1.

ANXIETY AND RELATED DISORDERS

● GAD
● PANIC & AGORAPHOBIA
● SPECIFIC PHOBIAS
● SOCIAL PHOBIA
2. STRESS RELATED DISORDERS
● CARDIOVASCULAR
● PTSD
3. OCD

ANXIETY DISORDERS (GENERAL OVERVIEW) (5/7.5)

DEFINITION

Anxiety disorders are abnormal states in which the most striking features are mental and
physical symptoms of anxiety, occurring in the absence of organic brain disease or another
psychiatric disorder.

They are characterized by unrealistic, irrational fears or anxieties that cause significant
distress and/or impairments in functioning.

Many people with one anxiety disorder will experience at least one more anxiety disorder
and/or depression either concurrently or at a different point in their lives.

ANXIETY DISORDERS IN DSM-5

Among the disorders recognized in DSM-5 are:

1. Specific phobia

2. Social anxiety disorder (social phobia)

3. Panic disorder

4. Agoraphobia

5. Generalized anxiety disorder

People with these varied disorders differ from one another both in terms of the amount of fear
or panic versus anxiety symptoms that they experience and in the kinds of objects or
situations that most concern them.
SYMPTOMS OF ANXIETY

1. Psychological Arousal

a. Fearful anticipation

b. Irritability

c. Sensitivity to noise

d. Restlessness

e. Poor concentration

f. Worrying thoughts

2. Autonomic Arousal

a. Gastrointestinal

i. Dry mouth

ii. Difficulty in swallowing

iii. Epigastric discomfort

iv. Excessive wind

v. Frequent or loose motions

b. Respiratory

i. Constriction in the chest

ii. Difficulty inhaling

c. Cardiovascular

i. Palpitations

ii. Discomfort in the chest

iii. Awareness of missed beats

d. Genitourinary

i. Frequent or urgent urination

 ii. Failure of erection

iii. Menstrual discomfort

e. Muscle tension

i. Tremor

ii. Headache

iii. Aching muscles

f. Hyperventilation

i. Dizziness

ii. Tingling in the extremities

iii. Feeling of breathlessness

g. Sleep disturbance

i. Insomnia

ii. Night terror

COMMONALITIES IN CAUSAL FACTORS

1. Biological Causal Factors: Genetics contributes to each of these disorders and that at least
part of the genetic vulnerability may be non-specific or common across the disorders.

a. In adults, the genetic vulnerability is manifested at a psychological level in part

by the personality trait called neuroticism—a proneness or disposition to
experience negative mood states that is a common risk factor for both anxiety and
mood disorders.

b. The brain structures most centrally involved in most disorders are in the limbic
system and certain parts of the cortex, and the neurotransmitter substances
that are most centrally involved are gamma aminobutyric acid (GABA),
norepinephrine, and serotonin

2. Psychological Causal Factors: Classical conditioning of fear, panic, or anxiety to a range

of stimuli plays an important role in many of these.

a. People who have perceptions of a lack of control over either their

environments or their own emotions (or both) seem more vulnerable to
developing anxiety disorders. The development of such perceptions of
 uncontrollability depends heavily on the social environment people are raised
in, including parenting styles.

b. For certain disorders, faulty or distorted patterns of cognition also may play
an important role.

3. Sociocultural Causal Factors: The sociocultural environment in which people are raised
also has prominent effects on the kinds of objects and experiences people become anxious
about or come to fear.

There are also many commonalities seen across the effective treatments for the various
anxiety disorders.

a. For each disorder, graduated exposure to feared cues, objects, and situations
—until fear or anxiety begins to habituate—is the most useful technique.

b. Cognitive Restructuring techniques are also useful.

c. Nearly all medications tend to fall into two primary medication categories: anti
anxiety medications (anxiolytics) and antidepressant medications.

DIFFERENCE BETWEEN FEAR AND ANXIETY (5/7.5 marks)

FEAR

1. According to prominent theorists who have proposed a more fundamental distinction between
them, fear is a basic emotion (shared by many animals) that involves activation of the “fight-
or-flight” response of the autonomic nervous system. This is an almost instantaneous
reaction to any imminent threat. Its adaptive value as a primitive alarm response to
imminent danger is that it allows us to escape.

2. When the fear response occurs in the absence of any obvious external danger, we say the
person has had a spontaneous or uncued panic attack. The symptoms of a panic attack are
nearly identical to those experienced during a state of fear except that panic attacks are often
accompanied by a subjective sense of impending doom, including fears of dying, going crazy,
or losing control.

3. Fear and panic have three components:

a. Cognitive/subjective components (e.g., “I’m going to die”)

b. Physiological components (e.g., increased heart rate and heavy breathing)

c. Behavioural components (e.g., a strong urge to escape or flee).

