenders—and rapists in particular—may have
developed integrated cognitive schemata that guide the offender's interactions with their victims and
justify their behaviour. Polaschek and Ward (2002) called these implicit theories. Offenders use these
schemata as causal theories about themselves, their victims and broader categories of people (such as
women or children). Polaschek and Gannon (2004) identified five types of implicit theory held by
rapists. These included the beliefs that (a) women are unknowable (i.e., ‘sexual encounters will end up
being adversarial because a woman's intentions are unknowable’), (b) women are sex objects (i.e.,
‘women are constantly sexually receptive and so will enjoy sex even when it is forced on them’), (c) the
male sex drive is uncontrollable (i.e., ‘a man's sex levels will build up to a dangerous level if women do
not provide them with reasonable sexual access’), (d) men are naturally dominant over women (i.e., ‘men
are more important in society than women, and a woman should meet a man's needs on demand’), and
(e) the world is a dangerous place (i.e., ‘it is a dog‐eat‐dog world and a man needs to take what he can
from it’). Implicit cognitive theories such as these can provide the sex offender with a justification for
both impulsive and premeditated sexual offences, and can be used as a way of denying both the
significance of the offence and the offender's responsibility for the offence, and further research is
beginning to identify the different forms of dysfunctional schemas that may act as vulnerability factors
for different forms of sexual offending (Sigre‐Leirós, Carvalho, & Nobre, 2015).

implicit theories In sexual offending, integrated cognitive schemas that guide sexual
offenders’ interactions with their victims and justify their behaviour.

Biological theories
As we mentioned earlier, the vast majority of those diagnosed with a paraphilia are male, and so it has
been hypothesised that paraphilia is caused by abnormalities in male sex hormones or by imbalances in
those brain neurotransmitters that control male sexual behaviour. For example, androgens are the
most important of the male hormones, and it may be that unusual sexual behaviour, such as impulsive
sexual offending involving non‐consenting others, may be due to imbalances in these hormones.
However, there is relatively little convincing evidence that abnormal androgen levels play a significant
role in the development of paraphilic behaviour, although androgen levels may help to maintain
paraphilic behaviour once it has been acquired (Buvat, Lemaire, & Ratajczyk, 1996; Thibaut, De La
Barra, Gordon, Cosyns, & Bradford, 2010), and antiandrogen drugs that reduce testosterone levels are
regularly used to reduce the sexual urges of those with paraphilia disorders (Bradford & Pawlak, 1993;
Jordan, Fromberger, Stolpmann, & Muller, 2011). Abnormalities in brain neurotransmitter metabolism
—such as serotonin—have also been associated with paraphilia (Maes, De Vos, Van Hunsel, & Van
West, 2001), although it is unclear whether such abnormalities are a cause of paraphilia or whether they
are a consequence of acquiring paraphilia behaviour and anxiety and depression that is frequently
comorbid with paraphilia.

androgens The most important of the male hormones. Unusual sexual behaviour, such as
impulsive sexual offending involving non-consenting others, may be due to imbalances in these
hormones.

Finally, there are a small number of studies that have identified abnormalities or deficits in brain
functioning with paraphilias. First, abnormalities in the brain's temporal lobe have been associated with
a number of paraphilias, including sadism, exhibitionism and paedophilia (Mason, 1997; Murphy,
1997; Mendez, Chow, Ringman, Twitchell, & Hinkin, 2000), and gray matter volume has been found to
be lower in the temporal lobes of paedophiles than nonpaedophiles (Schiffer et al., 2017). In particular,
these abnormalities appear to be related to dysfunction in the temporal lobes leading to sexual
disinhibition of previously controlled behaviour, and Schiffer et al. (2017) also found that lower gray
matter volume in the dorsomedial prefrontal cortex was associated with a higher risk of reoffending in
paedophilic child molesters. The dorsomedial prefrontal cortex plays a role in processing a sense of self,
theory of mind, empathy, and making morality judgements—and deficits in these abilities may all play a
role in sex offending.
Other studies (albeit based on small samples of participants) have identified deficits in cognitive abilities
in paedophiles that are mediated by striato‐thalamically controlled areas of the frontal cortex (Tost et
al., 2004). These areas are associated with neuropsychological functions that include response inhibition,
working memory and cognitive flexibility, and deficits in these domains are consistent with the finding
that paedophiles frequently have lower than expected IQ scores—often as much as two thirds of a
standard deviation below the population mean (Cantor, Blanchard, Robichaud, & Christensen, 2005).

Summary
Research on the aetiology of paraphilic disorders has largely been restricted to understanding the causes
of those paraphilias that involve sexual offending (e.g., paedophilia)—mainly because of the desire to
understand and prevent criminal activity. However, the research that is available has identified some risk
factors for paraphilia (e.g., hypersexuality, childhood abuse, and neglect), and has also indicated that
some paraphilias are associated with cognitive biases and dysfunctional beliefs that act to maintain
sexual offending and serve to legitimise or justify sexual activities.

11.3.3 The Treatment of Paraphilic Disorders

Attempts to treat paraphilic disorders have a long and complex history, dating back to the first half of
the twentieth century when castration was a popular method of treating paraphilias such as
paedophilia. However, castration was often reserved for repeated paraphilic behaviour that was a
criminal act and involved nonconsenting victims. In many of these cases, castration was seen more as a
criminal punishment than a method of treatment, and its effectiveness was often doubted because up to
30% of men treated in this way were still capable of erections and ejaculation up to 10 years after
surgery (Grubin & Mason, 1997).
Treatment of paraphilic disorders is further complicated by a number of factors that make successful
treatment difficult to achieve: (a) many paraphilic disorders involve criminal behaviour (e.g.,
paedophilia, exhibitionism, and voyeurism), and this will often mean that offenders are reluctant to be
wholly truthful about their activities or to honestly disclose their sexual activities; (b) to many people
with paraphilias, their sexual inclinations involve doing things that they particularly enjoy and which
provide sexual satisfaction. If they have been indulging in these activities since early adolescence, then
their behaviours may seem to them as normal as conventional sexual behaviour (Laws & O'Donohue,
1997); (c) with many of the paraphilias that involve a nonconsenting victim, the offender will often
develop a rigid set of beliefs about their activities that enables them to diffuse responsibility for their
behaviour and to blame others (e.g., the victim) (Abel et al., 1989; Shruti, Ward, & Gannon, 2008;
Petruccelli et al., 2017); because of this, the individual with a paraphilic disorder will often deny there is
a problem with their behaviour, lack motivation to change, and may even fake compliance with therapy
simple because it may allow them to subsequently continue their paraphilic activities (e.g., if treatment is
a requirement for release from prison for sexual offences); and (d) as we mentioned earlier, paraphilic
disorders are highly comorbid with a number of other psychopathologies, including substance abuse,
anxiety, depression, and personality disorders, and these comorbid disorders may have to be tackled
before treatment for the paraphilic disorder itself can be attempted.
We continue this section by describing some of the main treatment methods for paraphilic disorders.
However, many therapists currently use multifaceted approaches to treatment, and you should bear this
in mind when reviewing these specific treatment methods. For example, a multifaceted approach might
involve (a) treating the individual behavioural problem (e.g., shifting sexual arousal and satisfaction away
from specific or inappropriate stimuli and associating it with more acceptable stimuli), (b) dealing with
any dysfunctional beliefs or attitudes that are maintaining the paraphilic behaviour (see Table 11.18),
and (c) because many paraphilic disorders are associated with social skills deficits, the therapist may
provide social skills training that will help the individual function more appropriately with consenting
partners.

Behavioural techniques
In Section 11.3.2 we discussed a number of early theories of paraphilic disorders that viewed these
problems as resulting from classical conditioning processes. In these accounts unconventional stimuli or
events (such as specific stimuli in fetishes, watching others naked in voyeurism, etc.) have become
associated with sexual experiences, such as masturbation, during early adolescence. The assumption of
behaviour therapy is that if these behaviours are learnt through conditioning, then they can also be
‘unlearnt’ through the use of basic conditioning procedures. Three types of technique are described
here. These are aversion therapy, masturbatory satiation and orgasmic reorientation.
Aversion therapy is based on the assumption that inappropriate stimuli have become positively
associated with sexual arousal and sexual satisfaction, and in order to break this association, those
stimuli must now be paired with negative or aversive experiences. For example, treatment of a fur fetish
may involve pairing pictures of fur or women wearing fur clothing with aversive experiences such as an
electric shock or drug induced nausea. Alternatively, a paedophile may be given electric shocks when
shown pictures of naked children. An avoidance component can be added to this treatment in which
the client can avoid the negative outcome by pressing a button which changes the picture from their
preferred sexual stimulus (e.g., fur, naked child) to an acceptable one (e.g., an attractive female). Aversion
therapy can also be used in a covert conditioning form, where the client does not actually experience
the pairing of sexual stimuli with aversive outcomes, but imagines these associations during controlled
treatment sessions. For example, the client may be asked to imagine one of their sexual fantasies and
then to vividly imagine a highly aversive or negative outcome, such as his wife finding him indulging in
his paraphilic sexual activities or being arrested, etc. (Barlow, 1993). Aversion therapy has been used to
treat fetishes, transvestism, exhibitionism, and paedophilia, and there is some evidence that it may have
some treatment benefit when combined with other approaches such as social skills training (Marks,
Gelder, & Bancroft, 1970). However, as we have reported elsewhere in this book, aversion therapy rarely
achieves long‐term success when used alone—and high rates of relapse are associated with the sole use
of aversion therapy (Wilson, 1978; Beech & Harkins, 2012).

covert conditioning Using the client’s ability to imagine events in order to condition
associations between events.
Satiation is an important conditioning principle in which the unconditioned stimulus (in this case sexual
satisfaction) comes to be ineffective because it is experienced in excess, and this leads to extinction of the
sexual urges that had been conditioned to stimuli or events associated with that unconditioned stimulus
(e.g., fetishes, etc.). This has led to the development of masturbatory satiation as a treatment for
paraphilic disorders, in which the client is asked to masturbate in the presence of arousing stimuli (e.g.,
women's underwear if the client has an underwear fetish) and to simultaneously verbalise fantasies on a
tape recorder. Immediately after orgasm, the client is instructed to masturbate again no matter how
unaroused or uninterested they feel and continue for at least an hour (Marshall & Barbaree, 1978). After
a number of these sessions, the client often reports that the stimuli that previously sexually aroused them
has become boring or even aversive (LoPiccolo, 1985). Latency to orgasm increases, and the number of
sexual fantasies elicited by the paraphilic stimulus significantly decreases (Marshall & Lippens, 1977).

masturbatory satiation A treatment for paraphilias in which the client is asked to

masturbate in the presence of arousing stimuli.

An important task for anyone treating paraphilic disorders is not only to suppress inappropriate or
distressing sexual activities (perhaps using the methods described here), but to replace these with
acceptable sexual practices. Orgasmic reorientation is a treatment method that aims to make the
client sexually aroused by more conventional or acceptable stimuli. This is a more explicit attempt to
recondition sexual urges to more conventional stimuli and can be used as an extension of the
masturbatory satiation technique. For example, a male client is first asked to masturbate while attending
to conventionally arousing stimuli (such as pictures of nude females), but if they begin to feel bored or
lose their erection, they are asked to switch to attending to pictures associated with their paraphilia. As
soon as they feel sexually aroused again, they must switch back to attending to the conventional
stimulus, and so on. Although there are a number of individual case studies suggesting that some
variations of orgasmic reorientation may be successful in helping clients to manage their paraphilic
behaviour, there are few controlled outcome studies available to evaluate the success of this method over
the longer term (Laws & Marshall, 1991). Perhaps more important, reorientation treatments beg the
question of what criteria should be used to decide whether a sexual behaviour requires reassignment,
and this is an issue of significant debate, especially in LGBT communities (e.g., Flentje, Heck, &
Cochran, 2013), and the outcome of this debate will have important ramifications for clinical policy and
practice.

Orgasmic reorientation A treatment method to replace inappropriate or distressing sexual

activities. It aims to make the client sexually aroused by more conventional or acceptable
stimuli.

Cognitive treatments
We saw in the section on aetiology that dysfunctional beliefs play a central role in developing and
maintaining a number of paraphilic disorders—especially those paraphilias that involve sexual
offending with nonconsenting victims. Cognitive treatment for these paraphilias often involves CBT,
which is adapted to help the client to identify dysfunctional beliefs, to challenge these beliefs and then
replace them with functional and adaptive beliefs about sexual behaviour and sexual partners. Table
11.18 shows a list of the kinds of dysfunctional beliefs held by paedophiles and exhibitionists. These
beliefs act as justifications for sexual offending and are part of a belief system that effectively ‘gives
them permission’ to carry out their offences. Challenging dysfunctional beliefs includes (a)
demonstrating to clients that their dysfunctional beliefs are based on their deviant sexual behaviour
rather than being justifiable reasons for the behaviour, (b) helping clients to see how they might
misinterpret the behaviour of their victims to be consistent with their dysfunctional beliefs, and (c)
discussing dysfunctional beliefs within existing individual and broader social norms in order to
demonstrate that the client's beliefs are not shared by most other members of society (e.g., that women
are not merely objects for sexual gratification). One integrated CBT‐based treatment for sexual offenders
is called the Core Sex Offender Treatment Programme (SOTP) which had been recommended
for use in UK prisons by the Ministry of Justice. Core SOTP extensively adopts CBT methods for
treating imprisoned sex offenders (Beech, Fisher, & Beckett, 1999) and targets risk factors for reoffending
such as sexual preoccupation, sexual preferences for children, offence‐supporting attitudes, lack of
emotional intimacy with adults, impulsive lifestyle, and poor problem‐solving abilities. Despite evidence
that initially supported the efficacy of the programme in marginally reducing recidivism (e.g.,
Schmucker & Lösel, 2008), a later randomised controlled study of the longer‐term effects of the
treatment programme over 8 years showed paradoxically that more treated sex offenders committed at
least one sexual re‐offence when compared with non‐treated control offenders (Mews, Di Bella, &
Purver, 2017). Even though the Core SOTP programme was based on tried‐and‐tested CBT principles,
the Ministry of Justice withdrew the treatment programme in 2017, and it's not clear why the
programme failed to have the predicted outcome on sex offender recidivism. This may simply attest to
the great difficulty in finding effective psychological treatments that have any significant impact on
longer‐term sexual offending behaviour (Dennis et al., 2012).

Cognitive treatment Treatment approach intended to help the client identify and challenge
dysfunctional beliefs.

Sex Offender Treatment Programme (SOTP) An integrated treatment for sexual

offenders which adopts CBT methods for treating imprisoned sex offenders and targets risk
factors for reoffending such as sexual preoccupation, sexual preferences for children, offence-
supporting attitudes, lack of emotional intimacy with adults, impulsive lifestyle, poor coping
skills and poor problem-solving abilities.

Relapse‐prevention training
Rather than focus on an all‐embracing ‘cure’ for paraphilias, many forms of treatment focus specifically
on relapse prevention, and this is especially relevant in the case of sexual offenders (see previous
section). Relapse‐prevention training consists primarily of helping clients to identify circumstances,
situations, moods, and types of thoughts that might trigger paraphilic behaviour. For example, a mood
trigger might be a period of stress or anxiety or alcohol abuse that precipitates sexual offending, or close
contact with children might activate paedophile behaviours. Sexual offenders are also taught to identify
the distorted cognitions that might lead to offending (e.g., ‘that child is running around half dressed, so
she must be interested in sex’) and are taught self‐management skills that will enable them to interrupt
sequences of thoughts that lead to offending or to avoid situations that place them at risk (e.g., in the
case of paedophilia, to avoid taking jobs that involve working with or near children, or living near a
school).

Relapse-prevention training In paraphilias, a treatment which consists primarily of helping

clients to identify circumstances, situations, moods and types of thoughts that might trigger
paraphilic behaviour.

Hormonal and drug treatments

As we mentioned earlier, castration was the radical form of treatment for dangerous sex offenders
during periods of the twentieth century—especially in parts of Europe, and was often offered as an
alternative to imprisonment (Abel, Osborn, Anthony, & Gardos, 1992). The aim here was to curb the
sexual appetite of persistent offenders who were unable to respond to any other form of treatment. An
arguably more acceptable way of curbing sexual appetite in those paraphilics who persistently offend is
to use antiandrogen drugs that significantly decrease the levels of male hormones such as
testosterone. Currently used testosterone‐lowering drugs include medroxyprogesterone
acetate(MPA), cyproterone acetate(CPA), and gonadotropin‐releasing hormone(GnRH),
and these drugs have been shown to reduce the frequency of erection and ejaculation, and inhibit
sexual arousal (Hall, 1995; Bradford & Pawlak, 1993; Maletzky & Field, 2003). However, such a form of
treatment tends to depend very much on the compliance of the client or offender in taking such drugs
regularly. This is particularly important because evidence suggests that offenders will often revert to
paraphilic behaviour or sexual offending when they cease taking the drug—even after many years of
medication (Berlin & Meinecke, 1981), and a recent systematic review of available randomised trials of
these drugs concluded that no firm conclusions could be drawn on the effectiveness of these drugs for
reducing sexual offending (Khan et al., 2015)

antiandrogen drugs A group of drugs that significantly decrease the levels of male
hormones such as testosterone.

medroxyprogesterone acetate (MPA) An anti-androgen, testosterone-lowering drug.

cyproterone acetate (CPA) An antiandrogen, testosterone-lowering drug.

An alternative to antiandrogens is the use of antidepressant drugs such as SSRIs (e.g., fluoxetine), and
there is some modest evidence that such drugs will help the individual control sexual urges—especially
if depression is a trigger for indulging in paraphilic behaviour (Kafka & Hennen, 2000). In particular,
the available evidence suggests SSRIs may be helpful for conditions such as hypersexuality (increased
sex drive) (National Institute for Health and Care Excellence, 2015).

Summary of the treatment of paraphilic disorders

The treatment of paraphilic disorders is generally a difficult process, not least because many diagnosed
with paraphilia will also be sexual offenders (e.g., paedophiles, exhibitionists, voyeurs), and this can lead
clients to be less than truthful about their sexual activities and approach treatment with a relatively
ingrained set of beliefs about their activities. Paraphilic disorders are also highly comorbid with other
psychopathologies such as substance abuse, anxiety, depression and personality disorders, and this
makes treatment additionally complex. Most programmes of treatment adopt a multifaceted approach
that can involve behaviour therapy techniques to address the specific sexual behaviour problem (e.g.,
aversion therapy, masturbatory satiation, orgasmic reorientation), and use CBT to deal with the
dysfunctional beliefs that underlie many paraphilias and sexual offending in particular. Finally, social
skills training and relapse prevention procedures can be used in an attempt to ensure that the individual
is able to cope with the demands of normal sexual relationships and to identify situations and
circumstances that might trigger relapse.
It is also worth emphasising that treatment for paraphilias spans two quite different target groups (a)
those who are seeking help for a distressing and difficult paraphilia condition, and (b) those who are
convicted of sex offences against nonconsenting others (e.g., paedophiles, exhibitionists, rapists). While
treatment programmes may give some hope to those in the former group who are voluntarily seeking
help to manage their conditions, there is still very little convincing evidence that treatment programmes
for those in the second group significantly help to change sexual offending.

11.3.4 Summary of Paraphilic Disorders

When high rates of sexual behaviour are channeled into unusual or very specific sexual activities, these
are known as paraphilias. They range from sexual activities that are victimless (e.g., fetishes and
transvestic fetishism) to others that are defined in law as sexual offences (e.g., paedophilia, exhibitionism,
voyeurism). Many paraphilias are diagnosed on the basis of unusual, recurrent sexual urges that cause
personal distress or affect social and occupational functioning (e.g., fetishism, transvestic fetishism), but
others do not require that the individual experiences distress—merely that they have acted on their
urges with nonconsenting victims (e.g., paedophilic disorder, exhibitionistic disorder, voyeuristic
disorder). Research on the aetiology of paraphilic disorders has identified some risk factors (e.g.,
hypersexuality, childhood abuse and neglect) and has also indicated that dysfunctional beliefs may play
an important role in maintaining those paraphilic disorders that are linked to sexual offending (e.g.,
paedophilia, exhibitionism). Finally, treatments for paraphilic disorders are still relatively
underdeveloped, and adopt behaviour therapy or CBT techniques to change dysfunctional behaviour
and cognitions.
SELF‐TEST QUESTIONS

11.3.1 The Diagnosis and Description of Paraphilic Disorders

How are paraphilic disorders defined in DSM‐5?
What are the main categories of paraphilic disorders described in DSM‐5?
Can you differentiate between those paraphilic disorders that can be labelled ‘victimless’
and those that in many societies would be labelled ‘sexual offences’?
Can you list the main diagnostic criteria for fetishistic disorder, transvestic disorder,
voyeuristic disorder, frotteuristic disorder, paedophilic disorder, sexual masochistic disorder,
and sexual sadism disorder?

11.3.2 The Aetiology of Paraphilic Disorders

Can you list some of the main risk factors for paraphilic disorders?
Paraphilic disorders are highly comorbid with which other psychopathologies?
What is castration anxiety and how is it used by psychoanalytic theorists to explain
paraphilic disorders?
How is associative learning thought to be involved in the acquisition of some paraphilic
disorders?
Are childhood abuse and neglect an important factor in the development of paraphilic
disorders?
What are cognitive distortions and how are they used by sexual offenders to justify their
actions?
Is there any substantial evidence that sex hormone imbalances are involved in the
development of paraphilic disorders?
What brain area abnormalities have been associated with paraphilic disorders, and how
might they cause paraphilic behaviour?

11.3.3 The Treatment of Paraphilic Disorders

Why are paraphilic disorders so difficult to treat?
How have aversion therapy and covert conditioning been utilised to treat paraphilic
disorders?
What are masturbatory satiation and orgasmic reorientation techniques, and is there any
evidence that they can be successfully used to treat paraphilic disorders?
How has CBT been adapted to help treat paraphilic disorders?
What are the main drug treatments that have been used to treat paraphilic disorders, and
what is the evidence that such treatments prevent relapse?
What are the main principles of relapse‐prevention treatments for paraphilic disorders?
Do relapse‐prevention interventions work?
SECTION SUMMARY

11.3 PARAPHILIC DISORDERS

Paraphilic disorders tend to be associated with problematic high‐frequency sexual
behaviours or unusual sexual urges and activities that are often directed at inappropriate
targets.
Some paraphilic disorders are victimless (e.g., fetishistic disorder, transvestic disorder) and
others will be defined in law as sexual offences (e.g., exhibitionistic disorder, voyeuristic
disorder, frotteuristic disorder, paedophilic disorders).

11.3.1 The Diagnosis and Description of Paraphilic Disorders

Fetishistic disorder involves sexually arousing fantasies and urges directed at nonanimate
objects, and this causes the individual distress.
Transvestic disorder is when a heterosexual male experiences sexual arousal from cross‐
dressing in women's clothing, and this causes the individual distress.
Exhibitionistic disorder involves sexual fantasies about exposing the genitals to a stranger.
Voyeuristic disorder involves experiencing intense sexually arousing fantasies or urges to watch
an unsuspecting person who is naked, in the process of undressing or engaging in sexual
activity.
Frotteuristic disorder involves recurrent sexual urges to touch and rub up against other
nonconsenting people—usually in crowded places.
Paedophilic disorder is defined as sexual attraction towards prepubescent children, normally
13 years or younger.
Some paedophiles limit their activities to their immediate family (e.g., children,
stepchildren, nieces, etc) and incest is listed as a specific subtype of paedophilia in DSM‐5.
Nonincestuous paedophiles will normally become sexually aroused only by sexually
immature children and will often develop elaborate ways of gaining access to children
through ‘grooming’ activities.
Sexual masochism disorder is when an individual gains sexual arousal and satisfaction from
being humiliated, and this causes the individual significant distress.
Sexual sadism disorder is when a person gains sexual arousal and satisfaction from the
psychological or physical suffering of others, and this diagnosis is given if the symptoms
cause the individual significant distress or if the person acts on the impulses with a
nonconsenting person.

11.3.2 The Aetiology of Paraphilic Disorders

Most of the DSM‐5 diagnosable paraphilic disorders are male activities, and many are
also sexual offences (e.g., paedophilic disorder, exhibitionistic disorder).
Both hypersexuality and childhood abuse and neglect are risk factors for paraphilic disorders.
Psychodynamic theory views paraphilic disorders either as (a) defensive reactions that are
 attempting to defend the ego from repressed fears, or (b) as representing fixation at a
pregenital stage of development (e.g., the Oedipal stage).
Many paraphilic disorders develop during early adolescence, and inappropriate sexual
urges may have been developed through the association of sexual activities such as
masturbation with inappropriate stimuli or activities (the process of classical conditioning).
The level of childhood abuse experiences by sexual offenders is almost double the level
found in the general population. However, childhood abuse and neglect are not a sufficient
condition for committing a sexual offence, because it is reported by only 30% of sexual
offenders.
Sexual offenders, including paedophiles, develop a set of beliefs or cognitive distortions that
serve to legitimise or justify their sexual activities.
Even though antiandrogen drugs are regularly used to treat some paraphilic disorders,
there is little convincing evidence that abnormal androgen levels play a significant role in
the development of paraphilic behaviour.

11.3.3 The Treatment of Paraphilic Disorders

Many paraphilic disorders are difficult to treat because (a) they involve criminal behaviour
that will make individuals reluctant to be truthful about their activities, and (b) paraphilic
disorders are highly comorbid with other psychiatric disorders, which significantly
complicates treatment.
Behavioural treatments for paraphilic disorders include aversion therapy, covert conditioning,
masturbatory satiation, and orgasmic reorientation.
CBT has been adapted to treat paraphilic disorders (especially those involving sexual
offending) by addressing the dysfunctional beliefs or cognitive distortions that many sexual
offenders develop to legitimise their behaviour.
Antiandrogen drug treatments for paraphilic disorders include medroxyprogesterone acetate
(MPA), cyproterone acetate (CPA), and gonadotropin‐releasing hormone (GnRH) which reduce the
frequency of erection and inhibit sexual arousal.

11.4 SEXUAL PROBLEMS REVIEWED

Sexual behaviour is usually a central feature of our psychology. A satisfying sex life is an important
contributor to quality of life, and our sexual urges and attractions can determine how we view ourselves
and construct our self‐identity. This being the case, it is not surprising that when we encounter problems
related to sexual activity it can be an important source of psychological distress.
Sexual dysfunctions represent a set of diagnosable disorders of the normal sexual cycle, and can be
identified as problematic at various points in this cycle (namely disorders of desire, arousal, orgasm, and
resolution). The causes of sexual dysfunctions are diverse and include biological and organic factors,
psychological factors, and interpersonal problems. At one time, the open discussion and treatment of
sexual problems was considered taboo, but over the past 60 years the liberalisation of attitudes towards
sex has meant the development of a range of treatments for such disorders.
In contrast to those who report problems with normal sexual performance, there are those who exhibit
high frequencies of sexual activity that is triggered by or directed at inappropriate targets. These are
collectively known as paraphilic disorders, and some reflect sexual behaviour that becomes centred on
unusual objects or stimuli (e.g., fetishistic disorder, transvestic disorder), and others that may involve
nonconsenting persons (e.g., paedophilic disorder, exhibitionistic disorder, voyeuristic disorder). Some of
these activities acquire their status as psychopathologies because they are associated with personal
distress or impairment of normal daily activities (e.g., fetishistic disorders). Others are not necessarily
associated with personal distress but are diagnosed as disorders because they are activities directed at
nonconsenting others. As such, these latter examples tend to represent criminal behaviours as well as
diagnosable psychopathologies (e.g., paedophilic disorder, exhibitionistic disorder). Much of the research
on the aetiology of paraphilic disorders has centred on those disorders that represent criminal activities
or sexual offences—largely because of the need to help identify and treat such offenders. Treatments for
paraphilic disorders are also relatively under‐developed, largely because of the problems involved in
treating people whose behaviour represents sexual offending.

This book is accompanied by Student and Instructor companion

websites.
www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter References
Videos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
12
Personality Disorders

ROUTE MAP OF THE CHAPTER

This chapter begins by discussing some of the issues surrounding diagnosis of personality
disorders raised during the development of Diagnostic and Statistical Manual of Mental Disorders, 5th
Edition (DSM‐5). It then moves on to describe the 10 diagnostically independent personality
disorders listed by DSM‐5. We then discuss the diagnostic criteria for these disorders and
describe studies that have provided data on their prevalence. The section on aetiology reviews
the available evidence on how the different personality disorders are thought to develop and
what childhood and adolescent predictors and risk factors might help us to forecast personality
disorders in adulthood. The chapter then describes and reviews methods of treating people
with a diagnosis of personality disorder and the range of difficulties involved in these
treatments.

CHAPTER OUTLINE

12.1 CONTEMPORARY ISSUES IN THE DIAGNOSIS OF PERSONALITY

DISORDERS
12.2 PERSONALITY DISORDERS AND THEIR DIAGNOSIS
12.3 THE PREVALENCE OF PERSONALITY DISORDERS
12.4 THE AETIOLOGY OF PERSONALITY DISORDERS
12.5 TREATING PEOPLE WITH A DIAGNOSIS OF PERSONALITY
DISORDER
12.6 PERSONALITY DISORDERS REVIEWED
 LEARNING OUTCOMES
When you have completed this chapter, you should be able to:
1. Discuss contemporary issues in the diagnosis of personality disorders.
2. Describe the main diagnostic criteria for the DSM‐5 listed personality disorders, and
evaluate some of the controversial issues concerning both diagnosis and comorbidity.
3. Describe and evaluate the main theories of the aetiology of a number of personality
disorders, particularly Cluster A disorders, antisocial personality disorder, borderline
personality disorder, and Cluster C disorders.
4. Describe and evaluate the factors that make the treatment of people with a diagnosis of
personality disorder problematic.
5. Describe and evaluate 3 or 4 psychological therapies that have been developed to treat
people with a diagnosis of personality disorder.

I'm 35 now and for as long as I can remember I've been involved with services. As a child, I was in and out of
foster care as life at home was just one big mess. My parents drank heavily, and all my brothers and sisters—
including me—were neglected, physically, and emotionally. When I was seven, my mum's brother moved in, my
so‐called uncle, and that's when the sex abuse started. I was moved into care because no one could understand why
I was so unhappy all the time, but I couldn't tell anyone, he made me promise, and anyway he was pretty
controlling and scary. I should have been safe in care but there were people who hurt me and interfered with me.
I started self‐harming when I was 13 or 14. It was a complete distraction from all the mess and unhappiness
around me, cutting my arms, being in control of something, and letting the pressure out. Then I got pregnant by an
older guy when I was 16 and he promptly dumped me. That was a terrible time. I was utterly desperate and so
vulnerable, and I ended up giving my baby up for adoption. I will always feel guilty for that.
I had to leave school, though I was pretty rubbish there, and just couldn't focus or concentrate on anything, and
didn't really have anyone I could call a friend, someone who really knew me and what my life was like. I ended
up going from one job to the next, supermarkets, cleaning, you name it. So boring I couldn't hack it.
Then I really started hurting myself bad, so alone, so depressed, so much wanting not to exist, so needing to be
dead. Drinking helped, as did smoking weed, but that feeling of nothingness, the deadened peace, never really
lasted and I ended up doing some pretty stupid things with people. Don't even go there. I was 20 and going from
one fella to the next. Then I started being knocked around and was hurt so badly one time I just did it, tried to kill
myself, that's when I first went to the mental hospital. I was in and out of the wards, it was like a pattern, pick
myself up and start all over again and then bam, I was back to square one. The shrinks and the therapists tried to
help but it was useless, and I just hurt myself more and more. I think they were as close as I was to giving up,
maybe more so.
Jane's Story (from Solts & Harvey, 2015)

Introduction
We all have personalities. Personalities tend to be enduring features of individuals that determine how
we respond to life events and experiences, and they also provide a convenient means by which others
can label and react to us. To this extent, a personality is a global term that describes how you cope with,
adapt to, and respond to a range of life events, including challenges, frustrations, opportunities,
successes, and failures. A personality is something that we inwardly experience ourselves and outwardly
project to others. While personalities tend to be relatively enduring in their main features, most people
will learn and evolve with their experiences, and they will learn new and effective ways of behaving that
will enable them to adapt with increasing success to life's demands. In contrast, some others will have
experienced many difficulties in their lives, experienced much unhappiness, and will struggle to live the
‘normal’ lives of others that they see around them. Their attempts to cope with these difficulties are
often extreme and damaging. We can see many of these latter characteristics in Jane's Story. After a
childhood of neglect and abuse she spent much of her early life in care and then drifted from job to job
and relationship to relationship, experiencing a roller‐coaster of emotions. Her attempts to cope with
her life were damaging and often extreme, from self‐harm to drug abuse, and eventually suicide
attempts, and from childhood to adulthood her approach to life and its problems became more
entrenched and destructive. Jane's life story is characteristic of an individual with a diagnosis of
borderline personality disorder (BDP), which is the most common of the diagnosable personality
disorders.
The personality disorders diagnostic category is arguably the category that creates the most controversy
amongst clinical psychologists and mental health professionals, and we discuss many of these
controversies in this chapter. We also discuss the effects that these debates have had on the diagnostic
criteria for personality disorders found in the most recent edition of the DSM.
For the purposes of clinical diagnosis, DSM‐5 defines a personality disorder as ‘an enduring pattern of
inner experience and behaviour that deviates markedly from the expectations of the individual's culture,
is pervasive and inflexible, has an onset in adolescence or early adulthood, is stable over time, and leads
to distress and impairment’ (DSM‐5, American Psychiatric Association, 2013, p. 645). DSM‐5 has
grouped personality disorders into three distinct clusters (see Table 12.3). Cluster A includes paranoid,
schizoid, and schizotypical personality disorders, and DSM describes individuals with these disorders as
‘appearing odd or eccentric’. Cluster B includes antisocial, borderline, histrionic, and narcissistic
personality disorders, where individuals ‘often appear dramatic, emotional, or erratic’. Cluster C
includes avoidant, dependent, and obsessive‐compulsive personality disorders (OCPDs), and individuals
with these disorders ‘often appear anxious or fearful’ (DSM‐5, American Psychiatric Association, 2013,
p. 646).
Individuals diagnosed with a personality disorder will often deny their psychopathology, will often be
unable to comprehend that their behaviour may on some occasions be contrary to conventional and
acceptable ways of behaving, and will find it difficult to associate their own psychological difficulties
with their own inflexible ways of thinking, behaving, and coping.

12.1 CONTEMPORARY ISSUES IN THE DIAGNOSIS OF

PERSONALITY DISORDERS
There have been a number of concerns about how personality disorders have been traditionally
categorised and diagnosed, and while DSM‐5 has retained the categorical approach to diagnosis
outlined in its predecessor DSM‐IV‐TR, DSM‐5 also included an alternative model that could be used
to generate research on other diagnostic approaches. In order to fully explain these issues, we (a) briefly
describe the traditional diagnostic categories in DSM‐IV‐TR (also the ones retained in DSM‐5—see
Section 12.2), (b) explain the important problems that surround this traditional approach, and (c)
describe the alternative model proposed in DSM‐5.

12.1.1 The Categorical Approach to Personality Disorders in DSM‐IV‐TR and

DSM‐5
DSM‐IV‐TR listed 10 diagnostically independent personality disorders, and these were organised into
three primary clusters (and this is still the way that DSM‐5 categorises personality disorders in its main
diagnostic section): (a) odd/eccentric personality disorders, (b) dramatic/emotional personality
disorders, and (c) anxious/fearful personality disorders.
Those personality disorders grouped in Cluster A all have characteristics that resemble many of the
symptoms of schizophrenia (see Chapter 8), but unlike schizophrenia sufferers there is no apparent loss
of touch with reality nor the experiencing of sensory hallucinations. However, people with Cluster A
disorders may behave in ways that are indicative of delusional thinking (e.g., paranoid personality
disorder) or exhibit rambling or poorly organised speech (e.g., schizotypal personality disorder). The
three subtypes of Cluster A are (a) paranoid personality disorder, (b) schizotypal personality disorder,
and (c) schizoid personality disorder.
Cluster B includes people diagnosed with dramatic/emotional personality disorders who tend to be
erratic in their behaviour, self‐interested to the detriment of others, and emotionally labile. This
category includes (a) antisocial personality disorder (APD), (b) borderline personality disorder (BPD), (c)
narcissistic personality disorder, and (d) histrionic personality disorder.
Finally, as the name suggests, people with an anxious/fearful personality disorder (Cluster C) exhibit
anxious and fearful behaviour. However, unlike the main anxiety disorders, the anxious and fearful
behaviour exhibited will have been a stable feature of their behaviour from late childhood into
adulthood, and it is usually not possible to identify a specific experience or life event that might have
triggered this fear and anxiety. Anxious/fearful personality disorders may be comorbid with some
anxiety disorders (e.g., social anxiety disorder, panic disorder), where triggers for the latter can be
identified. But the pattern of behaviour exhibited by individuals with anxious/fearful personality
disorders generally tends to represent ingrained ways of dealing and coping with many of life's
perceived threats. The three disorders described in Cluster C are (a) avoidant personality disorder, (b)
dependent personality disorder and (c) obsessive‐compulsive personality disorder.

12.1.2 Problems with the Traditional Categorical Model

Many clinicians and researchers have argued that personality disorders do not exist as ‘categories’—i.e.,
they are not discrete disorders that an individual either possesses or does not possess, but they are in fact
dimensional extensions of ‘normal’ personality traits (e.g., Costa & MacRae, 1990). This is problematic
in a number of ways for the all‐or‐none approach to diagnosis of personality disorders that DSM‐IV‐
TR had taken.
First, there is evidence for a dimensional approach to personality disorders from the finding that
extreme scores on conventional measures of personality, such as the ‘five‐factor’ model are highly
associated with personality disorders (Trull et al., 1998; Costa & MacRae, 1990; Samuel & Widiger,
2008). This finding probably resonates with our own intuitive view that we ourselves and many of the
people we know exhibit to some extent and in some circumstances the traits that we might associate
with personality disorders (e.g., mood swings, impulsive behaviour, paranoia, lack of social conscience,
etc.). This suggests that personality disorders may not be disorders as such but simply represent extreme
cases on conventional personality dimensions.
Second, another conceptual difficulty with the traditional diagnostic model of personality disorders is
that many of them contain characteristics that overlap (e.g., impulsivity, poor self‐image, etc.), and so
there is a real temptation for clinicians to diagnose more than one personality disorder in a single
individual (Grilo, Sanislow, & McGlashan, 2002). Indeed, perhaps paradoxically, DSM‐IV‐TR often
defined personality disorders in ways that either (a) allowed a very heterogeneous group of individuals
to be diagnosed under a single diagnostic label, and for BPD in particular there were almost 100
different permutations of symptoms that would result in a diagnosis of BPD, or (b) allowed clinicians to
diagnose multiple comorbidity of personality disorders in a single individual.
Third, a number of the existing personality disorder categories are particularly rare in the general
population (e.g., histrionic personality disorder, dependent personality disorder), and may therefore not
represent useful independent disorder categories (Samuels et al., 2002; Trull et al., 2010).
Finally, one of the defining features of personality disorders in DSM is that they are highly stable over
time, and so in some sense ‘immutable’, and this may have deterred clinical psychologists and mental
health professional from giving a diagnosis of personality disorder because it may have implied that the
client was ‘untreatable’ (Tyrer, Mulder, Kim, & Crawford, 2018). Indeed, in the UK a diagnosis of
personality disorder was given for only 8% of psychiatric inpatients (NHS Digital, 2010) when research
suggested that personality disorder symptoms were present in 40–90% of psychiatric inpatients and
outpatients (Beckwith, Moran, & Kelly, 2014; Tyrer et al., 2011). Furthermore, personality disorders
may not be as stable over time as the definitions in both DSM‐IV‐TR and DSM‐5 might imply. Studies
suggest that as many as half of the individuals diagnosed with a personality disorder, do not receive the
same diagnosis 2 years later (Shea et al., 2002; Grilo et al., 2004). They may still be high on measures of
those personality traits but not high enough to meet the strict diagnostic criteria set by DSM‐IV‐TR.
This suggests that a dimensional approach to measuring and diagnosing personality disorders might be
more appropriate than the traditional all‐or‐none approach.

12.1.3 DSM‐5's Alternative Model

The alternative diagnostic model proposed as a basis for further research in DSM‐5 has three discrete
types of personality ratings that contribute to a diagnosis (Skodol et al., 2011). These are level of
personality functioning, personality disorder types, and personality trait domains and
facets. This system is designed to provide ratings of an individual's personality on a series of
personality dimensions (rather than diagnosing in an all‐or‐none categorical way), and reduces the
number of personality disorder categories from 10 down to 6. This model also provides information
about personality functioning (i.e., do an individual's personality traits allow them to function
adequately at both an emotional and behavioural level?) and whether they possess pathological
personality traits. These various assessment processes are shown schematically in Figure 12.1.

level of personality functioning Disturbances in self and interpersonal functioning are at

the core of personality disorders, with the severity of impairment indicating whether the
individual may have more than one personality disorder.

personality disorder types Each of six personality disorder traits specified in the alternative
diagnostic schemes published in DSM‐5.

personality trait domains In the alternative classification of personality disorders published

in DSM‐5, there are five personality trait domains covering negative affectivity, detachment,
antagonism, disinhibition, and psychoticism.
FIGURE 12.1 In the alternative diagnostic model for personality disorders described in DSM‐5, diagnosis progresses
through three relatively independent steps. These are (a) assessing personality functioning to determine whether there is
impairment typical of psychopathology, (b) a more comprehensive analysis of personality traits rated along a series of
dimensions, and finally (c) determining whether the information collected in steps 1 and 2 meet the diagnostic criteria for
any of six specific personality disorders.

Level of personality functioning

Disturbances in both self and interpersonal functioning are at the core of personality disorders, and
functioning in these areas predicts the presence of a personality disorder, with the severity of this
impairment indicating whether the individual may have more than one personality disorder.
Impairments to one's sense of self include inability to regulate emotions and self‐esteem, and
disturbances of interpersonal functioning include inability to empathise and lack of desire and capacity
for intimacy (Bender, Morey, & Skodol, 2011).

Pathological personality traits

Once impairments in personality functioning have been established, a more comprehensive analysis of
personality trait domains can be made. Scores on each of these dimensions will help the clinician to
decide which specific personality disorders should be diagnosed. There are five personality trait domains
covering negative affectivity, detachment, antagonism, disinhibition, and psychoticism, and each of
these domains is then supplemented by a further 25 trait facets which will help the clinician to provide a
more detailed rating within each domain (see Table 12.1).

Specific personality disorders

The alternative diagnostic model in DSM‐5 has reduced the number of individual diagnosable
personality disorders from 10 down to 6. These are APD, avoidant personality disorder, BPD,
narcissistic personality disorder, OCPD, and schizotypal personality disorder. Each individual
personality disorder then has its own set of criteria by which it can be diagnosed, and these criteria are
dependent on the presence of high scores on the measures of personality functioning and high scores
on specified personality traits. For example, under this proposed scheme, a diagnosis of APD would be
dependent on high ratings on two of the four elements of personality functioning, and six or more of
the following seven pathological personality traits: manipulativeness, callousness, deceitfulness, and
hostility (all aspects of antagonism), and risk taking, impulsivity, and irresponsibility (all aspects of
disinhibition) (see Table 12.2).
TABLE 12.1 Definitions of DSM‐5 personality disorder trait domains and facets
Domain Facets
Negative affectivity Emotional Lability
Anxiousness
Separation Insecurity
Submissiveness
Hostility
Perseveration
Depressivity
Suspiciousness
Restricted Affectivity
Detachment Withdrawal
Intimacy Avoidance
Anhedonia
Depressivity
Restricted Affectivity
Suspiciousness
Antagonism Manipulativeness
Deceitfulness
Grandiosity
Attention Seeking
Callousness
Hostility
Disinhibition Irresponsibility
Impulsivity
Distractibility
Risk Taking
Rigid Perfectionism
Psychoticism Unusual Beliefs and Experiences
Eccentricity
Cognitive and Perceptual Dysregulation

TABLE 12.2 Summary: DSM‐5 diagnostic criteria for general personality disorder

An ongoing rigid pattern of thought and behaviour that is significantly different from the
expectations of the person's culture, displaying manifestation in two or more of the following
areas:
Cognition
Affectivity
Interpersonal functioning
Impulse control
The pattern is constant and long lasting and can be traced back to adolescence or early childhood
The pattern leads to distress or impairment in social, occupational, and other areas of life
The symptoms are not better accounted for by another mental disorder or due to the effects of a
substance or other medical condition
12.1.4 Summary
This discussion should have given you an insight into how the diagnosis of personality disorders may
develop in the immediate future and has provided you with some of the reasons why diagnosis might
need to change. However, the American Psychiatric Association decided against introducing these
changes with the publication of DSM‐5 in 2013 and agreed to provide more time for further research
on the alternative, dimensional approach.
But it is expected that when the new revision of the International Classification of Diseases (ICD‐11) is
published by the World Health Organization (WHO) in 2022, it will adopt a fully dimensional
classification of personality disorders, in which a severity dimension will be the most significant
diagnostic dimension (mild, moderate, and severe), with five personality trait domains serving as
qualifiers (negative affectivity, detachment, dissociability, disinhibition, and anankastia, which are similar
to the higher‐order trait domains in the DSM‐5 alternative model, see Table 12.1) (Bach, 2018; Tyrer,
Mulder, Kim, & Crawford, 2018). This should allow the clinician to make a diagnosis that (a) is more
clinically meaningful in terms of how the severity of the symptoms affects functioning, (b) does not
require the need for multiple comorbid diagnoses (this would be covered by the severity dimension), and
(c) would enable treatment to be directed towards aiding functioning rather than treating dysfunctional
traits.

SELF‐TEST QUESTIONS
What are the problems associated with the current categorical approach to diagnosing
personality disorders?
What is the process for diagnosing personality disorders in DSM‐5's alternative model?

SECTION SUMMARY

12.1 CONTEMPORARY ISSUES IN THE DIAGNOSIS OF PERSONALITY

DISORDERS
DSM‐5 retains previous diagnostic criteria by defining personality disorders on a
categorical rather than dimensional basis
DSM‐5 also discusses a dimensional approach to diagnosing personality disorders which it
hopes will generate further research

12.2 PERSONALITY DISORDERS AND THEIR DIAGNOSIS

The diagnostic approach adopted in the main body of DSM‐5 is the traditional categorical one also
found in DSM‐IV‐TR (as opposed to the dimensional alternative described in Section 12.1.3) and the
categorical perspective is the one we use here. According to this approach, only when personality traits
are inflexible and maladaptive and cause significant functional impairment or distress are they
diagnosed as personality disorders. To help the clinician identify when personality traits have become
maladaptive in this way, DSM‐5 provides a set of general criteria which are shown in Table 12.2. The
main criterion is that a person's inner experience and behaviour must differ markedly from expectations
of the individual's culture and be reflected in at least two of the following four areas: cognition (e.g.,
ways of perceiving the self, other people, etc.), affectivity (e.g., the range, intensity, and changeability of
emotions), interpersonal functioning, and impulse control. Further criteria stress that the patterns of
behaviour and inner experience must be inflexible and pervasive, and lead to distress or social,
occupational, or other forms of impairment.
Apart from these general criteria, DSM‐5 then specifies criteria for 10 separate types of personality
disorder. These are grouped into clusters which cover (a) odd/eccentric personality disorders, (b)
dramatic/emotional personality disorders, and (c) anxious/fearful personality disorders (see Table 12.3).
The following sections describe each of these clusters and the diagnosable personality disorders listed in
each.

12.2.1 Odd/Eccentric Personality Disorders (Cluster A)

Those personality disorders grouped in Cluster A all have characteristics that resemble many of the
symptoms of schizophrenia (see Chapter 8), but unlike schizophrenia sufferers there is no apparent loss
of touch with reality nor the experiencing of sensory hallucinations. However, people with Cluster A
disorders may behave in ways that are indicative of delusional thinking (e.g., paranoid personality
disorder) or exhibit rambling or poorly organised speech (e.g., schizotypal personality disorder). The
three subtypes of Cluster A are (a) paranoid personality disorder, (b) schizoid personality disorder, and
(c) schizotypal personality disorder.
TABLE 12.3 The three clusters of personality disorders in DSM‐5
CLUSTER A Paranoid personality disorder
Odd/eccentric personality disorders Schizoid personality disorder
Schizotypal personality disorder
CLUSTER B Antisocial personality disorder (APD)
Dramatic/emotional personality disorders Borderline personality disorder (BPD)
Narcissistic personality disorder
Histrionic personality disorder
CLUSTER C Avoidant personality disorder
Anxious/fearful personality disorders Dependent personality disorder
Obsessive‐compulsive personality disorder (OCPD)

Paranoid personality disorder

Those with a diagnosis of paranoid personality disorder exhibit an enduring pattern of distrust
and suspiciousness of others. They will interpret innocent remarks as threatening, and they will
interpret the intentions of others as malevolent. They find ‘threatening’ hidden meaning in things and
events, and their distrust of others is pervasive and unchanging. If someone points out to them that their
paranoid interpretation of events may be wrong, they will inevitably begin to distrust the person who
brought this to their attention. As a result, individuals with paranoid personality disorder avoid close
relationships, are often spontaneously aggressive to others, become preoccupied with their mistrust of
others to the point of it severely disrupting their work performance, and often feel that they have been
deeply and irreversibly betrayed by others—even when there is no objective evidence for this.
Individuals with paranoid personality disorder will even misinterpret well‐intentioned and
complimentary statements as criticism, such as interpreting an offer of help as implying that they are
not doing a job or task well enough. Because such individuals are hypervigilant for the potential
malevolent intentions of others, they may often bear grudges, be quick to attack others for what are seen
as critical comments, and gather trivial and often circumstantial evidence to support ‘jealous’ beliefs—
especially about partners and colleagues. Because of their perceived need to constantly defend
themselves against malevolent others, individuals with paranoid personality disorder feel a need to have
a high degree of control over those around them and are frequently involved in litigious disputes. They
also appear to deploy an attributional style that blames others for things that go wrong in life (Fenigstein,
1996) and this external locus of control is very similar to the attributional style found in psychosis
(Bentall, 1994). Estimates of the prevalence of paranoid personality disorder range from 1.2% to 4.4%
which means it is not a particularly rare psychopathology, and it is known to be a disorder that is closely
associated with childhood trauma and social stress (Lee, 2017) (Table 12.4).

paranoid personality disorder A personality disorder characterised by an enduring pattern

of distrust and suspiciousness of others.

Schizoid personality disorder

Individuals diagnosed with schizoid personality disorder are often described as ‘loners’ who have
very few, if any, close relationships with others (except perhaps a single first‐degree relative). They fail to
express a normal range of emotions and appear to get little sensory or intellectual reward from any
activities. They prefer to spend most of their time with themselves and choose jobs and pastimes that do
not involve them in interactions with others—but they can be quite successful and efficient at their jobs
if it does involve relatively little social contact with others. However, they seem to be largely unaffected
by both praise and criticism and prefer mechanical abstract activities—such as computer or
mathematical games—to real‐life experiences. It has been suggested that there may be some link
between the symptoms of autism and a diagnosis of schizoid personality disorder (Cook, Zhang, &
Constantino, 2020; Ford & Crewther, 2014). For example, the lack of emotional responsiveness and the
tendency to be withdrawn and uncommunicative resembles the symptoms of autism, and there is some
evidence that there may be a modest genetic link between autism and schizoid personality disorder
(Wolff, 1998) (Table 12.5).

schizoid personality disorder A personality disorder in which individuals are often

described as ‘loners’ who fail to express a normal range of emotions and appear to get little
reward from any activities.
TABLE 12.4 Summary: DSM‐5 criteria for paranoid personality disorder

A universal distrust and suspicion of others to the extent that their motives are seen as malicious,
as indicated by at least four of the following:
Suspicions that others are misusing, hurting, or misleading him/her
Fixation with unjustifiable doubts about the trustworthiness of friends and such like
Unwilling to confide in others because of fear that the information will be used against
him/her
Sees hidden threats in nonthreatening words or events
Bears persistent grudges
Sees attacks on their character or status that are not apparent to others and is quick to react
angrily
Has ongoing suspicions about the faithfulness of their sexual partner or spouse
Symptoms do not occur exclusively during the course ofany other psychotic disorder

Schizotypal personality disorder

Individuals with a diagnosis of schizotypal personality disorder usually exhibit ‘eccentric’
behaviour marked by odd patterns of thinking and communication and discomfort with close personal
relationships. In particular, they often exhibit unusual ideas of reference, where they believe that
unrelated events pertain to them, that they have extrasensory abilities, or that they can influence events
external to them in a ‘magical’ way. For example, they may believe that their partner taking the dog for
a walk was a result of them thinking earlier that this needed to be done, or they may indulge in
ritualised, superstitious behaviour such as walking back and forth past a lamppost five times in an
attempt to prevent harm from occurring to a friend or relative. Because of these magical beliefs, they
will often become involved with unconventional groups interested in such topics as astrology,
extraterrestrial phenomena such as alien abduction, and fringe religious groups. Their speech may have
eccentric characteristics and be excessively rambling, and they may use words in unusual ways—but
they are able to communicate information and do not exhibit the incomprehensible ‘word salads’ and
derailment typical of schizophrenia (see Chapter 8). Individuals with schizotypical personality disorder
find it very difficult to interact in normal social situations, they become anxious, and may even develop
paranoid symptoms. As a result they often have few, if any, close friends, they are often viewed by others
as ‘loners’, and tend to drift aimlessly and lead unproductive lives (Skodol et al., 2002). Like all of the
personality disorders, these characteristics appear to develop in early adulthood and persist over much
of the individual's lifetime. There is a tendency for schizotypal personality disorder to manifest
differently in males and females, with females tending to exhibit the positive symptoms typical of
magical thinking and ideas of reference, whereas males tend to show more negative symptoms such as
emotional withdrawal (Table 12.6). Finally, one persistent problem with the diagnosis of schizotypical
personality disorder is that it tends to be highly comorbid with the other personality disorders, in
particular paranoid personality disorder and avoidant personality disorder (Morey, 1988), which
suggests there may be some common aetiological factors across these different diagnostic categories.

schizotypal personality disorder A personality disorder characterised by ‘eccentric’

behaviour marked by odd patterns of thinking and communication.
TABLE 12.5 Summary: DSM‐5 criteria for schizoid personality disorder

A persistent pattern of separation from social relationships and a restricted range of expression of
emotions in relational situations, as indicated by at least four of the following:
Does not like or want close relationships
Prefers solitary activities
Take little or no pleasure in sexual experiences with another person
Takes pleasure in few, if any activities
Lacks close friends or confidents other than immediate relatives
Indifferent to the praise or criticism of others
Displays emotional coldness, detachment, or flat expression
Symptoms do not occur exclusively during the course of any other psychotic disorder

TABLE 12.6 Summary: DSM‐5 criteria for schizotypal personality disorder

A persistent pattern of social and relational shortfalls, evidenced by a lack of ease with, and
reduced ability for, close relationships, as well as distortions and peculiarities of behaviour as
shown by at least five of the following:
Beliefs or perceptions which are irrelevant, innocuous, or unrelated
Odd beliefs that influence behaviour and are not within subcultural norms
Strange perceptions of what is occurring around them
Vague or other odd thinking and speech
Suspicious or paranoid ideas
Inappropriate or constricted emotional expression
Odd, eccentric, or strange behaviour or appearance
Lacks close friends or confidents other than immediate relatives
High levels of social anxiety despite familiarity
The pattern does not occur during the course of schizophrenia or other psychotic disorder
There is some evidence that the schizotypal disorder may be very closely related to schizophrenia. First,
schizotypal personality disorder is found to be significantly more common in individuals who have
biological relatives with schizophrenia than those who do not (Nicolson & Rapoport, 1999), suggesting a
possible inherited link between the two. Second, schizotypal personality disorder is significantly more
likely to be found in the offspring of individuals with schizophrenia than in the offspring of individuals
diagnosed with anxiety disorders or no mental disorder (Hans, Auerbach, Styr, & Marcus, 2004). Third,
some of the symptoms of schizotypal personality disorder can be successfully treated with antipsychotic
drugs also used to treat schizophrenia (Schulz, Schulz, & Wilson, 1988). Fourth, cognitive studies have
shown that many of the attentional and working memory deficits found in schizophrenia are also
apparent in individuals diagnosed with schizotypal personality disorder (Barch et al., 2004). Finally,
neuroimaging studies show that schizotypal personality disorder shares many forms of brain pathology
in common with schizophrenia, suggesting it may be a schizophrenia‐spectrum condition (Fervaha &
Remington, 2013). Schizotypal personality disorder is closely related in many ways to schizophrenia and
may even represent a genetic risk factor for schizophrenia (Walter, Fernandez, Snelling, & Barkus, 2016)
(Case History 12.1).
 CASE HISTORY 12.1 SCHIZOTYPAL PERSONALITY
DISORDER

‘Ian is 23 and lives at home with his parents. He is unemployed. He spends most of his time
watching TV, and often simply sits and stares into space. He says he just feels ‘out of it’ a lot of
the time. He reports that he seems to see himself from outside, as if watching himself in a film
and reading from a script. He has tried a few jobs but never manages to persist at one for very
long. At his last job, which was in a DIY store, several customers complained to the manager
about Ian talking to them in a rambling and vague way—often about irrelevant things. This led
to Ian being sacked from this job. Ian doesn't understand why people don't seem to like him and
get along with him. He notices that people move away from him on public transport or avoid
talking to him in queues, but nothing he seems to do or say changes this and he now tries to
avoid interactions with others because they make him anxious. He has no close relationships
and complains of feeling lonely and isolated’.

Clinical Commentary
Ian shows many of the diagnosable symptoms of schizotypal personality disorder including unusual
ideas of reference (feeling he is in a film), vague and circumstantial speech in conversations,
suspiciousness, and paranoia about others, a lack of close relationships, and feelings of anxiety in
interactions with others. Currently, these characteristics have led to Ian being unemployed and leading the
life of a relatively uncommunicative ‘loner’ who shows little emotion.

12.2.2 Dramatic/Emotional Personality Disorders (Cluster B)

Individuals diagnosed with dramatic/emotional personality disorders tend to be erratic in their
behaviour, self‐interested to the detriment of others, emotionally labile and attention‐seeking. These are
arguably the most problematic of the personality disorders in terms of the extremes of behaviour that
they generate, the impact of this behaviour on basic functioning, and the emotional and personal
distress this causes. In this category we describe the symptoms of (a) Antisocial Personality Disorder
(APD), (b) Borderline Personality Disorder (BPD), (c) narcissistic personality disorder, and (d) histrionic
personality disorder.

dramatic/emotional personality disorders Personality disorders grouped in Cluster B,

including (1) antisocial personality disorder, (2) borderline personality disorder, (3) narcissistic
personality disorder and (4) histrionic personality disorder.

Antisocial personality disorder (APD)

The fundamental feature of APD is an enduring disregard for, and violation of, the rights of others.
This begins in childhood (with a history of symptoms of conduct disorder (CD), see Chapter 16) and
continues into adulthood. The behaviour of individuals with APD deviates substantially from what we
would consider to be normal standards of social behaviour, morality, and remorse and is very closely
linked with adult criminal behaviour. For example, a survey of prison populations in 12 Western
countries found that 47% of male inmates and 21% of female inmates met the diagnostic criteria for
APD, and this is around 10 times the prevalence rate found in the general population (Fazel & Danesh,
2002). Similarly, a DSM diagnosis of APD has also been shown to be a significant predictor of
subsequent criminal behaviour (Fridell, Hesse, Jaeger, & Kuhlhorn, 2008). To be diagnosed with APD,
an individual must be at least 18 years of age and display some of the following characteristics: (a)
failure to conform to social and legal norms, (b) deceitfulness and impulsivity, (c) irritability and
aggressiveness, (d) consistent irresponsibility (e.g., repeated failure to honour obligations), and (e) lack of
remorse. The term ‘sociopath’ or ‘psychopath’ is sometimes used to describe this type of personality
disorder, and such people are often compulsive and persistent liars (Seto, Maric, & Barbaree, 2001) who
are self‐centred to the point of happily gaining profit at the expense of others. Some researchers have
distinguished different types of APD, and there appear to be those whose antisocial behaviour is a result
of unresolved emotional conflicts resulting from adverse early experiences (e.g., childhood neglect or
abuse), and those antisocial behaviours stem primarily from impulsivity in reaction to negative emotions
(Karpman, 1941; Poythress et al., 2010). Individuals with APD show a disregard for the safety of
themselves and others, and this is evidenced by their impulsive, often aggressive behaviour and failure to
plan ahead. Such individuals are frequently involved in motor accidents as a result of reckless driving
(McDonald & Davey, 1996) or commit physical and sexual assaults (including violent domestic abuse).
Impulsivity and irresponsibility can be identified in the daily lives of individuals with APD, where they
frequently may quit a job without a realistic plan for getting another one, or default on debts, fail to
provide child support, or fail to support other dependents on a regular basis.

Antisocial personality disorder (APD) A personality disorder, the main features of which
are an enduring disregard for, and violation of, the rights of others. It is characterised by
impulsive behaviour and lack of remorse, and is closely linked with adult criminal behaviour.

sociopath A person with a personality disorder manifesting itself in extreme antisocial

attitudes and behaviour.

sociopath A person with a personality disorder manifesting itself in extreme antisocial

attitudes and behaviour.

Prior to 1980, APD or psychopathy was defined primarily by personality traits such as egocentricity,
deceit, shallow affect, manipulativeness, selfishness, and lack of empathy. However, with the
introduction of DSM‐IV, APD has been defined more in terms of violations of social norms. The
reason given for this shift in emphasis is that personality traits are difficult to measure, and it is easier to
agree a diagnosis on the basis of well‐defined behaviours (such as breaking laws or aggressive
behaviours) (Widiger & Corbitt, 1993)—and these well‐defined, antisocial behaviours are well
represented in the DSM‐5 diagnostic criteria for APD (see Table 12.7). This shift in the diagnostic
criteria has meant that APD has become very closely associated with criminal activity rather than being
purely a psychopathology requiring treatment. This indicates that the changes to the diagnostic criteria
for APD over the years have moved this category more towards identifying criminals and criminal
behaviour and away from identifying psychological factors that might give rise to such behaviour (such
as lack of empathy, superficial interpersonal style, inflated sense of self‐importance, etc.). There is a real
possibility that this move towards defining APD in terms of antisocial activities could fudge the
distinction between psychopathology in need of treatment and criminal behaviour in need of restraint.
TABLE 12.7 Summary: DSM‐5 criteria for antisocial personality disorder (APD)

Pattern of indifference to and violation of the rights of others as shown by at least three of the
following since the age of 15 years:
Lack of conformity to social norms and regularly indulging in unlawful behaviours
Lying, pretending to be someone else, or deceiving others for personal gain
Failure to plan ahead or impulsiveness
Irritability and aggressiveness leading to physical fights and assaults
Reckless indifference to own and other's personal safety
Consistent irresponsible behaviour
Lack of remorse
The person is at least 18 years old
The antisocial behaviour is not associated with symptomsof schizophrenia or mania

Borderline personality disorder (BDP)

The cardinal features of Borderline personality disorder (BPD) are an enduring pattern of
instability in personal relationships, a lack of a well‐defined and stable self‐image, regular and
predictable changes in moods, and impulsive behaviour. These characteristics are pervasive and will
have endured from childhood into adulthood and can be seen in the personal account given in Jane's
Story at the beginning of this chapter. (Table 12.8). In particular, individuals with BPD appear to have a
significant fear of abandonment and rejection. This leads them to fall into close and conflict‐ridden
relationships after as little as a single meeting with someone; but they are just as likely to fall out with
that person if they interpret the person's behaviour as uncaring or not attentive enough—and this may
often be the case, because the feelings of the individual with BPD may not be shared by the other
person (Modestin & Villiger, 1989). Although their behavior becomes unpredictable and emotional
when their expectations for a relationship are not met, they are also riddled with fear about being
rejected and losing that relationship. This leads to rapid, ill‐tempered mood changes if the individual
does not feel that things ‘are going their way’. The results of this emotional roller‐coaster and fear of
abandonment and rejection are (a) regular and unpredictable shifts in self‐image characterised by
changing personal goals, values, and career aspirations; (b) prolonged bouts of depression (Luca, Luca,
& Calandra, 2012), deliberate self‐harm (Sansone, Wiederman, & Sansone, 2000), suicidal ideation, and
actual suicide attempts (Venta, Ross, Schatte, & Sharp, 2012); and (c) impulsive behaviour such as drug
abuse (Trull et al., 2000), physical violence, and inappropriate promiscuity (Sansone & Wiederman,
2009).

Borderline personality disorder (BPD) A personality disorder, the main features of which
are instability in personal relationships, a lack of well-defined and stable self‐image, regular and
unpredictable changes in moods and impulsive behaviour.
TABLE 12.8 Summary: DSM‐5 criteria for borderline personality disorder (BPD)

A long‐term display of instability of relationships, self‐image, and behaviour, as well as high levels
of impulsivity beginning in early adulthood and indicated by at least five of the following:
Desperate attempts to avoid real or imagined abandonment
A pattern of unstable and intense interpersonal relationships, fluctuating between adulation
and deprecation
Constantly unstable self‐image and identity disturbance
Potentially self‐damaging impulsivity in at least two areas such as sex, substance abuse, and
reckless driving
Repeated suicidal behaviour or self‐mutilation
Emotional instability due to reactivity of mood
Unsuitable, intense anger or difficulty controlling anger
Stress‐related paranoid idealisation or severe dissociative symptoms
Because of its close association with mood disorders, depression, and suicide, some researchers have
argued that BDP may well be a form of depression (Gunderson & Elliott, 1985), but in fact it is just as
likely to be comorbid with anxiety disorders or with depressive symptoms (Grant et al., 2008). Zanarini
et al., (1998) found that 96.3% of individuals diagnosed with BPD met the criteria for a mood disorder
(major depression, dysthymia, bipolar II disorder), but 88.4% also met the criteria for an anxiety
disorder, with panic disorder (47.8%) and social phobia (45.9%) being the most prevalent. Interestingly,
64.1% met the criteria for substance abuse disorders—reaffirming the link between BPD and impulsive
behaviour, whereas 53% met the criteria for eating disorders. Another important finding is that BPD is
often comorbid with post‐traumatic stress disorder (PTSD), with 30.2% of those with a diagnosis of
BPD also having a diagnosis of PTSD, and 24.2% of those with PTSD also having a diagnosis of BPD
(Pagura et al., 2010), a finding which is consistent with the view of some clinicians that BPD may be a
form of PTSD—and PTSD and BPD may be products of a history of traumatic childhood experience
related to neglect or physical and sexual abuse (Scheiderer, Wood, & Trull, 2015; Heffernan & Cloitre,
2000). At the very least, these data suggest that BPD represents a behavioural style that may put an
individual at severe risk for a wide range of other psychopathologies, and while the prevalence rates for
BPD in the general community are between 0.2% and 1.8%, this prevalence rises to 15–25% in
psychiatric inpatients (Leichsenring, Leibing, Kruse, New, & Leweke, 2011; Lieb, Zanarini, Schmahl,
Linehan, & Bohus, 2004)

Narcissistic personality disorder

The individual with a diagnosis of narcissistic personality disorder routinely overestimates their
abilities and inflates their accomplishments and is characterised by a pervasive need for admiration and
a lack of empathy with the feelings of others. Such people believe they are superior to others and expect
others to recognise this. They will constantly fish for compliments and are likely to become angry when
such compliments are not forthcoming (Gramzow & Tangney, 1992). In their relationships, they will
expect great dedication from others and may often exploit others for their own gain. They also have a
lack of empathy and either cannot recognise, or simply ignore, the desires and feelings of others.
Because of this, they tend to have a history of problematic relationships, and Campbell (1999) found
that individuals with narcissistic personality disorder tend to prefer partners who are openly admiring
rather than openly loving. (Table 12.9). However, beneath the façade of bragging about their
achievements and their talents is a very fragile self‐esteem and individuals with narcissistic personality
disorder constantly need to check for reassurance. When this is not forthcoming, they become angry
and aggressive. Because of the apparent lack of empathy and the tendency to exploit others for self‐
benefit, narcissistic personality disorder has been compared with APD, and it may be a subtype of APD
in that some features of the disorder (such as a grandiose self‐image) predict future criminal or
delinquent behaviour (Calhoun, Glaser, Stefurak, & Bradshaw, 2001).

narcissistic personality disorder A personality disorder in which individuals overestimate

their abilities, inflate their accomplishments, have a pervasive need for admiration and show a
lack of empathy with the feelings of others.

TABLE 12.9 Summary: DSM‐5 criteria for narcissistic personality disorder

An ongoing pattern of grandiosity, need for adoration and lack of empathy, beginning in early
adulthood and indicated by at least five of the following:
Has a highly exaggerated sense of self‐importance and self‐achievement
Preoccupied with illusions of unlimited success, power, beauty, or ideal love
Believes that they are special and can be understood only by people of similar speciality
Commands excessive admiration
Has unreasonable expectations of favourable treatment
Exploits others for personal gain
Lacks compassion and cannot identify with the needs and feelings of others
Often jealous of others and believes that others are jealous of them
Shows conceited, self‐important behaviour or attitudes

Histrionic personality disorder

Individuals with a diagnosis of histrionic personality disorder are attention‐seeking and
uncomfortable or unhappy when they are not the centre of attention. Their behaviour is often dramatic
and their language theatrical and exaggerated. For example, they may always seek to be the centre of
attention at a party, and if not, may suddenly do something dramatic to gain attention (such as make up
an intriguing story about themselves or someone else or create a scene). Similarly, they will make
extravagant expressions of emotion towards friends and colleagues and have a style of speech that is
excessively impressionistic but lacking in detail. For example, they may describe someone as a
‘wonderful person’ but then be unable to describe any features that contribute to this assessment. As a
result, such individuals are often viewed as shallow, self‐dramatising, and easily influenced. They will
draw attention to themselves by exaggerating their illnesses (Morrison, 1989) or dressing provocatively
or seductively. Because of their shallow and flirtatious nature, individuals with histrionic personality
disorder often find it difficult to make lasting relationships, and this is frequently a main reason why such
individuals seek therapy. Although there was traditionally a bias towards diagnosing this disorder more
often in women than in men (Anderson, Sankis, & Widiger, 2001), surveys suggest that it is equally
distributed across men and women (Mattia & Zimmerman, 2001). The prevalence rate of histrionic
personality disorder is low (0.4%) and it is highly comorbid with other personality disorders such as
borderline, narcissistic, and dependent personality disorders (Bakkevig & Karterud, 2010). This poor
construct validity may mean that is it likely to be excluded from future versions of DSM, although the
characteristics of exhibitionism and attention‐seeking may be ones that might be included in any
reformulation (Bakkevig & Karterud, 2010) (Table 12.10).
 histrionic personality disorder A personality disorder in which an individual is attention-
seeking and uncomfortable or unhappy when not the centre of attention.

12.2.3 Anxious/Fearful Personality Disorders (Cluster C)

As the name suggests, people diagnosed with a personality disorder in this cluster exhibit anxious and
fearful behaviour. However, unlike anxiety disorders, the anxious and fearful behaviour exhibited will
have been a stable feature of their behaviour from late childhood into adulthood, and it is usually not
possible to identify a specific experience or life event that might have triggered this fear and anxiety.
Anxious/fearful personality disorders may be comorbid with anxiety disorders (e.g., social
anxiety disorder, panic disorder), where triggers for the latter can be identified. But the pattern of
behaviour exhibited by individuals with anxious/fearful personality disorders generally tends to
represent ingrained ways of dealing and coping with many of life's perceived threats. The three
disorders to be described in Cluster C are (a) avoidant personality disorder, (b) dependent personality
disorder, and (c) OCPD.

Anxious/fearful personality disorders The exhibition of persistent anxious and fearful

behaviour which is not usually linked to a specific trigger experience or life event.

TABLE 12.10 Summary: DSM‐5 Criteria for Histrionic Personality Disorder

A continuous pattern of high levels of emotionality and attention‐seeking, beginning in early

adulthood and indicated by at least five of the following:
Unhappy in situations where they are not the centre of attention
Shows high levels of inappropriate sexually suggestive or provocative behaviour in
interactions with others
Displays rapidly shifting and shallow demonstrations of emotion
Frequently uses personal appearance to draw attention to self
Has an excessively impressionistic and detail‐lacking style of speech
Is self‐dramatic, overtheatrical, and uses exaggerated expressions of emotion
Is easily influenced by others
Feels that relationships are more intimate than they actually are

Avoidant personality disorder

The main features of avoidant personality disorder are persistent social inhibition (characterised
by avoidance of a wide range of social situations), feelings of inadequacy, and hypersensitivity to
negative evaluation and criticism. These tendencies appear in late childhood or early adolescence and
are exhibited across a range of different contexts, including occupational and social contexts and in
interpersonal interactions generally. Individuals with avoidant personality disorder are fearful of
criticism, disapproval, and rejection, and they automatically assume that others will be critical and
disapproving. They will avoid school, work, and all group activities because of these fears and are
unable to form close relationships unless there is an assurance of uncritical acceptance. They are
generally shy and cannot easily talk about themselves for fear of being ridiculed or shamed. They also
have a clear bias for interpreting ambiguous information and comments in a negative way (e.g.,
someone saying ‘I was surprised by the quality of your work’ would be interpreted as being critical or
disapproving, even though their comments could equally be interpreted as praise). Individuals with
avoidant personality disorder are particular ill at ease with strangers, and will usually avoid interactions
with strangers at all costs. As a result they are reluctant to take risks, engage in new activities, or even
accept job promotions that might involve greater responsibility and interaction with others (Table 12.11)
(Client's Perspective 12.1).

avoidant personality disorder A personality disorder the features of which are avoidance
of a wide range of social situations, feelings of inadequacy, and hypersensitivity to negative
evaluation and criticism.

TABLE 12.11 Summary: DSM‐5 criteria for avoidant personality disorder

A persistent pattern of social reticence, feelings of inadequacy, and hypersensitivity to criticism,

beginning in early adulthood and indicated by at least four of the following:
Avoiding occupational activities that involve high levels of interpersonal contact due to fears
of criticism or rejection
Unwilling to engage with others unless certain of approval and being liked
Shows restraint in intimate relationships for fear of ridicule or shame
Fixation with disapproval or rejection in social situations
Inhibited in new relationships due to feelings of inadequacy
Feels that they are socially incompetent, unappealing, or inferior to others
Highly reluctant to take part in any new activities because of the potential for
embarrassment

People with avoidant personality disorder generally have low self‐esteem, and will frequently feel angry
at themselves for being withdrawn and not enjoying the apparent social rewards and intimate
relationships experienced by others (Lynum, Wilberg, & Karterud, 2008). As you can imagine, avoidant
personality disorder has many features in common with social anxiety disorder (see Chapter 6), and
many individuals diagnosed with avoidant personality disorder also receive a diagnosis of social anxiety
disorder (Widiger, 2001; Marques et al., 2012). However, individuals with social anxiety disorder tend to
be made anxious by social situations where particular levels of performance might be required (e.g.,
making a work presentation or having a job interview), whereas the personality disorder is more
associated with (a) fear of personal interactions and social relationships generally, (b) the criticism and
rejection that they believe will be associated with these types of experiences, and (c) difficulties in being
open with people they are close to (Turner, Beidel, Dancu, & Keys, 1986; Marques et al., 2012). In
addition, there is some evidence that avoidant personality disorder is associated with avoidance
behaviour generally, and individuals diagnosed with the disorder show greater avoidance of emotion,
novelty, and other nonsocial events than nonsufferers (Taylor, Laposa, & Alden, 2004). However, some
clinicians believe that avoidant personality disorder and social anxiety disorder are both components of
a broader social anxiety spectrum (Tillfors & Ekselius, 2009), and there is evidence to suggest that
(a) the severity of the symptoms of avoidant personality disorder is significantly increased if it is
comorbid with social anxiety disorder (Ralevski et al., 2005), and (b) there is a genetic link between the
two disorders evidenced by the fact that if an individual is diagnosed with one of the disorders, first‐
degree relatives of that individual are 2–3 times more likely to be diagnosed with either of them (Tillfors
et al., 2001).

social anxiety spectrum A spectrum of disorder proposed to include both avoidant

personality disorder and social anxiety disorder.
 CLIENT'S PERSPECTIVE 12.1 THOUGHTS ABOUT AVOIDANT
PERSONALITY DISORDER

‘The way I see it, people like us (with avoidant personality disorder) were born with brains that
were very sensitive to social situations. As a child I used to get so frightened and scared that I
probably unconsciously decided to build up a defence system against terrible feelings in order to
protect myself. I just instinctively knew I had to do something, so my personality was formed in
a way designed to avoid the harm. I hated the fact that other kids would be out to criticise me,
so I adopted avoidance as a defence system. I had very low self‐esteem, so I didn't think anyone
liked me anyway. So I tried to stay away from potentially harmful situations, and lived in a
world of my own. When I was younger, my classmates used to tell me that at parties they would
turn the lights down and dance, but I would sit in the corner playing with my bike‐lights. I
would often stay off school and read books all day—that would comfort me because I liked the
stories. My real life became less important to me, and I didn't participate in social events apart
from just trying to be pleasant when needed. As I grew older, I should have developed a
different defence system, but I couldn't because I had become pretty much a social outcast, and
the fear of being criticised and rejected had got stronger. It was like I was in a vicious circle that
I couldn't get out of ’.

Clinical Commentary
In this personal account of avoidant personality disorder, the individual describes how her desire to avoid
social encounters developed during childhood from a fear of being criticised (and possibly bullied) by her
peers. When avoiding social encounters (e.g., by staying off school), she would reward these avoidance
responses by indulging in enjoyable activities, such as reading stories she liked. At adolescence she
discovers she has become something of a social outcast, and this maintains her low self‐esteem and
feelings of not being liked, which further maintains social avoidance. She shows a number of the
symptoms of avoidant personality disorder, including avoiding activities that involve significant
interpersonal contact because of fears of criticism, disapproval, or rejection, a preoccupation with being
criticised or rejected in social situations, and views herself as socially inept and personally unappealing to
others.

Dependent personality disorder

Dependent personality disorder is characterised by a pervasive and excessive need to be taken
care of that extends significantly beyond the caring relationships that most individuals would have with
one another. Individuals with dependent personality disorder exhibit submissive and clinging behaviour
and have great difficulty making everyday decisions (e.g., what clothes to wear) without receiving advice
from significant others. They are usually passive and will allow others to make all important decisions
for them, including where they should live, what job they should choose, and how they should spend
their free time. They have difficulty expressing disagreement with others and will often agree with things
that they know to be wrong or inappropriate rather than risk losing the support and help of those they
look to for guidance. They will also go to excessive lengths to secure support and guidance from others
—even to the point of taking on jobs and tasks that they find unpleasant—and will make regular self‐
sacrifices and continually tolerate verbal, physical, and even sexual abuse in order to retain their
relationship with those they are dependent on (such as the person who will tolerate their partner's
infidelities and physical abuse because of fear of losing the support they need). However, dependent
personality disorder may affect men and women differently, with women being more likely to be in
multiple abusive relationships, whereas men with dependent personality disorder have the potential to
become abusive in order to maintain their dependent relationships (Klonsky, Jane, Turkheimer, &
Oltmanns, 2002). Individuals suffering dependent personality disorder tend to be pessimistic and self‐
doubting, and belittle their own achievements. They will regularly ‘tag along’ with significant others in
order not to be alone, and will usually rebound from one relationship to another in order to ensure the
continual care and attention they need. (Table 12.12).

Dependent personality disorder A personality disorder characterised by a pervasive and

excessive need to be taken care of, submissive and clinging behaviour, and difficulty making
everyday decisions without advice from others.

The characteristics of dependent personality disorder appear to fall into two distinctive categories: (a)
attachment/abandonment, in which the individual fears abandonment and constantly seeks attachment
with significant others, and (b) dependency/incompetence, in which the individual has constant feelings
of incompetence which drives them to rely on others (Gude, Hoffart, Hedley, & Ro, 2004). Because of
their self‐doubting and overdependence, individuals with dependent personality disorder often dislike
themselves (Overholser, 1996), which may lead to depression, anxiety, eating disorders, and suicidal
ideation (e.g., Godt, 2002). Disney (2013) provides a thorough critical review of dependent personality
disorder and relevant research (Photo 12.1).
TABLE 12.12 Summary: DSM‐5 criteria for dependent personality disorder

An inescapable and extreme need to be taken care of, leading to submissive and clingy behaviour
and fear of separation, beginning in early adulthood and indicated by at least five of the
following:
Cannot make everyday decisions without an unnecessarily high level of advice and
reassurance from others
Needs others to assume the majority of responsibility for the major areas of his/her life
Struggles to express disagreement with someone for fear of loss of support
Has difficulty initiating/doing things on his/her own
Feels uncomfortable or afraid when left alone due to a fear of not being able to care for
oneself
Urgently seeks to secure another caring and supportive relationship when the previous one
ends
Is unrealistically obsessed with fears of being left to take care of oneself
PHOTO 12.1 From letters and biographies of Wolfgang Mozart it was assumed he may have suffered from bipolar
disorder because of periods of depression followed by bouts of mania. However, more recent analyses suggest he may have
been suffering from dependent personality disorder because of his mood lability, impulsiveness, and negative reactions to his
wife's absences (Huguelet & Perroud, 2005).
Obsessive‐compulsive personality disorder
Individuals diagnosed with obsessive‐compulsive personality disorder show exceptionally
perfectionist tendencies including a preoccupation with orderliness and control at the expense of
flexibility, efficiency, and productivity. They will stick to rules, work schedules and prearranged
procedures to such a degree that the overall purpose of the activity is lost. Diverging from a preset
schedule causes them significant distress, as does failing to achieve the highest of standards in the things
they do, and their attention to detail and their inflexibility will often annoy other people because of the
delays and inconvenience that this may cause. For example, they may hold up a work project by insisting
that their component of the project has to be completed meticulously and in the way in which it was
originally specified. Individuals with obsessive‐compulsive personality disorder nearly always plan ahead
meticulously and are unwilling to contemplate changes to their plan. This means that even hobbies and
recreational activities are approached as serious tasks requiring organisation and scheduling. For
example, they will need to plan a visit to a restaurant well in advance, the menu needs to be checked to
ensure that everyone will be happy with what is on offer, and the quality of the restaurant's service must
be checked with friends who have been there or by consulting dining reviews. If this planning is
disrupted (e.g., if the restaurant is closed when the party arrives), this will cause the individual
considerable distress and a spontaneous alternative will be difficult for them to consider. If things are
not done ‘their way’ this also causes distress, and this may be taken to unnecessary extremes (such as
asking a child to ride its bike in a straight line or telling people that there is only one way to wash the
dishes, etc.), and they will then become upset or angry if people do not comply, although the anger is
rarely expressed directly. Because of this they will rarely delegate tasks, but insist on doing them
themselves, and often become viewed as ‘workaholics’. Their perfectionist tendencies also means that
they often end up hoarding things rather than throwing them away and will adopt a miserly attitude to
spending, believing that money should not be wasted. Because of this, they often end up living at a
standard well below what they can afford. OCPD is one of the most prevalent of the personality
disorders, with a recent large‐scale epidemiology study recording a lifetime prevalence rate of 7.8%
with rates being similar between males and females (Grant, Mooney, & Kushner, 2012) (Table 12.13).

obsessive compulsive personality disorder (OCPD) A personality disorder in which

individuals show exceptionally perfectionist tendencies including a preoccupation with
orderliness and control at the expense of flexibility, efficiency and productivity.

TABLE 12.13 Summary: DSM‐5 criteria for obsessive‐compulsive personality disorder (OCPD)

An ongoing pattern of concern with orderliness, perfection, and mental and interpersonal
control, at the expense of flexibility, openness, and efficiency, beginning in early adulthood and
indicated by at least four of the following:
An obsession with details, rules, lists, organisation, or schedule to the exclusion of the main
point of the activity
Perfectionism that hinders task completion
Excessive devotion to work to the prohibition of social and leisure activities
Inflexibility about matters of morals, ethics, or values
Is unable to dispose of wornout or worthless objects despite them having no sentimental
value
Reluctant to delegate to others unless they submit to exactly his/her way of doing things
Hoards money and is reluctant to spend on their self or others
Is rigid and stubborn
 CASE HISTORY 12.2 OBSESSIVE‐COMPULSIVE
PERSONALITY DISORDER (OCPD)

‘Jane likes to describe herself as a perfect mother. She takes pride in keeping an orderly
household and attending all of her daughters' horse‐riding events, while being office manager
in an insurance company. She knows the schedules of each family member and follows rigid
routines to make sure everyone gets to work or school on time. Jane gets very upset when her
teenage daughters want to go out with friends at weekends or in the evenings. She says it takes
away from their family time and all of her efforts and planning are wasted. She refuses to go
out for the evening if this interferes with her planned weekly activities in the house. Her
husband doesn't mind Jane planning his schedule but he does complain when he helps out with
the household chores because she consistently complains that he hasn't followed her instructions
properly. For example, if he does the shopping but does not get the right discounted items, Jane
gets upset and accuses him of being careless and extravagant. Jane continually tells everyone
that if she wants something doing properly, she has to do it herself, and she will religiously clean
the house in exactly the same way every week—whether things are dirty and untidy or not’.

Clinical Commentary
Jane exhibits many of the symptoms of OCPD and probably has the minimum four symptoms required
for a DSM‐5 diagnosis. These are a pre‐occupation with details, rules, lists, order, organisation, or
schedules to the extent that the major point of the activity is lost (e.g., she will do the housework each
week in exactly the same way regardless of whether this is necessary), she is excessively devoted to work
and productivity to the exclusion of leisure activities, she is reluctant to delegate tasks or to work with
others unless they submit to exactly her way of doing things, she shows rigidity and stubbornness, and
adopts a miserly spending style. From this brief case description you can see that Jane frequently gets
upset and anxious about family life because of her rigid perfectionism (and this may well lead to a
comorbid diagnosis of generalised anxiety disorder, see Chapter 6), and her rigid and inflexible behaviour
also puts severe strains on family relationships.

While these characteristics may seem very similar to the symptoms of obsessive‐compulsive disorder
(OCD) (see Chapter 6), the exact relationship between OCPD and OCD has been the subject of debate
for some time. Some clinicians have argued that OCPD is a precursor for the development of OCD
(Krockmalik & Menzies, 2003). However, OCPD is not a necessary precursor of OCD and studies have
found the prevalence of OCPD in patients diagnosed with OCD as ranging only between 23% and
34% (Albert, Maina, Forner, & Bogetto, 2004; Lochner et al., 2011). However, regardless of whether
OCPD is a risk factor for OCD, individuals diagnosed with comorbid OCPD and OCD do appear to
exhibit more severe symptoms, are more functionally impaired, and are likely to develop other problems
such as alcohol dependence and depression (Garyfallos et al., 2010; Gordon, Salkovskis, Oldfield, &
Carter, 2013) (Case History 12.2).

12.2.4 Summary
While the different personality disorders we have discussed may seem to take quite contrasting forms
(e.g., some represent withdrawn and avoidant forms of behaviour, some are characterised by
behavioural and emotional lability and impulsivity, and others are characterised by intense fears of
criticism, rejection, and abandonment), they are all assumed within DSM‐5 to represent enduring
patterns of behaviour that we would consider to be close to the borderline of what is
adaptive/maladaptive, normal/abnormal, or culturally acceptable/unacceptable. Because the
behavioural styles of individuals with personality disorders can be conceptualised as being on normal
personality dimensions—albeit at the extremes of these dimensions (Costa & MacRae, 1990), there is an
issue about what it is that is ‘disordered’ or ‘abnormal’ about personality disorders, and this is likely to
be addressed with dimensional measurements for personality traits in future editions of DSM (see
Section 12.1.3) (see Activity Box 12.1 on the book's website).

SELF‐TEST QUESTIONS
Personality disorders generally consist of a loosely bound cluster of subtypes. What are the
four common features of all personality disorders?
What are the three clusters of personality disorders listed in DSM‐5, what are the
disorders listed in each cluster, and what are their main defining features?
Can you list the diagnostic criteria for (a) APD and (b) BPD?
Schizophrenia spectrum disorder, bipolar disorder spectrum, and social anxiety spectrum
are broader disorder categories associated respectively with which individual personality
disorders?
 SECTION SUMMARY

12.2 PERSONALITY DISORDERS AND THEIR DIAGNOSIS

DSM‐5 lists 10 diagnostically independent personality disorders that are organised into
three primary clusters (a) odd/eccentric—containing paranoid, schizoid, and schizotypal
personality disorders; (b) dramatic/emotional—containing antisocial, borderline,
narcissistic, and histrionic personality disorders; and (c) anxious/fearful—containing
avoidant, dependent, and OCPD.
Paranoid personality disorder is characterised by an enduring pattern of distrust and
suspiciousness of others.
Individuals with schizoid personality disorder are often described as ‘loners’ who fail to express
a normal range of emotions and appear to get little reward from any activities.
Schizotypal personality disorder is characterised by ‘eccentric’ behaviour marked by odd
patterns of thinking and communication.
The main features of antisocial personality disorder are an enduring disregard for, and violation
of the rights of others. It is characterised by impulsive behaviour, lack of remorse, and is
closely linked with adult criminal behaviour.
The defining characteristics of borderline personality disorder are instability in personal
relationships, a lack of well‐defined and stable self‐image, regular and unpredictable
changes in moods, and impulsive behaviour.
Individuals with narcissistic personality disorder overestimate their abilities, inflate their
accomplishments, have a pervasive need for admiration, and also show a lack of empathy
with the feelings of others.
Individuals with histrionic personality disorder are attention‐seeking, and are uncomfortable or
unhappy when they are not the centre of attention.
The main features of avoidant personality disorder are avoidance of a wide range of social
situations, feelings of inadequacy, and hypersensitivity to negative evaluation and criticism.
Dependent personality disorder is characterised by a pervasive and excessive need to be taken
care of, submissive and clinging behaviour, and difficulty making everyday decisions
without advice from others.
Individuals with obsessive–compulsive personality disorder show exceptionally perfectionist
tendencies including a preoccupation with orderliness and control at the expense of
flexibility, efficiency, and productivity.
Many personality disorders are highly comorbid with other psychiatric disorders such as
anxiety and mood disorders (including bipolar disorder, major depression, social phobia,
panic disorder, and PTSD).

12.3 THE PREVALENCE OF PERSONALITY DISORDERS

There has generally been some uncertainty about the actual prevalence rates of personality disorders
within the general population, and this uncertainty stems from issues to do with (a) reliability in the
diagnosis of personality disorders (McGlashan et al., 2005; Paris, 2001), (b) potential gender bias in
diagnosis of some of the disorders—particularly histrionic, borderline, and dependent personality
disorders (Widiger & Trull, 1993; Hartung & Widiger, 1998), and (c) the poor temporal stability of
personality disorder diagnoses over time (Zimmerman, 1994). This variability in estimated prevalence
rates is reflected in the data presented in Table 12.14, showing a selection of sources providing
prevalence rates from European and Westernised countries. These data suggest that the prevalence rate
for personality disorders in the general population is between 10.7% and 13.4%—which make
personality disorders one of the most common of the psychopathologies (see also Sansone & Sansone,
2011). But the variability in these figures across different studies makes it difficult to draw many
conclusions about the prevalence of specific personality disorders, except perhaps that OCPD is
probably the most common. In addition, the prevalence rates of personality disorders are consistently
lower in low‐ and middle‐income countries compared with high‐income countries (Winsper et al., 2020),
which may be the result of cultural or social factors, or the fact that symptoms of mental health
problems can present very differently in different cultures.
There are some significant gender differences in these prevalence rates. Coid, Yang, Tyrer, Roberts, and
Ullrich (2006) report that all personality disorder categories were more prevalent in men, but in their
study, Widiger and Trull (1993) found that 75% of individuals diagnosed with BPD were female. Coid et
al. (2006) also found that personality disorders were highly comorbid, with the mean number of
personality disorders per individual with a diagnosis being 1.92 (see Table 12.15). The differences in
prevalence and comorbidity rates recorded by different studies may be explained by differences in
sampling procedures, diagnostic procedures, number of disorder categories, and cultural differences in
the identification and diagnosis of personality disorders. Unfortunately, with the future changes
proposed to the diagnosis of personality disorders, we're unlikely to get a clear picture of prevalence
rates for some time to come!
There are also a number of risk factors for personality disorders and these include (a) low socio‐
economic class, (b) living in inner cities, (c) being a young adult, and (d) being divorced, separated,
widowed or never married (Torgersen, Kringlen, & Cramer, 2001; Grant et al., 2004). Childhood,
physical, verbal, and sexual abuse is also a significant risk factor for developing a personality disorder
(Johnson et al., 1999), and borderline and schizotypal personality disorders were strongly predicted by
childhood sexual abuse, APD by physical abuse, and avoidant and schizoid personality disorder by
emotional neglect (Waxman, Fenton, Skodol, Grant, & Hasin, 2014), and significant levels of childhood
verbal abuse increase the risk of a number of personality disorders, including paranoid, borderline,
narcissistic, and obsessive‐compulsive (Johnson et al., 2001). These findings suggest that childhood abuse
may well be an important factor in the development of a personality disorder in some individuals.
However, it is unclear whether other types of risk factors—e.g., low socio‐economic status, living in
inner cities, being divorced, separated, or never married—are causal factors in developing personality
disorders or are simply outcomes of having a personality disorder.
TABLE 12.14 Personality disorders prevalence rates
Cluster Personality Prevalence Prevalence Prevalence Prevalence
disorder rate in rate in rate in rate in a
general general general community
population population population sample
(DSM‐5 (Western (Norway) (United
estimate) countries) (Torgersen Kingdom)
(%) (Volkert et et al., 2001) (Coid et al.,
al., 2018) (%) (%) 2006) (%)
All 15.0 12.1 13.4 10.7
personality
disorders
CLUSTER A Paranoid 2.3–4.4 3.0 2.4 0.7
(odd/eccentric Schizoid 3.1–4.9 2.8 1.7 0.8
personality
disorders) Schizotypal 0.6–4.6 3.0 0.6 0.06
CLUSTER B Antisocial 0.2–3.3 3.0 0.7 0.6
(dramatic/emotional Borderline 1.6–5.9 1.9 0.7 0.7
personality
disorders) Histrionic 1.8 0.8 2.0 0
Narcissistic 0–6.2 1.2 0.8 0
CLUSTER C Avoidant 2.4 2.7 5.0 0.8
(anxious/fearful Dependent 0.4–0.6 0.7 1.5 0.1
personality
disorders) Obsessive– 2.1–7.9 4.3 2.0 1.9
compulsive
personality
disorder
TABLE 12.15 Comorbidity of borderline personality disorder and other personality disorders with psychological disorders
Data taken from Zanarini et al. (1998). Diagnoses were determined using DSM‐III‐R criteria which may give rise
to some inconsistencies in comorbidity rates when compared with current DSM‐5 criteria.

Disorder Disorder % Borderline personality % Other personality

Category disorder patients with disorder patients with
other diagnoses other diagnoses
Mood Major depression 83 67
disorders Dysthymia 39 25
Bipolar II disorder 10 1
Substance Alcohol 52 45
abuse Abuse/dependence
disorders Drug 46 42
Abuse/dependence
Anxiety Panic disorder 48 20
disorders Agoraphobia 12 3
Social phobia 46 19
Specific phobia 32 15
OCD 15 6
PTSD 56 21
Generalised 13 3
anxiety disorder
Somatisation Somatisation 4 0
disorders disorder
Hypochondriasis 5 2
Somatoform pain 4 2
disorder
Eating Anorexia nervosa 21 13
disorders Bulimia nervosa 26 17
Studies of individuals suffering from psychopathology suggest that individuals with personality disorders
are amongst the most frequently treated by mental health professionals. In a study of psychiatric
outpatients, Zimmerman, Rothschild, and Chelminski (2005) found that slightly less than one third of
all psychiatric outpatients in their sample were diagnosed with at least one personality disorder. This is
consistent with the fact that personality disorders are highly comorbid with other psychopathologies,
and particularly anxiety and mood disorders (Zanarini et al., 1998), and it is usually the comorbid and
more specific disorder that has brought the individual into treatment. This reflects the view that the
individual with a personality disorder will often view their behaviour as quite normal (because they have
‘always’ behaved like that), but what brings them to therapy are the more specific and distressing
consequences of their behaviour such as unstable or turbulent relationships, sexual dysfunction,
substance abuse, eating disorders, anxiety disorders such as panic disorder or social phobia, mood
disorders, deliberate self‐harm, and suicide attempts.
Some studies have identified ethnicity as a factor affecting rates of diagnosis of personality disorder. For
example, Chavira et al. (2003) identified significantly higher rates of BPD in Hispanic than in
Caucasian and African Americans, and higher rates of schizotypal personality disorder in African
Americans compared to Caucasians. McGilloway, Hall, Lee, and Bhui (2010) found a lower prevalence
of personality disorders among Black compared to White patients in UK studies, but they conclude that
this may indicate a neglect of personality disorder diagnosis among minority ethnic groups in the UK.

SELF‐TEST QUESTIONS
What is the estimated prevalence rate for personality disorders in the general population?
Do prevalence rates for personality disorders vary with culture and ethnicity?

SECTION SUMMARY

12.3 THE PREVALENCE OF PERSONALITY DISORDERS

The prevalence rate for personality disorders in the general population is around 10–15%
which makes them one of the most common of the psychopathologies.
Risk factors for developing a personality disorder include (a) low socio‐economic status; (b)
living in inner cities; (c) being a young adult; (d) being divorced, separated, widowed, or
never married; and (e) childhood neglect and childhood physical, verbal, and sexual abuse.

12.4 THE AETIOLOGY OF PERSONALITY DISORDERS

Explaining the development of the extreme and enduring behavioural styles characteristic of
personality disorders is still very much in its infancy. There will almost certainly be no overarching or
all‐inclusive theory of the aetiology of personality disorders because the different clusters represent
quite different patterns of behaviour (e.g., eccentric behaviours, dramatic and impulsive behaviours,
dependent and avoidant behaviours, etc.), so we might expect that different clusters, and indeed,
different personality disorders may be acquired in quite different ways. One characteristic that was
thought to be common to all personality disorders was that the respective behaviour patterns were
relatively enduring and can be traced back to childhood and early adolescence, suggesting that either
inherited or developmental factors may be quite important across all of the personality disorders.
However, the belief that personality disorders might be a lifetime affliction has recently been challenged,
with evidence that personality disorder diagnoses have poor stability over time (Zimmerman, 1994), and
75% of individuals with an early diagnosis of BPD no longer meet diagnostic criteria after 10–15 years
(Zanarini, Frankenburg, Hennen, Rich, and Silk, 2006). So there is evidence that at least some
personality disorders will either remit over time or will be responsive to effective treatments.
We will continue by looking at aetiological factors in each of the three personality disorder clusters.

12.4.1 Odd/Eccentric Personality Disorders (Cluster A)

As we mentioned earlier individuals diagnosed with Cluster A personality disorders have characteristics
that resemble many of the symptoms of schizophrenia, such as paranoid beliefs (paranoid personality
disorder), they may be socially withdrawn with flat affect (schizoid personality disorder) or exhibit
rambling or disorganised thoughts and speech (schizotypal personality disorder). As we shall see, these
formalistic similarities between Cluster A disorders and schizophrenia have led researchers to argue that
they are part of a broader schizophrenia spectrum disorder and so have causes that are closely
linked to the aetiology of schizophrenia itself (Siever & Davis, 2004; Bergman et al., 1996). Before we
discuss the schizophrenia spectrum approach, let us briefly mention some other approaches to
explaining Cluster A disorders.

Psychodynamic approaches
In the case of both paranoid and schizoid personality disorders, psychodynamic theorists have argued
that the causes of these disorders lie in the relationships that the sufferer had with their parents. In the
case of paranoid personality disorder, parents may have been demanding, distant, overrigid, and
rejecting (Manschreck, 1996), and the lack of love provided by parents makes the individual suspicious
and lacking in trust of others (Cameron, 1974). In contrast, parents of individuals with schizoid
personality disorder may have rejected or even abused their children, resulting in the child being unable
to give or receive love (Carstairs, 1992). As we shall see later, there is certainly some evidence that
individuals with personality disorders may have suffered childhood abuse and neglect (Johnson et al.,
1999; Waxman, Fenton, Skodol, Grant, & Hasin, 2014), so there is some supportive evidence for this
view.

The schizophrenia spectrum disorder

There are three lines of evidence suggesting that Cluster A‐type personality disorders are closely related
to schizophrenia and make up a schizophrenia spectrum disorder. First, there is considerable evidence
suggesting a genetic link between Cluster A disorders and schizophrenia. Studies have indicated that risk
for all three types of Cluster A disorder is increased in relatives of individuals diagnosed with
schizophrenia (Bernstein, Useda, & Siever, 1993; Battaglia et al., 1995; Nigg & Goldsmith, 1994). Even
in adopted children whose biological mothers have been diagnosed with schizophrenia, there is a
significantly higher risk of developing schizotypal personality disorder than if the biological mother was
not diagnosed with schizophrenia (Tienari et al., 2003). All of these studies suggest a genetic link
between Cluster A personality disorders and schizophrenia, and longitudinal studies indicate that
positive schizoptypal symptoms predict future psychotic‐like symptoms (Racioppi et al., 2018). Second,
individuals with Cluster A disorders have been shown to possess brain abnormalities that closely
resemble those found in schizophrenia (Fervaha & Remington, 2013). For example, individuals with
schizotypal personality disorder show abnormalities in frontal lobe and temporal lobe activation that are
very similar to those found in individuals with a diagnosis of schizophrenia (Siever & Davis, 2004). In
addition, they also exhibit the enlarged ventricles frequently found in the brains of schizophrenia
sufferers (Buchsbaum et al., 1997), suggesting similarities in abnormal brain development across
schizophrenia and schizotypal personality disorder. Third, individuals with Cluster A disorders
(particularly schizotypal personality disorder) also exhibit some of the physiological abnormalities
possessed by individuals with schizophrenia, and these include impairment of smooth pursuit eye
movements (see Chapter 8) and inability to inhibit the startle response to weak stimuli (Siever et al.,
1982; Cadenhead et al., 2000). Fourthly, individuals with Cluster A disorders also show many of the
deficits in cognitive and executive functioning exhibited by individuals with schizophrenia, and these
include impaired working memory, episodic memory, spatial attention, and reduced verbal intelligence
quotient (IQ) (Dickey et al., 2005; Mitropoulou et al., 2005). Taking all of these factors into account,
there is strong evidence linking schizotypal personality disorder to the aetiological factors implicated in
schizophrenia generally, and schizotypical personality disorder has been explicitly included in the DSM‐
5 chapter on schizophrenia spectrum disorders.
12.4.2 Dramatic/Emotional Personality Disorders (Cluster B)
Some of the Cluster B disorders share a number of characteristics in common, such as impulsivity
(antisocial and borderline disorders), lack of empathy (antisocial and narcissistic disorders), emotional
outbursts and aggressiveness (histrionic and borderline disorders). This suggests that there may be some
common elements in the aetiology of these disorders, and, indeed, some theorists argue that some of
the different Cluster B disorders may be different manifestations of a single underlying psychopathology
with a common aetiology. For example, some researchers consider that APD and BPD are the same
underlying disorder that manifests in men as APD and women as BPD (Widiger & Corbitt, 1997), and
narcissistic personality disorder shares antisocial behaviour, deceitfulness and lack of empathy and
remorse with APD. However, as we shall see, most of the research on the aetiology of Cluster B
disorders has been directed at attempting to explain the development of the behaviour patterns in
individual disorders (Focus Point 12.1).

Antisocial personality disorder

The main behavioural characteristics of APD are impulsivity, aggressiveness, deceitfulness, lying,
irritability, repeated irresponsibility and lack of remorse, and a history of criminal activity and
childhood conduct disorder. As with all personality disorders, the theoretical challenge with APD is to
explain why certain individuals develop these behavioural styles and why they can be so enduring and
often resistant to change. Because APD is closely associated with criminal and antisocial behaviour,
considerable effort has been invested in attempting (a) to identify childhood and adolescent behaviours
that may help to predict later adolescent and adult APD (e.g., patterns of childhood antisocial behaviour
or childhood abuse), (b), to identify the developmental factors that may give rise to APD (e.g., factors
associated with family and early environment), (c) to ascertain whether there is an inherited or genetic
component to APD, and (d) to identify any biological or psychological processes that may be involved in
APD (e.g., brain abnormalities or dysfunctional cognitive processes such as faulty beliefs). We will look
separately at these approaches to understanding APD. One caution we must post at this stage is that
much of the research on APD has been conducted using a variety of different methods of defining
APD, some studies have used DSM diagnostic criteria, while others have used earlier definitions of
antisocial behaviour such as the concept of psychopathy (Checkley, 1976), and only 20% of people with
a DSM diagnosis of APD will score high on measures of psychopathy (Rutherford, Cacciola, &
Alterman, 1999).

FOCUS POINT 12.1 IMPULSE‐CONTROL DISORDERS

Many of the personality disorders—especially Cluster B disorders—are characterised by
impulsivity, including unpredictability in behaviour and aggressive outbursts. However, DSM‐5
classifies a number of impulse‐based problems separately. These are known as disruptive,
impulse‐control, and conduct disorders, and are characterised by the failure to resist an
impulse, drive, or temptation to perform an act that is harmful to the person or to others.
Examples of impulse‐control disorders are:
Intermittent explosive disorder: Discrete episodes of failure to resist aggressive
impulses that frequently result in criminal assaults or destruction of property.
Kleptomania: Recurrent failure to resist impulses to steal objects that either have little or
no monetary or personal value (e.g., impulsive shoplifting).
Pyromania: Recurrent patterns of fire setting for pleasure, gratification, or relief of
tension.
In most of these disorders, the individual feels an increasing sense of tension or arousal before
committing the impulsive act and then experiences pleasure, gratification, or relief when the act
is committed. Following the act, the individual will often suffer regret or guilt, suggesting that
the sufferer is aware that their behaviour is wrong but are unable to control it (known as ego
dystonia).
Many of the impulse‐control disorders are frequently comorbid with personality disorders. For
example, in one study 42% of those diagnosed with kleptomania also met the criteria for a
personality disorder (the most common were paranoid, schizoid, and borderline) (Grant, 2004).
However, impulse disorders are classified separately from personality disorders because they are
also highly comorbid with a number of other disorders. For instance, kleptomania frequently
cooccurs with substance abuse disorders, and sufferers often have first‐degree relatives who are
themselves suffering from a substance abuse disorder (Grant, 2006; Dannon, Lowengrub, Aizer,
& Kotler, 2006). High rates of manic and depressive disorders have also been recorded amongst
those with impulse‐control disorders (Kim, Grant, Eckert, Faris, & Hartman, 2006), but it is not
clear whether these mood problems are causes or effects of the impulsive behaviour. For
example, pathological gamblers often begin to feel depressed as their financial losses mount and
 their personal relationships are disrupted. Alternatively, some individuals who are initialled
depressed may find compulsive gambling gives them an exhilarating ‘buzz’ that distracts briefly
from the pain of depression.
Those diagnosed with kleptomania steal regularly and impulsively and will usually steal items
that have no financial or personal worth. Sufferers experience an often intense period of tension
building up before the theft, but then experience relief and gratification afterwards. Thefts are
usually undertaken alone, are not preplanned and stolen goods may often be returned after the
event. Individuals with kleptomania are usually aware that the act of stealing is wrong and
senseless, and feel guilty and depressed about their actions. Opportunistic shoplifting is one
common form of kleptomania, but studies suggest that only around 5% of those convicted of
shoplifting meet DSM criteria for kleptomania (DSM‐IV‐TR, p. 668). Kleptomaniacs have
been shown to rate their feelings of inner tension before stealing as significantly higher than
undiagnosed shoplifters, and they also exhibit significantly greater feelings of relief after the
crime (Sarasalo, Bergman, & Toth, 1997).
A large‐scale survey in the US estimated that the lifetime prevalence rate for impulse‐control
disorders was 24.8%, with a median age of onset as early as 11 years of age (Kessler, Berglund,
Demier, Jin, & Walters, 2005).

Childhood and adolescent behavioural precursors of APD

Because APD is closely associated with criminal behaviour, and on many occasions with violent or
homicidal criminal behaviour, there has been a keen interest in attempting to identify risk factors for
APD. Identifying potential risk factors might allow clinicians to predict the development of APD from
childhood behaviour patterns or childhood experiences and might identify individuals who may respond
to early clinical interventions.
One of the best predictors of APD in adulthood is a diagnosis of conduct disorder (CD) during
childhood in which the child exhibits a range of behavioural problems that include fighting, lying,
running away from home, vandalism, and truancy (Farrington, Loeber, & Van Kammen, 1990; see
Chapter 16). This, however, begs the question of how such antisocial behaviours had developed in
childhood, and we may have to refer back to ineffective parenting practices, discordant and unstable
family life, poor peer relationships, and educational failure to trace the origins of these behaviours (Hill,
2003). Persistent and aggressive behaviour before the age of 11‐years is also a good predictor of APD in
adulthood (Robins, 1966), as is early fighting and hyperactivity (Loeber, Green, Lahey, & Kalb, 2000),
and low IQ and low self‐esteem (Fergusson, Lynskey, & Horwood, 1996). In particular, Loeber et al.
(1993) have argued that there are three pathways that predict APD in adulthood. These are (a) an ‘overt’
aggressive pathway that progresses from bullying to fighting to serious violence, (b) a ‘covert’ aggressive
pathway that progresses from lying and stealing to more serious damage to property, and (c) an
‘authority conflict’ pathway that progresses through various degrees of oppositional and defiant
behaviour. Behaviours in the early stages of each of these pathways predict more serious specific
antisocial behaviours later in life.

conduct disorder (CD) A pattern of behaviour during childhood in which the child exhibits
a range of behavioural problems, including fighting, lying, running away from home, vandalism
and truancy.

Many studies have emphasised that adolescent problem behaviours are strong predictors of adult APD.
McGue & Iacono (2005) found that adolescent smoking, alcohol use, illicit drug use, police trouble, and
sexual intercourse (all before 15 years of age) each significantly predicted APD symptoms in later life. In
fact, for those who exhibited four or more of these problem behaviours prior to age 15, there was a 90%
likelihood of subsequent APD diagnosis in males and a 35% probability in females. A possible link
between childhood attention‐deficit/hyperactivity disorder (ADHD) and APD is discussed in Focus
Point 12.2. Furthermore, harsh parental discipline and poverty strongly predict adult APD (Jaffee,
Strait, & Odgers, 2012), so there may be some form of vicious cycle occurring where the antisocial
behaviour of a child can provoke harsh discipline from parents which exacerbates antisocial behaviours.
Perhaps disappointingly, most of these studies merely indicate that adult antisocial behaviour defined by
APD is predicted by adolescent and childhood antisocial behaviour. However, such studies do
demonstrate that the behaviour patterns are often enduring and that these behaviours during childhood
and early adolescence should be taken as indicators of the possible need for intervention. For factors
involved in causing APD we need to explore developmental, psychological and biological factors (Focus
Point 12.3).

Developmental factors
There are a range of views about how familial factors might influence the development of APD, and
because APD is an antisocial disorder, there has been much speculation about how maladaptive
socialisation might have contributed to this pattern of behaviour. One important fact is that there is a
high incidence of APD in the parents of individuals with APD (Paris, 2001), suggesting that one
important developmental factor may be the learning of antisocial behaviours through modelling and
imitation (although this may also indicate a genetic or inherited component—see below). For example,
the children of parents with APD may often see aggressive and deceitful behaviour rewarded—
especially if a parent has had a relatively successful criminal career. Alternatively, parents may have
patterns of parenting which inadvertently reward their children for aggression, impulsivity, and
deceitfulness (Capaldi & Patterson, 1994). For instance, parents may try to calm down an aggressive or
impulsive child by giving him/her toys or sweets—a reaction which is likely to increase the frequency of
such behaviours rather than suppress them.
Parents may play a more discrete role in developing APD tendencies through the emotional relationship
they have with their children. Psychodynamic explanations of APD argue that a lack of parental love
and affection during childhood is likely to lead to the child failing to learn trust (Gabbard, 1990). This
lack of love and affection can take a number of forms, and there is evidence that individuals with APD
come from backgrounds of family violence, poverty, and conflict—including separation and divorce
(Farrington, 1991; Paris, 2001). In such circumstances, the child is likely to have had little experience of
positive emotional relationships and is more likely to have experienced conflict and aggression as a
normal way of life. Finally, some studies have identified both inconsistent parenting and harsh parenting
(e.g., corporal punishment, hitting, kicking, slapping, and emotional coercion, such as insulting,
threatening, or belittling) as being important in developing antisocial behaviours (Burnette, Oshri,
Richards, & Ragbeer, 2012), and parents of individuals with APD frequently fail to be consistent in
disciplining their children and also fail to teach them empathy and responsibility (Marshall & Cooke,
1999). At least one reason for this lack of consistency in parenting is that many of the fathers of
individuals with APD also exhibit the disorder.

FOCUS POINT 12.2 IS ATTENTION‐DEFICIT/HYPERACTIVITY

DISORDER (ADHD) A RISK FACTOR FOR ANTISOCIAL
PERSONALITY DISORDER?

Some researchers have suggested that conduct disorder (CD) in childhood is not the only
psychological diagnosis that predicts APD in later life. Lynam (1998) has argued that children
with hyperactivity/attention deficits (such as ADHD) are ‘fledgling psychopaths’ who because
of their impulsivity and attentional problems are likely to develop into long‐term psychopaths—
not least because their underlying problems are of a neuropsychological nature which are likely
to be resistant to behavioural treatments. However, more recent studies that have been based on
structured diagnostic interviews do not necessarily support this view. Lahey, Loeber, Burke, &
Applegate (2005) investigated whether a diagnosis of CD or ADHD in males between 7 and 12
years of age predicted a diagnosis of APD at 18–19 years. While CD predicted subsequent
APD in around 50% of the participants, ADHD predicted APD at rates no better than if the
child had neither ADHD or CD at ages 7–12 years (see figure), suggesting that ADHD during
childhood is not a significant differential predictor of APD in later life. More recent analyses
suggest only a weak link between ADHD and APD in prospective studies (Klein et al., 2012), or
that if youths with comorbid conduct disorder and ADHD do develop APD it is due to the
levels of conduct disorder, not the influence of ADHD (Smith & Hung, 2012).

Lahey et al. (2005) investigated whether a childhood diagnosis of CD or ADHD predicted a diagnosis of APD
at 18–19 years of age. The results show that while around 50% of those diagnosed with either CD or CD and
ADHD went on to develop APD, ADHD did not predict subsequent APD any better than if a child had neither
disorder.
 FOCUS POINT 12.3 PREDICTORS OF ANTISOCIAL
BEHAVIOUR AND VIOLENT CRIME

APD is closely associated with criminal and antisocial behaviour, and so some efforts have been
focussed on attempting to identify childhood predictors of these behaviours. The hope here is
that being able to identify such individuals at an early stage may prevent crime and enable
either treatment or reeducation programmes to be directed at individuals at risk of developing
APD.
Some childhood and early adolescent predictors of APD that have been identified include:
A diagnosis of CD in childhood
Persistent and aggressive behaviour before age 11 years
Fighting and hyperactivity
Low IQ and low self‐esteem
Persistent lying
Running away from home
Vandalism
Truancy
Discordant and unstable family life
Educational failure
Adolescent smoking, alcohol use, illicit drug use, police trouble, and sexual intercourse all
before age 15 years.
Having at least one parent diagnosed with APD
Coming from a background of family violence, poverty, and conflict

However, we must be cautious about how we interpret these developmental factors. They may not
represent causal factors in the development of APD but merely represent failures and inconsistencies in
parenting that are a consequence of having a child with severely disruptive and impulsive behaviour. We
must also remember that because an individual with APD may have a parent with the disorder does not
mean that they have learnt such behaviours from the parent—the disorder may involve psychological
and biological dysfunctions that may be inherited rather than learnt (such as maladaptive physiological
reactions that give rise to impulsivity and risk seeking, see below).

Genetic factors
There is clear evidence that APD appears to run in families and apart from the developmental factors
that may contribute to this effect, there is also the real possibility that there is a genetic or inherited
component to APD. Twin studies have demonstrated significantly higher concordance rates for APD in
monozygotic (MZ) twins than in dizygotic (DZ) twins (Lyons et al., 1995), and adoption studies have also
shown that incidence of APD in the adopted child is better predicted by APD in the biological than in
the adopted mother (Ge et al., 1996). Heritability of APD and antisocial psychopathy traits appear to be
relatively high, with recent estimates of heritability between 51% and 81% (Rosenstrom et al., 2017;
Tuvblad, Bezdjian, Raine, & Baker, 2014; Torgersen et al., 2012), with the highest estimates being
related to aggressive aspects of APD (Burt & Donnellan, 2009). In addition, studies suggest that the
heritability of APD and substance use disorder may be related, and this may account in part for the
high comorbidity between these two disorders (Kendler et al., 2003; Gizer et al., 2012).
Molecular genetic studies are beginning to identify the specific gene locations of some APD
characteristics, with the long allele of the serotonin transporter gene 5‐HTTLPR linked specifically with
the emotional deficits found in APD (Sadeh, Javdani, & Verona, 2013). Possession of a genotype
conferring low levels of monoamine oxidase A (MAO‐A) together with the experience of childhood
abuse does appear to predict adult antisocial behaviour (Caspi & Moffitt, 2006), and this genotype is
associated with volume reductions in the amygdala, anterior cingulate, and orbitofrontal cortex (Meyer‐
Lindenburg et al., 2006) and provides a potential pathway from genes, to brain, to antisocial behaviour
that implicates prefrontal and amygdala regions in antisocial behaviour (Raine, 2018, see subsequent
sections).
Finally, epigenetics is the process by which early experiences may affect the expression of certain genes,
and one process that can prevent the expression of a gene is DNA methylation (a process by which
methyl groups are added to the DNA molecule and typically act to repress gene transcription). Greater
methylation of the OXTR gene in children with CD has been associated with callous, unemotional
traits and lower circulating oxytocin—a hormone involved in empathy and amygdala functioning
(Dadds et al., 2014). Similarly, aggressive males have been found to have greater methylation of the
SLC6A4 serotonin transporter gene, as have women with a diagnosis of APD (Wang et al., 2012; Beach,
Brody, Todorov, Gunter, & Philibert, 2011), indicating that antisocial personality may be associated with
abnormalities in the serotonin system. If DNA methylation occurs as a result of particular types of early
experiences (e.g., childhood stress and abuse), then research may be able to identify how certain adverse
early experiences affect DNA expressions that have neurodevelopmental consequences which in turn
facilitate the development of antisocial traits.

Physiological and neurological factors

Individuals with APD show some interesting physiological characteristics which may help to explain
aspects of their behaviour such as their failure to learn from experience and their inability to empathise
with the feelings of others. First, they exhibit significantly lower levels of anxiety than normal control
participants. This is exhibited as a relative inability to learn to avoid physically aversive stimuli such as
electric shock (Lykken, 1957; Koenig & Gao, 2019), lower reactivity and baseline levels of physiological
indicators of anxiety such as skin conductance (Herperts et al., 2001; Hare, 1978), and a failure to
exhibit increased startle reactions when being shown stimuli designed to elicit negative emotions
(Levenston, Patrick, Bradley, & Lang, 2000). Indeed, low skin conductance responses to loud noises at
age 3 years have been found to predict psychopathology scores at age 28 years, suggesting it is a
potential risk factor for the development of APD (Glenn et al., 2007).
Second, individuals with APD regularly respond to emotional or distressing stimuli with slow autonomic
arousal and appear to possess low levels of electroencephalographic (EEG) activity (Dinn & Harris,
2000; Lindberg et al., 2005). This suggests that they may have difficulty maintaining normal daytime
arousal and may also be able to ignore threatening or distressing stimuli more easily than most people
(e.g., Smith & Lillenfeld, 2015), and brain imaging studies have indicated that individuals with a
diagnosis of APD show deficits in areas of the prefrontal cortex that are involved in attention to
negative and threatening information (Ermer, Cope, Nyalakanti, Calhoun, & Kiehl, 2012). This in turn
may explain why individuals with APD are unable to identify with the distress of others and are very
poor at recognising the fear and pain of other people (Brook & Kosson, 2013). They may also be more
risk seeking than normal because of the need to experience higher levels of stimulation before they feel
aroused (Hasselbrock & Hasselbrock, 1992).
Third, individuals with APD frequently fail to show any signs of fear learning in aversive conditioning
procedures (where, for example, a conditioned stimulus predicts the presentation of an aversive
unconditioned stimulus such as an electric shock) (Lykken, 1995), and functional brain imaging studies
have shown that this failure to learn is accompanied by inactivity in the brain circuits believed to
mediate fear learning (e.g., the amygdala) (Birbaumer et al., 2005) (Research Methods in Clinical
Psychology 12.1). These findings are consistent with the fact that individuals with APD will usually fail
to learn from experience about events that have negative outcomes, and they will continue to persevere
with their ingrained set of responses in such circumstances.
A number of studies have also indicated that individuals with APD have impaired performance on
neuropsychological tests of prefrontal cortex functioning (Dinn & Harris, 2000; Raine & Yang, 2007),
and these areas of the brain play an important role in inhibiting impulsivity. This may represent a brain
abnormality that contributes to the impulsive behaviour exhibited by such individuals, and may help to
explain some aspects of their antisocial behaviour by their apparent inability to inhibit inappropriate
behaviours in social contexts.

Cognitive models
Some recent models have argued that individuals with APD have developed dysfunctional cognitive
schemas that cause their responses to various situations to be extreme, impulsive, and changeable. For
example, Young, Klosko, and Weishaar (2003) have suggested that individuals with APD possess five
important and relatively independent dysfunctional schemas, and—when responding to important
events—they are assumed to switch quickly and unpredictably between schemas in a way that makes
their behavior appear impulsive and unpredictable. Young et al. proposed five important schema
modes that determine the responses and reactions of individuals with APD. As we will see from the
nature of these schema modes, it is claimed that they are developed as a result of abuse and neglect
experienced during childhood (Horowitz, Widom, McLaughlin, & White, 2001; Marshall & Cooke,
1999). The five dysfunctional schemas are (a) the Abandoned and Abused Child mode (generating
feelings of pain, fear of abandonment, and inferiority), (b) the Angry and Impulsive Child mode (where
bottled up aggression is discharged as anger), (c) the Punitive Parent mode (where the individual views
themselves as having done something wrong, evil, and worthless), (d) the Detached Protector mode (a
state where the individual endeavors not to feel the pain and emotion caused by the first three modes),
and (e) the Bully and Attack mode (where the individual hurts other people to overcompensate for, or to
cope with, mistrust, abuse, deprivation, and defectiveness) (Lobbestael, Arntz, & Sieswerda, 2005). The
development of instruments to measure these various schema modes has shown that individuals
diagnosed with APD do indeed score higher on measures of these five dysfunctional modes than
nonclinical participants (Lobbestael, Arntz, & Sieswerda, 2005). Individuals with APD are assumed to
switch rapidly and unpredictably from a ‘Healthy Adult’ mode—where their behaviour appears normal
—to pathological modes, and this can occur rapidly when the individual experiences negative emotions
such as anger (Lobbestael & Arntz, 2012). Because schemas such as these form part of the individual's
normal way of thinking, the person with APD does not recognise them as faulty. If such dysfunctional
schemas do represent important causal factors in the antisocial behaviour exhibited by individuals with
APD, then challenging and replacing these dysfunctional schemas may represent a useful starting point
for treating the disorder (Beck & Freeman, 1990).

dysfunctional schemas In personality disorders, a set of dysfunctional beliefs that are

hypothesised to maintain problematic behaviour characteristic of a number of personality
disorders (e.g. antisocial personality disorder and borderline personality disorder).
 RESEARCH METHODS IN CLINICAL PSYCHOLOGY 12.1
DEFICITS IN FEAR CONDITIONING IN ANTISOCIAL
PERSONALITY DISORDER (APD)

A seminal study by Lykken (1957) suggested that individuals with what was then labelled as a
sociopathic personality were unable to learn to avoid psychically aversive stimuli, and this
learning deficit may explain why individuals with APD are able to ignore threatening signals
and also appear to lack the ability to learn from experience about events that have negative
outcomes.
This learning deficit can be demonstrated in a simple laboratory‐based conditioning
experiment, and laboratory studies such as this often serve as good analogues of real‐life
learning situations.
A study by Birbaumer et al. (2005) replicated Lykken's original study. They used a differential
aversive conditioning procedure in which male faces acted as the conditioned stimuli (CSs). For
some participants, faces with a moustache were followed by an aversive unconditioned stimulus
(US) (in this case a painful pressure applied to the hand or arm) (CS+), while faces without a
moustache were followed by nothing (CS‐). For other participants the painful US followed the
faces without moustaches, and the moustached faces were followed by nothing (a
counterbalanced procedure so that conditioning could not be affected by the specific features of
the CS).
Normally, participants would show signs of anxiety during the CS+ (as recorded by
physiological measures such as skin conductance levels), and would also rate the CS+ face as
less pleasant than the CS‐ face. Birbaumer et al. compared the performance of 10 psychopaths
(six of whom met DSM‐IV criteria for APD) with 10 healthy control participants. While the
normal, healthy participants rated the CS+ as significantly less pleasant than the CS‐, the
psychopaths showed no difference in pleasantness ratings even after 16 pairings of CS+ with
the US, suggesting that they had failed to learn the significance of the aversive‐signalling CS+.

Summary of theories of antisocial personality disorder

Predictive theories of the aetiology of APD are still relatively underdeveloped, but we have already
learned some interesting facts about the kinds of factors that put an individual at risk for developing
APD. APD appears to run in families, with a genetic element being involved and the family
environment also playing a significant role. Children raised in families low on parental love, with
inconsistent or harsh parenting, or with parental conflict are more likely to develop APD, as are
individuals who have suffered childhood abuse or neglect. Individuals with APD also appear to have
dysfunctional cognitive schemas that lead them to behave either aggressively or impulsively, and we still
need to discover whether there is a link between the development of these dysfunctional schemas and
their early experiences. Finally, individuals with APD show a number of physiological and neurological
characteristics, such as physiological indicators of low anxiety, low levels of baseline arousal and
reactivity, lack of learning in simple aversive conditioning procedures, and neurological impairments
indicative of impulsivity, and these characteristics all appear to be consistent with the behavioural
characteristics of APD (such as aggressive and impulsive behaviour, lack of empathy, and failure to
learn acceptable adaptive responses).
One way of combining and conceptualising these different levels of explanation is as a form of neural
maldevelopment influenced by early experiences (Raine, 2018). For example, the high heritability
estimates for APD suggest that a vulnerability for the disorder is likely to be genetically transmitted, and
early forms of childhood experience, particularly the stress and social adversity imposed by harsh
parenting and poverty, may in turn—through the process of epigenetics—influence the expression of
various relevant genes. These epigenetic factors may lead to volume reductions in brain structures such
as the amygdala (Hanson et al., 2015), and result in poor connectivity between the amygdala and
prefrontal cortex (Tottenham & Galvan, 2016). These neurodevelopmental abnormalities then
contribute to emotional dysregulation, lack of empathy, failure to learn in aversive conditioning
procedures, and promote aggressive behaviour characteristic of APD.

Borderline personality disorder

Individuals with BPD exhibit a wide range of behavioural and psychological problems including fear of
abandonment and rejection, unpredictable mood swings, impulsivity, frequent and prolonged bouts of
depression often associated with suicidal ideation, self‐harm, and suicide attempts. This is a diverse
range of characteristics for a single theory to encompass, and this is without considering the fact that
BPD is commonly comorbid with at least one other psychological disorder. As we shall see, theories
developed to try to address the aetiology of BDP often try to explain the development of one aspect of
the disorder (such as fear of abandonment, mood lability or impulsivity), but it is worth starting this
section by giving ourselves an overview by reviewing some of the risk factors that predict the
development of BPD and then moving on to more specific biological and psychological theories.

Risk factors for borderline personality disorder

Many studies have reported that individuals with BDP report a history of difficulties in childhood—
many associated with problematic parenting. These include childhood physical, verbal, and sexual abuse
(Herman, Perry, & van der Kolk, 1989; Zanarini et al., 1997), childhood neglect or rejection (Zanarini
et al., 2000; Guttman, 2002), inconsistent or loveless parenting (Kernberg, 1985), inadequate parent–
child boundaries (Vanwoerden, Kalpakci, & Sharp, 2017), and inappropriate parental behaviour such as
persistent substance and alcohol abuse or promiscuity (Graybar & Boutilier, 2002). Individuals with
BDP report rates of childhood physical, sexual, verbal abuse, and neglect ranging from 60% to 90%
(Gabbard, 1990), including 67–87% for sexual abuse (Bryer, Nelson, Miller, & Krol, 1987). Herman,
Perry, & van der Kolk (1989) found rates of 71% for physical abuse amongst people diagnosed with
BPD compared to only 38% amongst psychiatric patients who had not been diagnosed with BPD.
Other studies have identified a number of developmental antecedents of BPD, including abuse, neglect,
environmental instability, paternal psychopathology, academic underachievement, low intelligence, and
artistic skills (Helgeland & Torgersen, 2004). Prenatal adversity in the form of prenatal maternal
distress, drug taking, tobacco smoking, or medical complications has also been shown to be a risk factor
for the subsequent development of BPD (Schwarze et al., 2013).
However, despite these developmental risk factors being significant predictors of BPD, we must
remember that around 20% of individuals who develop BPD have never reported experiencing
childhood abuse or neglect (Gabbard, 1990; Graybar & Boutilier, 2002), so such experiences are not a
necessary condition for developing BPD (Zanarini & Wedig, 2014).

Biological theories of BPD

Biological theories cover genetic factors, brain and neurological abnormalities, and biological
contributions to impulsivity.
First, there is evidence for a genetic component to BPD. The disorder does appear to run in families
(Baron, Risch, Levitt, & Gruen, 1985), and twin studies have indicated concordance rates of 35% and
7% for MZ and DZ twins respectively (Torgersen et al., 2000). In a recent total‐population Swedish
study a strong familial association was found, with BPD diagnosis covarying directly with the relatedness
between individuals, and heritability was estimated at a significant 46% (Skogland et al., 2019). Genetic
analyses have also indicated that traits common in BPD, such as neuroticism and emotional
dysregulation (labile moods and unpredictable rapid mood changes) have a strong inherited component
(Nigg & Goldsmith, 1994; Livesley, Jang, & Vernon, 1998). Studies have also attempted to disentangle
the effects of genetics and childhood abuse as contributors to BPD. In a study of identical twins of
whom only one of the pair had suffered childhood abuse, researchers found that the twin pairs had very
similar levels of BPD—that is, childhood abuse did not appear to contribute any more than 1% of the
variance in BPD measures, and the levels of BPD were almost entirely accounted for by genetic factors
(Berenz et al., 2013; Bornovalova et al., 2013). These findings suggest that childhood abuse and neglect
may not be a direct risk factor for BPD (we have already noted that not all individuals who develop BPD
have a history of childhood abuse and neglect). Instead, childhood abuse and neglect may be a
consequence of genetically inherited characteristics such as impulsivity and poor emotion regulation.
Inherited characteristics of impulsivity and emotionality in the parents of offspring who develop BPD
may make their parenting inconsistent and even neglectful, and these same inherited characteristics in
the children may generate impulsive and emotional behaviour that their parents may attempt to
manage in either harsh or neglectful ways.
More recent research has linked BPD with bipolar disorder, and the two are often comorbid (Smith,
Muir, & Blackwood, 2004). Deltito et al. (2001) have estimated that around 44% of individuals with
BPD belong to a broader bipolar disorder spectrum, which may help to account for their regular
and unpredictable mood changes. Because we already know that there is a significant genetic
component to bipolar disorder (see Section 7.2), this provides circumstantial evidence for a genetic
component to at least some of the symptoms characteristic of BPD.

bipolar disorder spectrum A proposed spectrum of disorder encompassing both bipolar

disorder and borderline personality disorder.

Evidence suggests that individuals with BPD have a number of brain abnormalities that may give rise to
impulsive behaviour. They tend to possess relatively low levels of the brain neurotransmitter serotonin,
and this is associated with impulsivity (Norra et al., 2003) and may account for their regular bouts of
depression (see Chapter 7). There is also some evidence for dysfunction in brain dopamine activity in
BPD, and such dopamine activity is known to play an important role in emotion information processing,
impulse control, and cognition (Friedel, 2004). However, much of this evidence is currently
circumstantial and derives mainly from the fact that administration of drugs that influence serotonin
and dopamine activity also appear to influence BPD symptoms.
Neuroimaging studies of individuals with BPD have revealed abnormalities in a number of brain areas,
primarily in frontal lobe functioning and in the limbic system, including the hippocampus and amygdala
(Juengling et al., 2003; Soloff et al., 2003). The frontal lobes play an important part in decision‐making,
and abnormalities in this area in individuals with a diagnosis of BPD could underlie their impulsivity,
and the amygdala is an important part of the brain system controlling and regulating emotion and these
abnormalities may contribute to some of the defining behavioural features of BPD and their emotional
regulation problems (Davies, Hayward, Evans, & Mason, 2020). In addition, activation of the limbic
areas and the amygdala is often excessive, which may be responsible for the extreme emotional reactions
often displayed by individuals with BPD (Lis, Greenfield, Henry, Guile, & Dougherty, 2007; Silbersweig
et al., 2007). Other studies have also identified abnormalities in the medial prefrontal cortex and
anterior cingulate areas, areas of the brain which are crucial for self‐referential processing, successful
social cognition, interpersonal transactions, and emotional regulation (Visintin et al., 2016).
Nevertheless, while these abnormalities are important correlates of BPD symptoms, it is still far from
clear whether these abnormalities represent a consequence of the disorder or a genetically or
developmentally determined cause of the disorder (Lieb et al., 2004).
Psychological theories of BPD
We have seen that a majority of individuals with BPD report experiencing relatively high levels of
childhood abuse and difficult or neglectful parenting, and a number of psychological theories of BPD
attempt to explain how these experiences might relate to the behavioural and emotional problems
characteristic of the disorder.
Some forms of psychodynamic theory, such as object‐relations theory, argue that people are
motivated to respond to the world through the perspectives they have learnt from important other
people in their developmental past. However, if these important others have offered only inadequate
support and love, or in fact been actively abusive, then this is likely to cause the child to develop an
insecure ego, which is likely to lead to lack of self‐esteem, increased dependence and a fear of
separation and rejection—all central features of BPD (Bartholomew, Kwong, & Hart, 2001: Kernberg,
1985). Object‐relations theory also argues that individuals with weak egos engage in a defence
mechanism called splitting, which means that they evaluate people, events or things in a completely
black or white way, often judging people as either good or bad with no shades of grey. This may give
rise to their difficulties with relationships, in which their all‐or‐none assessments mean that someone
they evaluate as ‘good’ can just as quickly become ‘bad’ on the basis of a single act or statement (e.g., if
a partner does not return from a work social event at exactly the time they said they would, the
individual with BDP is likely to respond with anger and threaten to withdraw from the relationship).
People with a diagnosis of BPD also have a tendency to perceive others as quarrelsome, which triggers
negative affect and leads to more quarrelsome behaviour during their interactions with others (Sadikaj,
Moskowitz, Russell, Zuroff, & Paris, 2013). Interestingly, Suvak et al. (2011) found that individuals with
a diagnosis of BPD judged their own emotions primarily on dimensions of valency, and hardly at all on
dimensions of arousal. This suggests that they are likely to judge their emotions in an ‘all or nothing’
way with relatively little intensity control, leading to extreme swings in emotions.

object‐relations theory Argues that individuals with borderline personality disorder (BPD)
have received inadequate support and love from important others (such as parents) and this
results in an insecure ego, which is likely to lead to lack of self‐esteem and fear of rejection.

splitting An element of object relations theory which argues that individuals with weak egos
engage in a defence mechanism by which they evaluate people, events or things in a completely
black or white way, often judging people as either good or bad with no shades of grey.

While object‐relations theory is consistent with the fact that a majority of individuals with BPD have
experienced childhood abuse, conflict and neglect, one problem is that such experiences are common
features of many of the personality disorders (including antisocial, paranoid, narcissistic, and OCPD)
(Klonsky, Oltmanns, Turkheimer, & Fiedler, 2000). This being the case, an account such as object‐
relations theory does not easily explain how such negative early experiences get translated into BPD
rather than these other disorders which also have such experiences as part of their history.
We have already noted the high levels of comorbidity between the different personality disorders
(Marinangeli et al., 2000), and, in particular, between 10% and 47% of individuals with BPD also
display antisocial behaviour and meet the diagnostic criteria for APD (Zanarini & Gunderson, 1997).
This suggests that there may be some commonality of aetiology between the two disorders, and we have
already noted that significant childhood abuse and neglect is apparent in both groups. This has led
Young, Klosko, and Weishaar (2003) to suggest that individuals with BPD may develop a similar set of
dysfunctional schema modes to those acquired by individuals with APD. We have already described
these dysfunctional schemas in relation to APD (Section 12.4.2), and Young et al. have argued that these
dysfunctional schema also determine reactions to events in individuals with BDP, such as dissociation
(Johnston et al., 2009). Subsequent studies have confirmed that individuals with APD and BPD do score
higher than control participants without a personality disorder diagnosis on measures of these
dysfunctional schemas, and also report levels of childhood abuse that were higher than controls
(Lobbestael, Arntz, & Siewerda, 2005). This suggests a significant amount of similarity in both the
developmental history of BPD and APD and in the dysfunctional cognitive schemas that characterise
these disorders. This has led some researchers to argue that APD and BPD may be different
manifestations of one single underlying disorder which may express itself as BPD in women and APD
in men (Paris, 1997; Widiger & Corbitt, 1997).

Diathesis–stress models of BPD

This section describing the aetiology of BPD has so far emphasised that genetics, brain abnormalities,
childhood abuse and neglect, and problematic parent–child relationships are all associated in some form
or another with BPD and its symptoms. These facts have given rise to diathesis–stress models of
BPD which argue that BPD develops as a result of genetic predispositions that give rise to behavioural
characteristics such as impulsivity and poor emotion regulation but that these inherited characteristics
are then amplified by parenting that is harsh, neglectful, or invalidating (where the child's feelings are
discounted, disrespected, or even punished) (Linehan, 1987; Crowell, Beauchaine, & Linehan, 2009).
Figure 12.2 provides a schematic representation of the processes involved in this diathesis–stress model.
The inherited factors (biological diathesis) will influence brain processes that result in emotional
dysregulation (e.g., impulsivity and poor emotional regulation), and the behavioural consequences of
this dysregulation impose significant demands on the family. Parents who are unable to cope with these
demands will ignore or punish the demands which in turn creates even stronger emotional outbursts by
the child, and a vicious cycle is created which simply reinforces the emotional outbursts of the child.
Thus, the model emphasises a biological predisposition to emotional dysregulation that is facilitated by a
parenting style that reinforces this dysregulation. There is some empirical evidence for the existence of
these interacting factors in the families of individuals who develop BPD. A prospective study of girls and
their mothers found that poor self‐control in the child predicted increases in harsh parenting by the
mother, and in turn, harsh parenting by the mother predicted poorer self‐control in the child (Hallquist,
Hipwell, & Stepp, 2015). As encouraging as this model is in incorporating the existing evidence across
biological, developmental and psychological research into BPD, there is still much that needs to be
verified. For example, research on the diathesis part of the model is still in its infancy, and clear causal
links need to be identified between genetic factors, dysregulation of brain areas dealing with impulsivity
and emotion regulation, and the effects this has on parenting styles.
FIGURE 12.2 Linehan's Diathesis–Stress Model of Borderline Personality Disorder.

Narcissistic personality disorder

As we described earlier, the individual suffering narcissistic personality disorder is someone who
overestimates their abilities and inflates their accomplishments, but has a complete lack of empathy with
the desires and feelings of others. However, underneath this grandiose exterior is a very frail self‐esteem
which means they constantly need to check for reassurance.
Psychodynamic theories of narcissistic personality disorder have argued that the traits associated with
this disorder result from childhood experiences with cold, rejecting parents who rarely respond with
praise at their children's achievements or displays of competence (Kohut & Wolf, 1978). Indeed, such
parents may often dismiss their children's successes in order to talk about their own achievements.
Because of these experiences, such children then try to find ways of defending against feelings of
worthlessness, dissatisfaction, and rejection by convincing themselves that they are worthy and talented
(Wink, 1996; Kernberg, 1985). The end product is someone with a vulnerable self‐esteem who seeks
reassurance about their talents and achievements from themselves and others and who has developed a
lack of empathy with others because of the cold and uncaring parenting they have experienced. In
support of this view, there is some evidence that individuals with narcissistic PD are more likely to come
from backgrounds involving child abuse, conflict, and neglect (Kernberg, 1989). However, evidence of
childhood abuse and neglect is not a sufficient condition for a child to develop narcissistic PD, and some
other theorists have argued that the disorder results from ‘doting’ parents who treat their children too
positively in a way that fosters unrealistic grandiose self‐perceptions (Millon, 1996). Interestingly, there is
some circumstantial evidence to support this view, in that measures of narcissism often show that scores
are often higher in firstborns or only children, where parents may have been able to devote more time
and attention to their children (Curtis & Cowell, 1993).
Narcissistic personality disorder is also closely associated with APD, and narcissistic individuals will
regularly act in self‐motivated, deceitful and aggressive ways very reminiscent of APD, and also exhibit
lack of empathy (Ritter et al., 2011). However, individuals with narcissistic PD can be reliably
differentiated from individuals with APD by their sense of grandiosity and self‐importance (Gunderson
& Ronningstam, 2001), so we need to look closely at factors that determine these characteristics
(Thomaes, Bushman, de Castro, & Stegge, 2009). Narcissists appear to hold grandiose, but
simultaneously tentative, unstable self‐views that require them to seek continuous self‐validation and
dominance over others. As such they may be addicted to self‐esteem and continually create social
situations in which they hope they can receive boosts to their self‐esteem (Baumeister & Vohs, 2001). But
how does this tendency develop? Thomaes et al. (2009) argue that it develops out of an interaction
between an inherited sensitivity to positive or desirable stimuli and an aversiveness to negative or
undesirable stimuli combined with extreme forms of parenting, such as parental overvaluation and
overindulgence (Twenge, 2006) or parental coldness, extremely high expectations, or lack of support
(Kernberg, 1985). This diathesis–stress model is consistent with the fact that narcissistic traits begin to
develop at age 8 years of age—at just the time that children are beginning to form a conscious, global
evaluation of themselves (Thomaes et al., 2008) (Case History 12.3).

CASE HISTORY 12.3 NARCISSISTIC PERSONALITY

DISORDER

In July 2005, Brian Blackwell—a 19‐year‐old public schoolboy from Liverpool—killed both his
parents and then used their credit cards to fund a £30,000 spending spree. After his arrest he
was subsequently diagnosed as suffering from narcissistic personality disorder and was reported
to have regularly fantasised about unlimited success, power, and brilliance. He had falsely
claimed to be a professional tennis player and applied for numerous credit cards to help fund
his fantasies. After the killings, Blackwell went on holiday to the US with his girlfriend, spending
huge sums of money while staying at expensive hotels in New York.
Clinical CommentaryMany researchers believe that narcissistic personality disorder is closely
associated with APD, and individuals with the disorder usually show clear signs of deceitfulness,
lying, lack of empathy with the feelings of others, acting impulsively and aggressively, showing
no remorse for acts of harm or violence, and going to any lengths to achieve their own personal
goals. Narcissistic personality disorder is differentiated from APD by the individuals’ grandiose
view of themselves and their need to brag about fantasised achievements. The parents of some
individuals with narcissistic personality disorder undoubtedly dote on them and may treat them
too positively in a way that fosters unrealistic grandiose self‐perceptions (Millon, 1996).

Histrionic personality disorder

There has been relatively little research into the aetiology of histrionic personality disorder, and its poor
construct validity suggests that it may well be excluded as a diagnostic category in future editions of the
DSM (Bakkevig & Karterud, 2010). Theories of histrionic personality disorder that are currently
available tend to have developed from psychodynamic accounts originally designed to understand
hysteria generally (Novais, Araújo, & Godinho, 2015). These types of accounts argue that the dramatic
displays of emotion and attention‐seeking behaviour characteristic of the person with histrionic PD are
manifestations of underlying conflict—especially conflicts related to acceptance by and relationships
with members of the opposite sex. Psychodynamic theories often differ as to the causes of the conflicts
that underlie attention seeking and dramatic behaviour. Some suggest that the disorder is fostered by
inconsistencies in parental attitudes towards sex, where parents convey the view that sex is both dirty
and exciting (Apt & Hurlburt, 1994). Others suggest that the disorder arises from a childhood
experience of parenting that is cold and controlling and leaves the child searching desperately for love
and assurance (Bender, Farber, & Geller, 2001). Finally, other psychodynamic views focus specifically on
the relationship between father and daughter. Because of a lack of maternal attention, some daughters
may actively seek the attention and approval of their fathers, and this leads to a flirtatious relationship
between father and daughter that the daughter carries on to other relationships later in her life (Phillips
& Gunderson, 1994). There is little objective evidence at present to differentiate between any of these
particular psychodynamic accounts, and they do appear to be focussed more on explaining the disorder
in females than in males. As such, they may all be relatively inadequate accounts of histrionic PD —
especially since more recent surveys have indicated that it is a disorder that is relatively equally
distributed across men and women (Mattia & Zimmerman, 2001).

12.4.3 Anxious/Fearful Personality Disorders (Cluster C)

Personality disorders in Cluster C exhibit mainly anxious and fearful symptoms, and are frequently
linked to comorbid anxiety disorders. Very little research has been carried out on the aetiology of
disorders in this cluster, although there have been attempts to view them as part of larger anxiety‐based
spectra of disorders (such as avoidant personality disorder within a social anxiety spectrum, and OCPD
within an obsessive‐compulsive spectrum) (e.g., Schneier, Blanco, Antia, & Liebowitz, 2002). As such, it
would be assumed that the personality disorders would then share some of the aetiological features of
their corresponding anxiety disorders—although this has yet to be confirmed empirically.

Avoidant personality disorder

Avoidant personality disorder is characterised by feelings of inadequacy, fear of criticism, disapproval
and rejection, and avoidance of most personal interactions with others. It is also associated with
avoidance behaviour generally and may be part of a broader social anxiety spectrum (Schneier,
Blanco, Antia, & Liebowitz, 2002). Like many of the personality disorders, the aetiology of avoidant
personality disorder has not been extensively researched. However, there have been a few studies
investigating the correlates and risk factors associated with avoidant PD. For example, avoidant PD has
been shown to be closely associated with scores on a variety of personality dimensions, including
introversion, neuroticism, low self‐esteem, pessimism, and to self‐reports of elevated emotional
responsiveness to threat and reduced emotional responsiveness to incentives (Meyer, 2002). Family
studies have also found that having a family member diagnosed with either social phobia or avoidant
PD increases the risk for both these disorders 2–3 fold (Tillfors, Furmark, Ekselius, & Frederickson,
2001), suggesting a close relationship between the development of social phobia and avoidant PD. This
may also be linked to a genetic predisposition for avoidant personality disorder, which is estimated to be
between around 27–35%, and overlaps with genetic vulnerability to social anxiety disorder (Reichborn‐
Kjennerud et al., 2007), although heritability levels have been found to be as high as 64% when
different methods of assessing avoidant PD have been used (Gjerde et al., 2012).
Finally, when compared with individuals with either major depression or other personality disorders,
individuals with avoidant PD report poorer child and adolescent athletic performance, less involvement
in hobbies during adolescence, and less adolescent popularity (Rettew et al., 2003), and this study also
demonstrated higher levels of childhood physical and emotional abuse in the avoidant PD group than
the depressed group—but this factor did not differentiate individuals with avoidant PD from individuals
with other forms of PD. What these studies do suggest is that (a) avoidant PD is closely associated with
social phobia, and both may be part of a broader social anxiety spectrum, and (b) there are some
important childhood precursors which suggest that underperformance across a variety of childhood
social domains may be predictive of later avoidant PD.
Finally, avoidant PD is closely associated with low self‐esteem and feelings of shame and guilt, and
psychodynamic accounts suggest that negative childhood experiences and childhood underachievement
may contribute to a negative self‐image (Gabbard, 1990). We have seen that there is some evidence for
childhood negative experiences and underachievement being precursors to later avoidant PD, but it is
still far from clear (a) whether these experiences are consequences of the developing disorder or (b) if
they are causal factors, how such experiences might lead to the development of low self‐esteem, shame
and guilt. Furthermore, avoidant PD has been commonly linked with the construct of ‘malignant self‐
regard’ where repeated experiences of disappointing and frustrating relationships with others are
attributed to the self, leading to a negative self‐concept (Huprich, 2014; Lengu, Evich, Nelson, &
Huprich, 2015).

Dependent personality disorder

Some clinicians have highlighted what appear to be many formalistic similarities between dependent
personality disorder and depression. These similarities include indecisiveness and passiveness, pessimism
and self‐doubting, and low self‐esteem. We have already seen in Chapter 7 that individuals suffering
depressed mood continually seek reassurance from family and friends in a way that is similar to the
manner in which individuals with dependent personality disorder continually seek support and guidance
(Joiner, Metalsky, Katz, & Beach, 1999). A possible link between dependent personality disorder and
depression is also supported by the fact that drugs used to treat depression will also significantly decrease
symptoms of dependent personality disorder (Ekselius & von Knorring, 1998). This has led
psychodynamic theorists to develop models of the aetiology of dependent personality disorder that
closely resemble those for depression. For example, object relation theorists claim that dependence and
fear of rejection is fostered by childhood neglect or loss of a parent during childhood. Alternatively,
some other psychodynamic theorists claim that overprotective parenting may cause subsequent
separation anxiety, depression and the development of dependent personality disorder (Bornstein,
1996). Clearly, these very different accounts require some further evidence to differentiate them, but
unfortunately there are currently no systematic data on the childhood experiences of individuals who
subsequently develop dependent personality disorder that might help to shed light on these different
accounts.
Apart from formalistic similarities with depression, dependent personality disorder has been found to be
regularly comorbid with a number of anxiety disorders, particularly social anxiety disorder, OCD, and
panic disorder (McLaughlin & Mennin, 2005). But once again, it is unclear whether dependent
personality disorder is associated with an increased risk for developing an anxiety disorder (and what the
mechanism for this increased risk might be) or whether anxiety disorders increase the risk for dependent
personality disorder. Further research is needed to clarify these relationships and to help understand
aetiological factors important to the development of dependent personality disorder.

Obsessive‐compulsive personality disorder

A first place to look for evidence relating to the aetiology of OCPD would be its apparently related
disorder, OCD – but a review of the facts does not indicate a particularly close link between the two
disorders. While the symptoms of OCPD are very similar to those of OCD, the reported comorbidity
of OCPD in individuals with OCD is relatively low at 22% (Albert, Maina, Forner, & Bogetto, 2004). In
fact, this study found that comorbidity of OCPD in individuals with panic disorder was 17%, suggesting
that OCPD is found at approximately the same level in individuals with panic disorder as it is
individuals with OCD. In addition, family studies have indicated that individuals with OCPD are no
more likely than chance to have close relatives with OCD, which does not suggest a genetic link between
OCPD and OCD (Nestadt et al., 2000). At present there is very little evidence available that enables us
to identify important factors in the aetiology of OCPD and significantly less that enables us to predict
those individuals who will develop OCPD as opposed to OCD. Some studies of nonclinical populations
indicate there may be a single underlying vulnerability factor for both OCPD and OCD, and this may
be related to a parenting style that includes psychological manipulation and guilt induction (Aycicegi,
Harris, & Dinn, 2002) or family transmission of symptoms to children by parents who also have OCPD
symptoms (Calvo et al., 2009). But this still begs the questions of (a) why OCPD and OCD are not
highly comorbid if they share similar vulnerability factors and (b) why some people develop OCPD and
not OCD.

Summary of the aetiology of personalitydisorders

This section has illustrated that the aetiology of personality disorders—compared with many other
psychopathologies—is relatively underresearched. APD and BPD have received the most attention,
while research on the aetiology of other personality disorders is still at a very early stage (e.g., the
Cluster C disorders). Because personality disorders can be enduring features of an individual's
behaviour from childhood into adulthood, researchers have tended to look for either genetic or
biological factors (e.g., brain abnormalities) and factors in childhood that might either put an individual
at risk for developing a personality disorder or be a direct causal factor in determining the behavioural
styles characteristic of the different disorders. Most personality disorders do appear to have a genetic
predisposition and are also associated with specific neurological features which may or may not be direct
causes of the behavioural traits of individual personality disorders. Furthermore, childhood abuse and
neglect appears to be an important risk factor for many personality disorders, but it is still not clear
whether these childhood experiences are a direct cause of personality disorders or whether childhood
abuse and neglect is a consequence of the behavioural problems that the individual with a personality
disorder brings to the parent‐child relationship. The most promising models of personality disorders
appear to be diathesis–stress models, where a genetic predisposition creates neurological abnormalities
that create behavioural and psychological problems (such as impulsivity or emotion dysregulation), and
these behavioural and psychological problems during childhood create parent–child relationships that
may foster harsh or neglectful parenting.
SELF‐TEST QUESTIONS
Can you describe the evidence suggesting that Cluster A disorders are genetically linked
with schizophrenia?
What are the risk factors and childhood precursors predictive of adult APD?
What is the evidence for a genetic element to APD?
Some theories argue that dysfunctional cognitive schemas underlie APD, can you name the
important schema modes described by these theories?
What are the physiological and neurological factors associated with APD, and how might
they contribute to typical APD behaviour patterns?
Can you describe the evidence suggesting that negative childhood experiences might be
important in the aetiology of BPD?
What is the evidence for a link between BPD and bipolar disorder?
How do psychodynamic theories attempt to explain the development of BPD?
What is the diathesis–stress model of BPD and how does this model predict the
development of BPD traits?
What might be the role of abnormal parenting in the development of narcissistic and
histrionic personality disorders?
What is the evidence for a genetic link between avoidant personality disorder and social
anxiety disorder?
What is the evidence for a link between dependent personality disorder and mood
disorders?
Is there any evidence for a link between OCPD and OCD?

SECTION SUMMARY

12.4 THE AETIOLOGY OF PERSONALITY DISORDERS

Cluster A Disorders
Behavioural and genetic links between Cluster A disorders (paranoid, schizoid and
schizotypal personality disorders) and schizophrenia suggest that they may be part of a
broader schizophrenia spectrum disorder.
Psychodynamic approaches to paranoid personality disorder suggest that parents may have
been demanding, distant, overrigid, and rejecting, giving rise to a lack of trust in others.
The risk of all three types of Cluster A disorder is increased in relatives of individuals
diagnosed with schizophrenia, suggesting a genetic link between schizophrenia and the
Cluster A personality disorders.
Antisocial Personality Disorder
One of the best predictors of APD in adulthood is conduct disorder in childhood.
Adolescent smoking, alcohol use, illicit drug use, police trouble, and sexual intercourse
before the age of 15 significantly predict APD in later life.
APD appears to run in families, suggesting that APD may be acquired through social
learning and imitation.
Psychodynamic approaches to APD suggest that lack of parental love and affection during
childhood and inconsistent parenting is likely to lead to the child failing to learn trust.
Heritability of APD traits appears to be relatively high, with estimates between 51% and
81%, with highest estimates related to aggressive traits.
DNA methylation may occur as a result of particular types of early experiences (e.g.,
childhood stress and abuse), and this has neurodevelopmental consequences which may
facilitate the development of antisocial traits in individuals with a diagnosis of APD
through epigenetic processes.
Individuals with both APD and BPD appear to possess a set of dysfunctional cognitive schemas
that give rise to their unpredictable mood swings and impulsive behavior.
Individuals with APD show a number of physiological and neurological characteristics,
such as physiological indicators of low anxiety, low levels of baseline arousal and reactivity,
lack of learning in simple aversive conditioning procedures, and neurological impairments
indicative of impulsivity.

Borderline Personality Disorder

Individuals with BPD report rates of childhood physical, sexual, verbal abuse and neglect
ranging from 60% to 90%, suggesting that these experiences may be important in the
development of BPD.
Whole population studies indicate that BPD diagnosis covaries directly with the relatedness
between individuals, and heritability of BPD is estimated at 46%
Recent research has linked BPD with mood disorders, and around 44% of individuals with
BPD belong to a broader bipolar disorder spectrum, which may account for the regular and
unpredictable mood swings in BPD.
Neuroimaging studies of BPD have identified brain abnormalities in the limbic system,
including the hippocampus and amygdala.
Object‐relations theory argues that individuals with BPD have received inadequate support
and love from important others (such as parents) and this results in an insecure ego, which
is likely to lead to lack of self‐esteem and fear of rejection.
Between 10% and 47% of individuals with BPD also meet the diagnostic criteria for APD,
suggested a link between the two disorders.
Linehan's (1987) diathesis–stress model of BPD states that BPD develops as a result of
genetic predispositions that give rise to behavioural characteristics such as impulsivity and
poor emotion regulation, but that these inherited characteristics are then amplified by
parenting that is harsh, neglectful, or invalidating.

Narcissistic Personality Disorder

 Psychodynamic theories of narcissistic personality disorder argue that the traits associated with
this disorder result from childhood experiences with cold, rejecting parents who rarely
praised their children's achievements.
Narcissistic personality disorder is also closely associated with APD, and narcissistic
individuals will regularly act in self‐motivated, deceitful, and aggressive ways reminiscent
of APD.
Narcissists appear to hold grandiose, but simultaneously tentative, unstable self‐views that
require them to seek continuous self‐validation and dominance over others.

Histrionic Personality Disorder

There is relatively little research on the aetiology of histrionic personality disorder, and theories
that are currently available tend to have developed from psychodynamic accounts.

Cluster C Disorders
Having a family member diagnosed with either social anxiety disorder or avoidant personality
disorder increases the risk for both disorders 2–3 fold, suggesting that both social phobia and
avoidant personality disorder may be part of a broader social anxiety spectrum that has a
genetic element.
Dependent personality disorder has many features similar to depression, including
indecisiveness, passiveness, pessimism, self‐doubting, and low self‐esteem, and drugs used
to treat depression are also successful at alleviating the symptoms of dependent personality
disorder.
Dependent personality disorder is also regularly comorbid with a number of other
psychopathologies, particularly social anxiety disorder, panic disorder and OCD.
The reported comorbidity of obsessive‐–compulsive personality disorder in individuals with OCD
is as low as 22%, suggesting that the two disorders may not be closely related.

12.5 TREATING PEOPLE WITH A DIAGNOSIS OF PERSONALITY

DISORDER
There are a number of important factors that make helping a person with a diagnosis of a personality
disorder problematic and may require approaches slightly different to those employed for many other
psychopathologies. First, as we have mentioned throughout this chapter, personality disorders can be
enduring patterns of behaviour that an individual has usually deployed from childhood into adulthood.
One consequence of this is that the individual may not view their behaviour as problematic, and as a
result, they are unlikely to believe they need to change their behaviour let alone seek treatment for it.
Second, individuals with personality disorders usually possess patterns of behaviour that are likely to
make them susceptible to a range of other psychiatric disorders (such as anxiety disorders or
depression), and we have discussed the extent of this comorbidity earlier. It is often for treatment of the
comorbid problems that an individual with personality disorders is first referred for treatment (e.g.,
depression and suicidal ideation in BPD; social phobia in avoidant personality disorder; panic disorder,
or social phobia in dependent personality disorder, etc. see Table 12.15). To add to these problems,
disorders that are comorbid with a personality disorder can be difficult to treat successfully (Crits‐
Christoph & Barber, 2002), and there may be many reasons for these difficulties. These include (a) such
individuals are significantly more disturbed and may require more intensive treatment than individuals
with other types of psychiatric disorder alone, (b) many personality disorders consist of ingrained
behavioural and psychological styles that are likely to continue to cause future life difficulties that may
trigger symptoms of other disorders (e.g., the individual with a diagnosis of BPD may continue to have
turbulent and unstable relationships that may cause future bouts of depression and suicidal ideation),
and (c) some of the personality disorders have features which make such individuals manipulative and
unable to form trusting relationships (e.g., APD, narcissistic personality disorder, and to a lesser degree
BPD), and this makes the development of a working, trusting relationship between therapist and client
very difficult—even when it comes to just treating any comorbid disorder. Third, it is worth asking what
it is about personality disorders that is disordered and requires treatment—Especially if the behavioural
styles typical of the personality disorders are really only extremes of what otherwise might be
considered to be normal personality dimensions (Costa & MacRae, 1990). Because individuals with
personality disorders exhibit extremes of behaviour on normal personality dimensions (such as
extraversion/introversion, conscientiousness, agreeableness/antagonism), it may be more realistic to try
to moderate and manage the existing behaviours of such individuals rather than try to change them
completely. For example, the behaviours of individuals with OCPD may be quite adaptive in some
circumstances and situations (e.g., when dealing with an important work project), but inappropriate and
maladaptive in others (e.g., when trying to obsessively organise family and friends on a holiday). Taking
this into account, the therapist may be more successful in trying to moderate the extreme behavioural
styles of the individual with a personality disorder, rather than trying to change their ingrained
behaviour patterns completely (Millon, 1996). Even given that these factors are taken into account when
devising interventions for personality disorders, 37% of people undergoing treatment for personality
disorders still fail to complete (McMurran, Huband, & Overton, 2010), and factors associated with
noncompletion include young age, lower education levels, unemployment, having juvenile convictions,
and emotional neglect in childhood. These are all factors to bear in mind when reviewing the
treatments that have been applied to personality disorders.
Finally, the scope of the personality disorders and their varied behavioural characteristics mean that
treatments are very often geared towards the requirements of individual personality disorders. This
being so, therapists have utilised a broad range of differing therapeutic procedures with varying degrees
of success, and we will discuss these differing approaches in turn. However, in general, individuals with
personality disorders will probably need to (a) acquire a range of life skills, (b) learn emotional control
strategies, and (c) acquire the skill of mentalisation, which is the ability to reflect on their experiences,
feelings, and thoughts and to assess their meaning and importance. These are all goals of therapy that
can be identified across a range of conceptually different treatments for the personality disorders.

12.5.1 Drug Treatments

Drugs are frequently used in an attempt to treat individuals with personality disorders, but they tend to
be used to tackle symptoms of any comorbid disorder rather than the symptoms of the personality
disorder itself (but see Newton‐Howes & Tyrer, 2003). Individuals with comorbid anxiety disorders,
such as social anxiety disorder or panic disorder can be prescribed anxiolytics, and those with comorbid
major depression may receive antidepressants such as the selective serotonin reuptake inhibitor
fluoxetine (Prozac) (Rinne, van den Brink, Wouters, & van Dyke, 2002, see Chapter 4, Section 4.1.1 for
a fuller description of drug treatments for psychopathologies). Lithium chloride can also be
administered to individuals who have comorbid bipolar disorder (a frequent comorbid disorder with
BPD and APD) in order to stabilise their moods and reduce antisocial behaviour. Antipsychotic drugs
(such as risperidone) can also be effective in reducing the symptoms of Cluster A personality disorders
which are known to have some relationship to the symptoms of schizophrenia (Koenigsberg et al.,
2001), and more recently, atypical antipsychotic drugs (such as quetiapine, see Table 4.2) have been
shown to reduce impulsivity, hostility, aggressiveness, irritability, and rage outbursts in individuals with
APD (Walker, Thomas, & Allen, 2003; Timäus et al., 2019). However, although such drug treatments
will improve symptoms, they will rarely produce remission of the personality disorder (Paris, 2011). In
terms of drug treatment for direct symptoms of the personality disorders themselves, antidepressants
have been found to be effective with Cluster C symptoms (avoidant personality disorder and OCPD)
(Pelissolo & Jost, 2011). Drugs for dealing with aggression and impulsivity, including lithium, beta
blockers, carbamazepine, antipsychotic drugs, and selective serotonin reuptake inhibitors (SSRIs) have
also been found to reduce symptoms in Cluster B disorders (Pelissolo & Jost, 2011). Having said this,
there are very few randomised controlled trials that have looked at the effects of medication on
personality disorder symptoms, and what little evidence is available is often equivocal, poorly controlled,
or conducted on only small numbers of participants (Olabi & Hall, 2010).

12.5.2 Psychodynamic and Insight Approaches

As we saw in Section 12.4, psychodynamic approaches have a long history of attempting to explain the
development of personality disorders, and so it is not surprising that psychodynamic and insight
therapies generally should also be prominently involved in treatments for these disorders. Problematic
relationships with parents and childhood neglect and abuse are factors that are prominent in attempts to
explain many of the personality disorders, and exploring and resolving these developmental experiences
is seen as an important role for psychodynamic therapies. Such therapists view ‘insight’ as the
important mechanism of change in personality disorders—not least because most individuals with
personality disorders do not initially view their behaviour as problematic. This approach is particularly
important when treating individuals with BPD because such clients represent a serious challenge to
therapists of any theoretical orientation. Many clients with BPD diagnosis may appear manipulative
and will frequently game‐play with the therapist in order to ascertain how special they are to the
therapist (e.g., by phoning the therapist regularly at inconvenient times) or they will make dramatic
gestures to seek attention (e.g., by threatening suicide attempts). They also lack trust which will make it
difficult to develop a working therapist‐client relationship whatever the therapeutic approach being
used. Finally, BPD is typical of most of the Cluster B personality disorders, in that the individual will
view the causes of their problems as external to them (i.e., they will be the fault of other people or of
other events such as the way they were treated in childhood), and this makes any form of insight therapy
difficult (see Colli, Tanzilli, Dimaggio, & Lingiardi, 2014, for a discussion of the difficulties faced by
therapists treating individuals with a personality disorder diagnosis).
However, psychodynamic therapists have tended to take a more active approach to treating personality
disorders and have attempted (a) to identify and block manipulative behaviours at an early stage, and (b)
to explore the ‘weak egos’ and fragile self‐image that usually underlie many of the personality disorders.
As a particular example of psychodynamic treatment, object‐relations psychotherapy attempts to
strengthen the individual's weak ego so that they are able to address issues in their life without constantly
flipping from one extreme view to another (Kernberg, 1985). In the case of BPD, for example, object‐
relations psychotherapy will (a) attempt to show the client how their normal way of behaving is
defensive (e.g., when they blame others for problems in their life), (b) how their judgements are often
simplistic and fall into simple dichotomous categories (such as either ‘good’ or ‘bad’) that cause them to
swing regularly from positive to negative ways of thinking, and (c) provide the client with more adaptive
ways of dealing with important life issues by, for example, teaching them that other people may possess
both good and bad characteristics, rather than either being all ‘good’ or all ‘bad’.

object‐relations psychotherapy A form of psychodynamic treatment that attempts to

strengthen the individual’s weak ego so that they are able to address issues in their life without
constantly flipping from one extreme view to another.

While it is difficult to objectively assess the effectiveness of psychodynamic approaches to treatment,

there is some evidence that psychodynamic psychotherapies do have a beneficial effect on the symptoms
of personality disorders. Some studies have suggested that clients do show significant improvements in
symptoms during treatment (Svartberg, Stiles, & Seltzer, 2004), and that short‐term psychodynamic
therapy is at least as effective as cognitive behaviour therapy(CBT) (Leichsenring & Leibing, 2003)
and a range of other treatments‐as‐usual, including general community based psychiatric treatment
(Fonagy, Roth, & Higgitt, 2005).

12.5.3 Dialectical Behaviour Therapy

One particular form of therapy that has been successfully used to treat individuals with personality
disorders is dialectical behaviour therapy (Linehan, 1987). This approach takes the client‐centred
view of accepting the client for what they are, but attempts to provide them with insight into their
dysfunctional ways of thinking about and categorising the world, and it is designed to provide them with
the necessary skills to overcome these problematic ways of thinking and behaving. This is not an easy
thing to do with a group of people who are usually very sensitive to criticism and can be emotionally
labile and who will probably react to any challenge to their current ways of thinking in extreme ways
(even threatening suicide). As a result, the dialectical behaviour therapist has to convey complete
acceptance of what the client does to enable a successful dialogue to ensue about the client's problems
and difficulties. Dialectical behaviour therapy subsequently includes skills training designed to teach
individuals to be mindful of their problematic ways of thinking about the world (e.g., that others are not
always to blame for the bad things that happen), to learn to solve problems effectively, to control their
emotions (such as their anger outbursts), and to develop more socially acceptable ways of dealing with
their life problems.

dialectical behaviour therapy A clientcentred therapy for personality disorder that

attempts to provide clients with insight into their dysfunctional ways of thinking about the
world.

Dialectical behavior therapy (DBT) can be split into four distinct stages: (a) addressing dangerous and
impulsive behaviours and helping the client to learn how to manage these behaviours, (b) helping the
client to moderate extremes of emotionality (e.g., learning to tolerate emotional distress), (c) improving
the client's self‐esteem and coaching them in dealing with relationships, and (d) promoting positive
emotions such as happiness.
This approach has been particularly successful with individuals with BPD (Robins & Chapman, 2004;
Bloom, Woodward, Susmaras, & Pantalone, 2012), has been shown to have long‐lasting positive effects
on suicidal and nonsuicidal self‐harm behaviours, depression, interpersonal functioning, anger control,
and rehospitalisation (McMain, Guimond, Streiner, Cardish, & Links, 2012; Linehan, Heard, &
Armstrong, 1993), and it is particularly effective as a treatment for BPD over the longer term when
combined with appropriate medication (Soler et al., 2005).

12.5.4 Cognitive Behaviour Therapy

Because of the resistance of many personality disorders to ‘insight’ therapies, it was originally felt
inappropriate to try and apply CBT to this category of psychopathologies. However, over the past 20
years, there has been significant progress in developing CBT in ways that are directly relevant to the
behavioural, emotional, and cognitive problems found in personality disorders. Applying CBT to the
treatment of people with a diagnosis of personality disorder was arguably first pioneered by Aaron Beck
and colleagues, who attempted to apply CBT methods first developed to treat depression (see Chapter
7) (Beck & Freeman, 1990). This meant exploring the range of logical errors and dysfunctional
schemata that might underlie problematic behaviour within individual personality disorders. For
instance, an example of a logical error would be the individual with obsessive–compulsive personality
disorder (OCPD) believing that they are incompetent if they do just one thing wrong. They may also
have developed dysfunctional schemata that generate problematic behaviour and cause emotional
distress. In the case of OCPD, the individual may have developed beliefs that everything has to be done
correctly (perhaps because of parental pressure to be perfectionist), and when one thing is not done
properly this causes emotional distress and anxiety. In most cases the way in which CBT is constructed
depends very much on the individual personality disorder diagnosed and on the cognitive factors
relevant to that individual client (see Beck & Freeman, 1990). However, Treatment in Practice 12.1
provides a brief summary of the stages through which conventional CBT for personality disorders
would proceed.
As a specific example, the way in which dysfunctional schemata may develop in BDP is outlined in
Figure 12.3. Childhood abuse is assumed to contribute to the development of a number of schemata
typical of BPD. This leads to the self being viewed as bad, vulnerable and helpless; others as
malevolent, abusing, and rejecting; experienced emotion is dangerous, and ‘clinging’ becomes a strategy
designed to get support from others but is alternated with ‘keeping distance’ because of distrust. These
negative, dysfunctional schemata give rise to hypervigilance, and the constant expectation of threat and
danger (Arntz, 1999). In addition, because childhood traumas have never been fully emotionally
processed, this has resulted in stunted emotional‐cognitive development, so that individuals with BPD
show dichotomous thinking (‘black’‐‘white’, ‘good’‐‘bad’ thinking with no shades of grey). CBT can be
used in its traditional way to challenge the status of these dysfunctional schemata and to attempt to
replace them with more functional schemata and views of the world. However, when treating
individuals with BDP in particular, the therapist (a) must avoid direct challenges with the client about
their beliefs because of their intense sensitivity to criticism, and so must usually approach this stage of
therapy empathetically (McGinn & Young, 1996), and (b) may attempt to approach the process of
changing dysfunctional schemata by ‘reparenting’ the client, which allows the therapist to form an
emotional attachment to the client in order to challenge dysfunctional schemata (Young, Klosko, &
Weishaar 2003).
CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 12.1
CBT FOR PERSONALITY DISORDERS

The normal stages through which CBT would progress in the treatment of a personality
disorder are the following:
1. During the initial sessions the therapist will deal with any coexisting psychiatric problems
(usually specific anxiety disorders such as panic disorder or social anxiety disorder or major
depression).
2. The therapist then teaches the client to identify and evaluate key negative automatic
thoughts (e.g., ‘nobody likes me’ or ‘I am worthless’ in avoidant or dependent personality
disorders).
3. The therapist will then structure the sessions carefully to build a collaborative and trusting
relationship with the client—especially in the case of those disorders where the client is
distrusting or manipulative (e.g., BPD).
4. The therapist may then employ guided imagery to unravel the meaning of new and earlier
experiences that may have contributed to the dysfunctional behaviour patterns (such as
problematic early childhood and parenting experiences).
5. In collaboration with the client, the therapist will prepare homework assignments tailored
to the client's specific issues.
6. Finally, the therapist will apply specific cognitive, behavioural, and emotion‐focused
schema restructuring techniques to dispute core beliefs and to develop new and more
adaptive beliefs and behaviour (see also Schema Therapy).
Two main treatment objective are, first, to help the client develop new and more adaptive core
beliefs, and second, to help the client develop more adaptive problem‐solving interpersonal
behaviours.
FIGURE 12.3 A schematic representation of the way that dysfunctional schema are thought to develop in borderline
personality disorder (BDP). See text for further elaboration.
After Arntz, 1999.
The development of specific CBT procedures for personality disorders is still an active process.
Procedures have been developed that are specific to the cognitive and behavioural requirements of
individual disorders (Beck & Freeman, 1990), and current attempts are being made to identify
maladaptive schemata and dysfunctional beliefs that are important determinants of the behavioural
styles typical of individual personality disorders (Young, Klosko, & Weishaar, 2003; Beck, Broder, &
Hindman, 2016; see Table 12.16). It is still very early to be able to say with any confidence that CBT
offers an important and effective method of treatment for personality disorders. However, a number of
controlled studies have shown that CBT for personality disorders are superior to non–therapy control
conditions in reducing symptoms (Linehan, Tutek, Heard, & Armstrong, 1994; Linehan et al., 1999)
and are equally as effective as psychodynamic therapy (Leichsenring & Leibing, 2003).

12.5.5 Schema‐Focused Cognitive Therapy

A more recent development of CBT for personality disorders is known as Schema‐Focused
Cognitive Therapy or Schemata Therapy. Central to this approach is the concept of early
maladaptive schemas (EMSs) that are thought to develop during childhood and result in dysfunctional
beliefs and behaviours during adulthood (Young, Klosko, & Weishaar 2003). We touched on these
maladaptive schemas and their putative role in determining the unpredictable, antisocial, and impulsive
behaviours typical of the more severe personality disorders earlier in this chapter (Section 12.4). For
example, if a child is continually overly criticised by parents, then he/she may develop the schema ‘I am
defective’. In order to deal with and cope with this schema, the child will develop strategies that in the
longer term are maladaptive and act to reinforce the schema. For example, they may develop a variety
of strategies that enable them to avoid thinking about this schema, such as storming off at the slightest
hint of criticism, summarily breaking off relationships if there is an indication that their partner is not
being affectionate, or inflicting self harm as a means of distracting from the schema. Schemata therapy
outlines three specific stages for therapy in these circumstances. First, the client needs to be convinced
that their problems and symptoms are not evidence for their maladaptive schemas, but in contrast their
maladaptive schemas are actually a cause of their symptoms. Developing self‐knowledge is important in
understanding that maladaptive schema are related to unfortunate childhood circumstances rather than
representing truths about the way that person is. The second stage is to attempt to identify and prevent
schemata avoidance responses, so that the client can experience, accept, and tolerate the negative and
painful emotional states that ensue when schemata avoidance is prevented. Third, through the
therapist's questioning and comments, the client is helped to examine the life experiences that have
given rise to the maladaptive schemata, and this final stage of therapy is intended to reduce the belief in
maladaptive schemata and to develop adaptive alternative perspectives on their problematic life
experiences. There is modest empirical evidence for the existence of many of the elements in schemata
theory, and there are a small number of effectiveness studies available which suggest it may be a
promising and cost‐effective treatment for personality disorders such as BPD (Sempértegui, Karreman,
Arntz, & Bekker, 2013). Benefits of schemata therapy perceived by clients with personality disorders
include improved self‐understanding and better awareness and management of their own emotional
processes (Tan et al., 2018)

Schema‐focused cognitive therapy In the treatment of personality disorders, a specially

developed cognitive therapy which is used to address dysfunctional ways of thinking and
maladaptive cognitive schema.

Schemata therapy Central to this approach is the concept of early maladaptive schemas
(EMSs) that are thought to develop during childhood and result in dysfunctional beliefs and
behaviours during adulthood.
TABLE 12.16 Core beliefs and strategies of individuals with personality disorder diagnoses—target beliefs for CBT
From Beck, Broder, & Hindman, 2016.
Personality Core Belief Assumptions Coping Strategies
Disorder About Self
Antisocial I'm a potential If I manipulate, attack, and Lie, cheat, manipulate, threaten
victim. take advantage of others, I others, act in an overly aggressive
can protect myself and get fashion
what I want.
Avoidant I'm unlovable and If I avoid intimacy, I will be Avoid social interaction and negative
vulnerable to less likely to be rejected. If I emotion
negative emotion. avoid dysphoria, I won't fall
apart.
Borderline I'm bad, helpless, If I depend on others, guard Rely on others, be overly vigilant for
defective against being hurt, and act harm, reject others to forestall
(unlovable), likely aggressively, I can survive. inevitable rejection from others
to be abandoned.
Dependent I'm weak and If 1 subjugate myself to Avoid independent problem solving
incapable. others, they'll take care of and decision making, go overboard
me. in pleasing others
Histrionic I'm nothing. If I entertain others, they'll Be inappropriately dramatic,
be drawn to me. seductive, entertaining
Narcissistic I'm inferior. If I demand entitlements and Put others down to display own
accolades, it will show I'm superiority; expect special favours
special. and accommodations, brag about
accomplishments
Obsessive‐ I'm vulnerable to If I'm highly responsible, Act in overly responsible ways,
compulsive bad things maintain order and control, rigidly control self and others, strive
happening. and perform to the highest, for perfection
I'll be okay.
Paranoid I'm vulnerable. If I'm on guard, I can protect Mistrust others, look for hidden
myself. motives
Schizoid I don't fit in. If I avoid others, I'll be okay. Distance themselves from others
Schizotypal I am different and If I get close to others, they'll Mistrust others, try to be different in
vulnerable. be unfriendly. a ‘special’ way

12.5.6 Summary of Treatments for People with a Diagnosis of Personality

Disorder
We have reviewed a range of difficulties that are involved in the treatment of individuals with a
personality disorder diagnosis, and these difficulties often make successful treatment challenging to
achieve. These difficulties include (a) denial of any psychopathology, (b) personality characteristics that
make forming a trusting relationship with a therapist difficult, (c) persistent behavioural patterns that are
likely to continue to cause future life difficulties, and (d) comorbid psychiatric disorders that usually need
to be addressed and treated before tackling any underlying personality disorder. Despite these
difficulties, therapists have been imaginative in attempting to develop a range of psychological
treatments designed to tackle the important features of personality disorders. First, drugs may be used
to reduce the symptoms of any comorbid disorder such as major depression, bipolar disorder, or
anxious psychopathologies generally, and have recently been successfully deployed in the reduction of
direct symptoms of personality disorders themselves (although they rarely result in remission of the
personality disorder). Subsequently, a range of insight based therapies (such as dialectical behaviour
therapy) or specially developed cognitive therapies (such as schema‐focussed cognitive therapy) can be
used to address dysfunctional ways of thinking and maladaptive cognitive schema. In general,
individuals with a personality disorder will benefit from (a) acquiring a range of adaptive life skills
(which allow them to interact and socialise successfully), (b) learning emotional management strategies
(that manage anger outbursts and acute periods of depression), and (c) acquire skills that enable them to
reflect objectively on their experiences, feelings, and thoughts, rather than reacting impulsively and
emotionally to challenging events.
Finally, a piece of optimistic news about the treatment of personality disorders. We have already
mentioned how difficult it might be to change the personalities of individuals who have been thinking
and behaving in relatively ingrained ways since childhood. However, a recent large‐scale review study
has found that psychological therapy techniques can successfully modify personality traits such as
neuroticism and extraversion, and they can do it in an average time of 24 weeks (Roberts et al., 2017)!