These components are only “loosely coupled”, which means that someone might show
physiological and behavioural indications of fear or panic without much of the subjective
component, or vice versa.

ANXIETY

In contrast to fear and panic, the anxiety response pattern is a complex blend of unpleasant
emotions and cognitions that is both more oriented to the future and much more diffuse than
fear. But like fear, it has 3 components.

1. Cognitive/ subjective level: Negative mood, worry about possible future threats or danger,
self-preoccupation, and a sense of being unable to predict the future threat or to control it if it
occurs.

2. Physiological level: State of tension and chronic overarousal, which may reflect risk
assessment and readiness for dealing with danger should it occur (“Something awful may
happen, and I had better be ready for it if it does”). Although there is no activation of the fight-
or-flight response as there is with fear, anxiety does prepare or prime a person for the fight-
or-flight response should the anticipated danger occur.

3. Behavioural level: Strong tendency to avoid situations where danger might be

encountered, but the immediate behavioural urge to flee is not present with anxiety as it is
with fear.

The adaptive value of anxiety may be that it helps us plan and prepare for a possible threat. In
mild to moderate degrees, anxiety actually enhances learning and performance. For example,
a mild amount of anxiety about how you are going to do on your next exam, or in your next
tennis match, can actually be helpful. However, it is maladaptive when it becomes chronic and
severe, like with people diagnosed with anxiety disorders.

SIMILARITIES
-cognitive/subjective, physiological, behavioral components
-can serve adaptive function
While threatening situations can provoke fear or anxiety unconditionally, many of our sources of
fear and anxiety are learned. These response patterns are highly conditionable where
previously neutral stimuli which are repeatedly paired with frightening or unpleasant events
(such as various kinds of physical or psychological trauma) can acquire the capacity to elicit fear
or anxiety themselves.

DIFFERENCES:
Support for the idea that anxiety is descriptively and functionally distinct from fear or panic
comes both from statistical analyses of subjective reports of panic and anxiety and from a
great deal of neurobiological evidence. There is much evidence that fear and anxiety reactions
differ psychologically and physiologically. Historically, the most common way of distinguishing
between the fear and anxiety response patterns has been to determine whether a clear and
obvious source of danger is present that would be regarded as real by most people. When the
source of danger is obvious, the experienced emotion has been called fear (e.g., “I’m afraid of
snakes”). With anxiety, however, we frequently cannot specify clearly what the danger is (e.g.,
“I’m anxious about my parents’ health”). Thus, anxiety is a future-oriented mood state,
characterized by apprehension because we cannot predict or control upcoming events. Fear,
on the other hand, is an immediate emotional reaction to current danger characterized by
strong escapist action tendencies and, often, a surge in the sympathetic branch of the
autonomic nervous system.

GENERALISED ANXIETY DISORDER

Clinical picture

Definition- Earlier known as Generalised worry disorder or pathological worry disorder,

Generalised anxiety disorder refers to a form of anxiety characterised by worry that is
generalised, chronic, excessive and unreasonable.

Diagnostic Criteria (DSM V)

A. Excessive anxiety and worry (apprehensive expectation), occurring more days than
not for at least 6 months, about a number of events or activities (such as work or
school performance).
B. The individual finds it difficult to control the worry.
 C. The anxiety and worry are associated with three (or more) of the following six
symptoms (with at least some symptoms having been present for more days than not for
the past 6 months): Note: Only one item is required in children.

1. Restlessness or feeling keyed up or on edge.

2. Being easily fatigued.

3. Difficulty concentrating or mind going blank.

4. Irritability.

5. Muscle tension.

6. Sleep disturbance (difficulty falling or staying asleep, or restless, unsatisfying sleep).

D. The anxiety, worry, or physical symptoms cause clinically significant distress or

impairment in social, occupational, or other important areas of functioning
E. The disturbance is not attributable to the physiological effects of a substance (e.g., a
drug of abuse, a medication) or another medical condition (e.g., hyperthyroidism).
F. The disturbance is not better explained by another mental disorder (e.g., anxiety or
worry about having panic attacks in panic disorder, negative evaluation in social anxiety
disorder [social phobia], contamination or other obsessions in obsessive compulsive
disorder, separation from attachment figures in separation anxiety disorder, reminders of
traumatic events in posttraumatic stress disorder, gaining weight in anorexia nervosa,
physical complaints in somatic symptom disorder, perceived appearance flaws in body
dysmorphic disorder, having a serious illness in illness anxiety disorder, or the content of
delusional beliefs in schizophrenia or delusional disorder)

Haven’t added clinical signs

Important Characteristics

People with GAD live in a relatively constant, future-oriented state of anxious apprehension,
chronic tension, worry, and diffuse uneasiness that they cannot control.