SELF‐TEST QUESTIONS
Can you name the factors that make personality disorders difficult to treat?
What is the evidence in favour of a role for drug treatment in the management of
personality disorders?
What are the difficulties involved in adapting CBTs to the treatment of personality
disorders such as APD and BPD?
What are the main features of object‐relations psychotherapy and dialectical behaviour
therapy as applied to the treatment of personality disorders?
What is schema‐focused cognitive therapy and how does it approach the treatment of
personality disorders?
 SECTION SUMMARY

12.5 TREATING PEOPLE WITH A DIAGNOSIS OF PERSONALITY

DISORDER
Personality disorders are particularly difficult to treat successfully because (a) individuals
with personality disorders regularly deny they have problems that require treatment, and
(b) personality disorders are also highly comorbid with other psychiatric disorders, which
makes treatment more complex.
Drug treatments can be used to tackle symptoms of any comorbid anxiety or mood
disorder, which in turn makes the personality disorder itself more accessible to treatment.
Object‐relations psychotherapy and dialectic behaviour therapy are both
treatments that have been developed specifically to deal with the difficulties posed by the
treatment of individuals with personality disorders such as BPD.
More recently, cognitive therapies have been developed which attempt to identify and
change any logical errors, dysfunctional beliefs and maladaptive schemas possessed by the
individual with personality disorders (e.g., schema‐focused cognitive therapy or schemata therapy).

12.6 PERSONALITY DISORDERS REVIEWED

Personality disorders represent long‐standing, pervasive and relatively inflexible patterns of behaviour
that deviate from acceptable norms within individual cultures. They are regularly associated with
unusual ways of interpreting events (e.g., paranoid and schizotypal personality disorders), unpredictable
mood swings (e.g., BPD), or impulsive behaviour (e.g., APD). These patterns of behaviour can be traced
back to childhood and early adolescence, and they represent ways of behaving that are likely to have
consequences that put the individual at risk for a range of other psychiatric disorders (particularly major
depression or anxiety disorders). While DSM‐5 lists 10 diagnostically independent personality disorders
that are organised into three primary clusters (odd/eccentric, dramatic/emotional, and
anxious/fearful), recent research has suggested that personality disorders are dimensional rather than
categorical (that is they represent extremes of normal personality traits). This has led DSM‐5 to include
an alternative approach to diagnosing personality disorders that has been the subject of research since
the publication of DSM‐5 in 2013. This alternative model requires that clients be rated on various
personality dimensions, and how these dimensions combine will provide the basis for diagnosis of a
reduced number of specific personality disorders (see Section 12.1.3)
Lifetime prevalence rates for personality disorders are difficult to estimate because of differences in
diagnostic reliability and also the poor temporal stability of personality disorders, but with estimates
around 10–15% (see Table 12.14), they are likely to be one of the most prevalent psychopathologies
treated by mental health professionals (Zimmerman, Rothschild, & Chelminski, 2005).
Personality disorders are particularly difficult to treat for a number of reasons. They are frequently
comorbid with other psychiatric disorders such as depression and anxiety (which complicates treatment),
individuals with personality disorders frequently deny their behaviour is problematic, and some can be
distrusting and manipulative in therapy. However, a number of recently developed insight and cognitive
therapies do appear to have some success in treating some of the more problematic personality
disorders, and these include object‐relations psychotherapy (Kernberg, 1985), dialectical behaviour
therapy (Linehan, 1987), cognitive therapy (Beck & Freeman, 1990), and schema‐focussed cognitive
therapy (Young, Klosko, & Weishaar, 2003).
Explaining the aetiology and development of personality disorders is still largely in its infancy. However,
because personality disorders can often be traced back to childhood as persistent patterns of behaviour,
many theories of personality disorders look to childhood experiences and developmental factors for the
causes of these extreme behaviour patterns, and it is certainly the case that childhood abuse, neglect and
conflict can be found in the history of many personality disorders such as BPD and APD (Gabbard,
1996; Paris, 2001). However, childhood abuse is not a necessary prerequisite for any personality disorder
and recent integrated diathesis–stress models of personality disorders view the aetiology as being a
combination of a genetic predisposition that creates neurological abnormalities that in turn generate
behavioural and psychological problems (such as impulsivity or emotion dysregulation), and these
behavioural and psychological problems during childhood create parent‐child relationships that may
foster harsh or neglectful parenting.
However, some other theorists note that individual personality disorders appear to have close links with
other psychopathologies, and may form part of broader spectrums of disorder. For example, (a) Cluster
A disorders (paranoid, schizoid, and schizotypal personality disorders) have strong behavioural and
genetic links with schizophrenia and may form part of a broader schizophrenia spectrum disorder
(Siever & Davis, 2004), (b) BPD is frequently comorbid with bipolar disorder and may belong to a
broader bipolar disorder spectrum which may explain the regular mood swings in BPD (Deltito et al.,
2001), and (c) avoidant personality is closely associated with social anxiety disorder and may form part
of a broader social anxiety spectrum (Schneier, Blanco, Antia, & Liebowitz, 2002). All of these factors
indicate that personality disorders are challenging to the researcher and therapist in many respects: they
are difficult to categorise as discrete disorders, they are difficult to successfully treat, and theories of their
aetiology are still only at the speculative and early stages of development.

This book is accompanied by Student and Instructor companion

websites.
www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter References
Videos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
13
Somatic Symptom Disorders

ROUTE MAP OF THE CHAPTER

This chapter begins by describing some of the features of those disorders collectively known in
the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM‐5) as somatic symptom
disorders. The diagnostic criteria, characteristics, and prevalence rates of the main disorders
are then described (these are somatic symptom disorder, illness anxiety disorder, conversion
disorder, and factitious disorder). We then discuss some of the factors important in the aetiology
of somatic symptom disorder. Finally, the chapter describes the range of treatments that have
been used with somatic symptom disorders, together with an assessment of their modes of
operation and their efficacy.

CHAPTER OUTLINE
13.1 THE DIAGNOSIS AND CHARACTERISTICS OF SOMATIC SYMPTOM
DISORDERS
13.2 THE AETIOLOGY OF SOMATIC SYMPTOM DISORDERS
13.3 THE TREATMENT OF SOMATIC SYMPTOM DISORDERS
13.4 SOMATIC SYMPTOM DISORDERS REVIEWED

LEARNING OUTCOMES
When you have completed this chapter, you should be able to:
1. Describe the main diagnostic criteria and symptom characteristics for the DSM‐5 listed
somatic symptom disorders and evaluate some of the issues concerning diagnosis and
comorbidity.
2. Describe and evaluate the main factors contributing to the aetiology of somatic symptom
disorders, and be able to compare psychological and biological explanations.
3. Describe and evaluate three or four treatments that have been developed to address
somatic symptom disorders.
 I have a core belief that I am dying, I know it's silly but you can't reason with a core belief, on top of that a huge
mistrust of doctors after one diagnosed my father with anxiety instead of checking him for bowel cancer (which he
actually had) and therefore delaying his treatment. It doesn't get any better when you get one doctor diagnosing you
with a UTI and the other saying that all UTIs are in my imagination so I end up avoiding doctors because all I
am told is that I am making it up to then get a rather nasty infection because it actually wasn't in my head after
all. I would love to know how I am supposed to think rationally when I can't even trust doctors anymore. I don't
spend my entire life worrying, I don't sit around doing nothing, despite the assumption that many GPs make, I am
not stressed but I am busy but as soon as I get a worrying symptom that is it, I can no longer function.
Kirsty's Story

Introduction
How often do we have physical symptoms such as aches and pains that trigger worries about contracting
cancer or heart disease? How often do we worry about becoming ill or even dying—even when we have
no physical symptoms of illness? For some people these everyday experiences are enough to cause
significant distress and to interfere with their normal day‐to‐day living. When such concerns and worries
become obsessive or a source of chronic anxiety or depression, they may be diagnosed as a somatic
symptom disorder. This category of disorders includes somatic symptom disorder, illness anxiety
disorder (formerly known as hypochondriasis or health anxiety), and conversion disorder. This is a new
category of disorders listed in DSM‐5, and all of these disorders share a common feature—the
prominence of somatic symptoms associated with significant distress and impairment. With somatic
symptom disorder individuals find somatic symptoms—either real or imagined—distressing and
spend significant amounts of time in medical settings attempting to seek a diagnosis for symptoms that
may either be trivial or not continuously present. Illness anxiety disorder is a preoccupation with
having or acquiring an illness to the extent that there is a high level of anxiety about health that both
causes distress and interferes with normal daily living. Conversion disorder is when the individual
begins to experience symptoms of altered motor or sensory functioning (e.g. unable to voluntarily move
a hand, or temporary blindness)—even when there is little or no evidence of relevant neurological
impairment. As you can imagine there is often a good deal of overlap in symptoms between these three
disorders, and that is one reason why they have been grouped together in their own chapter in DSM‐5.
In all cases, DSM‐5 emphasises that diagnosis should be made on the basis of positive symptoms such as
distress related to somatic symptoms and dysfunctional thoughts about health and not on excessive
anxiety in the absence of somatic symptoms (as had previously been the case in DSM‐IV‐TR). This is
because it is rarely the case that somatic symptom disorders occur in the absence of actual somatic
symptoms (even with conversion disorder), and so the exaggerated responses that develop to health and
physical symptoms in these disorders can frequently have their basis in actual somatic symptoms. This
can be seen in Kirsty's Story at the beginning of this chapter. She reports having a number of experiences
with GPs in relation to illness that she believes have given rise to her illness anxiety—an illness anxiety
that has become significantly disabling whenever she develops any symptoms of illness. Many
individuals with somatic symptom disorders believe that their problems are genuinely medical and are
often disbelieving when told there is no diagnosable evidence for a medical problem. In addition, those
with symptoms that mimic neurological disorders, such as full or partial blindness or loss of feeling
(anesthesia), genuinely believe they have a disability, but their normal functioning can often be
demonstrated in situations where drugs or hypnosis is used to alter levels of consciousness or where
elegant experimental methods are used to infer ability (e.g., Grosz & Zimmerman, 1970). It is also
important when diagnosing some somatoform disorders to differentiate true disorders from malingering
(Merten & Merckelbach, 2013). Claiming to have a physical illness when a person does not is not just a
ploy to avoid work or other situations that the individual may not enjoy but can also be an actively
deployed coping strategy at times of stress. The difference is that malingerers are fully aware that they
are exaggerating or inventing their symptoms, but individuals with somatoform disorders are not. This
is not an easy distinction to make, but malingerers will tend to be defensive when interviewed about
their symptoms, whereas many with somatoform disorders may often display a surprising indifference
about their symptoms (e.g., those with conversion disorder)—especially when the symptoms to most
people would be disturbing (e.g., blindness, paralysis). This is sometimes known as la belle
indifference, or “beautiful indifference.”

somatic symptom disorder A group of loosely associated disorders all of which can be
characterised by psychological problems manifesting as physical symptoms or as psychological
distress caused by physical symptoms or physical features.

Illness anxiety disorder A preoccupation with fears of having or contracting a serious

illness based on a misinterpretation of bodily signs or symptoms. Formerly known as
hypochondriasis.

Conversion disorder The presence of psychological symptoms or affecting voluntary motor

or sensory function.

One somatic symptom disorder that is thought to be related to malingering is factitious disorder
(previously known as Munchausen's Syndrome). Rather than being concerned with existing somatic
symptoms, factitious disorder is associated with the deliberate falsification of physical or psychological
symptoms and the induction of injury, illness, or disease through deception, and this may include
reporting fictitious neurological symptoms or deliberately manipulating laboratory tests (e.g., by adding
blood to urine). In the case of malingering, the individual may intentionally produce symptoms for a
specific reason (e.g., to avoid jury service, to avoid working in a stressful environment). In contrast, in
factitious disorder the individual's motivation is to adopt the sick role—perhaps from the attention that
this role may bestow on them, and individuals diagnosed with factitious disorders often have a history of
pathological lying who have developed an extensive knowledge of medicine and medical terminology. A
related disorder is factitious disorder imposed by another, in which parents or carers make up or
induce physical illnesses in others (such as their children). The reasons that drive individuals to
deliberately make others ill is unclear, although such individuals often crave the attention and praise
they receive in caring for someone who is ill (see Focus Point 13.1).

la belle indifference An indifference about real symptoms (especially when the symptoms
would be disturbing to most people) sometimes displayed by individuals with somatic symptom
disorders.

factitious disorder A set of physical or psychological symptoms that are intentionally

produced in order to assume the sick role

factitious disorder imposed by another The intentional falsification of physical or

psychological signs or symptoms, or induction of injury or disease, in another person.

We continue by describing the DSM‐5 diagnostic criteria and the main characteristics of somatic
symptom disorder, illness anxiety disorder, conversion disorder and factitious disorder.
13.1 THE DIAGNOSIS AND CHARACTERISTICS OF SOMATIC
SYMPTOMDISORDERS

13.1.1 Somatic Symptom Disorder

The cardinal feature of somatic symptom disorder is multiple, current, somatic symptoms that are
distressing or result in significant disruption to daily life. Symptoms can either be specific (e.g.,
localisable pain) or nonspecific (e.g., general fatigue). While it may not always be possible to explain the
somatic symptoms medically, in most cases the individual's suffering is authentic and not feigned. Those
with a diagnosis of somatic symptom disorder tend to have very high levels of worry about illness, and
will often catastrophise the most minor of physical symptoms. Sufferers often seek medical attention for
their symptoms, but are particularly unresponsive to medical interventions, and will often seek care from
many different doctors for the same symptoms, and frequently claim that their medical care has been
inadequate (Iezzi, Duckworth, & Adams, 2001; Smith & Józefowicz, 2012). The main DSM‐5
diagnostic criteria for somatic symptom disorder are listed in Table 13.1. Somatic symptom disorder
differs from illness anxiety disorder because in the former it is the symptoms themselves (e.g., the pain
they cause) that troubles the sufferer, whereas in the latter it is the prospect of contracting a disease or
illness from the symptoms that is distressing. While the symptoms they report are not usually indicators
of any underlying medical condition, they will often develop medical disorders as a result of exploratory
surgery and medication use (Holder‐Perkins & Wise, 2001; Rosic, Kalra, & Samaan, 2016). Somatic
symptom disorder may be underdiagnosed in older adults, largely because pain and fatigue are
considered a normal part of the aging process, but if excessive thoughts and catastrophising of somatic
symptoms are present, then a diagnosis of somatic symptom disorder might be considered.
 FOCUS POINT 13.1 FACTITIOUS DISORDER IMPOSED ON
ANOTHER

Beverley Allitt was a nurse who was convicted in 1993 of killing four children and injuring nine
others at Grantham Hospital, Lincolnshire. While working on a children's ward in the hospital
she was found to be secretly injecting infants with insulin—a drug that induced cardiac arrest,
causing death and brain damage. During the time that she was involved in these killings, she
was also befriending the parents of her victims and displaying what appeared to be a caring and
sympathetic manner. She received 13 life sentences for these crimes, yet her motives for the
killings have never been fully explained. One theory is that she suffered from factitious
disorder imposed by another (previously known as Munchausen's Syndrome by Proxy),
which is a controversial diagnosis in which sufferers are prompted to deliberately falsify illnesses
in others in order to attract attention to themselves.
What motivates some carers and parents to deliberately inflict illness, pain, and even death
knowingly on young children? Most mothers diagnosed with factitious disorder imposed by
another are emotionally needy and require attention and praise, and they receive this when
appearing caring and loving towards their ill child. They often have poor relationships with
their partners, receive little in the way of support outside of the medical environment, and
regularly exhibit low self‐esteem. Many have a good knowledge of medicine and medical
procedures that allows them to cause their child's illness with a minimum of suspicion (Adshead
& Brooke, 2001; Bluglass, 2001).
The syndrome is notoriously difficult to diagnose. This is because most of the victims are very
young children, many of whom may have genuinely experienced acute life‐threatening events
whose causes are difficult to detect (such as sudden infant death syndrome, SIDS) (Galvin,
Newton, & Vandeven, 2005). In such circumstances, carers who present the problems of their
children in unusual ways are often treated with suspicion—especially if their own emotional
needs are consistent with those often found in factitious disorder imposed by another (Pankratz,
2006).

TABLE 13.1 Summary: DSM‐5 diagnostic criteria for somatic symptom disorder

Shows at least one somatic symptom (present for at least 6 months) that causes distress or
disruption in everyday life
Unwarranted thoughts, feelings or behaviours related to the somatic symptoms or associated
health concerns, indicated by at least one of the following:
Disproportionate and persistent thoughts about how serious the symptoms are
Constantly high levels of anxiety about symptoms or health in general
Unwarranted levels of time and energy devoted to symptoms or health concerns

Somatic symptom disorder is also closely associated with other psychiatric diagnoses such as anxiety
disorders and major depression (Gureje, Simon, Ustun, & Goldberg, 1997). In younger individuals it
can be associated with impulsive and antisocial behaviour, suicide threats and deliberate self‐harm,
making the lives of such individuals chaotic and complicated. It is difficult to estimate the prevalence
rates of somatic symptom disorder because it is such a new diagnostic category. Based on previous
similar diagnostic categories DSM‐5 predicted lifetime prevalence rates of around 1% (DSM‐5,
American Psychiatric Association, 2013, p. 312), but subsequent reviews suggest it may be as high as 5–
7% in the general population (Kurlansik & Maffei, 2016), and 17% in the primary care patient
population (Creed & Barsky, 2004). There may also be cultural variations in the way in which somatic
symptoms are either described or accepted which may affect the diagnosis of somatic symptom disorder.
For example, some cultures give negative meaning to many bodily symptoms that in other cultures are
not described in those ways (e.g., too much heat in the body, burning in the head, etc.), and which serve
as the basis for worry about somatic symptoms.

13.1.2 Illness Anxiety Disorder

This disorder centres on a preoccupation with having or acquiring a serious, undiagnosed illness—
especially when somatic symptoms are either not present or only mild. The distress is largely generated
by beliefs about the meaning, significance, or cause of a symptom, or alternatively a fear of contracting
an illness that the individual believes might be disabling or life threatening. This preoccupation with
health status means that the individual will regularly become alarmed by hearing of someone else
becoming ill or by encountering health‐related news stories. This may commonly lead to a search for
medical information and advice, either by seeking reassurances from family or friends, or by attempts to
find medically relevant information on the Internet. Seeking medical reassurance about health status is
also very common, but this rarely reassures the sufferer, and a doctor's attempts at reassurance may
often exacerbate their anxiety (Table 13.2). Fear of aging and death is also associated with illness anxiety
disorder and may be associated with strict health regimes and use of alternative medicines (Fallon &
Feinstein, 2001). Sufferers are also prone to intrusive thoughts about illness, death, and dying and
usually catastrophise their symptoms. For example, they are likely to believe that an ambiguous bodily
sensation (e.g., an increase in heart rate) is attributable to an illness, rather than a nonthreatening
consequence (e.g., having just walked up a flight of stairs) (MacLeod, Haynes, & Sensky, 1998), and that
a blotch on the skin may be the start of a cancer (Rief, Hiller, & Margraf, 1998). Such individuals are
not necessarily better able to detect bodily sensations than non‐sufferers, but they do possess a negatively
based reporting style which means they interpret sensations significantly more negatively than
nonsufferers (Aronson, Barrett, & Quigley, 2006).
Illness anxiety disorder differs from its diagnostic predecessor hypochondriasis significantly. Around
75% of those diagnosed with hypochondriasis in DSM‐IV‐TR would now be rediagnosed in DSM‐5
with somatic symptom disorder if the somatic symptoms on which the anxiety and distress is based on
genuine somatic symptoms. Because illness anxiety disorder is a new diagnostic category it is difficult to
estimate prevalence rates or comorbidity. However, the prevalence rate for DSM‐IV‐TR
hypochondriasis in the general population is estimated to be 1–5% (DSM‐IV‐TR, p. 505) but can be as
high as 36% in chronic pain patients (Rode, Salkovskis, Dowd, & Hanna, 2006), and clinically
significant health anxieties may be as high as 13% in the general adult population (Scarella, Boland, &
Barsky, 2019). Illness anxiety disorder can begin at any age, but onset is most common during early
adulthood. It is frequently comorbid with other disorders, including mood disorders and obsessive‐
compulsive disorder (Abramowitz & Braddock, 2006; Noyes, 1999).
TABLE 13.2 Summary: DSM‐5 diagnostic criteria for illness anxiety disorder

Obsession with having or contracting a serious illness

Somatic symptoms are very mild or not present at all
High levels of anxiety about health and easily alarmed about personal health
Performs excessive health‐checking behaviour or shows maladaptive avoidance
Illness preoccupation has been present for at least 6 months
The symptoms are not better explained by another mental disorder
13.1.3 Conversion Disorder
The basic feature of conversion disorder is the presence of symptoms or deficits affecting voluntary
motor or sensory function suggestive of an underlying medical or neurological condition. To be
diagnosed with conversion disorder, these symptoms must cause the individual significant distress or
impair social, occupational or other functioning (Table 13.3). Common motor symptoms are paralysis,
impaired balance, localised motor function weaknesses, atonia (lack of normal muscle tone), difficulty
swallowing, and urinary retention. Common sensory symptoms include loss of touch or pain sensation,
double vision, blindness, deafness, hallucinations, and on some occasions seizures or convulsions.
However, in conversion disorder, thorough medical and neurological examination may fail to reveal any
significant underlying medical cause for these deficits, and the symptoms are often preceded by conflicts
or other life stressors (Roelofs et al., 2005) suggesting a psychological rather than a medical cause.
Sufferers do not appear to intentionally produce these symptoms, but more educated individuals may
tend to display more subtle symptoms and deficits that closely resemble known neurological deficits.
However, DSM‐5 specifies that conversion disorder should be diagnosed only when the clinical findings
show clear incompatibility with neurological disease (DSM‐5, American Psychiatric Association, 2013,
p. 319), and conversion symptoms often fail to behave in ways expected by the known neurology. For
example, in the conversion symptom known as glove anaesthesia, numbness begins at the wrist and
is experienced evenly across the hand and all fingers (Figure 13.1). However, if a specific nerve to the
hand, such as the ulnar nerve, is damaged, numbness should extend only to the ring finger and little
finger. Similarly, damage to the radial nerve should affect only the thumb, index finger, middle finger,
and part of the ring finger. Conversion symptoms are also frequently inconsistent, so a sufferer may
often use a ‘paralyzed’ limb when dressing and may reflexively catch a ball unexpectedly thrown to
them with their ‘paralyzed’ hand. Individuals with conversion disorder also tend to exhibit what is
known as la belle indifference (‘beautiful indifference’) about their disability. Whereas most people who
experience a sudden loss of physical ability would be frightened and distraught, individuals with
conversion disorder tend to be largely philosophical about their symptoms and willing to talk at length
about them. At least some psychodynamic approaches to the explanation of conversion disorder suggest
that this appears to reflect a form of ‘relief ’ that their symptoms may prevent them from having to deal
with current conflicts and stress in their lives (Kuechenoff, 2002; Temple, 2002), and prior to its
inclusion in the DSM, conversion disorder was popularly known as hysteria in psychodynamic circles.
TABLE 13.3 Summary: DSM‐5 diagnostic criteria for conversion disorder

At least one symptom of altered voluntary or sensory function

Evidence of incompatibility between the symptoms and known neurological or medical
conditions
The symptoms are not better accounted for by another medical condition or mental disorder
The symptoms cause significant distress or impairment in important areas of functioning
FIGURE 13.1 Glove anesthesia (a) Areas of the arm's skin that send sensory information to the brain by way of
different nerves. (b) A typical region of anesthesia in a patient with conversion disorder. If there were a nerve injury (in the
spinal cord), the anesthesia would extend over the length of the arm, following the nerve distribution shown in (a).

glove anaesthesia A conversion disorder symptom in which numbness begins at the wrist and
is experienced evenly across the hand and all fingers.

hysteria A common term used in psychodynamic circles to describe conversion disorder (prior
to the latter’s inclusion in the DSM).

Some diligence must be taken to ensure that conversion symptoms are not the result of developing
neurological problems, and it is estimated that between 13% and 30% of individuals diagnosed with
conversion disorder have later been found to develop some relevant neurological deficit (Kent,
Tomasson, & Coryell, 1995; Maldonado & Spiegel, 2003). Conversion disorder symptoms can develop
throughout the life course and are often seen to develop after some stressful life event (see Kanaan &
Craig, 2019, for a discussion of this issue). Severity of the symptoms can be linked to the severity of the
life stressor, and important stressful life events that can contribute to conversion disorder include work
experiences and relationship difficulties (Roelofs et al., 2005). However, symptoms can often
spontaneously remit, only to return at a later time, and there is some evidence to suggest that a history
of trauma and childhood abuse may be a vulnerability factor (Bowman & Markand, 1996).
The lifetime prevalence rate of conversion disorder is thought to be less than 1%, and it is significantly
more common in women than in men (Maldonado & Spiegel, 2003). There are also important cultural
differences in the way that conversion disorder manifests itself. For example, Janca, Isaac, Bennett, and
Tacchini (1995) found that sexual and menstrual symptoms were prominent in Western cultures,
complaints of body temperature irregularities are only found in Nigeria, kidney problems only in China,
and body odour complaints only in Japan. In addition, the lower the economic or educational standards
in a culture or community, the higher the prevalence of conversion disorder (Maldonado & Spiegel,
2003). Similarly, the higher the educational standards in a community the more likely it is that the
symptoms will resemble a known medical or neurological disorder (Iezzi et al., 2001). Conversion
disorder is also highly comorbid with other disorders, particularly anxiety disorders such as panic
disorder, and depressive disorders. A study by Sar, Akyuz, Kundakci, Kizltyan, and Dogan (2004) found
at least one other psychiatric diagnosis in 89.5% of a group of individuals with a diagnosis of
conversion disorder.

13.1.4 Factitious Disorder

This disorder is characterised by the individual falsifying medical or psychological symptoms in
themselves or others. The defining feature is that this falsification of evidence is intentionally deceptive.
Ways of falsifying symptoms can include exaggeration of symptoms, fabrication, simulation, and
induction. Examples include claiming symptoms of depression following the death of a loved one when
this event did not happen, deceptively reporting neurological symptoms such as dizziness or blacking
out, and manipulation of laboratory tests (e.g., by adding blood to urine) or ingesting a substance (such
as insulin) (Table 13.4). An alternative diagnosis is factitious disorder imposed on another, where the
individual is a perpetrator who falsifies medical or psychological symptoms in another (with the victims
of this action often being children). Focus Point 13.1 provides a detailed example of factitious disorder
imposed on another, previously known as Munchhausen's by Proxy. It is still unclear why individuals
take these deceptive actions, although it may well be to gain attention to themselves or to gain praise for
their actions in the case of factitious disorder imposed on another.

SELF‐TEST QUESTIONS
What are the main diagnostic criteria for somatic symptom disorder?
What are the main psychiatric disorders that tend to be comorbid with somatic symptom
disorders?
Can you describe the main diagnostic criteria for illness anxiety disorder, and by what
other name was this disorder previously known?
Can you describe the main diagnostic criteria for conversion disorder together with its
main features?
How do cultural factors affect the prevalence rate and manifestation of conversion
disorder symptoms?
What is factitious disorder and what are its main diagnostic criteria?
How does factitious disorder imposed by another differ from basic factitious disorder?
SECTION SUMMARY

13.1 THE DIAGNOSIS AND CHARACTERISTICS OF SOMATIC

SYMPTOM DISORDERS
Somatic symptom disorder is a pattern of recurring multiple, clinically significant somatic
symptoms that require medical treatment.
Individuals diagnosed with somatisation disorder are usually major users of health care
services.
Somatic symptom disorder is closely associated with other mental health problems such as
anxiety disorders and major depression.
Illness anxiety disorder (formerly known as hypochondriasis) is a preoccupation with fears of
having or contracting a serious illness based on a misinterpretation of bodily signs or
symptoms.
Individuals with hypochondriasis will regularly read about medical conditions and consult
medical opinion on a regular basis. They will also be entirely unconvinced by reassurances
that they do not have a medical illness.
The basic feature of conversion disorder is the presence of symptoms or deficits affecting
voluntary motor or sensory function.
It is estimated that between 13% and 30% of individuals diagnosed with conversion
disorder have later been found to have some neurological deficit.
Conversion symptoms usually develop in adolescence and severity of symptoms can be
linked to the severity of life stressors.
The lifetime prevalence rate for conversion disorder is less than 1%.
There are significant cultural differences in the way that conversion disorder symptoms
manifest themselves.
Conversion disorder is frequently comorbid with anxiety disorders, major depression,
dissociative disorders, substance abuse, and personality disorders.
Factitious disorder is characterised by the individual falsifying medical or psychological
symptoms in themselves or others.
Factitious disorder imposed by another is where the individual is a perpetrator who falsifies
symptoms in another.
TABLE 13.4 Summary: DSM‐5 diagnostic criteria for factitious disorder

Fabrication of physical or physiological symptoms or sign of injury or disease

Presenting oneself as ill or injured to others
The deception is evident despite a lack of obvious reward
The behaviour is not better explained by another mental disorder, such as delusional disorder
Factitious disorder imposed on another
Fabrication of physical or physiological symptoms or sign of injury or disease in another
Presenting another as ill or injured to others
The deception is evident despite a lack of obvious reward
The behaviour is not better explained by another mental disorder, such as delusional disorder
Note: In factitious disorder imposed on another it is the perpetrator, not the victim, who receives the
diagnosis

13.2 THE AETIOLOGY OF SOMATIC SYMPTOM DISORDERS

The most traditional explanations of somatic symptom disorders have been couched in psychodynamic
terms—primarily because some of Freud's most influential writings concerned hysteria and the causes
of unexplained physical symptoms. However, since that time a number of different approaches to
explaining somatic symptom disorders have developed, including learning accounts and cognitive
accounts. Nevertheless, regardless of how the theorist approaches the aetiology of somatic symptom
disorders, explanations of these disorders must address certain important questions: (a) are physical
symptoms a manifestation of underlying psychological conflict and stress? (b) are physical symptoms
generated in an involuntary fashion? (c) what is the role of life stress and childhood maltreatment in the
development of somatoform disorders? and (d) how do sufferers acquire the biased thinking and
dysfunctional beliefs about health that help to maintain many of the symptoms of these disorders?

13.2.1 Psychodynamic Interpretations

Some of Freud's most famous writings were on the subject of hysteria and how inner conflict, repressed
emotions, and life stress could be manifested in somatic symptoms. The basic psychodynamic view of
somatic symptom disorders is a conflict‐resolution one in which distressing memories, inner conflict,
anxiety, and unacceptable thoughts are repressed in consciousness but outwardly expressed as somatic
symptoms. For example, Freud believed that somatic symptoms such as those found in conversion
disorder (then known as hysteria) were associated with distressing memories of childhood seduction.
These might be actual experiences of childhood abuse or simply imagined as fantasies during the
Oedipal period of development. When these memories are reawakened during puberty this causes
intense anxiety and conflict resulting in somatic symptoms and repression of these memories. The
somatic symptoms served the purpose of helping to suppress these memories and to relieve anxiety, and
this was consistent with the fact that most individuals with conversion disorder exhibited a calm
philosophical attitude to their disability (“la belle indifference”), suggesting that it was a state in which
they experienced some relief from stress and conflict.
 conflict‐resolution Psychodynamic interpretations of somatic symptom disorders in which
distressing memories, inner conflict, anxiety and unacceptable thoughts are repressed in
consciousness but outwardly expressed as somatic symptoms

Underlying sexual conflict was also seen by psychodynamic theorists as being an important contributor
to other disorders such as somatic symptom disorder and illness anxiety disorder. Freud believed that
repressed sexual energy was often turned inward on the self, transforming it into physical symptoms that
created physical pain or were interpreted as indictors of illness and disease. Indeed, psychodynamic
theorists often view those suffering from somatic symptom disorders as regressing to the state of a sick
child, unconsciously seeking attention and relief from symptoms and responsibilities, and thus reducing
experienced anxiety (Kanaan & Craig, 2019; Kellner, 1990; Kuechenoff, 2002; Phillips 1996).
These psychodynamic accounts appear to make intuitive sense in that those who develop somatic
symptom disorders often appear to have either a history of conflict, stress, and abuse or have recently
experienced an important life stressor (Bowman & Markand, 1996; Roelofs et al., 2005), and an
important aspect of the psychodynamic conflict‐resolution model is that the physical symptoms either
cause relief from anxiety or from having to deal with current conflicts and stress (Temple, 2002).
Consistent with this view, some studies of conversion disorder have shown that onset of the disorder is
preceded by stress or trauma events and that the nature of these events are such that their negative or
distressing effects can be ameliorated by becoming ill (Nicholson et al., 2016). However, in contrast,
other studies have found that as few as 13% of conversion disorder sufferers can point to a traumatic
event preceding symptom onset (Kranick et al., 2011), although this latter study defined traumatic
events as ‘life threatening’ and most life stressors that may precipitate conversion disorder may not be
life threatening at all but just difficult for the individual to cope with (e.g., the break‐up of a relationship
or the birth of a child) (Kanaan & Craig, 2019). Nevertheless, disorders such as somatic symptom
disorder and illness anxiety disorder appear to involve high levels of anxiety (Noyes et al., 1994), and a
sizable minority of those with conversion disorder also fail to exhibit the calming effects of “la belle
indifference” (Gureje et al., 1997). Thus, there is some evidence that somatisation may be an attempt to
alleviate the pain and distress of a recent negative life event, but it is also clear that for many individuals
suffering somatisation symptoms, these symptoms themselves are distressing.

13.2.2 Consciousness and Behaviour

One important feature of some somatic symptom disorders, such as conversion disorder and somatic
symptom disorder, is that the sufferer appears able to generate physical symptoms or deficits (e.g.,
medical symptoms, blindness, etc.) in an involuntary fashion. That is, there is a dissociation between the
individual's behaviour and their awareness of that behaviour. For example, in conversion disorder the
sufferer appears genuinely unable to experience certain sensory input (e.g., when exhibiting blindness or
loss of feeling). However, studies suggest that these individuals can experience the sensory input at some
level of processing, but are consciously unaware of it. For example, Theodor and Mandelcorn (1973)
describe a study undertaken with a 16‐year‐old girl who complained of a loss of peripheral vision with
no underlying neurological explanation for this. In their study they presented a buzzer followed by a
bright visual stimulus to either the girl's central or peripheral visual field on a percentage of the trials.
The girl's task was to report whether a visual stimulus had followed the buzzer or not. They found that
the girl always correctly reported when the buzzer was followed by a stimulus to the central visual field.
However, she was only 30% correct when reporting a visual stimulus to the peripheral visual field.
Theodor and Mendelcorn argued that a person who truly had no peripheral vision would have reported
a visual stimulus at chance level—that is, on 50% of the trials. The girl with a somatic symptom
disorder in fact performed significantly worse than this—suggesting that at some level of consciousness
she was aware of the peripheral visual stimulus but was suppressing reporting it. In a similar study,
Zimmerman and Grosz (1966) also found that an individual with hysterical blindness performed a visual
task at significantly below chance level when a truly blind individual should be performing at chance
level. They also found that when visual stimuli were presented in a nonrandom predictable sequence,
their patient still performed at well below chance level—even a truly blind person would have
performed above chance on this task. These studies indicate that the person with, for example,
conversion disorder can discriminate the relevant incoming sensory information at some level—even if
they use that information in a way that results in them performing significantly below what would be
expected of someone who was blind! At first sight, evidence such as this suggests that the sufferer may
simply be faking the symptoms and trying to behave in ways that are consistent with these symptoms.
However, if it is faking, then the individual has taken great pains to be consistent in this behaviour often
over long periods of time and in difficult situations.
A very early explanation of these types of symptoms was proposed by Janet (1907) who suggested that
patients suffering from ‘hysteria’ experience a spontaneous narrowing of attention after being exposed
to trauma. This attentional narrowing limits the number of sensory channels that can be attended to
and leads to the loss of voluntary control over neglected channels. This results in the patient being
rendered anesthetic for any information coming in to the unattended modality even though it is still
processed outside of conscious awareness. As a result the patient may be unable to consciously access
information from these channels and experience blindness or paralysis, depending on the sensory
channel that has been neglected. A similar explanation of these anomalous findings is provided by
Oakley (1999). He draws attention to the many similarities between the behaviour of the individual with
conversion disorder or somatic symptom disorder and the effects of hypnosis. First, many of the
symptoms of conversion disorder are similar to physical states that can be easily established by hypnosis
(e.g., blindness, paralysis, etc.), and they also display a degree of involuntariness. That is, both the
conversion disorder patient and the person under hypnosis regularly report that they have no voluntary
control over a movement or a sensation (e.g., they may be unable to raise their arm). In drawing these
two areas together, Oakley (1999) has proposed that similar mechanisms could be responsible for both
conversion/somatisation symptoms and behaviour under hypnosis. So an action or incoming sensory
information may often be processed at a range of different levels of mental functioning but for some
reason may not be selected for conscious processing (presumably one of the last stages of this process).
Under hypnosis this last stage of processing can often be prevented by suggestions from an external
source (such as the hypnotist), and it will appear to the individual that they have no control over their
actions or their perceptions. Oakley proposes a similar effect in conversion disorder in which some
presumably internal processes have prevented sensory information from being analysed by conscious
awareness. Because the sensory information is processed at lower mental levels, this explains why the
individual with hysterical blindness can respond in ways that suggest visual information is being received
(e.g., by performing at significantly below chance on a visual recognition task) but is not consciously
aware that visual stimuli are being perceived and responded to. As appealing as this explanation is, it still
begs the question of how and why sensory information is blocked from conscious awareness in
individuals with conversion disorder. This aspect of this view still needs to be fully explored and
understood, and impairment of consciousness in conversion disorder might be the result of neurological
factors such as those found in psychogenic nonepileptic seizures when sufferers lose awareness or the
ability to react (Roberts & Reuber, 2014), or may be related to dissociative disorders such as dissociative
amnesia and depersonalisation disorder (see Chapter 14) which are often comorbid with conversion
disorder (Yayla et al., 2015).

hypnosis A therapeutic technique in which the client is placed in a trance

13.2.3 Risk Factors for Somatic Symptom Disorders

A significant factor in the history of most somatic symptom disorders is either a history of trauma or
abuse, or significant periods of stress and anxiety, and these appear to be important risk factors in
developing a somatic symptom disorder. For example, a history of childhood trauma appears to increase
vulnerability to conversion disorder (Bowman & Markand, 1996), and high levels of negative life events
in the year prior to onset have been found in individuals with globus pharyngis (a form of conversion
disorder in which the sufferer experiences a sensation of a lump in the throat) (Harris, Deary, & Wilson,
1996). Individuals with somatic symptom disorder tend to report histories of physical and sexual abuse
(Holder‐Perkins & Wise, 2001), as do many of those with illness anxiety disorder (Salmon &
Calderbank, 1996). In addition, many somatic symptom disorders develop following exposure to acute
stressors, such as recent loss (Van Ommeren et al., 2001), relationship difficulties (Craig, 2001), and
exposure to dead bodies following military combat (Labbate, Cardena, Dimitreva, Roy, & Engel, 1998).
Nevertheless, we must be cautious about what these findings mean in the aetiology of somatic symptom
disorders. First, not everyone who develops a somatic symptom disorders reports having had high levels
of childhood abuse or neglect nor having had a significant number of negative life events generally (e.g.
Sar et al., 2004), so such experiences are not a necessary condition for developing a somatic symptom
disorder. Second, the actual levels of stress reported by individuals with somatic symptom disorders are
not necessarily significantly higher than those reported by individuals with other psychopathologies, so
stress levels per se do not differentially predict the development of a somatic symptom disorders (Roelofs
et al., 2005). Third, high levels of childhood trauma and negative life events can be found in the
histories of a wide range of psychopathologies (e.g., personality disorders, eating disorders, anxiety
disorders, etc.), so why should someone who has this kind of traumatic history develop a somatic
symptom disorder rather than any of these others (although it must be admitted that somatoform
disorders are regularly comorbid with many other psychiatric disorders)? Some theories do specify a
central role for stress and early negative experiences in the development of somatic symptom disorders,
and the conflict‐resolution model adopted by many psychodynamic theorists is one example (see the
Psychodynamic Interpretations section). However, the role of stress and childhood trauma in other
theories is often underdeveloped, and this is an aspect of our understanding of the aetiology of somatic
symptom disorders that needs to be explored.
There are also a number of familial risk factors that have been identified for somatic symptom
disorders, and these include parents with somatisation characteristics, having a significant other/relative
with an organic disease, psychopathology of close family members, a dysfunctional family climate, and
insecure attachment (Schulte & Petermann, 2011). However, these factors are also risk factors for the
development of many other psychiatric disorders and so are not specific to somatic symptom disorders
alone.
Somatic symptoms can also be found in the general population and, although at sub‐clinical levels in
many cases, these symptoms may be the precursors of full‐blown diagnosable somatic symptom
disorders. Factors associated with these symptoms in the general population include lack of social
support, adverse life events, loneliness, depression, generalised anxiety, panic symptoms, and social
phobia, all of which may act as risk factors for somatic symptom disorders (Beutel et al., 2019).

13.2.4 Learning Approaches

A number of theorists have suggested that somatic symptom disorders may develop because many of
the aspects of these disorders are learnt through specific types of experiences. For example, Craig et al.
(1993) have argued that many individuals learn to interpret emotional symptoms as indicative of
physical illness. This learning could occur in a number of ways. First, individuals suffering conversion
disorder, somatic symptom disorder, or illness anxiety disorder often report having had early childhood
experiences where close members of their family have experienced physical illness or somatic symptoms
(Iezzi et al., 2001), and so expressing any negative feelings (emotional or physical) may occur through
somatisation because of exposure to modelling by important family members. In support of this view,
Craig, Cox, and Klein (2002) compared the childhood histories of three groups of women—those with
somatic symptom disorder, those with a long‐term illness, or healthy controls. They found that those
with somatic symptom disorder were three times more likely than those in the other groups to have had
a parent with a serious physical illness.
A related view is that expressing symptoms of physical illness may be reinforced by parents. For
example, some parents may view all underlying problems (including psychological ones) as being
physical rather than emotional, and subtly encourage their children to report psychological problems in
physical terms (Latimer, 1981). In an insightful study, Craig et al. (2004) observed mothers playing with
their four‐ to eight‐year‐old children. Mothers who exhibited somatisation symptoms were less
emotionally expressive than control mothers during most play tasks. However, they were significantly
more responsive to their children when they played with medically related toys (e.g., a medical box). In
this way, mothers who already display somatisation symptoms may pass this predisposition on to their
children through the differential display of attention in medically‐related contexts.
Finally, early learning of the kind described above means that many individuals may learn to describe
emotional symptoms in physical terms and in extreme cases begin to adopt what is known as a sick
role. Adopting a sick role has a number of disadvantages—it means a loss of power and influence as
the individual relinquishes tasks and duties to others; it also involves a loss of pleasure—especially if an
individual becomes housebound or even bedridden because of their symptoms. However, Ullman &
Krasner (1975) have argued that adopting a sick role can have significant advantages and rewards in
terms of the attention the sufferer is likely to receive from others, and the absolving of responsibility can
be viewed as a way of opting out of having to directly deal with life stressors and conflicts. In this case,
adopting the sick role becomes a coping style for adult life. While this view is consistent with the fact
that somatising mothers may teach their children similar tendencies, adopting a sick role implies that the
individual is unable to cope with the normal rigours and challenges of daily life. Convincing evidence
that this is indeed the case still needs to be collected.

sick role Playing the role of being sick as defined by the society to which the individual
belongs.

Nevertheless, there does seem to be some reasonable evidence that children may learn somatising
attitudes from their parents in various ways, and this may provide a basis for the possible development
of somatic symptom disorders in later life.

13.2.5 Cognitive Factors

One important feature of most of the somatic symptom disorders is that the sufferer believes they have
physical deficits or symptoms that are significant and threatening, but in most cases there is little or no
medical justification for these beliefs. This strongly suggests that sufferers may have developed thinking
and information processing biases that lead them to believe they have medical symptoms when in fact
they do not. Such cognitive biases can take a number of forms. They may involve interpretation
biases, in which the individual interprets ambiguous bodily sensations as threatening and evidence for
a potential serious illness (Marcus et al., 2007). For example, when an individual with illness anxiety
disorder experiences a stomach pain they may interpret this catastrophically as a possible symptom of
stomach cancer, rather than, say, the result of eating something that was ‘off ’. This biased thinking then
gives rise to a range of consequences which are likely to reinforce the biased belief, including increased
fear and anxiety, preoccupation with similar symptoms, overestimating the probability that a symptom is
a sign of a disease, and reassurance seeking (Rief et al., 2006; Warwick, 1995) (see Figure 13.2). In a
similar vein, Barsky (1992) argued that patients with somatic symptom disorder have a bias towards
describing minor automatic bodily sensations in a catastrophic manner, which leads to a significantly
higher level of reported symptoms. In support of these views, Lim & Kim (2005) demonstrated that
individuals diagnosed with a somatoform disorder showed significant attentional interference effects for
physical threat words (e.g., injury, seizure, inflammation), suggesting that these individuals consciously
and selectively attended to physical‐symptom related cues. In addition, when given ambiguous health‐
related vignettes about illness and death, Haenen et al. (2000) found that individuals with illness anxiety
disorder were significantly more likely than controls to interpret these vignettes as serious and
threatening.
 interpretation biases Cognitive biases in which an individual interprets ambiguous events as
threatening and evidence for potential negative outcomes.

As well as interpretation biases, individuals with somatic symptom disorders also exhibit attentional
biases which lead to the processing of health‐relevant information, including increased attention to
bodily sensations and a limited ability to distract from illness‐signalling information (Marcus et al.,
2007; Warwick & Salkovskis, 1990). This attentional bias is also associated with hyperactivation in brain
regions such as the amygdala that are crucial for an arousal‐related fear response (Mier et al., 2017).
Recent studies also suggest that individuals with somatic symptom disorders may also have a memory
bias towards remembering and retrieving illness relevant material. This bias also appears to make it
difficult for somatic symptom disorder sufferers to suppress illness‐related material, which may be
rapidly retrieved from memory when thinking about potential symptoms or illnesses (Wingenfeld,
Terfehr, Meyer, Lowe, & Spitzer, 2013).
FIGURE 13.2 This cognitive model of illness anxiety disorder illustrates how physical symptoms or bodily sensations
evoke negative automatic thoughts about illness. These thoughts then trigger feelings of anxiety, which in turn trigger a range
of behavioural, cognitive, and mood reactions that reinforce biased beliefs and illness anxiety symptoms.
After Warwick (1995).

memory bias Individuals with many psychopathologies may have a bias towards
remembering and retrieving illness relevant material.

One interesting feature of individuals with illness anxiety disorder and somatic symptom disorder is
their tendency to reject diagnoses that disagree with their own beliefs about their health and to seek
further opinions—presumably in the belief that someone will agree with their own view. Smeets, de
Jong, and Mayer (2000) found that individuals with illness anxiety disorder possessed a reasoning bias
that supported this ‘doctor shopping’. They would actively seek out and accept information that agreed
with their own view of their medical state but would ignore or reject arguments against their own
beliefs. This process will inevitably maintain hypochondriacal thinking and generalised anxiety about
health issues. In addition, individuals with somatic symptom disorders show greater attention allocation
to words and phrases that support their own beliefs about their health than those that don't (Witthöft,
Rist, & Bailer, 2009)—a process that is likely to reinforce existing dysfunctional beliefs.

reasoning bias The tendency of individuals with hypochondriasis to reject diagnoses that
disagree with their own beliefs about their health and to seek further opinions – presumably in
the belief that someone will agree with their view.

The preceding evidence strongly suggests that many somatic symptom disorders are maintained by
cognitive factors that take the form of (a) attentional biases to physical threats, (b) biases towards
interpreting body sensations and symptoms as threatening, (c) reasoning biases that maintain beliefs
about illness and being ill, (d) memory biases that facilitate the retrieval of illness relevant material, and
(e) catastrophising of symptoms. However, none of these accounts explain how the individual with a
somatic symptom disorder acquires these thinking and information processing biases. Some insight into
how these biases might develop has been provided by Brown (2004). Brown argues that “rogue
representations” are developed by a range of experiences, and these representations provide
inappropriate templates by which information is selected and interpreted. Rogue representations can be
created by experiences that include (a) a history of physical illness that causes a tendency to interpret
any sensation as a symptom of illness, (b) a history of experiencing emotional states that have strong
physical manifestations (e.g., anxiety is associated with shaking, palpitations, nausea, muscle tension,
chest pain, dizziness, etc.); such experiences might arise from childhood trauma and maltreatment and
result in a tendency to interpret such symptoms fearfully, and (c) exposure to physical illness in others
(e.g., abnormal levels of illness in the family) which creates a memory template by which one's own
physical sensations are interpreted. In support of this account, there is good evidence to suggest that
individuals with somatic symptom disorders do experience these factors with significantly greater
frequency than nonsufferers (Holder‐Perkins & Wise, 2001; Hotopf, Mayou, Wadsworth, & Wessely,
1999; Schrag, Brown, & Trimble, 2004; Iezzi, Duckworth, & Adams, 2001).

rogue representations In somatic symptom disorders, representations that provide

inappropriate templates by which information about body shape and health are selected and
interpreted.

For an integrated view of cognitive‐behavioural models of somatic symptom disorders, the review by
Witthöft and Hiller (2010) is recommended.

13.2.6 Sociocultural Approaches

There is some evidence that sociocultural factors can influence both the prevalence of somatic symptom
disorders and the nature of the symptoms exhibited in specific disorders. Being ill involves playing a
social role that is often shaped by the society to which the individual belongs (Fox, 1989). This role is
known as the sick role, and even across societies it is defined in ways that may help individuals to cope
with psychological distress and conflict. For example, the sick role in most societies means that (a) the
sick person is exempt from the normal social roles that the person has for the duration of the illness, and
(b) the sick person is often seen as not responsible for their illness (Parsons, 1951). Thus, playing the sick
role can provide relief from the stresses and strains of everyday living. However, the likelihood of an
individual adopting the sick role as a way of coping with stress and conflict will depend on attitudes
towards unexplained somatic symptoms in different cultures. In some cultures, expressing physical pain
is an accepted way of communicating psychological distress, and rates of somatic symptom disorders
tend to be higher in such cultures—for example, in Latin countries and amongst American Hispanic
women (Escobar, Burnam, Karno, Forsythe, & Golding, 1987; Tomasson, Kent, & Coryell, 1991).
Furthermore, members of non‐Western cultures tend to exhibit higher levels of somatic awareness but
lower levels of interoceptive accuracy, and this heightened somatic awareness among non‐Western
cultures is linked to greater emphasis on somatic symptoms in a wide array of psychopathologies
(mainly anxiety and depression) (Ma‐Kellams, 2014). In non‐Western communities, individuals may be
encouraged to somatise psychological distress in a way that allows them to more readily adopt a sick role
(Goldberg & Bridges, 1988). In addition to cultural factors that affect the somatisation of psychological
distress, socio‐economic standards also influence prevalence rates. Individuals who live in rural areas,
are less well educated, and have a poorer standard of living are more likely to exhibit somatic symptom
disorders (Maldonado & Spiegel, 2003)—possibly because in such socio‐economic groups the expression
of psychological distress is less acceptable and so psychological symptoms are expressed as physical
illness.
One final social factor can be identified in the aetiology of conversion disorder. Physical symptoms
associated with conversion disorder can often be ‘contagious’ and affect a number of people within a
single social setting or social group. This is similar to the physical symptoms of hysteria that were often
reported in young women at pop concerts during the 1960s and 1970s. Examples of contagion appear
to occur following an acute period of stress within a closely knit social group, where all those involved
display very similar unexplained somatisation symptoms. A recent example of this was reported by
Cassady et al. (2005) within an Amish community in the US. Four of them developed motor deficits
(inability to hold up their heads) and weight loss symptoms following a period of acute stress within the
closely knit Amish community. Examples of ‘contagious hysteria’ such as this continue to be reported,
but as yet there is no convincing explanation for these multiple cases of somatic symptom disorders
(Focus Point 13.2).

13.2.7 Biological Factors

Because somatic symptom disorders involve what are apparently physical symptoms, it is reasonable to
ask whether there are any underlying biological causes for these disorders. We know that (a) a certain
percentage of those with conversion disorder and somatic symptom disorder do have medical conditions
that could contribute to their psychopathology (Holder‐Perkins & Wise, 2001; Maldonado & Spiegel,
2003), and (b) many who develop somatic symptom disorders have a history of physical illness in their
family (Hotopf et al. 1999), and both of these factors give grounds for exploring the role of biological
factors.
Torgersen (1986) investigated a possible genetic component to somatic symptom disorders by
investigating the presence of somatic symptom disorder in monozygotic (MZ) and dizygotic (DZ) twins.
He found that MZ twins had a higher concordance rate for somatic symptom disorders than DZ twins,
which is consistent with there being a genetic component to these disorders, but the sample he used was
particularly small. Some studies have investigated inherited aspects of somatic symptom disorder using
adoption studies, but these have only served to further confuse the role of inheritance in somatic
symptom disorders. Bohman, Cloninger, von Knorring, and Sigvardsson (1984) and Cloninger,
Sigvardsson, von Knorring, and Bohman (1984) traced the histories of the biological and adoptive
parents of 859 women with somatic symptom disorder. However, they rather surprisingly found that the
biological fathers of these women had significantly higher levels of alcoholism or violent crime than
would be expected by chance, suggesting a biological or genetic link between antisocial behaviour and
somatic symptom disorder!
More recently there has been research suggesting that genetic variation in two neuroendocrine systems,
the serotoninergic system and the hypothalamic‐pituitary‐adrenal (HPA) axis, are associated with
medically unexplained somatic symptoms, and the genes identified may be implicated in susceptibility to
somatisation and pain (Holliday et al., 2010). Consistent with this is that functional magnetic resonance
imaging (fMRI) studies of the brains of individuals with a diagnosis of somatic symptom disorder show
abnormal changes in brain activity in areas such as the anterior cingulate cortex(ACC) (Li et al.,
2016), and heightened activity in the ACC is associated with a greater propensity for somatic symptoms
and experiencing more intense pain (Landgrebe et al., 2008). Taken together, these results suggest that
genetic factors may contribute to a predisposition to somatisation and pain that is mediated by those
regions of the brain relevant to detecting bodily sensations and mediating pain perception (Boeckle,
Schrimpf, Liegl, & Pieh, 2016; Bourke, Langford, & White, 2015).

FOCUS POINT 13.2 ‘HYSTERIA’

The mystery of screaming schoolgirls in Malaysia

It was a quiet Friday morning in July 2019 when pandemonium broke out at a school in
Kelantan in northeast Malaysia. A 17‐year‐old female student was at the centre of the
outbreak. This is her account of what happened.
The assembly bells rang.
I was at my desk feeling sleepy when I felt a hard, sharp tap on my shoulder.
I turned round to see who it was and the room went dark.
Fear overtook me. I felt a sharp, splitting pain in my back and my head started spinning. I fell to the floor.
Before I knew it, I was looking into the ‘otherworld’. Scenes of blood, gore, and violence.
The scariest thing I saw was a face of pure evil.
It was haunting me, I couldn't escape. I opened my mouth and tried to scream but no sound came out.
I passed out.
This student's outburst triggered a spontaneous and immediate chain reaction in which students
throughout the school started screaming and running from their classrooms. One girl fainted
and others barricaded themselves into classrooms. By the end of the day up to 39 people were
 suffering physical symptoms as a result of this outbreak of ‘mass hysteria’.
‘Mass hysteria’ (sometimes called ‘mass psychogenic illness’) is the rapid spread of physical
symptoms amongst a large group of people. These symptoms are very similar to those
frequently found in panic disorder (see Chapter 6) such as hyperventilation, rapid heartbeat,
sweating, headaches, abdominal pain, chest pains, dizziness, trembling, and feelings of nausea.
These symptoms originate from an arousal‐based nervous system disturbance involving
excitation, loss or alteration of function, and these physical complaints are exhibited
unconsciously and have no obvious corresponding organic origin—and these latter effects are
very similar to those found in somatic symptom disorders (Bartholomew & Wessely, 2002). Such
symptoms are associated with strong feelings of fear and anxiety which help to spread the
condition amongst members of a cohesive group, in this case schoolchildren.
‘Mass hysteria’ is a phenomenon that is not well understood, and it is not listed as a specific
psychopathology in DSM‐5. But while the symptoms experienced are real, there is no obvious
biomedical explanation for them.
The causes of ‘mass hysteria’ appear to lie in psychological and social factors, with deeply
religious and spiritual communities being especially vulnerable to these phenomena, especially
where communities believe in the powers of traditional folklore and the supernatural.
Predisposing factors that have been noted include intense stress within the community affected
(in this example, the students were in the middle of a stressful exam period), conflicts, low
education status, lower socio‐economic status, being a minority group, and history of abuse and
trauma (Haque et al., 2013; Swartz, Blazer, George, & Landerman, 1986; Tarafder et al.,
2016).
So, while many of the physical symptoms of ‘mass hysteria’ resemble autonomic arousal
responses typical of panic disorder, the phenomenon also has many characteristics in common
with somatic symptom disorders—especially the fact that these physical symptoms are
generated unconsciously and with no obvious biomedical explanation.
(Original news item published at https://www.bbc.co.uk/news/world‐asia‐48850490)

Finally, because of the startling symptoms of conversion disorder, such as paralysis and blindness, there
have been a number of studies that have investigated the role of the brain in this particular disorder.
Studies that have monitored the brain waves of individuals with conversion disorder suggest that
sensory information is reaching the appropriate areas of the brain, but they are not being registered in
consciousness. Marshall, Halligan, Fink, Wade, and Frackowiak (1997) carried out a positron emission
tomography (PET scan) study of a conversion disorder patient who had a paralysed left leg. They found
increased activation in the right orbitofrontal and anterior cingulated cortices, but an absence of activity
in the right primary cortex when the patient attempted to move the leg. This suggests that unexplained
paralysis involves some form of inhibition of primary motor activity by brain areas such as the
orbitofrontal and anterior cingulated cortices. Interestingly, this same pattern of excitation and
inhibition can be found in PET scans of individuals who have leg paralysis induced by hypnosis
(Halligan, Athwal, Oakley, & Frackowiak, 2000), suggesting that paralysis caused by conversion disorder
and hypnosis may reflect very similar underlying brain processes. These findings suggest that brain areas
that would normally instigate movement are being activated, but other areas of the brain that would not
be involved are being activated in order to inhibit the movement (e.g., orbitofrontal and anterior
cingulated cortices—see Research Methods in Clinical Psychology 13.1).

RESEARCH METHODS IN CLINICAL PSYCHOLOGY BOX 3.1

BRAIN IMAGING USING POSITRON EMISSION
TOMOGRAPHY
At least some psychopathologies are either associated with brain abnormalities or are caused by
unusual patterns of activation in the brain, and so understanding a particular disorder can be
helped significantly by procedures that allow the researcher to look directly at the structure and
functioning of the brain.
Positron emission tomography (commonly known as “PET scans”) involves injecting radioactive
molecules into the bloodstream. These molecules are then tracked by a scanner as they are
metabolised in the brain. Differences in metabolism rates in the brain are detected and show up
on a screen as different colour contrasts. Lighter and warmer colours denote areas when
metabolism (and therefore brain activity) is high. This technique is useful for detecting which
areas of the brain are active when the individual engages in a particular behaviour.
A study by Marshall et al. (1997) used PET scanning methods to try and identify the areas of
the brain that became active when an individual with conversion disorder attempted to move
their paralysed left leg. They found that when the patient tried to move their paralysed leg,
areas not normally associated with movement became active (the right cingulated cortex and
the right orbitofrontal cortex). They hypothesised that the activation of these areas somehow
actively inhibited or prevented leg movement. In a similar study, Halligan et al. (2000) used the
same PET procedure with a patient whose left leg had been paralysed by hypnosis. The
resulting scan (below) shows that exactly the same areas of the brain are activated when the
hypnotised individual tries to move their leg—suggesting that paralysis in both conversion
disorder and under hypnosis may be a result of movement being inhibited by the activation of
certain cortical brain areas.
13.2.8 Summary
Theories of the aetiology of somatic symptom disorders attempt to explain the development of these
disorders at a number of different levels. Common to many of these accounts are (a) the role of anxiety,
depression, and existing psychological conflict in generating somatoform symptoms; (b) the part that
playing the ‘sick role’ might have in coping with psychological stress and the way that this role might be
reinforced by family, associates, and medical practitioners; and (c) the role of biased thinking and
dysfunctional beliefs in maintaining beliefs about illness in those with somatic symptom disorders. The
startling and disabling nature of the symptoms in conversion disorder has meant that some theoretical
accounts have been addressed solely at the unique features of this disorder. These include accounts that
attempt to explain how sensory information is blocked from consciousness and how an individual may
lose voluntary control over their movements (e.g., brain scan studies, and comparisons of conversion
disorder with hypnosis). Finally, neurological studies indicate that there may be a modest genetic
predisposition for somatic symptom disorders that are mediated by brain regions involved in the
perception of bodily sensations and the experience of pain.
SELF‐TEST QUESTIONS
What are the main features of psychodynamic explanations of somatoform disorders, and
what is meant by a ‘conflict‐resolution’ view of somatoform symptoms?
Can you describe at least one experimental study showing that those suffering from
conversion disorder are aware of sensory stimuli at some level of processing?
Why is it helpful in understanding conversion disorder symptoms to make comparisons
between conversion disorder and behaviour under hypnosis?
What kinds of negative life events and stressors have been noted as risk factors in the
development of somatic symptom disorders?
What is the evidence that those suffering from somatic symptom disorders may have
‘learnt’ to adopt a ‘sick role’ during childhood?
What is the experimental evidence that individuals with somatic symptom disorders have
information processing biases?
What are ‘rogue representations’ and how might they affect thinking about illness
symptoms?
What is the ‘sick role’, and how might it help an individual cope with stress?
How have brain scanning technologies been used to throw light on the mechanisms
underlying conversion disorder symptoms?
SECTION SUMMARY

13.2 THE AETIOLOGY OF SOMATIC SYMPTOM DISORDERS

Psychodynamic interpretations of somatic symptom disorders is mainly a conflict‐
resolution one in which distressing memories, inner conflict, anxiety, and unacceptable
thoughts are repressed in consciousness but outwardly expressed as somatic symptoms.
In disorders such as conversion disorder, there appears to be a dissociation between the
individual's behaviour and their awareness of that behaviour.
Studies suggest that in conversion disorder, sensory input is processed at some level but is
unavailable at the level of conscious awareness.
There are many similarities between the behaviour of individuals with conversion disorder
and the effects of hypnosis, suggesting that similar mechanisms may be responsible for
both.
Risk factors in the history of many somatic symptom disorders are a history of trauma or
maltreatment, significant periods of stress and anxiety, and a range of familial risk factors.
Some learning accounts of somatic symptom disorders suggest that expressing symptoms of
physical illness may be reinforced during childhood by parents or carers.
Many individuals with somatic symptom disorders may have learnt to adopt a ‘sick role’
which may be a form of coping with life stressors.
Most of the somatic symptom disorders are characterised by cognitive and information
processing biases, including (a) interpretation biases, (b) attentional biases, (c) reasoning
biases, (d) memory biases, (e) catastrophising of symptoms, and (f) the development of
inappropriate `rogue representations’ which maintain the dysfunctional thinking that
maintains somatoform symptoms.
Sociocultural factors can influence both the prevalence of somatic symptom disorders and the
nature of the symptoms exhibited.
Physical symptoms associated with conversion disorder can often be ‘contagious’ and affect
a number of people within a single social setting or social group (sometimes known as
‘hysteria’).
Both twin and adoption studies have provided only indirect evidence for a genetic
component to somatoform disorders.
Studies indicate that there may be a modest genetic predisposition for somatic symptom
disorders that are mediated by brain regions involved in the perception of bodily
sensations and the experience of pain (e.g., the anterior cingulate cortex).
PET scans suggest that increased activation in some areas of the cortex may inhibit the
movement of ‘paralysed’ limbs in individuals with conversion disorder. A similar effect can
be found in individuals whose limbs are paralysed by hypnosis.
13.3 THE TREATMENT OF SOMATIC SYMPTOM DISORDERS
One of the main problems in treating somatic symptom disorders is that they manifest as physical or
medical symptoms, and thus a sufferer will initially undertake a lengthy period of medical treatment in
order to discover whether there are any underlying physical causes for their symptoms. This not only
allows symptoms to become entrenched before psychological therapy is attempted, but may also
contribute to the resistance of sufferers to psychological therapy. For example, many sufferers of
disorders such as somatic symptom disorders, illness anxiety disorder and conversion disorder frequently
deny they have a psychological problem, and continue to search for a medical ‘solution’ to their
symptoms. This denial of an underlying psychological cause can make treatment problematic.
Second, we have already noted that somatic symptom disorders are highly comorbid with other
disorders such as anxiety and depression. This raises a ‘chicken and egg’ question about which
symptoms come first. For instance, many people who are anxious and depressed come to have concerns
about their physical health as a result of their anxiety and depression (Noyes et al., 1994) and it is often
the case that treating the anxiety or depression will significantly reduce illness symptoms and worries
(Smith, 1992). In addition, somatic symptom disorders, illness anxiety disorder, and somatic symptom
disorder are often comorbid with obsessive‐convulsive disorder (OCD), and as we shall see later in this
section, treatments for OCD are also successful in treating the symptoms of these somatoform problems
(Phillips, 1996; Rosen, 1996).
This section now considers the types of treatments that are often used with somatic symptom disorders.

13.3.1 Psychodynamic Therapy

In the section on aetiology we noted that psychodynamic accounts of somatic symptom disorders take a
‘conflict‐resolution’ view of these disorders in which inner conflict, anxiety, and distressing memories are
repressed in consciousness and outwardly expressed as somatic symptoms. Psychodynamic therapy
therefore focuses on procedures designed to bring these repressed thoughts and memories into
consciousness where they can be effectively dealt with. This will in turn alleviate the somatic symptoms
that are a consequence of repression. Nevertheless, somatic symptoms are often quite resistant to a
psychodynamic approach—not least because the client may continue to believe that they have a physical
and not a psychological problem. In a study following‐up the progress of individuals with somatic
symptom disorders, Kent et al. (1995) found that 63% of conversion patients and 92% of somatisation
patients still met the diagnostic criteria for these disorders 4 years after initial diagnosis. However, meta‐
analyses have indicated that psychodynamic therapy for somatoform disorders is (a) more effective than
no treatment or treatment as usual, and (b) is likely to be more successful the greater the competence of
the therapist and his/her ability to form a therapeutic alliance with the client (Leichsenring, 2005).

Psychodynamic therapy Therapeutic approach that focuses on procedures designed to

bring repressed thoughts and memories into consciousness where they can be effectively dealt
with.

13.3.2 Behaviour Therapy

Many somatic symptom disorders involve some learning and behavioural‐based components that can be
treated by the use of the learning principles implicit in behaviour therapy. Two prominent examples of
such components include (a) the reinforcing function of attention given to individuals (e.g., by family
members or medical professionals) which will maintain their ‘illness’ behaviours (such as staying away
from work or complaining about pain), and (b) continuous checking for physical signs of illness or
deformity, which are prominent in illness anxiety disorder and somatic symptom disorder.
In the case of the former, Liebson (1967) reports an intervention that attempted to change the
reinforcement contingencies controlling the illness behaviour of a client who had given up his job
because of pain and weakness in his legs. Liebson persuaded the client's family to stop giving him
attention for illness‐related behaviours such as being inactive at home or complaining of pain. In
addition, the therapist arranged for him to get a pay rise if he went back to work. This approach makes
the reinforcement contingencies more functional by providing motivation to work and removing any
incentive to feel ill or incapacitated. Similar approaches can be used to extinguish reassurance seeking
behaviour in individuals with illness anxiety disorder. This type of programme attempts to minimise the
anxiety relief that clients get from reassurance seeking from the therapist, friends, and family. It can also
be supplemented by coping skills training, in which the client receives training and advice on how to
cope with anxiety and by training in the skills required to use in social or work settings. Also useful are
relaxation training and behavioural techniques designed to reduce worrying. This form of
behavioural stress management has been found to be significantly more effective than no
treatment control conditions (Clark et al., 1998), and follow‐up studies suggest that clients treated by
these procedures were still symptom free 5 years after treatment (Warwick & Marks, 1988).

behavioural stress management Behavioural techniques designed to reduce worrying and

increase relaxation.

13.3.3 Cognitive Behaviour Therapy

As we saw in the previous section on aetiology, cognitive factors appear to play an important role in the
acquisition and maintenance of somatic symptom disorders. Sufferers appear to acquire interpretation
biases (in which they view ambiguous stimuli as evidence of illness or physical problems), they possess
reasoning biases in which they tend to accept only information that is consistent with their illness beliefs,
they possess negative thought patterns that lead to the catastrophising of physical symptoms into beliefs
about full‐blown illness, and they possess a set of underlying beliefs about their disorder that help to
support their symptoms (e.g., the illness anxiety disorder sufferer may hold dysfunctional beliefs that all
physical sensations are indicators of impending illness). Such cognitive factors appear to play an
important role in most somatic symptom disorders. This being the case, cognitive behaviour
therapy(CBT) seems particularly well suited to treating these dysfunctional beliefs and thought
patterns.
 CASE HISTORY 13.1 ILLNESS ANXIETY DISORDER

A is a 32‐year‐old married engineer. He developed an acute urticarial rash, consisting of typical

eruptions of intensely itchy weals surrounded by red areas. (Urticaria may occur as a sensitivity
response to certain foods or as a reaction to drugs such as penicillin: However, in 50% of
chronic cases, a cause is never found. It is not associated with any malignant condition.) His rash
persisted for several months despite advice and treatment from his family doctor and
dermatologist. He had had a previous episode of urticaria, which was salicylate induced, but
apart from this has been completely healthy. Physical examination and investigations revealed
no significant abnormality, and a diagnosis of idiopathic urticaria was made. Despite this
reassurance, he became increasingly anxious that he had a serious underlying condition such as
leukaemia, and sought repeated consultations. His belief in the idea that he had leukaemia had
arisen in the first instance because a skin specialist had attempted to reassure him by giving him
some medical details. Specifically, this doctor had told him that the rash arose because his white
blood cells were attacking foreign matter in his blood cells. The patient had interpreted this as
meaning that there was something wrong with his white blood cells, signifying that he had
leukaemia. He inspected his rash frequently, read textbooks in an effort to discover ‘the real
cause’, and could talk of little else to his wife, family, and friends. Eventually, he became
suicidal, unable to work and was admitted psychiatrically.
From Salkovskis & Warwick, 1986, p. 598

Clinical Commentary: This patient exhibits many of the classic symptoms of an individual
with illness anxiety disorder (formerly known as hypochondriasis). He is obsessed with his symptoms by
continually checking his rash to see if it has grown and can talk of nothing else to friends and families.
The continual checking of symptoms and reassurance seeking from friends and family merely act to
maintain his anxiety. He also displays a number of cognitive biases typical of illness anxiety disorder.
He interprets his rash and the explanation given to him by a skin specialist in threatening terms—even
though there are many other explanations for them. He is also unmoved by reassurances from doctors that
his condition is not life‐threatening. He has a bias to dismiss evidence that is not consistent with his own
view of his symptoms and to accepting only evidence that is consistent with his view. Treatment consisted
of CBT (described more fully in the text) to deal with these cognitive biases.

CBT has proven to be particularly effective with those diagnosed with illness anxiety disorder (formerly
hypochondriasis). Such sufferers tend to interpret anything to do with bodily symptoms or health issues
as threatening (Smeets et al. 2000), and CBT can be used to challenge these dysfunctional beliefs and
replace them with more functional health beliefs. Case History 13.1 relates the symptoms of an illness
anxiety disorder patient who was convinced he had leukaemia after developing a harmless rash
(Salkovskis & Warwick, 1986). The treatment for this case involved the client being asked to test either
of two competing hypotheses—(a) that he was suffering from a life‐threatening illness, or (b) he had a
problem with anxiety which was maintained by repeated medical consultation and checking of his
symptoms. He was also asked to stop indulging in behaviours that might maintain his anxiety such as
checking to see if his rash had extended, continually seeking consultations with his doctor, and reading
medical textbooks. After around 30 days his symptoms had significantly reduced. He was no longer
regularly seeking medical reassurance about his symptoms and his self‐rated scores on measures of
health anxiety and illness beliefs had also significantly decreased.
Randomised control trials (RCTs) indicate that CBT for somatic symptom disorders is significantly
more effective at treating symptoms than normal medical care and is still effective at 6‐ and 12‐month
follow‐up (Barsky & Ahern, 2004), but RCTs suggest that it may not necessarily be more effective than
other treatments such as progressive muscle relaxation (Schröder, Heider, Zaby, & Göllner, 2004). Other
studies have begun to look at the feasibility of new third‐wave CBT interventions such as
mindfulness‐based cognitive therapy(MCBT) (see Chapter 4) in the treatment of somatic
symptom disorders, and initial results indicate the effects of mindfulness may be favourably comparable
to those of CBT (Fjorback et al., 2013), and it has a small to moderate effect in reducing pain, symptom
severity, depression, and anxiety associated with somatisation disorders (Lakhan & Schofield, 2013).

13.3.4 Drug Treatments

Throughout this chapter we have continually emphasised the important relationship between
somatoform disorders and anxiety and depression. Anxiety and depression are regularly comorbid with
conversion disorder (Sar et al., 2004), somatic symptom disorders (Gureje et al., 1997), and illness
anxiety disorder (Abramowitz & Braddock, 2006). This suggests that pharmacological interventions
effective with anxiety and depression may to some extent help to alleviate the symptoms of somatic
symptom disorders. A range of drug treatments have regularly been applied to somatic symptom
disorders, and these include tricyclic antidepressants (TCA), selective serotonin reuptake inhibitors
(SSRIs), serotonin and noradrenalin reuptake inhibitors (SNRIs), atypical antipsychotics, and herbal
medications (e.g., St. John's Wort) (Somashekar, Jainer, & Wuntakal, 2013). Antidepressants (TCAs,
SSRIs, and SNRIs) seem to be the most effective with somatic symptom disorders generally, but more
research is required to understand how these drugs have their therapeutic effects, what the longer‐term
effects of these drugs are, and there is also a need to develop drugs that will alleviate symptoms of
specific somatic symptoms disorders (Kleinstäuber et al., 2014).

13.3.5 Summary
A range of different treatments have been utilised with somatic symptom disorders. Traditionally,
psychodynamic therapy has been an important method of treating hysteria‐based disorders such as
conversion disorder, although the evidence for the medium‐term success of such interventions is
meagre. Both behaviour therapy and CBT have become important interventions over the past 20 years
with CBT being successfully used across a range of somatic symptom disorders to challenge
dysfunctional beliefs and to correct interpretational biases. Third‐wave CBT treatments, such as MCBT,
are being tested as possible new effective interventions for somatic symptom disorders, and finally, drug
treatments can also be effective in helping to alleviate some of the symptoms of somatic symptom
disorders, with the most effective being antidepressants.

SELF‐TEST QUESTIONS
What are the two main difficulties encountered when attempting to treat somatic symptom
disorders with psychological therapies?
Can you describe the main features of behavioural stress management procedures for
somatic symptom disorders?
How are CBT interventions used to treat somatic symptom disorders? What particular
aspects of somatic symptom disorders does CBT target?
What kinds of drug treatments are most effective in treating the symptoms of somatic
symptom disorders?
 SECTION SUMMARY

13.3 THE TREATMENT OF SOMATIC SYMPTOM DISORDERS

Somatic symptom disorders can be difficult to treat because the sufferer (a) believes their
problems have medical rather than psychological origins, and (b) usually has other
comorbid disorders that complicate treatment.
Psychodynamic therapy attempts to bring repressed thoughts and memories that may
cause somatic symptoms into consciousness where they can be effectively dealt with.
Behavioural stress management attempts to deal with somatic symptom disorders by eliminating
reassurance seeking from clients and supplementing this with coping skills training,
relaxation training, and techniques designed to reduce worrying.
CBT can be used across a range of somatic symptom disorders in order to challenge and
replace the dysfunctional beliefs and cognitive biases that maintain somatic symptoms.
Antidepressant drugs such as selective serotonin reuptake inhibitors (SSRIs) or tricyclic
antidepressants have been used to reduce the symptoms of many somatoform disorders,
although evidence for the long‐term effectiveness of this kind of treatment is still modest.

13.4 SOMATIC SYMPTOM DISORDERS REVIEWED

Somatic symptom disorders are a group of loosely associated disorders all of which can be
characterised by psychological problems manifesting as physical symptoms or as psychological distress
caused by physical symptoms or physical features. In many cases, the physical symptoms may have no
detectable medical cause, but neither are symptoms being faked by the sufferer. The causes of the
symptoms appear to lie in psychological factors such as life stress, anxiety, and a history of conflict or
maltreatment. In many cases individuals may have learnt through experience to adopt a ‘sick role’
which allows the person to opt out of stressful daily living, in others it is clear the sufferer has developed
a range of cognitive biases and dysfunctional beliefs that maintain a focus on their symptoms (e.g.,
illness anxiety disorder). There is evidence for a modest genetic component to somatic symptom
disorders, and this genetic predisposition may be mediated via brain areas that process bodily sensations
and pain experience. Interventions effective in addressing symptoms of somatic symptom disorders
include psychoanalysis, behaviour therapy, CBT, and antidepressant pharmacological treatments.
This book is accompanied by Student and Instructor companion
websites.
www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter References
Videos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
14
Dissociative Experiences

ROUTE MAP OF THE CHAPTER

This chapter describes the diagnosis and characteristics of three dissociative disorders, namely
dissociative amnesia, dissociative identity disorder (DID, formally multiple personality disorder),
and depersonalisation disorder. The aetiology section then discusses a range of theories of the
development of dissociative experiences including psychodynamic theory, cognitive models, and
the possible role that therapy can play in constructing dissociative symptoms. Finally, we discuss
treatments for dissociative experiences. These are relatively underdeveloped, but in particular
we discuss the use of psychoanalysis and hypnotherapy.

CHAPTER OUTLINE
14.1 THE DIAGNOSIS AND CHARACTERISTICS OF DISSOCIATIVE
DISORDERS
14.2 THE AETIOLOGY OF DISSOCIATIVE DISORDERS
14.3 THE TREATMENT OF DISSOCIATIVE DISORDERS
14.4 DISSOCIATIVE DISORDERS REVIEWED

LEARNING OUTCOMES
When you have completed this chapter, you should be able to:
1. Describe the main diagnostic criteria and symptom characteristics for the DSM‐5 listed
dissociative disorders and evaluate some of the issues concerning diagnosis, comorbidity,
and prevalence.
2. Describe and evaluate the main theories of the aetiology of dissociative disorders.
3. Evaluate the difficulties associated with treating dissociative experiences and describe at
least two types of therapies that have been used to treat dissociative experiences.
 This is DID … dissociative identity disorder … multiple personality disorder. We are a freak. I've started writing
this a million times … I don't know how to explain this. I know I hide. I don't want you to know me. I feel
shame about who I am … maybe that word defines me … shame. I lived through childhood abuses that one only
hears about … between the ages of 4 and 20. I think. I am not sure. I don't even know if I remember everything
yet. That's a part of the disorder … forgetting. The other part of the disorder is having 11 other people living
inside of me. Therapy is working. Most of the time I remember when they are out now … in the past they used to
come out and I wouldn't know about it unless they left a clue behind … lots of clues for me to see. Sometimes they
would hurt me … intentionally. Sometimes I would hear them screaming in my head or saying things to me …
sometimes derogatory, sometimes soothing … sometimes they would only cry. Sometimes I would find things that I
couldn't understand. Waking with a teddy bear beside me that I didn't remember. Buying toys and items that I
would never buy … losing money … people saying hello to me in the street who I didn't know. My spouse looks at
me and asks me who I am half the time. My spouse no longer knows me but still loves me and I reciprocate.
Without the support I couldn't make it.
Michael's Story

Introduction
Dissociative disorders generally are characterised by significant changes in an individual's sense of
identity, memory, perception, or consciousness, and these changes can either be gradual or sudden and
transient or chronic. Symptoms of these disorders include an inability to recall important personal or
life events (e.g., dissociative amnesia), a temporary loss or disruption of identity (e.g., dissociative identity
disorder), or significant feelings of depersonalisation in which the person feels that something about
themselves has been altered (depersonalisation disorder). Dissociative symptoms such as these are
often found in the aftermath of severe or prolonged traumatic experiences, such as childhood abuse,
natural disasters, or life‐threatening accidents. Because of this close association with trauma, dissociative
symptoms are often found in individuals with a diagnosis of post‐traumatic stress disorder
(PTSD), and the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM‐5) recognises this
relationship by placing dissociative disorders in the chapter next to trauma and stressor‐related disorders
(see Chapter 6). The diagnostic criteria for both PTSD and acute stress disorder contain reference to
dissociative symptoms such as amnesia, flashbacks, numbing, and depersonalisation. We discuss the
relationship between PTSD and dissociative symptoms later in this chapter (Section 14.1.1).
Michael's Story presented at the beginning of this chapter describes one particular form taken by
dissociative symptoms, and this is the presence of many distinct identities that each periodically take
control of his behaviour. These are often known as multiple personalities and identities, and the sufferer
often appears to be unaware that they present these different personalities to the world. This is known as
Dissociative identity disorder (DID) and represents a failure to integrate various aspects of
identity, consciousness, and memory. As we shall see, in many cases dissociative disorders develop
because the individual is attempting to cope with psychological distress and conflict that may be related
to earlier traumatic life experiences. Being able to adopt different personalities and repress specific
memories is viewed by many theorists as a way of coping with the anxiety and stress derived from these
earlier life experiences (e.g., Gleaves, 1996).

Dissociative identity disorder (DID) A dissociative disorder characterised by the

individual displaying two or more distinct identities or personality states that take turns to
control behaviour (formerly known as multiple personality disorder).

To a certain degree we all have dissociative experiences at some time during our lifetime, we will
sometimes have brief periods of memory loss, become confused about our identity, and sometimes just
feel ‘strange’ or depersonalised (Kihlstrom, 2001). A community sample study by Seedat, Stein, &
Forder (2003) found that 6% of respondents endorsed four to five lifetime dissociative symptoms, and
approximately one in three endorsed at least one lifetime symptom—suggesting that dissociative
symptoms are relatively common in the general population. Very often, these experiences will coincide
with periods of stress or trauma, and it is common for individuals who have experienced severe trauma
—such as combat troops and survivors of natural disasters or terrorist attacks—to experience these
kinds of dissociative symptoms (Kozaric‐Kovacic & Borovecki, 2005) (Photo 14.1). However, for some
individuals these symptoms either become so severe that they significantly disrupt their day‐to‐day
living, or they become chronic conditions rather than temporary responses to stress and cause significant
distress to the individual. In such circumstances, they may become diagnosable as a dissociative disorder.
In this chapter we discuss three dissociative disorders, namely (1) dissociative amnesia, (2) Dissociative
identity disorder (DID), and (3) depersonalisation disorder. Table 14.1 shows the prevalence and
comorbidity rates for dissociative disorders taken in an American community sample (Johnson, Cohen,
Kasen, & Brooks, 2006). These figures suggest a 12‐month prevalence rate of 9.1% for dissociative
disorders generally in individuals with a mean age of 33 years; however, prevalence rates can vary
considerably depending on the screening methods used in individual studies (Sar, 2011). Such disorders
are also comorbid in around one in three cases with anxiety disorders, eating disorders, mood disorders,
or personality disorders.

PHOTO 14.1 Cases of dissociative disorder increase significantly after war, natural disasters, or terrorist attacks when
individuals experience life‐threatening trauma well beyond that experienced during normal daily living, one such example
being the trauma experienced by those involved in the terrorist suicide bombing attack at the Ariana Grande concert in the
Manchester Arena in May 2017.

14.1 THE DIAGNOSIS AND CHARACTERISTICS OF DISSOCIATIVE

DISORDERS
14.1.1 Dissociative Amnesia
The main feature of this disorder is an inability to recall important personal information that is usually
of a stressful or traumatic nature. This memory loss cannot be explained by normal forgetfulness, nor is
it the result of any demonstrable damage to the brain. Dissociative amnesia normally manifests itself as
a retrospectively reported gap or series of gaps in the individual's ability to verbally recall aspects of
their life history, and these gaps are often related to traumatic or stressful experiences such as physical or
sexual abuse, involvement in a natural or human‐made disaster, being in an accident, experiencing
military combat or terrorist attacks, etc. Periods of amnesia may also extend to aspects of the
individual's own behaviour, such as memory loss for violent outbursts, suicide attempts, or self‐harm,
and the perpetrators of some violent crimes have often claimed that they cannot recall anything about
the event itself (and may use this in their legal defence against prosecution for violent crimes such as
murder see Focus Point 14.1 and Activity Box 14.1 on the book’s website).

Dissociative Amnesia An inability to recall important personal information that is usually of

a stressful or traumatic nature.

Dissociative amnesia is associated with several types of memory disturbances. Localised amnesia is
when the individual is unable to recall events that occurred during a specific time period (e.g., memory
loss for a period of 2 days following a serious car accident). Selective amnesia is when an individual
can recall some, but not all, of the events during a specific time period (e.g., a combat veteran may be
able to recall some events during a violent military encounter, but not others). The final three types of
dissociative amnesia are the least common but represent the most severe types of symptoms.
Generalised amnesia is a failure of recall that encompasses the person's entire life, and such
individuals may suddenly report to police stations or to hospitals as a result of this disorientation.
Continuous amnesia is the inability to recall events from a specific time up to and including the
present, and is also associated with the forgetting of new events as they occur. Systematic amnesia is
a loss of memory that relates to specific categories of information, such as family history (Table 14.2).

Localised amnesia When an individual is unable to recall events that occurred during a
specific time period (e.g. memory loss for a period of 2 days following a serious car accident).

Selective amnesia A memory disturbance where an individual can recall some, but not all, of
the events during a specific time period (e.g. a combat veteran may be able to recall some events
during a violent military encounter, but not others).

Generalised amnesia A failure of recall that encompasses the person’s entire life, and
such individuals may suddenly report to police stations or to hospitals as a result of this
disorientation.

Continuous amnesia A memory disturbance where there is an inability to recall events from
a specific time up to and including the present.

Systematic amnesia A memory disturbance where there is a loss of memory that relates to
specific categories of information, such as family history.
TABLE 14.1 Prevalence and comorbidity of dissociative disorders
From Johnson, Cohen, Kasen, & Brooks (2006).