They not only show marked vigilance for possible signs of danger in the envt but also
frequently engage in subtle avoidance activities such as procrastination, checking or calling a
loved one ( frequently) to see if he or she is safe (Barlow, 2002)

Experience difficulty making decisions and worry endlessly about the possible errors and
unforeseen circumstances if they manage to make one.

Inability to appreciate logic that may help come out of the unending loop of anxiety, as they
fail to escape the illusory world created in their thoughts and images and thus, may rarely
experience the present moment as potentially joyous.

Common symptoms-
 - Worry and apprehension
- Psychological arousal-irritability, poor concentration
- Autonomic overactivity-epigastric discomfort, sweating, palpitation etc
- Muscle tension,
- Hyperventilation, which may lead to dizziness, tingling in the extremities and
paradoxically ,a feeling of shortness of breath.
- Sleep disturbances, which include difficulty in falling asleep and persistent worrying
thoughts often intermittent, unrefreshing, and accompanied by unpleasant dreams, night
terrors, sudden disruptions and so on.
- Early-morning waking is not a feature of GAD, and its presence strongly suggests a
depressive disorder.
- Other features, which include tiredness, depressive symptoms, obsessional symptoms,
and depersonalization. These symptoms are never the most prominent feature of GAD. If
they are prominent, another diagnosis should be considered

Prevalence, Age of Onset, and Gender Difference

Approximately 3 percent in any 1-year period and 5.7 percent lifetime risk (Kessler et al., 1994)
GAD is one of the most common anxiety disorders. Similar rates are reported from around the
world. Tends to be chronic. One 12-year follow-up study found that 42 percent had not remitted
13 years later and of those who had remitted, nearly half had had a recurrence (Bruce et al.,
2005) After age 50 the disorder seems to disappear for many people (Rubio & Lopez-Ibor,
2007); however, it often tends to be replaced by a somatic symptom disorder and
characterized by physical symptoms and health concerns.

Gender differences
GAD is approximately twice as common in women as in men, but this sex ratio may be specific
to developed countries. In a South African study, GAD was found to be more common in
males.

Onset
Age of onset may be described as slow and insidious as GAD is difficult to determine given the
chronic nature of the disorder. However, it has been found most prevalent in adults (older
adults in particular) In the Harvard brown anxiety research programme- mean age of onset was
found to be 21 years although many patients had been unwell since their teenage years.

Differential diagnosis

1. Depressive disorder- Anxiety is a common symptom in depressive disorder, and GAD

often includes some depressive symptoms. the diagnosis is decided on the basis of the
severity of two kinds of symptoms and the order in which they appeared. Depressive
disorders are often worst in the morning, and anxiety that is worst at this time suggests a
depressive disorder.
 2. Schizophrenia People with schizophrenia sometimes complain of anxiety before the
other symptoms are recognized- ask reasons for worry
3. Dementia Anxiety may be the first abnormality to be complained of by a person
developing dementia.- Memory to be assessed
4. Substance misuse- A substance/medication-induced anxiety disorder is distinguished
from generalized anxiety disorder by the fact that a substance or medication (e.g., a drug
of abuse, exposure to a toxin) is judged to be etiologically related to the anxiety. For
example, severe anxiety that occurs only in the context of heavy coffee consumption
would be diagnosed as caffeine-induced anxiety disorder
5. Posttraumatic stress disorder and adjustment disorders. Anxiety is invariably present
in posttraumatic stress disorder. Generalized anxiety disorder is not diagnosed if the
anxiety and worry are better explained by symptoms of posttraumatic stress disorder.

Comorbidity
Generalized anxiety disorder often co-occurs with other disorders, especially other anxiety and
mood disorders such as panic disorder, social phobia, specific phobia, PTSD, and major
depressive disorder (Kessler, Chiu, et al., 2005). In addition, many people with GAD
experience occasional panic attacks without qualifying for a diagnosis of panic disorder.

Case Study

Rodney was a 26-year-old, single graduate student in the social sciences at a prestigious
university. He reported that he had had problems with anxiety nearly all his life, but they had
become worse since he had left home and gone to an Ivy League college. During the past year
his anxiety had seriously interfered with his functioning, and he worried about several different
spheres of his life such as his own and his parents’ health. During one incident a few months
earlier, he had thought that his heart was beating more slowly than usual, and he had
experienced some tingling sensations; this led him to worry that he might die. In another
incident he had heard his name spoken over a loudspeaker in an airport and had worried that
someone at home must be dying. He was also very worried about his future because his
anxiety had kept him from completing his master’s thesis on time. Rodney also worried
excessively about getting a bad grade even though he had never had one either in college or in
graduate school. In classes he worried excessively about what the professor and other students
thought of him. Although he had a number of friends, he had never had a girlfriend because of
his shyness about dating. He had no problem talking or socializing with women as long as it was
not defined as a dating situation. He worried that he should date a woman only if he was quite
sure, from the outset, that it could be a serious relationship. He also worried excessively that if a
woman did not want to date him, it meant that he was boring. In addition to his worries,
which he perceived as uncontrollable, Rodney reported muscle tension and becoming easily
fatigued. He also reported great difficulty concentrating and a considerable amount of
restlessness and pacing. At times he had difficulty falling asleep if he was particularly anxious,
but at other times he slept excessively, in part to escape from his worries. He frequently
experienced dizziness and palpitations, and in the past he had had fullblown panic attacks.
Rodney’s mother was also quite anxious and had been treated for panic disorder.
ETIOLOGY (CLINICAL DYNAMICS)
PSYCHOLOGICAL CAUSAL FACTORS