Prevalence of dissociative disorders at mean age 33

Prevalence of disorder in the past year
Dissociative Males (N = 309) n (%) Females (N = 349) n (%) Total
disorder sample (N
= 658) n
(%)
Depersonalisation 2 (0.6%) 3 (0.9%) 5 (0.8%)
disorder
Dissociative amnesia 3 (1.0%) 9 (2.6%) 12 (1.8%)
Dissociative identity 5 (1.6%) 5 (1.4%) 10 (1.5%)
disorder (DID)
Dissociative disorder not 21 (6.8%) 15 (4.3%) 36 (5.5%)
otherwise specified
(DDNOS)
Any dissociative disorder 30 (9.7%) 30 (8.6%) 60 (9.1%)
Prevalence of dissociative disorders among
individuals with or without co‐occurring
psychopathologies in the past year at mean age 33
Prevalence of dissociative disorder in the past year
among individuals
Psychopathology Without co‐occurring With co‐occurring
psychopathology % (n/N) psychopathology %
(n/N)
Anxiety disorder 5.6% (30 of 533) 33.3% (25 of 75)
Eating disorder 7.0% (39 of 558) 32.0% (16 of 50)
Mood disorder 5.3% (28 of 527) 33.3% (27 of 81)
Personality disorder 3.9% (20 of 512) 36.5% (35 of 96)
Substance use disorder 7.6% (40 of 526) 18.3% (15 of 82)
Any anxiety, eating, 2.1% (8 of 373) 20.0% (47 of 235)
mood, personality, or
substance use disorder

FOCUS POINT 14.1 AMNESIA AND CRIME

In May 2002, the BBC News website reported how Jan Charlton was convicted of the
manslaughter of her boyfriend after hacking him to death with an axe. She claimed in court at
Leeds that she did not know she had killed him and ‘was in a daze, a total and utter daze’.
Professor Michael Kopelman, the psychiatrist who interviewed her, said she claimed she did not
remember the killing until the memory came back more than a month after the incident and he
told the court that amnesia in homicides was most common in ‘crimes of passion’.
Claims of crime‐related amnesia such as this are relatively common, and between 20% and
30% of individuals who commit violent crimes report no recollections of the event (Cima,
Merckelbach, Hollnack, & Knauer, 2003). Although post‐crime amnesia is most common for
violent crimes, it can also be found in those charged with nonviolent crimes such as fraud
(Kopelman, Green, Guinan, Lewis, & Stanhope, 1994). Amnesia may occur when the
individual is in a highly altered physiological state, either because of extreme rage or anger or
because they are under the influence of alcohol or other substances (Kopelman, 2002)
Nevertheless, there are good incentives for a criminal to fake symptoms of amnesia for a
criminal act, and it is estimated that about 20% of criminals who claim amnesia are feigning
their memory loss (Hopwood & Snell, 1933). So how can we identify true amnesiacs from those
 that are faking? One method is to use what is called Symptom Validity Testing (SVT). SVT is a
forced‐choice questionnaire in which defendants are asked a series of questions about their
crime. In each question, the defendant must choose between two equally plausible answers one
of which is correct and the other is incorrect. Examples include ‘The magazine that was stolen
was (1) Penthouse, or (2) Playboy’; ‘In the bar there is a huge mirror (1) yes or (2) no’. If the
individual is truly suffering amnesia they should perform at around chance level (i.e., get around
50% correct). However, studies suggest that individuals who are faking amnesia (and so do
know the correct answer), perform at levels significantly below chance (e.g., get less than 40%
correct) (Merckelbach, Hauer, & Rassin, 2002; Jelicic, Merckelbach, & van Bergen, 2004). This
is because they attempt to overcompensate for their knowledge of the crime by tended to
choose the wrong answer rather than choosing answers at random.

Dissociative amnesia can present in any age group from young children to adults—but it is difficult to
diagnose in young children because it can be confused with attentional and educational difficulties. An
episode may last for minutes or years, but symptoms can often be alleviated simply by removing the
individual from the circumstances or situation that may have caused trauma or stress (e.g., dissociative
amnesia may spontaneously remit when a soldier is removed from the locality of the battlefield).
Interestingly, individuals with dissociative amnesia are much less disturbed by their symptoms than we
might expect, and this may imply that the amnesia serves some kind of coping function that enables the
individual to deal with stress and trauma (Kihlstrom, 2001).
TABLE 14.2 Summary: DSM‐5 diagnostic criteria for dissociative amnesia

Unable to remember important personal information, usually relating to traumatic or stressful

occurrences, that is not in line with natural forgetting, causing significant distress or impairment
in important areas of functioning
The symptoms are not the result of the use of a substance or due to another neurological or
medical condition
The disorder is not better accounted for by another mental disorder, such as dissociative identity
disorder, post‐traumatic stress disorder, acute stress disorder.

The prevalence rate for dissociative amnesia in a community sample is around 1.8%, with rates being
higher in females than in males (Johnson et al., 2006—see Table 14.1).

14.1.2 Dissociative Identity Disorder (DID)

DID (formerly known as Multiple Personality Disorder) is a disorder where the individual displays two
or more distinct identities or personality states that take turns to control behaviour. It is also associated
with an inability to recall important autobiographical information. DID reflects an inability to integrate
aspects of identity, memory and consciousness to the extent that each personality state is experienced as
if it has its own life history, self‐image, and identity. Different identities usually have different names and
will quite often have very contrasting personalities (e.g., controlling, destructive, or passive). DID is
associated with gaps in memory for various life events, and the extent of this amnesia may vary with the
nature of the different identities (hostile personalities tend to have more complete memories whereas
passive personalities have fewer). The different identities will often deny knowledge of each other but
may battle for control of behaviour, and an identity that is not in control may gain access to
consciousness by producing auditory hallucinations (e.g., by giving instructions). Michael's Story at the
beginning of this chapter describes how the sufferer is often unaware that different identities are taking
control of his behaviour, and he only becomes aware afterwards by finding certain items around (such as
waking up with a teddy bear in his bed). He is also surprised when people he doesn't know say hello to
him—people whom one of his other identities has presumably met. The time required to switch from
one personality to another is usually very brief, and may be preceded by various physical signs, such as
rapid blinking, changes in voice or demeanour, an interruption of ongoing speech or thought, and
changes in facial expression. A distinction can be made between the host identity (the one that existed
before the onset of the disorder), and alter identities (those that develop after the onset). In the
simplest form of the disorder, two alternating identities take turns to control behaviour, and in many
cases the alter may know about the host personality, but not vice versa (Dorahy, 2001). The host may
become slowly aware of the existence of the alter identity, as did Michael, by encountering evidence that
a different personality state has been controlling behaviour. However, many DID sufferers have
significantly more than just one alter identity, and surveys suggest that the average is around 13 per
sufferer (Putnam, 1997). In addition, 85% of sufferers report having at least one alter identity that is a
child and over 50% report having an alter identity that is of the opposite sex (Putnam, Guroff,
Silberman, Barban, & Post, 1986). In general, alter identities tend to take on a range of contrasting
personalities and may individually take charge only of certain areas in the sufferer's life (such as one
dealing with sex life, one with work, one with anger, etc.). In some cases, alter identities have been found
to have different handedness, like different foods, and even have allergies to different substances (Boysen
& VanBergen, 2014). DID can also manifest in the form of possession by ‘spirits’,’ supernatural beings,
‘ghosts’, demons, or personalities from previous lives. In some cultures, these ‘possession’ states are
viewed as relatively normal, and as manifestations that have an explanation in the religious beliefs of the
locality. One such example is that described in Chapter 1 in Focus Point 1.2, where spirit possession is a
common trauma‐related phenomenon in child soldiers in war‐affected areas of Africa.

Dissociative Identity Disorder (DID) A dissociative disorder characterised by the

individual displaying two or more distinct identities or personality states that take turns to
control behaviour (formerly known as multiple personality disorder).

host identity The identity that existed before the onset of dissociative identity disorder.

alter identities The identities that develop after the onset of dissociative identity disorder.

A significant factor in the history of DID sufferers appears to be childhood trauma, and surveys suggest
that over 95% of individuals diagnosed with DID report childhood sexual and physical abuse, including
incest (Putnam, 1997; Putnam et al., 1986). Many sufferers report their disorder beginning in childhood,
often before 12‐years of age, and at times of severe trauma (Putnam, 1997), and over 70% of
outpatients with DID report having attempted suicide at least once (DSM‐5, American Psychiatric
Association, 2013). This seems to suggest that DID may be a coping strategy adopted by children and
adolescents to distance themselves from experienced trauma (Atchison & McFarlane, 1994). We will
discuss this issue more fully in the section on aetiology (Table 14.3) (Case History 14.1). Individuals with
DID also exhibit a large number of comorbid conditions, including PTSD, depressive disorders,
trauma‐ and stressor‐related disorders, personality disorders (especially avoidant and borderline
personality disorders), conversion disorder, somatic symptom disorder, eating disorders, obsessive‐
compulsive disorder, and substance use disorders (DSM‐5, American Psychiatric Association, 2013; see
also Table 14.1).
TABLE 14.3 Summary: DSM‐5 diagnostic criteria for dissociative identity disorder

Disturbance of identity marked by at least two distinct personality states, which in some cultures
may be seen as evidence of possession
Recurring breaks in remembering everyday events, personal information, or traumatic events that
is not in line with natural forgetting.
The symptoms cause significant distress or impairment in important areas of functioning
The disturbance is not a normal part of broadly accepted cultural or religious practice, for
example, children having an imaginary friend
The symptoms are not the result of the use of a substance or due to another medical condition.
The prevalence rate for DID is around 1.5% in a community sample (Johnson et al., 2006), but the
number of reported cases has risen significantly in recent years. For example, Elzinga, van Dyck, &
Spinhoven (1998) found that the number of reported cases worldwide rose from 79 in 1980 to 6,000 in
1986, and the vast majority of these have been reported in the US. What then has caused this
significant increase in diagnosed cases of DID? There may be a number of factors, including (a) the
inclusion of DID for the first time as a diagnostic category in DSM‐III published in 1980; (b) early cases
of DID may simply have been diagnosed as examples of schizophrenia rather than a dissociative
disorder (Rosenbaum, 1980), (c) during the 1970s, interest in multiple personality disorder was fuelled
by the publication of Sybil (Schreiber, 1973), a case history describing an individual with 16 personalities
which was later popularised in a Hollywood film; (d) therapists have increasingly used hypnosis in an
attempt to get victims of childhood abuse to reveal details of this abuse or to reveal alter identities, and
there is some evidence that the power of suggestion under hypnosis may be enough to generate
‘multiple personalities’ that were not there in the first place (Piper, 1997; Powell & Gee, 1999); (e)
dissociative disorders such as DID are closely associated with trauma and PTSD, and interest in these
syndromes grew following the experience of veterans of the Vietnam war; and (f) many of the
symptoms of DID can be relatively easily faked, and some experts estimate that as many as 25% of
DID cases are either faked or are induced by therapy (Ross, 1997) (see also Brand et al., 2016, for a
discussion of some of the ‘myths’ surrounding DID).
 CASE HISTORY 14.1 THE EMERGENCE OF ‘EVELYN’

The psychiatrist Robert F. Jeans reported the case of a single, 31‐year‐old professional woman
called Gina. Her initial symptoms included sleepwalking and screaming in her sleep, and he
noted that she was uncomfortable about being a woman and about the thought of having a
sexual relationship with her married boyfriend known as T.C. During the course of therapy, he
noticed a second personality emerging, which was called Mary Sunshine by Gina and her
therapist. Mary was more feminine, outgoing, and seductive than Gina. Over time Gina found
evidence that Mary had been controlling her behaviour across various aspects of her life: she
found hot chocolate drinks in the sink (Gina did not like hot chocolate), large sums of money
withdrawn from her bank account, and a sewing machine was delivered—that was presumably
ordered by Mary. Mary also seemed to take over Gina's relationship with T.C. and acted as a
seductive and warm partner, whereas Gina had often been cynical and cold. Eventually a third
personality emerged which appeared to be a synthesis of the features of Gina and Mary. Gina
described how this happened:
I was lying in bed trying to go to sleep. Someone started to cry about T.C. I was sure that it was Mary. I
started to talk to her. The person told me that she didn't have a name. Later she said that Mary called her
Evelyn but that she didn't like that name. I asked her what she preferred to be called. She replied that she will
decide later.
I was suspicious at first that it was Mary pretending to be Evelyn. I changed my mind, however, because the
person I talked to had too much sense to be Mary. She said that she realized that T.C. was unreliable but she
still loved him and was very lonely. She agreed that it would be best to find a reliable man.
She told me that she comes out once a day for a very short time to get used to the world. She promised that she
will come out to see you sometime when she is stronger.
I asked her where Mary was. She said Mary was so exhausted from designing her home that she had fallen
asleep.
(Jeans, 1976, pp. 254–255)
Over time Evelyn appeared more and more and appeared to be an adaptive alter identity that
allowed Gina to cope better with the range of issues in her life. Within months she was Evelyn
all the time, had no recollection of Mary, and later became successfully married to a physician.

Clinical Commentary
Like many alter identities in DID, Mary evolved primarily to take charge of certain areas of Gina’s life
—particularly controlling her feminine role and her relationship with T.C. Typically, Gina had no
recollection of her behaviour when Mary was in control and came to be aware of Mary only by
encountering evidence that a different personality had been controlling behaviour. In this particular case,
Evelyn eventually merged as a synthesis of both Gina and Mary's personalities and this proved to be an
adaptive change that enabled Gina to deal with a range of matters across her life.

14.1.3 Depersonalisation Disorder

The central feature of this disorder is persistent or recurrent episodes of depersonalisation. These
symptoms are characterised by feelings of detachment or estrangement from the self. The sufferer may
feel that they are living in a dream or in a film and that they are not in control of their behaviour but
merely standing outside of themselves, watching themselves. As we mentioned earlier, symptoms of
depersonalisation are commonly experienced, so depersonalisation disorder should be diagnosed only if
the symptoms are recurrent, cause severe distress, and disrupt day‐to‐day living. Depersonalisation
symptoms also occur regularly in other disorders, such as panic disorder, schizophrenia, and other
dissociative disorders, so it is important to determine whether symptoms of these other disorders are
present when an individual presents with depersonalisation experiences (Table 14.4).

Depersonalisation Disorder Feelings of detachment or estrangement from the self (such as

living in a dream or standing outside of oneself, watching oneself).

TABLE 14.4 Summary: DSM‐5 diagnostic criteria for depersonalisation/derealisation disorder

Recurring occurrences of depersonalisation, derealisation, or both, causing significant distress or

impairment in important areas of functioning:
Depersonalisation—experiences of detachment or outside observation of one’s own
thoughts, feelings, body, or actions
Derealisation—Experiences of detachment with regard to surroundings
During the occurrences, the individual is still able to distinguish what is real from what is not
The disturbance is not directly due to the use of a substance
The disorder is not better accounted for by another mental disorder, such as schizophrenia, panic
disorder, or major depressive disorder

As is the case in panic disorder, sufferers of depersonalisation disorder often think they are ‘going
crazy’—especially if this is also associated with a sense of derealisation (a feeling that the world is
strange or unreal). Other common symptoms include disturbances in the sense of time, obsessive
rumination, and somatic concerns. Depersonalisation disorder is also highly comorbid with anxiety
symptoms and depression, and a past history of anxiety and depression is regularly reported in those
suffering depersonalisation disorder (Baker et al., 2003).
In everyday life, depersonalisation experiences can occur when the individual is in transitional
physiological states such as on waking up, when feeling tired, practicing meditation, or following an
acute stressor or scary experience. Interestingly, depersonalisation disorder has been associated with
severe life trauma such as childhood physical and emotional abuse (Simeon, Gralnik, Schmeidler, Sirof,
& Knutelska, 2001), and research suggests that depersonalisation during periods of stress or trauma may
be adaptive in reducing symptoms of anxiety or depression immediately after the event (Shilony &
Grossman, 1993). In fact, depersonalisation may account for the periods of emotional ‘numbing’ that
individuals feel immediately after a severe traumatic experience, and before developing symptoms of
PTSD (see Chapter 6, Section 6.7).
Depersonalisation disorder often develops in late adolescence or early adulthood, with a mean onset age
of 16 years, and less than 20% of sufferers reporting onset after 20 years of age. The 12‐month
prevalence rate for depersonalisation disorder is relatively low at 0.8% (Johnson et al., 2006), but it must
be remembered that individual depersonalisation experiences are significantly more prevalent than this.

14.1.4 Dissociative Disorders and PTSD

As we have already mentioned, there is a close relationship between symptoms of PTSD and
dissociative disorders, and studies have suggested that between 15 and 30% of individuals with PTSD
also experience high levels of dissociation in the form of dissociative symptoms (Lipschitz, Winegar,
Hartnick, Foote, & Southwick, 1999; Stein et al., 2013). This has led clinical researchers to speculate
about the relationship between these two diagnostic categories, with at least some clinicians arguing for
a dissociative subtype of PTSD (Lanius et al., 2010).
We noted earlier that dissociative‐type symptoms are already listed in the diagnostic features of PTSD,
and these symptoms include amnesia, flashbacks, numbing, and depersonalisation. PTSD is related to
dissociative disorders in at least three possible ways. First, persistent dissociative symptoms immediately
after a traumatic experience are a significant predictor of the subsequent acquisition of full‐blown
PTSD (Murray, Ehlers, & Mayou, 2002), so a tendency to dissociative symptoms may make individuals
vulnerable to the development of other PTSD‐relevant symptoms. Second, dissociation is a feature of
‘complex’ or severe PTSD (van der Hart, Nijenhuis, & Steele, 2005), in which individuals suffer from a
range of persistent symptoms, enduring personality changes, affect disruption, somatisation, and
changes in self‐perception (Herman, 1992; Giourou et al., 2018). Complex PTSD is often associated
with early age interpersonal trauma and with dissociative symptoms from that early age (Ford & Kidd,
1998; McLean & Gallop, 2003) and has led some clinicians to argue that dissociation and other PTSD
symptoms may share a common central psychobiological pathology (Brewin, 2003). Third, there may
exist a specific dissociative subtype of PTSD that is defined by the severity of both PTSD and
dissociative symptoms, and which may account for up to 30% of cases of PTSD (Wolf et al., 2012). We
must await further research on the psychological and biological pathways through which dissociative
and PTSD symptoms are acquired before we will be able to fully understand the relationship between
dissociative symptoms and PTSD, and one outcome of this research might be a dissociative subtype of
PTSD in future editions of the DSM.

Complex PTSD A severe form of PTSD often associated with early age interpersonal trauma
and with dissociative symptoms from that early age.

SELF‐TEST QUESTIONS
What are the main diagnostic features of dissociative amnesia?
Can you name the five types of memory disturbance that occur in dissociative amnesia?
What are the main features of DID and what was it previously called?
Can you describe the difference between host identities and alter identities in DID?
What is the estimated prevalence rate of DID and what problems are involved in
estimating its prevalence?
What are the main features of depersonalisation disorder?
What is complex PTSD and how is it related to dissociative experiences?
 SECTION SUMMARY

14.1 THE DIAGNOSIS AND CHARACTERISTICS OF DISSOCIATIVE

DISORDERS
Dissociative amnesia is an inability to recall important personal information that is usually of
a stressful or traumatic nature.
The symptoms of dissociative amnesia can often be alleviated by removing the individual
from the situation that may have caused trauma (e.g., removing a soldier from the locality
of a battlefield).
Dissociative identity disorder (DID) was formerly known as ‘multiple personality disorder’ and
is characterised by the individual displaying two or more distinct identities.
DID is often associated with childhood maltreatment, and most sufferers usually exhibit
many more than just two distinct alter identities.
The number of reported cases of DID increased dramatically between 1980 and 1986,
and the reasons for this increase are unclear.
Depersonalisation disorder is characterised by persistent or recurrent episodes of
depersonalisation, including feelings of detachment and not being in direct control of their
behaviour.
Dissociative experiences are often associated with symptoms of PTSD and sometimes give
rise to what is known as complex PTSD.

14.2 THE AETIOLOGY OF DISSOCIATIVE DISORDERS

The questions of how and why people develop dissociative disorders are interesting ones. The
symptoms are often striking and quite frequently found in individuals who have undergone experiences
of extreme trauma or stress. There are two important issues that need addressing when we attempt to
look at the causes of dissociative disorders. The first is that we need to be able to explain how the
components of consciousness (e.g., cognition, emotion etc.) become dissociated. Consciousness is
normally a fully integrated entity, but in individuals with dissociative disorders some memories can be
completely lost or suppressed (as in dissociative amnesia), some aspects of consciousness can be isolated
from others (such as the different identities experienced in DID), and the individual can feel that they
are dissociated from both themselves and the outside world (e.g., in depersonalisation disorder). Any
theory of dissociative disorders needs to explain why some individuals develop these symptoms, and
how the different components of consciousness become dissociated. The second issue associated with
the aetiology of dissociative disorders is whether the symptoms actually have a functional significance—
that is, do the symptoms serve a purpose? In the previous sections of this chapter we have alluded to the
possibility that dissociative symptoms may protect individuals from stressful memories and experiences
and help them to cope with day‐to‐day living, anxiety and depression (e.g., Kihlstrom, 2001; Riether &
Stoudemire, 1988; Atchison & McFarlane, 1994). As we go through the various theories of dissociative
disorders, it is important to bear these two central issues in mind.
14.2.1 Risk Factors for Dissociative Disorders
Risk factors for dissociative disorders include a history of anxiety and depression that predates the
disorder (Putnam et al., 1986), and a history of childhood abuse (physical and sexual) and childhood
neglect, and up to 95% of individuals diagnosed with DID report instances of childhood sexual and
physical abuse (Putnam, 1997; Putnam et al., 1986). Dissociative amnesia is associated with a history of
trauma and is more common after major stressful life events such as war or natural disasters (Coons,
1999). What is not clear is whether childhood abuse actively contributes to the development of
dissociative disorders in a causal way. However, the strength of dissociative symptoms appears to be
directly related to the age of onset of physical and sexual abuse, with higher levels of symptoms
reported in those whose abuse began early in life, or who suffer disorganised or insecure attachment
early in life (Chu, Frey, Ganzel, & Matthews, 1999; Pasquini et al., 2002), and dissociative symptoms are
commonly found in homeless and runaway youths who had suffered various forms of abuse prior to
leaving home (Tyler, Cauce, & Whitbeck, 2004). This provides some indirect support for the view that
childhood abuse does play a causal role in the development of dissociative disorders, and there may be a
chain of reactions involved because children who develop dissociative symptoms during childhood are
more likely to develop psychological symptoms after trauma (Dalenberg et al., 2012). The issue of
whether being male or female is a risk factor for dissociative disorders is still unclear; some studies
suggest a greater risk of dissociative disorders in women than in men (Putnam & Loewenstein, 2000;
Simeon et al., 1997), but other community‐based studies suggest that this may be true only for
dissociative amnesia (Johnson et al., 2006, see Table 14.1).

childhood abuse The physical or psychological maltreatment of a child.

14.2.2 Psychodynamic Theories

The general view of most psychodynamic theorists is that dissociative symptoms are caused by
repression, which is the most basic of the ego defence mechanisms. In these cases, repression helps to
unconsciously suppress painful memories and to prevent stressful thoughts entering consciousness. As a
result, repression helps to control conflict, anxiety, and depression. According to Freudian views,
dissociative amnesia is a simple example of repression, where stressful or traumatic memories are simply
suppressed until the individual has the strength to cope with them. These tendencies to repress
unwanted or painful memories may be acquired in childhood, when excessively strict parents may instil
a strict moral code in their children. When the individual violates this code during adulthood (such as by
having an extramarital affair), the expression of these ‘unacceptable’ id impulses are repressed by
unconscious mechanisms that prevent the retrieval of such memories. DID is viewed as a further form
of repression, but one in which repression persists for significantly longer (e.g., throughout a lifetime) in
order to repress the memories of very traumatic childhood events (Brenner, 1999; Reis, 1993). In
psychodynamic terms, the DID sufferer develops alter egos in order to avoid the distressing world they
were brought up in, and also to protect themselves from the impulses that they believe may have been
the reason for their excessive punishments during childhood. Thus, a DID sufferer can disown any ‘bad’
thoughts or impulses by attributing them to a ‘rogue’ alter ego.

Psychodynamic Theories See Psychodynamic approaches.

repression A basic psychodynamic defence mechanism that helps to suppress painful

memories and prevent stressful thoughts.
There is certainly some evidence that individuals with dissociative disorders do experience less conflict
and anxiety than individuals with other forms of psychopathology (e.g., substance abuse), and this
evidence supports the psychodynamic view (Alpher, 1996). However, we must once again return to the
difficulties inherent in testing predictions from psychodynamic accounts because of the difficulties in
objectively measuring the concepts and mechanisms described in psychodynamic theory. This is just as
much true of psychodynamic accounts of dissociative disorders as it is of any other psychopathology
(see Chapter 1).

14.2.3 The Role of Fantasy and Dissociative Experiences

There is some evidence that dissociative disorders may develop more readily in individuals who have
early dissociative or depersonalisation experiences and such individuals may learn to use such
experiences in order to suppress anxiety and painful memories. For example, in a selection of prison
inmates diagnosed with DID, Lewis, Yeager, Swica, Pincus, and Lewis (1997) found that 12 out of 14
cases had longstanding dissociative experiences that predated the full‐blown DID symptoms, and 10 of
the 14 reported having imaginary companions during childhood. Reporting imaginary companions
during childhood is common in individuals with DID (Sanders, 1992), and some theorists have argued
that such experiences will predispose an individual to develop DID. For example, Kluft (1992) has
argued that a child who constructs imaginary companions may find that they can occasionally use these
imaginary personalities to ameliorate periods of stress and conflict, and the child may then learn to
actively construct these personalities into adaptive alter identities to protect themselves from stress.
However, currently the only evidence in support of this view is that individuals with dissociative
disorders do appear to have a history of dissociative experiences, and they also appear to have strong
imaginations and a rich fantasy life, which will contribute to the development of symptoms such as alter
identities (Lynn, 1988). More recent studies have also demonstrated a significant but modest relationship
between measures of fantasy‐proneness and dissociative symptoms (Giesbrecht, Merckelbach, &
Geraerts, 2007), but fantasy‐proneness appears to be a feature associated with many different
psychopathologies and not just dissociative disorders (Merckelbach, à Campo, Hardy, & Giesbrecht,
2005). In addition, recent research has tended to favour the view that a dissociative disorder such as
DID has its origins in childhood trauma rather than fantasy‐proneness (Vissia et al., 2016), and studies
that have attempted to simulate DID symptoms in low‐ and high fantasy participants have found little
evidence that fantasy‐proneness facilitates these dissociative symptoms (Reinders & Willemsen, 2014).
However, more detailed analysis seems to indicate that particular aspects of fantasy‐proneness, such as
vivid mental imagery and parapsychological beliefs may be better predictors of dissociative
psychopathology than fantasy‐proneness per se (Klinger, Henning, & Janssen, 2009).

14.2.4 Cognitive Approaches

A central issue in explaining dissociative disorders is an understanding of how various components of
conscious experience come to be detached from each other (e.g., how memory for some events become
suppressed while others remain intact). Such characteristics suggest that an answer may lie in how
normal memory and recall processes are affected in individuals suffering dissociative symptoms, and
many cognitive theorists believe that dissociative disorders represent a disruption of all or part of the
sufferer's memory processes (Dorahy, 2001).
For example, do individuals displaying dissociative symptoms show poorer recall for trauma‐ or abuse‐
related material in experimental studies? If so, then they may have developed a tendency to avoid
encoding traumatic material in memory or they may have developed impaired retrieval processes for
such information (McNally, Clancy. & Schachter, 2001). Unfortunately, much of the experimental
evidence does not support such a simple explanation. In explicit memory tasks—where participants are
asked to either remember or forget words presented in a recall task—individuals with a history of
childhood abuse showed no difference in recall of trauma‐related words than non‐abused control
participants (McNally et al., 1998; Cloitre, Cancienne, Brodsky, Dulit, & Perry, 1996). Although these
studies did not directly investigate individuals with dissociative symptoms, the findings do suggest that
individuals with a history of abuse do not have an automatic tendency to suppress or avoid encoding or
recalling traumatic material. However, subsequent studies have suggested that individuals high in
dissociative symptoms do have impaired recall for words associated with trauma under conditions of
divided attention (i.e., when they are asked to perform a concurrent task as well as the memory task)
(DePrince & Freyd, 2004) (see Figure 14.1). This suggests that attentional context is important in helping
high dissociators to forget trauma‐related material, and dividing their attention across a range of sources
may help individuals with dissociative symptoms facilitate forgetting of emotional‐relevant or traumatic
information.

FIGURE 14.1 Percentage correct recall of to‐be‐remembered neutral and trauma‐related words presented under
conditions of divided attention. Grey bars represent participants who scored high on dissociative experiences, and red bars
represent those who scored low on dissociative experiences.
After DePrince and Freyd, (2004).
An alternative explanation of the memory failures experienced by dissociative disorder sufferers is in
terms of how changes in their physiological and emotional state can influence recall of memories.
State‐dependent memory is a well‐established cognitive phenomenon in which the individual is
more likely to remember an event if they are in the same physiological state as when the event occurred
(Bower, 1981). We have already noted that individuals with dissociative disorders often experience
severely traumatic life events that cause significant changes in mood and physiology when such events
occur (e.g., being involved in a natural disaster such as an earthquake may be experienced during states
of hyperarousal and panic). If the events relating to this experience are encoded in memory during
these unusual emotional states, then it may be that the individual will have difficulty properly recalling
them in less traumatic emotional states (Radulovic, Lee, & Ortony, 2018). State‐dependent learning has
also been used to explain the between‐identity amnesia that is often experienced in DID (Szostak, Lister,
Eckhart, & Weingartner, 1995), and it has been suggested that most between‐identities amnesia will
occur between those alter identities that differ most in their normal mood states (e.g., there will be less
cross‐identity knowledge between identities that display negative emotions, such as sadness or anger, and
those that exhibit mainly positive emotions such as joy and happiness) (Bower, 1981). Nevertheless, while
state‐dependent memory may seem like an appealing explanation of dissociative amnesia, there are
some difficulties with this explanation. First, dissociative amnesia is usually much more severe than has
been reported in basic studies of state‐dependent memory. Second, individuals with DID have problems
with both free recall memory and recognition memory, but state‐dependent memory is usually only
found with the former (Peters, Uyterlinde, Consemulder, & van der Hart, 1998). Third, studies have
effectively demonstrated that different identities in DID can recall autobiographical information from
the other identities when a concealed recognition test is used, suggesting that dissociative amnesia in
DID probably does not entail inter‐identity memory systems or is constrained by state‐dependent
learning (Huntjens, Verschuere, & McNally, 2012).

State‐dependent memory A well-established cognitive phenomenon in which the individual

is more likely to remember an event if he or she is in the same physiological state as when the
event occurred.

Finally, one other cognitive theory of dissociative symptoms involves the concept of reconstructive
memory. This view argues that an individual autobiographical memory is stored as a series of discrete
elements associated with that experience (e.g., context, emotional state, sensory and perceptual features,
etc.). These various elements will then be recognised as an autobiographical memory to the extent that
the various elements can be retrieved and associated together (the act of reconstruction). In some cases,
not all of the elements that go to make up an autobiographical memory may be activated, and this may
lead the individual to doubt that the retrieved fragments of memory refer to a memory from his or her
own past. Being unable to recall the relevant elements of an autobiographical experience from memory
is known as a deficit in source‐monitoring ability (Johnson, Hashtroudi, & Lindsay, 1993), and an
example of this is when an individual cannot remember whether they read something in a newspaper or
whether it was just a rumour they heard from a friend. It has been suggested that dissociative amnesia
may result from deficits in both reconstructive memory and source‐monitoring abilities. For some
reason, individuals with dissociative symptoms may not be able to recover from memory sufficient
elements of an autobiographical event to convince them it was an experience that happened to them. In
addition, a deficit in reality monitoring (a form of source monitoring required to distinguish mental
contents arising from experience from those arising from imagination), may also lead them to doubt that
they have actually had a particular experience (Johnson & Raye, 1981), and both of these processes may
contribute to dissociative amnesia. Consistent with this view are findings that women who have
experienced childhood sexual abuse and score high on dissociative experiences have greater difficulty
than nonabused control participants in distinguishing between words they had seen in a memory test
and words they imagined seeing (McNally, Clancy, Barrett, & Parker, 2005; Clancy, Schachter, McNally,
& Pitman, 2000)—a finding which suggests that they may well have a deficit in reality monitoring.

reconstructive memory A concept of a cognitive theory of dissociative symptoms which

argues that an individual autobiographical memory is stored as a series of discrete elements
associated with that experience (e.g. context, emotional state, sensory and perceptual features).
 source‐monitoring ability The ability to recall the relevant elements of an autobiographical
experience from memory.

reality monitoring A form of source monitoring required to distinguish mental contents

arising from experience from those arising from imagination.

However, deficits in reality monitoring can work both ways. They can prevent a person from identifying
an autobiographical memory as one they have actually experienced, but they may also lead to the
individual identifying an imagined event as an actual experience. This may be the basis for what have
now become known as false recovered memories of trauma (Loftus, 1993), in which various
therapeutic techniques are used to try to recover repressed childhood memories of trauma but which
may actually generate false memories of events that did not occur. Such techniques may inadvertently
lead the client to falsely recognise imagined experiences as ones that actually happened, and this issue is
discussed more fully in Focus Point 14.2 and Research Methods in Clinical Psychology 14.1.

false recovered memories of trauma The recovery of repressed childhood memories of

trauma that turn out to be false.

FOCUS POINT 14.2 REPRESSED MEMORIES, RECOVERED

MEMORIES, AND FALSE MEMORY SYNDROME

There has been a belief amongst many therapists and clinicians that individuals can forget
traumatic or stressful events in their life for relatively lengthy periods of time, and this view
stems back to the original works of Freud who believed that severe trauma was repressed to the
unconscious mind because it was too painful to tolerate. Many of the symptoms of dissociative
disorders seem to support this belief—especially because many of these disorders are
characterised by amnesia, and childhood abuse is a common factor in the history of many with
dissociative disorders. However, attempting to confirm that memories have been repressed is a
difficult process. For example, it is often difficult to find corroborative evidence even when
repressed memories of abuse have been recovered, because many of the recovered memories
may be of abuse that the perpetrators will be unwilling to substantiate. There are therefore a
number of issues to address when considering repressed memories. In particular these are:
Can memories of early childhood trauma or abuse be repressed?
If they can be repressed, can they subsequently be recovered?
If so‐called repressed memories are recovered, are they accurate?

CAN MEMORIES OF CHILDHOOD TRAUMA OR ABUSE BE

REPRESSED?
Williams (1995) used hospital files to identify 206 women who, as children, had received
medical treatment for sexual abuse in the 1970s. Twenty years later, the researcher located these
individuals and interviewed them about a range of topics including childhood sexual abuse.
38% of those interviewed did not report the incident of sexual abuse for which they were
hospitalised, but did report other incidents, suggesting that they were not simply holding back
sensitive information. Of those who did report the incident of sexual abuse, 16% reported that
there were times in their lives when they had effectively forgotten it (see Goodman, Wolpe, &
Gonzalves, 2019, for a review and discussion of the Williams, 1995, study). This study suggests
that there may be occasions when individuals do fail to recall traumatic events such as
childhood abuse. However, this may simply be due to normal processes of forgetting rather
than active repression of painful memories. In contrast, Zola (1998) reports a study
investigating the memories of individuals whose childhood traumas were a matter of historical
record (e.g., kidnap and Holocaust survivors). In all of these cases there was no evidence of
repressed memories for these events in the survivors, and they remembered most of the
traumatic events quite vividly. Freyd (1996), however, has argued that childhood sexual abuse is
qualitatively different from the traumas experienced by Zola's participants. She suggests that
childhood sexual abuse is often perpetrated by a trusted caretaker, such as a parent or close
relative, and this gives rise to what is called ‘betrayal trauma’, which is more likely to be
repressed than other forms of trauma because the perpetrator was someone who also provided
‘care’. So, studies such as these provide conflicting evidence as to whether trauma memories are
repressed or not. If they are subject to periods of amnesia, then it needs to be established
whether this is due to normal processes of forgetting or whether it is the result of an active
repression process.

IF MEMORIES OF TRAUMA OR ABUSE CAN BE REPRESSED, CAN

THEY SUBSEQUENTLY BE RECOVERED?
During the 1980s and 1990s many therapists came to believe that a wide range of
psychopathology symptoms were caused by past sexual abuse that has been repressed in the
memories of the victims. They also believed that a range of therapeutic methods could be used
to recover these repressed memories, and these included hypnotism and directive
psychotherapy. These approaches generally came to be known as recovered memory therapy,
and proponents of this approach had a crusading belief that a wide range of psychopathologies
were indicative of childhood sexual abuse (Kaplan & Manicavasagar, 2001). Much of the
impetus for this loose therapeutic movement came from a book called The Courage to Heal,
written in 1988 by two feminist counsellors, Ellen Bass and Laura Davis. They argued that (a) a
large number of people are the victims of childhood sexual abuse but do not realise they were
abused, and (b) a list of symptoms (e.g., being held in a way that made them feel uneasy) may
well be indicative of actual childhood abuse. Their overriding principle was ‘if you feel
something abusive happened to you, it probably did!’ (1988, p. 21). Therapists who
subsequently adopted this approach to treating psychopathology were thus given free rein to
indulge in a directive approach attempting to uncover evidence of suppressed memories of
childhood abuse—even to the point where clients were told they were ‘in denial’ if they could
not remember instances of abuse! Under such conditions it is almost inevitable that clients may
begin to ‘recall’ instances of abuse that did not actually happen.

IF SO‐CALLED REPRESSED MEMORIES ARE RECOVERED, ARE THEY

ACCURATE?
There have been a number of high profile court cases—especially in the US, where parents or
carers have been convicted of childhood abuse on the basis of memories of this abuse
recovered by their children while undergoing therapy. In 1990, George Franklin was convicted
of murdering a child 20 years earlier on the basis that his daughter suddenly remembered him
committing the act while she was undergoing therapy. This conviction was subsequently
quashed in 1995 as a result of substantial doubts about the validity of his daughter's memories.
This case is an example of what has come to be known as false memory syndrome, in
which individuals recall memories which subsequently turn out to be false. This does not mean
that the individual is actively lying or faking the memory, but a variety of psychological
processes might contribute to the individual developing a false memory and believing that it is
an accurate record of past events.
This debate on whether recovered memories of trauma are genuine or false is still ongoing and
has been reignited in the UK in recent years in the wake of the revelations of sexual abuse by
former DJ Jimmy Savile and the setting up of an inquiry into child sexual abuse by the UK
Government in 2015 (Brewin & Andrews, 2017a). Given the available evidence, there is no
doubt that some people probably do repress memories of childhood abuse, some probably recover
those memories—either with or without therapy—and some probably recall memories of
childhood abuse that never actually happened but are post hoc reconstructions often shaped by
the narratives of others (see Brewin & Andrews, 2017a,b, for thorough reviews of where the
debate on false memories of childhood abuse has reached).
RESEARCH METHODS IN CLINICAL PSYCHOLOGY 14.1
MEASURING PRONENESS TO FALSE RECOGNITION IN
RECOVERED MEMORIES

Individuals who have suffered amnesia for stressful life events may occasionally recall what have
now come to be known as false recovered memories of trauma. That is, they may actually recall
events that they believed happened, but which objective evidence subsequently suggests did not
happen. A classic example of this is described in Focus Point 14.2.
We have described in Section 14.2 why we think some people might be prone to recalling
memories that are false, but how do we go about studying this phenomenon experimentally?
False recognition—the mistaken belief that one has previously encountered a novel item—has
been studied extensively in the laboratory and the methods used to investigate this have been
applied to the study of false recovered memories in individuals with dissociative disorder
symptoms.
In the laboratory procedure, participants are presented with lists of words, and each list is
composed of words associated to a single non‐presented ‘theme word’. For example, a list may
consist of words associated with sweet (such as sour, sugar, bitter, candy, etc.). After hearing the lists,
participants are then given a recognition test where they are presented with words (a) that were
presented in the previous lists, (b) words that have not been presented before but are related to
the theme words (known as false targets), and (c) a control set of words that have never been
presented before but which are not related to the theme words.
Using college students as participants, many studies have suggested that rates of false
recognition to false targets is high—so even nonclinical populations often believe they have seen
words in the original lists when in fact they have not (i.e., exhibit false recognition) (Roediger &
McDermott, 1995; Schachter, Norman, & Koutstaal, 1998).
A number of studies have used this paradigm to test whether individuals with dissociative
disorder symptoms have particularly high levels of false recognition. Clancy, Schachter,
McNally, & Pitman (2000) indeed found that a group of women who reported recovered
memories of childhood sexual abuse was more prone to false recognition in this laboratory
procedure than other groups (such as women who believed they were sexually abused as
children but could not remember it, and women with no history of childhood sexual abuse).
Interestingly, people who report having been abducted by space aliens also exhibit proneness to
false recognition (Clancy, McNally, Schachter, Lenzenweger, & Pitman, 2002).
Experimental studies such as these suggest that false recognition of past experiences are not
uncommon, and clinicians need to be aware of this when dealing with the recall of traumatic
experiences in clients with dissociative disorders. In addition, it suggests that some groups of
people (i.e., those who claim to have recovered memories of past traumas) are particularly
prone to false recognition. It is not at all clear why this is so, but individuals who have
undergone severe stress may have deficits in source monitoring—i.e., remembering how, when,
and why a memory was acquired, and this can be manifested in this simple false recognition lab
test as well as in real life.
14.2.5 Biological Explanations
Dissociative disorders generate symptoms—such as amnesia—that prima facie look as though they may
have been generated by neurological defects or abnormalities in brain processes. Even so, there is very
little evidence that these amnesic symptoms are caused by underlying deficits in brain function. First,
memory loss tends to be selective and in many cases it is transitory. This suggests that if there are brain
abnormalities causing these symptoms, these too must be selective and transitory. One such candidate
that has been suggested is undiagnosed epilepsy (Sivec & Lynn, 1995). Epileptic seizures are known to
be associated with DID and with symptoms of depersonalisation disorder such as blackouts and déjà vu.
Even so, the symptoms of some dissociative disorders—such as DID—are very complex, and it is
unlikely that undiagnosed bouts of epilepsy could explain the intricate way in which knowledge about
alter identities is suppressed or recovered by the sufferer.

epilepsy A disorder of the nervous system characterised either by mild, episodic loss of
attention or sleepiness or by severe convulsions with loss of consciousness.

An alternative biological explanation alludes to the role of the hippocampus. Brain scan studies have
suggested that the hippocampus is the area of the brain that brings together the various elements of an
autobiographical memory and integrates them to provide the individual with a memory that they
recognise as a past personal experience. Given that individuals with dissociative disorders appear to
have problems recalling and integrating memories of certain experiences (such as childhood abuse), this
may be caused by abnormalities in the hippocampus. Bremner, Krystal, Charney, & Southwick (1996)
have argued that neurotransmitters released during stress can modulate memory function—particularly
at the level of the hippocampus—and this release may interfere with the laying down of memory traces
for high stress incidents such as childhood abuse. In addition, extended periods of stress may also cause
long‐term, semi‐permanent alterations in the release of these neurotransmitters, causing long‐term
amnesic effects for experiences related to trauma. More recent functional magnetic resonance imaging
research has suggested that the prefrontal cortex may play an important role in inhibiting the activity of
the hippocampus in individuals with dissociative amnesia, a process that will result in memory
repression (Kikuchi et al., 2010).

14.2.6 Dissociative Symptoms as Role‐Playing and Therapeutic

Constructions
A number of theorists have argued over a number of decades now that the more elaborate symptoms of
dissociative disorders, such as alter identities in DID, are a form of role‐playing by the sufferer in order
to evoke sympathy and to escape responsibility for their actions (Spanos, 1996). Such role playing is
usually reinforced by family, friends, and therapists, as it evokes the required attention and allows the
individual to absolve themselves of day‐to‐day responsibilities for their behaviour. In addition, people
simulating DID in the laboratory are mostly indistinguishable from individuals with a diagnosis of DID,
suggesting that it is not a difficult condition to feign (Boysen & Van Bergen, 2013, but see Reinders &
Willemsen, 2014). In particular, alter identities in DID may be developed in response to particular types
of therapeutic intervention. For instance, in the ‘emergence of Evelyn’ example (Case History 14.1) the
therapist's interactions with Gina lead to an alter identity emerging, and this new identity was given the
name Mary by both the client and the therapist. In fact, therapists dealing with DID often ask their
clients to give a name to an alter identity so they can talk about this personality more easily. Spanos
(1996) suggests that this interactive therapeutic process actually creates the client's alter identities—so
alter identities may be constructions of the therapeutic process itself rather than genuine, full‐blown
symptoms that precede treatment. The client then finds that these well‐defined alter identities serve a
useful function in their life by allowing them to explain away their behaviour and alleviating stress and
anxiety.
 Therapeutic Constructions The view that the multiple personalities found in dissociative
identity disorders are merely constructions of the therapeutic process.

What evidence is there that alter identities in DID are a construction of the therapeutic process?
Supportive evidence includes:
1. Alter identities are significantly less well defined in childhood and appear in adulthood usually after
treatment by a therapist has begun (Spanos, 1994; Lilienfield et al., 1999).
2. Relatives of individuals with DID rarely report having seen evidence of alter identities before
treatment (Piper & Mersky, 2004).
3. Individuals who develop DID usually have strong imaginations and a rich fantasy life that enables
them to play different roles with some ease (Lynn, 1988).
4. There is some evidence that many cases of DID may be diagnosed by only a relatively small
number of clinicians who may have a therapeutic style that allows alter egos to develop; for
example, in a Swiss survey, Modestin (1992) found that 66% of the DID diagnoses in the country
were made by less than 10% of the clinicians in the survey.
5. Individuals diagnosed with dissociative disorders are very susceptible to suggestion and hypnosis
(Bliss, 1980; Butler, Duran, Jasiukaitis, Koopman, & Spiegel, 1996), and hypnotherapy is a
common form of treatment for DID; Spanos (1996) argues that such susceptible individuals may
adopt the “hypnotic role” and simple produce the kind of behaviour that the therapist wants.
6. Spanos (1994) noted that those who support DID as a diagnostic category have described a wide
range of symptoms that may be indicative of DID and this justifies constant probing in therapy to
confirm a diagnosis, and this may occur to the point where therapists insist to doubting clients that
they do have multiple alter egos (Mersky, 1995); consistent with the desire of many clinicians to
diagnose DID is the finding that the prevalence of diagnosed DID has increased dramatically since
1980 (Elzinga, van Dyck, & Spinhoven, 1998).
Nevertheless, there is still debate about whether most cases of DID are strategic enactments or not.
Gleaves (1996) has provided a vigorous defence of the psychiatric view that DID is a legitimate
diagnostic category and not a construction of the therapeutic process. He argues that (a) it is not
surprising that the rate of DID diagnosis has increased significantly in recent years because this may be
a result of less scepticism about the diagnostic category and a reduction in the misdiagnosis of DID as
schizophrenia; (b) there is relatively little evidence that hypnotherapy actively contributes to the
development of DID symptoms because the number of clients diagnosed with DID after hypnotherapy
is as low as one in four; (c) core symptoms of DID, such as amnesia, are frequently found in DID
sufferers before their first treatment session (Coons, Bowman, & Milstein, 1988), so DID cannot be
entirely constructed as a result of therapy; and (d) rather than being openly collusive with the therapist
about their symptoms, many individuals with DID are highly reluctant to talk about their symptoms
and have an avoidant style that is not conducive to revealing a history of abuse or the existence of
multiple personalities (Kluft, 1994).
As an epilogue to this ongoing debate, it is worth discussing an interesting study conducted by Spanos,
Weekes, & Bertrand (1985). They designed an experiment based on the famous case of Kenneth
Bianchi, who was accused of a series of murders and rapes in Los Angeles in the 1980s. During his
psychiatric evaluation under hypnosis, Bianchi revealed evidence of DID symptoms and eventually of
an alter identity called Steve whom he claimed committed the rapes and murders. When he came out
of the hypnotic state, Bianchi claimed to know nothing about Steve or the murders or what he had said
under hypnosis. Table 14.5 provides a transcript of part of the discussion between the clinician and
Bianchi while the latter was under hypnosis. Spanos, Weekes, & Bertrand (1985) claim that this is an
excellent example of how Bianchi's alter identity was constructed via the therapeutic discussion.
Constructing ‘Steve’ served a useful purpose for Bianchi, because it allowed him to plead not guilty to
murder by reason of insanity (i.e., his supposed DID). In their experimental study, Spanos et al. (1985)
asked three groups of students to act out variations of the hypnotherapy procedure undergone by
Bianchi. All groups were instructed to play the role of individuals accused of murder. Group 1 was then
hypnotised and underwent questioning taken almost verbatim from the Bianchi transcript. Group 2
were also hypnotised and told that under hypnosis many individuals reveal evidence of hidden multiple
personalities, but this aspect was then not directly addressed in the interview. Group 3 were a control
condition that were not hypnotised and were given little or no information about hidden multiple
personalities. After the interviews, all participants were questioned about whether they had a hidden
personality or second identity. In Group 1—which underwent a procedure similar to Bianchi—81%
admitted a second personality. In Group 2—whose interview did not allude to hidden personalities—
only 31% revealed an alter identity. Only 13% of those in Group 3 admitted a hidden personality.
Spanos et al. (1985) argued that these results provided evidence that alter identities can be developed as
a result of the demand characteristics of the interview style of the therapist, and that such alter
identities are strategic enactments that serve the purposes of the client (e.g., by diverting or avoiding
blame for their behaviour). Nevertheless, while this study provides convincing evidence that some alter
identities can be developed by the therapist's interviewing style, it is still not evidence that all alter
identities are strategic enactments.
TABLE 14.5 Transcript of the discussion that took place between accused murderer, Kenneth Bianchi, and a clinician
while Bianchi is under hypnosis (see text for further elaboration)
After Schwarz (1981), pp. 139–143.
Clinician: I've talked a bit to Ken, but I think that perhaps there might be another part of Ken that I
haven't talked to. And I would like to communicate with that other part. And I would like
that other part to come to talk to me….And when you're here, lift the left hand off the chair
to signal to me that you are here. Would you please come, Part, so I can talk to you … Part,
would you come and lift Ken's hand to indicate to me that you are here… Would you talk to
me, Part, by saying ‘I'm here’?
Bianchi: Yes.
Clinician: Part, are you the same as Ken or are you different in any way
Bianchi: I'm not him.
Clinician: You're not him. Who are you? Do you have a name?
Bianchi: I'm not Ken.
Clinician: You're not him? OK. Who are you? Tell me about yourself. Do you have a name I can call
you by?
Bianchi: Steve. You can call me Steve.

14.2.7 Summary
We posed two questions at the outset of this section on aetiology: (a) How do the normally integrated
components of consciousness become dissociated in the dissociative disorders? and (b) Do the distinctive
symptoms of dissociative disorders (such as amnesia and multiple personalities) have a specific function?
We have reviewed a range of theories about how the elements of consciousness become dissociated in
these disorders and how memories might become suppressed. Cognitive theories try to explain these
dissociative symptoms primarily by attempting to describe the mechanisms that might mediate effects
such as selective amnesia. We reviewed two specific accounts, state‐dependent memory and
reconstructive memory. The latter additionally argued that individuals with dissociative disorders may
suffer deficits in source‐monitoring ability and reality monitoring—both may prevent an individual from
identifying an autobiographical memory as one they have actually experienced. Some relatively
undeveloped biological accounts also intimate that selective amnesia may result from abnormal brain
processes (such as epilepsy) or specific brain functions which inhibit the ability of the hippocampus to
lay down or recall specific memories. An alternative view of the striking symptoms of dissociative
disorders is that many of them may be a construction of the therapeutic process. In particular, directive
therapeutic approaches (including hypnotherapy) may encourage the client to create alter identities that
did not exist prior to therapy or to recall false memories of events that had never happened. We
concluded that while some symptoms of dissociative disorders may be developed by overly directive
therapy techniques, it is highly unlikely that this explains all dissociative symptoms. Finally, in relation to
our second question, it is quite probable that the symptoms of dissociative disorders (particularly
selective amnesia and alter identities) do serve some kind of palliative role, and in the psychodynamic
view they may allow the sufferer to repress traumatic memories that are too painful to tolerate.

SELF‐TEST QUESTIONS
Can you describe some of the main risk factors for dissociative disorders?
What is the psychodynamic concept of repression, and how does it account for the
symptoms of dissociative disorders?
What is the evidence that fantasy and early dissociative experiences may play a role in the
development of dissociative disorders?
Can you describe the procedure for a laboratory‐based experiment designed to investigate
deficits in memory processes in individuals with dissociative disorders?
What is state‐dependent memory and how does it attempt to account for dissociative
amnesia?
Can you explain how deficits in source monitoring ability or reality monitoring might
account for both dissociative amnesia and false recovered memories of trauma?
What is the evidence that alter identities in DID are a construction of the therapeutic
process?
 SECTION SUMMARY

14.2 THE AETIOLOGY OF DISSOCIATIVE DISORDERS

Risk factors for dissociative disorders include physical and sexual childhood abuse and a
history of trauma generally (e.g., experiencing major stressful life events such as war or
natural disasters).
Psychodynamic theorists view dissociative disorders as being caused by repression, which is
one of the most basic of the ego defence mechanisms.
Dissociative disorders may develop more readily in those who have experienced
dissociative symptoms as a child or who have strong imaginations and a rich fantasy life.
Cognitive theorists believe that dissociative symptoms are caused by a disruption to the
sufferer's memory processes.
Individuals with dissociative symptoms only appear to have poor memory for trauma
information under conditions of divided attention.
Some theorists argue that dissociative amnesia is caused either by a deficit in source‐
monitoring ability or reality monitoring.
Deficits in some memory processes may be the reason some sufferers are prone to recover
false memories of trauma that never happened.
Biological accounts suggest that dissociative symptoms may be caused by undiagnosed
epilepsy or that stress causes permanent changes in the release of neurotransmitters that
inhibit the laying down of memory traces.
Some theorists argue that alter identities in DID may be the construction of the
therapeutic process itself rather than full‐blown symptoms that precede treatment.

14.3 THE TREATMENT OF DISSOCIATIVE DISORDERS

The main issues to be addressed in the treatment of dissociative disorders are (a) helping to alleviate
selective amnesia for life events and helping the client to adapt to recovered memories if they are painful
or traumatic ones, and (b) helping individuals with DID to identify alter identities and to merge them
fully into a single, integrated identity.
Clinicians attempting to treat dissociative disorders face a number of problems:
1. For some complex disorders such as DID therapeutic techniques are relatively underdeveloped and
there are no formal evidence‐based guidelines yet available for DID in many countries.
2. Outcome studies designed to assess effectiveness of therapy methods are relatively rare, often
because the interventions for dissociative disorders require long‐term and specialised treatment (but
see Myrick et al., 2017).
3. Some dissociative disorders such as dissociative amnesia often spontaneously remit, so it is difficult
in these cases to assess whether those therapeutic methods that have been applied are effective or
 not.
4. Dealing with recovered memories is often a severely traumatic experience for the client and may
involve the intense re‐experiencing of traumatic events (known as abreaction), and this may
continually plunge the client into emotional crisis.

abreaction The intense re‐experiencing of traumatic events.

5. Some overly directive therapeutic styles may lead to the recovery of false memories, with the
potential broad range of negative consequences that this might have for the client and their family
(see Focus Point 14.2).
6. In DID, integrating alter identities into a single, functional identity is an extremely difficult process
—many clients find that having a series of alter identities is a useful way of explaining their
behaviour to others and absolving the ‘host’ identity from blame and responsibility, and breaking
this down in difficult (Hale, 1983). For example, in a survey of 153 clients undergoing therapy for
DID, Piper (1994) found that only 38 of 153 (25%) achieved a stable integration of their alter
identities, but other longer term studies have intimated at more optimistic outcomes, with Kluft
(2000) finding a successful integration rate of 68% over a period of 3 months after therapy.
7. All dissociative disorders are usually comorbid with a range of other common psychopathologies,
and particularly with anxiety disorders, depression, and PTSD; dealing with these comorbid
problems will also usually be a requirement in therapy.
As we mentioned at the beginning of this section, therapies for dissociative disorders are relatively
underdeveloped, but we will discuss the most commonly used ones. These are psychodynamic therapy,
hypnotherapy, and—to a lesser extent—drug therapy.

hypnotherapy A form of therapy undertaken while the client is hypnotised.

14.3.1 Psychodynamic Therapy

One of the most common forms of treatment for dissociative disorders is individual psychodynamic
therapy (Brand, Classen, McNary, & Zaveri, 2009). Freud viewed dissociative symptoms, especially
dissociative amnesia, as a form of repression in which memories that were considered too painful to
tolerate were repressed to the unconscious mind. Like most approaches to dissociative disorders,
psychodynamic therapy requires a measured step‐by‐step approach to revealing repressed memories or
integrating multiple personalities. The usual process is first to establish a trusting and workable
relationship between therapist and client followed by attempts to deal directly with repressed memories
or alter identities. This second stage is clearly the most challenging. First, memory retrieval may be as
traumatising as the original experience, and this is known as abreaction. Re‐experiencing trauma in this
way will clearly be distressing to the client, and may well initiate further emotional turmoil. In an
attempt to avoid full‐blown abreaction, some therapists have proposed that repressed memories of abuse
should be retrieved only piece by piece, with the client learning to adapt emotionally to each memory
fragment before moving on to retrieve the next (Kluft, 1999). Second, in the case of clients with DID,
this second stage will often be characterised by the client's resistance to integrating multiple identities.
For the individual with DID, multiple personalities appear to serve a coping function in allowing the
sufferer to abdicate responsibility for actions and emotions to individual identities, and successful
therapy will need to deal with these ‘responsibilities’ before integration can be achieved. Indeed, in
many cases, the subpersonalities will view ‘fusion’ of their identities as a form of death that has to be
avoided (Kluft, 2001; Spiegel, 1994). Finally, if these stages of treatment are progressed successfully, the
client will normally need to have training in a range of skills to enable them to cope with day‐to‐day
living with either their recovered memories or their newly integrated personality. In particular, training
will be needed in how to avoid dissociation when encountering future stressors (Kihlstrom, 2001).
Almost any form of psychotherapy is a lengthy process where dissociative disorders are concerned.
Issues have to be approached cautiously, and there may be many occasions when the therapeutic process
takes steps backward as well as forward. In the case of DID, the greater the number of multiple
identities that need to be integrated, the longer the therapeutic process will take, and an average
treatment programme of 500 hours per client over an average of 2 years has been reported (Putnam et
al., 1986; see International Society for the Study of Trauma & Dissociation, 2011, for some guidelines
for treating DID in adults).

14.3.2 Hypnotherapy
This is a method that is used relatively regularly with those who suffer dissociative disorders. This is
because sufferers are unusually susceptible to suggestion and hypnosis (Bliss, 1980), and at least some
clinicians believe that dissociative symptoms such as amnesia or multiple identities may be the result of
a form of ‘self‐ hypnosis’ by which individuals are able to restrict certain thoughts and memories
entering consciousness (Frischholz, Lipman, Braun, & Sachs, 1992). Using hypnotherapy, the clinician
can help guide the client through the recall of repressed memories. Hypnosis is also used to help people
to regress to childhood states in an attempt to help them recall significant events that they may have
repressed. Drugs such as sodium amobarbital and sodium pentobarbital can also be used
concurrently with hypnotherapy to help clients recall past events (Ruedrich, Chu, & Wadle, 1985). One
assumption in the hypnotherapy approach is that hypnosis will recreate the physical and mental state
the client was in prior to experiencing any trauma, and this will help the individual to recall events
during earlier stages of their life. This is known as age regression, and while some clients find this
helpful in recalling and dealing with repressed memories, there is no objective evidence that hypnosis
does recreate any of the physical or mental states experienced earlier in life. Hypnotherapy is also used
in the treatment of DID in order to help bring potential alter identities into consciousness and to
facilitate the fusion of identities. However, although widely used in the treatment of dissociative
disorders there have been no systematic group‐ or single‐case studies of the effectiveness of this
technique (Cardena, 2000).

sodium amobarbital A drug which can be used concurrently with hypnotherapy to help
clients recall past events.

sodium pentobarbital A drug which can be used concurrently with hypnotherapy to help
clients recall past events.

age regression In hypnotherapy, the recreation of the physical and mental state that a client
was in prior to experiencing any trauma in order to help the individual recall events during
earlier stages of his or her life.

14.3.3 Drug Treatments

Because anxiety and depression are common features of dissociative disorders and may be diagnosable
comorbid conditions, some antidepressant and anxiolytic drugs have been used successfully to treat
some of these supplementary symptoms. Antidepressants and tranquilisers have been used to address
the depression and anxiety associated with DID, but these drugs tend to have little effect on the main
symptoms of DID itself (Simon, 1998). There is, however, some evidence that selective serotonin
reuptake inhibitors such as Prozac may help to alleviate the symptoms of depersonalisation disorder
(Simeon, Stein, & Hollander, 1995), and because there is some evidence for abnormalities in the
endogenous opioid systems in depersonalisation disorder, opioid antagonists such as naltrexone have
been found to reduce depersonalisation symptoms by an average 30% (Simeon & Knutelska, 2005).

14.3.4 Summary
Treating dissociative disorders can often be a lengthy process, whether through conventional
psychotherapy or hypnotherapy. This picture is additionally clouded by the fact that many health
insurers are increasingly requiring treatments that are empirically supported, and in some countries—
such as the Netherlands—psychoanalysis is no longer being reimbursed as a treatment for dissociative
disorders (Brand, 2012). More recently, staged treatments have been developed that are assessed using
empirically based methods (e.g., schema therapy for DID), and may provide more evidence‐based
alternatives to traditional psychoanalysis and hypnotherapy (Baars et al., 2011; Brand, Lanius,
Vermetten, Loewenstein, & Spiegel, 2012; Huntjens, Rijkeboer, & Arntz, 2019). Apart from the
therapies we have discussed in this section, many individuals with dissociative disorders can often be
treated with cognitive behaviour therapy (CBT) for their depression and anxiety symptoms. Because
both dissociative and PTSD symptoms may be an outcome of extreme trauma, those therapies used to
treat PTSD also have some success in dealing with dissociative symptoms (e.g., therapies such as
cognitive restructuring, eye movement desensitisation and reprocessing—EMDR, see Chapter 6).

SELF‐TEST QUESTIONS
What are the main problems facing clinicians who attempt to treat dissociative disorders?
Can you describe the main characteristics of psychodynamic therapies for dissociative
disorders?
What is the evidence that hypnotherapy is an effective treatment for dissociative disorders?

SECTION SUMMARY

14.3 THE TREATMENT OF DISSOCIATIVE DISORDERS

Abreaction and the recovery of false memories are important issues to consider in the
treatment of dissociative disorders.
Psychodynamic therapies attempt to bring repressed memories back to the conscious mind so
that they can be effectively dealt with.
Hypnotherapy is a common form of treatment for dissociative disorders, and those diagnosed
with dissociative disorders are unusually susceptible to suggestion and hypnosis.
Some antidepressant and anxiolytic drugs have been successful in treating some of the
depression and anxiety related symptoms of dissociative disorders.
14.4 DISSOCIATIVE DISORDERS REVIEWED
In this chapter we have described the main features of three dissociative disorders—dissociative
amnesia, DID, and depersonalisation disorder. All represent a failure to integrate various aspects of
identity, consciousness, and memory, and most involve some form of amnesia for past life events or
autobiographical memories. All of these disorders are associated with severe psychological stress.
Symptoms may manifest immediately after severe traumatic experiences (such as war or a natural
disaster) or they may develop over a number of years. In the latter case, DID is a particular example
where selective amnesia and multiple identities may develop many years after severe childhood trauma
such as sexual or physical abuse.
There are a number of theories of the aetiology of dissociative symptoms, but most relate in some way
to early trauma. Psychodynamic theories claim that dissociative symptoms such as amnesia are ways of
coping with severe traumatic experiences by repressing these memories to the unconscious mind.
Cognitive accounts are much more interested in the mechanisms by which memories are selectively
repressed in dissociative disorders, and laboratory studies have identified deficits in source‐monitoring
ability and reality monitoring (e.g., not being able to effectively differentiate imagined events from
experienced events). In contrast, some theorists believe that many of the symptoms of dissociative
disorders (such as the multiple alter identities in DID) are merely constructions of the therapeutic
process. That is, therapy that is either too directive or attempts to probe too deeply to confirm a
diagnosis of DID actually plays a causal role in the development of alter identities.
Treatments for dissociative disorders are relatively underdeveloped, and the most popular are
psychodynamic approaches and hypnotherapy. For many dissociative disorders, therapy can be a lengthy
process as the sufferer often has to deal with recovered memories of trauma that may involve intense re‐
experiencing of these events. The therapeutic process can also be problematic as we discussed in Focus
Point 14.2, where overdirective psychotherapy can often create false recovered memories of trauma and
abuse, and these false memories can often have catastrophic consequences for both the client and their
family.
This book is accompanied by Student and Instructor companion
websites.
www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter References
Videos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
15
Neurocognitive Disorders

ROUTE MAP OF THE CHAPTER

The chapter begins by describing some of the cognitive impairments that characterise
neurocognitive disorders and identifying some of the brain areas associated with these deficits.
We then discuss some of the various methods used by clinical neuropsychologists to assess
cognitive functioning, and some of the difficulties associated with diagnosis. The second part of
the chapter looks more closely at the various types of neurocognitive disorder described in
DSM‐5 and their causes. These can involve cerebral infection, traumatic brain injury,
cerebrovascular accidents such as strokes, and degenerative disorders such as Alzheimer's
disease. Finally, we cover some of the treatment and rehabilitation programmes that have been
developed to tackle neurocognitive disorders, including drug treatments, cognitive rehabilitation
procedures, and the role of caregiver support programmes.

CHAPTER OUTLINE
15.1 THE DIAGNOSIS AND ASSESSMENT OF NEUROCOGNITIVE
DISORDERS
15.2 TREATMENT AND REHABILITATION FOR NEUROCOGNITIVE
DISORDERS
15.3 NEUROCOGNITIVE DISORDERS REVIEWED

LEARNING OUTCOMES

When you have completed this chapter, you should be able to:
1. Describe some of the cognitive impairments that characterise neurocognitive disorders.
2. Describe some of the main methods that clinical neuropsychologists use to assess cognitive
functioning in neurocognitive disorders.
3. Describe a range of types of neurocognitive disorders and evaluate their causes.
4. Describe, compare, and contrast the various types of treatment and rehabilitation
programmes that have been developed to deal with neurocognitive disorders.
 Within the last 8 months I've been at war with the cooker. I put the oven on at a temperature which I know is
right only to find the meat burnt or not cooked because what I thought was the right temperature was not. It gets
me so annoyed. I also forget what time I put things in the oven—even if I repeat it to myself a few times and keep
looking at the clock. If I do something else, go upstairs, for example, I cannot remember what time the food went in
no matter how I try.
I've had to give up driving. I kept losing concentration and my speed just got faster and faster. I could have caused
an accident—especially when feeling disoriented. I still work part‐time, but that is slipping something awful. I do
things at work alone as much as possible so no one can see the mistakes I'm making. I've had all the tests now, but
the neurologist tells me all the findings so far are consistent with AD (Alzheimer's disease). To be honest, trying to
get through the day is like knitting with a knotted ball of wool. Every now and again I come to a knot. I try to
unravel it but can't, so I knit the knot in. As time goes by, there are more and more knots.
Paddy's Story

Introduction
The majority of the disorders we have discussed in this book so far appear to have psychological origins.
That is, people have experiences that give rise to problematic ways of thinking and behaving, and these
ways of thinking and behaving may cause distress and form the basis for diagnosable psychopathologies.
In contrast, neurocognitive disorders have their origins in damage or abnormalities in the biological
substrates that underlie thinking and behaving. This damage or degeneration can be caused by disease,
physical trauma (such as brain injury), or genetic predispositions causing irreversible changes in the
brain and central nervous system. By definition, the causes of neurocognitive disorders are biological
and can usually be identified as biochemical imbalances in the brain and central nervous system or
direct or indirect damage to brain tissue. Despite the fact that the causes of neurocognitive disorders are
primarily physical, psychology is centrally important in the diagnosis, assessment, and rehabilitation of
individuals suffering such disorders. For example, some of the first signs of neurocognitive disorders
(such as dementia, brain injury, or stroke) are deficits in basic cognitive functions such as perception,
learning, memory, attention, language, and visuospatial skills, and also deficits in what are known as
executive functions (i.e., those skills that involve problem‐solving, planning, and engaging in goal‐
directed behaviour). Clinical psychologists are therefore actively engaged in assessing these abilities and
interpreting whether any deficits are early signs of neurocognitive disorders. In addition, neurocognitive
disorders do not only generate deficits in basic cognitive functioning, they can also affect disposition and
personality. An individual diagnosed with a neurocognitive disorder may become both depressed and
anxious and require suitable treatment for these conditions. They may also display radical changes in
personality and behaviour, such as impulsivity or outbursts of aggressive behaviour. These also need to
be managed and treated. Finally, clinical psychologists are also centrally involved in the development of
rehabilitation programmes that may have a variety of aims, including (a) restoring previously
affected cognitive and behavioural functions (although this is often a difficult task), (b) helping clients to
develop new skills to replace those that have been lost as a result of tissue damage (e.g., learning to use
memory aids), (c) providing therapy for concurrent depression, anxiety or anger problems, and (d)
providing clients and carers with skills and advice that will help them structure their living environment
in a way that will help to accommodate changes in cognitive and behavioural abilities.

executive functions Cognitive skills that involve problem-solving, planning and engaging in
goal‐directed behaviour.
 rehabilitation programmes Treatment programmes that usually combine a mixture of
group work, psychological interventions, social skills training and practical and vocational
activities.

At the beginning of this chapter we described Paddy's Story, which recounts the experiences of someone
who is in the early stages of Alzheimer's disease. This describes her awareness of her memory lapses,
mistakes, and periodic disorientation that give rise to frustration, anxiety, and depression. For many who
are in the early stages of a degenerative neurocognitive condition, these experiences can be both
frequent and frightening.
We continue this chapter by discussing some of the more general characteristics of neurocognitive
disorders and the diagnostic and assessment issues that are relevant to them.

15.1 THE DIAGNOSIS AND ASSESSMENT OF NEUROCOGNITIVE

DISORDERS
First, let's look at some of the cognitive impairments that are commonly found in neurocognitive
disorders. We then discuss some broader diagnostic and assessment issues.

15.1.1 Cognitive Impairments in Neurocognitive Disorders

Learning and memory deficits

Amnesia is a common feature of many neurocognitive disorders, including an inability to learn new
information, a failure to recall past events, but more commonly a failure to recall events in the most
recent past. If the neurological condition is caused by a specific traumatic event (such as a head injury),
the individual may be unable to recall anything from the moment of the injury or to retain memories of
recent events. This is known as anterograde amnesia or anterograde memory dysfunction.
The effects of anterograde amnesia are dramatically displayed in the 2000 film Memento in which the
lead character, Leonard, is unable to form new memories as a result of an earlier head injury caused by
an assailant. The film graphically describes how Leonard has to develop a series of ad hoc ways of
coping with his inability to recall recent events. More commonly, in degenerative disorders such as
dementia, memory deficits slowly develop from what initially appears like normal forgetfulness to
become a more full‐blown inability to recall events. In the latter case, sufferers may often seem
“rambling” as they attempt to make up events to fill the gaps in their memory.

anterograde amnesia Memory loss for information acquired after the onset of amnesia.
Also known as anterograde memory dysfunction.

anterograde memory dysfunction Memory loss for information acquired after the onset
of amnesia. Also known as anterograde amnesia.

Deficits in attention and arousal

Some first indications of neurocognitive problems are when the individual shows signs of lack of
attention, being easily distracted, and performing well‐learned activities more slowly than before (such
as having difficulty using the controls of a smartphone or TV). They may also have difficulty focussing
on or keeping up with a conversation, and need more time to make simple decisions.

Language deficits
The individual may appear to be rambling during conversations and have difficulty conveying what they
have to say in a coherent manner. They may also have difficultly reading and understanding the speech
of others. Language deficits are one of the most common features of neurocognitive disorders, and are
collectively known as aphasias. Language impairments can take many forms, including (a) an inability
to comprehend or understand speech or to repeat speech accurately and correctly; (b) the production of
incoherent, jumbled speech (known as fluent aphasia); and (c) an inability to initiate speech or
respond to speech with anything other than simple words (known as nonfluent aphasia). A distinction
can be made between Broca's aphasia and Wernicke's aphasia. Disruption of the ability to speak
is known generally as Broca's aphasia, and consists of difficulties with word ordering (agrammatism),
finding the right word (anomia) and articulation. It is characterised by laborious nonfluent speech
involving mispronounciation rather than mis‐selection of words. In contrast, Wernicke's aphasia is a
deficit in the comprehension of speech involving difficulties in recognising spoken words and converting
thoughts into words. Damage to different areas of the left hemisphere (which controls speech) are
specific to each of these deficits. Wernicke's aphasia is associated with damage to regions behind the
frontal lobes whereas Broca's aphasia is more likely to result from damage to the left frontal lobe itself
(see Table 15.1).

aphasias A speech disorder resulting in difficulties producing or comprehending speech.

fluent aphasia The production of incoherent, jumbled speech.

nonfluent aphasia An inability to initiate speech or respond to speech with anything other
than simple words.

Broca’s aphasia Disruption of the ability to speak consisting of difficulties with word
ordering, finding the right word and articulation.

Wernicke’s aphasia A deficit in the comprehension of speech involving difficulties in

recognising spoken words and converting thoughts into words.
TABLE 15.1 Terminology: cognitive impairments in neurocognitive disorders
Term Definition Main brain areas affected
Aphasia Speech disorder resulting in difficulties Language centres of the left hemisphere
producing or comprehending speech (usually Broca's Area or Wernicke's Area)
(Figure 1)
Agnosia Loss of ability to recognise objects, Occipital or parietal lobes (Figure 2)
persons, sounds, shapes, or smells while the
specific sense is not defective nor is there
any significant memory loss
Apraxia Loss of the ability to execute or carry out Parietal lobes of the left hemisphere (Figure
learned (familiar) movements, despite 2)
having the desire and the physical ability to
perform the movements
Anterograde Memory loss for information acquired Hippocampus; medial temporal lobes; basal
Amnesia after the onset of amnesia forebrain (Figure 2)
Retrograde Inability to recall events that occurred Hippocampus; temporal lobes (Figure 2)
Amnesia before the onset of amnesia
Deficits in The inability to effectively solve problems, Frontal Lobes (especially the prefrontal
Executive plan, initiate, organise, monitor and inhibit cortex) (Figure 2)
Functioning complex behaviours
Figure 1 Figure 2

Deficits in visual‐perceptual functioning

In some cases the individual may be unable to recognise everyday objects and name them correctly.
This is known as agnosia and it can affect a wide variety of functional skills, such as face perception
(prosopagnosia) and musical discrimination (amusia). A famous example of agnosia is recounted in the
book The Man Who Mistook His Wife for a Hat and Other Clinical Tales by Oliver Sacks. He describes the
case of Dr. P., a music professor who had developed visual agnosia. He was able to identify and describe
complex shapes but often could not recognise his own students' faces, and could only identify them
when they spoke. The title of the book comes from an occasion when Dr. P. was leaving a house and
reached for his wife's head, mistaking it for a hat and trying to lift it off. Interestingly his agnosia affected
only his visual perceptions and did not affect his music abilities in any way.
 agnosia The loss of the ability to recognize objects, persons, sounds, shapes or smells while the
specific sense is not defective and there is no significant memory loss.

Motor skill deficits

Some neurocognitive disorders are characterised by impairments in motor performance and
coordination. This may involve the inability to move a limb, a tendency to suddenly become paralysed,
or difficulty in coordinating movements effectively. This is known as apraxia, and in more complex
cases the individual with apraxia may be able to emit a behaviour when it is under routine conditions
(e.g., cleaning their teeth as part of their washing routine first thing in the morning) but are unable to do
this on command.

apraxia Loss of the ability to execute or carry out learnt (familiar) movements, despite having
the desire and the physical ability to perform the movements.

Deficits in executive functions

This reflects the inability to effectively solve problems, plan, initiate, organise, monitor, and inhibit
complex behaviours. These functions are normally associated with the prefrontal cortex, and so
damage to this area of the brain is frequently involved when executive function deficits are found. A
widely used test of executive functioning is the Wisconsin card sorting test, where individuals must
sort cards for a number of trials using one rule (e.g., colour) and then sort cards using a different rule
(e.g., shape). This requires the ability to shift attention and to inhibit an established response pattern.
Deficits in executive functioning are revealed in everyday behaviour by examples of poor judgement
(e.g., erratic or unsafe driving), inappropriate behaviour (e.g., leaving the house in inappropriate clothing
such as pyjamas), and erratic mood swings (e.g., from laughter to hostility).

Wisconsin card sorting task A widely used test of executive functioning where individuals
must sort cards for a number of trials using one rule (e.g. colour) and then sort cards using a
different rule (e.g. shape).

Deficits in higher‐order intellectual functioning

Impairment in more abstract mental tasks is another possible indication of a neurological disorder, and
individuals may be unable to make simple mathematical calculations, to reason deductively, or to draw
on general knowledge when undertaking a task or activity (Table 15.1).

15.1.2 Assessment in Clinical Neuropsychology

Identifying that someone has a neurocognitive disorder is a difficult and often lengthy process.
Assessment is important (a) for determining the actual nature of any deficits and the location of any
related tissue damage in the brain, (b) for providing information about onset, type, severity, and
progression of symptoms, (c) for helping to discriminate between neurological deficits that have an
organic basis and psychiatric symptoms that do not, and (d) for helping identify the focus for
rehabilitation programmes and to assess progress on these programmes (Reason, Healey, & Rich, 2015;
Shepherd, Stapleton, & Jeal, 2015). In many cases, a diagnosis has to be made on the basis of cognitive
and behavioural impairments that are detected by a range of neuropsychological tests, and the results of
these tests can be supplemented by findings from electroencephalogram (EEG) analyses, brain scans
such as PET scans and fMRI, blood tests, and chemical analyses of cerebrospinal fluids. Assessment of
cognitive abilities is also supplemented with behavioural observation, and information from clients and
their families about onset, type, severity and progression of symptoms, together with a detailed history
of educational, occupational, psychosocial, demographic, and previous and current medical factors.
Neuropsychological tests themselves can be remarkably accurate in detecting quite specific deficits and
also identifying the brain areas where tissue damage may have led to the deficit. Brain scans can then
supplement and confirm the results of neuropsychological tests (D'Esposito, 2000). One of the most
widely used tests worldwide is the WAIS IV (the Wechsler Adult Intelligence Scale, Fourth Edition)
(Wechsler, 2008) (see Chapter 2, Section 2.2.3). This contains scales that measure vocabulary, arithmetic
ability, digit span, information comprehension, letter‐number sequencing, picture completion ability,
reasoning ability, symbol search and object assembly ability. These measures can be aggregated to
provide scores on broader indices of ability such as verbal comprehension, perceptual organisation (a
measure of nonverbal reasoning), working memory, and information processing speed. In the UK, the
Adult Memory and Information Processing Battery (AMIPB) (Coughlan & Hollows, 1985) is
widely used, and this comprises two tests of speed of information processing, verbal memory tests (list
learning and story recall), and visual memory tests (design learning and figure recall). One of the
common neuropsychological tests used in the US is the Halstead‐Reitan Neuropsychological Test
Battery (Broshek & Barth, 2000), which has been compiled to evaluate brain and nervous system
functioning across a fixed set of eight tests. The tests evaluate function across visual, auditory and tactile
input, verbal communication, spatial and sequential perception, the ability to analyse information, the
ability to form mental concepts, make judgements, control motor output, and to attend to and
memorise stimuli.

FOCUS POINT 15.1 THE TRAIL MAKING TASK

This is an example of the trail making test. It consists of a page with circles containing the
letters A to L and 13 numbered circles intermixed and randomly arranged. The patient is
instructed to connect the circles by drawing lines alternating between numbers and letters in
sequential order until they reach the circle labelled ‘End’. This test would normally take 5–10
minutes to complete.
The trail making test helps to evaluate information processing speed, visual scanning ability,
integration of visual and motor functions, letter and number recognition and sequencing, and
 the ability to maintain two different trains of thought.
For adults, scores above 91 seconds have traditionally indicated brain impairment, but
completion times may vary significantly with age, education, and culture.

Test batteries such as these also provide useful information on the source of any deficits (such as closed
head injury, alcohol abuse, Alzheimer's disease, stroke, etc.), whether the damage occurred during
childhood development, and whether any deficits are progressive. Focus Point 15.1 provides an example
of one of the basic tests—the trail making test—that provides a measure of information processing
speed and a range of recognition and visuo‐motor integration abilities. Many of these tests are so
extensive that they may take as long as 6 hours to administer, requiring substantial patience and stamina
on the part of both the clinician and the patient. In contrast, some other tests have been developed to
be quick and simple to implement, and to provide a reasonably reliable indication of general level of
impairment. One such test is the Mini‐Mental State Examination(MMSE), which is a brief 30‐
item test used to screen for dementia (e.g., in Alzheimer's disease) and takes about 10 minutes to
administer (see Focus Point 15.2) (see also Tsoi, Chan, Hirai, Wong, & Kwok, 2015, for a systematic
review and meta‐analysis of cognitive tests to detect dementia).

15.1.3 The Diagnosis of Neurocognitive Disorders

Difficulties of diagnosis
Diagnosis is made difficult by the fact that the symptoms and deficits found in neurocognitive disorders
often closely resemble those of other psychopathologies. For example, cognitive deficits typical of
neurocognitive disorders are a regular feature of dissociative disorders (e.g., amnesia), and schizophrenia
(e.g., language deficits, information‐processing deficits, and deficits in executive functions). Motor
coordination deficits, paralysis, and impairments of sensory input are also found in somatic symptom
disorders such as conversion disorder (e.g., hysterical paralysis and blindness, see Chapter 13). In
addition, in the early stages of a degenerative neurological disorder people will start to experience
cognitive impairments that affect their daily lives, and this will often lead to the development of
psychological problems (e.g., depression and anxiety) that compound the difficulties of diagnosis (see
Paddy's Story at the beginning of this chapter). Indeed, prior to the development of modern brain
scanning technology, it was often the case that a neurological disorder could be diagnosed only by
autopsy after the death of the sufferer (Patton & Shepherd, 1956). Even so, with the range of tests
available today psychological problems can still be misdiagnosed as neurological ones (e.g., Iverson,
2006), and vice versa (e.g., Sumpter & McMillan, 2005), and this has important implications for
rehabilitation and subsequent care.

FOCUS POINT 15.2 MINI MENTAL STATE EXAMINATION

(MMSE)

The MMSE is a good instrument for assessing cognitive function in dementia and takes about
10 minutes to administer.
Orientation
What is the (year) (season) (date) (day) (month)?
5□
Where are we: (country) (city) (part of city) (number of flat/house) (name of street)?
5□
Registration
Name three objects: 1 second to say each.
Then ask the patient to name all three after you have said them.
Give one point for each correct answer.
3□
Attention and calculation
Serial 7s: Ask the patient to begin with 100 and count backwards by 7. Stop after 5 subtractions
(93, 86, 79, 72, 65). One point for each correct.
5□
Recall
Ask for the three objects repeated above (under Registration).
Give one point for each correct.
3□
Language
Name a pencil and watch (Show the patient a wrist‐watch and ask him or her what it is). Repeat for
pencil. (two points).
Repeat the following: ‘No ifs, ands or buts’ (one point).
Follow a three‐stage command: ‘Take a paper in your right hand, fold it in half and put it on the
floor’ (three points).
Read and obey the following: Close your eyes (one point).
Write a sentence (one point).
Copy a design (one point). On a clean piece of paper, draw intersecting pentagons (as below),
each side about 1 in. and ask him or her to copy it exactly as it is. All 10 angles must be present
and two must intersect to score 1 point. Tremor and rotation are ignored.

9□
Total score____________
A score of 20 or less generally suggests dementia but may also be found in acute confusion,
schizophrenia or severe depression. Mild Alzheimer's is usually linked to an MMSE score of
21–26, Moderate Alzheimer's to scores of 10–20, and severe Alzheimer's to an MMSE score of
less than 10.
To add to the difficulties of diagnosis, the symptoms of a range of neurological disorders overlap
considerably. For example, damage to specific areas of the brain as a result of a closed head injury can
give rise to similar cognitive deficits as those found in broader degenerative disorders such as
Alzheimer's disease. Similarly, a single causal factor (such as a brain tumour) can manifest as a range of
different symptoms including speech disorder, deficits in sensory perception, or emotionality and
aggressiveness. These are some of the reasons why neurological assessment is thorough and multifaceted
and continues to be administered throughout the period of diagnosis and rehabilitation.

DSM‐5 neurocognitive disorder diagnostic categories

The Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM‐5) identifies two broader
diagnostic syndromes into which many neurological disorders fall. They are delirium—which is
characterised by confused and disorganised behaviour, and major or mildneurocognitive
disorders (NCDs) (formally known in DSM‐IV as dementias)—which are characterised by the
impairment of basic cognitive functions. We will look at these two diagnostic categories more closely.

delirium A disturbance of consciousness that develops over a short period of time.

major neurocognitive disorder (NCDs) DSM‐5 defines neurocognitive disorders (NCDs)

as conditions where there is evidence of a significant decline in performance across one or more
cognitive domains, such as complex attention, executive functioning, learning and memory,
language, perceptual‐motor, or social cognition. Major NCDs reflect a substantial impairment.

Delirium
The main feature of a delirium is a disturbance of attention and awareness, and the disturbance in
attention is reflected in a reduced ability to direct, focus, sustain, and shift attention, and the disturbance
develops over a short period of time. The person may not understand simple questions, and may be
unable to shift attention from answering one question to answering another. Delirium often occurs in
the context of other neurocognitive disorders, and may be accompanied by memory and learning
deficits, disorientation, and perceptual disturbances such as hallucinations. There may be evidence that
the delirium is a result of the physiological consequences of a general medical condition, substance
intoxication or withdrawal, or use of a medication or a toxin and may be associated with disturbances
in the sleep‐wake cycle, such as a reversal of the day‐night cycle, restlessness, and hyperactivity. The
individual may also exhibit emotional disturbances such as anxiety, fear, depression, irritability, anger,
euphoria, and apathy, accompanied by rapid and unpredictable shifts from one emotional state to
another.

dementias The development of multiple cognitive deficits that include memory impairment
and at least one other specific deficit.

The symptoms of delirium can develop rapidly over hours to days but may begin abruptly after specific
traumatic events, such as head injury. Equally, delirium may resolve in just a few hours, but alternatively
persist for weeks to months especially in the elderly. Delirium appears to result from widespread
disruption of brain metabolism and neurotransmitter activity that can be triggered by a range of events.
These can include traumatic head injury, substance intoxication or withdrawal, surgery, sleep loss,
malnutrition, and psychological stress generally. Delirium is particularly common in older people, and
particularly hospitalised older people. The community prevalence rate for delirium is 1–2%, but
increases with age, rising to 14% amongst those over 85 years‐of‐age (DSM‐5, American Psychiatric
Association, 2013, p. 600) (Table 15.2).

Major or minor neurocognitive disorders (NCDs)

DSM‐5 defines neurocognitive disorders as conditions where there is evidence of a significant decline in
performance across one or more cognitive domains, such as complex attention, executive functioning,
learning and memory, language, perceptual‐motor, or social cognition. This decline can be diagnosed as
either major—reflecting a substantial impairment, or minor—reflecting a modest impairment in
cognitive performance. Major neurocognitive disorders correspond to the categories labelled as
dementias in previous editions of the DSM. Examples of cognitive deficits include difficulty
remembering a short grocery list or keeping track of the plot of a TV programme; executive
functioning problems include difficulty resuming a task when interrupted, organising finances, or
planning a meal out. At the mild NCD level, the individual will describe these tasks as requiring extra
time or additional compensatory strategies. However, at the major NCD level, the individual will
normally require assistance to complete these kinds of tasks. The DSM‐5 diagnostic criteria for major
and minor neurocognitive disorders are provided in Tables 15.3 and 15.4.
TABLE 15.2 Summary: DSM‐5 diagnostic criteria for delirium

A reduced ability to focus, direct, and sustain attention and awareness, developing over a short
period of time (hours to a few days) and fluctuates in severity throughout that time
Additional disturbances in cognitive functioning are also observed
Disturbances are not a result of a preexisting neurological condition and do not occur during the
course of a coma or other reduced level of arousal state
There is no evidence that the disturbance is as a direct physiological result of another medical
condition, substance use, or withdrawal
In the major neurocognitive disorders, language function may deteriorate to the point where the
individual's conversation is vague or empty, and they may be unable to name individual everyday
objects (such as tie, dress, desk, lamp, etc.). The condition may also (but not necessarily) be associated
with apraxia (impaired ability to execute motor activities) and agnosia (the failure to recognise or
identify objects despite intact sensory functioning). Disturbances in executive functioning are also
common and are evidenced by the individual having difficulty coping with new tasks, shifting mental
sets, generating novel verbal information, and using or recalling basic general knowledge. Simple tests
for executive functioning include asking the individual to count to 10, recite the alphabet, do
subtraction, or state as many animals as possible in 1 minute. Poor judgement and poor insight are also
common features of major neurocognitive disorders. They may underestimate the risks involved in
certain activities (e.g., driving) and indulge in inappropriate behaviours, such as making inappropriate
jokes, neglecting personal hygiene, or disregarding conventional rules of social conduct.
TABLE 15.3 Summary: DSM‐5 diagnostic criteria for major neurocognitive disorder

Significant cognitive deterioration from previous level in at least one of the cognitive domains
based on:
Concern of the patient, informant, or doctor that there has been a substantial decline in
cognitive function
A substantial impairment in cognitive performance, preferably as documented by standard
testing
The cognitive deterioration interferes with self‐reliance in everyday activities
The deficit does not occur in the context of delirium
The deficit is not better accounted for by another mental disorder such as major depressive
disorder or schizophrenia

TABLE 15.4 Summary: DSM‐5 diagnostic criteria for mild neurocognitive disorder

Limited cognitive deterioration from previous level in at least one of the cognitive domains based
on:
Concern of the patient, informant, or doctor that there has been a limited decline in
cognitive function
A limited impairment in cognitive performance, preferably as documented by standard
testing
The cognitive deterioration does not interfere with self‐reliance in everyday activities
The deficit does not occur in the context of delirium
The deficit is not better accounted for by another mental disorder such as major depressive
disorder or schizophrenia
DSM‐5 lists a number of specific major neurocognitive disorders, and we will look at these individually
in more detail next. These are Alzheimer's disease, vascular neurocognitive disorders, NCD due
to Parkinson's disease, NCD due to traumatic brain injury. NCD due to human immunodeficiency virus
(HIV) infection, NCD due to Huntington's disease, NCD due to prion disease, and NCD with Lewy
bodies.