1. Psychoanalytic Viewpoint: According to Psychoanalysts, generalized anxiety results

from an unconscious conflict between ego and id impulses that is not adequately dealt
with because the person’s defence mechanisms have either broken down or have
never developed. Defence mechanisms may become overwhelmed when a person
experiences frequent and extreme levels of anxiety, as might happen if id impulses are
frequently blocked from expression.
2. Perception of uncontrollability & unpredictability: Researchers hypothesize that
people with GAD may have a history of experiencing many important events in their
lives as unpredictable or uncontrollable (more stressful in nature). Research indicates
that people with GAD may be more likely to have had a history of trauma in childhood
than individuals with several other anxiety disorders. Moreover, people with GAD have
far less tolerance for uncertainty than non-anxious people and even people with panic
disorder which suggests that they are especially disturbed by not being able to predict
the future.
3. Sense of Mastery: A person’s history of control over important aspects of their
environment is another significant experiential variable strongly affecting reactions to
anxiety-provoking situations. In children, experiences with control and mastery often
occur in the context of the parent–child relationship and thus parents’ responsiveness
to their children’s needs directly influences their children’s developing sense of mastery.
Parents of anxious children often have an intrusive, overcontrolling parenting style,
which may serve only to promote their children’s anxious behaviours by making them
think of the world as an unsafe place in which they require protection and have little
control themselves.
4. Reinforcing Properties of Worry: Several of the benefits that people with GAD most
commonly think derive from worrying are:
a. Superstitious avoidance of catastrophe
b. Avoidance of deeper emotional topics
c. Coping and preparation

Some evidence suggests that for a subset of people with GAD, these positive beliefs
about worry play a key role in maintaining high levels of anxiety and worry.

a. When people with GAD worry, their emotional and physiological responses to
aversive imagery are suppressed. This suppression reinforces the process of
worry.
b. Worrying also insulates the person from fully experiencing or processing the
topic that she or he is worrying about, and it is known that such full processing is
necessary if extinction of that anxiety is to occur. Thus, the threatening
meaning of the topic being worried about is maintained.
5. Negative Consequences of Worry: Worry itself is unpleasant and can actually lead to a
greater sense of danger and anxiety (and lower positive mood) because of all the
possible catastrophic outcomes that the worrier envisions.
a. People who worry about something tend subsequently to have more negative
intrusive thoughts than people who do not worry.
b. Paradoxically, these intrusive thoughts can serve as further trigger topics for
more worry, and a sense of uncontrollability over worry may develop in people
caught in this cycle that occurs in GAD.
c. Evidence suggests that attempts to control thoughts and worry may
paradoxically lead to increased experience of intrusive thoughts and enhanced
perception of being unable to control them.
d. Perceptions of uncontrollability are also known to be associated with increased
anxiety, so a vicious circle of anxiety, worry, and intrusive thoughts may
develop.
6. Cognitive Biases/Distortions:

a. People with GAD have frequent frightening thoughts and process threatening
information in a biased way, because they have prominent danger schemas.
Anxious people tend to preferentially allocate their attention toward
threatening cues when both threat and nonthreat cues are present in the
environment. Further, this attentional vigilance for threat cues can occur at a very
early stage of information processing, even before the information has entered the
person’s conscious awareness. If a person is already anxious, having her or his
attention automatically focused on threat cues in the environment would seem
only to maintain the anxiety or even make it worse. Moreover, recent evidence
also strongly supports the idea that such attentional biases play a causal role in
anxiety.
b. Anxious people are also more likely than non-anxious people to think that bad
things are likely to happen in the future, and they have a much stronger
tendency to interpret ambiguous information in a threatening way
(misinterpretation). This tendency has actually been shown to increase anxiety
in several situations.
7. Personality Traits: Anxiety symptoms are associated with neuroticism, and twin
studies have shown an overlap between the genetic factors related to neuroticism and
those related to GAD. Personality disorder - GAD occurs in people with anxious–
avoidant personality disorders, but also in individuals with other personality disorders.
BIOLOGICAL CAUSAL FACTORS

1. Genetic Factors: Evidence for genetic factors in GAD is mixed, but there does seem to
be a modest heritability. Several large twin studies have revealed that heritability
estimates vary as a function of one’s definition of GAD, and indicate that 15 to 20
percent of the variance in liability to GAD is due to genetic factors. At least part of this
common genetic predisposition for GAD is personality trait – neuroticism.

2. Neurotransmitters & Neurohormonal Abnormalities

a. A Functional Deficiency in GABA: In the 1950s, the benzodiazepine was found
to reduce anxiety. This discovery was followed in the 1970s by the finding that
these drugs probably exert their effects by stimulating the action of GABA It
appears that highly anxious people have a kind of functional deficiency in
GABA. Benzodiazepine drugs appear to reduce anxiety by increasing GABA
activity in certain parts of the brain implicated in anxiety, such as the limbic
system, and by suppressing the stress hormone cortisol. Whether the functional
deficiency in GABA in anxious people causes their anxiety or occurs as a
consequence of it is not yet known, but it does appear that this functional
deficiency promotes the maintenance of anxiety.
b. Serotonin: It is also involved in modulating generalized anxiety. At present, it
seems that GABA, serotonin, and perhaps norepinephrine all play a role in
anxiety, but the ways in which they interact remain largely unknown.
c. Corticotropin-Releasing Hormone System: An anxiety-producing hormone
called corticotropin-releasing hormone (CRH) has also been strongly
implicated as playing an important role in GAD.

i. When activated by stress or perceived threat, CRH stimulates

the release of ACTH (adrenocorticotropic hormone) from the pituitary gland,
which in turn causes release of the stress hormone cortisol from the adrenal
gland.

ii. CRH may play an important role in generalized anxiety

through its effects on the bed nucleus of the stria terminalis (an extension
of the amygdala which is now believed to be an important brain area
mediating generalized anxiety).

3) Brain Structures

a. Amygdala: Studies in animals have indicated a key role for the amygdala,
which receives sensory information both directly from the thalamus and from a
longer pathway involving the somatosensory cortex and anterior cingulate cortex.
b. Prefrontal cortex: Cortical involvement in anxiety is important because it
indicates a role for cognitive processes in its expression.
c. Hippocampus: The hippocampus is also believed to have an important role in the
regulation of anxiety, because it relates fearful memories to relevant present
 contexts. Breakdown of this mechanism could lead to an overgeneralization of
fear in response to non threatening stimuli.

d. Functional imaging of the brain during the presentation of aversive stimuli (e.g.
fearful faces) has shown inconsistent changes in amygdala reactivity in patients
with GAD. Evidence of altered activity in cortical regulatory regions such as
the ventrolateral prefrontal cortex and altered connectivity between this region
and the amygdala. This picture is probably best explained by attempts to regulate
excessive emotional responses, and perhaps represents the neural expression of
the tendency of patients with GAD to use worry as an emotional coping
strategy.

PHOBIA
Phobic anxiety disorders have the same core symptoms as GAD (Worry and apprehension,
Muscle tension, Autonomic overactivity, Psychological arousal, Sleep disturbance), but these
symptoms occur only in specific circumstances. In some phobic disorders these circumstances
are few and the patient is free from anxiety for most of the time. In other phobic disorders many
circumstances provoke anxiety, and consequently anxiety is more frequent, but even so there are
some situations in which no anxiety is experienced. Two other features characterize phobic
disorders. First, the person avoids circumstances that provoke anxiety and, secondly, they
experience anticipatory anxiety when there is the prospect of encountering these circumstances.
This avoidance is a cardinal characteristic of phobias; it occurs both because the phobic response
itself is so unpleasant and because of the phobic person’s irrational appraisal of the likelihood
that something terrible will happen.

Classification of phobic disorders

For clinical purposes, in DSM- 5, phobic disorders are divided into- specific phobia, social
phobia, and agoraphobia. Panic disorder and agoraphobia are coded as two separate diagnoses. A
patient who meets criteria for both panic disorder and agoraphobia has both diagnoses assigned.

SPECIFIC PHOBIAS
A specific phobia is an irrational, strong, and persistent fear of a specific object or situation that
leads to significant distress and markedly interferes with an individual’s ability to function.
When people with specific phobias encounter a phobic stimulus, they often show an immediate
fear response that often resembles a panic attack except for the existence of a clear external
trigger (APA, 2013). Such individuals also experience anxiety if they anticipate they may
encounter a phobic object or situation and so go to great lengths to avoid encounters with their
phobic stimulus, even avoiding seemingly harmless representations of it such as photographs or
television images.
Generally, people with specific phobias recognize that their fear is somewhat excessive or
unreasonable although occasionally they may not have this insight.