Types of major neurocognitive disorder

In this section, we look in more detail at some of the prevalent neurocognitive disorders that are
categorised by their causes. These causes can range across cerebral infection, traumatic brain injury,
cerebrovascular accidents (such as strokes), and degenerative disorders (such as Alzheimer's disease).

NCD due to HIV infection

Among the viruses that can infect the brain is the human immunodeficiency virus type 1 (HIV‐1). The
HIV virus tends to enter the central nervous system early in the illness, and neurological difficulties can
develop in up to 60% of those infected with the virus (Ghafouri, Amini, Khalili, & Sawaya, 2006). On
many occasions, the impairments caused by infection are usually minor, but over the many years that a
sufferer may be hosting the virus, it may induce multiple symptoms of motor and cognitive dysfunction
and create a syndrome of impairment that is known in DSM‐5 as neurocognitive disorder due to
HIV infection (sometimes also known as AIDS dementia complex, ADC, or HIV‐1 associated
dementia, HAD). Individuals who develop this NCD diagnosis show impaired executive functioning,
slowed speed of processing information, problems with attentional tasks, and difficulty learning new
information. Other symptoms include impaired short‐term memory, lack of concentration, leg
weakness, slowness of hand movement, and depression (Reger, Welsh, Razani, Martin, & Boone, 2002)
(Table 15.5). Depending on the stage of their infection, around a third to a half of HIV‐infected
individuals will develop at least mild neurocognitive impairment, but fewer than 5% would normally
meet the criteria for major neuorocognitive disorder (DSM‐5, American Psychiatric Association, 2013,
p. 633). HIV infection appears to cause these cognitive impairments in a variety of ways. Magnetic
resonance imaging (MRI) scans indicate that HIV infection is associated with progressive cortical
atrophy in the gray and white matter in the brain, particularly in the later stages of the disease (Dalpan
et al., 1992) (Figure 15.1), and autopsies of people with HIV indicate that between 80% and 90%
exhibit signs of neurological disorders (Gray, Gherardi, & Scaravilli, 1988). However, while the HIV
virus can itself attack the central nervous system, neurological deficits are often caused by the body's
weakened immune system allowing other infections to attack the brain (Ghafouri et al., 2006).
TABLE 15.5 Summary: DSM‐5 diagnostic criteria for neurocognitive disorder due to HIV infection

The criteria are met for major or mild neurocognitive disorder

The patient is infected with human immunodeficiency virus (HIV)
The disorder is not better explained by non‐HIV conditions including secondary brain diseases
The disorder is not due to another medical condition and is not better explained by another
mental disorder

FIGURE 15.1 Functional MRI (fMRI) scans showing activation during a motor task for HIV patients with normal
cognitive (NL), minor cognitive–motor disorder (MCMD), and HIV associated dementia (HAD). Darkened regions
indicate areas of activation. Compared with NL, patients with MCMD and HAD have significantly less activation.
From Tucker et al., 2004.

NCD due to prion disease

In the UK in the 1980s and 1990s what was called ‘mad cow disease’ received considerable attention in
the media. ‘Mad cow disease’ is a fatal infectious disease known as spongiform encephalopathy
that attacks the brain and central nervous system. Outbreaks of the disease hit epidemic proportions
amongst cattle in the UK during the 1980s, and evidence suggests that the disease was transmitted to
humans through contaminated beef. In humans, this became known as variant Creutzfeldt‐Jakob
Disease (vCJD). The disease may have an incubation period of up to 10–15 years, but once symptoms
begin to appear, death may occur within 4 months. Early signs of vCJD include changes in mood,
temperament, and behaviour followed by impairments in memory and concentration and confused
thinking. Deficits in verbal fluency, numeracy ability, face recognition, memory ability, and executive
functioning appear rapidly once symptoms have been identified (Kapur, Abbott, Lowman, & Will, 2003)
(Table 15.6). Thankfully, the annual incidence of Creutzfeld‐Jakob Disease is very low at around one or
two cases per million people (DSM‐5, American Psychiatric Association, 2013, p. 635), but because of
its lengthy incubation period the number of deaths as a result of Creutzfeld‐Jakob Disease in the UK is
still relatively high even though the original causes (such as the availability of contaminated beef) are no
longer a major risk factor (131 deaths in 2019 compared with 33 deaths in 1990, National CJD
Research & Surveillance Unit, 2020). The infectious agent in vCJD is thought to be the prion (a prion
is an abnormal, transmissible agent that is able to induce abnormal folding of normal cellular proteins
in the brain, leading to brain damage), and rapid dementia in vCJD appears to result from prions or
protein deposits encrusting or replacing neurons in the brain and central nervous system. This occurs at
both the cortical and subcortical level, causing deficits in cognitive functioning and basic motor
coordination.

spongiform encephalopathy A fatal infectious disease that attacks the brain and central
nervous system. Commonly known as ‘mad cow disease’ or variant Creutzfeldt–Jakob disease
(vCJD).

prion disease Prion disease represents a group of conditions that affect the nervous system in
humans and animals.

TABLE 15.6 Summary: DSM‐5 diagnostic criteria for neurocognitive disorder due to prion disease

The criteria are met for major or mild neurocognitive disorder

The onset is slow, with rapid progression of the impairment
Motor features of prion disease are obvious, such as involuntary muscle twitching or ataxia
The disorder is not due to another medical condition and is not better explained by another
mental disorder

NCD due to traumatic brain injury

One of the most common causes of neurological impairment is traumatic brain injury. This can result
from blunt or penetrating trauma to the head as a result of direct injury at the impact site. Indirect
injury can also be caused by sudden impacts causing movement of the brain within the skull, leading to
injury on the opposite side of the brain to the impact. Between 2000 and 2017 the incidence of
traumatic brain injuries in England has increased modestly and accounts for just under half of all
acquired brain injuries (see Figure 15.2). Road traffic accidents account for around 40–50% of all head
injuries, while domestic and industrial accidents account for between 20% and 30%. A majority of the
rest are caused by sports and recreational activities (10–15%) and assaults (10%) (The Health & Social
Care Information Centre, 2012). Twice as many males as females are likely to be treated in hospital for
traumatic brain injury, and around 40–50% are children. While the vast majority of these cases will
suffer only a minor head injury, more serious cases will lapse into coma, develop epilepsy, or suffer other
forms of long‐term disability (both physical and intellectual). Although many victims of head injury will
show a slow but gradual improvement over time (e.g., recovery of any memory loss, recovery of motor
functions such as balance, dissipation of feelings of confusion and disorientation), severe head injury
can be associated with a range of semi‐permanent cognitive and neurological deficits, including general
deficits in speed of information processing, attention, memory, language skills, and executive
functioning, and may meet the diagnostic criteria for neurocognitive disorder due to traumatic
brain injury, with around 2% of the population of the US living with a traumatic brain injury‐
associated disability (DSM‐5, American Psychiatric Association, 2013, p. 625) (Table 15.7). If recovery
from such deficits occurs, it is likely to happen in the first 6 months following the injury. However,
perhaps more dramatic than some of the cognitive deficits resulting from brain injury are the emotional
sequelae, and these include depression, irritability, fatigue, aggressive behaviour, anxiety, rapid mood
shifts, and difficulty concentrating (Satz et al., 1998). These factors can cause a significant decline in the
overall quality of life for those with severe brain injury, give rise to intense bouts of depression and
suicidal ideation, posing significant challenges for postinjury care and rehabilitation (e.g., Baguley,
Cooper, & Felmingham, 2006; Horneman, Folkesson, Sintonen, von Wendt, & Emanuelson, 2005;
Juengst, Kumar, & Wagner, 2017; Levin et al., 2005).

FIGURE 15.2 Hospital admissions for acquired brain injuries in England.

NHS Digital: Hospital Admitted Patient Care Statistics.
TABLE 15.7 Summary: DSM‐5 diagnostic criteria for neurocognitive disorder due to traumatic brain injury

The criteria are met for major or mild neurocognitive disorder

Traumatic brain injury has occurred with at least one of the following:
Unconsciousness
Post‐traumatic amnesia
Disorientation and confusion
Neurological signs such as neuroimaging demonstrating injury
The disorder occurs immediately after the traumatic brain injury occurs

Vascular neurocognitive disorder

Damage to brain tissue can also occur as a result of a cardiovascular accident(CVA)—otherwise
known as a stroke. Strokes result from either a blockage or breaking of the blood vessels in the brain
and can be defined in two broad ways. An infarction is when the blood flow to the brain is impeded in
some way, resulting in damage to the brain tissue fed by that blood flow. In contrast, a haemorrhage is
when a blood vessel in the brain ruptures and affects local brain tissue.
 cardiovascular accident (CVA) Otherwise known as a stroke. Strokes result from either a
blockage or breaking of the blood vessels in the brain.

stroke A sudden loss of consciousness resulting when the rupture or occlusion of a blood vessel
leads to oxygen lack in the brain.

The most common causes of infarction are an embolism or a thrombosis. A cerebral embolism is a
blood clot that forms somewhere in the body before travelling through the blood vessels and lodging in
the brain, causing the brain cells to become damaged as a result of oxygen starvation. Cerebral
thrombosis occurs when a blood clot (thrombus) forms in an artery (blood vessel) supplying blood to
the brain. Furred‐up blood vessels with fatty patches of atheroma (an abnormal inflammatory
accumulation of macrophage white blood cells within the walls of arteries) may make a thrombosis
more likely. The clot interrupts the blood supply and brain cells are starved of oxygen.

infarction The injury caused when the blood flow to the brain is impeded in some way,
resulting in damage to the brain tissue fed by that blood flow.

haemorrhage When a blood vessel in the brain ruptures and affects local brain tissue.

cerebral embolism A blood clot that forms somewhere in the body before travelling through
the blood vessels and lodging in the brain, causing the brain cells to become damaged as a result
of oxygen starvation.

Cerebral thrombosis An injury caused when a blood clot (thrombus) forms in an artery
(blood vessel) supplying blood to the brain. The clot interrupts the blood supply and brain cells
are starved of oxygen.

Haemorrhaging in the brain is often the result of hypertension or high blood pressure, and is often due
to an aneurysm or bulging in the wall of the blood vessel—usually an artery at the base of the brain.

aneurysm A localized bulging in a blood vessel caused by disease or weakening of the vessel
wall.

Strokes are remarkably common—especially in individuals over the age of 55 years. In the UK, an
estimated 100,000 people a year suffer a stroke—although the incidence of strokes in the UK has fallen
by 19% from 1990 to 2010 (The Stroke Association, 2017). Strokes are the fourth most common cause
of death in the UK, and the single most common cause of disability, and over 1.2 million people in the
UK are stroke survivors (The Stroke Association, 2017). Symptoms of a stroke often occur very
suddenly and unexpectedly. Symptoms include numbness, weakness, or paralysis on one side of the
body (signs of this may be a drooping arm, leg, a lowered eyelid, or a dribbling mouth), slurred speech
or difficulty finding words or understanding speech, sudden blurred vision or loss of sight, confusion or
unsteadiness, and a severe headache. The type and severity of symptoms will depend entirely on the
brain area affected by the CVA. The most common longer‐term symptoms of stroke include aphasia,
agnosia, apraxia (see Table 15.1), and paralysis, and a DSM‐5 diagnosis of vascular neurocognitive
disorder is established if there is good evidence for a cerebrovascular event as the cause of the disability,
and the criteria are met for major or mild neurocognitive disorder (see Table 15.3 and 15.4) (Table
15.8). One of the most common forms of stroke is thrombosis in the left‐middle cerebral artery,
affecting the left hemisphere. This will cause disability to the right hand side of the body (which is
controlled by the left hemisphere) and also cause significant impairment in language ability (e.g.,
aphasia) because the left hemisphere is critically involved in language generation and comprehension.
As well as physical and cognitive deficits, individuals who have suffered a stroke also exhibit emotional
disturbance, often manifested as depressed mood or as emotional lability. Depression in particular is a
common and significant consequence of strokes, and a recent meta‐analysis indicated that 29% of
stroke victims suffer depression up to 10 years after their stroke, with cognitive impairment being one of
the main predictors of poststroke depression (Ayerbe, Ayis, Wolfe, & Rudd, 2013). Levels of depression
are also correlated with the severity of both physical and cognitive deficits (Kauhanen et al., 1999),
suggesting that there may be a link between degree of disability and depression, and depression is
associated with a significantly increased risk of early mortality (Pan, Sun, Okereke, Rexrode, & Hu,
2011). Recovery from physical and cognitive impairment is also significantly retarded in those with
depression (Morris, Robinson, Andrezejewski, Samuels, & Price, 1993; Robinson, Lipsey, Rao, & Price,
1986). There is a tendency here to conclude that the disabilities resulting from a stroke may cause
depression that in turn inhibits recovery. However, the picture is rather more complex than this and
there seems to be a bidirectional link between stroke and depression (Wium‐Andersen et al., 2019). For
example, depression is a risk factor for strokes. In a prospective study, May et al. (2002) found that men
with significant depressive symptoms were significantly more likely to suffer a stroke within the following
14 years than those without significant depression symptoms. Similarly, treating poststroke depression
with antidepressant medication also has the effect of significantly decreasing mortality rates over a 9‐
year period (Robinson et al., 2000). All of this suggests that depression is an important feature of
disability caused by strokes as well as a risk factor for strokes and is an area where clinical psychologists
might be suitably employed to manage depression in attempts to improve recovery rates and reduce
mortality rates.
TABLE 15.8 Summary: DSM‐5 diagnostic criteria for vascular neurocognitive disorder

The criteria are met for major or mild neurocognitive disorder

The clinical features suggest vascular aetiology as marked by one of the following:
Arrival of the cognitive deficit is timely related to at least one cardiovascular event
Decline is evident in complex attention and frontal‐executive function
There is evidence of cerebrovascular disease to account for the neurocognitive deficits
The symptoms are not better accounted for by another brain disease or disorder

Degenerative disorders
Degenerative disorders represent those neurocognitive disorders that are characterised by a slow, general
deterioration in cognitive, physical, and emotional functioning as a result of progressive physical
changes in the brain. Deterioration occurs gradually over a number of years, and degenerative disorders
are most frequently a feature of older age, and around 5–8% of the general population aged 60 and
over are estimated to have dementia at any one time (World Health Organization, 2019). Degenerative
disorders can affect both the cerebral cortex and subcortical regions of the brain. Those that affect
cortical areas cause impairments in cognitive abilities such as memory, language, attention, and
executive functioning (causing amnesia, aphasia, agnosia, slowed thinking, and confusion see Table
15.1). Disorders affecting subcortical regions of the brain may in addition cause emotional disturbances
and motor coordination difficulties. There are currently an estimated 850,000 people in the UK with
dementia, and one in six people over 80 years‐of‐age have dementia (Alzheimer's Society, 2020a), with
the most common cause of degenerative dementia in the UK being Alzheimer's disease (contributing
55%). Degenerative disorders that in addition significantly affect subcortical areas, and so affect
emotional behaviour and motor coordination, are Parkinson's disease and Huntington's disease.
Diagnosis of degenerative disorders is difficult and complex. First, a degenerative disorder has to be
distinguished from the normal process of ageing. Normal ageing naturally results in a moderate
deterioration of cognitive abilities (such as forgetting or cognitive slowness) and a deterioration in
physical abilities (such as problems with balance and motor coordination). However, degenerative
disorders compound this natural process because they represent an active pathological organic
deterioration of the brain. Second, it is often difficult to distinguish between the different degenerative
disorders that may affect cognitive and physical functioning. Many manifest with very similar cognitive
impairments, such as amnesia. Third, degenerative disorders are most frequently found in the elderly,
and this particular population will often present with a wide range of psychological and medical
problems that complicate diagnosis. For example, anxiety and depression are common features of old
age and may complicate neurological testing. Performance during assessment may also be affected by
other physical illnesses or the effects of medications for other ailments (Shepherd et al., 2015). Finally,
how a degenerative disorder manifests on presentation may differ significantly between individuals
depending on factors such as their level of education, level of family and social support, and their
psychological history. In effect, two individuals with the same disorder may present themselves quite
differently and perform quite differently in assessments depending on a range of social and
psychological factors. Overall prevalence estimates for diagnosed dementia disorders are around 1–2%
at age 65 years and as high as 30% by age 85 years (DSM‐5, American Psychiatric Association, 2013, p.
608).
The following sections continue by describing in detail some of the main degenerative disorders. These
cover neurocognitive disorder due to Alzheimer's disease, frontotemporal neurocognitive disorder,
neurocognitive disorder due to Parkinson's disease, neurocognitive disorder with Lewy bodies, and
neurocognitive disorder due to Huntington's disease.

NCD due to Alzheimer's disease

Characteristics of Alzheimer's disease

Alzheimer's disease is the most common form of dementia. It is a slowly progressive disorder and
neural damage may start 20–30 years before any overt cognitive or behavioural signs of impairment
(Davies et al., 1988). The disease manifests as progressive impairments in short‐term memory, with
symptoms of aphasia, apraxia, and agnosia, together with evidence of impaired judgements, decision‐
making, and orientation. Early signs of the disease are irritability, lack of concentration, and basic
failures of short‐term memory, such as forgetting that food is cooking or forgetting names. Eventually,
the individual becomes more and more confused and disoriented, and may be unable to remember
basic general knowledge (e.g., be unable to recite the alphabet), may confuse night and day, and get lost
in relatively familiar environments. Many individuals also show personality changes, may exhibit
paranoid behaviour and become generally irritable and difficult to control. Eventually sufferers usually
become physically weak and bedridden. Their erratic and unpredictable behaviour will often become
problematic for their carers, many of whom are likely to be the elderly spouses of the sufferer
themselves. The average duration of the disease from onset of symptoms to death is around 8–10 years.

Alzheimer’s disease A slowly progressive form of dementia involving progressive

impairments in short-term memory, with symptoms of aphasia, apraxia and agnosia, together
with evidence of impaired judgements, decision-making and orientation.

Known risk factors for Alzheimer's disease include the following (Barranco‐Quintana, Allam, Del
Castillo, & Navajas, 2005): (a) age—which is the principal marker for risk of the disease, (b) sex
—prevalence is higher in women than in men, (c) genetics—having a first‐degree relative with the
disease significantly increases risk, (d) family history of dementia—nearly 40% of those with
Alzheimer's disease have a family history of dementia, (e) a history of head injury (McDowell, 2001), (f)
high levels of anxiety (Becker et al., 2018), and (g) low educational status and low wealth (Cadaret al.,
2018). Interestingly, some activities appear to have a direct or indirect protective value by predicting
lower rates of Alzheimer's disease (even in those with a family history of dementia), and these include
physical activity, smoking, drinking moderate levels of alcohol, and diets high in vitamins B6, B12, and
folic acid (Barranco‐Quintana et al., 2005). However, we must be cautious about how we interpret these
factors. For example, smoking probably protects against Alzheimer's disease largely because it is likely to
prevent smokers from reaching old age, which is when the disease becomes prevalent. In addition, low
educational status may be correlated with Alzheimer's disease because it may adversely affect
performance on the cognitive tasks used to diagnose the disease. Several studies also suggest that factors
such as diet (e.g., a Mediterranean diet), regular exercise, and engagement in intellectual activities also
appear to be useful in warding off cognitive decline (Hamer & Chida, 2009; Lee et al., 2018; Williams,
Plassman, Burke, Holsinger, & Benjamin, 2010). For example, high levels of cognitive activity appears to
protect against cognitive decline even in individuals who have a high genetic risk for Alzheimer's disease
and have already developed the plaques and tangles in their brain that are associated with Alzheimer's
(Wilson, Scherr, Schneider, Tang, & Bennett, 2007).
The DSM‐5 diagnostic criteria for Neurocognitive disorder due to Alzheimer's disease is given in Table
15.9. However, Alzheimer's disease itself is difficult to differentiate from other forms of degenerative
dementia, and it is often easier to identify Alzheimer's disease by successively eliminating other types of
disorder that cause dementia symptoms, such as Parkinson's disease, Huntington's disease,
hypothyroidism, HIV infection, substance abuse, or head trauma. This can be achieved using thyroid
function tests, blood tests, and a battery of neuropsychological tests of cognitive function. However, the
recent identification of some of the genes that carry a high risk for the development of Alzheimer's
disease mean that genetic testing can be used to identify Alzheimer's as the possible cause of the
dementia or cognitive decline. In addition, neuroimaging plays an important part in the diagnosis of
Alzheimer's disease, by helping to exclude alternative causes of dementia such as brain tumour, cerebral
atrophy, and cerebrovascular disease.

Aetiology of Alzheimer's disease

It is only in the past 30 years that we have come to understand some of the causes of Alzheimer's
disease, and, indeed, to be able to identify it as a specific form of degenerative dementia. The changes
that occur to the brain during Alzheimer's disease appear to be structural and involve the development
of beta amyloid plaques and neurofibrillary tangles. Beta amyloid plaques appear to be caused by
abnormal protein synthesis in the brain and they clump together with the consequence of killing
healthy neurones. Neurofibrillary tangles consist of abnormal collections of twisted nerve cell
threads which result in errors in impulses between nerve cells and eventual cell death (Blennow, de
Leon, & Zetterberg, 2006; Hernández‐Ortega, Garcia‐Esparcia, Gil, Lucas, & Ferrer, 2016) (Figure
15.3). The result of these abnormal cell developments is that there is a gradual shrinkage of healthy
brain tissue. The grooves or furrows in the brain, called sulci, are noticeably widened and there is
shrinkage of the gyri, the well‐developed folds of the brain's outer layer. In addition, the ventricles, or
chambers within the brain that contain cerebrospinal fluid, are noticeably enlarged.

Beta amyloid plaques Abnormal cell development, possibly caused by abnormal protein
synthesis in the brain, which clump together with the consequence of killing healthy neurons.
 Neurofibrillary tangles Abnormal collections of twisted nerve cell threads which result in
errors in impulses between nerve cells and eventual cell death.

TABLE 15.9 Summary: DSM‐5 diagnostic criteria for neurocognitive disorder due to Alzheimer's disease

The criteria are met for major or mild neurocognitive disorder

The onset is slow, with gradual progression of the impairment
For major neurocognitive disorder:
Probable Alzheimer's disease is diagnosed if either of the following are present:
Evidence of the Alzheimer's disease genetic mutation in the family history of the patient or
via genetic testing
All three of the following are present:
Decline in memory and learning and at least one other cognitive ability
Steady, gradual decline in cognition
No evidence of other neurodegenerative or cerebrovascular disease
Otherwise, possible Alzheimer's disease should be diagnosed.
For mild neurocognitive disorder:
Probable Alzheimer's disease is diagnosed if there is evidence of the Alzheimer's disease genetic
mutation in the family history of the patient or via genetic testing. Otherwise, possible Alzheimer's
disease should be diagnosed if all three of the following are present:
Decline in memory and learning and at least one other cognitive ability
Steady, gradual decline in cognition
No evidence of other neurodegenerative or cerebrovascular disease
The disturbance is not better explained by cerebrovascular disease, another neurodegenerative
disease, or disorder

Another factor that is thought to be important in Alzheimer's disease is the faulty production of the
brain neurotransmitter acetylcholine, and Alzheimer's disease appears to affect structures involved in
the production of acetylcholine (Hampel et al., 2018). The enzyme acetylcholinesterase normally breaks
down acetylcholine after use so it can be recycled, but in Alzheimer's disease acetylcholine levels fall too
low and memory and other brain functions are impaired. A number of drug treatments can be utilised
to help facilitate acetylcholine production in the brain, and we discuss these in more detail in the
following section on treatment and rehabilitation.

acetylcholine A neurotransmitter that appears to be involved in learning and memory.

There also appears to be a significant inherited component to Alzheimer's disease with an estimate of
up to 50% of the first‐degree relatives of sufferers also developing the disorder (Korten et al., 1993). In
addition, twin studies suggest that the heritability of the disease is high ‐ between 58% and 79% (Gatz
et al., 2006). Up to 43 susceptibility genes have been identified for late‐onset Alzheimer's disease
(Kamboh, 2018), and these include ApoE4 and GAB2 (Bertram & Tanzi, 2008; Bookheimer &
Burggen, 2009), and currently, genetic testing to identify such genes is often used to enable diagnosis.
Some of these genes may increase susceptibility to Alzheimer's disease while others may have a more
direct cause in generating proteins that cause the beta amyloid plaques that result in damage to brain
tissue (e.g., causing overproduction of the beta amyloid plaques that leads to loss of healthy neurones).
In addition, some genes may play a role in early‐onset Alzheimer's disease, whereas others appear to be
linked to late onset (Bertram & Tanzi, 2008). All this suggests that, while there is no doubt about the
importance of an inherited component to Alzheimer's disease, it may have multiple causes, and a
number of genetic mechanisms may contribute to the factors which cause degenerative brain damage
(Focus Point 15.3).
FIGURE 15.3 Beta amyloid plaques and neurofibrillary tangles in the cerebral cortex in Alzheimer's disease. Plaques
appear to be caused by abnormal protein synthesis in the brain and they clump together killing healthy neurones. Tangles
consist of abnormal collections of twisted nerve cell threads causing errors in impulses between nerves. Certain genes such
as ApoE4 have also been identified that promote the formation of abnormal amyloid plaques (Bookheimer & Burggen,
2009).
From Blennow, de Leon, & Zetterberg, 2006.
 FOCUS POINT 15.3 THE PROS AND CONS OF GENETIC
TESTING FOR DEGENERATIVE BRAIN DISORDERS

Some people may wish to use genetic testing to assess their risk of developing dementia later in
life. Genetic testing is not a straightforward issue and individuals need to think very carefully
before deciding to take such a test. The experience might be very difficult emotionally, may not
provide conclusive results either way, and may cause practical difficulties.
Possible advantages of genetic testing include that it might:
help genetic researchers understand the disease better and so lead to improved treatment
encourage someone to adopt a healthier lifestyle
allow people who are at a high risk of developing dementia to benefit from new treatments
that may become available in the future
help people to plan for the future
However, genetic testing may create problems, for the following reasons:
A genetic defect cannot be repaired, and effective treatment to slow the disease is not yet
generally available. A genetic test might therefore raise anxiety without offering a clear
course of action.
There is a risk of reading too much into the test results. Testing positive for one or two
gene variants does not mean a person will definitely develop Alzheimer's and testing
negative does not guarantee that they will be free from Alzheimer's.
People testing positive for any genetic test could face discrimination affecting their ability
to buy property, get insurance, or plan financially for their old age. However, following a
brief moratorium on the use of genetic information by UK insurance companies, a
voluntary code of practice was agreed between the UK Government and insurers in 2018
clarifying how information on genetic testing can be used in a way that does not
discriminate against those who have received positive tests (HM Government, 2018).

Frontotemporal neurocognitive disorder

Frontotemporal NCD is associated with a loss of neurones from the frontal and temporal regions of
the brain that lead to progressive development of behavioural and personality changes and language
impairment. Unlike Alzheimer's disease, frontotemporal NCD does not usually affect memory
processes, but has its main impact on emotional factors such as apathy and the ability to empathise with
others. It is also characterised by a lack of insight into social conventions (e.g., someone might not realise
that a particular behaviour was embarrassing to them or to others), and an inability to regulate
emotions. Regular neurocognitive symptoms include lack of planning and organisation, distractability,
and poor judgement, and this may lead to a lack of self‐care, changes in social style, hoarding, and
changes in eating behaviour (Table 15.10).

Frontotemporal neurocognitive disorder Associated with a loss of neurones from the

frontal and temporal regions of the brain that leads to progressive development of behavioural
and personality changes and language impairment.
Frontotemporal NCD is a common cause of early onset dementia in individuals under 65 years of age,
but accounts for only 5% of all cases of dementia in autopsy studies (DSM‐5, American Psychiatric
Association, 2013, p. 616). The disorder has a strong genetic component of around 50–60% (Le Ber,
2013) but with a high probability of a number of different genes and genetic pathways being involved
(Cruts et al., 2006). This fact also suggests that the neurological degeneration in frontotemporal NCD
probably results from many different gene‐controlled molecular processes that contribute to the death of
healthy brain neurones in the frontal and temporal regions (Seelaar, Rohrer, Pijnenburg, Fox, & van
Swieton, 2011). A whole range of diseases or pathological processes can cause frontotemporal NCD,
one of which is Pick's disease which is characterised by the development of spherical bodies within
neurons (Bang, Spina, & Miller, 2015).
TABLE 15.10 Summary: DSM‐5 diagnostic criteria for frontotemporal neurocognitive disorder

The criteria are met for major or mild neurocognitive disorder

The onset is slow, with gradual progression of the impairment
Either a behavioural or a language variant is present:
Behavioural:
At least three of the following:
Lack of inhibition
Sluggishness or lethargy
Compulsive/ritualistic behaviour
Inserting inappropriate things into the mouth or diet changes
Obvious decline in social cognition
Language:
Obvious decline in language ability
Limited learning and memory functions and perceptual motor function
The disturbance is not better explained by cerebrovascular disease, another neurodegenerative
disease or disorder, or by the effects of a substance

NCD due to Parkinson's disease and NCD with Lewy bodies

Parkinson's disease is a progressive neurological condition affecting movements such as walking,
talking, and writing, and it causes psychological disturbance in between 40% and 60% of sufferers. The
main symptoms of Parkinson's disease are (a) tremor, including jerky movements of the arms, hands,
and head which are also present during resting periods; (b) slowness of movement (bradykinesia)—
people with Parkinson's may find that they have difficulty initiating movements or find that performing
movements takes longer; and (c) stiffness or rigidity of muscles, including problems in standing up from
a chair or rolling over in bed. The disease is named after Dr. James Parkinson (1755–1824), the London
doctor who first identified Parkinson's as a specific condition. Parkinson's disease occurs as a result of
damage in the basal ganglia—particularly the region of the basal ganglia known as the substantia
nigra. Cells in this area are responsible for producing the neurotransmitter dopamine, which allows
messages to be sent to the parts of the brain that co‐ordinate movement. With the depletion of
dopamine‐producing cells, these parts of the brain are unable to function normally. It is estimated that
over 10 million people worldwide suffer from Parkinson's disease, including 145,000 in the UK
(Parkinson's UK, 2018). Symptoms first appear when the individual is over 50 years of age, with men
being marginally more likely to develop the disorder than women.

Parkinson’s disease A progressive neurological condition affecting movements such as

walking, talking and writing, and causing psychological disturbance in between 40 and 60 per
cent of sufferers.

substantia nigra A region of the basal ganglia.

Those sufferers who develop psychological problems experience memory problems and exhibit deficits
in learning, judgement, and concentration, as well as becoming socially withdrawn and apathetic. It is
estimated that up to 75% of individuals with Parkinson's disease may eventually develop dementia, and
these symptoms can occur as early as 1–2 years after onset of the disease (Ehrt & Aarsland, 2005;
Williams‐Gray, Foltynie, Lewis, & Barker, 2006). As well as signs of cognitive impairment, Parkinson's
sufferers also regularly exhibit symptoms of psychosis and depression. Hallucinations occur in between
16% and 40% of sufferers, and this has often been considered as a medication‐induced phenomenon.
That is, the drugs used to facilitate substantia nigra dopamine production in sufferers are also known to
produce psychosis‐like symptoms. However, there is reason to believe that psychosis symptoms such as
hallucinations may also be intrinsic to the disease and result from progressive dementia or impairments
in primary visual processing (Williams‐Gray et al., 2006). Studies also suggest that depression is a
significant feature of Parkinson's disease in between 25% and 40% of sufferers (Leentjens, 2004), and
this is often considered to be an understandable reaction to having to cope with a chronic and
debilitating disease. However, as in the case of Alzheimer's disease, depression is also a significant
predictor of subsequent Parkinson's diagnosis, with the incidence of depression increasing significantly
in the 3 years prior to diagnosis of Parkinson's (Leentjens, Van den Akker, Metsemakers, Lousberg, &
Verhey, 2003). The fact that depression appears to be a biological risk factor for a number of
degenerative dementias has given rise to the view that depression may be accompanied by an
allostatic state (a biological state of stress) that can accelerate disease processes and cause atrophy of
nerve cells in the brain, in turn leading to dementia (McEwen, 2003).

allostatic state A biological state of stress.

Post‐mortem studies of individuals with Parkinson's disease suggest an association between dementia
and Lewy body deposition. Lewy bodies are abnormal protein deposits that disrupt the brain's normal
functioning. These Lewy body proteins are found in an area of the brain stem where they deplete the
neurotransmitter dopamine, causing Parkinson's symptoms. These abnormal proteins can also diffuse
throughout other areas of the brain, including the cerebral cortex, causing disruption of perception,
thinking, and behaviour. Around 80% of individuals with Parkinson's disease will develop dementia with
Lewy bodies, but others without Parkinson's disease can develop neurocognitive disorders purely as a
result of the development of Lewy bodies. This led DSM‐5 to introduce a new diagnostic category
known as Neurocognitive disorder with Lewy bodies. A diagnosis of NCD due to Parkinson's
disease is given if Parkinson's disease clearly precedes the onset of the neurocognitive disorder, and a
diagnosis of NCD with Lewy bodies is given if there is no convincing evidence of Parkinson's disease in
the aetiology (Tables 15.11 and 15.12). The prevalence of Parkinson's disease in the US begins at
around 0.5% between 65 and 69 years of age and rises to 3% by 85 years of age. Estimates of NCD
with Lewy bodies in the general elderly population range from 0.1% to 5% (DSM‐5, American
Psychiatric Association, 2013, p. 619), and this form of neurocognitive disorder may account for up to
30% of all dementias (Figure 15.4).

Lewy bodies Abnormal protein deposits that disrupt the brain’s normal functioning.
NCD due to Huntington's disease
Huntington's disease is an inherited, degenerative disorder of the central nervous system, caused by
a dominant gene. This means that everyone who inherits the gene from one of his/her parents will
develop the disease with 50% likelihood (see Focus Point 1.4 in Chapter 1 for a fuller explanation of the
genetics of Huntington's disease). Symptoms of the disorder do not normally occur until after the age
of 35 years and can have an even later onset (however, the earlier the onset, the more severe the disease
tends to be). It is principally a movement disorder, with the first observable behavioural symptoms
manifesting themselves as clumsiness and an involuntary, spasmodic jerking of the limbs. However,
many early signs of the disease tend to be radical changes in temperament. The individual may become
rude, exhibit unpredictable mood changes, and switch dramatically from depression to euphoria.
Cognitive functioning is affected as the disease develops, and this is manifested as impairments in
memory, attention, and decision making leading to full dementia. In addition, as the disease progresses,
the sufferer may also begin to exhibit psychotic symptoms, including hallucinations and delusions. The
general psychological syndrome associated with Huntington's disease includes affective symptoms,
cognitive deficits, personality disorganisation, bloody‐mindedness, early loss of common sense,
hallucinations, delusional ideation, odd behaviours, and obsessions (Wagle, Wagle, Markova, & Berrios,
2000). Psychopathological symptoms associated with the disease include depression, mania,
schizophrenia, paranoia, anxiety, and obsessive‐compulsive behaviours (Barquero‐Jimenez & Gomez‐
Tortosa, 2001). Huntington's disease affects an estimated 3 to 7 people per 100,000 who have European
ancestry. The disorder is less common in other populations, including those of Japanese, Chinese, and
African descent (US National Library of Medicine, 2020).

Huntington’s disease An inherited, degenerative disorder of the central nervous system,

caused by a dominant gene.

TABLE 15.11 Summary: DSM‐5 diagnostic criteria for neurocognitive disorder due to Parkinson's disease

The criteria are met for major or mild neurocognitive disorder

The disturbance occurs during diagnosed Parkinson's disease
The onset is slow, with gradual progression of the impairment
The disturbance is not better explained by another medical condition or mental disorder
Major or mild neurocognitive disorder probably due to Parkinson's disease should be diagnosed if both of the
following are met. Major or mild neurocognitive disorder possibly due to Parkinson's disease should be
diagnosed if one of the following is met:
No evidence of other neurodegenerative or cerebrovascular disease
The Parkinson's disease diagnosis predates the neurological disorder
TABLE 15.12 Summary: DSM‐5 diagnostic criteria for neurocognitive disorder with Lewy bodies

The criteria are met for major or mild neurocognitive disorder

The onset is slow, with gradual progression of the impairment
Probable major or mild neurocognitive disorder with Lewy bodies is diagnosed if the patient has two of the
core features or at least one suggestive feature with other features. Possible major or mild neurocognitive
disorder with Lewy bodies is diagnosed if the patient has one of the core features or at least one
suggestive feature
Core features:
Varying cognition with obvious changeability in attention and alertness
Reoccurring, detailed hallucinations
Features of Parkinsonism prior to the development of cognitive decline
Suggestive features:
Rapid eye movement sleep behaviour disorder
Adverse reactions to neuroleptics
The disturbance is not better explained by cerebrovascular disease, another neurodegenerative
disease or disorder, or by the effects of a substance
FIGURE 15.4 This figure illustrates how Lewy bodies progress from the brain stem, the dorsal motor nucleus and
olfactory bulb in the initial stages of dementia (presymptomatic phase, stage 1), and then spread in six separate stages
throughout the brain to the neocortex (stages 5 and 6, darker colouring shows areas of greater concentration of Lewy
bodies). Between 4% and 7% of those with dementia will have dementia with Lewy bodies (Hogan et al., 2016), but
Lewy bodies are much more common in those with Parkinson's disease who develop dementia.
From Goedert, Spillantini, Del Tredici, & Braak (2013).
The genetic abnormality in Huntington's chorea is found on the fourth chromosome. This results in the
production of a protein, mutant Huntingtin (mHtt), which causes cell death in the basal ganglia
—an area of the brain responsible for posture, muscle tone, and motor coordination. Presymptom
testing is possible by means of a blood test which counts the number of mutant repetitions on the
relevant gene. A negative blood test means that the individual does not carry the gene, will never
develop symptoms, and cannot pass it on to children. A positive blood test means that the individual
does carry the gene, will develop the disease, and has a 50% chance of passing it on to children,
assuming he or she lives long enough to do so. Because a positive blood test will have such a dramatic
psychological impact, potential sufferers are given intensive counselling and psychological support
before undergoing presymptom testing. A diagnosis of neurocognitive disorder due to Huntington's
disease is given if the individual meets the criteria for major or mild neurocognitive disorder, and there
is good evidence based on family history or genetic testing that Huntington's disease is a relevant
aetiology (Table 15.13).

mutant Huntingtin (mHtt) A protein which causes cell death in the basal ganglia and
contributes to Huntington’s disease.

TABLE 15.13 Summary: DSM‐5 diagnostic criteria for neurocognitive disorder due to Huntington's disease

The criteria are met for major or mild neurocognitive disorder

The onset is slow, with gradual progression of the impairment
The disturbance occurs during diagnosed Huntington's disease or the risk of Huntington's disease
based on family history or genetic testing
The disturbance is not better explained by another medical condition or mental disorder

Summary of types of neurocognitive disorder

In this section we have discussed a number of different types of neurocognitive disorder and their
DSM‐5 diagnostic categories. The main aetiology categories we covered were infection (e.g., HIV
infection), traumatic brain injury, vascular causes (e.g., strokes), and degenerative disorders (e.g.,
Alzheimer's disease, Parkinson's disease). All of these can cause cognitive impairment to differing
degrees, and the nature of the impairment will depend on the areas of the brain affected by each factor.
Neurocognitive deficits may be relatively specific and result from damage to tissue in areas of the brain
dealing with specific functions such as language, memory, or visuo‐motor coordination (see Table 15.1).
Such specific disabilities are found most often with traumatic brain injury, cerebrovascular accidents,
and brain tumours. Other types of disorder are progressive and can develop from being diagnosed as
mild neurocognitive disorders to major cognitive disorders (see Section 15.1.3). A common feature of
most types of neurocognitive disorder is that they are often associated with other forms of
psychopathology, including anxiety, depression, and psychosis. Depression is very closely associated with
some of the degenerative disorders, such as Alzheimer's and Parkinson's diseases, and is not only a
frequent consequence of these disorders but also a presymptom predictor of the disorder. One feature
common to almost all of these types of neurocognitive disorder is that the cognitive, behavioural, and
emotional deficits that ensue are almost entirely the result of damage to brain tissue caused either
through trauma, disease, or biochemical abnormalities in the brain. In some cases, the means by which
brain tissue is damaged may be common across a number of different types of disorder. For example,
there is gathering evidence that the deposition of Lewy bodies in the brain may be one part of the
mechanism causing dementia in both Alzheimer's and Parkinson's disease.

SELF‐TEST QUESTIONS
Can you define the terms amnesia, aphasia, agnosia, and apraxia?
What is the difference between Broca's aphasia and Wernicke's aphasia?
What specific skills are impaired when neurological disorders cause deficits in executive
functioning?
Can you name some of the difficulties involved in diagnosing specific neurological
disorders?
What kinds of individual abilities are assessed using the Wechsler Adult Intelligence Scale
(WAIS) IV or the Adult Memory and Information Processing Battery (AMIPB)?
Can you describe the DSM‐5 diagnostic criteria for delirium?
Can you name two or more types of cerebral infection that may cause cognitive deficits?
What are the main causes of traumatic brain injury?
What are some of the emotional and psychological consequences of suffering a stroke?
Can you name the main neurocognitive degenerative disorders?
What is frontotemporal neurocognitive disorder and how does it differ from other
neurocognitive disorders?
Can you describe the main characteristics of Alzheimer's disease?
What are the main risk factors for Alzheimer's disease and what changes in the brain are
thought to occur during the disorder?
What areas of the brain are affected by Parkinson's disease, and what are the cognitive and
emotional symptoms associated with the disorder?
What are Lewy bodies, and how are they involved in neurocognitive deficits?

SECTION SUMMARY

15.1 THE DIAGNOSIS AND ASSESSMENT OF NEUROCOGNITIVE

DISORDERS

15.1.1 Cognitive Impairments in Neurocognitive Disorders

The main cognitive impairments in neurological disorders are deficits in learning and
memory, attention and arousal, language and communication, visual‐perceptual
 functioning, motor skills, and executive functioning.
Language deficits are known as aphasias and include Broca's aphasia and Wernicke's aphasia.
Agnosia is a disorder of the ability to recognise and name everyday objects
Apraxia is an impairment in motor performance and coordination.
Deficits in executive functioning reflect the inability to solve problems, plan, initiate, organise,
monitor, and inhibit complex behaviours.
Assessment in clinical neuropsychology is based on a range of cognitive tests and can be
supplemented by blood tests, chemical analyses of cerebrospinal fluids, and brain scans
such as positron emission tomography (PET) and functional magnetic resonance imaging
(fMRI).

15.1.3 The Diagnosis of Neurocognitive Disorders

Delirium is a disturbance of consciousness that develops over a short period of time.
Major or minor neurocognitive disorders are the two overarching categories into which DSM‐5
conceptualises neurocognitive disorders
Neurocognitive disorders caused by infections include neurocognitive disorder due to HIV
infection and neurocognitive disorder due to prion disease
Traumatic brain injury is one of the most common causes of neurological impairment.
Damage to brain tissue can occur as a result of a cardiovascular accident (CVA)—
otherwise known as a stroke, and these are remarkably common in individuals over the age
of 65 years.
Degenerative disorders represent those dementias that are characterised by a slow, general
deterioration in cognitive, physical, and emotional functioning, and these affect around 5–
8% of individuals over 60 years of age.
Alzheimer's disease is the most common cause of dementia in the UK (contributing 55%),
and one in six people over 80 years‐of‐age have dementia in the UK.
The changes that occur in the brain during Alzheimer's disease appear to be structural and
involve the development of beta amyloid plaques and neurofibrillary tangles. It is also associated
with the faulty production of the brain neurotransmitter acetylcholine.
Frontotemporal neurocognitive disorder is associated with a loss of neurones from the frontal and
temporal regions of the brain causing behavioural, personality, and language impairments.
Parkinson's disease causes psychological and cognitive disturbance in up to 75% of sufferers
and appears to be caused as a result of degenerative damage to the region of the basal
ganglia known as the substantia nigra.
Lewy bodies are abnormal protein deposits that disrupt the brain's normal functioning and
can occur in around 80% of individuals with Parkinson's disease.
Neurocognitive disorder with Lewy bodies is diagnosed when Lewy bodies are present in the brain
without convincing evidence for a diagnosis of Parkinson's disease.
15.2 TREATMENT AND REHABILITATION FOR NEUROCOGNITIVE
DISORDERS
Many of the neurocognitive disorders described in this chapter represent irreversible changes in
impairment and central nervous system damage. As a consequence, attempts at treatment tend to be
oriented towards rehabilitation rather than cure. Nevertheless, impairment in some types of
neurocognitive disorder can be reversible, and deficits caused by some kinds of cerebral infection are
one example (e.g., meningitis and encephalitis). In the case of degenerative disorders such as
Alzheimer's disease, recent developments in drug treatments have indicated that progressive impairment
can be slowed, affording some respite from the degenerative nature of the disease. However, in many
cases, neurological damage is relatively permanent and the sufferer must learn to live with the
behavioural and cognitive deficits that the disorder brings (e.g., traumatic brain injury, strokes, etc.). This
has led to the development of a range of rehabilitation procedures designed to provide the individual
with (a) exercises that help to improve impaired cognitive functions (e.g., impaired language or memory
function), (b) training in the use of cognitive and behavoural aids (e.g., using memory aids or labelling
cupboards and drawers in order to remember where things are), (c) assistive technology (e.g., equipment
that may aid hearing, speaking or moving about), and (d) basic drug treatment and psychotherapy to
help deal with related mood disorders (such as depression). Finally, in some severe cases of neurological
disorder very little in the way of ameliorative therapeutic help can be provided for the sufferer, but
support can be provided for caregivers, and many national associations provide structured support and
advice for such caregivers (e.g., the UK Alzheimer's Society, www.alzheimers.org.uk). We now discuss the
various forms of treatment and rehabilitation in more detail.

15.2.1 Biological Treatments

Biological treatments for neurocognitive disorders take a number of forms. The most common are drug
treatments that help stabilise or slow degenerative disorders, others include drug treatments to combat
cerebral infections, and electrical brain stimulation for some forms of dementia.

Drug treatments
There has been some success in recent years in developing drugs that can help to slow the progress of
degenerative disorders such as Alzheimer's disease and Parkinson's disease. In the case of Alzheimer's
we have already noted that the disease is often associated with abnormalities in the production of the
brain neurotransmitter acetylcholine. During the course of the disease, an enzyme called
acetylcholinesterase breaks down acetylcholine and leads to depletion of the neurotransmitter
dopamine. In order to combat this effect, drugs have been developed that prevent acetylcoline
breakdown in the synaptic cleft by acetylcholinesterase and increase its uptake in the postsynaptic
receptor. The most common of these drugs are donepezil, rivastigmine, and galantamine and they are
collectively known as cholinesterase inhibitors (Petersen, Thomas, Grundman, & Thal, 2005).
Randomised, double‐blind, placebo‐controlled trials suggest that treatment for 6 months with
cholinesterase inhibitors produces moderate improvements in cognitive function in those with mild to
moderate Alzheimer's disease (Hitzeman, 2006). They may also help to slow memory decline (Birks,
2006), and prospects are best when treatment begins early in the course of the disease (Seltzer, 2006).
Although the emphasis has been on identifying early signs of Alzheimer's so that drug treatment can
begin as soon as possible, there is also some evidence that cholinesterase inhibitors such as donepezil can
improve cognition in individuals with severe Alzheimer's (Winblad et al., 2006), and accumulating
evidence that donepezil can also help to alleviate behavioural symptoms, mood disturbances, and
delusions associated with Alzheimer's (Cummings, McRae, & Zhang, 2006). However, recent systematic
reviews of cholinesterase inhibitors found no evidence that they could prevent dementia (Cooper, Li,
Lyketsos, & Livingston, 2013; Sharma, 2019). In 2011 the UK National Institute for Health and Care
Excellence (NICE) recommended to the NHS that donepezil, rivastigmine, and galantamine be made
available as part of the management of mild and moderate Alzheimer's disease, and those to be
targeted should score 10 points or higher on the MMSE (NICE, 2011)(see Focus Point 15.2). However,
more recent guidelines question whether prescribing anticholinergic drugs is appropriate before
randomised controlled trials are conducted to compare the potential efficacy of such medications
(NICE, 2018). While some cholinesterase inhibitors (especially galantamine) may have some effects in
slowing cognitive decline in Alzheimer's disease (e.g., Li, Zhang, Zhang, & Zhao, 2019), there is as yet
no reliable evidence for the efficacy of any drug treatments for frontotemporal neurocognitive disorder
(Schwarz, Froelich, & Burns, 2012).

cholinesterase inhibitors A group of drugs that prevent acetylcholine breakdown in the

synaptic cleft by acetylcholinesterase and increase its uptake in the postsynaptic receptor. The
most common of these drugs are donepezil, rivastigmine and galantamine.

Parkinson's disease is associated with degeneration in the substantia nigra area of the brain, where the
important neurotransmitter dopamine is produced. The main drug that is used to counteract this
decline in dopamine is levodopa, a natural amino acid that the brain converts into dopamine to
replace the depleted neurotransmitter. Although the drug has been relatively successful in helping suffers
to control tremor and other motor symptoms, there is little evidence that levodopa alleviates any of the
cognitive impairments associated with Parkinson's dementia (Morrison et al., 2004), but may prevent a
decline in cognitive function (Ikeda, Kataoka, & Ueno, 2017). Levadopa administration has to be closely
supervised because it also has a number of potential side effects including, hypertension, and delusions
and hallucinations similar to those found in schizophrenia and amphetamine psychosis.

levodopa A natural amino acid that is converted by the brain into dopamine and is used in the
treatment of Parkinson’s disease.

Medication can also be successful in reducing disability following cerebrovascular accidents such as
strokes. Thrombolytic therapy is the use of drugs to break up or dissolve blood clots—one of the
main causes of strokes. The most commonly used thrombolytic drug is tissue plasminogen activator (t‐
PA), and if this is administered within the first 3 hours of a stroke then disability is significantly reduced
(Albers, 1997; Hacke et al., 2004). Nevertheless, the success of this treatment is critically dependent on
the individual being able to identify the early signs of a stroke and seek rapid treatment, and stroke
patients begin to have cognitive impairments within 24‐hr on stroke onset. Although early
administration of thrombolytic therapy can significantly aid survival and physical recovery, there is only
modest evidence that administration of t‐PA is associated with improvement in cognitive function
(Rosenbaum Halevi et al., 2019; Nys, van Zandvoort, Algra, Kappelle, & de Haan, 2006).

Thrombolytic therapy The use of drugs to break up or dissolve blood clots – one of the
main causes of strokes.

Medication is also used in the treatment of brain deficits caused by cerebral infections. Bacterial
infections, such as certain types of encephalitis and meningitis, are treatable with antibiotics. However,
many viral infections are much more problematic, and steroids can be used to combat viral infections
such as herpes encephalitis. In the case of HIV‐1 associated dementia, newly developed
antiretroviral drugs are proving to be effective in reducing the severity of HIV dementia and the
prevalence of diagnoses of neurocognitive disorder (Nath & Sacktor, 2006; Crum‐Cianflone et al.,
2013). Usually, up to three to four antiretroviral drugs are used that act at different stages of the virus
life cycle. This produces a dramatic reduction in viral load (the level of virus in the blood) and prevents
further immune damage.
 antiretroviral drugs Chemicals that inhibit the replication of retroviruses, such as HIV.

Finally, mood disorders (such as depression) are a common feature of neurological disorders, including
stroke, traumatic brain injury, and degenerative disorders, and depression can often adversely affect the
course of the disorder, prevent recovery, and increase mortality rates (Leentjens, 2004; Ramasubbu &
Patten, 2003; Robinson, Lipsey, Rao, & Price, 1986). The use of drugs such as selective serotonin
reuptake inhibitors (SSRIs) and tricyclic antidepressants to help alleviate depressed mood has proven to
be successful in improving recovery from strokes (Hackett, Anderson, & House, 2005), alleviating
symptoms of depression in Parkinson's disease and Alzheimer's disease (Modegro, 2010; Weintraub et
al., 2005), and improving mood and cognitive performance following traumatic head injury (Horsfield
et al., 2002). In at least some of these disorders (e.g., Parkinson's disease) there is a view that depression
is an integral symptom of the disorder—especially because depression often precedes and predicts other
symptoms of the disease as well as affecting outcome. So tackling depression can be considered a direct
treatment of the disorder itself rather than dealing with a side effect of disability (e.g., Leentjens, 2004).

Deep brain stimulation (DBS)

A recently developed form of treatment for Parkinson's Disease involves deep brain
stimulation(DBS). This uses a surgically implanted, battery‐operated device called a neurostimulator
to deliver electrical stimulation to the ventral intermediate nucleus of the thalamus or the subthalamic
nucleus area in the basal ganglia. These areas of the brain control movement, and through mechanisms
that are as yet unclear, electrical stimulation in this area appears to block the abnormal nerve signals
that cause tremor and Parkinson's symptoms (Ananthaswamy, 2004; Perlmutter & Mink, 2006). DBS
has been shown to result in improvements in physical abilities (e.g., mobility) and global measures of
quality of life (Hamani, Neimat, & Lozano, 2006), but there is little evidence at present that DBS has
any significant effect on cognitive abilities (Laxton, Lipson, & Lozano, 2013) and may even be associated
with a mild decline in some cognitive abilities such as communication skills and language abilities
(Castelli et al., 2006; Drapier et al., 2005; Kurtis, Rajah, Delgado, & Dafsari, 2017).

deep brain stimulation (DBS) A form of treatment for Parkinson’s disease which uses a
surgically implanted, batteryoperated device called a neurostimulator to deliver electrical
stimulation to the ventral intermediate nucleus of the thalamus or the subthalamic nucleus area
in the basal ganglia.

15.2.2 Cognitive Rehabilitation

The nature and structure of cognitive rehabilitation programmes will inevitably depend on the
nature of the cognitive deficits that the individual has suffered, and a range of relatively successful
procedures are available that afford some significant gains across a range of functions (Cicerone et al.,
2005). Many of these programmes are basic training procedures which give the client structured
extensive training in the area of their deficit (e.g., attention, memory, executive functioning, etc.). This
may be in the form of extended practice at a task (e.g., attention process training [APT]), perhaps with
the additional use of concurrent feedback on performance so that the client can adjust their
functioning, or with the use of assistive technology (e.g., memory aids). In particular, the use of
computer‐based technology to assist rehabilitation training is a thriving area of development, and
clinicians may use computers, smartphones, personal digital assistants, and tablet computers to present
specific training programmes—a newly emerging approach sometimes called digital therapeutics
(Cha & im, 2013; Choi, Kim, Nah, & Kang, 2019; Tam & Man, 2004). These methods may include
memory training programmes or virtual environments in which the client can learn to coordinate the
relevant sequence of actions to successfully complete a task (Zhang et al., 2003) (Treatment in Practice
15.1). While many rehabilitation programmes target quite specific impairments, some others attempt to
address multiple aspects of dysfunction and are known as holistic rehabilitation methods. These
may address a combination of cognitive, emotional, motivational, and interpersonal impairments in the
context of an integrated programme of treatment (e.g., Braverman et al., 1999; Prigatano, 2013).

holistic rehabilitation Treatment methods for neurological disorders which attempt to

address multiple aspects of dysfunction.

This section continues by providing some examples of cognitive rehabilitation procedures that have
been shown to be effective in the rehabilitation of specific impairments. We then look at an example of
the holistic rehabilitation method.

Attention deficits
One form of rehabilitation training for attention deficits is known as Attention Process Training
(APT), and this uses a number of different strategies to promote and encourage attentional abilities
(Sohlberg & Mateer, 2010). Exercises include listening to an auditory piece that contains target words
that must be responded to by pressing a buzzer. Learning to shift attention appropriately is also
encouraged by learning to attend to a new word following identification of a preceding target word.
APT has been shown to be superior to basic therapeutic support in promoting attention and memory
functioning (Sohlberg, McLaughlin, Pavese, Heidrich, & Posner, 2000) and has also been shown to
provide gains in other everyday skills such as independent living and driving ability (Sohlberg & Mateer,
2001). An alternative approach to dealing with attention deficits is not to try and improve attention
itself, but to provide the client with some compensatory skills that will allow them to effectively manage
their slowed information processing (Fasotti, Kovacs, Eling, & Brouwer, 2000). This is known as time
pressure management(TPM) and is an alternative to ‘concentration’ training of the kind taught by
the APT procedure.

Attention Process Training (APT) A form of rehabilitation training for attention deficits
that uses a number of different strategies to promote and encourage attentional abilities.

time pressure management (TPM) An approach to dealing with attention deficits which
aims not to try to improve attention itself, but to provide clients with some compensatory skills
that will allow them to effectively manage their slowed information processing.
 CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 15.1
THE VIRTUAL REALITY KITCHEN

This virtual reality computer programme provides a safe and controlled environment for
patients with brain injury to learn and improve basic daily skills such as preparing a meal of a
can of soup and a sandwich. All necessary objects are found on the computer screen and can
be accessed by using the computer mouse. Prompts appear on the screen initiating actions,
sequencing actions, and providing reinforcing feedback for correct actions. For example, one of
the first steps for preparing a can of soup is to remove the can from the cupboard. If this does
not occur within a predetermined time, the cupboard door is highlighted by a pulsating colour.
If the action is still not initiated, a verbal cue tells the patient to ‘open the cupboard’. Each
action performed by the patient is recorded and their performance can be quantitatively
assessed over time. Training in virtual environments such as this results in improved
performance on the tasks over time and performance on the virtual task correlates well with
performance on the tasks in a real kitchen.

From Zhang et al. (2003).

Visuospatial deficits
A number of programmes have been developed for the rehabilitation of unilateral visual neglect and to
compensate for partial deficits in visual perception caused by neurological disorders. One such example
is the computer‐assisted training programme designed to aid visual scanning (Pizzamiglio, Guariglia,
Antonucci, & Zoccolotti, 2006). This consists of a series of tasks in which the patient is asked to (a) read
out coloured numbers projected on to a wall (scanning the full frontal environment), (b) manually track
a red ball projected onto a wall (helping coordination of scanning and physical movement), (c) react to
moving images as they are projected in front of them (facilitating detection of stimuli in space), and (d)
move the projected image of a wheelchair down a simulated three‐lane road while avoiding obstacles.
Visual scanning training has been shown to reduce unilateral visual neglect symptoms and to generalise
to improved performance on a real‐life wheelchair obstacle course.

Apraxia and deficits in coordinated self‐help behaviours

Apraxia involves an inability to undertake learned and purposeful activities such as dressing, cooking
etc., and means that sufferers must rely increasingly on caregivers to help with these activities. For
example, limb apraxia is a common symptom of left hemisphere damage and consists of a deficit in
performing gestures to verbal command or imitation. Sufferers are particularly impaired when asked to
demonstrate how to use an object or carry out actions. They appear to be unable to plan a sequence of
actions or they may exhibit inappropriate gestures (e.g., they may try to pour water from a bottle into a
glass without removing the lid or to stir the bottle opener in the glass). This is assumed to be an
impairment of gesture learning which is generally considered to be the consequence of a motor
memory disorder (Heilman, Schwartz, & Geshwind, 1975). One form of rehabilitation training for limb
apraxia is gestural training, in which the client is taught to recognise gestures and postures that are
appropriate and in context. For example, the patient may be required to demonstrate the use of a
common object (such as a guitar), or be shown a picture of the gesture (e.g., someone playing a guitar)
and to replicate that action, or to be shown simply a picture of the object and asked to mimic how it is
used. Patients may also be shown pictures of people appropriately or inappropriately using objects and
asked to identify which of these are correct (Treatment in Practice 15.2). Gestural training has been
shown to significantly reduce errors in performing everyday actions and to improve recognition of
gestures (Smania, Girardi, Domenicali, Lora, & Aglioti, 2000), although outcome studies of this
procedure are relatively rare (Rose, Raymer, Lanyon, & Attard, 2013).

gestural training A form of rehabilitation training for limb apraxia in which the client is
taught to recognise gestures and postures that are appropriate and in context.

In contrast, computer‐based virtual reality (VR) environments have been developed to enable disabled
individuals with brain injury to learn and improve basic daily living skills in a safe and controlled
environment. For example, Zhang et al. (2003) developed a virtual kitchen in which the patient can
learn the sequence of behaviours required to make a bowl of soup or prepare a sandwich (see
Treatment in Practice 15.1). Zhang et al. (2003) found that training in virtual environments such as this
resulted in improved performance on both tasks, and performance on the virtual task correlated well
with performance at the tasks in a real kitchen, and learning in virtual environments may be equally as
effective as other cognitive retraining procedures (Jacoby et al., 2013). Recent systematic reviews of
virtual reality training suggest that VR is a feasible and effective tool in the treatment of a range of
neurological disorders, including dementia, stroke, spinal cord injury, Parkinson's disease, and multiple
sclerosis (Schiza, Matsangidou, Neokleous, & Pattichis, 2019).

CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 15.2

GESTURAL TRAINING
 One form of rehabilitation training for limb apraxia is gestural training, in which the client is
taught to recognise gestures and postures that are appropriate and in context. This example
shows three gestures used in the gesture‐recognition test, and the patient must identify which is
an appropriate use of the object. (A) is an appropriate gesture, (B) is a semantically related but
inappropriate gesture, and (C) is a semantically unrelated and inappropriate gesture.

From Smania et al. (2000).

Language and communication deficits

Impairments in language and communication may manifest in a variety of ways, including deficits in
the production of speech (e.g., fluent aphasia), an inability to comprehend or understand speech, and an
inability to initiate speech (e.g., nonfluent aphasia) (see Table 15.1). Many patients undergo standard
forms of speech therapy to help promote the production and comprehension of speech, and many of
these approaches may combine speech therapy with procedures that permit massed practice of
production and comprehension skills, such as the combination of therapist‐delivered speech‐language
training and home‐based computer‐assisted massed practice (e.g., Wallesch & Johannsen‐Horbach,
2004).
Another specific form of treatment that has been shown to provide significant gains in the production
and comprehension of speech is known as group communication treatment. This focuses on
increasing initiation of conversation and exchanging information using whatever communication means
possible, being aware of personal goals in communication, and gaining confidence in the ability to
communicate in personally relevant situations. Elman and Berstein‐Ellis (1999) demonstrated that those
patients who received group communication treatment showed significantly more improvement in
functional communication compared with patients not receiving structured treatment. Subsequent
developments indicate that group communication treatment can be used as an effective service delivery
model, with aphasic patients acquiring the use of many different modalities to communicate (Mooney,
Beale, & Fried‐Oken, 2018).

group communication treatment A form of treatment used in the production and

comprehension of speech, focusing on increasing initiation of conversation and exchanging
information using whatever communication means possible.

Finally, a number of specific techniques exist to help individuals with aphasia and traumatic brain
injury improve their ability to name objects, improve writing skills, and improve sentence production,
and these may range from the use of cuing techniques to help the patient name specific objects to
semantic feature analysis (SFA) designed to improve lexical retrieval by increasing the level of activation
within a semantic network (e.g., Boyle, 2010; Coelho, McHugh, & Boyle, 2000).

Memory deficits
Procedures for dealing with memory impairments mainly revolve around what are known as
compensatory strategies—that is, providing patients with specific strategies for remembering
material on a daily basis. Compensatory strategies of this kind tend to be more efficient than simple
remedial strategies and more easily generalisable to daily activities (Cotelli, Manenti, Zanetti, &
Miniussi, 2012; Nadar & McDowd, 2010). Compensatory strategies may involve assistive technology
such as using diaries to aid recall of daily events, labelling cupboards to remember where everyday
items are stored or located, or using a pager to remind the individual of important daily events. Wilson,
Emslie, Quirk, and Evans (1999) report the case study of a young man called George who had severe
memory impairments after a head injury sustained in a road traffic accident. The pager could be used
to remind George about a range of tasks and activities during the day. Using assistive technology such
as a pager as a memory prompt has been shown to be effective, easy to use, and significantly reduces the
number of memory and planning problems experienced by people with traumatic brain injury (Wilson,
Emslie, Quirk, Evans, & Watson, 2005). Assistive technology (e.g., smartphones) can also be used
effectively in many different ways for memory support. For example, a range of assistive technology
devices has now been developed to support people with dementia and their carers to manage their daily
activities and to enhance safety, for example, electronic pill boxes, picture phones, and mobile tracking
devices (Van der Roest, Wenborn, Pastink, Droes, & Orrell, 2017). In one example, a smartphone app
has been developed to help individuals with dementia recognise friends and family. The app is installed
on the phones of patients and friends, family, and caregivers and uses GPS tracking to flash an alert to
the patient when one of the group members is nearby. The app then tells the patient who is
approaching and what their relationship is to the person approaching. It then provides information and
pictures of the relevant group member (Steele, 2016). Assistive technology can be used in a variety of
ways to aid impaired memory. Computers, tablets, and smartphones can function as simple memory
aids to enhance prospective memory (e.g., by acting as an electronic diary), by providing memory
training exercises, or by instructing the patient in the use of memory strategies (Kapur, Glisky, & Wilson,
2004).
Teaching remembering strategies is also beneficial. One technique involves training the patient in the
use of visual imagery mnemonics in order to help store and retrieve items and events to be
remembered. Ten weeks of training in visual imagery techniques has been shown to result in significant
improvement in memory functioning 3 months after treatment (Kaschel et al., 2002). Errorless
learning is also a technique that has proven to be helpful in training individuals with amnesia.
Errorless learning is a training procedure where people are prevented—as far as possible—from making
any errors while learning a new skill or new information (Baddeley & Wilson, 1994), and in the context
of memory impairments it is useful for teaching new knowledge or training specific skills such as helping
the patient to find and use the right word to name objects. There is still some debate over whether
memory aids (e.g., smartphones, tablets, pagers, diaries, and personal organisers) are superior to
memory treatments (e.g., attempts to train better memory functioning), but in many cases a combination
of both aids and ‘treatments’ seems to be most effective (e.g., Middleton & Schwartz, 2012; Ownsworth
& McFarland, 1999).

visual imagery mnemonics A technique for teaching remembering strategies in order to

help store and retrieve items and events to be remembered.

Errorless learning A training procedure used in training individuals with amnesia where
people are prevented – as far as possible – from making any errors while learning a new skill or
new information.

Deficits in executive functioning

As we described earlier, executive functioning involves the integrated use of several cognitive processes
by which people problem‐solve, plan, initiate, organise, and monitor goal‐directed activities. Deficits in
this collection of integrated skills will obviously require some training in a range of basic abilities, such
as attention and memory, and more specifically will require training in problem‐solving skills and
planning and goal‐management skills. Many effective interventions involve training in problem‐solving,
and one particular procedure is known as goal management training(GMT). This involves
training to help evaluate a current problem (“What am I doing?”), followed by specification of the
relevant goals, and partitioning of the problem‐solving process into subgoals or steps. Patients are then
assisted with the learning and retention of subgoals (“Do I know the steps?”) followed by self‐monitoring
of the results of their actions (“Am I doing what I planned to do?”) (Levine et al., 2000). GMT appears
to have beneficial effects on a range of cognitive measures, such as sustained attention to tasks as well as
transfer of training across problems (Levine et al., 2011), and leads to moderate overall improvements in
executive functions that are maintained over time (Stamenova & Levine, 2018). Other procedures for
aiding problem‐solving skills involve cognitive‐behavioural training in problem‐solving skills, exercises
for analysing real‐life problems, and role‐playing of real‐examples of problem situations, and such
training results in significant beneficial effects on measures of executive cognitive functioning up to 6
months after the intervention (e.g., Rath et al., 2003). Relatively new procedures designed to facilitate
executive functioning by training improvements in working memory in dementia sufferers have also
shown promise (Huntley, Hampshire, Bor, Owen, & Howard, 2017).

goal management training (GMT) A procedure that involves training in problem solving
to help evaluate a current problem, followed by specification of the relevant goals, and
partitioning of the problemsolving process into subgoals or steps.

Many types of intervention for executive functioning deficits focus on both behavioural and emotional
regulation, and aim to train the individual in self‐regulation when confronting a problem and managing
their way through the sequence of cognitive and behavioural actions required to solve a problem. One
such procedure is known as self‐instructional training(SIT) where the individual learns a set of
instructions for talking themselves through particular problems. Such types of intervention have been
shown to raise personal self‐awareness of deficits and increase use of successful problem‐solving
strategies, but importantly these methods have the additional beneficial effects of improving emotional
self‐regulation and reducing outward expressions of anger and frustration (Medd & Tate, 2000;
Ownsworth, McFarland, & Young, 2000).

self–instructional training (SIT) A procedure used in the intervention for executive

functioning deficits where individuals learn a set of instructions for talking themselves through
particular problems.
Holistic rehabilitation methods
Most cognitive rehabilitation techniques have been developed to address individual deficits in cognitive
functioning (such as attentional, memory, or language deficits). However, there are substantial benefits to
adopting a more comprehensive holistic approach to rehabilitation that collectively addresses cognitive,
emotional, and functional impairments, as well as physical disability. For example, Malec and Basford
(1996) advocated a comprehensive integrated treatment for individuals with traumatic brain injury that
addressed cognitive, interpersonal, and emotional concerns, used group interventions that addressed
disability awareness and social skills training, and included procedures to enhance vocational
functioning (occupational therapy) and independent living skills. Such approaches are holistic in the
sense that they attempt to develop the individual's awareness of their disabilities and to provide them
with compensatory skills that will enable them to negotiate daily living and regain occupational skills. To
this extent, holistic methods differentiate between restorative procedures that attempt to provide training
to improve cognitive impairments (e.g., intensive training of memory skills), and compensatory procedures
that enable the patient to achieve daily goals through different means (e.g., using assistive technology
such as a smartphone as a memory aid). Holistic rehabilitation methods have been shown to promote
significant improvement in overall functioning in individuals with traumatic brain injury (Ben‐Yishay &
Daniels‐Zide, 2000), develop awareness of disabilities and impairments (which is important when
attempting to engage patients in rehabilitation programmes) (Fleming & Ownsworth, 2006), and to be
superior to standard neurorehabilitation programmes in improving community integration and raising
the patient's level of satisfaction with cognitive functioning (Cicerone, Mott, Azulay, & Friel, 2004).
In the case of dementia, holistic approaches can improve cognitive functioning and slow the decline in
abilities during the early stages of dementia before obvious functional impairment is present (labelled as
mild neurocognitive disorder in DSM‐5). For example, exercise can help to prevent memory problems
and predicts slower decline in cognitive functioning (Sofi et al., 2011; Heyn, Abreu, & Ottenbacher,
2004), as does active participation in intellectual activities such as reading books, newspapers, magazines
or playing board games or card games (Lee et al., 2018). Some forms of training can also provide skills
that generalise across a range of activities, such as metacognitive programmes that teach strategies for
enhancing memory that will generalise across a range of tasks (Hertzog, Kramer, Wilson, &
Lindenberger, 2009), and training in multitasking that improves both multitasking and the ability to
hold information in memory (Anguera et al., 2013). Finally, programmes that address a range of
activities related to healthy living such as diet, exercise, health monitoring, and cognitive training are
showing promise in facilitating cognitive skills such as executive functioning in individuals with mild
neurocognitive disorder (Ngandu et al., 2015), although whether such progammes can actually prevent
dementia is still very much an open question.

15.2.3 Caregiver Support Programmes

Many individuals with neurological disorders are not in primary care but live with their families or with
caregivers such as their spouses or partners. This puts considerable burden on caregivers generally and
will usually require them to cope with behavioural and cognitive deficits, physical disability, challenging
behaviour (such as anger and aggression), and problematic behaviour generally (such as inappropriate
social behaviour). In the case of degenerative disorders that do not usually begin to manifest until later
life, the carers of such individuals will often be their elderly spouses or partners (e.g., in the case of
Alzheimer's disease). In 2011 there were approximately 5.8 million people providing unpaid care for
chronic illness sufferers in England and Wales—just over 1 in 10 of the population were unpaid carers.
This number had grown by over 10% in the 10 years since 2001 (Office for National Statistics, 2013),
and was expected to grow to over 9 million unpaid carers in the UK by 2037 (CarersUK, 2015) ‐ largely
because of the significant increase anticipated in care for dementia over the next 30 years or so. Families
and individuals bear the biggest burden of caring for this increase in people living with chronic illness,
and about 40% of carers of family members with dementia have clinically significant anxiety or
depression (Cooper, Balamurali, & Livingstone, 2007).
Caregivers need to give both physical and emotional support to suffers, as well as having to learn how to
communicate with the sufferer and listen to them without becoming frustrated and angry. Carers may
also pay a substantial economic cost in terms of loss of income as well as living a restricted social life. It
goes without saying that the overall burden on a caregiver will usually be proportional to the disabilities
experienced by the sufferer, and caregivers usually report that their physical and emotional health
suffers as a result of caregiving and many begin to exhibit symptoms of depression. In a study of
caregiver‐burden in Parkinson's disease, perceived burden and quality of life was proportional to
disability, range of symptoms, and the mental health problems exhibited by the individual with
Parkinson's disease (e.g., depression, hallucinations, and confusion) (Schrag, Hovris, Morley, Quinn, &
Jahanshahi, 2006). Poor quality of life and depression in caregivers can often be traced in part to a lack
of skills or strategies for managing the sufferer, and many become avoidant copers by avoiding new
situations and wishing the problems would simply go away. Avoidant coping such as this is significantly
correlated with levels of depression in elderly caregivers or spouses of those with dementia (Mausbach
et al., 2006). To address these problems associated with care‐giving, interventions have been designed to
provide caregivers with a range of skills that will help their day‐to‐day living with sufferers. These may
include advice on how to modify the home environment to support the sufferer (Gitlin, Hauck, Dennis,
& Winter, 2005), training in skills to develop self‐care behaviours by the suffer, to control aggression and
wandering (Pinkston, Linsk, & Young, 1988), or manual based coping interventions delivered in a series
of sessions with trained facilitators (Livingston et al., 2013). Such programmes have been shown to
maintain caregiver positive affect for a period of at least 12 months after the intervention (Lopez‐
Hartmann, Wens, Verhoeven, & Remmen, 2012), and reduce levels of depression and anxiety in carers
over a 6‐year period (Livingston et al., 2020).
Peer support groups are also an important means of maintaining quality of life and positive affect in
caregivers. National societies such as the UK Alzheimer's Society (www.alzheimers.org.uk) provide
information and advice for caregivers including advice on how to understand and respect persons with
neurological disabilities or degenerative disorders and also how to cope with caring for a sufferer. For
example, the Alzheimer's Society recommends that caregivers (a) need to ensure they have sufficient
support (either from family or local support groups), (b) should make time each day for themselves, (c)
understand their right to local services (such as assessment of needs), (d) should try to involve other
family members in caregiving, (e) look after their health (by eating regularly and healthily), (f) check
whether they are entitled to any financial benefits, (g) confront and deal with feelings of guilt, and (h)
take a regular break or holiday by seeking short‐term respite care for the sufferer. In addition, local
groups comprised of similar caregivers can provide significant support across a range of needs,
including (a) information and education, (b) referral and/or assistance on engaging with local health
services, and (c) emotional support (Salfi, Ploeg, & Black, 2005). The effects of such support groups can
be beneficial even if communication is by telephone or by Internet videoconferencing (Marziali,
Donahue, & Crossin, 2005).
Finally, caregiver interventions may not only address the skills and knowledge that will help the
caregiver physically and emotionally manage a sufferer but may also help the caregiver understand and
respect the person with a neurological or degenerative disorder. Once someone's cognitive and physical
abilities begin to decline—especially in old age—it is quite easy to forget that they are still individuals
who should be valued and respected, and support groups such as Alzheimer's Society provide good
advice on how to communication with and listen to individuals with dementia, e.g., Alzheimer's Society
(2020b).
15.2.4 Summary of Treatments and Rehabilitation for Neurocognitive
Disorders
The neurocognitive disorders we have covered in this chapter often represent chronic impairments that
are caused by irreversible damage to brain tissue or are the result of progressive degenerative disorders.
Because of this, rehabilitation may often be a lengthy process and sufferers are likely to require long‐
term care of some kind. We have noted that there have been attempts to develop drugs that can slow
the progress of degenerative disorders such as Alzheimer's disease and Parkinson's disease, and
antiretroviral drugs have similar effects in reducing the severity of HIV symptoms—but the evidence on
whether these drug developments have beneficial effects on cognitive deficits is still modest at best.
Medication is also an important treatment for depression, which is a common and important symptom
of neurological disorders. Antidepressants not only help to improve mood but can also indirectly help to
improve cognitive performance.
Cognitive rehabilitation programmes have been developed to help the individual with a range of
specific cognitive deficits, including attention deficits, visuospatial deficits, apraxia, language and
communication deficits, memory deficits, and executive function impairments. These may take a variety
of forms, such as (a) massed training to improve cognitive impairments (e.g., memory training); (b)
compensatory skills training, which accepts that the individual has particular impairments and helps
them to achieve daily goals by other means; (c) computer‐assisted training can provide the means for
remedial cognitive training in both the therapeutic and home environment, or provide virtual
environments in which the sufferer can learn skills in relative safety; and (d) assistive technology is being
increasingly utilised as a means of helping the disabled individual to cope with and negotiate daily living
(e.g., using a smartphone to provide reminders for daily activities in individuals with memory deficits).
 A WEEK IN THE LIFE OF A CLINICAL PSYCHOLOGIST
WORKING AS A CONSULTANT CLINICAL
NEUROPSYCHOLOGIST
Monday. “How do you spell neuropsychologist?” asked the Detective Sergeant on the telephone.
He requests a statement relating to whether a client could be a reliable witness in a sexual
assault case. I explained to him that since suffering from encephalitis her attention and memory
abilities are so poor that it was unlikely she could provide a reasonable account for the police.
The call has taken my administration time and once again I begin a new week behind schedule
as I rush off to the first meeting of the week.
The community disability team meeting focuses on the most complex cases. A man who has
motor neurone disease has now found out his wife has developed multiple sclerosis. Concerns
are expressed about a lady with a brainstem stroke. There are concerns her female partner is
emotionally abusing her. All agree a vulnerable adults strategy meeting is required. The
afternoon is spent supervising colleagues and a new trainee.
Tuesday is spent completing four initial consultations to decide whether psychological
intervention can be appropriately offered. A lady with Parkinson's disease who has started
having panic attacks. A man who suffered a head injury in a car accident, his parents are
struggling to cope with his bad language and temper outbursts. A lady with multiple sclerosis is
saddened by having to give up work and finally a man of 80 who suffered a stroke last summer.
His wife feels desperately isolated, as he can no longer drive.
Wednesday. Appropriate psychometric tests are chosen for the man who has come for an
outpatient assessment this morning. He has experienced a 2‐year history of memory problems.
Sadly, the man struggles with most tests but particularly those we know are associated with
dementia of the Alzheimer's type. A sense of sadness stays with me for the afternoon at the
thought of what my feedback has meant to that couple. I resolve to reduce my administration
pile by the end of today.
Seven ladies have arrived for my Thursday morning relative's group, a meeting for people living
with someone who has a neurological diagnosis. The usual issues are discussed, how to cope
with the feelings of loss, what to do in response to a partner's temper outbursts and how to
minimise cognitive difficulties. Thursday afternoons are usually set aside for outpatient
intervention appointments. Today a lady in her 40s talks about her sense of isolation since her
stroke and requests help to explain the nature of her difficulties to her children. The last
appointment of the day brings a feeling of optimism as a young woman who suffered a severe
head injury 2 years ago is pleased to inform me that she is finally living independently and has
started a part time job.
Friday morning is spent making an assessment as to the capacity of a lady with Huntington's
disease to manage her finances. Two further outpatient appointments leave just an hour to write
up client files and complete an assessment report before meeting the final challenge of the
week, Friday evening rush hour!

Finally, because of the nature of neurocognitive disorders and the frequent need for long‐term care,
programmes of support and training are increasingly becoming available for caregivers. These include
programmes to provide emotional support for caregivers, programmes to provide appropriate
management and coping skills for living with individuals with disabilities, and local or national support
groups that provide advice and information.
SELF‐TEST QUESTIONS
What is the difference between a restorative treatment and compensatory skills training?
How have drugs been used in the treatment of neurological disorders? Do such drugs help
in the treatment of the cognitive deficits caused by the disorder?
Can you describe at least one specific intervention designed to address each of the
following: attention deficits, visuospatial deficits, apraxia, language and communication
deficits, memory deficits, and deficits in executive functioning?
What are holistic rehabilitation methods, and how do they differ from specific restorative
interventions?
What are the main problems encountered by those giving care to people suffering from
neurological disorders, and what interventions have been developed to help them?
 SECTION SUMMARY

15.2 TREATMENT AND REHABILITATION FOR NEUROCOGNITIVE

DISORDERS
Treatment of neurological disorders tends to be based on restorative treatment for individual
cognitive deficits (e.g., memory training) or compensatory skills training based on helping the
sufferer to deal with the daily living difficulties posed by the deficit.
Drug treatments include the use of cholinesterase inhibitors (Alzheimer's disease), levodopa
(Parkinson's disease), thrombolytic therapy (CVAs and strokes), and antiretroviral drugs (HIV
dementia).
Depression is also a common feature of many neurological disorders and can be treated
with antidepressants and appropriate psychological therapy.
Deep brain stimulation (DBS) alleviates symptoms of Parkinson's disease by delivering
electrical stimulation to the thalamus and basal ganglia.
Cognitive rehabilitation programmes are usually directed at improving function within
specific cognitive deficits (e.g., memory, language).
Rehabilitation programmes for attention deficits include Attention process training (APT)
and time pressure management (TPM).
Gestural training and the use of virtual reality environments can be utilised to treat apraxia and
deficits in coordinated self‐help behaviours.
Treatment of language and communication deficits will depend on the specific nature of
the problem, but common examples of rehabilitation procedures include constraint‐induced
movement therapy (CIMT) and group communication treatment.
Memory deficits can be addressed with the use of assistive technology (such as smartphones)
or specific memory training procedures such as visual imagery mnemonics or errorless learning
procedures.
Deficits in executive functioning often utilise interventions that involve problem‐solving
training such as goal management training (GMT) or self‐instructional training (SIT).
Holistic rehabilitation methods collectively attempt to address cognitive, emotional, and
functional impairments, as well as physical disability.
Because those suffering neurological disorders live with their families or caregivers, caregiver
interventions have been developed that help to provide the caregiver with training and
support for the task.

15.3 NEUROCOGNITIVE DISORDERS REVIEWED

Unlike many of the other disorders described in this text, neurocognitive disorders have their origins
almost solely in damage or abnormalities in the biological substrates that underlie thinking and
behaviour. These disorders give rise to a range of disabilities and impairments, both physical and
cognitive, and many are irreversible and permanent deficits. The main causes of neurocognitive
disorders are cerebral infections, traumatic brain injuries, cerebrovascular accidents such as strokes, and
degenerative disorders such as Alzheimer's disease and Parkinson's disease. Clinical psychologists have a
major interest in neurocognitive disorders because many of the major symptoms are deficits in critical
cognitive functions such as learning and memory, attention, language and communication, visual
perception, motor skills, and executive functions. Because of this, clinicians are involved in the
assessment of neurocognitive disorders and the treatment and rehabilitation of these disorders.
Assessment of neurocognitive disorders is often difficult and involves a combination of tests of cognitive
functioning (such as the WAIS IV or the AMIPB), blood tests and analyses of cerebrospinal fluids (to
determine the presence of inherited degenerative diseases or infections), genetic testing (to determine
whether the individual possesses genes likely to put them at risk for neurocognitive or degenerative brain
disorders), and brain scans using EEG, PET, or fMRI. While some of the disorders result in immediate
impairment (such as traumatic brain injury or stroke), many others are progressive degenerative
disorders that develop from mild symptoms of cognitive impairment to full‐blown dementia and
physical disability (e.g., Alzheimer's disease). While most degenerative disorders afflict the older adult,
some can affect younger individuals (e.g., neurocognitive disorder due to HIV infection or prion
disease). Many of the neurocognitive disorders are closely associated with other forms of
psychopathology, especially depression and psychosis. Depression appears to be both a predictor and a
consequence of some neurocognitive disorders (such as stroke or Parkinson's disease) and is considered
by some to be an integral feature of those disorders.
Because most neurocognitive disorders are caused by irreversible damage to brain tissue, treatment, and
rehabilitation often takes the form of compensatory skills training which accepts that the individual has
a particular impairment and helps them to achieve their daily goals by other means (e.g., by using
compensatory strategies, such as memory aids, or assistive technology, such as equipment to aid hearing,
speaking, or moving about). Nevertheless, there are many specific cognitive rehabilitation procedures
that can be used with reasonable success in attempts to restore basic cognitive functions such as memory,
attention, language, and motor skills. However, because of the long‐term nature of many
neurocognitive disorders there is a basic need for long‐term care for sufferers, and this is often care
provided by close family, spouses, and partners. This need has given rise to a range of programmes to
provide support to caregivers, including basic caregiver skills training (e.g., how to structure the
environment for a disabled individual) and emotional support programmes.
This book is accompanied by Student and Instructor companion
websites.
www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter References
Videos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
16
Childhood and Adolescent Psychological Problems

ROUTE MAP OF THE CHAPTER

This chapter begins by discussing some of the difficulties involved in identifying and diagnosing
childhood and adolescent psychological problems. We then go on to discuss the characteristics,
prevalence rates, and aetiology of disruptive behaviour problems (discussing ADHD and
conduct disorder in detail) and childhood and adolescent anxiety and depression. The chapter
ends by discussing the main treatment methods used with children and adolescents and how
coordinated provision of treatment extends across a range of services, including education,
health, and social services.

CHAPTER OUTLINE
16.1 THE DIAGNOSIS AND PREVALENCE OF CHILDHOOD AND
ADOLESCENT PSYCHOLOGICAL PROBLEMS: SOME GENERAL ISSUES
16.2 DISRUPTIVE BEHAVIOUR PROBLEMS
16.3 CHILDHOOD AND ADOLESCENT ANXIETY AND DEPRESSION
16.4 THE TREATMENT OF CHILDHOOD AND ADOLESCENT
PSYCHOLOGICAL PROBLEMS
16.5 CHILDHOOD AND ADOLESCENT PSYCHOLOGICAL PROBLEMS
REVIEWED

LEARNING OUTCOMES
When you have completed this chapter, you should be able to:
1. Describe and evaluate some of the difficulties involved in diagnosing and treating
childhood and adolescent psychological problems.
2. Describe the characteristics of at least two disruptive behaviour disorders.
3. Describe the characteristics of childhood and adolescent anxiety and depression.
4. Compare and contrast theories of the aetiology of disruptive behaviour disorders,
childhood anxiety, and childhood depression.
5. Describe the characteristics of some of the main therapeutic methods used to treat
childhood and adolescent psychological problems and evaluate their efficacy.
 My own troubles began when I was 3 years old and my father died abruptly of a brain tumour. A few years later
my mother was diagnosed with breast cancer and died when I was 11 years old. Watching so many important
people die was frightening and confusing. Even so, the most traumatic event of my childhood was my placement
into foster care. Although my aunts and uncles hinted at the possibility, I never believed they would give me away. I
threatened to jump off a high building if they went ahead with the plan. I knew they were conspiring to banish me
and I did not trust a single one of them. But they did it anyway. I'd had enough of the cycle of attachment and
desertion and decided I wasn't going to become attached to my new foster parents. To the outside world I was
withdrawn and detached. Yet towards myself I was overwhelmed by intense feelings of rage and hatred. My foster
mother repeatedly spoke of her disappointment in me and angrily talked about sending me away. I knew from my
brother that foster children often go from place to place and that being physically or sexually abused was common.
During the following 2 years I continued to float through time and space in a state of numb, disorganised misery,
going through the emotions but not really alive. I was aware of my impairment, and ashamed of it. I believed I
was peculiar. When I was about 16, I became absorbed with the idea that my central problem was a bodily
defect, and I focussed on one aspect of my anatomy after another, determined to find the specific flaw. At 17 I
developed the sensation of a lump in my throat and became convinced I was about to choke to death. I had no
labels for any of my experiences, so I did not realise this latest state was a form of anxiety. Every night I stayed
awake to the point of exhaustion.
Frank's Story

Introduction
The study of childhood and adolescent psychopathology is fraught with a range of difficulties that are
not experienced in the study of adult psychopathology. First, any behavioural or psychological problems
have to be assessed in the context of the child as a developing organism. For example, bed‐wetting is
quite normal in infancy but might be a sign of anxiety or adjustment problems after the age of 5 years.
Similarly, shyness and withdrawal from social contact are often normal during periods of social
development as the child attempts to understand the rules of social interaction and learns how to
verbally communicate with others. However, in early adolescence these may represent the first signs of
psychopathology. In addition, children may often go through brief stages of development when they
exhibit behavioural problems or fears and anxieties, but these problems often disappear as rapidly as
they appeared. Most parents have experienced a child who refuses to eat or very suddenly becomes
frightened of noises, strangers, or certain types of animals, only for this to disappear within a matter of
weeks or even days. Second, because of their immaturity, children will tend to have poor self‐knowledge.
They may feel that something is wrong but be unable to label it as anxiety or depression, or convey
clearly how they feel to others. In such circumstances, the clinician has to infer psychological states from
overt behaviour and decide whether that behaviour is unusual for the developmental stages through
which the child is passing. With these issues in mind, clinicians have tended to organise childhood
psychological problems into two broad domains based on the general behavioural characteristics of the
child. The first domain covers externalising disorders, which are based on outward‐directed
behaviour problems such as aggressiveness, hyperactivity, noncompliance, or impulsiveness. The second
domain covers internalising disorders, which are represented by more inward‐looking and
withdrawn behaviours and may represent the experience of depression, anxiety, and active attempts to
socially withdraw. The former are now more commonly known as disruptive behaviour disorders, and
include the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM‐5) diagnosable disorders
such as conduct disorder (CD) and attention deficit hyperactivity disorder(ADHD). The
internalising disorders are still difficult to diagnose reliably, but DSM‐5 does include guidelines for
diagnosing childhood separation anxiety, generalised anxiety disorder(GAD), and major
depressive disorder. The childhood and adolescent disorders discussed in this chapter are covered in
a number of different chapters in DSM‐5, including the chapter on disruptive, impulse control, and
conduct disorders (oppositional defiant disorder [ODD], conduct disorder), neurodevelopmental
disorders (attention‐deficit/hyperactivity disorder, ADHD), anxiety disorders (childhood separation
anxiety, childhood GAD), depressive disorder (childhood major depression), and obsessive‐compulsive
and related disorders (childhood OCD).

externalising disorders Disorders based on outward‐directed behaviour problems such as

aggressiveness, hyperactivity, non‐compliance or impulsiveness.

internalising disorders Disorders represented by more inward‐looking and withdrawn

behaviours, and may represent the experience of depression, anxiety, and active attempts to
socially withdraw.

separation anxiety A childhood anxiety problem involving an intense fear of being separated
from parents or carers.