The diagnostic criteria for the same is as follows- (all have to present)
A. Marked fear or anxiety about a specific object or situation (e.g., flying, heights, animals,
receiving an injection, seeing blood).
B. The phobic object or situation almost always provokes immediate fear or anxiety.
C. The phobic object or situation is actively avoided or endured with intense fear or anxiety.
D. The fear or anxiety is out of proportion to the actual danger posed by the specific object
or situation and to the sociocultural context.
E. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.
F. The fear, anxiety, or avoidance causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
G. The disturbance is not better explained by the symptoms of another mental disorder,
including fear, anxiety, and avoidance of situations associated with panic-like symptoms
or other incapacitating symptoms (as in agoraphobia); objects or situations related to
obsessions (as in obsessive-compulsive disorder); reminders of traumatic events (as in
posttraumatic stress disorder); separation from home or attachment figures (as in
separation anxiety disorder); or social situations (as in social anxiety disorder).

Specify type:
1. Animal
2. Natural environment (e.g., heights, storms, and water)
3. Blood–injection–injury (e.g., needles, invasive medical procedures)
4. Situational (e.g., planes, elevators, or enclosed places)
5. Other (e.g., phobic avoidance of situations that may lead to choking, vomiting, or
contracting an illness; or in children, avoidance of loud sounds or costumed characters)
NOTE: It is common for individuals to have multiple specific phobias. The average individual
with specific phobia fears three objects or situations, and approximately 75% of individuals with
specific phobia fear more than one situation or object. In such cases, multiple specific phobia
diagnoses, each with its own diagnostic code reflecting the phobic stimulus, would need to be
given.

Blood–Injection–Injury Phobia
People afflicted with this phobia typically experience at least as much (if not more) disgust as
fear (Teachman & Saporito, 2009). They also show a unique physiological response when
confronted with the sight of blood or injury. Rather than showing the simple increase in heart
rate and blood pressure seen when most people with phobias encounter their phobic object, these
people show an initial acceleration, followed by a dramatic drop in both heart rate and blood
pressure. This is very frequently accompanied by nausea, dizziness, or fainting, which does not
occur with other specific phobias (Öst & Hellström, 1997; Page & Tan, 2009). Blood–injection–
injury phobia runs in families more strongly than any phobic disorder and is highly heritable.
This is probably because people with this phobia inherit a strong vasovagal response to blood,
injury, or the possibility of an injection, all of which cause a drop in blood pressure and a
tendency to faint. The phobia develops over the possibility of having this response.

Situational Phobia
Phobias characterized by fear of public transportation or enclosed places are called situational
phobias. Claustrophobia, a fear of small enclosed places, is situational, as is a phobia of flying.
Psychopathologists first thought that situational phobia was similar to panic disorder and
agoraphobia. The main difference between situational phobia and panic disorder is that people
with situational phobia never experience panic attacks outside the context of their phobic object
or situation. Therefore, they can relax when they don’t have to confront their phobic situation.
People with panic disorder, in contrast, might experience unexpected, uncued panic attacks at
any time.

Natural Environment Phobia

Sometimes people develop fears of situations or events occurring in nature. These fears are
called natural environment phobias. The major examples are heights, storms, and water. These
fears also seem to cluster together (Antony & Barlow, 2002; Hofmann et al., 1997): if you fear
one situation or event, such as deep water, you are likely to fear another, such as storms. Many of
these situations have some danger associated with them and, therefore, mild to moderate fear can
be adaptive.
They are not phobias if they are only passing fears. They have to be persistent (lasting at least six
months) and to interfere substantially with the person’s functioning, leading to avoidance of boat
trips or summer vacations in the mountains where there might be a storm.

Animal Phobia
Fears of animals and insects are called animal phobias. These fears are common but become
phobic only if severe interference with functioning occurs. For example, we have seen cases in
our clinic in which people with snake or mice phobias are unable to read magazines for fear of
unexpectedly coming across a picture of one of these animals. There are many places that these
people are unable to go, even if they want to go very much, such as to the country to visit
someone. The fear experienced by people with animal phobias is different from an ordinary mild
revulsion.

Clinical Features
Onset: Specific phobia usually develops in early childhood, with the majority of cases
developing prior to age 10 years. The median age at onset is between 7 and 11 years, with the
mean at about 10 years, the youngest of any anxiety disorder except separation anxiety disorder.
Animal phobias usually begin in childhood, as do blood-injection-injury phobias and dental
phobias. However, situational phobias (such as claustrophobia and driving phobia) tend to have
onset at a later age such as adolescence or early adulthood.

Course and Duration: Once a phobia develops, it tends to last a lifetime (run a chronic course);
thus, the issue of treatment becomes important. Though specific phobias that develop in
childhood and adolescence are likely to wax and wane during that period, phobias that do persist
into adulthood are unlikely to remit for the majority of individuals.

Differential Diagnosis
1. Agoraphobia: If an individual fears only one of the agoraphobia situations, then specific
phobia, situational, may be diagnosed. If two or more agoraphobic situations are feared, a
diagnosis of agoraphobia is likely warranted. If the situations are feared for other reasons
than fear of developing panic-like symptoms or other incapacitating or embarrassing
symptoms (Criterion B of agoraphobia), such as fear of being harmed directly by the
object or situations (e.g., fear of the plane crashing, fear of the animal biting), a specific
phobia diagnosis may be more appropriate.
2. Social anxiety disorder: If the situations are feared because of negative evaluation, social
anxiety disorder should be diagnosed instead of specific phobia.
3. Separation anxiety disorder: If the situations are feared because of separation from a
primary caregiver or attachment figure, separation anxiety disorder should be diagnosed
instead of specific phobia.
4. Panic disorder: A diagnosis of specific phobia would be given if the panic attacks only
occurred in response to the specific object or situation, whereas a diagnosis of panic
disorder would be given if the individual also experienced panic attacks that were
unexpected.
5. Obsessive-compulsive disorder. If an individual's primary fear or anxiety is of an object
or situation as a result of obsessions, and if other diagnostic criteria for obsessive-
compulsive disorder are met, then obsessive-compulsive disorder should be diagnosed.
6. Trauma- and stressor-related disorders. If the phobia develops following a traumatic
event, posttraumatic stress disorder (PTSD) should be considered as a diagnosis, only if
all the criteria are met.
7. Eating disorders. A diagnosis of specific phobia is not given if the avoidance behavior is
exclusively limited to avoidance of food and food-related cues, in which case a diagnosis
of anorexia nervosa or bulimia nervosa should be considered.
8. Schizophrenia spectrum and other psychotic disorders. When the fear and avoidance are
due to delusional thinking, a diagnosis of specific phobia is not warranted.

Comorbidity
Specific phobia is frequently associated with a range of other disorders, especially depression in
older adults. Individuals with specific phobia are at increased risk for the development of other
disorders, including other anxiety disorders, depressive and bipolar disorders, substance related
disorders, somatic symptom and related disorders, and personality disorders (particularly
dependent personality disorder).

Case Study
The client was a 9-year-old Hispanic American boy with an avoidance of buttons. The phobia
began when the boy was 5 years old, in kindergarten, during an art project that involved buttons.
He described the situation in which he ran out of buttons to paste on his posterboard and was
asked to come to the front of the class to retrieve more buttons from a large bowl on his teacher’s
desk. When he reached for the bowl, his hand slipped and all the buttons in the bowl fell on him.
He described this experience as distressful, and since then both the boy and his mother reported
that his avoidance of buttons continually increased. At first, his avoidance of buttons did not
present many difficulties, but as time progressed, it became more difficult for him to handle
buttons. This led to several areas of interference for the boy and his family, such as not being
able to dress himself and difficulties concentrating in school due to excessive preoccupation with
not touching his school uniform or anything that his buttoned shirt touched. Outside school, he
avoided wearing clothing containing buttons and avoided contact with buttons that others wore.

Prevalence and Conclusion

Specifc phobias are common, occurring in about 12 percent of people at some point in their
lifetime (Kessler, Chiu, et al., 2005). Phobias are much more common in women than in men,
although the gender ratio varies by type of phobia. For example, about 90 to 95 percent of people
with animal phobias are women, but the gender ratio is less than 2:1 for blood-injection-injury
phobia.

ETIOLOGY
Biological Causal Factors
Several behavior genetic studies suggest a modest genetic contribution to the development of
specific phobias. For example, large twin studies show that monozygotic (identical) twins are
more likely to share animal phobias and situational phobias than were dizygotic (nonidentical)
twins. Another study found that the heritability of animal phobias was separate from the
heritability of complex phobias such as social phobia and agoraphobia (Czajkowski et al., 2011)
Genetic and temperamental variables also affect the speed and strength of conditioning of fear.
For example, Lonsdorf and colleagues (2009) found that individuals who are carriers of one of
the two variants of the serotonin transporter gene (the s allele, which has been linked to
heightened neuroticism) show superior fear conditioning than those without the s allele.
Relatedly, Kagan and his colleagues (2001) found that behaviorally inhibited toddlers (who are
excessively timid, shy, easily distressed, etc.) at 21 months of age were at higher risk of
developing multiple specific phobias by 7 to 8 years of age than were uninhibited children (32
versus 5 percent).
Psychological Causal Factors
PSYCHOANALYTIC VIEWPOINT
Phobias represent a defense against anxiety that stems from repressed impulses from the id.
Because it is too dangerous to “know” the repressed id impulse, the anxiety is displaced onto
some external object or situation that has some symbolic relationship to the real object of the
anxiety (Freud, 1909). However, this view was criticized as being far too speculative.