Frank's Story described at the beginning of this chapter illustrates the kinds of experiences that might give
rise to psychological distress in childhood and adolescence and how this distress may be manifested in
behaviour. This personal account describes the negative emotional impact of the death of his mother
and father, his feelings of abandonment and impotency, and how this affected his ability to form
relationships. This in turn gave rise to feelings of guilt, shame, and inadequacy, and in adolescence
finally manifested as specific psychological problems such as body dysmorphic disorder and somatic
symptom disorder. He related this story as an adult and as such was able to look back on his childhood
and put his behaviour and emotions into a perspective that enabled him to understand them. But events
often seem confusing and uncontrollable to a child, and a clinician has to interpret what a child might
be feeling and experiencing from their behaviour alone (for example, much of Frank's behaviour might
be seen as internalising, and suggestive of anxiety and depression). Nevertheless, even during an
upbringing that is relatively trauma free, children will frequently experience childhood as a threatening
and frightening time. They will develop anxieties as they experience new people and new situations
(Crijnen, Achenbach, & Velhulst 1999), will worry about many of their everyday activities such as
attending school (Ollendick, King, & Muris, 2002; Vasey, 1993), and develop behavioural problems such
as temper tantrums, eating irregularities, nightmares, and phobias. As the child moves into adolescence
even more challenges await as the individual develops sexually, changes physically, encounters
educational and occupational challenges, and moves into a new period where feelings of responsibility
and self‐worth are expected of them. It is perhaps not surprising at this stage that many adolescents
encounter feelings of confusion, anxiety, and depression while attempting to cope with these changes
(Lerner, 2002), and it is also not surprising therefore that the initial symptoms of many of the adult
mental health disorders we have covered earlier in this book first begin to develop during adolescence
(e.g., schizophrenia, paraphilic disorders, somatic symptom disorders, etc.).
In the following section of this chapter we look briefly at the difficulties involved in addressing
psychological problems of childhood and adolescence, and then look at the prevalence rates of specific
disorders. The remainder of the chapter looks in detail at the diagnosis, aetiology, and treatment of the
following: (a) attention deficit and disruptive behaviour disorders, and (b) childhood anxiety and
depression.

16.1 THE DIAGNOSIS AND PREVALENCE OF CHILDHOOD AND

ADOLESCENT PSYCHOLOGICAL PROBLEMS: SOME GENERAL
ISSUES
16.1.1 Difficulties Associated with Identification and Diagnosis of Childhood
and Adolescent Psychological Problems
We have already alluded to some of the difficulties involved in identifying whether a child needs help
and treatment for a mental health problem and it is worth considering some of these difficulties before
we discuss individual diagnoses. For example, when considering what might be clinically relevant
behaviour in children, we first have to consider what is normal for a particular age. For example, bed‐
wetting is considered relatively normal in children up to the age of 5 years but may be a symptom of
psychological distress if it occurs after that age. Diagnosing a psychological problem is often dependent
on the individual being able to communicate with the practitioner and to articulate how they experience
the distress that their problems are causing them. However, many children are unable to communicate
clearly how they feel (e.g., they may not be able to differentiate feelings of anxiety from feelings of
depression). They may also lack self‐knowledge, and be unable to understand precisely what they are
feeling. In extreme cases, some disorders are explicitly associated with an inability to communicate with
others (e.g., autistic syndrome disorders), and so identification of psychological problems has to take
place almost solely on the basis of external observation of the child's behaviour and their rate of
development. Differences in cultural norms will also affect whether childhood behaviours are seen as
problematic or not. Externalising behaviour problems are most prominent in many Western societies,
but some Eastern cultures have relatively low levels of this type of problem where parents are less likely
to endorse aggressive or authoritarian attitudes (Lansford et al., 2018; Weisz, Suwanlert, Wanchai, &
Bernadette, 1987). For example, in those countries that practice Buddhism, externalising behaviours
such as disrespect and aggression are rarely tolerated by parents and teachers and are often managed at
an early stage in the child's life. Finally, during childhood and early adolescence, developmental changes
occur rapidly, and this means that psychological problems can escalate quickly and dramatically. For
example, behaviour problems can be generated very rapidly if the development of language skills, self‐
control skills, social skills, and emotional regulation do not proceed normally. This requires that
childhood problems need to be identified early and quickly in order to minimise the psychological
damage that prolonged abnormal development could inflict.

16.1.2 Childhood Psychopathology as the Precursor of Adult

Psychopathology
The section on Adult Mental Health describes how important childhood experiences appear to be in
the aetiology of many diagnosable psychological disorders, so childhood maltreatment and adversity not
only affects childhood behaviour but may serve as the basis for the development of long‐term
psychological maladjustment including major depression, anxiety disorders, personality disorders such
as borderline and antisocial personality disorders, somatic symptom disorders, dissociative disorders,
eating disorders, and sexual and gender disorders (Dunn et al., 2017; Jaffee, 2017). Childhood
maltreatment and adversity can take a number of forms. Arguably, the most severe is childhood physical
and sexual abuse, but neglect and inconsistent parenting are also stressful experiences for a child, as are
many more ‘normative’ types of childhood adversity within the family that can generate
psychopathology in the child across the course of their lifetime, and these include such things as
maternal depression, family financial stress, parental conflict, family anger, maternal role overload, and
negative parenting. The last factor includes disciplining strategies such as threatening a child—‘You stop
crying or I'll give you something to cry about’—or attending to the child only when they are doing
something wrong (Essex, Klein, Cho, & Kalin, 2002). Quite strikingly, childhood adversity such as
parental mental health problems and household dysfunction have affected as many as two out of every
three children by the age of 18 (Anda et al., 2006). This may have some of its effects on mental health
by affecting amygdala‐hippocampus connectivity (the brain system that enables enhanced memory for
negative emotional events) and biasing brain areas such as the amygdala towards reactivity to negative
content (Herringa et al., 2013; Herringa et al., 2016). Extreme forms of childhood adversity can also
have their effects on later mental health through epigenetic processes, where severe stress during
childhood may affect the expression of genes that would help to regulate mental health problems. For
example, self‐starvation and severe weight loss during childhood and adolescence can affect the
expression of genes that affect a variety of systems relevant to eating disorders, including
behavioural/affective regulation, sensitivity to nutritional insufficiencies, and body weight maintenance
(Saffrey, Novakovic, & Wade, 2014; Tremolizzo et al., 2014, see Chapter 10, Section 10.3.1). Regardless
of the nature of the mechanisms which may mediate the relationship between childhood maltreatment
and mental health problems in adulthood, recent studies indicate that childhood maltreatment
effectively doubles the risk of mental health problems in adulthood (Chandan et al., 2019; Dunn et al.,
2017), but we also need to be clear that mental health problems are not an inevitable outcome of being
maltreated during childhood, and access to supportive relationships can buffer people from the adverse
effects of maltreatment (Jaffee, 2017).
Table 16.1 lists some of the childhood risk factors that have been identified in the aetiology of adult
psychopathology, and these are all discussed more fully in the relevant chapters of this book. Childhood
risk factors such as these enable researchers and clinicians to identify those groups of children and
adolescents that are most likely to be at risk for adult mental health problems. With this in mind, an
emerging area of research is developmental psychopathology. This is an area that is concerned
with mapping how early childhood experiences may act as risk factors for later diagnosable
psychological disorders and attempts to describe the pathways by which early experiences may generate
adult psychological problems (Drabick & Kendall, 2010).

developmental psychopathology An area of research concerned with mapping how early

childhood experiences may act as risk factors for later diagnosable psychological disorders. It
also attempts to describe the pathways by which early experiences may generate adult
psychological problems.

TABLE 16.1 Childhood Risk Factors for Adult Mental Health Problems
Childhood experience (risk Adult mental Reference Chapter
factor) health problem
Abnormal Parent‐Child Social anxiety disorder Moore, Whaley, & Sigman (2004) 6
Interaction Style Narcissistic and Johnson et al. (2003) 12
obsessive compulsive
personality disorder
Antisocial personality Gabbard (1990) 12
disorder
Borderline personality Graybar & Boutilier (2002) 12
disorder
Histrionic personality Bender, Farber, & Geller (2001) 12
disorder
Childhood abuse (physical OCD Grisham et al. (2011) 6
and sexual) PTS Wolf et al. (2012) 6
Depression (reduced Raes, Hermans, Williams, & 7
autobiographical Eelen (2005)
specificity)
Psychosis McGrath et al. (2017) 8
Substance use Sartor et al. (2013) 9
disorder
Suicide and suicidal Gould & Kramer (2001) 7
 ideation

Eating disorders Steiger et al. (2000); Brown, 10

Russell, Thornton, & Dunn
(1997); Perroud et al. (2011)
Hypoactive sexual Stuart & Greer (1984) 11
desire disorder
Sexual aversion Berman et al. (1999) 11
disorder
Vaginismus DSM‐IV‐TR 11
Sexual dysfunction Najman et al. (2005); Pulverman, 11
generally Kilimnik, & Meston (2018)
Dyspareunia Binik, Bergeron, & Khalifé 11
(2000)
Paedophilic disorder Freund & Kuban (1994); Cohen 11
et al. (2010)
Paraphilias generally Mason (1997); Murphy (1997) 11
Gender dysphoria Bradley & Zucker (1997) 11
Personality disorders Johnson et al. (1999) 12
generally
Borderline personality Heffeman & Cloitre (2000); 12
disorder Scheiderer, Wood, & Trull (2015)
Antisocial personality Horowitz, Widom, McLaughlin, 12
disorder & White (2001)
Narcissistic personality Kernberg (1989) 12
disorder
Avoidant personality Rettew et al. (2013) 12
disorder
Schizotypal Waxman, Fenton, Skodol, Grant, 12
personality disorder & Hasin (2014)
Conversion disorder Bowman & Markand (1996) 13
Hypochondriasis Salmon & Calderbank (1996) 13
Somatisation disorder Iezzi, Duckworth, & Adams 13
(2001)
Dissociative disorders Tyler, Cauce, & Whitbeck (2004); 14
generally Dalenberg et al. (2012)
Dissociative identity Putnam (1997); Vissia et al. 14
disorder (DID) (2016)
Depersonalisation Simeon et al. (2001) 14
disorder
Childhood neglect (e.g., Post‐traumatic stress King et al. (1996) 6
separation, inadequate, and disorder (PTSD)
ineffectual parenting) Major depression Lara & Klein (1999); Goodman 7
(2002); Nelson, Klumparendt,
Doebler, & Ehring (2017)
 Cannabis, nicotine, Cadoret et al. (1995) 9
and alcohol abuse
Hypersexuality Långström & Hanson (2006) 11
Paraphilias generally Mason (1997); Murphy (1997) 11
Antisocial personality Hill (2003) 12
disorder
Borderline personality Guttman (2002) 12
disorder
Dependent Bornstein (1996) 12
personality disorder
Body dysmorphic Cororve & Gleaves (2001) 13
disorder
Childhood trauma generally Schizophrenia Read, van Os, Morrison, & Ross 8
(2005)
Alcohol dependency Sher (1991); Wilsnack, 9
Vogeltanz, Klassen, & Harris
(1997); Brady & Back (2012)
Nicotine dependency Anda et al. (1999) 9
Conversion disorder Bowman & Markand (1996) 13
Dissociative identity Putnam (1997) 14
disorder
Childhood conflict and Specific phobias Freud 6
emotional disturbance Cannabis dependency Meltzer, Gatward, Goodman, & 9
Ford (2003)
Childhood poverty Major depression Hammen (2016) 7
Schizophrenia Byrne, Agerbo, Eaton, & 8
Mortensen (2004)
Alcohol, nicotine, and Alverson, Alverson, & Drake 9
cannabis abuse (2000)
Substance Petronis & Anthony (2003) 9
dependency generally
Antisocial personality Paris (2001); Hanson et al. (2015) 12
disorder
Summary points on childhood maltreatment (from Jaffee, 2017):
In the United States in 2014, 9.4 per 1,000 children were found to be victims of childhood maltreatment. Children
under the age of 3 have the highest risk of victimisation.
Although having a childhood history of maltreatment increases the odds that an individual will
engage in abuse or neglect as an adult, the majority of children who are maltreated do not grow up
to perpetrate abuse or neglect.
Child victims of maltreatment and adults who were maltreated in childhood are at risk for a range
of mental health problems, including depression, anxiety, substance abuse, antisocial behaviour,
psychotic symptoms, and personality disorders. The risk for psychopathology associated with a
history of abuse or neglect is not due to cooccurring sociodemographic risk factors.
Maltreatment is likely to increase risk for different forms of psychopathology by increasing threat
 sensitivity, decreasing responsivity to reward, and producing deficits in emotion recognition and
understanding.
Mental health problems are not inevitable consequences of being maltreated. Access to socially
supportive relationships can buffer individuals from the adverse effects of maltreatment, and some
individuals carry gene variants that are associated with reduced susceptibility to maltreatment.
There are a number of possible ways in which childhood psychopathology may link to adult mental
health problems, and we have already briefly discussed the possibility of childhood maltreatment
affecting gene expression and brain connectivity. However, the simplest relationship is where a
childhood disorder merely persists into adulthood in the same form (e.g., where childhood anxiety or
depression develops into experienced anxiety and depression in adulthood). One striking example of
this was described in Chapter 12, where we noted that childhood conduct disorder and antisocial
behaviour often persist into adulthood in the form of antisocial personality disorder (Farrington, Loeber,
& Van Kammen, 1990). Second, a childhood psychopathology may have an adverse effect on
subsequent development and indirectly lead to different forms of maladjustment in later life. For
example, children who fail to form adaptive relationships with their parents early in life exhibit
disruptive behaviour in late infancy, and such disruptiveness can result in more general adjustment
problems and the development of learning difficulties later in life. Third, a childhood psychopathology
may simply represent the less cognitive precursor of a related adult disorder. For example, adolescent
height phobia has been shown to be a risk factor for full‐blown panic disorder in adulthood (Starcevic &
Bogojevic, 1997), and this may result from the fact that the catastrophising of bodily sensations is a
central feature of both disorders and may extend across an increasing number of cognitive and
behavioural domains as the individual develops from childhood into adolescence (Davey, Menzies, &
Gallardo, 1997). Fourth, a childhood disorder may not necessarily extend into adulthood but may
render the individual vulnerable to later life stressors. For example, maltreatment is likely to increase the
risk for different forms of psychopathology by increasing threat sensitivity, decreasing responsiveness to
rewards and resulting in deficits in emotion recognition and understanding (Jaffee, 2017). Fifth, a
childhood disorder may be quite specific to childhood and disappear or change form dramatically once
the individual has reached adulthood.
Finally, we must also be open to the possibility that although childhood maltreatment may be a risk
factor for adult psychopathology, it may not be a direct cause of that adult psychopathology. For
example, genetically inherited characteristics such as impulsivity and poor emotion regulation in a child
may be difficult characteristics for a parent to deal with, and as a consequence parents may attempt to
cope with such problems in their children in either harsh or neglectful ways. In situations such as this,
childhood maltreatment may predict later psychopathology, but it is the genetic predispositions that are
the cause of the adult psychopathology, not the childhood maltreatment per se (cf. Berenz et al., 2013;
Bornovalova et al., 2013; see Chapter 12, Section 12.4.2).
However, most of these examples demonstrate that childhood experiences and childhood
psychopathology can have an important influence on adult mental health, but the nature of this
influence is not always direct and not always in the same form as the childhood difficulties. You may
want to refer to Table 16.1 and consider what possible developmental processes might link certain
childhood experiences with adult psychopathology.

16.1.3 The Prevalence of Childhood and Adolescent Psychological Disorders

Studies of the prevalence of diagnosable childhood psychological disorders estimate that as many as
10–20% of children and adolescents have a diagnosable psychological problem (World Health
Organization, 2020). Boys exhibit higher prevalence rates than girls in the 5–11‐ year age range with
conduct disorders predominating (Centre for Mental Health, 2016), but once in adolescence and early
adulthood (15–25 years of age) girls report significantly higher rates for psychological distress, anxiety,
and depression (Van Droogenbroeck, Spruyt, & Keppens, 2018). Figure 16.1 shows the prevalence of
having any psychopathology in children and adolescents aged between 5 and 19 years in England
(Office for National Statistics, 2018). The pattern of association between age and disorder was different
for boys and girls. In girls the association was pronounced, but it was not apparent in boys. Among 5–
10‐year‐olds, boys (12.2%) were more likely than girls (6.6%) to have a mental health problem (as a
result of the higher levels of behavioural and conduct disorders in boys). Boys (14.3%) and girls (14.4%)
aged 11–16 were equally likely to be diagnosed with a psychopathology. In 17–19‐year‐olds, girls
(23.9%) were more than twice as likely as boys (10.3%) to have a mental health problem—and this
difference was largely due to the high prevalence of emotional problems (anxiety and depression) in
girls. Over a third (38.2%) of those living in households with the least healthy family functioning had a
diagnosable mental health problem, compared with less than 1 in 10 (8.3%) of those living in
households with the healthiest family functioning, and children living in households with the lowest
levels of income were around twice as likely to have a diagnosable mental health problem as those living
in the highest income households (Office for National Statistics, 2018).
Comorbidity between childhood disorders is also common, and many children have more than one
mental health diagnosis, although the percentage of children suffering comorbid conditions differs
significantly between epidemiology studies (Arcelus & Panos, 2005). In addition, childhood
psychopathology is also associated with physical health problems, poor educational performance, and
comorbidity is associated with greater risk for suicide, substance abuse, and conduct disorder (Arcelus &
Panos, 2005; Office for National Statistics, 2018).

FIGURE 16.1 The prevalence of any diagnosable mental health problem in childhood. Percentage of children (boys and
girls) with a diagnosable mental health problem in age groups 5–10 years, 11–16 years, and 17 to 19 years of age.
From Office for National Statistics (2018) Mental health of children and young people in England, 2017.
https://files.digital.nhs.uk/A0/273EE3/MHCYP%202017%20Trends%20Characteristics.pdf
 SELF‐TEST QUESTIONS
Can you describe four difficulties involved in the detection and diagnosis of childhood
psychological disorders?
What kinds of childhood events act as precursors or risk factors for adult mental health
problems?
How prevalent are childhood psychological disorders?

SECTION SUMMARY

16.1 THE DIAGNOSIS AND PREVALENCE OF CHILDHOOD AND

ADOLESCENT PSYCHOLOGICAL PROBLEMS: SOME GENERAL
ISSUES
There are a number of difficulties associated with recognising and diagnosing childhood
psychological problems, including communication difficulties and the child's
underdeveloped self‐awareness.
Childhood psychopathology is often a significant precursor to adult psychopathology.
Between 10 and 20% of children and adolescents have a diagnosable psychological
disorder
Comorbidity between disorders is common.

16.2 DISRUPTIVE BEHAVIOUR PROBLEMS

In this section we cover those behavioural problems that are characterised by impulsive, disruptive, and
poorly controlled behaviour. We all expect children of certain ages to have poor self‐control, to throw
temper tantrums, or to disrupt ongoing activities by failing to show restraint. However, by the time most
children enter school, they are expected to be able to restrain their behaviour, attend to tasks when
asked, and to attend to and follow appropriate commands. Nevertheless, some individuals find this hard
to do—even in late childhood or adolescence. Their inability to restrain themselves and follow
instructions can lead to the disruption of cooperative and group activities (such as group learning in
school), and in extreme cases may represent overtly aggressive behaviour to peers and adults, including
criminal violence and damage to property. We discuss two particular disruptive behaviour
problems that can be found in DSM‐5: attention deficit hyperactivity disorder (ADHD) and
conduct disorder. In this section we discuss these two syndromes individually, covering their diagnosis
and aetiology.
16.2.1 Attention Deficit Hyperactivity Disorder (ADHD)
The main feature of ADHD is a persistent pattern of inattention and/or hyperactivity‐impulsivity that
is at a significantly higher rate than would be expected for the child at that developmental stage. ADHD
can manifest itself behaviourally in many ways, including lack of attention in academic, occupational,
or social situations; making careless mistakes in school work or other tasks; difficulty maintaining
attention until task completion; appearing to have their attention elsewhere, and a failure to take in or
respond to instructions; a tendency to shift from one task to another without completing any of them.
The child with ADHD will typically have a strong dislike for tasks that require sustained self‐application
and mental effort and will be easily distracted by irrelevant stimuli or events. Hyperactivity may be
manifest as excessive fidgetiness and by not remaining seated when asked. The child with ADHD will
exhibit excessive running or climbing when inappropriate, or will talk excessively. Toddlers with the
disorder will appear to be constantly ‘on the go’ and jump and climb on furniture as well as having
difficulty in participating in sedentary activities such as listening to a story. Impulsivity manifests as
impatience, a difficulty in appropriately delaying responses (e.g., attempting to run out of the house
before their coat is on), and constantly interrupting others before they have finished what they have to
say; it may also reflect a desire for immediate rewards over delayed rewards. Impulsivity can also result
in accidents such as knocking over objects or indulging in dangerous activities (such as riding a bike fast
over rough terrain) (Case History 16.1).

Hyperactivity A higher than normal level of activity.

Impulsivity The act of reacting to a situation without considering the consequences.

The diagnosis of ADHD

The main issue in diagnosing ADHD is to ensure that hyperactivity or inattention is significantly greater
than normal for the child's developmental stage, and to ensure that it is a generalised and persistent
predisposition rather than one that is confined to a single context. Table 16.2 describes the DSM‐5
diagnostic criteria for ADHD, and this emphasises that impairment is present before 12‐years of age
(Criterion B) and is found in two or more contexts (Criterion C). Most individuals with ADHD present
with symptoms of both inattention and hyperactivity, but in some one or the other pattern may be
dominant. This has given rise to two diagnostic subtypes, namely attention‐deficit/hyperactivity
disorder, predominantly inattentive presentation and attention‐deficit/hyperactivity
disorder, predominantly hyperactive/impulsive presentation. If both inattentive and
hyperactive/impulsive elements are present this is known as a combined presentation. Each subtype
should be used if six (or more) of the dominant symptoms are present with fewer than six of the less
dominant symptoms present.
Around half of those diagnosed with the combined presentation of ADHD will also be diagnosed with
ODD or conduct disorder (see Section 16.2.2), and these rates of comorbidity are significantly higher
than comorbidity with other psychopathologies (Hinshaw, 1987). This indicates that in many cases
ADHD is associated with the violation of social norms and the basic rights of others, and raises the
question of whether there might be an underlying link between the two disorders (e.g., Quay, 1979).
Opinion on this is currently undecided, but what is clear is that when a child is diagnosed with both
ADHD and an ODD/conduct disorder, the individual will usually exhibit the worst of both disorders
(Biederman, Newcorn, & Sprich, 1991). In other cases, children with ADHD can be distinguished from
those with ODD/conduct disorder by the fact that the latter are likely (a) to be more aggressive, (b) live
in families with a lower socio‐economic status, and (c) have parents who also exhibit antisocial behaviour
(Faraone, Biederman, Jetton, & Tsuang, 1997; Hinshaw, 1987). In addition, recent studies have
suggested that children with a single diagnosis of ADHD are likely to have a better long‐term prognosis
than those with oppositional defiant disorder/conduct disorder, and childhood ADHD alone is not a
differential predictor of antisocial personality disorder in adulthood (Lahey, Loeber, Burke, &
Applegate, 2005). However, there is evidence that in some cases ADHD can lead to earlier onset of
conduct disorder and around a quarter of those children with a combined presentation ADHD
diagnosis will be diagnosed with conduct disorder (DSM‐5, American Psychiatric Association, 2013, p.
65). This may be because some children with ADHD become involved in an escalation of symptoms
caused by a vicious cycle where their disruptive behaviour causes aggressive reactions in others, and this
in turn evokes aggressive and increasingly antisocial reactions in the sufferer (Hinshaw, Lahey, & Hart,
1993). Anxiety and depressive disorders are comorbid in a minority of children with ADHD, and this is
at a slightly higher rate than in the general population (DSM‐5, American Psychiatric Association, 2013,
p. 65; Furman, 2005).

CASE HISTORY 16.1 ATTENTION DEFICIT HYPERACTIVITY

DISORDER (ADHD)

‘Mark, age 14, has more energy than most boys his age. But then, he's always been overly
active. Starting at age 3, he was a human tornado, dashing around and disrupting everything in
his path. At home, he darted from one activity to the next, leaving a trail of toys behind him. At
meals, he upset dishes and chattered nonstop. He was reckless and impulsive, running into the
street with oncoming cars, no matter how many times his mother explained the danger or
scolded him. In the playground, he seemed no wilder than the other kids. But his tendency to
overreact—like hitting playmates simply for bumping in to him—had already gotten him into
trouble several times. His parents did not know what to do. Mark's doting grandparents
reassured them, “Boys will be boys. Do not worry, he'll grow out of it”. But he did not’.

From http://www.nimh.nih.gov/publicat/adhd.cfm#adhd2
TABLE 16.2 Summary: DSM‐5 Diagnostic Criteria for Attention Deficit Hyperactivity Disorder (ADHD)

An ongoing pattern of inattention and/or hyperactivity and impulsivity that interferes with
normal functioning or development, as marked by the following:
Inattention. At least six of the following for at least 6 months:
Not paying close attention to details or making careless mistakes
Difficultly in maintaining attention in activities
Does not listen when spoken to directly
Ignores instructions
Has difficulty organising
Dislikes or avoids tasks which require sustained mental effort
Loses things needed for tasks
Easily distractible
Forgetful in daily activities
Hyperactivity and Impulsivity. At least six of the following for at least 6 months:
High level of fidgeting
Not sitting still or leaving seat when expected to sit
Runs or climbs in situations where it is inappropriate
Unable to engage in activities quietly
Excessive talking
Blurts out an answer before the question is finished
Has difficulty awaiting their turn
Interrupts or intrudes on others frequently
Symptoms were present before the age of 12
Symptoms are present in at least two settings
Symptoms reduce the quality of educational, social, or occupational ability
Symptoms do not occur during schizophrenia or another psychotic disorder and are not better
explained by another mental disorder

In terms of its course, ADHD is usually first recognised by parents when the child is a toddler, but not
all hyperactive toddlers go on to develop ADHD. The disorder is usually first recognised and diagnosed
after the child first begins schooling, and this is because learning and adjustment at school is significantly
affected by the disorder. As the child develops into adolescence, symptoms usually attenuate and become
less pronounced, although about half will continue to show symptoms well into adulthood and this can
detrimentally affect intellectual functioning and intelligence quotient (IQ) (Bridgett & Walker, 2006).
There is much discussion in the literature about whether ADHD is a culturally constructed disorder—
that is, whether the rates of diagnosis differ in different cultures because of differing cultural perceptions
of children's behaviour. The evidence on this is equivocal. Some studies suggest very similar rates of
diagnosis across different cultures and ethnic groups (Bailey & Owens, 2005; Rohde et al., 2005),
whereas others indicate differing rates of ADHD in different countries (Dwivedi & Banhatti, 2005).
Studies indicating different rates of diagnosis may do so because different cultural environments may
directly affect a child's behaviour (e.g., Buddhist cultures tend not to tolerate externalising behaviours),
or may affect the attitudes of parents and clinicians towards what is acceptable behaviour. For example,
Zwirs, Burger, Buitelaar, & Schulpen (2006) found that detection of externalising disorders was
significantly lower in a sample of non‐Dutch parents (Moroccan, Turkish, and Surinamese) than Dutch
parents and that cultural contexts may have an important influence on whether ADHD symptoms are
detected and reported.

The prevalence of ADHD

DSM‐5 estimates that around 5% of school‐age children and 2.5% of adults worldwide are diagnosed
with ADHD, but these estimates can vary widely between epidemiological studies and data collected
from different countries. Rates of diagnosis found in preschool children (aged 2–5 years) range from
1.8% to 5.4% (e.g., Wichstrøm et al., 2012), and whereas ADHD was once considered a childhood
condition, it is now acknowledged that around 50–60% of those diagnosed with ADHD in childhood
will carry that diagnosis into adulthood (Fayyad et al., 2017; Kessler et al., 2006). There is considerable
evidence to indicate that ADHD is more common in boys than girls, and reasons for this may include
the fact that boys are more likely to be referred for treatment than girls—perhaps because girls tend to
have less extreme symptoms than boys and a narrower distribution of symptoms (Arnett, Pennington,
Willcutt, DeFries, & Olson, 2015).
However, there is still a good deal of controversy over the prevalence of ADHD and, in particular,
whether rates are genuinely higher for males than females. The lifetime prevalence rates for ADHD in
US adults (aged 18–44 years) has been estimated to be 8.1% (Kessler et al., 2005), with point prevalence
rates for males (5.4%) slightly higher than for females (3.2%) (Kessler et al., 2006). At least some of the
confusion over prevalence rates may be explained by the fact that estimated rates of ADHD appear to
have increased dramatically over the last couple of decades, from 7.8% in 2003 to 11.0% in 2011
(Visser et al., 2014). However, this increase may be illusionary and may result in part from many
children getting a diagnosis when they may not meet strict DSM‐5 criteria for the disorder and only
after a fleeting consultation with a paediatrician or psychologist (Hinshaw & Scheffler, 2014). This
cursory labelling of some children with ADHD in many cases serves a particular purpose for schools
and educational services by effectively removing a child that may be disruptive and inattentive from
school performance statistics.

The consequences of ADHD

Like most psychopathologies the symptoms of ADHD also have detrimental consequences for the
sufferer across a range of life domains. First, their attentional deficits and hyperactivity may make them
prone to temper outbursts, frustration, bossiness, stubbornness, changeable moods, and poor self‐
esteem. As a result, academic achievement is usually impaired leading to conflict with teachers and
family. Because the disruptive consequences of their behaviour are pervasive, family members often
view their behaviour as intentional, wilful, and irresponsible, and this can cause resentment within the
family (see Activity Box 16.1 on the book’s website). Individuals with predominantly inattentive
symptoms tend to suffer most in terms of academic achievement, while hyperactivity and impulsivity
are associated most with peer rejection and accidental injury. However, in general, children with ADHD
have great difficulty making friends and integrating successfully into social groups—usually because
their behaviour is aggressive and disruptive (Hinshaw & Melnick, 1995). Indeed, in new social settings
children with ADHD are often singled out and rejected relatively rapidly by their peers (Erhardt &
Hinshaw, 1994). In part, this is due to their disruptive behavioural symptoms, but in addition, children
with ADHD frequently fail to understand the intentions of their peers and are unable to translate the
correct social response into appropriate behaviour (Whalen & Henker, 1998).
In adulthood, ADHD also has a number of impairing consequences, including less success and safety at
work (Kessler, Lane, Stang, & Van Brunt, 2009), poorer interpersonal relationships (Biederman et al.,
2006), poorer academic outcomes (Lewandowski, Lovett, Codding, & Gordon, 2008), and poorer
general life satisfaction (Biederman et al., 2006).
The aetiology of ADHD
The causes of ADHD can be clustered under two broad headings—biological and psychological, but
the current view is that biological factors are particularly important in the aetiology of ADHD,
especially inherited factors that may play a strong role in mediating susceptibility to ADHD (Faraone &
Khan, 2006).

Biological factors

Genetic factors
There is now considerable evidence pointing to the involvement of an inherited susceptibility to ADHD.
ADHD appears to be one of the most heritable psychiatric disorders, and pooled data from 20 twin
studies report a mean heritability estimate of 76% (Faraone & Mick, 2010). Adoption studies also
suggest that ADHD in the adopted child is more likely to occur if a biological parent has ADHD than if
an adopted parent has ADHD (Faraone et al., 2005). However, what is inherited is significantly less easy
to determine (Faraone & Larsson, 2019). A meta‐analysis of gene linkage studies has revealed a region
on chromosome 16 that has the most consistent linkage evidence (Coghill & Banaschewski, 2009).
However, identifying individual genes is much more problematic, and reviews of genome‐wide
association studies have suggested that any individual gene variant for ADHD must have a very small
individual effect (Neale et al., 2010). However, many of those genes identified may underlie
abnormalities in neurotransmitter systems—particularly the dopamine, norepinephrine, and serotonin
systems (Waldman & Gizer, 2006). Specific genes that may be involved are the dopamine transporter
gene, the dopamine D4 and D5 receptors and SNAP‐25, a gene that controls the way dopamine is
released in the brain and promotes the plasticity and adaptability of neuron synapses.
However, while susceptibility to ADHD appears to have a significant genetic component, additional
studies strongly indicate a genes‐environment interaction. That is, what is inherited is a vulnerability to
ADHD, but ADHD becomes manifest only when certain environmental influences are found. For
example, Kahn, Khoury, Nichols, & Lanphear (2003) found that children with two copies of the 10‐
repeat allele of a DAT1 gene (a gene related to dopamine regulation in the brain) who were exposed to
maternal prenatal smoking exhibited significantly higher levels of hyperactivity, impulsiveness, and
oppositional behaviours than a control group of children who possessed these genes but whose mothers
did not smoke during pregnancy. In addition, children who possessed only one of the risk factors (the
high‐risk genotype or a mother that smoked during pregnancy) did not show significantly higher levels
of ADHD symptoms than children who possessed neither of the risk factors. Studies such as this
indicate that, while inherited factors are critically important in the aetiology of ADHD, they may
constitute a vulnerability that converts into ADHD only if certain environmental factors are present
(Coghill & Banaschewski, 2009). Other environmental risk factors that have been proposed include pre‐
or perinatal complications and maternal drinking during pregnancy (Mick et al., 2002; Milberger,
Biederman, Faraone, Guite, & Tsuang, 1997; Milberger, Biederman, Faraone, & Jones, 1998).

Neuroscience
Magnetic resonance imaging (MRI) studies of the brains of individuals with ADHD have revealed a
number of significant differences between ADHD sufferers and nonsufferers (e.g., Cortese, 2012; Krain
& Castellanos, 2006; Rubia, 2018). First, there is consistent evidence that the brains of children with
ADHD are smaller than those of healthy comparison children, and develop more slowly. Overall brain
volume has been shown to be smaller by an average of 3.2%, with the main areas affected being the
frontal, parietal, temporal, and occipital lobes (Durston et al., 2004), and ADHD is also associated with
a global reduction in gray matter (Nakao, Radua, Rubia, & Mataix‐Cols, 2011). Other brain areas
exhibiting decreased volume in ADHD include the frontal cortex, basal ganglia, and cerebellum (Krain
& Castellanos, 2006). Comparisons of the development of brain structures in children with ADHD and
typically developing controls also suggests that the median age by which 50% of the cortex reaches peak
thickness is 10.5 years in children with ADHD, but only 7.5 years in normally developing controls (Shaw
et al., 2007). A range of studies has also indicated that brain volume in specific brain areas is inversely
correlated with a variety of ADHD symptoms. For example, children with ADHD are known to have
deficits in executive functioning (involving planning and problem solving) which involves the frontal
lobes, and specifically have difficulty in selective attention, working memory, and inhibiting responses
(Fair, Bathula, Nikolas, & Nigg, 2012; Mueller, Hong, Shepard, & Moore, 2017) (Research Methods in
Clinical Psychology 16.1). Another area of the brain that regularly exhibits abnormalities in association
with ADHD symptoms is the cerebellum (Cherkasova & Hechtman, 2009). In ADHD, abnormalities
are usually found in the cerebellum's influence on the cortico‐striatal‐thalamo‐cortical circuits, and these
circuits are involved in choosing, initiating, and carrying out complex motor and cognitive responses
(Alexander, DeLong, & Strick, 1986; Graybiel, 1998). In this case it is not hard to imagine how
dysfunctions in these pathways may result in the disruption of the planning and execution of behaviour.
 RESEARCH METHODS IN CLINICAL PSYCHOLOGY 16.1
COGNITIVE TESTS OF ADHD

A variety of tests have been devised that are capable of differentiating between children with
ADHD and control participants. The aim of most of these tasks is to test attention or to
determine whether the individual is able to successfully inhibit responses when required to do so
(see Seidman, 2006).
The Continuous Performance Test (CPT): The CPT is a computerised visual
vigilance/attention task in which the child is seated before a computer monitor and instructed
to observe a string of letters presented randomly and at varying speeds. Children are instructed
to press the space bar as quickly as possible following all letters except the letter X. Children
with ADHD are less able to inhibit responses following the presentation of the target letter X
and also emit longer reaction times following letters that should be responded to (Epstein,
Johnson, Varia, & Conners, 2001).
The Stroop Task: This is generally considered a test of ability to inhibit responses. In the
task, a word describing a colour (e.g., red) is presented in a different colour (e.g., green), and the
participant has to respond as quickly as possible by naming the colour ink that the word is
written in. Children with ADHD take more time to respond and make more errors than control
participants (Shin, 2005).
The Trail Making Test: This is a measure involving connecting circles on a page (Reitan,
1958). The child is instructed to connect the circles by drawing lines alternating between circles
labelled with numbers and letters in sequential order until they reach the circle labelled ‘End’
(see Focus Point 15.1). Most studies show that children and adults with ADHD perform
significantly worse than control participants (Rapport, Van Voorhis, Tzelepis, & Friedman,
2001).
The Controlled Word Association Test (COWAT): This test measures verbal fluency in
response to single letters, which taps into phonological associations, and category fluency
(‘name all the animals you can beginning with the letter…’) (Benton, Hamsher, & Sivan, 1983).
This test appears to measure speed of access to words, persistence at a task, and processing
speed. The majority of studies show impaired performance on this task in children with ADHD
compared to controls (Dinn, Robbins, & Harris, 2001).
Conners' Parent Rating Scale (CPRS): The CPRS (Conners, Sitarenios, Parker, &
Epstein, 1998) is an 80‐item scale completed by the child's parent using a 4‐point scale. This
instrument has well‐accepted reliability and validity and is considered to be standard in ADHD
diagnosis (Barkley, 1991). Norms by age are available for males and females in 3‐year intervals.

Prenatal factors
As we have already noted, at least some prenatal experiences appear to interact with a genetic
predisposition to put an individual at risk for ADHD. These experiences include maternal smoking and
drinking during pregnancy (Mick et al., 2002) and general complications associated with childbirth,
such as low birthweight, respiratory distress, and birth asphyxia (Getahun, et al., 2013; Tannock, 1998).
Schmitz et al. (2006) found that pregnant mothers smoking greater than 10 cigarettes per day were
significantly more likely to give birth to children with ADHD than nonsmoking mothers – even when
other potential confounding factors such as maternal ADHD, ODD, birth weight, and alcohol use
during pregnancy were controlled for. In addition, a study by Milberger, Biederman, Faraone, Chen,
and Jones (1997) found that 22% of mothers of children with ADHD reported smoking a pack of
cigarettes a day during pregnancy compared with only 8% of mothers whose children did not develop
ADHD. Milberger, Biederman, Faraone, Guite, and Tsuang (1997) hypothesised that prenatal exposure
to nicotine caused abnormalities in the dopaminergic neurotransmitter system, resulting in the offspring
having difficulties inhibiting behaviour.

Environmental toxins
Some early accounts of ADHD did allude to the possibility that hyperactivity resulted from various
biochemical imbalances caused by such factors as food additives (Feingold, 1973), refined sugar cane
(Goyette & Conners, 1977), and lead poisoning (Thompson et al., 1989). However, there is only modest
evidence that artificial food colorings contribute to hyperactivity (Nigg, Lewis, Edinger, & Falk, 2012),
but there is some support for the fact that both the levels of lead in the blood and chronic exposure to
nicotine or tobacco smoke may increase hyperactivity (e.g., Fung & Lau, 1989; Polanska, Jurewicz, &
Hanke, 2012), although it must be emphasised that most children with ADHD do not show raised levels
of lead in the blood.

Psychological factors

Parent–child interactions
ADHD appears to run in families, and this may have implications beyond the fact that there is a genetic
component to the disorder. For example, it also means that children with ADHD are more likely to be
brought up by parents who also have the disorder, and this may exacerbate any symptoms that are
caused by the genetic component alone. For example, fathers who are diagnosed with ADHD have been
found to be less effective parents (in terms of exhibiting ineffective discipline and adopting traditionally
conservative father roles) than parents without an ADHD diagnosis (Arnold, O'Leary, & Edwards,
1997), and this may exacerbate any disruptive characteristics the ADHD child may exhibit.
Psychodynamic approaches to ADHD have also pointed to the possible role of inconsistent and
ineffective parenting of children with ADHD. Bettelheim (1967) proposed that hyperactivity resulted
when a predisposition to ADHD is accompanied by authoritarian parenting methods. He argued that
such parents are likely to become impatient with a disruptive and hyperactive child, resulting in a
vicious cycle whereby constant attempts to discipline the child cause even more defiant reactions on the
part of the child who reacts by defying rules across a range of life contexts (e.g., school, social situations,
etc.).
Learning theorists have suggested that parents may exacerbate ADHD symptoms in a rather different
way. Individuals with ADHD exhibit impulsive and disruptive behaviour that in many cases will require
the need for control by the parent. In such circumstances the attention from the parent that these
behaviours demand may be rewarding or reinforcing them, thus increasing their frequency and
intensity. While there is no direct evidence to support this view, indirect support comes from studies
showing that time out from positive reinforcement can act as an effective procedure for reducing negative
and disruptive behaviour in children with ADHD (Fabiano et al., 2004).
Nevertheless, while parent–child interactions of various kinds may exacerbate ADHD symptoms, there
is no evidence to suggest that they are the sole cause of these symptoms (Johnston & Marsh, 2001).

Theory of mind (TOM) deficits

We have already mentioned that children with ADHD may fail to understand the intentions of their
peers in social situations, and this has led some theorists to argue that children with ADHD have
theory of mind(TOM) deficits. TOM is the ability to understand one's own and other people's
mental states (Premack & Woodruff, 1978), and it is not difficult to see that if a child has deficits in such
abilities they will often react in inappropriate ways to peers and family. However, studies have tended to
be inconsistent in showing a relationship between poor performance on TOM tasks (see Chapter 17,
Section 17.4.4) and ADHD. For example, Buitelaar, Van Der Wees, Swaab‐Barnveld, & Van Der Gaag
(1999) found that children with ADHD diagnoses showed poorer performance on a TOM task than
control participants. In contrast, in a later study, Perner, Kain, and Barchfeld (2002) found that children
with ADHD showed no impairment at all on an advanced TOM task. However, in contrast, studies
have been fairly consistent in showing that children with ADHD do show impaired performance
compared to controls on tasks of executive functioning (Fahie & Symons, 2003; Perner et al., 2002).
Executive functioning is that range of skills that require goal‐directed behaviour, planning, attentional
control, and inhibition of inappropriate responses. Such studies have tended to suggest that children
with ADHD have specific deficits related to planning and inhibition of behaviour (Papadopoulos,
Panayiotou, Spanoudis, & Natsopoulos, 2005), and it is deficits in these areas of functioning that give
rise to their behavioural problems. This has been reinforced by studies showing that individuals with
ADHD do show executive functioning deficits, and in some cases these deficits are related to deficits in
TOM. This suggests that ADHD symptoms may be linked more directly to executive functioning
problems rather than deficits in social functioning such as TOM, but executive functioning deficits can
also cause secondary TOM deficits in some individuals with a diagnosis of ADHD (Gonzalez‐Gadea et
al., 2013; Pineda‐Alhucema, Aristizabal, Escudero‐Cabarcas, Acosta‐López, & Vélez, 2018). The fact
that tests of executive functioning have indicated that this is where the cognitive deficits in ADHD lie is
consistent with the neurological evidence we reviewed earlier, which strongly indicates that children with
ADHD have abnormalities in the frontal lobes of the brain, and it is the frontal lobes that control
executive functioning.

Summary of ADHD
The evidence on the aetiology of ADHD strongly indicates that there is a significant genetic component
to the disorder, and it may be one of the most heritable psychological disorders. However, it is not fully
clear yet whether this genetic component merely bestows a vulnerability for the disorder or whether it
may be a direct cause of abnormalities that underlie ADHD; it is also not yet been possible to clearly
identify the genes through which this heritability is transmitted. There are clearly some brain
abnormalities that characterise ADHD, including reduced overall brain volume and gray matter, and
reduced brain volume particularly in areas such as the frontal cortex, basal ganglia and cerebellum, and
abnormalities in the frontal lobes may contribute to the deficits in executive functioning that are found
in ADHD using cognitive tests. Some pre‐ and perinatal factors have been identified that may
contribute to abnormal development, and these include maternal smoking and drinking during
pregnancy, and complications at birth, including low birthweight, respiratory distress, and birth
asphyxia. There is also some evidence that dysfunctional parenting may contribute to the behavioural
symptoms of ADHD in children, but there is no evidence that dysfunctional parenting is a sole cause of
ADHD.

16.2.2 Conduct Disorder

While ADHD is characterised by behaviour that tends to be disruptive and inappropriate, many
children and adolescents exhibit behaviour that appears almost intentionally vicious, callous, and
aggressive, and it is when such characteristics appear that a diagnosis of conduct disorder may be
appropriate. Behaviours typical of conduct disorder include violent or aggressive behaviour, deliberate
cruelty towards people or animals, wanton vandalism or damage to property, lying, stealing and
cheating, criminal theft, and violation of the rights of others (e.g., trespass, threatening behaviour, and
verbal abuse) (Photo 16.1). The following sections discuss the diagnosis, prevalence, and known causes
of conduct disorder.

The diagnosis of conduct disorder

DSM‐5 devotes a chapter to disruptive, impulse‐control, and conduct disorders, and these disorders are
linked to a common externalising spectrum characterised by a lack of inhibition or inability to control
impulses. This common theme throughout these problem behaviours is one reason why conduct
disorder is regularly comorbid with impulse disorders, such as intermittent explosive disorder (DSM‐5,
American Psychiatric Association, 2013, p. 466), and other impulse control disorders such as Pyromania
(deliberate and purposeful fire‐setting) (DSM‐5, p. 476) and kleptomania (recurrent failure to resist
impulses to steal objects) (DSM‐5, p. 478). In this chapter we discuss two disorders, namely conduct
disorder and oppositional defiant disorder (ODD).
The main feature of conduct disorder is a repetitive and persistent pattern of behaviour involving the
violation of accepted social norms or the basic rights of others. There are four main categories of such
behaviour: (a) aggression to people and animals, (b) destruction of property, (c) deceitfulness or theft,
and (d) the serious violation of accepted rules (such as driving violations). These behaviours must also
cause severe impairment in social, academic, or occupational functioning and should be found in a
range of different contexts such as home, school or the community (Table 16.3). For a diagnosis of
conduct disorder, characteristic behaviours must have been present for at least 12 months.
Children or adolescents with this disorder would normally initiate violence or aggressive behaviour and
react violently to others. Their behaviour will often include bullying or threatening behaviour, and they
will often initiate physical fights, carry weapons, be physically cruel to people or animals, and intimidate
people into activities by threats of physical force (e.g., force others into sexual activity). Individuals with
conduct disorder also have little respect for property, and they will indulge in acts of vandalism and
petty theft from others. Their lying will also extend to breaking promises to obtain goods or benefits, or
simply ‘conning’ others into providing benefits or favours. Finally, children with conduct disorder will
usually have a history of breaking rules, including staying out late despite prohibitions, running away
from home, or staying away from school.
PHOTO 16.1 Behaviours typical of conduct disorder include violent or aggressive behaviour, wanton vandalism or
damage to property, and violation of the rights of others
TABLE 16.3 Summary: DSM‐5 Diagnostic Criteria for Conduct Disorder

An ongoing pattern of behaviour where the rights of others or social norms are infringed, as
shown by at least three of the following over a 12‐month period:
Bullying or threatening others
Starting fights
Using a weapon to do serious physical harm
Physical cruelty to others
Physical cruelty to animals
Mugging or similar crimes
Forcing another into sexual activity
Fire setting to destroy/seriously damage property
Deliberate destruction of another's property
Breaking into buildings or cars
Lies to get goods or favours
Shoplifting or similar
Stays out at night despite parental intervention, starting from before the age of 13
Has run away from home at least twice or once for a long period of time
Often misses school, starting from before the age of 13
The disturbances cause significant impairment in social, academic, or occupational functioning
If the patient is 18 years or older, the condition is not better explained by antisocial personality
disorder

There are two main subtypes of conduct disorder based on the age of onset. Childhood‐onset type
is defined by the onset of at least one criterion characteristic of conduct disorder prior to 10 years of
age. Adolescent‐onset type is defined by the appearance of conduct disorder symptoms only after
the age of 10 years. Such individuals are less likely to be physically aggressive than those with
childhood‐onset type, and will usually have better peer relationships.
Like individuals with antisocial personality disorder (see Chapter 12), children and adolescents with
conduct disorder display little empathy with the feelings and intentions of others and will usually believe
that their aggressive reactions to others are justified. They will frequently try to blame others for their
misdeeds, and exhibit little or any genuine guilt for their antisocial actions. Risk‐taking, frustration,
irritability, impulsivity, and temper tantrums are regularly associated with conduct disorder and result in
higher accident rates for such individuals. Conduct disorder is also associated with early onset of a
range of behaviours, including sexual behaviour, drinking, smoking, substance abuse, and general risk‐
taking behaviour (e.g., dangerous and erratic driving). Finally, the disorder is more common in males
than in females, and males with a diagnosis will outnumber females by a ratio of at least 4 to 1 and
often up to 10 to 1 (Merikangas et al. 2010; Zoccolillo, 1993).
It is important to mention at least three issues related to diagnosis of conduct disorder. First, individuals
diagnosed with conduct disorder will usually be under 18 years of age and diagnosed with the disorder
only at a later age if the criteria for antisocial personality disorder are not met. Second, the clinician will
need to take account of the social context in which behaviours characteristic of conduct disorder are
found. For example, in certain deprived inner‐city areas, behaviours characteristic of conduct disorder
may be seen as being protective. That is, they may represent the norm for that environment and may
serve an adaptive function in dealing with poverty and the threatening behaviour of others. In addition,
immigrants from war‐ravaged countries can have a reputation for violence because such behaviour has
been necessary for survival in their previous countries. Clinicians must be sure that a diagnosis of
conduct disorder is made only when the characteristic behaviours are symptomatic of dysfunction
rather than a reaction to a specific social context. Third, a related category of disruptive behaviour
disorders in DSM‐5 is known as oppositional defiant disorder (ODD). ODD is a diagnosis usually
reserved for those children who do not meet the full criteria for conduct disorder (e.g., extreme
aggression and violence) but who have regular temper tantrums, refuse to comply with requests or
instructions, or appear to deliberately indulge in behaviours that annoy others. ODD is common in
preschool children and may even be a precursor to later childhood conduct disorder (Lahey, McBurnett,
& Loeber, 2000). It is found more often in families where childcare has been disrupted (through the
child experiencing a number of different caregivers) or in families where at least one parent has a
history of mood disorders, antisocial personality disorder, ADHD or substance abuse.

oppositional defiant disorder (ODD) A mild form of disruptive behaviour disorders

reserved for children who do not meet the full criteria for conduct disorder.

The prevalence and course of conduct disorder

Epidemiological studies indicate that conduct disorder may be relatively common, with prevalence rates
ranging from 4% to 16% in boys and 1.2%–9% in girls (Loeber, Burke, Lahey, Winters, & Zera, 2000).
A more recent US study estimated the lifetime prevalence rate of conduct disorder at 9.5% (12.0%
amongst males and 7.1% amongst females) and a median age of onset of 11.6 years (Nock, Kazdin,
Hiripi, & Kessler, 2006).
The most significant symptoms of conduct disorder begin to appear between middle childhood to
middle adolescence, although ODD is a common precursor to conduct disorder in the preschool years.
In a majority of individuals the disorder remits by adulthood, but some do go on to meet the criteria for
antisocial personality disorder. Indeed, studies suggest that childhood conduct disorder (but not
childhood ADHD) predicts antisocial personality disorder in adulthood, but only in lower socio‐
economic status families (Lahey et al., 2005). Children with conduct disorder are also more likely to
develop into adulthood with antisocial personality disorder if they have a parent with antisocial
personality disorder or have low verbal IQ (Lahey et al., 1995).
Finally, we have already indicated that conduct disorder prevalence rates for boys are significantly
higher than for girls, and the disorder also manifests differently in boys and girls. In boys, the main
behaviours are aggressive and violent behaviour, fighting, stealing, damage to property, and school
problems. However, for girls, the most common behaviours are petty theft (such as shoplifting), lying,
running away from home, avoiding school, and prostitution (Robins, 1991). Indeed, these differential
behaviours may have a direct impact on gender differences in prevalence rates since the crimes indulged
in by girls (e.g., shoplifting) are often considered less serious than the violent crimes committed by boys,
and boys are usually considered more likely to commit crimes than girls and so may be more likely to be
given a diagnosis (Zahn‐Waxler, 1993).

The aetiology of conduct disorder

Biological factors

Genetic factors
There is now some evidence that conduct disorder and its associated behaviours of aggressiveness and
criminality may have a genetic component. Twin studies specifically involving conduct disorders have
found heritability estimates between 45% and 67% (Viding & McCrory, 2012), while twin studies also
suggest that aggressive and violent behaviour (e.g., fighting, cruelty to animals) has a significant inherited
component (Edelbrock, Rende, Plomin, & Thompson, 1995). Adoption studies have also reported
significant genetic and environmental influences on both conduct disorder and criminal behaviour
(Simonoff, 2001). Some studies have even identified a specific gene, GABRA2, which is associated with
childhood conduct disorder (Dick et al., 2006), and, interestingly, this gene is also related to adult
alcohol dependence and drug dependence in adolescence. Two other candidate genes, 5HTTLPR and
MAOA have also been linked to conduct disorder. These genes influence serotonin and monoamine
neurotransmitters, and it may be the effect of this on socioemotional information processing in the
prefrontal cortex that facilitates responses such as aggression and threat reactivity found in conduct
disorder (Ficks & Waldman, 2014).
However, the results from more candidate gene association studies have been modest, with only a small
number of candidate genes identified to date (Viding et al., 2013). What these studies suggest is that
there is probably an inherited component to conduct disorder – perhaps in the form of inherited
temperamental characteristics—but that environmental factors also play an important role in
determining behaviour patterns typical of conduct disorder, and may interact with inherited
predispositions. For example, using a large sample of over 1,000 children from the Dunedin
Multidisciplinary Health and Development Study, Caspi et al. (2002) found that levels of the MAOA
gene interacted with childhood maltreatment, and those individuals who had low levels of MAOA and
had been maltreated were more likely to develop conduct disorder than individuals who had any other
combination of MAOA and maltreatment.

Neuropsychological deficits
Just as with ADHD, conduct disorder is associated with neuropsychological deficits in cognitive
functioning, including deficits in executive functioning (planning and self‐control), verbal IQ , and
memory (Lynam & Henry, 2001). Low IQ is also associated with conduct disorder, and is particularly
associated with early‐age onset conduct disorder independently of related socio‐economic factors such
as poverty, race, or poor educational attainment (Lynam, Moffitt, & Stouthamer‐Loeber, 1993).
Nevertheless, there is some doubt about whether executive functioning deficits occur in conduct
disorder in the absence of ADHD symptoms. For example, Oosterlaan, Scheres, & Sergeant (2005)
found that while executive functioning deficits were found in children with comorbid conduct disorder
and ADHD, no deficits were found in children diagnosed solely with either ODD or CD. Similarly,
meta‐analyses have found that antisocial behaviour generally is associated with poor executive
functioning, but this association is predominantly driven by relationships between poor executive
functioning and criminality and externalising behaviours generally rather than conduct disorder
specifically (Ogilvie, Stewart, Chan, & Shum, 2011)
Children with a diagnosis of conduct disorder also exhibit reduced activation in brain areas such as the
amygdala, ventral striatum, and prefrontal cortex—brain regions that contribute to emotion, reward,
and learning to associate behaviour with rewards (Alegria, Radua, & Rubia, 2016; Blair, 2013), all
features that may contribute to lack of empathy, misconstruing of the intentions of others, and a failure
to learn from rewarding and aversive experiences.

Prenatal factors
A number of prenatal factors have been identified in the aetiology of conduct disorder. These include
maternal smoking and drinking during pregnancy and prenatal and postnatal malnutrition. Maternal
smoking has been found to predict the early emergence of conduct problems in the offspring, especially
socially resistant and impulsively aggressive behaviour (Wakschlag, Pickett, Kasra, & Loeber, 2006) and
conduct disorder is specifically associated with maternal drinking of one or more drink during the first
trimester (Larkby, Goldschmidt, Hanusa, & Day, 2011), but this may be restricted to mothers and
children of low socio‐economic status (Monuteaux et al., 2006). Similarly, delinquent behaviour and
poor moral judgement has been found to be higher in children prenatally exposed to alcohol (Schonfeld,
Mattson, & Riley, 2005). Recent studies also suggest that externalising behaviours are associated with
prenatal malnutrition, especially deficits in proteins, iron, and zinc (Liu & Raine, 2006). However, we
must be cautious about how we interpret all of these findings because correlations between prenatal
exposure and conduct disorder may be significantly confounded with other risk factors, such as parental
depression, family disadvantage, and genetic influences (Maughan, Taylor, Caspi, & Moffitt, 2004). If
so, prenatal exposure may simply be a risk factor for the development of conduct disorder rather than a
direct cause of the condition.

Psychological factors

The family environment and parent–child relationships

While studies of the heritability of conduct disorder suggest an important genetic component to the
disorder, these studies also indicate that significant environmental factors are also involved, and arguably
one of the most important of the latter is the family environment and the nature of parent–child
interactions during childhood. It is already well documented that risk factors for conduct disorder and
ODD include parental unemployment, having a parent with antisocial personality disorder, disrupted
childcare, and childhood abuse or maltreatment (Frick, 1998; Lahey et al., 1995). For example,
inconsistent and harsh parenting is associated with the development of aggressive behaviour and other
symptoms of conduct disorder (Coie & Dodge, 1998). This may be because inconsistent discipline may
permit the child to get away with behaving antisocially on many occasions, but when disciplining does
occur, the child may learn aggressive or violent behaviour from parents who behave aggressively when
disciplining their child. Indeed, there is evidence that children who are physically abused by their
parents are more likely to be aggressive when they grow up (Coie & Dodge, 1998), and parents who are
physically abusive to their children also report more behaviour problems in their children than
nonabusive parents (Lau, Valeri, McCarty, & Weisz, 2006). However, longitudinal studies are generally
consistent in indicating that childhood maltreatment is a risk factor for criminal behaviour, violence, and
diagnosis of conduct disorder in later childhood and adolescence (Fergusson, Horwood, & Lynskey,
1996; Maxfield & Widom, 1996), and there is some evidence that childhood abuse may give rise to
conduct disorder in children only with a specific genetic predisposition (Caspi et al., 2002; Dodge, 2009;
Taylor & Kim‐Cohen, 2007). In addition to childhood abuse, conduct disorder has also been shown to
be associated with family environments that are less cohesive, have few intellectual/cultural pursuits,
greater levels of family conflict, and higher levels of parental stress (Blader, 2006; George, Herman, &
Ostrander, 2006). Interestingly, many of these familial characteristics that are associated with conduct
disorder are also very closely linked to poverty and social deprivation, and we will look at how this socio‐
economic factor may influence aetiology later.

Media and peer influences

Many children may develop antisocial and aggressive behaviour because they simply mimic the violent
activities that they see around them in the media or displayed by their peers. Interestingly, statistics from
the US suggest that between 1980 and 1995 violent crime by juveniles increased by over 50% (US
Bureau of the Census, 1997), and at least part of this increase may have been due to the increasing
levels of violence viewed by children on TV and in video games. In the UK, acts of juvenile violence
have also been on the increase. Between 2008 and 2018 violence against the person offences in first‐time
offenders (aged 10–17 years) increased from 6% to 10%, and possession of weapons offences increased
from 3% to 13% (Ministry of Justice, 2019). Although the relationship between exposure to violent
media and aggressive behaviour is still heavily debated—even after 50 years of research (Murray, 2008),
there is a general view that exposure to violent media increases the likelihood of aggressive behaviour in
both the short and the long term, increases hostile perceptions and attitudes, and desensitises individuals
to violence (Warburton, 2014). However, while there is a view that violent media exposure may increase
aggressiveness in general terms, there is only weak evidence that violent video game use in children is
associated with subsequent measures of conduct disorder (Etchells, Gage, Rutherford, & Munafò, 2016).
Other studies tend to supplement these general findings of the effects of violent media exposure on
aggressive behaviour by suggesting that media violence has its effect primarily on children who are
already emotionally and psychiatrically disturbed. Recent longitudinal studies indicate that simply
watching more than 3 hours TV a day at age 5 years predicts an increase in conduct problems by age 7
years, but this effect is only significant for TV watching and not playing electronic games (Parkes,
Sweeting, Wight, & Henderson, 2013). Finally, studies have demonstrated an effect of violent TV
programmes on behavioural and physiological measures of aggression only in children who already
have a diagnosis of ADHD, ODD, conduct disorder, or disruptive behavioural disorders generally
(Grimes, Vernberg, & Cathers, 1997; Grimes et al., 2004).
A more important source of mimicry may be peer behaviour, and there is already evidence suggesting
that associating with peers who indulge in violent or criminal behaviour is likely to increase one's own
delinquent behaviour (Burt & Klump, 2013). In fact, a vicious cycle may develop in which associating
with aggressive peers may expose the individual to increasing levels of community violence (e.g., gang
fights, violent assaults, and robbery, etc.). This in turn will facilitate mimicry of violence and will
increase the perception of violent behaviour being the norm (Lambert, Ialongo, Boyd, & Cooley, 2005).
However, what is not clear from this research is whether children who already have antisocial and
aggressive tendencies choose to mix with similar peers in the first place, and so the peer association may
merely increase preexisting tendencies rather than create delinquent behaviour from scratch. There is
some evidence that deviant peer affiliation is associated with later antisocial behaviour and substance
abuse only in children who already display symptoms of ODD and conduct disorder. Deviant peer
affiliation only weakly predicts future antisocial behaviour in individuals without these initial symptoms
(Marshall & Molina, 2006).
Another view is that peer factors may facilitate symptoms of conduct disorder in a more indirect way.
For example, being rejected by peers has been shown to cause increased aggressiveness—especially in
children that have an existing disruptive behaviour disorder such as ADHD (Hinshaw & Melnick, 1995),
and this may also become a vicious cycle, as peers continue to reject adolescents whose behaviour
exhibits increasing levels of antisocial behaviour (Kelly, Jorm, & Rodgers, 2006). In particular, recent
longitudinal studies have discovered that children who react negatively to events and situations are more
likely to be rejected by peers and as a consequence then tend to react in more antisocial ways (Buil, van
Lier, Brendgen, Koot, & Vitaro, 2017).
In summary, media and peer mimicry may be risk factors for conduct disorder but may facilitate
antisocial and aggressive behaviour more in those children and adolescents who are already displaying
symptoms of conduct disorder. As such, they probably represent mediating variables rather than true
causes of the disorder.

Cognitive factors
Conduct disorder is associated with the development of deviant moral awareness. For example, most
children grow up learning that certain behaviours are morally acceptable and others are morally and
socially unacceptable. However, children with conduct disorder fail to acquire this moral awareness.
They are content to achieve their goals using violence and deceit, they have little respect for the rights
of others and show little or no remorse for their antisocial acts. Much of this lack of awareness of moral
standards may come from the fact that they may have developed highly biased ways of interpreting the
world. For example, a child with conduct disorder regularly interprets the behaviour of others as hostile
or challenging, and this appears to give rise to their aggressive reactions. Dodge (1991, 1993) has
proposed a social‐information processing model of antisocial and aggressive behaviour in which a
history of trauma, abuse, deprivation, and insecure attachment may give rise to specific information
processing biases. These include hypervigilance for hostile cues and attributing minor provocations to
hostile intent, and these biases give rise to unwarranted fear and to aggressive reactions. If the child is
brought up in a family environment where they learn aggressive behaviour in child‐parent interactions
(Patterson, Reid, & Dishion, 1992), and if they also have their own experiences with successful
aggressive tactics, they will evaluate aggression as an adaptive social strategy and use it proactively (see
Figure 16.2). In support of this hypothesis, Gouze (1987) found that aggressive children direct their
attention selectively towards hostile social cues and have difficulty diverting their attention away from
these cues. Aggressive children also exhibit what is called a ‘hostile attributional bias’ (Nasby, Hayden, &
DePaulo, 1979), in which they will interpret not only ambiguous cues as signalling hostility but also
many cues which are generated by benign intentions (e.g., Dodge, Bates, & Pettit, 1990). Once a hostile
attribution is made, studies also suggest that there is a 70% probability of an aggressive response,
compared with only 25% probability following a benign attribution (Dodge, 1991). Because of such
information processing and attributional biases, the individual with conduct disorder may be locked into
a cycle of hostile interpretations and aggressive responding that becomes difficult to break—especially
as continued aggressive behaviour by the sufferer is likely to generate genuine hostile intentions from
others in the future.

Socio‐economic factors
Delinquent, violent behaviour has been shown to be highly associated with poverty, low socio‐economic
class, unemployment, urban living, and poor educational achievement, and such factors may be a cause
of conduct disorder rather than a consequence of it (Lahey, Miller, Gordon, & Riley, 1999). A
longitudinal study of familial and socio‐economic predictors of conduct disorder in a Scottish cohort
indicated that individuals with conduct problems were more likely to have mothers that smoked during
pregnancy, less likely to be living with both parents, have poor general health, and have a parent who
agrees with smacking as a form of punishment (Wilson et al., 2013). So, poverty is likely to affect
conduct disorders through mediating factors such as disrupted family life, parental stress, poor
educational opportunities, and parental neglect. For example, Granero, Louwaars, & Ezpeleta (2015)
found that the relationship between low socio‐economic status and ODD in boys was mediated by harsh
parenting practices and inconsistent parental discipline, suggesting that some of the effects of poverty
on conduct disorder may be a result of the type of parenting found in poverty conditions rather than by
poverty per se.
FIGURE 16.2 Dodge's (1991) social‐information processing model of antisocial and aggressive behaviour in which a
history of trauma, abuse, deprivation, and insecure attachment can give rise to information processing biases including a
tendency to interpret even benign cues as signalling hostility.
Figure taken from Krol, Morton, & De Bruyn, 2004.
However, an instructive study by Costello, Compton, Keeler, and Angold (2003) suggests that poverty
may also have a direct causal effect on the level of conduct disorder in a local population. They studied
conduct disorder in American Indian children before and after a casino opened on their reservation
which provided income that moved many families out of poverty. This constituted an interesting natural
experiment on the role of poverty in childhood disorders. Before the casino opened, children of poor
families suffered more symptoms of psychopathology than those of non‐poor families. However, after
the casino had opened the children of those families who moved from the poor to non‐poor class
showed a significant drop in symptoms of conduct disorder and ODD. Levels of these symptoms in
families who remained poor after the casino opened did not change. This study provides a striking
example of how poverty may represent a genuine causal factor for conduct disorder. However, the exact
mechanisms that mediate the relationship between poverty and conduct disorder remain unclear.

Summary of conduct disorder

This section has indicated that conduct disorder may have a number of contributing causes. First, there
is an important genetic element that may be related to the inheritance of temperament factors.
However, these studies also tend to implicate significant environmental factors in the aetiology of
conduct disorder. Certain types of familial environments and parent–child relationships are risk factors
for the development of conduct disorder, particularly family environments with disrupted childcare,
childhood abuse and maltreatment, and inconsistent parenting. Some theories suggest that early
experience with maladaptive and abusive parenting may give rise to information processing biases that
lead the child to attend to and interpret most social cues as indicative of hostile intent, and this
generates aggressive responding. There is some modest evidence that media and peer influences may
also facilitate aggressive and antisocial behaviour. However, more recent research suggests that these
factors may facilitate aggressive antisocial behaviour mainly in children who are already displaying
symptoms of conduct disorder and ODD. Finally, low socio‐economic status and poverty is closely
linked with the development of conduct disorder, and at least one study suggests that the link may be
causal. However, as yet, the mechanisms by which poverty may cause antisocial and aggressive
behaviour in children are unclear.

SELF‐TEST QUESTIONS
Can you name the main symptoms of ADHD?
What are the different subtypes of ADHD and what other disorders is ADHD likely to be
comorbid with?
What is the evidence that ADHD is genetically determined?
How might deficits in executive functioning cause ADHD symptoms?
What prenatal factors have been identified as risk factors for ADHD?
How might parent–child interactional styles exacerbate the symptoms of ADHD?
Do children diagnosed with ADHD have a theory of mind (TOM) deficit?
What are the four main categories of symptoms found with conduct disorder?
What is ODD and how does it differ from conduct disorder?
Can you summarise the biological factors that may be involved in the aetiology of conduct
disorder?
What is the evidence that children develop symptoms typical of conduct disorder by
mimicking the violent activities they see around them in the media or displayed by peers?
How can interpretation biases account for behaviours typical of conduct disorder?
What socio‐economic variables act as risk factors for conduct disorder?
 SECTION SUMMARY

16.2 DISRUPTIVE BEHAVIOUR PROBLEMS

Disruptive behaviour disorders are characterised by impulsive, disruptive, and poorly controlled
behaviour.
The two main disruptive behaviour disorders are ADHD and conduct disorder.
ADHD can manifest itself as lack of attention, hyperactivity, or impulsivity.
Around 5% of school‐age children worldwide are estimated to be diagnosed with ADHD.
ADHD significantly affects educational achievement and social integration.
ADHD appears to have a mean heritability estimate as high as 76%.
ADHD is associated with smaller brain size, deficits in executive functioning, and
abnormalities in the cerebellum.
Dysfunctional parent–child interactions may contribute to ADHD, but there is no evidence
to suggest these are a sole cause of the disorder.
Conduct disorder can be described by behaviour that is aggressive, causes vandalism,
property loss or damage, deceitfulness and lying, and serious violation of accepted rules.
Oppositional defiant disorder (ODD) is a milder form of disruptive behaviour disorders
reserved for children who do not meet the full criteria for conduct disorder.
Prevalence rates for conduct disorder are estimated at 4–16% for boys and 1.2–9% in girls.
Both genetic and environmental factors appear to be important in the aetiology of
conduct disorder.
Psychological factors influencing conduct disorder symptoms include the nature of the
family environment, parent–child relationships, and media and peer influences.
Individuals with conduct disorder appear to develop an information bias in which they
interpret the benign intentions of others as hostile.
Conduct disorder is highly associated with poverty, low socio‐economic class,
unemployment, urban living, and poor educational achievement,

16.3 CHILDHOOD AND ADOLESCENT ANXIETY AND

DEPRESSION
Frank's Story at the beginning of this chapter graphically illustrates some of the distress experienced by
children who are exposed to uncertainty and stress early in their lives. As a result of the loss of his
parents and being moved to a foster home, he experiences a range of emotions, including rejection, fear,
confusion, anger, hatred, and misery. By their very nature children are emotionally naïve, and will often
be unable to label the feelings they experience—they may only know that they feel bad and confused. As
was the case with Frank, these feelings often lead the individual to become withdrawn and inward‐
looking (and this behaviour may be labelled by the clinician as representing an internalising disorder),
and may serve as the basis for future disorders in adolescence and early adulthood. All of these factors
make it difficult for the clinician to identify childhood anxiety and depression. Children who are anxious
and depressed tend to be clinging and demanding of their parents and carers, will go to great lengths to
avoid some activities such as school, and will express exaggerated fears—especially of events such as
separation from, or the death of, a parent or carer. There has been some success recently in identifying
specific disorders in childhood such as separation anxiety disorder, early onset GAD, and obsessive‐
compulsive disorder (OCD). However, anxiety and depression are frequently comorbid in childhood
(Manassis & Monga, 2001), and treatment may need to target both conditions. We continue by looking
separately at the characteristics and known causes of childhood anxiety and childhood depression.

16.3.1 Childhood Anxiety

In childhood, anxiety is primarily manifested as withdrawn behaviour (internalising). The child will
avoid activities where they may have to socialise with others (e.g., school), they will be clinging and
demanding of parents and carers (to the point of following a parent from room to room), they will
express a desire to want to stay at home, and communicate exaggerated fears over such things as the
death of carers or of being bullied by peers. Children tend to be less concerned than do adults about
the specific symptoms of their anxiety, but they do tend to report significantly more somatic complaints
than nonanxious children (Hofflich, Hughes, & Kendall, 2006). Many childhood anxiety disorders do
tend to be recognisable as those also found in adulthood (e.g., GAD, OCD, and social anxiety disorder).
However, at least some manifestations of childhood anxiety tend to be confined to childhood, and
separation anxiety is one such example.

The features and characteristics of childhood and adolescent anxiety problems

Separation anxiety
As the name suggests, separation anxiety is an intense fear of being separated from parents or
carers. It is commonly found in many children at the end of the first year of life, but in most children
this fear gradually subsides. However, in others it persists well into the school years and may also re‐
appear in later childhood following a period of stress or trauma. Older children with separation anxiety
will become distressed at being away from home and will often need to know the whereabouts of
parents. They may also develop exaggerated fears that their parents will become ill, die, or be unable to
look after them. Consequences of this anxiety include a reluctance to attend school, to stay at friend's
homes overnight, and many will require that a parent or carer stay with them at bedtime until they have
fallen asleep. As with most childhood anxiety disorders, sufferers will also report physical complaints
such as stomach aches, headaches, nausea, and vomiting (Table 16.4). Separation anxiety is often a
normal feature of early development, but it can be triggered and exaggerated by specific life stressors
(such as the death of a relative or pet, an illness, a change of schools, or moving home).
The estimated prevalence rate of diagnosable separation anxiety is approximately 4% in children 6‐ to
12‐months old, and has a 12‐month prevalence rate of 1.6% in adolescents (DSM‐5, American
Psychiatric Association, 2013, p. 192). However, once they have reached the age for school attendance,
many children suffering separation disorder go on to exhibit school refusal problems including social
anxiety disorder (Egger, Costello, & Angold, 2003) (See Chapter 6, Section 6.3).

Obsessive‐compulsive disorder (OCD)

Often beginning in childhood, obsessive‐compulsive disorder is now recognised as a relatively
common disorder and its phenomenology in childhood is very similar to adult OCD, with the main
features of the disorder in children manifesting as intrusive, repetitive thoughts, obsessions, and
compulsions (for brief reviews see Krebs & Heyman, 2014, and chapter 2 in Davey, Dash, & Meeten,
2014). The most common obsession themes in children are contamination, aggression (harm or death),
symmetry and exactness, and in adolescence religious and sexual obsessions also become common
(Geller et al., 2001). Common compulsive behaviours in children and adolescents include washing,
checking, ordering, touching, repeating, and reassurance seeking, as well as covert behaviours such as
reviewing or cancelling thoughts, silent prayers, or counting (Franklin et al., 1998). In adults,
compulsions (e.g., behavioural rituals) are rarely found without accompanying obsessions (e.g., intrusive
thoughts), but in children compulsions without obsessions can be quite common, and these are
frequently tactile (e.g., touching, tapping. or rubbing rituals) and may be accompanied by behavioural
tics (Leckman et al., 1995). While the range of obsessions and compulsions in childhood and
adolescence is very similar to that seen in adults, there are some differences between boys and girls, with
boys having an earlier age of onset than girls (Garcia et al., 2009), girls exhibiting more hoarding
compulsions than boys, but boys being more likely to have sexual obsessions than girls (Mataix‐Cols,
Nakatani, Micali, & Heyman, 2008). Case History 16.2 provides a typical example of the development
of OCD in a 13‐year‐old adolescent boy, and demonstrates how rapidly OCD symptoms can manifest
and establish themselves in childhood, which is in some contrast to the gradual acquisition found in
adulthood.

tic disorders Uncontrollable physical movements such as facial twitches, rapid blinking or
twitches of the mouth.

TABLE 16.4 Summary: DSM‐5 Diagnostic Criteria for Separation Anxiety

Excessive anxiety surrounding separation from those to whom the individual is attached, as shown
by at least three of the following:
Disproportionate distress when anticipating or experiencing separation from home or
attachment figures
Ongoing and unnecessary concern about losing attachment figures or potential harm to
them
Ongoing and unnecessary concern about an unexpected event which causes separation from
attachment figures
Ongoing aversion to going out or away from home because of fear of separation
Ongoing and unnecessary fear of being left alone or without attachment figures
Ongoing aversion to going to sleep alone or sleeping away from home
Repeated nightmares around separation
Complaints of physical symptoms such as headaches or nausea when separated or
anticipating separation from attachment figures
The anxiety lasts at least 4 weeks in children and 6 months in adults
The disturbance causes significant impairment in important areas of functioning
The disturbance is not better explained by another mental disorder
 CASE HISTORY 16.2 CHILDHOOD AND ADOLESCENT OCD

Andy was a 13‐year‐old boy diagnosed with isolated testicular relapse of acute lymphoblastic
leukaemia 40 days before coming to psychiatric attention. He was first diagnosed with acute
lymphoblastic leukaemia at age 10. After his initial diagnosis, he experienced remission at the
end of chemotherapy induction and finished his treatment for acute lymphoblastic leukaemia.
Three years later he began further drug treatment for his leukemia, and the psychiatric
consultation‐liaison service evaluated him after he expressed bothersome obsessive thoughts,
compulsive behaviours, and insomnia beginning 24–36 hours after he had completed a 28‐day
course of steroid drug treatment. Andy had no history of psychiatric illness or treatment.
At his initial interview, Andy described increasingly bothersome obsessions over the previous 2
days. He felt that he was ‘going crazy’ and feared that he would forget how to talk and lose his
cognitive abilities. He repeated mantras, reassuring himself that if he remained calm, these
bothersome thoughts would pass. He sought reassurance from his mother and the interviewers,
and he repeated the ‘ABCs’ to reassure himself that he could think clearly. His mood was
dysphoric, which he attributed both to insomnia and worry surrounding his constant
bombardment of unwanted thoughts. He reported no depressive symptoms, perceptual
disturbances, or suicidal thoughts. He displayed no manic symptoms.
Andy's symptoms rapidly worsened within 24 hours. His thoughts became dominated by fears
that he would be condemned to hell and that he deserved this fate. He noted images in his mind
of self‐harm and harming family members. He struggled against these thoughts and images, as
well as guilt from having them, by repeatedly telling family members that he loved them. He
continued to deteriorate and struck himself in the head with the blunt end of an ax. He stated
that he had no desire to die but had become convinced of the validity of the emerging thoughts
that he should harm himself. Although he did not sustain serious injury, he was admitted to a
child and adolescent psychiatric inpatient unit for safety.

Clinical Commentary
Andy’s symptoms are typical of many adolescents suffering OCD. In his case, these are
obsessive thoughts about going mad and harming himself and others. In an attempt to
try and prevent his obsessive thoughts entering consciousness, he indulges in protective
behaviours, such as repeating mantras, seeking reassurances from adults, and reciting
the alphabet. The symptoms appear to be precipitated by a stressful illness, and such
stressors are common precursors of OCD symptoms in both children and adults. OCD
symptoms would normally appear very slowly and have a gradual onset, unlike Andy’s
which appeared very rapidly over a period of a few weeks. Such rapid acquisition may
have been facilitated by the abrupt cessation of steroid drugs that he was receiving as
part of his treatment for leukaemia.

Adapted from Morris, Meighen, & McDougle, 2005

Age of onset for childhood OCD can be as early as 3–4 years of age, but the mean age of onset is more
likely to be around 10 years (Swedo et al., 1989). Childhood OCD is regularly found to be comorbid
with a range of other disorders, including tic disorders, Tourette's syndrome, other anxiety
disorders, and eating disorders (Geller et al., 1996). Specifically, over 60% of children seeking treatment
for OCD symptoms also have a lifetime history of tics or Tourette's syndrome (Leonard et al., 1992),
and 50% of children with Tourette's syndrome subsequently develop OCD (Leckman, 1993). This
suggests that childhood OCD and tic disorder may be different manifestations of the same underlying
disorder (Swedo, 1994) (see Focus Point 16.1).

Tourette’s syndrome A disorder in which motor and vocal tics occur frequently throughout
the day for at least 1 year.

Generalised anxiety disorder (GAD)

In children, as in adulthood, GAD usually takes the form of anticipatory anxiety, in which the main
feature is chronic worrying about potential problems and threats (see also Chapter 6). Even in
childhood, GAD is differentiated from other forms of childhood anxiety by being associated with
significantly increased levels of pathological worrying (Tracey, Chorpita, Douban, & Barlow, 1997;
Wilson, 2010), and what a child worries about appears to be determined by their age. For example,
Muris, Merckelbach, & Luijten (2002) found that 4–7‐year‐olds tended to worry about personal harm,
separation from parents and imaginary creatures, whereas 11–13‐year‐olds worried more about social
threats and being punished. The number of worries also increase with age, with the number of worries
reported by 8‐year‐olds almost double that reported by 5‐year‐olds (Muris et al., 1998). However, while
adult worry appears to be primarily verbal in nature and associated with thinking processes, worry in
children is more fear based, and the extent to which the child fears negative outcomes is relatively
stronger than the extent to which they think about them. Therefore, genuine worrisome thoughts will
depend on the child's age and ability to verbalise thoughts about their fears (Songo, Hudson, & Fox,
2020). Epidemiological studies have differed in their estimates of GAD in childhood populations with a
UK study estimating GAD in less than 1% of 5–10‐year‐olds, but an American study reporting 11% of
6–11‐year‐olds meeting the criteria for ‘overanxious disorder’.

pathological worrying Perseverative worrying that an individual finds uncontrollable.

 FOCUS POINT 16.1 CHILDHOOD OCD, TIC DISORDER, AND
TOURETTE'S SYNDROME

Tourette's syndrome (also known as Tourette's or TS) is a disorder with onset in childhood,
characterised by the presence of multiple physical (motor) tics and at least one vocal (phonic)
tic. It is important to understand that these are chronic and involuntary. Someone with TS may
be able to suppress them for a period but eventually they have to let the tics out.
Tics usually start in childhood around the age of 7 and are likely to persist throughout life,
though the symptoms often decrease towards the end of adolescence. The first symptoms are
usually facial tics such as rapid blinking or twitches of the mouth, but TS may start with sounds
such as throat clearing and sniffing, or even with multiple tics of movements and sounds. Tics
can be either simple or complex. Simple tics are of short duration and may include eye
blinks, shoulder shrugging, sniffing, grunting, or extensions of the extremities. Complex
motor tics are of longer duration and can consist of combinations of simple tics (e.g., head
turning plus shoulder shrugging). They can often appear purposeful when the tic consists of
imitating another person's movements, making tic‐like obscene or sexual gestures, or uttering
socially unacceptable words. For Tourette's disorder, both motor and vocal tics must be present.
Tic disorders are more common in children than in adults, in special education populations
than in general populations of children and among boys more than among girls (Knight et al.,
2012). Tic disorders are relatively common in children, with a point prevalence of transient tic
disorder of 2.99%. Tourette's disorder is less common, with a point prevalence of only 0.77%
(Knight et al., 2012).
Tourette's syndrome and behavioural tics are often comorbid with a diagnosis of OCD in
childhood. Studies suggest that up to 60% of children seeking treatment for OCD have a
lifetime history of tics (Leonard et al., 1992), and some theorists believe that OCD is a
heterogenous disorder with an inherited component that can manifest either as OCD
obsessions or compulsions, or as behavioural or vocal tics (Pauls et al., 1995).
OCD symptoms and behavioural and vocal tics can cause obvious problems for a child, with
them being a source of anxiety and fear for the sufferer, and provoking ridicule and
victimisation by peers (Storch et al., 2006). The severity of behavioural and vocal tics is usually
directly related to levels of stress, so learning how to control stress can greatly reduce symptoms
(e.g., by learning relaxation techniques). In some cases, a less socially acceptable tic can be
replaced with a more socially acceptable one using behaviour therapy methods, and medication
can also be used to help control the condition. Treatments normally used with OCD symptoms
(such as exposure with response prevention or cognitive behaviour therapy(CBT)—see
Chapter 6, Section 6.6.4) can also be used with behavioural tics (Turner, 2006; Verdellen,
Keijsers, Cath, & Hoogduin, 2004).

The factors that contribute to pathological worrying in children are as yet unclear, but recent evidence
suggests that negative information processing biases and executive functioning deficits may play a role
(Songo et al., 2020). Children and adolescents with a diagnosis of GAD show an attentional bias
towards negative information (Dalgleish et al., 2003; Waters, Bradley, & Mogg, 2014; but see Abend et
al. 2018, for evidence of a failure to find attentional bias in GAD). They have a bias towards
interpreting ambiguous information as threatening (Pasarelu, Dobrean, Balazsi, Podina, & Mogoase,
2017), and have poor attentional control over worrisome thoughts (Geronimi, Patterson, & Woodruff‐
Borden, 2016).
Specific phobias
Specific fears and phobias are often common in the normal development of children. For example, fears
of heights, water, spiders, strangers, and separation often occur in the absence of individual learning
experiences and appear to represent characteristics of normal developmental stages through which the
child develops. A fear may appear suddenly and intensely, but then disappear almost as quickly (Poulton
& Menzies, 2002). However, for some children a fear may persist and become problematic in that it
prevents normal daily functioning. One such example in childhood is social phobia (social anxiety
disorder), and this often begins in childhood as a fear of strangers (Hudson & Dodd, 2011). Most
children will grow out of this fear by around 2–3 years of age, but some still persist with their fear of
social situations and may find it very difficult to speak to strangers or to be in the presence of strangers.
If pushed into social situations, they will often become mute, blush, withdraw or show extreme
emotional responses (e.g., burst into tears) (Vasey, 1995). However, children and adolescents with social
phobia are usually well adjusted in all other situations that do not involve significant social interaction
(e.g., at home), and this differs from separation disorder where the latter is characterised by clinging and
demanding behaviour at home.
The prevalence for specific phobias in 8–9‐year‐olds is estimated to be around 7% for boys and 10%
for girls (Lichtenstein & Annas, 2000), but up to 76% of adolescents in some cultures report at least one
fear and up to 36% meet the lifetime criteria for specific phobia, indicating that specific phobias are a
common and enduring problem during childhood and adolescence (Benjet, Borges, Stein, Mendez, &
Medina‐Mora, 2012).

The aetiology of childhood and adolescent anxiety problems

Childhood anxiety and its associated disorders appear to result from a combination of inherited factors
and childhood experiences. Children inherit a temperament that may make them more or less
vulnerable to life stressors such as inadequate parenting or physical trauma. In addition, children seem
to be particularly vulnerable to learning fear and anxiety through indirect routes, such as information
from adults, peers, TV etc. (Field, 2006a). Finally, we also need to be aware that the kinds of life events
that might mean relatively little to an adult can be viewed as extremely stressful for a child, and these
include such events as the death of a pet, an illness, starting school, or moving house.

Genetic factors
Twin and familial studies of childhood anxiety disorders tend to indicate a significant and stable
inherited component. In a familial study of childhood OCD, Pauls et al. (1995) found that rates of
OCD were significantly greater in the first‐degree relatives of children with OCD than the relatives of
control participants without OCD. However, the inherited component appeared to be nonspecific, since
children with OCD were just as likely to have first‐degree relatives with behavioural tics as with specific
OCD symptoms. More recent twin studies of anxiety disorders in 7–9‐year‐olds have suggested a stable
heritability averaging 54% across anxiety disorders (Trzaskowski, Zavos, Haworth, Plomin, & Eley,
2012) that may be transmitted by many genetic variants, each with only a modest or small effect in itself
(Trzaskowski et al., 2013). Recent research involving linkage studies, genome‐wide association studies,
and candidate gene studies have identified a number of genes that may interact with environmental
factors such as childhood trauma, environmental adversity, and stressful life events to create heightened
risk for GAD and neuroticism (Gottschalk & Domschke, 2017). These genes include 5‐HTT, NPSR1,
COMT, MAOA, CRHR1, and RGS2 which have their effects within the serotonergic and
catecholaminergic systems of the central nervous system.
Trauma and stress experiences
Table 16.1 provides striking examples of how childhood trauma and stress represent significant risk
factors for a range of later diagnosable adult psychological disorders. It is also self‐evident that these
experiences will inevitably cause significant psychological stress during childhood (see Frank's Story at the
beginning of this chapter). Many of these experiences (such as childhood physical and sexual abuse)
represent extreme experiences for any individual, and there are clear links between such experiences
and childhood anxiety generally (e.g., Feerick & Snow, 2005; Whiffen & MacIntosh, 2005). However,
during childhood, even many experiences that seem relatively unexceptional may seem stressful to a
child who is relatively inexperienced in the world, and these can provide significant events that trigger
bouts of anxiety and distress. For example, living with illnesses such as asthma or eczema has been
shown to significantly increase childhood anxiety and reduce quality of life (Gillaspy et al., 2002; Lewis‐
Jones, 2006), and the death of a pet—to whom a child may become significantly attached—can cause
prolonged anxiety and depression (Kaufman & Kaufman, 2006). Even an event such as a minor road
traffic accident may be a new and frightening experience to a child, and a common consequence of
such an experience in childhood is a mixture of post‐traumatic stress disorder (PTSD) symptoms,
anxiety, and depression (Schafer, Barkmann, Riedesser, & Schulte‐Markworth, 2006).

Modelling and exposure to information

Whether it is in school, at home, or through the media, young children are regularly exposed to
information about potential threats and dangers. Children are bombarded with violent and threatening
images on television and are being constantly warned about the dangers of sexual molestation,
abduction, or drugs. Recent experimental evidence suggests that information of this kind may be an
important source of childhood fears. Field (2006a) and his colleagues have developed a valuable
experimental procedure for studying how information about a stimulus or event might cause subsequent
fear and anxiety. Children are shown pictures of animals they are unfamiliar with (e.g., toy monsters or
rare Australian marsupials) and then given some information about that animal. Some participants may
be told the animal is benign and friendly, while others may be told it is scary and dangerous. In a study
with 7–9‐year‐old children, Field, Argyris, and Knowles (2001) found that fear beliefs about an animal
increased significantly if the children had been given negative information about the animal—but only
if that information had been provided by an adult and not by a peer. Subsequent studies have indicated
that the fear generated by negative information can be detected using both explicit and implicit
measures of fear, will result in behavioural avoidance of the animal, and can still be detected up to 6‐
months later (Field & Lawson, 2003; Field, Lawson, & Banerjee, 2008) (Photo 16.2). In addition, studies
indicate that the child's levels of trait anxiety will facilitate the learning of fear in such situations by
increasing biases to attend to stimuli associated with threat information (Field, 2006b). Studies such as
these indicate that negative information about a stimulus or event—especially if it is provided by an
authoritative source such as an adult—can cause changes in fear beliefs and behavioural avoidance that
are relatively long lasting (up to at least 6 months).

Parenting style
Children are highly dependent on their parents or carers for guidance and emotional support during
their development, so it is not surprising that dysfunctional forms of parenting may cause psychological
and adjustment problems during childhood. Parents may be detached, rejecting, overcontrolling,
overprotective, or demanding, and each of these different parenting styles may cause anxiety and
maladjustment in the child. Research into how parenting style may influence childhood anxiety is
relatively underdeveloped at present. However, some studies do suggest links between overprotective
and overanxious parenting and a child who is overanxious or suffers anxiety separation (Giotakos &
Konstantopoulos, 2002; Rapee, 1997), and this appears to result from the parents' overprotectiveness
generating a lack of confidence and feelings of inadequacy in the child (Dadds, Heard, & Rapee, 1991;
Woodruff‐Borden, Morrow, Bourland, & Cambron, 2002). Specifically, Rapee (2001) has argued that
there may be a reciprocal relationship between child temperament and parenting whereby parents of
children with an anxious temperament are more likely to become over‐involved with the child in an
attempt to reduce the child's distress. However, this over‐involvement is likely to increase the child's
vulnerability to anxiety by increasing the child's perception of threat, reducing the child's perceived
control over threat, and increasing avoidance of threat (e.g., Gallagher & Cartwright‐Hatton, 2009).
Hudson & Rapee (2002) provided some experimental support for this view by reporting that mothers of
children with an anxiety disorder were more likely to be intrusive while the child was completing a
puzzle task than were mothers of non‐anxious control children. Most of these studies of overprotective
parenting tend to suggest that it is only the mother's overprotection that is likely to generate anxiety in
the child, and studies are less likely to find these effects with fathers. However, these effects of parenting
are often moderated by other factors (such as the child's existing level of trait anxiety), and broad
generalisations about the effects of overprotective parenting on offspring anxiety are difficult to make
because of significant methodological differences between studies (Percy, Cresswell, Garner, O'Brien, &
Murray, 2016) (see https://www.psychologytoday.com/gb/blog/why‐we‐worry/201705/helicopter‐
snowplow‐and‐bubble‐wrap‐parenting) for a discussion of ‘Helicopter, Snowplow, and Bubble‐Wrap
Parenting’.
PHOTO 16.2 Are you frightened of this animal? Professor Andy Field has developed a procedure for investigating how
exposure to information about potential threats affects fear acquisition in children. This photo shows an Australian Quoll,
an animal not well known to most children in the northern hemisphere. Some are then told they are potentially dangerous
and others told that they are harmless and benign. Children told they are dangerous subsequently fear them more and avoid
possible contact with them in experimental approach tasks, and this fear can often last up to 6 months.
While overprotective parents appear to generate anxiety in their children, so do parents who are
rejecting and hostile. Children who experience rejecting or detached parents also show increased levels
of anxiety and are often overly self‐critical and have poor self‐esteem (Chartier, Walker, & Stein, 2001;
Hudson & Rapee, 2001). For example, anxiety sensitivity (concern over the physical symptoms of
anxiety, such as trembling, shaking, etc.) is known to be a factor that mediates emotional distress in both
adulthood and childhood, and this has been linked to exposure to parental threatening, hostile, and
rejecting behaviours (Scher & Stein, 2003). Recently, studies have investigated the differential effects on
childhood anxiety that might be made separately by mothers and fathers. Moller, Majdandzic, de Vente,
& Bogels (2013) have argued that the evolved basis of sex differences in parenting means that mothers
and fathers will convey different aspects of anxiety to their offspring. Mothers will tend to transmit
caution and information about threat (with overanxious mothers transmitting more anxiety to their
offspring), whereas fathers may be more likely to teach their offspring how to explore the environment
and compete with others (and in doing so, reduce anxiety).
Clearly, parenting style is likely to be an important factor influencing the development of anxiety
symptoms in children. Both overprotective and overrejecting styles may have adverse effects and
facilitate anxiety and its cognitive and behavioural correlates (e.g., hypervigilance for threat, avoidance
behaviour, etc.). Further research is clearly required in this area to clarify the various mechanisms by
which such parenting styles might have their effects.

16.3.2 Childhood and Adolescent Depression

Depression in childhood is notoriously difficult to identify, and parents and teachers regularly fail to
recognise its symptoms—especially in very young children (Tarullo et al., 1995). In early childhood,
depression will manifest as clingy behaviour, school refusal, and exaggerated fears and is also associated
with an increased frequency of somatic complaints, such as stomach aches and headaches. However, as
the child reaches puberty and early adolescence, between 11% and 28% of adolescents aged up to 19
years will have experienced a diagnosable episode of major depression (Alaie et al., 2018; Lewinsohn,
Rohde, & Seeley, 1998). In adolescence, depression will manifest as sulkiness, withdrawing from family
activities, weight disturbance, loss of energy, feelings of worthlessness and guilt, and—in extreme cases
—suicidal ideation (Roberts, Lewinsohn, & Seeley, 1995). The following sections cover the diagnosis and
prevalence of childhood depression, and then we cover some of the theories of its aetiology.

The diagnosis and prevalence of childhood and adolescent depression

With some minor amendments, the diagnostic criteria for depression in childhood are essentially the
same as those specified for adult major depression (see Chapter 7, Table 7.2). However, some of the
symptoms may change with age. Somatic complaints, irritability, and social withdrawal are prominent in
younger children, but psychomotor retardation (slowed thinking and movement) and hypersomnia
(excessive sleeping) are more common in adolescents.
Rates of depression in children are variable and can depend on age, culture, and nationality. In 2017 in
the UK, 0.3% of 5–10‐year‐olds met clinical criteria for depression, as did 2.7% of 11–16‐year‐olds,
and 4.8% of 17–19‐year olds (Vizard et al., 2018). There are also some gender differences in
adolescence, with girls experiencing around twice the rate of depression as boys during the late teen
years (McGuinness, Dyer, & Wade, 2012). In addition, depressed girls more often report weight/appetite
disturbances and feelings of worthlessness/guilt than depressed boys (Lewinsohn et al., 1998).
Lewinsohn et al. (1994) estimated that the mean duration of major depression in adolescence was 26
weeks, with longer durations associated with earlier onset and suicidal ideation. A consequence of
adolescent depression is that as many as 8% of adolescents diagnosed with major depression will have
committed suicide by young adulthood (Perou et al., 2013), and many will also self‐harm (see Chapter 7,
Section 7.4).
Childhood depression is highly comorbid with other psychopathologies, and around half of adolescents
diagnosed with depression will experience at least one other disorder during their lifetime. 20% of
adolescents with depression will be diagnosed with another anxiety disorder (especially with GAD,
Copeland, Shanahan, Erkanli, Costello, & Angold, 2013) and between 13% and 30% will also exhibit a
substance use disorder (e.g., alcohol or drug abuse) (Lewinsohn et al., 1998). In addition, preadolescent
depression has been found to be a risk factors for earlier onset of alcohol use in adolescence (Wu et al.,
2006). Comorbid depression has a number of serious negative consequences for children and
adolescents. It has been shown to adversely affect academic performance, impairs social functioning
generally when sufferers may be rejected by their peers, is associated with increased conflict with
parents, and increases the risk of suicide attempts (Lewinsohn, Rohde, & Seeley, 1995).

The aetiology of childhood and adolescent depression

Childhood depression appears to have only a modest genetic component, and so early experience
appears to be a more significant contributor to the disorder. As a result, interest in the aetiology of
childhood depression has focussed mainly on early experiences, parent–child interactions, and cognitive
factors. We begin by reviewing the risk factors for childhood depression and then assess the evidence for
biological and psychological influences. Fuller discussion of theories of depression is outlined in
Chapter 7, and we focus in the following sections primarily on the known risk factors and determinants
for depression during childhood and adolescence.

Risk factors of childhood depression

Table 16.5 provides an overview of the risk factors known to be associated with depression in
adolescents, and these range across (a) dispositional factors and existing psychological problems, (b)
stress experiences, (c) poor coping skills, (d) poor social support, (e) physical health problems, and (f) poor
academic performance—and the greater the number of these risk factors experienced by an adolescent,
the greater the probability that he/she will become depressed in the future (Lewinsohn et al., 1998).
Taking the relevant risk factors into account, Lewinsohn et al. (1998) have drawn up a profile of the
‘prototypical adolescent most at risk for depression’. This is described in Focus Point 16.2.
TABLE 16.5 Risk Factors for Adolescent Depression
From Lewinsohn, Rohde, & Seeley (1998).

Domain Specific Risk Factor

Cognitive Depressive negative cognitions
Depressive attributional style
Dispositional factors and other psychopathologies Self‐consciousness
Low self‐esteem
Emotional reliance
Current depression
Internalising problem behaviours
Externalising problem behaviours
Past suicide attempts
Past depression
Past anxiety
Stress Daily hassles
Major life events
Social and coping skills Low self‐rated social competence
Poor coping skills
Interpersonal conflict with parents
Social support Low social support from family
Low social support from friends
Physical Physical illness
Poor self‐rated health
Reduced level of activities
Lifetime number of physical symptoms
Current rate of tobacco use
Academic School absenteeism
Dissatisfaction with grades

In younger children, childhood abuse or neglect is closely related to the development of depression and
appears to generate feelings of worthlessness, betrayal, loneliness, and guilt (Dykman et al., 1997; Wolfe
& McEachran, 1997). In addition, predictors of depression in children younger than 5 years of age
include parental marital partner changes, mother's health problems in pregnancy, child's health over the
first 6 months of life, maternal anxiety, and marital satisfaction early in the child's development, and
the mother's attitude towards caregiving (Najman et al., 2005). Many of these risk factors may affect the
quality of mother–child interactions during early development, and these may be a significant factor in
the development of childhood depression. Childhood adversity generally is also a risk factor for
childhood and adolescent depression, and this includes factors such as financial hardship and chronic
illness (Hazel et al., 2008). In such cases, the positive relationship between negative life events and
depressive symptoms is found only in those adolescents characterised by an elevated level of depressive
rumination (see Chapter 7, Section 7.1.2 for a discussion of depressive rumination), suggesting that a
tendency to ruminate mediates the relationship between negative childhood events and depression
(Kosiak, Blaut, Klosowska, & Kosiak‐Pilch, 2019)
 FOCUS POINT 16.2 THE PROTOTYPICAL ADOLESCENT AT
RISK FOR DEPRESSION

Lewinsohn, Rohde, and Seeley (1998) provide the following description of the prototypical
adolescent most at risk for adolescent depression:
‘The prototypical adolescent most likely to become depressed is a 16‐year‐old female who had
an early or late puberty. She is experiencing low self‐esteem/poor body image, feelings of
worthlessness, pessimism, and self‐blame. She is self‐conscious and overly dependent on others,
although she feels that she is receiving little support from her family. She is experiencing both
major and minor stressors, such as conflict with parents, physical illness, poor school
performance, and relationship breakups; she is coping poorly with the ramifications of these
events. Other psychopathologies include anxiety disorders, smoking, and past suicidality, are
probably present’ (p. 778).

Genetic factors
Studies of the heritability of childhood depression have been variable in their findings. Family, twin and
adoption studies suggest that genetic influences on childhood depression may be indirect and have their
effects in combination with environmental risks (Rice, 2009; Thapar & Rice, 2006), and in particular,
prepubertal depression is strongly associated with psychological adversity (such as negative childhood
experiences), and has a significantly lower heritability component than adult depression (Rice, 2010).
Just as with adult depression, we would expect any genetic influences on depression to be present from
birth, but it may be the case that these genetic predispositions may only have their effect at the
appropriate time during the developmental process that allows these genes to be expressed or allows
gene effects to interact with specific early life experiences (such as adversity or stress). Indeed, some
genetic influences may have their effects only when hormonal and physical developments occur in the
child (e.g., during puberty), and those genes that influence levels of cortisol and growth hormone
secretion may be responsible for an increased incidence of depression during puberty (Reinecke &
Simons, 2005). Childhood depression may also be influenced by genes associated with the serotonin
transporter system. One example is SLC6A4 which is associated with a reduction in serotonin expression
(Caspi, Harari, Holmes, Uher, & Moffitt, 2010). Reductions in serotonin expression are associated with
a vulnerability to depression, and during early development serotonin modulates neuroplasticity, and
dysfunction in these systems is known to contribute to the physiopathology of depression (Kraus,
Castrén, Kasper, & Lanzenberger, 2017).
Familial studies have indicated a strong link between parental depression and childhood depression, and
a child with a depressed parent is almost four times more likely to suffer childhood depression than one
without a depressed parent (Hammen & Brennan, 2001). While this is evidence that is consistent with
an inherited view of childhood depression, it could also imply that the behaviour of depressed parents
may create adverse early experiences that precipitate depression in the child (see later). Finally, the fact
that childhood experiences may be significantly more important than inherited factors in causing
childhood depression comes from adoption studies. Such studies have provided little or no evidence for
a genetic influence on depressive symptoms in childhood (Rice, Harold, & Thapar, 2002).

Psychological factors
Two major areas of research into the aetiology of childhood depression are (a) the role of parent‐child
interaction and (b) the development of dysfunctional cognitions that shape and support depressive
thinking in childhood.
We have already noted that children who have depressed parents are themselves more prone to
depression, and this relationship could be mediated in a variety of ways. First, parents who are
depressed may simply transmit their negative and low mood to their children through their interactions
with them, and children may simply model the behavioural symptoms of depression exhibited by their
parents (Jackson & Huang, 2000). Alternatively, depressed parents may not be able to properly respond
to their children's emotional experiences, and in so doing may leave the child either feeling helpless or
unable to learn the necessary emotional regulation skills required to deal with provocative experiences.
In support of this view, (a) Beeghly et al. (2017) found that infants aged 2 to 18 months received more
maternal social support the less the mother exhibited maternal depression symptoms, and (b) a study of
mother–child interactions by Shaw et al. (2006) found that depressed mothers were significantly less
responsive to their children's expressions of distress than nondepressed mothers. These findings suggest
that depressed mothers may be less sensitive or less knowledgeable about their offspring's emotional
distress, and this lack of responsiveness may facilitate internalising symptoms typical of childhood
depression. Unfortunately, many parents exhibit symptoms of depression—especially in the immediate
postpartum period, and this factor may be significant in generating internalising symptoms in their
infant offspring. For example, Paulson, Dauber, & Leiferman (2006) estimated that 14% of mothers and
10% of fathers exhibited significant levels of depressive symptoms up to 9 months after the birth of a
child. In addition, mothers who were post‐partum depressed were less likely to engage in healthy
feeding and sleeping practices with their infant, and depression in both mothers and fathers was
associated with fewer positive enrichment activities with the child (e.g., reading, singing songs, and
telling stories). Finally, those youths (especially girls) who are the offspring of depressed mothers also
show increased interpersonal impairment and risk of interpersonal dysfunction (Hammen, 2012), and
these romantic and interpersonal dysfunctions may not only be a consequence of depression, they may
well intensify and maintain the depression (Hammen, 2009).
As the child grows older, symptoms of depression often come to be associated with dysfunctional
cognitive characteristics that may function to maintain depressed behaviour. For example, attributional
models of adult depression suggest that the depressed individual may have acquired (a) a pessimistic
inferential style (attributing negative events to stable, global causes), (b) a tendency to catastrophise the
consequences of negative events, and (c) a tendency to infer negative self‐characteristics (see Chapter 7)
(Abramson, Metalsky, & Alloy, 1989), and studies of attributional style in childhood and adolescence
strongly suggest that a stable attributional style does not appear until early adolescence, suggesting that
attributional theories of depression may not apply to children until they reach adolescence (Cole et al.,
2008). Research on cognitive factors in adolescent depression has tended to focus mainly on the role of
pessimistic inferential styles and how this style interacts with negative experiences. For example,
children and adolescents with a pessimistic inferential style have been shown to be more likely to
experience increases in self‐reported depressive symptoms following negative events than children who
do not possesses this inferential style (Hilsman & Garber, 1995), and a pessimistic inferential style
interacts with daily hassles (daily annoyances, like being caught in a traffic jam) to predict increases in
depressive symptoms (Brozina & Abela, 2006). Such studies suggest that as the depressed child develops
cognitively, they may develop negative ways of construing events that, in conjunction with negative
experiences, act to maintain depressed symptomatology, and longitudinal studies have pin‐pointed a
time around 13–14 years of age, when depressive attributional styles begin to become stable attributes
of the individual and may be a risk factor for lifelong depression (Cole et al., 2008).

pessimistic inferential style The attribution of negative events to stable, global causes.
 SELF‐TEST QUESTIONS
Can you name four different types of diagnosable childhood anxiety disorder?
How might negative information provide a basis for the learning of anxious responding?
What is the evidence that ‘overprotective parents’ generate anxiety in their children?
How prevalent is depression in childhood and adolescence?
Can you name some risk factors that may make individuals vulnerable to adolescent
depression?
What is the pessimistic inferential style and how might it contribute to depression in
children and adolescents?

SECTION SUMMARY

16.3 CHILDHOOD AND ADOLESCENT ANXIETY AND DEPRESSION

Childhood anxiety and depression are known generally as internalising disorders.
Diagnosable forms of childhood anxiety include separation anxiety, OCD, GAD, specific phobias,
and social phobia.
Genetic factors play a relatively nonspecific role in childhood anxiety by determining
general levels of temperament probably transmitted through many gene variants.
Both trauma and stress experiences, as well as exposure to threat‐relevant information
have been shown to cause increases in anxious responding.
An overprotective parenting style may contribute to, or exacerbate, childhood anxiety.
As a child reaches puberty and early adolescence, between 11 and 28% of adolescents
aged up to 19 years of age will have experienced a diagnosable episode of major
depression
Childhood depression is highly comorbid with other psychological problems and can have
detrimental effects on educational and social functioning.
Studies suggest a modest genetic component to childhood depression and a substantial
environmental component.
Being reared by a depressed parent may contribute to childhood depression, and as the
child grows older it may develop a pessimistic inferential style.

16.4 THE TREATMENT OF CHILDHOOD AND ADOLESCENT

PSYCHOLOGICAL PROBLEMS
Many of the treatment methods used with adults have been successfully adapted to treat childhood
psychological problems. Children and adolescents with psychological problems will often require a
multifaceted approach to treatment, requiring procedures that address one or more of the following:
specific symptoms (e.g., enuresis), general emotional states and cognitions (such as anxiety or suicidal
ideation), behavioural problems (such as behavioural tics, aggressive, and disruptive behaviour), and
intrafamily relationships (such as issues relating to effective parenting, parent–child communication, or
childhood neglect and abuse). In addition, treatment will have to be provided while the child is still a
psychologically and physically developing organism and in the context of possible ongoing educational,
social, and familial difficulties. It can be seen that this multicomponent approach is most likely to require
a coordinated provision of supervision and treatment which extends across a range of services,
including education, health, and social services.
In the remainder of this section we look at individual treatment methods that have been applied to
childhood psychological problems. The emphasis here is on specific methodologies and how they have
been applied, and it is important to note that such procedures may often form part of a broader
collection of interventions depending on the needs of the individual child.

16.4.1 Drug Treatments

Drug‐based treatments of psychological problems in childhood and adolescence are becoming more
widely used as we come to understand the effects that various drugs may have on children (Walkup,
Labellarte, & Ginsburg, 2002). But the increase in the use of drug treatments for children has alarmed
many. For example, the paediatric use of selective serotonin reuptake inhibitors (SSRIs) had risen by
over 50% between 1994 and 2000 (Moynihan, 2003). Much of this increase in prescribing has been for
childhood and adolescent depression, and has often occurred without regulatory approval. So much so,
that in 2003, the British Medicines and Healthcare Products Regulatory Agency (MHRA) banned the
use of SSRIs in children under 18 years of age except for Prozac/fluoxetine. This was followed by a
meta‐analysis conducted by the US Food and Drug Administration (FDA) suggesting that there is an
increased risk of suicidal acts with the use of both SSRIs and serotonin and norepinephrine reuptake
inhibitors (SNRIs) in young people up to the age of 25 years,and that in the case of many the risks
outweighed the benefits of such drugs (FDA, 2007). However, more recent inclusive meta‐analyses seem
to challenge the FDA conclusion and suggest that the benefits may outweigh the risks of SSRIs when
treating a range of childhood problems such as depression and non‐OCD anxiety disorders (Bridge et
al., 2007; Gibbons, Brown, Hur, Davis, & Mann, 2012), so the debate is still open on this issue. While
the National Institute for Health and Care Excellence (NICE) advises that antidepressants should be
used only as a last resort for under‐18s, almost 65,000 young people under 18 years were prescribed
antidepressants in England between April 2015 and March 2016 (Marsh, 2017)—a statement not so
much on the effectiveness of antidepressants for children and adolescents, but the fact that medications
may be the only option available when having to negotiate the lengthy waiting times between referral
and psychological treatment.
SSRIs such as fluoxetine have also been used in the treatment of childhood anxiety disorders (excluding
the treatment of childhood OCD), and clinical trials have found it to be effective in reducing anxiety
symptoms and improving functioning generally (Seidel & Walkup, 2006). Nevertheless, there are a
number of reasons why we should be cautious about recommending the use of drug treatments with
childhood disorders: For example (a) complete remission of symptoms is rarely found, especially in the
treatment of childhood depression using SSRIs (Treatment for Adolescents with Depression Study
Team, 2004); (b) SSRIs (whether used for the treatment of depression or anxiety) have a number of
undesirable side effects in children, including nausea, headaches, and insomnia; (c) to date, outcome
studies vary considerably in their trial methodology to the extent that the safety and efficacy of such
drug treatments cannot yet be assured (Cheung, Emslie, & Mayes, 2005); and (d) doubts about the safety
of many antidepressant drugs when used to treat children have been raised in both the US and UK, to
the extent that official warnings have been released in relation to the use of such drugs (Fegert, Janhsen,
& Boge, 2006).
Despite the difficulties of using pharmacological treatments with childhood anxiety and depression,
much greater use has been made of drug treatments in ADHD. US studies indicate that stimulant
medication is the most adopted form of treatment for children diagnosed with ADHD with more than
half of them being treated in this way (Schwarz & Cohen, 2013), and stimulant medication has been
shown to be superior to placebos in reducing symptoms (Schulz et al., 2010). The most common form
of stimulant medication is Ritalin (methylphenidate), and this has been used to treat hyperactive
children since the 1950s. Ritalin is an amphetamine which paradoxically has a quietening effect on
overactive children, and decreases distractibility and increases alertness (Konrad, Gunther, Hanisch, &
Herpertz‐Dahlmann, 2004). We are still unsure about how drugs such as Ritalin have their beneficial
effects, but it may be that they act on the neurotransmitters noradrenaline and dopamine in areas of the
brain that play a part in controlling attention and behaviour. As we saw in Section 16.2, children with
ADHD appear to have some deficits in attention and executive functioning that may be redressed by the
effects that Ritalin has on neurotransmitter production. Studies have suggested that amphetamines such
as Ritalin are effective in reducing the amount of aggressive behaviour in children with ADHD (Fava,
1997), and it can significantly facilitate educational progress (Charach, Ickowicz, & Schachar, 2004).
However, despite these positive effects, there are still some drawbacks to the use of Ritalin with ADHD.
First, while it is effective in reducing symptoms in the short term, its longer‐term effects have not been
fully documented (Safer, 1997). Second, Ritalin also has a number of side effects including reduced
appetite, sleeping difficulties, disruption of growth hormone, memory loss, and stomach pains. Third,
Ritalin is an amphetamine and so can also be used as a drug of abuse, and there is evidence of
adolescents using Ritalin as a recreational drug to obtain a ‘high’ (Kapner, 2003), although recent
studies suggest that children with ADHD who have taken stimulant medication are no more at risk of
future substance abuse than those who have not taken that form of medication (Molina et al., 2013).

Ritalin (methylphenidate) A stimulant medication that is used to treat ADHD

16.4.2 Behaviour Therapy

Behaviour therapy is a useful means of changing quite specific behaviours and can provide learning‐
based interventions that allow the individual to change old behaviour patterns or learn new ones.
Examples of how this has been used in the treatment of childhood psychological problems include (a)
the treatment of symptom‐based disorders (such as enuresis), (b) the adaptation of adult behaviour
therapy methods (such as systematic desensitisation) to use with childhood anxiety disorders, and (c) the
development of behaviour change programmes for children with disruptive behaviour disorders.
A widely‐used classical conditioning method for treating nocturnal enuresis is known as the ‘bell‐and‐
battery technique’ (Mikkelsen, 2001). A sensor is placed in the child's underwear when they go to
bed and a single drop of urine will be detected by the sensor and set off an auditory alarm that will
wake the child (see Figure 16.3). This method allows the child to associate the alarm (the unconditioned
stimulus, UCS) with the sensation of a full bladder (the conditioned stimulus, CS), so that the child
eventually learns to wake up when he/she experiences a full bladder.

bell‐and‐battery technique A widely used classical conditioning method for treating

nocturnal enuresis.

Specific behaviour therapy techniques such as systematic desensitisation (see Chapter 4) can also
be successfully adapted to treat anxiety‐based problems in children (King, Muris, Ollendick, & Gullone,
2005), although in vivo methods appear to be significantly more successful than ‘imaginal’
desensitization, where the child has to imagine being in fearful situations. Sturges and Sturges (1998)
report the successful use of systematic desensitisation to treat an 11‐year‐old girl's elevator phobia.
Following an injury to her hand in an elevator door, she refused to ride in elevators. The clinicians
developed a behavioural hierarchy in which the sequential steps involved approaching and entering an
elevator while reciting self‐calming statements that she had agreed with the therapists. The child very
quickly resumed elevator use with no reoccurrence of anxiety up to 1 year later.

FIGURE 16.3 ‘Bell and battery technique’.

Drops of urine on the sensor pad set off an alarm that wakes the child; this enables the child with nocturnal enuresis to
learn to associate a full bladder with waking up.
Selective reinforcement techniques have been used to facilitate academic achievement in children with
ADHD and conduct disorder. One view of children with disruptive behaviour disorders is that their
disruptive behaviour is positively reinforced by the attention it receives from both peers and adults, and
this may especially be the case in the classroom setting. The purpose of introducing a behavioural
programme into such settings would be to regularise the reinforcement contingencies in the
environment—specifically to ensure that positive behaviours (e.g., attention to the teacher, or thinking
through tasks before responding) were rewarded and disruptive behaviours were not. Time out(TO)
from positive reinforcement has been found to be an effective means of reducing disruptive behaviours
including aggressiveness, destruction of property, and non‐compliance in the classroom (Fabiano et al.,
2004). In this case, the time‐out consisted of the child merely sitting in a specific time‐out chair in the
classroom for periods between 5 and 15 min. Other studies have established the effectiveness of ignoring
nonattention in the classroom (called ‘off‐task’ behaviour) and of rewarding all behaviours that may
contribute to the learning task in hand by praising the child. Such behaviours that would be reinforced
might include pausing for thought rather than impulsively beginning a task, communicating
appropriately with peers and teachers, etc. (Stahr, Cushing, Lane, & Fox, 2006).

Time Out (TO) A means of reducing disruptive behaviours, including aggressiveness,

destruction of property and non-compliance in the classroom, by removing the child from the
situation and directing him or her, for example, to sit in a specific timeout chair for periods of
between 5 and 15 minutes.

Finally, behaviour management techniques can be used in a range of environments and can even
be taught to parents as an aid to controlling and responding to their children in the home. For example,
teaching parents to identify and reward positive behaviour also helps to prevent parents from focussing
on the negative and disruptive behaviours exhibited by children with both ADHD and conduct disorder.
This has the effect of facilitating adaptive behaviour in the child and reducing the parent's negative
feelings towards the child (Kazdin & Weisz, 2003).
 behaviour management techniques Treatment methods that can be used in a range of
environments and can even be taught to parents as an aid to controlling and responding to their
children in the home.

16.4.3 Family Interventions

Family interventions are popular forms of interventions for many childhood psychological problems,
especially because many aetiological models of childhood psychological problems focus on parent‐child
relationships as one possible cause of the symptoms. Family interventions take a number of forms:
1. Systemic family therapy is based on the view that childhood problems result from
inappropriate family structure and organisation, and the therapist is concerned with the
boundaries between parents and children, and the ways in which they communicate (Minuchin,
Rosman, & Baker, 1978).

Systemic family therapy A family intervention technique based on the view that
childhood problems result from inappropriate family structure and organisation. The
therapist is concerned with the boundaries between parents and children, and the ways in
which they communicate.

2. Parent management training attempts to teach parents to modify their responses to their
children so that acceptable rather than antisocial behaviours are reinforced and this is used
especially with the families of children diagnosed with conduct disorder (Kazdin, 2006). This
method has been shown to effectively decrease antisocial behaviour and has long‐term beneficial
effects (Brestan & Eyberg, 1998; Dishion & Andrews, 1995).

Parent management training Therapeutic intervention which attempts to teach

parents to modify their responses to their children so that acceptable rather than antisocial
behaviours are reinforced and this is used especially with the families of children diagnosed
with conduct disorder

3. Functional family therapy(FFT) incorporates elements of systemic family therapy and CBT.
This approach views childhood problems as serving a function within the family, and they may
represent maladaptive ways of regulating distance or intimacy between other family members, and
this type of therapy attempts to change maladaptive interactional patterns and improve
communication (Alexander & Parsons, 1982). In this context, you may also want to have a look at
Treatment in Practice Box 10.1, where Sandy—suffering from anorexia—may be using her eating
problems as a means of distancing herself from her parents' conflicts and marriage problems.
These various forms of family therapy have been used successfully with children with conduct disorder,
ADHD, childhood depression, anxiety problems and eating disorders (see Carr, 2018, for an evidence‐
based review). Meta‐analyses of systemic and family therapies generally conclude that family
interventions have a positive effect when compared with no treatment and some alternative treatments
(Hazelrigg, Cooper, & Borduin, 1987), and a meta‐content analysis of 47 randomised controlled
outcome studies found that systemic family therapy was effective for treating children with eating
disorders, conduct problems, and substance use disorders (von Sydow, Behar, Rothers‐Schweitzer, &
Retzlaff, 2006).

16.4.4 Cognitive Behaviour Therapy (CBT)

CBT is becoming an increasingly useful treatment method for children and adolescents, and especially
those suffering from anxiety and depression. CBT is mainly used with adolescents and has been shown
to significantly reduce symptoms of depression (Brent et al., 1997) and anxiety (Manassis et al., 2002).
Even so, recent randomised controlled trials indicate that family‐based CBT can be successful even for
children as young as 5–8 years (Freeman et al., 2014). When used to treat adolescent depression, the
purpose of CBT is to help the depressed individual become aware of pessimistic and negative thoughts,
depressive beliefs, and causal attributions in which the adolescent blames themselves for failures but does
not take the credit for successes. Once these thoughts have been identified, the client is taught how to
substitute more realistic and constructive cognitions for the dysfunctional ones. A further goal of the
therapy is to increase the client's engagement with behaviours that will elicit positive reinforcement (e.g.,
Rohde, Feeny, & Robins, 2005). Other important components of CBT for adolescent depression that
help the efficacy of such treatments include (a) increasing and improving social interactions, (b)
improving problem‐solving skills, (c) improving goal‐setting and attainment skills, and (d) involving
parents closely in the therapy (parents are often the ones who refer their children for treatment, ensure
treatment attendance, and may contribute to the child's depression through their own problems and
difficulties) (Curry & Wells, 2005).

CBT See Cognitive behaviour therapy.

CBT for anxious children is also constructed to enable the child to become aware of problematic
thoughts and feelings (Kendall, Kane, Howard, & Siqueland, 1990). A typical treatment programme
involves (a) recognition of anxious feelings and somatic reactions, (b) understanding the role of
cognitions and self‐talk in exacerbating anxious situations, (c) learning the use of problem‐solving and
coping skills to manage anxiety, (d) using self‐evaluation and self‐reinforcement strategies to facilitate the
maintenance of coping, and (e) implementing a plan of what to do in order to cope when in an anxious
situation. CBT has been successfully used to treat a range of childhood anxiety disorders, including
OCD, GAD, specific phobias, social phobia, and separation anxiety and has been used with children
aged 8–18 years (Banneyer, Bonin Price, Goodman, & Storch, 2018; James, James, Cowdrey, Soler, &
Choke, 2015) and can also effectively reduce comorbid mood and behavioural symptoms (Mahdi,
Jhawar, Bennett, & Shafran, 2019). Long‐term follow‐up studies suggest that treatment gains are
maintained over 3 years after treatment (Kendall & Southam‐Gerow, 1996). CBT for childhood anxiety
appears to be equally as effective as medication alone (O'Kearney et al., 2006) and family
psychoeducation alone (Kendall et al., 2008) but is less effective for children under 4 years of age
(Rapee, Abbott, & Lyneham, 2006). More recent developments include computerised CBT and
Internet‐delivered CBT for children and adolescents (Stallard, Richardson, Velleman, & Attwood, 2011;
Vigerland et al., 2016), CBT for violent behaviour in children (Ozabaci, 2011) and childhood insomnia
(Paine & Gradisar, 2011). Finally, family interventions can also be used successfully to teach parents how
to use basic CBT procedures to address their children's anxiety, and such family‐based interventions
already show much promise (Cartwright‐Hatton et al., 2011).

16.4.5 Play Therapy

Play therapy offers a useful set of techniques that can be used with younger children who are less able
to communicate and express their feelings verbally (Carmichael, 2006). Play in itself can have curative
properties and can enable children to feel less anxious or depressed. However, it can also be used to help
children express their concerns, help them to manage their behaviour (e.g., by learning restraint when a
child is impulsive or aggressive), and to learn coping strategies and adaptive responses when
experiencing stress (e.g., Gil, 1991; Pedro‐Carroll & Reddy, 2005). Through play therapy, children
develop a positive relationship with a therapist, learn to communicate with others, express feelings,
modify behaviour, develop problem‐solving skills, and learn a variety of ways of relating to others. As
such, play therapy has been used in a range of mental health contexts to manage anger, deal with grief
and loss, divorce and family problems, crisis and trauma, and has proven useful across a range of
childhood psychological problems including anxiety, depression, ADHD, conduct disorder, autism, and
learning disorders (see Chapter 17) (Landreth, 2002; Bratton, Ray, & Rhine, 2005; Wilkes‐Gillan,
Bundy, Cordier, Lincoln, & Chen, 2016). Teenagers and adults have also benefited from play therapy
methods, and the use of these techniques has increased with these client groups (Pedro‐Carroll &
Reddy, 2005). Treatment in Practice 16.1 provides a couple of detailed examples of play therapies, and
more can be found in Hall, Kaduson, & Schaefer (2002).

Play therapy A range of play‐based therapeutic and assessment techniques that can be used
with younger children who are less able to communicate and express their feelings.

CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 16.1

PLAY THERAPY

Play therapy is a term used to cover a range of therapies that build on the normal
communicative and learning processes of children. Clinicians may use play therapy to help a
child articulate what is troubling them, to manage their behaviour (e.g., impulsive or aggressive
behaviour), and to learn adaptive responses when the child is experiencing emotional problems
or skills deficits. The following are two examples of specific play therapies, one designed to help
children practice self‐control (the ‘Slow Motion Game’) and the other to enable children to
communicate any distress they are feeling (the ‘Puppet Game’).
THE SLOW MOTION GAME

Therapeutic rationale
It is well known that children learn best by doing. The Slow Motion Game (by Heidi Kaduson;
see Kaduson & Schaefer, 2001, pp. 199–202) was designed to have children actively practice
self‐control over their movements in a playful group context.

Description
Materials needed: stopwatches for each child, cards (see below), dice, poker chips, paper, and
colouring materials.
To begin, the therapist introduces the concept of self‐control, discussing how it is very difficult
to maintain self‐control when we are moving too fast. Next, the children are asked to illustrate
what fast moving looks like. Once it is clear that the children understand the concept of self‐
control, each child is given a stopwatch. In the centre of the table are cards created by the
therapist with various scenes that the children must act out in slow motion. For example,
playing soccer, doing jumping jacks, or taking a math test. The children are instructed to roll
the die to see who goes first. The highest number goes first, and that child picks a card and goes
to the front of the room with the therapist. The therapist tells the group what that child is going
to do in ‘very slow motion’. On the count of three, all of the children start their stopwatches.
Every 10 seconds, the group reports to the child performing the task how much time has passed.
When the child has reached a full minute, the group yells ‘Stop’. Having successfully completed
the task, the child receives a poker chip. Then the next child (working in a clockwise direction)
picks a card and the game starts again. Once each child has had a turn, the time is increased to
2 minutes, and the second round begins. At the end of the second round, each player will have
two chips each, and a snack or treat is provided as a reward. The therapist can also give each
child a certificate for ‘Achievement in Slow Motion’.

Applications
The Slow Motion Game is successful with any group of children that has difficulty maintaining
self‐control. Also, common board games can be effectively used to increase children's self‐
control. For example, Jenga, Operation, Perfection, and Do Not Break the Ice.

USING A PUPPET TO CREATE A SYMBOLIC CLIENT

Therapeutic rationale
Puppets serve a crucial role in play therapy. Frequently, children project their thoughts and
feelings onto puppets. In this way, puppets allow children the distance needed to communicate
their distress. Furthermore, the puppets serve as a medium for the therapist to reflect
understanding and provide corrective emotional experiences in the context of the children's
play. Most children naturally project their experiences onto the puppets. However, some
children are too fearful and withdrawn to become involved in any aspect of therapy. By using
the puppet as a symbolic client (a game created by Carolyn J. Narcavage; see Kaduson &
Schaefer, 1997, pp. 199–203), the therapist is able to engage these children and overcome
resistance. The creation of the symbolic client removes the focus from the child, thereby
 increasing the child's comfort level and allowing him or her to remain at a safe emotional
distance.

Description
Materials needed: puppets
Once the therapist recognises that the child is frightened, the therapist might show the child a
puppet, remark that it is frightened, and reassure it of its safety. Next, the therapist should enlist
the help of the child in comforting the puppet. By completing these few simple steps, the
therapist has achieved three essential goals: The therapist has (a) responded and empathised
with the child's feelings in a nonthreatening manner, (b) begun the child's participation in
therapy, and (c) started fostering a positive therapeutic relationship with the child. The puppet
often becomes a safety object for the child throughout therapy.

Applications
This technique is particularly effective for any child between 4 and 8 years of age who is
anxious or withdrawn in the beginning stages of therapy. A variation of this technique would
be to have the puppet present with the same problem as the child and to enlist the child's help
in brainstorming solutions to solve the puppet's problem.

From Hall, Kaduson, & Schaefer (2002)

There has been some criticism of play therapy in the past, with critics suggesting that it lacks an
adequate research base to justify its use (Campbell, 1992; Reade, Hunter, & McMillan, 1999). However,
more recent randomised controlled trials and meta‐analyses of outcome studies suggest that children
treated with play therapy function significantly better after therapy than those who have had no
treatment (e.g., Bratton, Ray, Rhine, & Jones, 2005; Masoudifard, Mahmoodi, Bagheri, Dolatian, &
Kabir, 2019). Play therapy also appears to be effective across modalities, settings, age, and gender and
has positive effects on children's behaviour generally, their social adjustment, and their personality.

16.4.6 Prevention Strategies

Rather than simply identifying children and adolescents with mental health problems and attempting to
help and support them, attention has recently switched to prevention strategies, especially targeting
at risk families and developing school‐based prevention programmes—especially programmes to help
children to develop strategies for managing common mental health problems such as depression and
anxiety. Programmes in group settings such as schools are at the forefront of global preventative
initiatives (McLaughlin, 2017), and in the UK plans are in place for every school to appoint a mental
health lead and for a greater role for schools in cross‐sectoral mental health teams (Department of
Health & Social Care, 2017). Such programmes often use CBT methodologies to focus on problem‐
solving skills and to manage negative thoughts and negative moods, but can also involve other
therapeutic approaches such as mindfulness, relaxation, bias modification, behaviour therapy, or
psychoeducation (see Caldwell et al., 2019). However, as important as preventative programmes are,
they have so far only met with modest success (Brunwasser & Garber, 2016), and in a systematic review
of such programmes, Caldwell et al. (2019) conclude that ‘there is little evidence that educational
setting‐based interventions focused solely on the prevention of depression or anxiety are effective’ (p.
1011). They recommend that to be successful, future programmes should not just focus on the
individual child's cognitions, emotions, or moods but also address the wider familial and school systems
in which these kinds of interventions are implemented.
16.4.7 Summary of Treatment of Childhood and Adolescent Psychological
Problems
This section has described a number of different interventions that are regularly used to treat childhood
and adolescent psychological problems. Although drug treatments are becoming more common for a
number of disorders, there is still much uncertainty about their effectiveness and their safety. Common
treatment methods include behaviour therapy, family therapy, CBT, and play therapy, and these forms
of treatment will be adapted to the specific therapeutic needs of the child and often used in a
multifaceted approach to ensuring improvements across emotional, educational, and social functioning.
Preventative programmes are becoming a priority but as yet are still in their infancy and may need to
take account of the broader educational and familial context in which the child lives rather than simply
targeting individual cognitions and emotions.

SELF‐TEST QUESTIONS
What drugs are used in the treatment of ADHD and childhood depression? What are the
risks of using such drugs?
What is the evidence that SSRIs and SSNIs are dangerous for children and adolescents
below the age of 18 years?
How have behaviour therapy techniques been adapted to treat childhood behavioural
problems?
What are the different types of family intervention that might be used in dealing with
childhood mental health problems?
How can CBT be used to treat childhood and adolescent anxiety and depression?
What is play therapy and what aspects of childhood psychopathology can it be used to
treat?
What preventative strategies have been developed to help prevent child and adolescent
common mental health problems such as anxiety and depression?
 SECTION SUMMARY

16.4 THE TREATMENT OF CHILDHOOD AND ADOLESCENT

PSYCHOLOGICAL PROBLEMS
Treatment for childhood psychological problems requires a coordinated provision of
services that extends across educational, health, and social services.
Drug treatments are used for childhood anxiety and depression, and ADHD, but there are
still significant doubts about the safety of many medications used with children.
Ritalin is a stimulant medication that is used to treat ADHD in around half of those
diagnosed with the disorder.
Behaviour therapy techniques can be adapted to treat many childhood behaviour problems,
techniques used include the bell‐and‐battery techniques for enuresis, systematic desensitisation for
anxiety problems, and time out (TO) to reduce disruptive behaviours.
Important family interventions include Systemic Family Therapy, Parent Management Training,
and Functional Family Therapy (FFT).
CBT has been successfully adapted to treat childhood and adolescent depression and
anxiety, as well as a number of other childhood psychological problems.
Play therapy covers a range of techniques that can be used with younger children who are
less able to communicate and express their feelings.

16.5 CHILDHOOD AND ADOLESCENT PSYCHOLOGICAL

PROBLEMS REVIEWED
There is a range of difficulties involved in the identification, diagnosis, and treatment of childhood
psychological problems that are not usually encountered in adult mental health problems. First, children
are often unable to communicate any distress they are feeling and may lack the self‐awareness to identify
individual symptoms of psychopathology, such as anxiety or depression. Second, until recently
childhood psychopathology has been a relatively neglected area of clinical research and much of
childhood psychopathology has previously been rather simplistically labelled as either internalising
(reminiscent of anxiety or depression) or externalising (exhibiting signs of disruptive and aggressive
behavioural problems). However, research in this area has increased significantly in recent years, and we
are now able to identify rather specific childhood disorders such as childhood depression, OCD, and
GAD, as well as two important disruptive behaviour disorders—ADHD and conduct disorder.
We are still some way from fully understanding the aetiology of most childhood psychological problems,
although some do have important genetic components (e.g., ADHD) whereas others appear to be
related to significant developmental factors such as the nature of the family environment, parent–child
relationships, and the socio‐economic climate in which the child is being raised.
Treatment for childhood disorders is usually multifaceted, and takes place in the context of a
coordinated provision of supervision and treatment that extends across a range of services, including
education, health, and social services. While there are drug treatments for many childhood
psychological problems, there are still significant doubts about the effectiveness and safety of many of
these treatments. More widely adopted are adaptations of adult psychotherapies, including behaviour
therapy, family‐based interventions, and CBT. Play therapy also offers a useful eclectic intervention that
can be used with younger children who are less able to communicate and express their feelings verbally.
Prevention programmes for common mental health problems such as anxiety and depression are very
much in their infancy but once refined will be a priority for mental health services.

This book is accompanied by Student and Instructor companion

websites.
www.wiley.com/go/davey/psychopathology3e
The website includes many resources for individual chapters, including:
Chapter References
Videos
Student quizzes
Student flashcards
Recommended reading links
Lecturer Test Banks (available to Instructors only)
Lecture PowerPoint slides (available to Instructors only)
Study Management & Motivation Workbooks
Mood & Anxiety Summary Tables
Activity Boxes
Glossary of Key Terms
Essay questions, Exam questions, Discussion Topics, and more
17
Neurodevelopmental Disability and Diversity

ROUTE MAP OF THE CHAPTER

This chapter begins by describing the way in which learning, intellectual, and developmental
disabilities and diversities are defined and the terminology that is associated with these
conditions. The chapter then proceeds to discuss factors associated with the diagnosis, aetiology
and treatment of three groups of disabilities, namely specific learning problems (e.g., specific
disorders of reading, writing, and communication), intellectual disabilities, and finally autistic
spectrum disorder.

CHAPTER OUTLINE
17.1 THE HISTORY OF CATEGORISING AND LABELLING
NEURODEVELOPMENTAL DISABILITIES AND DIVERSITIES
17.2 SPECIFIC LEARNING PROBLEMS
17.3 INTELLECTUAL DISABILITIES
17.4 AUTISTIC SPECTRUM DISORDER (ASD)
17.5 NEURODEVELOPMENTAL DISABILITY AND DIVERSITY REVIEWED

LEARNING OUTCOMES
When you have completed this chapter you should be able to:
1. Discuss the different ways in which learning and developmental problems are categorised
and labelled.
2. Describe and compare the various types of specific learning problems, their aetiology and
treatment.
3. Describe the various forms of intellectual disability
4. Compare and contrast genetic, biological, and environmental causes of intellectual
disabilities.
5. Describe and evaluate the main forms of intervention, care and support for intellectual
disabilities
6. Describe the diagnostic criteria for autistic spectrum disorder (ASD)
7. Compare and contrast theories of the aetiology of ASD
8. Describe and evaluate the main forms of intervention, care, and support for individuals
with a diagnosis of ASD.
 During childhood, no one knew what I had, I was considered ‘crazy’ by a doctor at age one, because I had
constant tantrums, which only ended, 1 day, when my mother took me to the beach during a holiday. My nerves
suddenly calmed down, by the sight, and the soothing sounds of the sea. I was beginning to say my first words,
and started some progress.
Despite the progress, I still had strange behaviours, like spinning plastic lids, jars and coins. I rejected teddy bears
that other toddlers liked, but held on to other objects, like dice (which had a smooth surface and were pleasant to
touch). I was terrorised by everyday noises, like planes passing by, thunder, machinery, drills, balloons bursting,
and any sudden noise.
Being the firstborn, my mother did not take notice of behaviours like rocking back and forth, or spending time on a
rocking horse in the day care centre as a toddler instead of playing with other kids.
Despite socialising difficulties, my interest for reading, and learning the alphabet pleased my mother. Instead of
pointing out pictures in a newspaper my mother was reading, I asked her what the letters were, and that prompted
her to teach me to read before starting school.
Socially, I had problems that worried people. I was not able to recognise people easily, and was not able to decode
nonverbal cues. My mother complained about always having to spell things out to me. While my younger (non‐
autistic) brother seemed to know instinctively when to bring up a subject, or when to say a joke, I was a nuisance,
because I could not tell if somebody was angry, sad, tired, etc, just by looking at him/her. I took things literally
and was terrorised by my mother's ‘threats’ which my younger brother did not take seriously. She uttered threats
like ‘I will send you away’ when we behaved badly. My brother was able to understand that she never means it,
however I was terrorised by them.
One thing that discouraged socialising was that most others did not like to talk about insects, calculators, or space
all the time. Other people liked my subjects ‘once in a while’ and got angry if I went on and on. My mother
constantly reminded me not to talk about the same things over and over. Changing subjects was hard for me. I was
fixated on certain subjects like entomology, and arachnology. Nobody cares to hear about the chelate pedipalps of
pseudoscorpions.
George's Story

Introduction
Neurodevelopmental disorders are a category of disabilities that typically begin to manifest in early
development and may affect intellectual, social, and motor development and as a consequence will have
effects on academic achievement, the development of social behaviours, and subsequent occupational
functioning. In this chapter, we will cover three categories of neurodevelopmental disorder—specific
learning disorders, intellectual disabilities, and autistic spectrum disorder (ASD). Each of these
categories is characterised either by a specific impairment in learning or control (e.g., language or
communication disorders, such as dyslexia), different ways of processing information about the world
(e.g., autistic spectrum disorder), or global impairments to intellectual, social, and motor skills (e.g.,
intellectual disability). A neurodevelopmental disorder can be considered as a significant, lifelong
condition that is usually present from birth, but it may often not be recognised until the individual's
behaviour appears different at certain milestones in their development. Failing to sit up, to talk, read, or
attend to what is going on in the world are all possible signs of a learning disability if these activities do
not appear as expected at normal developmental intervals. Most neurodevelopmental disorders are
permanent conditions, but with suitable support and encouragement many people with these conditions
contribute to society in significant ways (see Focus Point 17.1).
 FOCUS POINT 17.1 NEURODIVERSITY

The term ‘neurodiversity’ was coined in 1998 by Australian sociologist Judy Singer who was
diagnosed with autistic spectrum disorder, and the neurodiversity movement had its origins in
the Autistic Rights Movement that began in the 1990s. Neurodiversity is a term used to reflect
the variation in neurocognitive functioning in human beings, and to promote the idea that there
is not just one ‘normal’ or ‘healthy’ type of brain or form of neurodevelopment and that one
form of neurocognitive functioning is no more right or wrong than any other form. As a
consequence, many clinicians and researchers who integrate the concept of neurodiversity into
their research and their practice refuse to view neurodivergence as intrinsically pathological.
Subsumed under the concept of neurodiversity are a number of conditions usually found in
mental health diagnostic manuals, including autistic spectrum disorder, dyslexia, ADHD (see
Chapter 16), and bipolar disorder (see Chapter 7), and therapists who embrace neurodiversity
attempt to help individuals with these characteristics to find ways of living that are more in
harmony with their neurological dispositions. For example, people with autistic spectrum
disorder have a greater than normal capacity for processing information even from rapid
presentations and are better able to detect information defined as critical—an attribute that
may help to explain the higher than average prevalence of people with autism spectrum
disorders in the IT industry (Remington, Sweetenham, & Lavie, 2012). Similarly, individuals
with dyslexia may struggle with word based tasks, but in some visuospatial skills they can often
outperform nondyslexic peers (Duranovic, Dedeic, & Gavrić, 2014) which suggests they may
not necessarily be learning disabled in the traditional sense of that phrase but may just be
learning differently.

George's Story describes the early life of someone diagnosed with ASD. This involves early difficulties in
interpreting nonverbal behaviour, impairment in communicating with others, and a repetitive
preoccupation with individual objects, activities, or topics. This personal account provides a striking
insight into how these characteristics can affect normal day‐to‐day living during childhood. George
prefers indulging in stereotyped behaviours, such as rocking, to playing with other kids. He is unable to
understand both normal verbal innuendo and the nonverbal body language that most people learn to
understand implicitly. This causes him to be seen by others as ‘difficult’, uncommunicating, and ‘a
nuisance’, all of which in turn causes him to feel more anxious and distressed. Most
neurodevelopmental disorders, no matter how specific, cause difficulties across the whole range of life
activities, including educational, social, and occupational, but the degree to which those with
neurodevelopmental diversity characteristics have problems in these areas of functioning will depend on
their background and family circumstances and the nature and degree of the disability.
This chapter will look in detail at the various neurodevelopmental diversities, their aetiology, and the
various support options that are available for these diversities (Focus Point 17.1).

17.1 THE HISTORY OF CATEGORISING AND LABELLING

NEURODEVELOPMENTAL DISABILITIES AND DIVERSITIES
In this chapter neurodevelopmental disabilities and diversities are divided into three broad categories.
These are (a) specific learning problems, such as language and communication problems, (b)
intellectual disabilities, covering some of the more severe learning difficulties, and (c) autistic
spectrum disorder, which covers a dimension of problems associated with one or more of social
communication, ways of interpreting the world, and in some cases is accompanied by information
processing difficulties and intellectual impairments.

intellectual disabilities A modern term replacing mental retardation to describe the more
severe and general learning disabilities.

There is considerable diversity across different areas of the world about how various learning disabilities
have been labelled. In the UK, Europe, and much of Australasia the term learning disability has
often been used as an umbrella term to cover disorders across all three of the main categories described
previously—and it is especially used in this way by health and social care services. In DSM‐IV‐TR, the
term mental retardation referred to a specific diagnostic category of disorder defined as significantly
below average intellectual functioning characterised by an IQ of 70 or below (DSM‐IV‐TR, p. 49).
However, the term mental retardation is now quite rightly frowned upon as stigmatising, demeaning,
and discriminatory and was replaced in the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition
(DSM‐5) by the label intellectual disability and in the International Classification of Diseases (ICD‐11) by
intellectual development disorder—a change that was required by a federal statute in the United States
that was known as Rosa's Law (https://www.govtrack.us/congress/bills/111/s2781, 2010). There is as
yet no genuine international consensus on the use of these categories and labels, and even within
countries these terms can change quite frequently to reflect shifts in social attitudes towards individuals
with different learning abilities.

learning disability An umbrella term to cover specific learning disabilities, intellectual

disabilities and pervasive developmental disorders.

SELF‐TEST QUESTIONS
How are the terms specific learning disability, intellectual disability, and autistic spectrum
disorder defined?

SECTION SUMMARY

17.1.THE HISTORY OF CATEGORISING AND LABELLING

NEURODEVELOPMENTAL DISABILITIES AND DIVERSITIES
The three main categories of learning disabilities are (a) specific learning problems (e.g., specific
learning disorder), (b) intellectual disabilities, and (c) autistic spectrum disorder (ASD).

17.2 SPECIFIC LEARNING PROBLEMS

DSM‐5 divides specific learning problems into two broad categories. The first is the diagnostic category
called (a) specific learning disorder, which covers difficulties in learning and using academic skills
such as reading and writing, and (b) communication disorders, which covers problems in language,
speech, and communication.

17.2.1 Specific Learning Disorder

Specific learning disorder refers to a number of problems that each affect the individual's performance
on standardised tests of academic ability such as reading, mathematics, or written expression.
Individuals with these problems show levels of achievement well below what would be expected for their
age, schooling, and level of intelligence. As we shall see, individuals with specific learning disabilities can
show deficits in perceptual organisation (organising information), auditory and visual perception,
memory, and attention. Without special remedial support, individuals with these problems will normally
perform badly at school, be viewed as failures by friends and family, and as a consequence exhibit low
self‐esteem and motivation (Bjorkland & Green, 1992). Similarly, school dropout rates for children with
specific learning disabilities are high and they will also experience difficulties in occupational and social
functioning. Specific learning disorder is diagnosed when there are deficits or impairments in the
individual's ability to either perceive or process information accurately and will eventually manifest in
academic circumstances as difficulties in reading, writing, or in mathematical ability. DSM‐5 has
incorporated a number of previously different disabilities (such as dyslexia and dyscalculia) into a single
specific learning disorder diagnostic category, and defines disabilities in this category as difficulties in
learning and using academic skills in one or more areas such as slow reading, difficulty understanding
the meaning of what is read, difficulties with spelling and written expression, difficulty mastering
number sense, and difficulties with mathematical reasoning. Table 17.1 provides the DSM‐5 diagnostic
criteria for specific learning disorder and Table 17.2 describes some of the specific disabilities covered
under this diagnostic category and provides some examples.

specific learning disabilities Disorders such as dyslexia and communication disabilities.

Specific learning disabilities such as these are often commonly comorbid with other childhood
psychological problems, and studies suggest that specific learning disabilities can be diagnosed in 79%
of children with bipolar disorder, 71% with attention‐deficit‐hyperactivity disorder (ADHD), 67% with
autism, and slightly lower percentages with anxiety and depression (18–19%) (Mayes & Calhoun, 2006).
Literacy problems generally are associated with increased risk for both externalising and internalising
disorders in childhood, and this may be due either to the stressors associated with academic failure
(causing anxiety and depression), or the fact that certain types of cognitive deficit (such as attention
deficits) may be common to a number of different disorders, including specific learning disorders and
disruptive behaviour disorders such as ADHD (Maughan & Carroll, 2006).
TABLE 17.1 Summary: DSM‐5 diagnostic criteria for specific learning disorder

Impediments in learning and using academic skills, marked by at least one of the following over a
6‐month period:
Inaccurate or slow and struggling reading
Difficulty understanding the meaning of read words
Spelling difficulties
Difficulties in expression through writing
Difficulties understanding numbers
Difficulties with mathematical reasoning
The affected academic skills are substantially below what would be expected for the individual's
age
The difficulties are not better accounted for by intellectual disabilities, vision or hearing
difficulties, or other mental or neurological disorders
TABLE 17.2 Specific learning disabilities
Disability Description Example
symptoms

Problems with accurate or fluent Reading achievement is substantially Omit, add, or

word recognition, poor decoding, below norm for chronological age, distort the
and poor spelling abilities intelligence, and educational level sound of
(formerly known as dyslexia) words when
reading

Read slowly
and with poor
comprehension

Problems with written expression Writing skills are substantially below Regular errors
those expected for chronological age, in spelling,
intelligence, and educational level grammar, or
punctuation

Difficulties mastering number Mathematics ability is substantially Difficulty

sense, number facts, or calculation below norm for chronological age, remembering
(formerly known as dyscalculia) intelligence, and educational level arithmetic facts
(e.g., to ‘carry’
a number)

Failure to
understand
arithmetic
concepts

Difficulties with verbal and Scores on tests of expressive language Markedly

written expression development are substantially below limited
those for chronological age, vocabulary
intelligence, and educational level
Making errors
in tense

Difficulty
recalling the
right word

Dyslexia
Dyslexia is a complex pattern of learning difficulties associated with difficulties in word recognition
while reading, poor spelling, and difficulties with written expression. Reading may be characterised by
word distortions, substitutions, or omissions, and is generally slow, with the child having difficulty fully
comprehending what has been read. Around 3 to 17.5% of school‐age children have specific
developmental reading problems (DeFries, Fulker, & BaBuda, 1987; Shaywitz et al., 1998), and between
60 and 80% of those diagnosed are likely to be boys (Shaywitz, Shaywitz, Fletcher, & Escobar, 1990),
and this gender difference may be due to a number of factors, including (a) there are higher referral
rates for males because they may be more disruptive than girls in learning environments, (b) girls may at
least partially offset their reading difficulties by enjoying reading more than boys (Chiu & McBride‐
Chang, 2006), (c) girls may have more effective coping strategies than boys for dealing with reading
difficulties (Alexander‐Passe, 2006), and (d) boys do have a slower and more variable processing speed
and worse inhibitory control than girls (Arnett et al., 2017). Most longitudinal studies suggest that
reading problems can often be persistent and chronic, which does not simply represent a developmental
lag in reading ability but is evidence for a specific learning disability (Bruck, 1992; Scarborough, 1990;
Francis, Shaywitz, Stuebing, Shaywitz, & Fletcher, 1996). Figure 17.1 shows that, even though children
with impaired reading skills show an improvement in reading ability with age, a gap in reading ability
remains across time between children with reading impairments and those without. In individuals
suffering dyslexic problems, writing skills fall significantly below those expected for the child's
chronological age, IQ , and educational history. The child will have difficulty composing written text and
will exhibit grammatical errors, punctuation errors, poor paragraph organisation, spelling errors, and
poor handwriting (Photo 17.1).

FIGURE 17.1 Trajectory of reading skills over time in nonimpaired and dyslexic readers. Both nonimpaired and
dyslexic readers improve their reading scores as they get older, but the gap between nonimpaired and dyslexic readers remains
suggesting that dyslexia is a deficit and not a developmental lag.
From Shaywitz (2003).
PHOTO 17.1 Dyslexia includes deficits in spelling and writing as well as reading. Other symptoms of dyslexia can
include poor comprehension, reversal of words or letters while reading, and difficulty decoding syllables or single words and
associating them with specific sounds (phonics). Here, a child with dyslexia attempts to reproduce a teacher's sentence.
Will and Deni McIntyre/Science Source, National Audubon Society Collection/Photo Researchers, Inc. Reproduced with permission.

Dyscalculia
The main feature of dyscalculia is that mathematical or arithmetical ability falls significantly short of
that expected for the child's chronological age, IQ , and educational history. Individual skills that may be
problematic in dyscalculia are (a) understanding or naming mathematical terms, (b) decoding problems
into mathematical terms, (c) recognising and reading numerical symbols or arithmetical signs, (d)
copying numbers or symbols correctly, (e) remembering to conduct certain mathematical operations
(such as ‘carrying’ figures when making calculations), and (f) following sequences of mathematical steps
in the correct order. It is estimated that around 3–4% of school‐age children may suffer from
developmental dyscalculia, with the male to female ratio as high as 4:1 (Reigosa‐Crespo et al., 2012).

dyscalculia A specific learning disability characterised by mathematical ability being

substantially below norm for chronological age, intelligence and educational level.

17.2.2 Communication Disorders

Communication disorders include impairments in language, speech and communication, and here
we cover the DSM‐5 diagnostic categories of language disorder, speech sound disorder, and childhood‐
onset fluency disorder (otherwise known as ‘stuttering’).
 Communication disorders Problems with the articulation of sounds.

Language disorder
Language disorder concerns problems with language acquisition and use as a result of problems in
vocabulary comprehension and production and in the construction of sentences. This usually results in
a significantly smaller vocabulary size, with grammatical and tense errors. These problems will appear
during early development and persist into adolescence and adulthood (Table 17.3). General features of
this particular problem include a limited amount of speech, limited vocabulary, difficulty learning new
words, difficulty finding the right word (e.g., unable to come up with the word car when pointing to a
car), shortened sentences, simple grammatical structures (e.g., use of relatively few verb forms), omission
of critical parts of sentences, unusual word order, and slow language development generally. Language
disorder is often comorbid in younger children with speech sound disorder (discussed next), reflecting a
general problem with the fluidity of language and erratic speech rhythms. Language disorder can be
identified as early as age 2–3 years (Eisenwort et al., 2004), but milder forms may not become apparent
until early adolescence.

Language disorder A disability concerned with problems in vocabulary comprehension and

production.

TABLE 17.3 Summary: DSM‐5 Diagnostic Criteria for Language Disorder

Ongoing difficulties in the attainment and use of language (including spoken and written), due to
difficulties in understanding and emitting that include the following:
Reduced vocabulary
Limited sentence structure ability
Difficulties in dialogue
Abilities are substantially below what would be expected for the patient's age
Symptoms start in early development
The difficulties are not better accounted for by vision or hearing difficulties, motor dysfunction, or
other mental or neurological disorders

Speech sound disorder

This is a speech problem characterised by persistent difficulty with speech sound production, and to be
diagnosed with speech sound disorder, these impairments must be problems in effective
communication that interfere with social, academic, or occupational achievement (Table 17.4). The
disorder includes errors of sound production (e.g., using a t sound to represent the letter k) and the
omissions of sounds—especially from the ends of words. Those diagnosed with speech sound disorder
will also be unable to categorise speech sounds and will be unable to decipher which sounds in the
language make a difference in meaning. The most severely misarticulated sounds are those learnt later
in the developmental process such as l, r, s, z, th, and ch, and lisping is particularly common (e.g., saying
wabbit instead of rabbit). Speech sound disorder may often be associated with physical causes, such as a
hearing impairment, cleft palate, neurological limitations such as cerebral palsy, and ear, nose, and
throat problems (Fox, Dodd, & Howard, 2002), but at least 3% of preschool children are diagnosed with
a speech sound disorder of unknown origin. Prevalence rate of similar or related speech sound disorders
is around 2% in 6–7 year‐olds falling to 0.5% by age 17 years (DSM‐IV‐TR, p. 66).

speech sound disorder Persistent difficulty with speech sound production that interferes with
speech intelligibility or prevents verbal communication of messages.

TABLE 17.4 Summary: DSM‐5 Diagnostic Criteria for Speech Sound Disorder

Ongoing difficulty with speech sound production that causes problems with speech understanding
or prevents verbal communication
The difficulty causes limitations in effective communication, interfering with social participation,
academic or occupational performance
Symptoms start in early development
Difficulties are not better accounted for by congenital or acquired conditions including cerebral
palsy, deafness, or other medical conditions

Childhood‐onset fluency disorder (stuttering)

This is a problem with the fluency and time‐patterning of speech which involves (a) frequent repetitions
or prolongations of sounds, (b) pauses within words, (c) filled or unfilled pauses in speech, (d) word
substitutions to avoid pronouncing problematic words, (e) words produced with an excess of physical
tension, and (f) monosyllabic word repetitions (e.g., ‘go‐go‐go‐go out of the room’) (Table 17.5). Fearful
anticipation of stuttering may develop in many sufferers and this may make stuttering worse in
stressful situations, such as when giving a speech or at an interview. Stuttering may be accompanied by
physical symptoms such as eye blinks, tics, tremors, jerking of the head, clenching fists, etc. As can be
envisaged, stuttering can also have highly detrimental effects on social and occupational functioning.
Onset of stuttering typically occurs between 2 and 7 years of age, with a peak onset around 5 years.
The onset is usually insidious and initially the child may be unaware of stuttering. However, as
awareness increases, the child will develop compensatory strategies for avoiding words and situations
that cause stuttering. Community studies estimate prevalence rates for all individuals at 0.7%, rising to
1.4% in young children and dropping to 0.5% in adolescents (Craig et al., 2002), although it has been
argued that the lifetime prevalence rate for stuttering may be much higher because of underdiagnosis
(Yairi & Ambrose, 2013). However, the prognosis for stuttering is good, with around 40% of sufferers
overcoming the problem before they start school and 80% overcoming it before adolescence (Couture &
Guitar, 1993). Stuttering is more common in males than females, with a male‐to‐female ratio of 4:1 in
adolescents and 2.3:1 in both younger children and adults. Of those children diagnosed with stuttering,
12.7% also have phonological disorder, 15.2% have another learning disability, and 5.9% have ADHD
(Blood, Ridenour, Qualls, & Hammer, 2003).

stuttering A disturbance in the normal fluency and time patterning of speech that is
inappropriate for the individual’s age.
TABLE 17.5 Summary: DSM‐5 Diagnostic Criteria for Childhood‐Onset Fluency Disorder (Stuttering)

Ongoing disturbance of normal fluency and time patterns in speech, inappropriate to the
patient's age and language skills, as marked by at least one of the following:
Sound and syllable repetitions
Sound prolongation of consonants and vowels
Broken words
Filled or unfilled pauses in speech
Word substitution to avoid difficult words
Word pronunciation with excessive physical tension
Monosyllabic whole‐word repetitions
The disturbance causes anxiety about speaking or limitation in effective communication
Symptoms start in early development
Difficulties are not better accounted for by speech‐motor or sensory deficit or other medical
condition

17.2.3 The Aetiology of Specific Learning Disabilities

In the following section, we discuss the aetiology and causes of some of the more common of the
specific learning problems we have described in this section.

Dyslexia
As we mentioned earlier, dyslexia is a condition which affects both reading and written expression and
is a persistent, chronic condition in which reading ability lags behind that of nonimpaired individuals
for the course of most of their lifetime. The development of dyslexia can be predicted by a number of
risk factors, including difficulty recognising rhymes at age 4 years (Bradley & Bryant, 1985), difficulty
naming everyday objects at age 5 years (Wolf, Bally, & Morris, 1986), and difficulty learning syntactic
rules at age 2–3 years (Scarborough, 1990). However, the main causes of dyslexia now appear to be
identified as abnormalities in specific areas of the brain such as the temporoparietal region (Shaywitz &
Shaywitz, 2005). These abnormalities may be the result of genetic factors, and they may give rise to the
difficulties that individuals have in decoding and comprehending written material. We will review these
theories of the aetiology of dyslexia by looking in turn at evidence related to genetic inheritance,
cognitive factors, and brain functions.

dyslexia A persistent, chronic learning disability in which there are developmental deficits in
spelling, reading and writing abilities.

Genetic factors
As early as 1950, it was reported that more than 80% of children with dyslexia also had other family
members with the disability, with further studies suggesting that between 23 and 65% of children with
dyslexia have a parent with the disorder (Scarborough, 1990). In addition, 40% of the siblings of
sufferers will also exhibit symptoms of dyslexia (Pennington & Gilger, 1996). This suggests that dyslexia
runs in families and so may have an important genetic component, and evidence for this genetic
component is supported by studies suggesting that dyslexia concordance rates are significantly higher in
monozygotic (MZ) than in dizygotic (DZ) twins (Stevenson, Graham Fredman, & McLoughlin, 1987),
and heritability estimates have in some cases been as high as 0.72 (Plomin & Kovas, 2005). Using
genetic markers for dyslexia (see Chapter 1, Section 1.3), linkage studies have implicated genes on a
number of chromosomes in the aetiology of dyslexia, including loci on chromosomes 2, 3, 6, 15, and 18
(Fisher & DeFries, 2002), and the involvement of several genes spanning these regions in the aetiology
of dyslexia has been reported (Mascheretti et al., 2017). There is evidence from molecular genetics to
suggest that many of these genes participate in brain development, and cause the differences in brain
development associated with dyslexia (Galaburda, LoTurco, Ramus, Fitch, & Rosen, 2006; Scerri &
Schulte‐Koene, 2010).

Cognitive factors
Research on the aetiology of dyslexia has converged on the view that reading disabilities in dyslexia are
caused primarily by difficulties in differentiating the elements of speech (phonemes) and associating
these sounds with the letters in a written word (Shaywitz, 2003). This is known as the phonological
theory of dyslexia where, in order to learn to read, the child must learn to recognise that letters and
letter strings represent the sounds of spoken language. The deficits in dyslexia impair the child's ability
to break up a spoken word into its basic phonological elements and link each letter to its corresponding
sound. This deficit is quite independent of other abilities, such as general intelligence, reasoning,
vocabulary, and use of syntax (Share & Stanovich, 1995; Shankweiler et al., 1995). Shaywitz & Shaywitz
(2005) characterise the experience of the dyslexic in the following way: ‘The problem is that the affected
reader cannot use his or her higher‐order linguistic skills to access the meaning until the printed word
has first been decoded and identified. Suppose, for example, an individual knows the precise meaning of
the spoken word ‘apparition’; however, she will not be able to use her knowledge of the meaning of the
word until she can decode and identify the printed word on the page and it will appear that she does not
know the word's meaning’ (p. 1302).

phonological theory The view that reading disabilities in dyslexia are caused primarily by
difficulties in differentiating the elements of speech (phonemes) and associating these sounds
with the letters in a written word.

However, phonological theory may not be the single answer to understanding dyslexia. First,
phonological theory has difficulty explaining all the behavioural symptoms of dyslexia (e.g., many
individuals with a diagnosis of dyslexia are both physically and socially immature, and have trouble
reading social cues) (Ramus & Ahissar, 2012), and not all individuals with dyslexia show a phonological
deficit (Pennington et al., 2012). Conversely, not all individuals with a phonological deficit are given a
diagnosis of dyslexia (van der Leij et al., 2013). This suggests that phonological theory may not be the
sole explanation of dyslexia, with the possibility that various constellations of underlying cognitive
abnormalities may lead to some of the symptoms of dyslexia (van Bergen, van der Leij, & de Jong,
2014).

Brain function
Associated with problems in relating written letters to corresponding sounds are problems in brain
functioning in dyslexia—especially in the temporoparietal areas of the brain. Post‐mortem studies
of the brains of individuals with dyslexia suggest abnormalities in the temporo‐parietal brain region
(Galaburda et al., 1985), and the number and organisation of neurones in the posterior language area
of the cortex (Galaburda, 1993). Nevertheless, these abnormalities found in post‐mortem studies might
simply represent the consequences of a lifetime of poor reading rather than a causal factor in dyslexia.
However, functional magnetic resonance imaging (fMRI) studies of the brains of young children with
dyslexia indicate that they show significantly less activation in a number of left hemisphere sites when
reading than do nonimpaired children. These areas include the inferior frontal, superior temporal,
parietotemporal, and middle‐temporal‐middle occipital gyri (Shaywitz et al., 2002). This represents a
common finding from functional brain imaging studies suggesting that a failure of proper functioning in
left hemisphere brain systems is associated with impaired reading in children with dyslexia (Xu, Yang,
Siok, & Tan, 2015). Studies of lesions of the temporoparietal areas of the brain also indicate that this
area may be critical for analysing the written word and transforming the symbol into the sounds
associated with the linguistic structure of the word (Damasio & Damasio, 1983; McCandliss, Cohen, &
Dehaene, 2003). Interestingly, brain imaging studies also suggest that individuals with dyslexia may
attempt to compensate for the lack of function in the temporo‐parietal areas of the brain by using other
brain areas to help them identify words and associate them with sounds. These compensatory effects
involve brain sites required for physically articulating a word, enabling the individual with dyslexia to
develop an awareness of the sound structure of a word by forming the word with their lips, tongue, and
vocal apparatus (Brunswick, McCrory, Price, Frith, & Frith, 1999). Compensatory effects such as this
may explain why reading performance in children with dyslexia improves with age but still fails to reach
the standard of nonimpaired children (see Figure 17.1).

Dyscalculia
Dyscalculia appears to be a specific but chronic condition, in which sufferers may perform better than
average on measures of IQ , vocabulary, and working memory but still perform significantly poorly on
tests of mathematical ability (Landerl, Bevan, & Butterworth, 2004). This problem appears to be the
result of specific disabilities in basic number processing, and can take three basic forms: (a) a problem in
the memorising and retrieval of arithmetic facts, (b) developmentally immature strategies for solving
arithmetic problems, and (c) impaired visuospatial skills resulting in errors in aligning numbers or
placing decimal points (Geary, 1993, 2004).
Dyscalculia appears to have a familial component, but as yet the underlying genetic contributors to this
are not well researched (Monuteaux, Faraone, Herzig, Navsaria, & Biedeman, 2005; Carvalho & Haase,
2019), even though abnormalities in brain function associated with dyscalculia may be partially
transmitted genetically (von Aster, Kucian, Schweiter, & Martin, 2005), and may be associated with the
genes that mediate mathematical ability generally (Plomin & Kovas, 2005). However, a number of
studies have also implicated prenatal factors such as fetal alcohol spectrum disorder (FASD) and low
birthweight (O'Malley & Nanson, 2002; Shalev, 2004). Brain functions specialising in number
processing are located in various areas of the brain, and fMRI studies have implicated abnormalities in
the left parietotemporal and inferior prefrontal cortex areas of the brain and the intraparietal sulcus in
mathematics disorder (Dehaene, Molko, Cohen, & Wilson, 2004; Molko et al., 2003). Thus, the current
evidence suggests a possible genetic or developmental cause that results in abnormalities of function in
those areas of the brain responsible for processing numbers and arithmetic calculations.

Communication disorders
Many communication disorders may be caused by organic problems relating to abnormal development
of the physical apparatus required to make and articulate sounds. For example, speech sound disorder
and stuttering can be associated with physical causes such as hearing impairment, cleft palate, cerebral
palsy, and ear, nose, and throat problems. In addition, some theories of stuttering argue that this
disorder results from problems with the physical articulation of sounds in the mouth and larynx
(Agnello, 1975). However, organic difficulties related to sound production may not represent the whole
picture. For example, there is growing evidence of a familial and genetic component to communication
disorders such as stuttering (Canhetti‐Oliveira & Richieri‐Costa, 2006; Frigerio‐Domingues & Drayna,
2017) that indicates that the heritability of stuttering may be as high as 80–85% (Ooki, 2005; Fagnani,
Fibiger, Skytthe, & Hjelmborg, 2011). There is also evidence from brain scan studies of abnormalities in
certain brain circuits that are related to stuttering. One such circuit is the basal ganglia‐thalamo‐
cortical motor circuit, which, if impaired, may affect the ability of the basal ganglia to produce timing
cues for the initiation of the next motor segment in speech (Alm, 2004). The fact that stuttering may be
a problem associated with the sequential production of sounds and words is supported by evidence
which suggests that stuttering rarely occurs in one‐word utterances and is affected by the length and
grammatical complexity of utterances (Bloodstein, 2006). Furthermore, stuttering is often a
consequence of brain injury in the basal ganglia, suggesting that it is an important area in the
production of normal speech (Tani & Sakai, 2011).
Finally, there is some evidence that the production of sounds in communication disorders may be
affected by emotional factors such as anticipatory anxiety or lack of control over emotional reactions
(Karrass et al., 2006). However, at least some researchers view this association between disorders such as
stuttering and anticipatory anxiety as secondary, and as a conditioned consequence of previous
stuttering experiences (Alm, 2004).

17.2.4 Treatment and Support for Specific Learning Problems

The inclusion of specific learning and communication difficulties in DSM over the years has been
controversial. Many view these problems as developmental ones that require attention in an educational
rather than a clinical setting, and, indeed, many learning problems and disabilities are tackled primarily
in the context of the child's educational development (Mishna, 1996). However, specific learning
difficulties are frequently associated with clinical problems such as anxiety, depression, and disruptive
behaviour, and they can create significant problems in social, educational and familial functioning that
may require referral to clinical services. Many of the treatments required by individuals with specific
learning problems can be provided by educational psychologists or speech therapists rather than clinical
psychologists, and it is not intended to cover these forms of treatment here.
In many cases, such as reading impairments, appropriate reading instruction for at‐risk younger
children can enable them to become accurate and fluent readers (Alexander & Slinger‐Constant, 2004).
However, with older individuals suffering from reading problems such as dyslexia, a common approach
in educational settings is to provide learning materials in a form that allows them to be most easily
negotiated by the dyslexic student. In addition, to compensate for the fact that the dyslexic student's
reading is less automatic and more effortful, extra time is given during assessments such as
examinations.
Treatment of communication disorders is normally the domain of speech therapists and related
disciplines, and a range of successful treatment programmes and equipment are available for problems
such as phonological disorder and stuttering (Saltuklaroglu & Kalinowski, 2005; Law, Garrett, & Nye,
2004). For example, hand‐held equipment can provide altered auditory feedback(AAF) for the
stutterer, either in terms of the delay of AAF it gives the sufferer when speaking or through a change in
frequency of the voice. Such devices appear to have success in reducing the levels of stuttering, but it is
still not fully clear by what mechanism they have this effect or whether they work equally well for
everyone with a stuttering problem (Lincoln, Packman, & Onslow, 2006; Lincoln, Packman, Onslow, &
Jones, 2010). Another successful set of techniques used to address stuttering is known as prolonged
speech. This teaches the sufferer a set of new speech patterns that result in changes in the phrasing
and articulation of speech and of the respiratory patterns produced by stutterers while speaking
(Packman, Onslow, & van Doorn, 1994). The success rates of treatments for stuttering are particularly
high and estimated to be around 60–80%, but this may at least in part be confounded by the fact that
much childhood stuttering will usually spontaneously remit after a few years (Saltuklaroglu &
Kalinowski, 2005).

altered auditory feedback (AAF) A form of treatment for stuttering in which delayed
auditory feedback or a change in frequency of the voice is given to clients when they are
speaking.
SELF‐TEST QUESTIONS
What are the defining characteristics of specific learning disorder as a diagnostic category?
What are the individual skills that may be impaired in dyscalculia?
What are the main characteristics of language disorder, speech sound disorder, and
childhood‐onset fluency disorder?
What is the evidence that dyslexia is an inherited disorder?
Can you describe the phonological theory of dyslexia?
What areas of the brain appear to be most affected in dyslexia?
What is the evidence that communication disorders might be associated with physical
rather than psychological causes?
Can you describe treatments for stuttering such as AAF and prolonged speech?

SECTION SUMMARY

17.2 SPECIFIC LEARNING PROBLEMS

Specific learning disorder refers to a range of disabilities that affect performance on tests of
academic ability such as reading, mathematics, or written expression.
Dyslexia is a learning disability associated with difficulty in recognising words, poor spelling,
and difficulty with written expression.
Dyscalculia is a disability that affects mathematical or arithmetic ability.
Communication disorders include impairments in language, speech, and communication.
Language disorder is a disability concerned with problems in vocabulary comprehension and
production.
Speech and sound disorder is a disability associated with difficulty in speech sound production.
Childhood‐onset fluency disorder is sometimes known as ‘stuttering’ and involves a problem with
the fluency and time‐patterning of speech.
Disorders of reading, such as dyslexia, are known to have an important genetic component
and are associated with brain abnormalities in the temporoparietal areas.
Dyslexia appears to be associated with difficulties differentiating the elements of speech
and associating these sounds with the letters in a written word (the phonological theory).
Treatment for specific learning disabilities often occurs in an educational rather than a
clinical setting.
17.2.5 Summary of Specific Learning Problems
In this section we have reviewed the characteristics, aetiology and general treatment of a number of
specific learning problems. These are largely problems associated with reading, writing, and
communication generally, and the most well known of these problems is the reading difficulty known as
dyslexia. While many of these problems will require attention in educational rather than clinical
settings, they may come to the attention of clinical psychologists because they may often become
associated with mental health problems and cause significant disruption to social, familial, and
educational functioning.

17.3 INTELLECTUAL DISABILITIES

17.3.1 DSM‐5 Diagnostic Criteria for Intellectual Disability

Intellectual disability is a condition with onset during the individual's developmental period (usually up
to age 18 years) that covers impairment in both intellectual and adaptive functioning. DSM‐5 defines
intellectual ability according to three primary criteria. They are (a) significantly below average
intellectual functioning in areas such as reasoning, problem solving, abstract thinking, planning, and
learning generally; and this below normal intellectual functioning is defined by scores on IQ tests
approximately 2 standard deviations below the population mean (i.e., an IQ <70 on IQ tests with a
mean of 100 and a standard deviation of 15), (b) impairments in adaptive functioning generally (e.g., an
inability to master social or educational skills that would be expected for the individual's chronological
age), and (c) these deficits should be manifest during the individual's developmental period (i.e.,
normally, up to 18 years of age) (Table 17.6). DSM‐5 makes it clear that a good deal of clinical
judgment is required when diagnosing intellectual disability. It should take into account whether the
individual meets community and cultural standards of independence and social responsibility, and IQ
test scores should be interpreted cautiously depending on whether the instrument is culturally relevant,
based on up‐to‐date norms, and takes into account any sensory or motor disabilities the individual may
possess.

intellectual disability A modern term replacing mental retardation to describe the more
severe and general learning disabilities.

TABLE 17.6 Summary: DSM‐5 Diagnostic Criteria for Intellectual Disability

Deficits in intellectual functions as confirmed by clinical assessment and standard intelligence tests
Deficits in adaptive functioning resulting in an inability to meet development and sociocultural
standards for personal independence and social responsibility
Symptoms start in developmental period
DSM‐5 also allows intellectual disability to be specified according to its severity into mild, moderate,
severe, and profound, with mild being the least disabling where sufferers may only be mildly cognitively
impaired, socially ‘immature’ rather than impaired, and may be able to deal with daily living tasks given
appropriate support. In the case of profound severity the individual may have little understanding of
symbolic communication and is dependent on others for all aspects of daily care, their health, and their
safety. Clinicians assessing individuals with intellectual disabilities would also gather information about
disabilities from other reliable independent sources, such as teachers and medical doctors.
17.3.2 Alternative Approaches to Defining Intellectual Disability
Rather than simply taking a negative approach to diagnosis and focusing on an individual's limitations,
impairments, and deficits, other views attempt to highlight those factors that might be required to
facilitate better intellectual and adaptive functioning in the individual. People with intellectual
disabilities differ significantly in the severity of their disabilities, with some able to function almost
without notice in everyday life, while others may require constant supervision and sheltered
environments in which to live. Similarly, individuals also differ significantly in their personalities. Some
will be passive, placid and dependent, while others may be aggressive and impulsive. These kinds of
issues mean that each individual with an intellectual disability is likely to differ in terms of both their
level of functioning and what is required to achieve any form of adaptive functioning. In this sense, the
notion of ‘intellectual disability’ is more of a social construction than a diagnostic category (a term that
is a product of particular historical and cultural conditions rather than medical or psychological science)
(Webb & Whitaker, 2012).
The American Association on Intellectual & Developmental Disabilities (AAIDD) has promoted a more
individualised assessment of a person's skills and needs rather than an approach based solely on
categorising intellectual and adaptive impairments. This approach emphasises that individuals have
both strengths and limitations and that an individual's limitations need to be described in a way that
enables suitable support to be developed. So, rather than simply forcing the individual into a diagnostic
category, this approach evaluates the specific needs of the individual and then suggests strategies,
services, and supports that will optimise individual functioning. Supports are defined as ‘the resources
and individual strategies necessary to promote the development, education, interests, and personal well‐
being of a person with intellectual disabilities’. Supports can be provided wherever necessary by parents,
friends, teachers, psychologists, doctors, and GPs or any other appropriate person or agency. People
with intellectual disabilities frequently face major stigma and prejudice, and they are often confronted
with significant barriers to realising their own potential, but approaches such as that advocated by the
AAIDD are designed to enable individuals with intellectual disabilities to achieve their potential. In the
UK, the Special Education Needs & Disability Act of 2001 extended the rights of individuals with
intellectual disabilities to be educated in mainstream schools, and schools are required to draw up
accessibility strategies to facilitate the inclusion of pupils with intellectual disabilities and to make
reasonable adjustments so that they are not disadvantaged. As a result of such changes in attitude,
support, and legislation, more than half of those people with intellectual disabilities in the UK now live
with their parents or carers.

accessibility strategies Programmes that extend the rights of individuals with intellectual
disabilities to be educated according to their needs in mainstream schools.

17.3.3 The Prevalence of Intellectual Disabilities

Estimates of the prevalence levels of intellectual disabilities will depend very much on how intellectual
disabilities are defined. DSM‐5 estimates the prevalence rate of a diagnosis of intellectual disability at
around 1%, and prevalence for severe intellectual disability at around 6 in 1,000. The World Health
Organization estimates that 1–3% of the global population has an intellectual disability—as many as
200 million people, with the highest prevalence rates found in the lowest income countries. Currently,
there are estimated to be around 1.5 million people in the UK with a learning disability (Office for
National Statistics, 2019), which is a prevalence rate of around 2.1% of adults. There are also around
325,000 children and adolescents (aged 0–17 years) with a learning disability in the UK. However, a
study looking specifically at the prevalence rate of IQ scores less than 70 in the UK suggested that
prevalence of such low IQ scores may be as high as between 5 and 10% in school children aged 13–15
years. Further analysis suggested that only around 15% of those with IQ scores <70 were already in
receipt of a statement of special educational needs (SENs) (Simonoff et al., 2006). The implications of
this are that the majority of the group with low IQ either did not need educational support or were as
yet unrecognised as in need of support.

17.3.4 The Aetiology of Intellectual Disability

First and foremost, the causes of intellectual disability in individual cases are often extremely difficult to
isolate and identify. Even when the cause of disability can be identified (such as a chromosomal
disorder) two individuals identified with the same cause may exhibit quite different levels of disability.
Differential diagnosis is also quite problematic, in many cases it is unclear whether an individual has a
specific learning disability, has more general intellectual impairments, is affected by a more severe form
of ASD (see Section 17.4), or has psychological or emotional problems. As we shall see in the following
sections, the major causes of intellectual disability are biological in nature, and over 1,000 forms of
impairment based on genetic, chromosomal, or metabolic abnormalities have been identified (Dykens &
Hodapp, 2001). However, many researchers believe that an individual's resultant intellectual disability is
also influenced considerably by environmental factors. For example, mild or moderate intellectual
disability tends to occur more frequently in lower socio‐economic groups, indicating that poverty and
associated deprivation may retard intellectual development. One example of this is the case of teenage
mothers who choose to rear their children. They more often live in poor environments, are more likely
to expose their children to alcohol and poor nutrition, and are less likely to provide sensitive parenting
(Brooks‐Gunn & Chase‐Lansdale, 1995; Borkowski et al., 1992). As a result, mild to moderate
intellectual disability is found significantly more frequently in children of teenage mothers than in the
children of older mothers (Broman, Nichols, Shaughnessy, & Kennedy, 1987). Subsequent analyses have
indicated that the offspring of teenage mothers have an average IQ score 3 points lower than offspring
born to mothers over 20 years of age. Even when adjustment is made for parental socio‐economic
status, maternal IQ , maternal smoking, and binge drinking in pregnancy, birthweight, and parenting
style, this effect is still significant (Khatun et al., 2017), suggesting that public policy initiative could be
targeted at delaying childbearing beyond teenage years or supporting the early lives of children born to
teenage mothers.
In the following section, we look first at the known biological causes of intellectual disability, followed by
some of the environmental factors thought to be involved. Table 17.7 provides a summary of some of
the known causes of intellectual disabilities categorised by the developmental period when they have
their effect.
TABLE 17.7 Causes of Intellectual Disability
Developmental Cause or risk factor
period
Before/during Inherited recessive gene disorders (e.g., phenylketonuria, Tay‐Sachs disease)
conception Chromosome abnormalities (e.g., Down syndrome, fragile X syndrome)
During pregnancy Severe maternal malnutrition
Maternal iodine deficiency
Maternal infections (e.g., rubella, syphilis, HIV, Herpes Simplex)
Maternal drug abuse (e.g., alcoholism, tobacco abuse, illegal drug abuse)
Maternal medications (e.g., cancer chemotherapy)
During birth Anoxia and hypoxia (oxygen starvation or insufficient oxygen supply)
Low birthweight
Brain infections (e.g., encephalitis, meningitis)
Early childhood Childhood malnutrition
Severe head injury (e.g., physical accidents, physical abuse such as shaken
baby syndrome)
Exposure to toxins (e.g., lead, mercury)
Social deprivation and poverty (e.g., poor parenting, unstimulating infant
environment)

Biological causes
Biological factors represent the largest known group of causes of intellectual disabilities, and we will
divide these into three main categories: (a) chromosomal disorders, (b) metabolic causes, and (c)
perinatal causes.

Chromosomal disorders
For many years now, it has been known that forms of intellectual disability are genetically linked to
abnormalities in the X chromosome (the chromosome that also determines biological sex), and these
abnormalities will often manifest as physical weaknesses in the chromosomes or abnormalities resulting
from irregular cell division during the mother's pregnancy. Chromosomal abnormalities occur in around
5% of all pregnancies, and the majority usually end in spontaneous miscarriages. However, it is
estimated that 0.5% of all newborn babies have a chromosomal disorder, but many of these die soon
after birth (Smith, Bierman, & Robinson, 1978). Chromosomal disorders account for around 25–30%
of all diagnosed cases of intellectual disability and the two most prominent forms are Down syndrome
and fragile X syndrome.
PHOTO 17.2 The typical facial features of children born with Down syndrome or fragile X syndrome. Individuals with
Down syndrome almost always possess an extra chromosome in pair 21, while in fragile X syndrome the X chromosome
shows physical weaknesses and may be bent or broken.
Down syndrome was first described by British doctor Langdon Down in 1866. However, it was not
until 1959 that French geneticist Jerome Lejeune first reported that individuals with Down syndrome
almost always possess an extra chromosome in pair 21 which is usually caused by errors in cell division
in the mother's womb (also known as Down syndrome trisomy 21) (Photo 17.2). Down syndrome
occurs in around 1.5 of every 1,000 births (a prevalence rate of 0.15%) (Simonoff, Bolton, & Rutter,
1996)—although this may vary from country to country. An estimated 37,000 people in the UK had
Down syndrome in 2011(a prevalence rate of 0.66 per 1,000 people, Wu & Morris, 2013). Risk is
related to the age of the mother, and for women aged 20–24 years the risk is 0.07%, and this rises to
1.1% for women aged 40 years, and up to 3.3% in women aged over 45 years (Morris, Wald, Mutton, &
Alberman, 2003). Although this link between maternal age and incidence of Down syndrome has been
known for some time, it is still unclear how maternal age contributes to the chromosomal abnormalities.
However, recent animal studies suggest that as a mother ages she will have lower amounts of the
proteins cohesin and securin in her eggs, and these proteins help to keep chromosomes together at
their centres. Lower levels of these proteins therefore lead to instability in chromosome pairs and the
possibility that chromosome division will happen unevenly (Nabti, Grimes, Sarna, Marangos, & Carroll,
2017).

Down syndrome A disorder caused by the presence of an extra chromosome in pair 21 and
characterised by intellectual disability and distinguishing physical features.

The majority of individuals with Down syndrome have moderate to severe intellectual impairment with
a measurable IQ usually between 35 and 55. They also have distinctive physical appearance with eyes
that slant upward and outward with an extra fold of skin that appears to exaggerate the slant. They are
usually shorter and stockier than average, with broad hands and short fingers. They may also have a
larger than normal furrowed tongue that makes it difficult for them to pronounce words easily. They
also suffer physical disability such as heart problems, and appear to age rapidly with mortality high after
40 years of age. Aging is also closely associated with signs of dementia similar to Alzheimer's disease (see
Chapter 15), and this may be a result of the causes of both disorders being closely located on
chromosome 21 (Zigman, Schupf, Sersen, & Silverman, 1995; Selkoe, 1991). Down syndrome can be
identified prenatally in high‐risk parents by using a procedure known as amniocentesis which involves
extracting and analysing the pregnant mother's amniotic fluid. It is a routine procedure for pregnant
mothers that is carried out after week 15 of pregnancy. It is frequently recommended for mothers over
the age of 35 years, and the results of this process can leave prospective parents with difficult decisions
about whether to maintain a pregnancy or not.

amniocentesis A procedure which involves extracting and analysing the pregnant mother’s
amniotic fluid used prenatally in identifying Down syndrome in high-risk parents.

Another important chromosomal abnormality that causes intellectual disability is known as fragile X
syndrome. This is where the X chromosome appears to show physical weaknesses and may be bent or
broken, and fragile X syndrome occurs in approximately 1 in 4000 males and 1 in 8000 females
(Hagerman & Lampe, 1999). Individuals with fragile X syndrome possess mild to moderate levels of
intellectual disability and may also exhibit language impairment and behavioural problems such as
mood irregularities (Eliez & Feinstein, 2001; Zigler & Hodapp, 1991). Like individuals with Down
syndrome, they also have specific physical characteristics, such as elongated faces and large, prominent
ears (see Photo 17.2). Studies suggest there may be a syndrome of fragile X chromosome in which
different individuals manifest rather different symptoms and degrees of disability (Hagerman, 1995). For
example, some may have normal IQ levels but suffer specific learning disabilities. Others may exhibit
emotional lability and symptoms characteristic of autism such as hand‐biting, limited speech and poor
eye contact (Dykens, Leckman, Paul, & Watson, 1988), and around one in three will exhibit symptoms
of ASD (Hagerman, 2006). Intellectual impairment will usually be greatest in males suffering fragile X
syndrome because they only have one X chromosome. Because females possess two X chromosomes the
risk of intellectual disability is less (Sherman, 1996).

fragile X syndrome A chromosomal abnormality that causes intellectual disability where the
X chromosome appears to show physical weaknesses and may be bent or broken.

Metabolic disorders
Metabolic disorders occur when the body's ability to produce or break down chemicals is impaired.
There are many different types of metabolic disorders and many can affect intellectual ability. Such
disorders are often caused by genetic factors and may be carried by a recessive gene. When both
parents possess the defective recessive gene, then their offspring are in danger of developing the
metabolic disturbances linked to that gene. We provide examples of two such genetically determined
metabolic disorders that affect intellectual ability. These are phenylketonuria (PKU) and Tay‐Sachs
syndrome.

recessive gene A gene that must be present on both chromosomes in a pair to show outward
signs of a certain characteristic.

Phenylketonuria (PKU) is caused by a deficiency of the liver enzyme phenylalanine 4‐hydroxylase

which is necessary for the effective metabolism of the amino acid phenylalanine. As a result of this
deficit, phenylalanine and its derivative phenylpyruvic acid build up in the body and irreparably
damage the brain and central nervous system by preventing effective myelination of neurons
(myelination is the development of a protective sheath around the axons of neurons that enables
effective transmission between nerve cells). This results in severe intellectual disability and hyperactivity.
In Europe generally PKU has an incidence of around 1 in 10,000 live births (van Wegberg et al., 2017),
and it is carried on the Phenylalanine hydroxylase gene (PAH) on chromosome 12 (Doss &
Sethumadhavan, 2009). Several hundred mutations of this gene have been identified, but just five
account for approximately 60% of PKU cases in European populations. It is estimated that as many as
1 in 70 people may be carriers of the recessive gene responsible for PKU. At risk parents who may carry
the gene are now routinely given blood tests to determine the risk of having a child with PKU. Diet is
also an important factor in controlling intellectual deficits in foetuses and offspring at risk of PKU. A
special diet low in phenylalanine is recommended for at‐risk pregnant mothers, and if children with
PKU are given diets low in phenylalanine from birth to at least 6 years of age, this can minimise
neurological damage and intellectual deficit (Mazzoco et al., 1994).

Phenylketonuria (PKU) A metabolic disorder caused by a deficiency of the liver enzyme

phenylalanine 4‐hydroxylase, which is necessary for the effective metabolism of the amino acid
phenylalanine.

Tay‐Sachs disease is also a metabolic disorder caused by a recessive gene (often found in children of
Eastern European Jewish ancestry). The defective gene results in an absence of the enzyme
hexosominidase A in the brain and central nervous system and this eventually causes neurones to die.
The disorder is degenerative, with infants of around 5 months showing an exaggerated startle response
and poor motor development. Only around 17% of sufferers live beyond 4 years of age (Sloan, 1991)
but those that do show rapid decline in cognitive, motor, and verbal skills. The disorder is relatively rare,
occurring in around 1 in 360,000 live births worldwide, and this rate is being significantly reduced by
effective screening.

Tay–Sachs disease A metabolic disorder caused by a recessive gene which results in an

absence of the enzyme hexosominidase A in the brain and central nervous system, eventually
causing neurons to die.

Perinatal causes
From conception to the early postnatal period is a dangerous time for an organism that is developing as
rapidly as a human baby. Because of this, there are considerable prenatal and immediately post‐natal
factors that put normal development at risk and may cause lifelong intellectual disability. One type of
risk involves those factors that can adversely affect the foetus's interuterine environment and its food
supply. These include factors such as maternal infections, substance abuse, or malnutrition. Disorders
acquired during prenatal development are known as congenital disorders because they are acquired
prior to birth but are not genetically inherited.

congenital disorders Disorders acquired during prenatal development prior to birth but
which are not genetically inherited.

Maternal diet is one example. For instance, if there is too little iodine in the mother's diet during
pregnancy this can give rise to the condition known as cretinism. The mother's iodine deficiency may
often be caused by a hormonal imbalance called thyroxine deficiency. Children suffering from this
disorder show slow development, intellectual disabilities, and often have a small stature. Thankfully the
condition is relatively rare nowadays because of the availability of iodised table salt and the fact that
most diets now contain sufficient iodine. Similarly, mineral and vitamin deficiencies caused by
maternal malnutrition during pregnancy can also result in intellectual disability and significantly
affect the child's physical and behavioural development (Barrett & Frank, 1987). However, the adverse
effects of maternal malnutrition can often be partially rectified by providing newborn infants with
intellectually supportive environments and appropriate food supplements (Zeskind & Ramsay, 1981;
Super, Herrera, & Mora, 1990). In most Westernised societies maternal malnutrition is relatively rare,
but when it does occur it probably occurs in conjunction with other factors likely to harm the child's
intellectual and physical development, such as maternal drug or alcohol addiction, low socio‐economic
status, and possibly maternal HIV or syphilis infection (see below).

cretinism A congenital disorder resulting in slow development, intellectual disabilities and

small stature.

maternal malnutrition During pregnancy maternal malnutrition can cause intellectual

disability and affect a child’s physical and behavioural development

Maternal infectious diseases during pregnancy are another potential cause of intellectual disability in
the offspring. Such diseases are most damaging during the first trimester of pregnancy when the foetus
has little or no immunological protection. Common maternal diseases that can cause intellectual
impairment in the offspring include rubella (German measles), syphilis and HIV amongst others. If a
mother contracts rubella during the first 10 weeks of pregnancy, there is almost a 90% chance that the
baby will develop congenital rubella syndrome(CRS) resulting in abortion, miscarriage, stillbirth,
or severe birth defects. Up to 20% of babies born live will have CRS causing heart disease, deafness,
and intellectual impairment. The incidence of rubella infections during pregnancy in the UK between
2003 and 2016 was 0.23 infections per 100,000 pregnancies, and 16% of these infections led to CRS in
the infant (Bukasa et al., 2018).

congenital rubella syndrome (CRS) The constellation of abnormalities caused by

infection with the rubella (German measles) virus before birth. The syndrome is characterised
by multiple congenital malformations (birth defects) and intellectual disability.

In contrast, maternal HIV infection became an important cause of intellectual disability in the
1980s and 1990s. If the mother is not being treated for HIV during pregnancy there is a likelihood that
the infection will be passed on to the foetus. The infection can also be passed on through breastfeeding.
There is then almost a 50% chance that the newborn child will develop moderate to severe
neurodevelopmental and intellectual disabilities (Knox et al., 2018). However, in utero transmission of
HIV can be reduced from 25 to 8% if the mother is given an antiretroviral drug such as zidovudine
during pregnancy and if the newborn child then receives the drug for up to 6 weeks postnatally (Belfer
& Munir, 1997).

maternal HIV infection The incidence of a mother having HIV during pregnancy, leading
to a likelihood that the infection will be passed on to the fetus.

A further significant cause of intellectual disability is maternal drug use during pregnancy. In many
cases the drugs responsible for offspring intellectual disability may be ones taken for medicinal purposes
(such as drugs taken during cancer chemotherapy treatment), but most other cases occur where the
mother is a substance abuser. For instance, US studies indicated that 18% of pregnant women smoke
tobacco, 9.8% drink alcohol, and 4% use illegal drugs (Jones, 2006). Fetal alcohol syndrome(FAS) is
one such example of maternal drug abuse causing childhood intellectual disabilities. Whenever a
pregnant mother drinks alcohol this will enter the foetus's bloodstream and slow down its metabolism
and affect development. If this occurs on a regular basis, then development of the foetus will be severely
impaired. Children suffering FAS will usually have lower birthweight, lower IQ (between 40 and 80) and
suffer motor impairments and deficits in attention and working memory (Niccols, 1994; Burden,
Jacobson, Sokol, & Jacobson, 2005). They will also frequently exhibit distinctive facial characteristics
including slit eyes, short noses, drooping eyelids and thin upper lips. In the UK around 1 in every 6–
7,000 babies born have FAS (National Organisation on Fetal Alcohol Syndrome, 2012). Recently,
attention has also been focussed on the intellectual and developmental effects on children of illegal
drugs use by pregnant mothers. Use of both cocaine and crack cocaine (see Chapter 9) by a pregnant
mother can lead to babies being physically addicted to the drug before birth (known as ‘crack
babies’). There is some evidence that this can adversely affect physical development and brain
development in particular (Hadeed & Siegel, 1989) and result in slow language development (van Baar,
1990). However, it is clear that maternal drug‐taking while pregnant may often occur in contexts that
may also contribute to poor intellectual development in the offspring, and these may include the abuse
of other drugs, pregnancy deprivations (such as dietary imbalances), and economic and social
deprivation (Vidaeff & Mastrobattisa, 2003). As such, this makes it difficult to assess the specific effect of
maternal cocaine use on offspring intellectual development (Jones, 2006).
One final example of a perinatal cause of intellectual disability is anoxia, which is a significant period
without oxygen occurring during or immediately after delivery. Lack of oxygen to the brain during the
birth process can damage parts of the brain that are yet to develop, and as a result can cause both
physical and intellectual impairment (Erickson, 1992). The main neurological birth syndrome caused by
anoxia is cerebral palsy which is characterised by motor symptoms that affect the strength and
coordination of movement. While the primary disabilities are mainly physical, around one third of
those suffering from cerebral palsy will also suffer some form of intellectual, cognitive, or emotional
disability as well.

anoxia A perinatal cause of intellectual disability, being a significant period without oxygen
that occurs during or immediately after delivery.

cerebral palsy The main neurological birth syndrome caused by anoxia which is
characterised by motor symptoms that affect the strength and coordination of movement.

Childhood causes
Although a child may be born healthy, there are potentially a number of early childhood factors that
might put the child at risk of intellectual disability. Very often these factors may operate in conjunction
with other causes such as perinatal problems. We will look briefly at four groups of potential childhood
causes of intellectual disability, namely accidents and injury, exposure to toxins, childhood infections,
and poverty and deprivation.
During their early developmental years, young children will often be involved in accidents, and these
can often be severe enough to cause irreversible physical damage and intellectual impairment (Ewing‐
Cobbs et al., 2006). Common childhood accidents that may cause permanent intellectual disability
include falls, car accidents, near drownings, suffocation, and poisoning. However, at least some of the
injuries that cause intellectual disability in children may not be genuine accidents but may be the result
of physical abuse by others. A retrospective study of head injuries in children aged between 1 and 6
years of age estimated that 81% of cases could be defined as accidents and 19% as definite cases of
abuse (Reece & Sege, 2000). One form of child abuse that is known to cause intellectual disability is
known as shaken baby syndrome. This refers to traumatic brain injury that occurs when a baby is
violently shaken. In comparison to babies who receive accidental traumatic brain injury, shaken baby
injuries have a much worse prognosis, including retinal haemorrhaging that is likely to cause blindness
and an increased risk of mental disability such as cerebral palsy or intellectual impairment (Lind,
Laurent‐Vannier, Toure, Brugel, & Chevignard, 2013). Nevertheless, we must remain cautious about the
degree to which shaken baby syndrome may contribute to intellectual disability because of controversies
over how the syndrome should be diagnosed (e.g., Kumar, 2005).

shaken baby syndrome A form of child abuse that is known to cause intellectual disability. It
refers to traumatic brain injury that occurs when a baby is violently shaken.

During early development children may also be exposed to toxins that can cause neurological damage
resulting in intellectual impairment. One such toxin is lead, which is still frequently found in the
pollution from vehicles that that burn leaded petrol. Lead‐based paint is also found in older properties,
and so may well be a risk factor in children living in deprived, low socio‐economic areas. Lead causes
neurological damage by accumulating in body tissue and interfering with brain and central nervous
system metabolism. Children exposed to high levels of lead have been found to exhibit deficits in IQ
scores of up to 10 points (Dietrich, Berger, Succop, Hammond, & Bomschein, 1993). Even in
Westernised societies aware of the risks associated with exposure to lead the prevalence of lead
poisoning in children aged 1–2 years is still as high as 1% (Ossiander, Mueller, & van Enwyk, 2005).
Prevalence rates are significantly higher than this is developing countries (Sun, Zhao, Li, & Cheng,
2004).
There is evidence to suggest that social deprivation and poverty can themselves contribute to
intellectual disability. Although such factors may not directly cause impairment to the biological
substrates underlying intellectual ability, they may contribute a form of intellectual impoverishment that
can be measured in terms of lowered IQ scores (Garber & McInerney, 1982; Farah, 2017). Social
deprivation and poverty are also inextricably linked to other risk factors for intellectual disability,
including poor infant diet, exposure to toxins (such as lead paint in old or run‐down housing), maternal
drug‐taking and alcoholism, and childhood physical abuse. A cycle of deprivation, poverty, and
intellectual disability is established when young adolescents in deprived environments themselves give
birth to children while still teenagers (Wildsmith, Manlove, Jekielek, Moore, & Mincieli, 2012). Such
teenage mothers are frequently found to live in deprived areas, are often unmarried, live in poverty as a
result of their premature motherhood, and have a significantly lower than average IQ themselves
(Carnegie Corporation of New York, 1994; Borkowski et al., 1992). Studies have shown that teenage
mothers are significantly more likely to punish their children than praise them and are significantly less
sensitive to their children's needs than older mothers (Borkowski et al., 1992; Brooks‐Gunn & Chase‐
Lansdale, 1995). As a result, children born to teenage mothers are at increased risk of problematic
parent‐child interactions, (Leadbeater, Bishop, & Raver, 1996), behavioural difficulties (Fergusson &
Lynskey, 1993), and cognitive disadvantage and educational underachievement (Fergusson &
Woodward, 1999; Brooks‐Gunn, Guo, & Fustenberg, 1993). Consequently, mild intellectual disability is
reckoned to occur three times more frequently in the children of teenage mothers (Borkowski et al.,
1992; Broman et al., 1987). As we said earlier, it is difficult to estimate solely how much this is due to the
teenage mother's age and her parenting practices, because the child of a teenage mother is significantly
more likely to be raised in the kinds of deprived environments that contain many other risk factors for
intellectual disability.

teenage mothers In relation to intellectual disabilities, young mothers who become pregnant
before 18 years of age, and who are likely to have lived in deprived areas prior to giving birth,
are often unmarried, live in poverty as a result of their premature motherhood, and are likely to
have a significantly lower than average IQ.

Finally, one important feature of deprived environments is that they will usually provide significantly
decreased levels of stimulation for young children, including lower rates of sensory and educational
stimulation, lack of one‐to‐one child‐parent experiences, and poverty of verbal communication—all
factors that are thought to be associated with poor intellectual development. However, there are some
views that claim that lack of stimulation can have a direct effect on the early physical development of the
brain and so result in permanent impairments to brain functioning. For instance, neural development of
the brain occurs most extensively and rapidly in the first year after birth (Kolb, 1989), and a rich,
stimulating environment is necessary for full development of the brain's structure (Nelson & Bosquet,
2000). Alternatively, an unstimulating, stressful environment can actually trigger the secretion of
hormones that prevent effective brain development (Gunnar, 1998). In a study comparing children
brought up in deprived inner city areas with a group exposed to good nutrition and provided with a
stimulating environment, Campbell & Ramsey (1994) found that by 12 years of age the deprivation
experienced by the former group had a significant negative effect on brain functioning.

Summary of the aetiology of intellectual disability

From the material covered in this section, you can see that the causes of intellectual disability are
diverse. As we mentioned earlier, very often it is impossible to pinpoint the specific cause of an
individual's intellectual disability, but intellectual disability caused by chromosomal disorders (such as
Down syndrome and fragile X syndrome) and inherited metabolic disorders are some of the more easily
identified. Individuals are most at risk of developing permanent intellectual disabilities during early
development of their central nervous system, which is why conditions in the uterus and in the
immediate postnatal period are critical for normal development. Risk factors that can disrupt normal
prenatal development of the brain and central nervous system include maternal infections, alcoholism,
drug abuse, and malnutrition. Early childhood factors that can affect normal neurological development
include accidents, physical abuse, exposure to toxins, infectious illnesses, and an early childhood spent in
deprivation and poverty. As we have mentioned many times in this section, many of these risk factors
may operate concurrently to determine levels of intellectual disability.

17.3.5 Support and Interventions for Intellectual Disabilities

Most forms of intellectual disability impose limitations on that individual's ability to function fully and
actively in society. This means that—depending on the severity of the disability—the individual will
need support to cope with many of the rigours of everyday living. As a result of the disability, sufferers
are at risk of underachieving in many areas of their life, including educationally, occupationally,
economically, and socially. In most societies, the days when people with intellectual disabilities were
simply institutionalised and provided with little more than custodial care are now gone (see Chapter 1,
Section 1.1.3), and provision for such people not only attempts to address their needs but also recognises
their fundamental rights as human beings and citizens who have a right to an inclusive lifestyle. Thus,
support and intervention for intellectual disabilities has a number of diverse aims. At the primary level
there are those interventions aimed at preventing intellectual disability in the first place by educating
potential parents about the risk factors for intellectual disability (e.g., educating parents about the effects
of maternal alcohol and drug abuse during pregnancy). A second broad aim of interventions is to make
available training programmes that will provide the sufferer with enough basic skills to cope with many
of the challenges of everyday life (e.g., self‐help skills, communication skills, etc.). Third, approaches to
helping those with intellectual disabilities are based on the principle of inclusion in an attempt to help
such individuals achieve their potential. For example, in many countries, education services are now
required to draw up accessibility strategies to allow pupils with intellectual disabilities to engage in the
educational process without being disadvantaged. Similarly, social inclusion is also encouraged to
provide those with intellectual disabilities the opportunity for personal, social, emotion, and sexual
development. We now discuss each of these three types of approach to support and intervention in
more detail.

inclusion Strategies intended to teach high‐functioning individuals self‐help strategies, social

and living skills, and selfmanagement that are designed to help the individual function more
effectively in society.
Prevention strategies
In Table 17.7 we have listed many of the causes and risk factors for intellectual disability, and you can
probably glean from this list that many of the causes are ones that are potentially preventable. This is
particularly the case with many perinatal causes, and especially those involving maternal factors during
pregnancy. For example, fetal alcohol syndrome (FAS) is a significant cause of intellectual disability, and
prevention programmes aim to identify those women at risk of alcohol abuse during pregnancy and to
provide interventions or alcohol‐reduction counselling (Floyd, O'Connor, Bertrand, & Sokol, 2006;
Lange, Rovet, Rehm, & Popova, 2017). Recognising those at risk can be achieved by using established
diagnostic and screening questionnaires (Ismail, Buckley, Budacki, Jabbar, & Gallicano, 2010) and
interventions include providing feedback on rates of drinking behaviour during pregnancy, discussing
strategies for avoiding alcohol cravings and binge drinking sessions, and more recently, web‐based
interventions (Tenkku et al., 2011). Controlled comparison studies suggest that such screening and
intervention methods significantly reduce the risk for alcohol‐exposed pregnancies compared with
nonintervention control participants (Ingersoll et al., 2005).
Prevention can also be achieved in a number of other ways. For example, genetic analysis and
counselling enables those parents at risk of abnormal births to be identified, informed of the risk, and
counselled about how to proceed. Blood tests and tests of amniotic fluid such as amniocentesis enable
parents to be informed of risks for a range of potential disorders, including Down syndrome, Tay‐Sachs
disease, phenylketonuria, and intellectual disability caused by CRS. In addition, those disabilities related
to dietary irregularities can also be identified and treated, and these include providing at‐risk pregnant
mothers with iodine supplements to prevent cretinism and providing diets low in phenylalanine for
pregnant mothers and offspring at risk of phenyketonuria.
Finally, as we saw earlier, conditions associated with poverty and social deprivation also put children at
risk of educational underachievement, lower than average IQ , and mild intellectual disability, and
support programmes in countries such as the US and Europe have been developed to try to counteract
this risk factor. For example, family support programmes in the US have indicated that mothers of low
socio‐economic status participating in such schemes are more affectionate and positive with their
children and provide more stimulating environments than mothers who are not in such schemes
(Johnson, Walker, & Rodriguez, 1996). Being a teenage mother is also a risk factor for raising children of
lower IQ than average, and this factor can be tackled in a number of ways, including providing teenage
girls with advice on and access to contraception, improving teenage mothers' access to education
(Department for Children, Schools & Families, 2010), improving housing quality, and encouraging the
presence of a co‐residential partner rather than raising a child alone (Berrington et al., 2004).

Training procedures
The quality of life of people with intellectual disabilities can be improved significantly with the help of
basic training procedures that will equip them with a range of skills depending on their level of
disability. Types of skills include self‐help and adaptive skills (such as toileting, feeding, and dressing),
language and communication skills (including speech, comprehension, sign language), leisure and
recreational skills (such as playing games, cooking skills), basic daily living skills (using a telephone,
handling money), and controlling anger outbursts and aggressive and challenging behaviour (reducing
the tendency to communicate through aggressive or challenging behaviours such as pushing or
shouting). Training methods can also be used in more severe cases to control life‐threatening behaviours
such as self‐mutilation or head‐banging.
Behavioural techniques that adopt basic principles of operant and classical conditioning are used
extensively in these contexts, and the application of learning theory to training in these areas is also
known as applied behaviour analysis (Davey, 1998; Cooper, 2019). Basic techniques that are used
include operant reinforcement (rewarding correct responses—for example, with attention or praise),
response shaping (breaking down complex behaviours into small achievable steps and then rewarding
each step successively), errorless learning (breaking down a behaviour to be learned into simple
components that can be learned without making errors—errorless learning is stronger and more
durable than learning with errors), imitation learning (where the trainer demonstrates a response for the
client to imitate), chaining (training the individual on the final components of a task first, and then
working backwards to learn the earlier steps), and self‐instructional training (teaching the client to guide
themselves through a task by verbally instructing themselves what to do at each step). Very often,
inappropriate, life‐threatening or challenging behaviours may be inadvertently maintained by
reinforcement from others in the environment (e.g., self‐mutilating behaviour may be maintained by the
attention it attracts from family or care staff). In these cases, a functional analysis can be carried out in
order to help identify the factors maintaining the behaviour, and this is done by keeping a record of the
frequency of the behaviours and noting the antecedents and consequences of the behaviour. Once it is
known what consequences might be maintaining the behaviour, these can be addressed to prevent the
behaviour being reinforced (Mazaleski, Iwata, Vollmer, Zarcone, & Smith, 1993; Wacker et al., 1990)
(Treatment in Practice Box 17.1).

applied behaviour analysis Applying the principles of learning theory (particularly operant
conditioning) to the assessment and treatment of individuals suffering psychopathology.
CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE BOX
17.1 A FUNCTIONAL ANALYSIS OF CHALLENGING
BEHAVIOUR

Some individuals with intellectual disabilities typically display behaviour that may put
themselves or others at risk, or which may prevent the use of community facilities or prevent
the individual having a normal home life. Challenging behaviours may take the form of
aggression, self‐injury, stereotyped behaviour, or disruptive and destructive behaviour generally.
In many cases, a functional analysis may help to identify the factors maintaining challenging
behaviour, and these may range from social attention, tangible rewards such as a hug, escape
from stressful situations, or they may simply provide sensory stimulation. A functional analysis is
undertaken by keeping a record of the frequency of the behaviours and noting the antecedents
and consequences of the behaviour. This will take the form of:
A. What happens before the challenging behaviour (the trigger)
B. What does the individual do? (the behaviour)
C. What does the person get as a result of the behaviour? (the consequence)
A typical ‘ABC’ chart on which family and carers will keep a record of these behaviours will
often look like this:
Date Antecedent (what Behaviour Consequence (what Signature
happened before the (describe exactly happened immediately
behaviour occurred?) what the person after the behaviour?)
did)

A FUNCTIONAL ANALYSIS CASE HISTORY:

Andy is a middle‐aged man with severe intellectual disability. He has recently moved into a
group home he shares with seven other people. Since he moved in, staff have observed several
incidents of self‐injury. They report that Andy starts to rock backwards and forwards in his
chair, and this then escalates into him slapping his face repeatedly. Staff have asked for help.
The staff team working with Andy were asked to complete ABC charts for 4 weeks. These were
then analysed and it was found that the behaviour tended to occur in the lounge when there
were a number of people in the room and the television was on. The consequence of Andy
starting to rock and slap himself was that staff would remove him from the room and take him
into the kitchen where it was empty and quiet.
It was hypothesised that the function of the behaviour for Andy was to escape from a noisy and
crowded situation. Staff decided to respond by watching Andy for early signs he may be feeling
overstimulated and to ask him if he wanted to leave the room.
This led to a reduction of self‐injury and later it was noted that Andy would now try to attract
staff attention when he wanted to leave.
Inclusion strategies
Policy on the development and education of individuals with intellectual disabilities has changed
significantly over the past 35 years. Prior to inclusion policies being introduced, even individuals with
mild intellectual disabilities were often deprived of any effective participation in the life of the society in
which they lived, and more often than not they would be institutionalised or educated separately.
However, many countries have introduced accessibility strategies that extend the rights of individuals
with intellectual disabilities to be educated according to their needs in mainstream schools. This
approach evaluates the individual's specific needs and then suggests strategies, services and supports that
will optimise the individuals functioning within society. In the UK, the Government's strategy for
individuals with special educational needs (SEN) involves improving the support system for
children and young people with SEN and their families and providing an integrated education, health,
and care plan for young people with SEN aged 0–25 years, improving educational provision for pupils
with SEN, including the development of suitable educational materials and the training of specialist
teachers and support staff (Department for Education, 2013). Social and educational inclusion also has
indirect benefits for the individual. Kim, Larson, & Lakin (2001) reviewed those studies carried out
between 1980 and 1999 that investigated the effects of the shift from institutionalised living to living in
the community. Most studies reported an improvement in three areas (a) overall improvements in coping
with day‐to‐day living and increases in self‐esteem, (b) a decrease in the frequency of maladaptive
behaviours, such as aggression or anger outbursts, and (c) an improvement in self‐care behaviours and
social skills. Case History 17.1 recites the story of Thomas, a Down syndrome sufferer, who lives with
his family and has benefited in a variety of ways from participating in a range of community activities
(Case History 17.1).

special educational needs (SEN) A term used in the UK to identify those who require
instruction or education tailored to their specific needs.
 CASE HISTORY 17.1 THOMAS'S STORY

Thomas is 23 and lives with his mum and dad. His brother now lives away, but sees him quite
regularly.
Thomas has Down syndrome and needs a great deal of support. He goes to college 4 days a
week and, on Fridays, attends a project where he is learning living skills and enjoying cooking.
Thomas has a supported work placement for 2 hours a week in a riding stable. He has a hectic
social life with weekly activities including riding, sports, going to the gym, trampolining, and
football. He goes to monthly discos with a group of young people with a learning disability and
is regularly to be found in the local pub playing pool with his friends.
We were transporting him to and from these activities and were concerned that he should be
able to mix more with his own age group. We arranged for 15½ hours' worth of direct
payments for Thomas to choose someone in his peer group to help him access these activities.
There was a great deal of interest in the advert we placed at the local university for a student to
help with this and we have had several different students helping over the past year, who have
become firm friends. Thomas's current helper, Laura, accompanies him on his outings and
Thomas has now become a part of a wider social circle, going to the pub, out for meals, and
watching videos at Laura's house with her friends, which he greatly enjoys.
Thomas's moods, self‐esteem, and well‐being are greatly improved by the stimulation and social
nature of all that he does, as well as the routine and structure it brings to his life.
Thomas and his friends have gained enormous confidence from attending several drama
courses and the group has enjoyed the feeling of empowerment and also the opportunity to
show their feelings. Last year, a group of 11 young adolescents, including Thomas, attended a
week‐long outward bound course run by the Calvert Trust without their families. Afterwards,
the group made a presentation to about 80 people who had been involved in organising or
fundraising their trip, with a very professional PowerPoint presentation and question and
answer session. They were all keen to contribute, wanted to find other groups to make their
presentation to and gained lots of confidence from this. It makes a change from the usual
painting eggs and bingo offered by local services, just not appropriate for a 22‐year‐old.
(From evidence from a family carer given to the Foundation for People with Learning Disabilities' Inquiry
into Meeting the Mental Health Needs of Young People with Learning Disabilities–Count Us In)

Clinical Commentary
Thomas is an example of how individuals with intellectual disabilities can benefit significantly from
accessibility and inclusion strategies. He has work in a supported employment setting and has a full
social life in which he can mix with people of his own age. This approach has the benefit of building
confidence and self‐esteem, as well as providing the individual with a real sense of empowerment.

Inclusion policies have resulted in significant improvements to the quality of life experienced by
individuals with intellectual disabilities, and such individuals now have opportunities to pursue social,
educational, and occupational goals and pursue their own personal development. For example,
individuals with intellectual disabilities now have the right to pursue their own sexual and emotional
development—usually with the support of their own family. Whereas in the past involuntary
sterilization was common for such individuals, appropriate training and counselling now means that
most individuals can be taught about sexual behaviour to a level appropriate for their functioning. This
often means that they can learn to use contraceptives, employ responsible family planning, get married,
and—in many cases—successfully rear a family, either on their own or with the help of local services
(Lumley & Scotti, 2001; Levesque, 1996; but see Schaafsma, Kok, Stoffelen, & Curfs, 2017, for a
discussion of how sex education for individuals with intellectual disabilities might be improved).
However, while inclusion in its broadest sense continues to benefit individuals with intellectual
disabilities, there is still much confusion over the way in which inclusion is defined and operationalised
(Bigby, 2012) and this makes objectively measuring the success of such policies difficult (Martin &
Cobigo, 2011).
Finally, although inclusion is still an important goal for governments and service providers, in 2016 it
was estimated that only 5.7% of individuals with an intellectual or learning disability were in any form
of paid employment in the UK, compared with 74.5% of the working‐age population (Hatton, 2016).
If these figures are correct, then they represent a disappointingly low level of inclusion. Of those that
are employed, most are conscientious and valued workers employed in normal work environments.
Others with more specific needs may need to pursue employment within sheltered workshops or
supported employment settings which provide employment tailored to the individuals own needs.
The UK Government seeks to promote employment as another form of social inclusion for individuals
with intellectual disabilities. Those working in sheltered workshops have been shown to exhibit higher
levels of job satisfaction than those who work outside such a scheme, and those living in a semi‐
independent home and also work in a sheltered workshop show the highest levels of self‐esteem (Griffin,
Rosenberg, & Cheyney, 1996).

sheltered workshops Settings that provide individuals with intellectual disabilities with
employment tailored to their own needs and abilities.

Summary of support and intervention for intellectual disabilities

This section has given you a brief insight into some of the supports and interventions deployed to help
people with intellectual disabilities. These include (a) the use of prevention strategies designed to
identify those at risk of having offspring with intellectual disabilities (e.g., those with recessive gene
disorders or mothers at risk during pregnancy), providing them with skills to minimise risk, and
counselling them about the possible outcomes; (b) a range of training programmes and techniques to
provide individuals with learning difficulties with a variety of everyday skills; and (c) the adoption of
inclusion strategies that provide the individual with educational and occupational environments tailored
to meeting their needs within mainstream society.

17.3.6 Summary of Intellectual Disabilities

We began this section by describing the DSM‐5 diagnostic criteria for intellectual disability and
discussing some alternative types of definition and terminology that focus on identifying needs and
facilitating adaptive functioning. The aetiology of intellectual disorders is a diverse topic, with no single
identifiable cause being found for a large proportion of those with intellectual disabilities. Biological
causes are primarily responsible for those aetiologies that can be identified, and these include
chromosomal disorders, recessive gene disorders, and perinatal factors. Childhood problems can also
contribute to intellectual disability, and we discussed the role of accidents, abuse, infectious diseases, and
the nonspecific detrimental effect that social deprivation and poverty can have on intellectual
development. In the final section we covered interventions for the prevention of intellectual disability,
and programmes for the care, development and support of individuals with intellectual disabilities.
SELF‐TEST QUESTIONS
Can you describe both the traditional and more recent alternative approaches to defining
intellectual disability?
What are the different levels of intellectual disability defined in DSM‐5?
What are the main chromosomal disorders that cause intellectual disability?
Can you describe at least two metabolic disorders that give rise to intellectual disability?
What is meant by the term ‘congenital disorder’ when used in relation to intellectual
disability? Can you give some examples of congenital causes of intellectual disability?
What are the main childhood causes of intellectual disability?
Can intellectual disability be prevented? If so, how?
Can you describe the kinds of training procedures that are used to help individuals with
intellectual disabilities acquire self‐help and communication skills?
Can you describe some examples of inclusion strategies that have been used in relation to
intellectual disability?
 SECTION SUMMARY

17.3 INTELLECTUAL DISABILITIES

Intellectual disability is a term that covers impairments in both intellectual and adaptive
functioning.
Intellectual disability involves significantly below average intellectual functioning, usually
defined by a score on a standardised IQ test of below 70.
Modern approaches to defining intellectual disabilities attempt to highlight those factors
that might be required to facilitate more adaptive functioning, and to draw up accessibility
strategies to ensure that such individuals are not excluded or disadvantaged in their
education
Chromosomal disorders such as Down syndrome and fragile X syndrome account for around
25–30% of all diagnosed cases of intellectual disability.
Metabolic disorders that cause intellectual disability are usually carried by a recessive gene
and include phenylketonuria (PKU) and Tay‐Sachs disease.
Congenital disorders are those that are acquired prior to birth but are not genetically
inherited. Congenital causes of intellectual disability include maternal malnutrition, congenital
rubella syndrome (CRS), maternal HIV infection, and fetal alcohol syndrome (FAS).
Childhood environmental causes of intellectual disability include childhood accidents
(including intentional physical abuse by others), exposure to toxins (such as lead),
childhood infections, and poverty and deprivation.
Prevention strategies for intellectual disability include prevention campaigns and screening
for such factors as maternal alcohol abuse and genetic risk factors.
Behavioural training procedures can equip sufferers with a range of self‐help and adaptive
skills, and the application of learning theory in these areas is known as applied behaviour
analysis.
Inclusion strategies provide those with intellectual disabilities with access to mainstream
educational and occupational opportunities.

17.4 AUTISTIC SPECTRUM DISORDER (ASD)

Some conditions are characterised by a range of different problems in the developmental process, and
those that fall under the heading of autistic spectrum disorder (ASD) are usually associated with
problems that can afflict several areas of development. From early infancy, some children will exhibit a
spectrum of developmental impairments and delays that include social and emotional disturbances (e.g.,
poor social interaction with others), intellectual disabilities (e.g., low IQ), language and communication
deficits (e.g., failure to learn to speak or develop language skills), and in severe cases the development of
stereotyped or self‐injurious behaviour patterns (e.g., hand biting and hair pulling). Prior to DSM‐5
there were a number of different ASD diagnostic categories, and these included autistic disorder
(autism), Rett's disorder, childhood disintegrative disorder, and Asperger's syndrome. However, DSM‐5
has combined these into one single dimensional diagnostic category called autistic spectrum disorder
(ASD). The reason for this change was that there was little research evidence that supported the
independence of all these different diagnostic categories, and most shared several common features.
DSM‐5 field studies also supported the validity of the new DSM‐5 diagnostic criteria, although these
new criteria appear to be reducing the number of individuals who would receive a diagnosis of ASD
(Kulage et al., 2019; see also Chapter 2, Section 2.1.3 for a discussion of how changes in the DSM
criteria for ASD may affect diagnosis). We discuss the DSM‐5 diagnostic criteria in Section 17.4.2, but
first let's look more closely at some of the defining characteristics of individuals with a diagnosis of
ASD.

autistic spectrum disorder (ASD) An umbrella term that refers to all disorders that display
autistic-style symptoms across a wide range of severity and disability.

17.4.1 The Characteristics of Autistic Spectrum Disorder

The early development of some children is so profoundly disturbed that from as young as less than 1
year of age it will become apparent to family and friends that the infant's development is not proceeding
normally. The child may seem withdrawn, may have failed to develop normal means of
communication, appears uninterested in its surroundings, and may have difficulty learning new skills.
Case History 17.2 relates some of the behavioural traits of Adam, a 1‐year‐old child who was later
diagnosed with autistic disorder. Typical of ASDs, Adam shows no interest in his surroundings other
than an obsessive interest in a small number of toys, he lacks normal communication skills for his age,
and appears withdrawn and unable to learn new responses or skills. He also has temper tantrums when
he appears unable to express his needs or has his very detailed play routines disrupted (Case History
17.2). The two central features of ASD are severe impairment in social interaction and in
communication. The range of disability caused by problems in social interaction and communication is
broad, and many individuals with a diagnosis of ASD are able to function effectively and have
successful educational and working careers. However, for others with more severe problems, the level of
disability may require lifelong support.
 CASE HISTORY 17.2 AUTISTIC SPECTRUM DISORDER

After Adam's first birthday party his mother began to pay attention to some characteristics of
her son's personality that did not seem to match those of the other children. Unlike other
toddlers, Adam was not babbling or forming any word sounds, while others his age were saying
‘mama’ and ‘cake’. Adam made no attempt to label people or objects but would just pronounce
a few noises which he would utter randomly through the day.
At the birthday party and in other situations, Adam seemed uninterested in playing with other
children or even being around them socially. He seemed to enjoy everyone singing ‘Happy
Birthday’ to him, but made no attempt to blow the candles out on the cake—even after others
modelled the behaviour for him.
His parents also noted that Adam had very few interests. He would seek out two or three Disney
toys and their corresponding videotapes and that was it. All other games, activities, and toy
characters were rejected. If pushed to play with something new, he would sometimes throw
intense, unconsolable tantrums. Even the toys he did enjoy were typically not played with in an
appropriate manner. Often he would line them up in a row, in the same order, and would not
allow them to be removed until he decided he was finished with them. If someone else tried to
rearrange the toys he would have a tantrum.
As the months went by and he remained unable to express his wants and needs, Adam's
tantrums became more frequent. If his mother did not understand his noises and gestures, he
would become angry at not getting what he wanted. He would begin to hit his ears with his
hands and cry for longer and longer periods of time.
Source: Adapted from Gorenstein & Cromer (2004).

Clinical Commentary
From a very early age, Adam exhibited symptoms of the triad of impairments typical of autistic
spectrum disorder. He shows (a) no sign of engaging in or enjoying reciprocal social interactions (e.g., the
lack of interest in socialising with others at his birthday party), (b) a significant delay in the development
of spoken speech (illustrated by his failure to form word sounds, label objects, or express his wants and
needs), and (c)a lack of imagination and flexibility of thought (as demonstrated by his inability to use
toys in imaginative play and his inflexibly stereotyped behaviour towards these toys).

Impairments of reciprocal social interaction

The impairment in reciprocal social interaction is one of the most marked and sustained features of
ASD. Sufferers will exhibit impairment in the use of nonverbal behaviours (e.g., eye contact,
appropriate facial expression) and will have difficulty regulating social interaction and communication.
In severe cases they will rarely approach others, almost never offer a spontaneous greeting, or make eye
contact when meeting or leaving another individual (Hobson & Lee, 1998). In young children, this is
often manifested as a clear disinterest in making friends, establishing friendships or any other form of
peer communication. Particularly striking is the autistic child's apparent inability to understand the
intentions or emotions of others and their universal disinterest in what others are doing. This has led
some theorists to suggest that children with autistic disorder fail to develop a ‘theory of mind, that is
they fail to develop an ability to understand the intentions, desires, and beliefs of others, and as a result
this makes them unable to understand why other people behave in the way they do. While children with
milder forms of the condition may be able to learn what physical features of a person are associated
with the expression of an emotion (e.g., that a frown is associated with anger or disapproval), they are
often unable to explain why someone is expressing a particular emotion (Capps, Losh, & Thurber,
2000).

Impairments in communication
There is often a prominent delay in the development of spoken language, and in those that do learn to
speak there can be an inability to sustain a conversation. When speech does develop, it may fail to follow
the normal rules of pitch, intonation, or stress, and a child's speech may sound monotonous and
disinterested. Grammatical structures are often immature and more than half of those diagnosed with
autistic disorder fail to speak at all but may utter a range of noises and screams that are often unrelated
to attempts to communicate. Some individuals exhibit what is known as echolalia, which is immediate
imitation of words or sounds they have just heard (e.g., if asked “Do you want a drink?” the child will
reply “Do you want a drink?”). Others that do develop language may only be able to communicate in a
limited way and may exhibit oddities in grammar and articulation. For instance, some exhibit pronoun
reversal in which they refer to themselves as ‘he’, ‘she’, or ‘you’, and this is a feature of speech that is
highly resistant to change (Tramonta & Stimbert, 1970). An autistic child's ability to learn language is a
good indicator of prognosis. Those that have learned meaningful speech by age 5 years are the ones
that are most likely to benefit from subsequent treatment (Werry, 1996; Kobayashi, Murata, &
Yoshinaga, 1992).

echolalia The immediate imitation of words or sounds that have just been heard.

Pronoun reversal An impairment in communication in which an individual refers to himself

or herself as ‘he’, ‘she’ or ‘you’.

Impairments in imagination and flexibility of thought

One feature of many individuals with ASD is that they often display restricted, repetitive, and
stereotyped patterns of behaviour and interests. This can manifest in childhood as a specific and
detailed interest in only a small number of toys. Like Adam in Case History 17.2, they may line up the
same set of toys in exactly the same way time after time and become very distressed if their routine is
disrupted or if they are not allowed to complete the routine. There appears to be a need to retain
‘sameness’ in all their experiences, and an autistic child may become extremely distressed if the
furniture in a room is changed around or they travel on a different route to school one day. Children
with ASD will often form strong attachments to inanimate objects such as keys, rocks, mechanical
objects, or objects with particular types of tactile characteristics (such as the smooth‐surfaced dice
described in George's Story at the beginning of this chapter). However, when they do play with individual
objects, such as a toy car, they rarely indulge in symbolic play (e.g., by moving the car along the floor as
if it were travelling somewhere), but instead will usually explore the tactile features of the toy in a
stereotyped manner (e.g., by simply rotating the car in their hands for long periods of time). A further
common characteristic of ASD in childhood is the appearance of stereotyped body movements, and
these can include hand clapping, finger snapping, rocking, dipping, and swaying. These patterns of
behaviour often appear to be self‐stimulatory in nature and can often become so intense and severe that
they may cause the individual physical injury, such as stereotyped hand and finger biting, head banging,
hair pulling, and scratching.
Intellectual deficits
In addition to these main symptoms, it is estimated that around 70% of individuals with a diagnosis of
ASD also have some level of intellectual disability, and the remaining 30% may have some other form
of disability such as a speech or behaviour disability or a cognitive impairment (e.g., a working memory
problem) (Srivastava & Schwartz, 2014). However, the nature of the intellectual deficits in children with
ASD is often different to those with a primary diagnosis of intellectual disability (see Section 17.3).
Individuals with a diagnosis of ASD will usually perform much better on tests of visuospatial ability
than tests of social understanding or verbal ability. Thus, they are much better at finding hidden figures
in drawings, assembling disassembled objects, and matching designs in block‐design tests (Rutter, 1983).
However, in many cases individuals with ASD may excel at one specific task (such as the ability to
calculate dates) or in one particular area (such as mathematics or music) (see Section 17.4.4). In
individuals with multiple cognitive disabilities, extraordinary proficiency in one isolated skill is known as
savant syndrome, and it is a phenomenon that appears to be closely linked to ASD (Heaton &
Wallace, 2004).

savant syndrome The phenomenon of extraordinary proficiency in one isolated skill in

individuals with multiple cognitive disabilities. It appears to be closely linked to autistic
spectrum disorder and is frequently found in Asperger’s syndrome.

17.4.2 The Diagnosis of Autistic Spectrum Disorder

The characteristics that we have just described form the basis for the DSM‐5 diagnosis of ASD. These
include persistent deficits in social communication and interaction that include deficits in social‐
emotional reciprocity (e.g., failure of normal back‐and‐forth conversation), deficits in nonverbal
communication (e.g., abnormal eye contact), and deficits in making, maintaining, and understanding
relationships (e.g., difficulties in adjusting behaviour to suit different social contexts). In addition to these
social communication deficits, individuals must also exhibit restricted, repetitive patterns of behaviour,
interests, or activities, such as stereotyped or repetitive motor movements or highly restricted, fixated
interests, and they will probably display an insistence on sameness and adherence to routines. Many will
also demonstrate a hyper‐ or hyporeactivity to sensory input or unusual interest in sensory aspects of the
environment. Most of these criteria are exhibited in the example of Adam shown in Case History 17.2.
In addition to these criteria related to social communication and restricted, repetitive patterns of
behaviour, the symptoms must be present in the early developmental period, and must cause significant
impairment in social, occupational or other areas of functioning. The diagnosis can also be
individualised with the use of specifiers that indicate whether the symptoms are accompanied by
intellectual impairment, or language impairment (Table 17.8). The DSM‐5 criteria also enable the
clinician to specify the severity level for the diagnosis from ‘requiring very substantial support’ (e.g.,
rarely initiates interaction and becomes highly distressed when having to cope with change), through
‘requiring substantial support’ (e.g., limited initiation of social interactions and some distress when
having to cope with change), to ‘requiring support’ (e.g., without support, deficits in social
communication cause noticeable impairments, and has difficulty switching between activities).
Finally, we must conclude by stressing that diagnosing an ASD is complicated. For example, ASDs can
manifest over a range of disabilities from severe to relatively mild high‐functioning autism, and at the
high‐functioning end of the spectrum it is often hard to distinguish those symptoms that may be
characteristic of autism. Similarly, diagnosis is complicated by the fact that (a) behaviour patterns may
change with age, (b) symptoms may be manifested with varying degrees of intellectual disability, and (c)
ASDs are often comorbid with other problems such as ADHD and epilepsy.
TABLE 17.8 Summary: DSM‐5 Diagnostic Criteria for Autism Spectrum Disorder

Ongoing deficits in social activities as marked by the following:

Social situation deficits—for example, abnormal social approach or failure to initiate or
respond to social situations
Nonverbal communication behaviour deficits—for example, abnormalities in eye contact or
poorly integrated verbal and nonverbal communication
Inability to develop, maintain, or understand relationships
Restricted and repetitive patterns of behaviour, interest, or activity, as marked by at least two of
the following:
Repetitive motor movement, use of objects or speech
Inflexibility and strong adherence to routine
Abnormally intense fixated interests
Hyper‐ or hyporeactivity to sensory input or unusual interest in sensory aspects of the
environment
Symptoms start in early development
Symptoms cause significant impairment in important areas of functioning
Symptoms are not better accounted for by intellectual disability or global development delay

17.4.3 The Prevalence of Autistic Spectrum Disorder

The latest studies of ASD in adults in the UK indicate a prevalence rate of around 1.1% indicating that
over 700,000 people in the UK may be potentially diagnosable with ASD (Brughas et al., 2016). In
childhood, a significant majority of those diagnosed with ASD are boys with a frequently cited ratio of
4: 1 (Halladay et al., 2015), and autism appears to occur equally in all socio‐economic classes and racial
groups (Fombonne, 2002). Epidemiological surveys of ASD suggest that the prevalence rate of the
disorder has been increasing significantly over the last 2–3 decades, and the US Centers for Disease
Control and Prevention (CDC) estimates that in 2000 1 in 150 children in the US were diagnosed with
ASD, but by 2016 this figure had risen to 1 in 54 (CDC, 2019). The reasons for this are unclear,
although one possible cause may be the expansion of the criteria for diagnosis of ASD in DSM‐IV that
was published in 1994, whereas some others suspect this may be a real increase in incidence resulting
from an increase in the prevalence of those factors that cause ASD (e.g., Blaxill, Baskin, & Spitzer,
2003). However, it is clear that the changes to the diagnostic criteria introduced in DSM‐5 in 2013 have
begun to cause a reduction in prevalence rates for ASD, and studies comparing DSM‐5 and DSM‐IV‐
TR diagnostic criteria indicate a reduction of up to 9% in the number of individuals diagnosed with
ASD under DSM‐5 compared with DSM‐IV‐TR (Huerta, Bishop, Duncan, Hus, & Lord, 2012; Wilson
et al., 2013; see Kulage et al., 2019, for more recent figures).

17.4.4 The Aetiology of Autistic Spectrum Disorder

In the 1960s, it was believed that autistic behaviour was caused by cold or rejecting parenting (e.g.,
Bettelheim, 1967)—a view that simply added to the distress of parents already having to cope with a
child with severe behavioural problems. However, subsequent studies have systematically failed to
uphold this view and have confirmed that the parents of autistic children are no different in their
parenting skills to those of nonautistic children (Cox, Rutter, Newman, & Bartak, 1975; Cantwell,
Baker, & Rutter, 1978). Nevertheless, the causes of ASD are still relatively poorly understood, but it is
becoming clear that there is a significant genetic element. However, in individual cases there is also
likely to be a contribution from environmental factors as well, such as perinatal risk factors (e.g.,
maternal infections during pregnancy), and the various combinations of genetics and environmental risk
factors may be the reason why ASD varies so much in its symptomatology and severity.

Biological causes

Genetic factors
There had been evidence available for some time that the social and language deficits and psychological
problems reminiscent of ASD often had a family history (Folstein & Rutter, 1988; Piven & Palmer,
1999). In particular, there is evidence for a strong familial aggregation of autistic symptoms, as
demonstrated in studies of sibling reoccurrence risk (i.e., studies investigating the probability of
developing autism given that an individual's sibling is autistic). These studies have estimated that the rate
of autism in the sibling of someone with autism ranges between 2 and 14% (Bailey, Phillips, & Rutter,
1996; Jorde et al., 1990), which is significantly higher than the prevalence rate found in the general
population. ASD also appears to co‐occur with several known genetic disorders such as
phenylketonuria, fragile X syndrome, and tuberous sclerosis (Smalley, 1998; Reiss & Freund, 1990),
implying a genetic link in its aetiology. There are also familial links between ASD and other
psychological problems. For instance, affective disorders are almost three times more common in the
parents of autism sufferers than in the parents of children suffering from tuberous sclerosis or epilepsy.
While we might expect that having a child with a disability might precipitate such psychological
problems, a majority of parents of autistic children developed their affective disorder before the birth of
the child (Bailey, Phillips, & Rutter, 1996).
Numerous twin studies have confirmed this genetic component to ASD. In studies comparing
concordance rates in MZ and DZ twins, Folstein & Rutter (1977) found concordance in 4 out of 11 MZ
twins but none in DZ twins. Subsequent twin studies have found concordance rates of between 60 and
91% for MZ twins and between 0 and 20% for DZ twins (Rutter et al., 1990; Bailey et al., 1995;
Steffenberg et al., 1989; Lichtenstein, Carlstrom, Ramstam, Gillberg, & Anckarsater, 2010), and a
recent meta‐analysis of twin studies has indicated that the heritability level of ASD is substantial, at
between 64 and 91% (Tick, Bolton, Happe, Rutter, & Rijsdijk, 2016). In addition, twin studies have also
demonstrated that each of the symptom components of autistic disorder—social impairments,
communication impairments, and restricted repetitive behaviours—all individually show high levels of
heritability (Ronald, Happe, Price, Baron‐Cohen, & Plomin, 2006).
Molecular genetics have implicated over 100 genes as risk factors for ASD (Satterstrom et al., 2020).
Most of these affect the development of brain synapses or regulate other genes, and while some have a
broad effect on early development, others are more specific to the symptoms of ASD. Figure 17.2
provides an overview of some of the mechanisms by which these gene effects are moderated. These
include (a) abnormalities resulting from gene copy number variations (CNVs), (b) epigenetics, in which
perinatal or early development experiences may modulate the expression of genes (e.g., Wong et al.,
2014), (c) double‐hit mutations (abnormalities resulting from rearrangements in two particular genes),
and (d) sex‐linked modifiers (i.e., sex‐linked genes that may make males more susceptible to ASD)
(Rylaarsdam & Guemez‐Gamboa, 2019). Most of this evidence strongly indicates that ASD is a
complex inherited condition that may involve a range of different genetic influences affecting symptom
expression and severity, including several different gene CNVs (Freitag, Staal, Klauck, Duketis, &
Waltes, 2010).

Perinatal factors
We noted in our discussion of intellectual disabilities, that perinatal factors may play a significant role in
determining intellectual impairment and the same may be true in the case of ASD. A range of birth
complications and pre‐natal factors have been identified as risk factors in the development of ASD, and
these include maternal infections, such as maternal rubella during pregnancy (Chess, Fernandez, &
Korn, 1978), intrauterine exposure to drugs such as thalidomide and valproate (Stromland, Nordin,
Miller, Akerstrom, & Gillberg, 1994; Williams et al., 2001), maternal bleeding after the first trimester of
pregnancy (Tsai, 1987), and depressed maternal immune functioning during pregnancy (Tsai &
Ghaziuddin, 1997). However, many of these risk factors have been identified only in individual case
reports, and they probably account for a very small percentage of cases of ASD (Fombonne, 2002;
Muhle, Trentacoste, & Rapin, 2004). For example, recent studies suggest that congenital rubella
infection has been found to be present in less than 0.75% of autistic populations—largely because of
the near eradication of the disease in Western countries (Fombonne, 1999; however, rubella still affects
up to 5% of pregnant women worldwide and may still be a cause of autism, Hutton, 2016). Some
studies also claim to have linked autism to postnatal events such as a link between ASD, inflammatory
bowel disease, and administration of the measles, mumps, and rubella (MMR) vaccine (Wakefield et al.,
1998). This claim caused some controversy in the UK at the time because it led to many parents
refusing to have their children immunised with the vaccine, and so put them at significant risk for these
infections (see Activity Box 17.1). However, subsequent studies have failed to corroborate an association
between administration of MMR and autism (e.g., Madsen et al., 2002; Hviid, Hansen, Frisch, &
Melbye, 2019). In addition, recent studies have also failed to find any association between infectious
diseases in the first 2 years of life and autism. Rosen, Yoshida, & Croen (2007) found that children with
subsequent diagnoses of autism had no more overall infections in the first 2 years of life than children
without autism.

FIGURE 17.2 Genetic modifiers in autism spectrum disorder. Autism spectrum disorder is estimated to be between 64
and 91% inherited (Tick, Bolton, Happe, Rutter, & Rijsdijk, 2016). However, both genetic and nongenetic factors
modulate the influence of risk genes, resulting in a highly heterogeneous set of symptoms. Examples of genetic modulators
include CNV (abnormalities resulting from gene copy number variations), epigenetics (e.g., maternal complications during
pregnancy may influence gene expression), and double‐hit mutations (where abnormalities result from rearrangements in two
particular genes). Examples of nongenetic modifiers include environmental exposures (e.g., maternal tobacco smoking) and
sex‐linked modifiers (e.g., sex‐linked factors that may protect females from ASD or make males more susceptible to ASD).
From Rylaarsdam & Guemez‐Gamboa, 2019.
Brain function
There is now a good deal of converging evidence from autopsy studies, fMRI studies, and studies
measuring EEG (electroencephalogram) and ERP (event‐related potentials) that autism is associated
with aberrant brain development. Autopsy studies of individuals diagnosed with ASD have revealed
abnormalities in a number of brain areas including the limbic system and the cerebellum. For example,
neurons in the limbic system are smaller and more dense than normal, and the dendrites which transmit
messages from one neurone to another are shorter and less well developed (Bauman & Kemper, 1994).
Abnormalities in the cerebellum appear to correspond to deficits in motor skills such as impaired
balance, manual dexterity and grip often found in individuals with ASD (Gowen & Miall, 2005). Finally,
autopsy studies have also shown overly large brain size and enlarged ventricles in the brain (Bailey et al.,
1998), and many of these abnormalities are typical of prenatal stages of brain development.
Interestingly, children with ASD are born with brains of normal size, but brain size increases
significantly between 12 and 24 months, and brain size at 24 months is positively correlated with autism
symptoms (Hazlett et al., 2017). A brain that is growing at a faster rate than normal may mean that
neurone connections are not being made selectively, and this may affect the functionality in important
parts of the brain such as the frontal and temporal lobes, and the cerebellum—brain areas important
for language, social, and emotional functions.
Anatomical and functional imaging studies have supplemented the evidence from autopsy studies and
given us an insight into how brain abnormalities in autism progress during different developmental
stages. They have confirmed that individuals with autism have abnormalities in a number of brain
regions, including the frontal lobes, limbic system, cerebellum, and basal ganglia (Sokol & Edwards‐
Brown, 2004), and they also confirm that autistic individuals have larger brain size and significantly
poorer neural connectivity than nonsufferers (McAlonan et al., 2005). We have already alluded to the
fact that individuals diagnosed with autism may lack a ‘theory of mind’ (the ability to attribute mental
states to others or to understand the intentions of others) (see Section 17.4.4), and fMRI studies indicate
that this is associated with decreased activation of the prefrontal cortex and amygdala, and these are
areas that an important component of the brain system underlying the intentions of others (Castelli,
Frith, Happe, & Frith, 2002). The larger brain size of individuals with ASD may provide some insight
into the developmental factors that may impair normal brain development in childhood.
In addition, one in four individuals with autistic disorder also exhibit abnormal EEG patterns in the
frontal and temporal lobes, and many of these have actual clinical seizures (Dawson, Klinger,
Panagiotides, Lewy, & Castelloe, 1995; Rossi, Parmeggani, Bach, Santucci, & Visconti, 1995). In
contrast, ERP studies provide information from brain activity about how individuals react to external
stimuli in the environment, and individuals with autism exhibit ERP patterns that indicate disrupted
and abnormal attention to a range of stimuli, including novel stimuli and language stimuli (Courchesne
et al., 1994; Dunn, 1994).
Taken together, these sources of evidence indicate that individuals with ASD exhibit abnormalities in a
number of different brain areas. These brain areas exhibit both anatomical (i.e., structural)
developmental abnormalities, as well as functional abnormalities (i.e., they do not appear to be able to
fulfil the cognitive functions they are intended for). These abnormalities appear to be determined by a
period of unusual brain overgrowth in early childhood (hence studies showing that autistic individuals
develop oversize brains), followed by abnormally slow or arrested growth, and these anomalies in brain
growth occur at a time during development when the formation of brain circuitry is at its most
vulnerable (Courchesne, 2004).

Cognitive factors
Depending on the severity of their symptoms, individuals with ASD often have problems attending to
and understanding the world around them. Most notably, they have difficulty with normal social
functioning. In severe cases they may be withdrawn and unresponsive, while less severe cases may
exhibit difficulty in reciprocal social interaction, including experiencing problems in communication
and in understanding the intentions and emotions of others. Some theorists have argued that these
deficits in social skills are a result of deficits in cognitive functioning (Rutter, Bailey, Bolton, & Couteur,
1994). First, individuals with ASD appear to exhibit deficits in executive functioning, resulting in
poor problem‐solving ability, difficulty planning actions, controlling impulses and attention, and
inhibiting inappropriate behaviour, and these deficits all have an impact on the ability to act
appropriately in social situations. Second, some theorists have argued that individuals with ASD lack a
‘theory of mind’ (TOM). That is, they fail to comprehend normal mental states and so are unable to
understand or predict the intentions of others. Third, and importantly, researchers such as Simon
Baron‐Cohen have argued that individuals with ASD do not just exhibit cognitive impairments, they
also have areas of strength, and one such strength is their ability to systematise information. We discuss
these three cognitive accounts separately.

Deficits in executive functioning

Individuals with ASD generally perform poorly on tests of executive functioning suggesting that they
may have difficulty effectively problem‐solving, planning, initiating, organising, monitoring and
inhibiting complex behaviours (Ozonoff & McEvoy, 1994; Shu, Lung, Tien, & Chen, 2001). Consistent
evidence for executive functioning deficits has been found in adults, adolescents, and older children with
autism (McEvoy, Rogers, & Pennington, 1993). However, determining the significance of poor
performance on tests of executive functioning is difficult, because executive functioning tasks require the
integration of a range of more basic cognitive abilities such as shifting attention, memory, sequencing
events, and inhibiting responses. Nevertheless, even when the basic cognitive processes required for
successful executive functioning are analysed separately, individuals with ASD exhibit deficits in a
number of these skills, including categorisation and concept formation (Minshew, Meyer, & Goldstein,
2002), shifting attention (Akshoomoff, Courchesne, & Townsend, 1997; Belmonte, 2000), planning and
abstract problem solving (Hill & Bird, 2006), short‐term and long‐term memory (Bachevalier, 1994;
Klinger & Dawson, 1996), and both phonological and visuospatial working memory (Habib, Harris,
Pollick, & Melville, 2019). However, evidence suggests that they fail to exhibit deficits in cognitive
inhibition (inhibiting inappropriate responses) (Kleinhans, Akshoomoff, & Delis, 2005; Ozonoff &
Strayer, 1997) or on tests of semantic fluency (Boucher, 1988; Manjiviona & Prior, 1999). Thus,
depending on the degree of severity of the disorder, individuals with ASD may only be deficient in
some of the basic cognitive skills required to successfully complete executive function tasks and not in
others.

Theory of mind deficits

One influential account of ASD claims that the fundamental problem for individuals with autism is that
they fail to develop a theory of mind (Baron‐Cohen, Leslie, & Frith, 1985; Baron‐Cohen, 2001; see
Boucher, 2012, for a review). That is, individuals with autism fail to develop an awareness that the
behaviour of other people is based on mental states that include beliefs and intentions about what they
should do, and as a result, individuals with autism fail to understand the intentions of others (refer back
to George's Story at the beginning of this chapter to see how George was unable to comprehend that his
mother's threats to ‘send him away’ were not intentional). There are a number of ways to test whether a
child has developed a ‘theory of mind’. One traditional method is known as the Sally‐Ann False
Belief Task (Baron‐Cohen, Leslie, & Frith, 1985), and this procedure is described more fully in
Research Methods Box 17.1.
 Sally–Anne False Belief Task An imaginative procedure that has been used many times to
assess theory of mind abilities in a range of clinical populations.

Even adults with high functioning autism also exhibit theory of mind deficits on some measures. For
example, many of the traditional tests of theory of mind are rather static and somewhat removed from
the dynamic situations an individual with autism will experience in real life. To make such tests more
akin to everyday experiences, Heavey, Phillips, Baron‐Cohen, & Rutter (2000) devised the Awkward
Moments Test, in which participants view a series of TV commercials and then are asked questions
about the events in each. Individuals with Asperger's syndrome were significantly less able to answer
questions about the mental state of the characters in the commercials than an age‐ and gender‐matched
control group without autism. However, the two groups did not differ on scores on questions related to
recall of events within the TV clips (a memory test), suggesting that the poorer scores on mental state
questions by Asperger's syndrome participants was not simply due to a memory deficit. Because of these
difficulties in understanding the mental states of others, individuals with ASD will undoubtedly have
difficulty indulging in symbolic play with others, actively participating in human interactions, and
forming lasting relationships.
However, some researchers argue that theory of mind deficits do not explain all the social interaction
problems found in individuals with ASD. Other processes that need to be considered are problems in
facial and emotion processing, poor attentional focus, and that individuals with ASD may simply have a
disinclination for social interactions rather than a deficit (e.g., Nuske, Vivanti, & Dissanayake, 2013;
Koldewyn, Jiang, Weigelt, & Kanwisher, 2013).

The empathising‐systematising theory

More recently, some researchers have argued that theory of mind deficits may help to explain many of
the social and communication difficulties experienced by individuals with ASD, but such deficits do not
easily explain the nonsocial features of behaviour, such as having very focussed interests, a need for
sameness, and attention to detail. Baron‐Cohen (2002, 2009) has argued that theory of mind deficits
only address the difficulties that people with autism experience and do not address their areas of
strength. He suggests that individuals with ASD may even have superior skills in systematising, that is,
analysing or constructing systems to understand the world, and they do this by noting regularities,
structures, and rules within systems. This leads such individuals to focus on fully understanding
individual systems, such as collectible systems (e.g., distinguishing between types of stones), mechanical
systems (e.g., a video‐recorder), numerical systems (e.g., a train timetable), abstract systems (e.g., the
syntax of a language), and motoric systems (e.g., bouncing on a trampoline) (Baron‐Cohen, 2009). This
is a helpful way of explaining the focussed interests, repetitive behaviour, and resistance to change/need
for sameness found in ASD, and it is this desire to systematise that differentiates autism from some other
conditions that also exhibit theory of mind deficits (e.g., schizophrenia, borderline personality disorder,
conduct disorder) (Corcoran & Frith, 1997; Fonagy, 1989; Dodge, 1993). The empathising‐
systematising theory also helps to explain the inability to ‘generalise’ in ASDs (Wing, 1997). Baron‐
Cohen (2009) provides the following example: ‘The typical clinical example is a teacher who teaches a
child with autism to perform a task in one setting (e.g., taking a shower at home) but has to reteach it in
a new setting (e.g., taking a shower at school). Consider though that if the child is treating the situation
as a system, the unique features of each (e.g., how the shower at home differs to the shower at school in
the detail of their temperature control functions or the angle and height of the shower‐head) may be
more salient than their shared features (e.g., that both require getting in, turning the shower on, turning
it off, and getting out)’ (Baron‐Cohen, 2009, pp. 72–73).

empathising–systematizing theory A theory of the social and communication difficulties

experienced by individuals with autistic spectrum disorder.
RESEARCH METHODS BOX 17.1 THE SALLY‐ANN FALSE
BELIEF TASK

How can we measure whether someone can understand the intentions of others? Baron‐Cohen,
Leslie, & Frith (1985) designed an imaginative procedure that has been used many times to
assess theory of mind abilities in a range of clinical populations. This is known as the Sally‐
Ann False Beliefs Task. In this procedure two dolls are used to act out the story shown in
the image, and at the end children are asked ‘Where will Sally look for her marble?’ Children
who have developed a theory of mind will say that when Sally comes back from her walk she
 will look in the basket for her marble because they will understand that she has not seen Ann
move it. Children who are unable to understand that others have different beliefs from
themselves will say that Sally will look in the box because that is where they themselves know it
is.
Baron‐Cohen, Leslie, & Frith (1985) conducted this test with three groups of children, all with a
mental age of over 3 years. One group was diagnosed with autistic disorder, one with Down
syndrome, and the third group consisted of normally developing children. Most of the children
with autism answered incorrectly (saying Sally would look in the box) while most of the children
in the other two groups gave the right answer (saying Sally would look in the basket). The
inclusion in the study of a group of children with Down syndrome showed that the failure on
this task of children with autism could not be attributed to their learning difficulties more
generally. In addition all children correctly answered two control questions ‘Where is the
marble really?’ and ‘Where was the marble in the beginning?’ demonstrating understanding of
the change in the physical location of the marble during the story.

Source: Frith (2003).

Summary of the aetiology of autistic spectrum disorder

As we noted at the outset of this topic, autism is a complex disorder, which varies considerably in its
symptomatology and severity across individuals. Recent research has indicated a significant genetic
component to ASD (up to 91% heritability in some studies), and molecular genetic studies are
beginning to identify some of the gene sequencing and structure abnormalities that may mediate
autistic syndrome symptoms. Autopsies, fMRI, EEG, and ERP studies suggest that individuals with
ASD exhibit deficits in a number of different brain areas as a result of abnormal brain growth between
12 and 24 months of age. While there is some evidence that theory of mind deficits may play a role in
the social interaction problems experienced by individuals with ASD, problems with executive function
skills may also contribute to these problems. Nevertheless, at least some theories of ASD also claim that
sufferers may well have cognitive ‘strengths’ as well as impairments, and the ability to systematise
information may be one of these strengths. ASD is undoubtedly a multifaceted syndrome, with a range
of different genetic, perinatal, and environmental causes.

17.4.5 Support and Interventions and Individuals with Autistic Spectrum

Disorder
A range of attempts have been made to support individuals with ASD when it comes to dealing with the
issues of day‐to‐day living that their neurological and cognitive differences can often raise. As we have
described earlier, many individuals with severe ASD may be unable to live a normal life without
continuous support and care. Interventions have generally taken three broad forms: in severe cases drug
treatments can be used to reduce problematic behaviour such as withdrawal, aggression or self‐injury,
behavioural training to promote basic communication and socialising skills, and inclusion strategies that
will support the client attempting to live a relatively normal life within society. But first, because of the
nature of ASD, there can be difficulties associated with attempting to treat individuals with severe forms
of ASD and we describe these first.

Difficulties in the treatment of individuals with severe autistic spectrum disorder

Many of the symptoms of ASD cause problems for almost any form of intervention designed to
improve their skills or quality of life. First, one of the main characteristics of the condition is that such
individuals do not easily tolerate changes from routine, and any intervention—by its very nature—is
designed to implement change. Second, many autistic spectrum children often appear to be oblivious to
the outside world, they respond very poorly to attempts at communication, and even something as
simple as trying to achieve eye contact can be problematic. Because of this, any training programme has
to begin at a very basic communication level by, for example, teaching the child to make eye contact
(Hwang & Hughes, 2000). Third, children with autistic symptoms often show interest in only a very
limited range of events and objects, and this makes it very difficult to find effective reinforcers that can
be used to reward them. Because of their apparent unresponsiveness to communications, praise is often
ineffective as a reinforcer and attempts have to be made to find rewards that are highly salient. In severe
cases, this may mean having to pair praise with food (so that praise acquires secondary reinforcing
properties) (Davison, 1964) or using tactile reinforcers such as a hug or a vibratory stimulus applied to
the skin (Johnson & Davey, 1978). Fourth, many children with autistic symptoms have overselective
attention that means if they do attend to the training task, it is likely that anything that is learned may
well be situation specific and will not generalise to other environments or to other similar tasks. Finally,
even in high‐functioning sufferers, difficulties in negotiating social encounters can mean that they may
be treated with some reserve by others in society—even though they are as capable as anyone else at
successfully undertaking employment. As we shall see later, this issue means that inclusion strategies will
require support for both client and employer if the high‐functioning individual with ASD is to integrate
successfully into the working environment.

Drug treatments
A number of drugs are used in the treatment of autism symptoms, mainly to help manage problem
behaviours in those with severe symptoms. Antipsychotic medications are the type of drug most
commonly used in the treatment of severe autistic symptoms, and these include haloperidol and,
more recently, risperidone (see also Chapter 4 for a description of antipsychotic drugs). Antipsychotic
drugs such as these have been shown to reduce repetitive and stereotyped behaviours, reduce levels of
social withdrawal, and also reduce symptoms associated with aggression and challenging behaviour,
such as hyperactivity, temper tantrums, mood changes, and self‐abusive behaviour (Malone, Gratz,
Delany, & Hyman, 2005). However, not all children with autism respond well to this class of drugs, and
they can have potentially serious side effects such as sedation, dizziness, increased appetite, and weight
gain and result in jerky movement disturbances (dyskinesias) (Campbell et al., 1997).

haloperidol An antipsychotic medication most commonly used in the treatment of autism.

risperidone A drug treatment for children with autism.

The opioid receptor antagonist naltrexone has also been found to be beneficial in the control of
hyperactivity and self‐injurious behaviour, and a study by Symons, Thompson, & Rodriguez (2004)
suggested that the drug decreased self‐injurious behaviours by over 50% in 47% of the participants in
their study. Some studies have even indicated that naltrexone can produce moderate increases in social
interaction and communication (Aman & Langworthy, 2000; Kolmen, Feldman, Handen, & Janosky,
1995).

Behavioural training methods

Most training programmes for children with severe symptoms of ASD will attempt to develop basic self‐
help, social, and communication skills in children who otherwise might be largely uncommunicative and
require lifelong care. Most training procedures adopt a conditioning‐based approach, in which the
clinician will attempt to reinforce basic behavioural skills such as attention (eye contact), toileting
behaviour, self‐help behaviours, initiating interactions with peers and adults, and play behaviour with
peers. These methods can also be used to reduce the frequency of disruptive or inappropriate
behaviours such as temper tantrums, self‐injurious behaviour, repetitive behaviours, and aggressive
responses (for example see the section on functional analysis in individuals with intellectual disorders in
Section 17.3.5) (Lovaas, 1987; Davison, 1964). To supplement basic conditioning principles, therapists
will also use a range of methods to try and promote the required behaviours in the first place, and these
may include modelling (i.e., demonstrating the required behaviour to the client before prompting them
to imitate it). This technique is especially helpful when attempting to teach autistic individuals to
communicate using sign language. Because many autistic children remain speechless, learning to
communicate through sign language has proved a useful way of facilitating interactions with others
(Goldstein, 2002). Despite the wide use of these methods to promote basic behaviours, there are very
few properly controlled outcome studies that have assessed the relative efficacy of these training
procedures (Howlin, 2005). However, in the absence of such studies the literature does suggest that early
intensive behavioural interventions may be the most effective way of promoting the social functioning
of autistic children over the long term (Howlin, 2005), and a meta‐analysis of behavioural interventions
for individuals with ASD indicated significant gains in IQ , language skills, communication, socialisation,
and daily living skills when compared with control interventions (Virués‐Ortega, 2010).

modelling The process of demonstrating a required behaviour to clients before prompting

them to imitate it.

Most of these training procedures are time consuming and repetitive and require a significant amount
of investment in time and effort by those conducting the training. However, a way of supplementing
treatment by professionals is to train parents themselves so that they can apply these behavioural
techniques at home (Erba, 2000; Boone, 2018). This has a number of benefits. It enables the autistic
child to learn appropriate behaviours in the environment in which he/she is most likely to be using
them (the home), and it frees up professional therapists' time and offers a tiered structure to treatment
that provides a potentially larger number of sufferers with day‐to‐day treatment. Some studies even
suggest that parents may be more effective and efficient trainers than professionals, and a study by
Koegel, Schreibman, Britten, Burkey, & O' Neil (1982) suggested that 25–30 hours of parent training
was as effective as 200 hours of similar treatment by professionals in a clinic setting. Parent‐
implemented early intervention has been shown to improve child communication behaviour,
increased maternal knowledge of autism, enhanced maternal communication style and parent–child
interaction, and reduced maternal depression (McConachie & Diggle, 2007). Parents can not only learn
to use behavioural techniques to train their own children but can also effectively train others who work
with or care for their children to use these techniques (Symon, 2005). This approach effectively expands
the group of individuals associated with an autistic child who are skilled in maintaining a consistent
training regime for that child.

Parent‐implemented early intervention Using parents as effective trainers to teach

children with intellectual disabilities, basic self‐help and communication skills.

Inclusion strategies
Many home‐based interventions for high‐functioning individuals with ASD teach self‐help strategies,
social and living skills, and self‐management that are designed to help the individual function more
effectively in society. However, even when an individual has effectively acquired many of these skills,
they may still need to be supported through important life transitions, such as finding and keeping a job.
One such support scheme is known as supported employment. This provides support to both the
employee with autism and the employer and includes (a) providing training and support for the
employer on how to manage the employee with autism, (b) provision of job preparation and interview
skills for the employee, (c) support for the employee for as long as it is needed, and (d) regular feedback
sessions with both employee and employer. Supported employment schemes such as this have been
shown to increase the employee's social integration, increase employee satisfaction and self‐esteem
(Kilsby & Beyer, 1996; Stevens & Martin, 1999), and promote higher rates of employment compared to
a matched control group (Mawhood & Howlin, 1999) (Focus Point 17.2—Compensatory Strategies).

FOCUS POINT 17.2 COMPENSATORY STRATEGIES FOR

EVERYDAY SOCIAL INTERACTION

Having hidden her ‘quirks’ her whole life, Eloise Stark—a student studying for a psychiatry
doctorate at Oxford University—struggled to make sense of why she felt different until she was
diagnosed with autism at the relatively late age of 27.
‘I adapted to try and fit in. I learned from an early age that you are expected to make eye
contact, then read that, actually, people do not keep constant eye contact and that was
something of an epiphany for me. So I started to look away for 2 seconds for every four
sentences of a conversation. I know that if someone makes a joke, I am expected to laugh,
whether I find it funny or not’. (BBC News, 2020).
Many adults with a diagnosis of ASD can appear quite neurotypical and rarely demonstrate
any behaviours during social encounters that appear atypical. They may show good eye contact
and appropriate social reciprocity, but it appears that many high‐functioning individuals with
ASD spent some time learning and developing compensatory strategies to deal with these
socially related issues.
In a study investigating the types of compensatory strategies used by adults with a diagnosis of
ASD, Livingston, Shah, Milner, and Happé (2020) found that many intellectually able
individuals with a diagnosis of ASD reported using learned compensatory strategies to modify
their social behaviour. Some of these strategies included:
Predicting, planning, and rehearsing conversations before they happen
Mimicking facial expressions, gestures, and tone of voice picked up from other people or
from TV characters
Looking at the bridge of the nose or standing at right angles to the person they are talking
with in order to avoid eye contact
Making eye contact even though it is not appropriate for that particular conversation
Using props in social situations that will take attention away from any potential social faux
pas, props such as pets, children, or an interesting object
Such compensatory strategies can operate at both conscious and subconscious levels, and help
to explain why some individuals do not receive a diagnosis of ASD until well into adulthood
(Livingston & Happe, 2017; Lai et al., 2017).

Summary of support & interventions for individuals with autistic Spectrum disorder
This section has given a flavour of the broad range of support and interventions that are available for
individuals with a diagnosis of ASD. Basic behavioural training methods have proven to be effective at
promoting a range of self‐help, social, and communicative skills in those most severely affected, and this
has been supplemented with the adoption of parent training programmes that extend the range of
individuals with the skills necessary for successful intervention. Drugs are commonly used primarily to
control negative behavioural symptoms such as self‐injurious, challenging, and hyperactive behaviours,
and they may also have some positive impact on communication and social behaviour. High functioning
individuals with ASD can also receive support in the form of supported employment programmes that
help the individual to seek a suitable job and to proposer in that employment.

17.4.6 Summary of Autistic Spectrum Disorder

ASD describes a broad ranging dimension of symptoms covering arrested development across a range
of skills, and the main characteristics are difficulties in reciprocal social interactions, communication
skills, and in severe cases, the presence of stereotyped or repetitive behaviour patterns. ASD is now
considered to be primarily a genetically‐determined condition, but we are only beginning to identity
some of the genes that may mediate autistic syndrome symptoms. Individuals with ASD exhibit both
functional and structural differences in a number of brain areas, and cognitive symptoms of ASD
include problems with some of the skills that contribute to executive functioning and theory of mind
deficits that make it difficult for some individuals with a diagnosis of ASD to understand the emotions
and intentions of others. More recently, the focussed interests and resistance to change/need for
sameness found in many high‐functioning adults with autism have been interpreted as a strong desire to
systematise, and it may be this analytical feature that differentiates autism from other conditions that
also exhibit theory of mind deficits and also represents a potential cognitive area of strength for
individuals with ASD (see Focus Point 17.1).
Psychological and behavioural interventions are arguably the most successful ways of supporting
individuals with ASD and are used to help children to learn useful social and behavioural skills. In some
cases, drugs can be used to help manage the more disruptive behavioural elements of severe ASD (such
as self‐injurious behaviour, aggressive behaviour, etc.), and early intensive behavioural interventions
appear to be the best way of promoting social functioning over the longer term. Finally, high‐
functioning individuals with ASD can be helped to establish a successful working career with the help of
community inclusion strategies and supported employment schemes.
SELF‐TEST QUESTIONS
What is the triad of impairments that are important in the diagnosis of autistic spectrum
disorder?
What are the current prevalence rates for autistic spectrum disorder and what factors
might have caused recent increases in those prevalence rates?
What is the evidence for autistic spectrum disorder being an inherited disorder?
What perinatal factors might contribute to autistic symptoms?
What kinds of studies have contributed to our understanding of brain abnormalities in
autistic spectrum disorder?
What cognitive problems have individuals with autistic spectrum disorder been shown to
have?
What are the main difficulties associated with the treatment of individuals with autistic
spectrum disorder?
What drugs are used to treat autistic spectrum disorder and what symptoms do they
attempt to treat?
What is parent‐implemented early intervention, and is it effective?
What is supported employment when used with higher functioning individuals with
autism? How successful is it?
 SECTION SUMMARY

17.4 AUTISTIC SPECTRUM DISORDER (ASD)

The triad of impairments in ASD are impairments in (a) reciprocal social interaction, (b)
communication, and (c) imagination and flexibility of thought.
The prevalence rate of diagnosed ASDs is estimated at around 1.1% with around 80% of
those diagnosed being boys.
There is an important genetic element to ASD, and we are beginning to identify some of
the gene sequencing and structure abnormalities that may mediate autistic symptoms.
Perinatal factors may account for a small percentage of ASD cases, and such factors may
include maternal rubella during pregnancy, interuterine exposure to drugs, maternal
bleeding after the first trimester, and depressed maternal immune functioning during
pregnancy.
There is good evidence from autopsy, fMRI, and EEG, and ERP studies that autism is
associated with problems in brain development between 12 and 24 months of age.
Cognitive factors contributing to autistic symptoms include impaired executive functioning and
theory of mind (TOM) deficits.
The focussed interests, repetitive behaviour, and resistance to change/need for sameness
found in high functioning ASD has been interpreted as a strong desire to systematically
analyse information.
Drug treatments for children with severe autism symptoms include haloperidol, risperidone,
and naltrexone, all of which attempt to treat the negative symptoms of the disorder.
Behavioural training methods used to teach basic self‐help and communication skills
include operant conditioning techniques, modelling, and parent‐implemented early interventions.
Supported employment has proven successful at helping higher functioning individuals with
autism to find and maintain employment.

17.5 NEURODEVELOPMENTAL DISABILITY AND DIVERSITY

REVIEWED
In this chapter we have covered three distinctive types of neurodevelopmental disability and diversity,
namely specific learning problems (such as reading disorder and expressive language disorder),
intellectual disabilities, and autistic spectrum disorder. All of these categories represent lifelong
conditions that are usually present from birth, and are characterised by the individual falling behind in
important developmental milestones in social behaviour, communication, and learning skills.
The range of disability covered by these three areas is broad, with some individuals being so severely
affected by the disability as to require lifelong specialised support. However, many others with these
disabilities can function sufficiently well to enjoy relatively normal daily living and with structured
support schemes can succeed in both educational and occupational environments. Recent years have
seen rapid development in inclusion policies designed to extend the rights of individuals with diverse
learning and developmental disabilities to be educated and employed in mainstream settings, and
this has led to a significant improvement in the quality of life and self‐esteem experienced by those
diagnosed with these conditions.

developmental disabilities A broad umbrella term used, in the USA, to refer to intellectual
disabilities and pervasive developmental disorders such as autism and Asperger’s syndrome.

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