PHOBIAS AS LEARNED BEHAVIOR

Wolpe and Rachman (1960) developed an account based on learning theory, which sought to
explain the development of phobic behavior through classical conditioning. The fear response
can readily be conditioned to previously neutral stimuli when these stimuli are paired with
traumatic or painful events. Once acquired, phobic fears would generalize to other, similar
objects or situations.

Vicarious Conditioning: Simply watching a phobic person behaving fearfully with his or her
phobic object can be distressing to the observer and can result in fear being transmitted from one
person to another through vicarious or observational classical conditioning. In addition, watching
a non fearful person undergoing a frightening experience can also lead to vicarious conditioning.

Individual Differences in Learning: Individual differences in life experiences strongly affect

whether conditioned fears or phobias actually develop. Importantly, some life experiences may
serve as risk factors and make certain people more vulnerable to phobias than others, whereas
others experiences may serve as protective factors for the development of phobias (Mineka &
Sutton, 2006). For example, children who have had more previous non traumatic experiences
with a dentist are less likely to develop dental anxiety after a bad and painful experience than are
children with fewer previous non traumatic experiences (Ten Berge et al., 2002).

Certain aspects of the conditioning experience, and our response to it, also are important in
determining the level of fear that is conditioned. For example, experiencing an inescapable and
uncontrollable event, such as being attacked by a dog that one cannot escape from after being
bitten, is expected to condition fear much more powerfully than experiencing the same intensity
of trauma that is escapable or to some extent controllable. It has also been shown that our
cognitions, or thoughts, can help maintain our phobias once they have been acquired. For
example, people with phobias are constantly on the alert for their phobic objects or situations and
for other stimuli relevant to their phobia. Phobics also markedly overestimate the probability that
feared objects have been, or will be, followed by frightening events. This cognitive bias may
help maintain or strengthen phobic fears with the passage of time
Evolutionary Preparedness for Learning Certain Fears and Phobias: Our evolutionary
history has affected which stimuli we are most likely to come to fear. Primates and humans seem
to be evolutionarily prepared to rapidly associate certain objects—such as snakes, spiders, water,
and enclosed spaces—with frightening or unpleasant events. This occurs because, over the
course of evolution, those primates and humans who rapidly acquired fears of certain objects or
situations that posed real threats to our early ancestors may have enjoyed a selective advantage
(meaning, they survived more often than those who had no fear of such things). Thus, “prepared”
fears are not inborn or innate but rather are easily acquired or especially resistant to extinction.
This does not extend to all stimuli as they were not present in our early evolutionary history and
so did not convey any such selective advantage.

SOCIAL PHOBIA
Social phobia (or social anxiety disorder) is characterized by disabling fears of one or more
specific social situations (such as public speaking, urinating in a public bathroom, or eating or
writing in public. In these situations, a person fears that they may be exposed to the scrutiny and
potential negative evaluation of others or that they may act in an embarrassing or humiliating
manner. Because of their fears, people with social phobia either avoid these situations or endure
them with great distress

Social anxiety disorder is associated with elevated rates of school dropout and with decreased
well-being, employment, workplace productivity, socioeconomic status, and quality of life.
Social anxiety disorder is also associated with being single, unmarried, or divorced and with not
having children, particularly among men. In older adults, there may be impairment in caregiving
duties and volunteer activities. Social anxiety disorder also impedes leisure activities

Diagnostic Criteria

A. Marked fear or anxiety about one or more social situations in which the individual is
exposed to possible scrutiny by others. Examples include social interactions (e.g., having
a conversation, meeting unfamiliar people), being observed (e.g., eating or drinking), and
performing in front of others (e.g., giving a speech).
B. The individual fears that he or she will act in a way or show anxiety symptoms that will
be negatively evaluated (i.e., will be humiliating or embarrassing: will lead to rejection or
offend others).
C. The social situations almost always provoke fear or anxiety. Note: In children, the fear or
anxiety may be expressed by crying, tantrums, freezing, clinging, shrinking, or failing to
speak in social situations.
D. The social situations are avoided or endured with intense fear or anxiety.
E. The fear or anxiety is out of proportion to the actual threat posed by the social situation
and to the socio-cultural context.
F. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.
G. The fear, anxiety, or avoidance causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
H. The fear, anxiety, or avoidance is not attributable to the physiological effects of a
substance (e.g., a drug of abuse, a medication) or another medical condition.
I. The fear, anxiety, or avoidance is not better explained by the symptoms of another mental
disorder, such as panic disorder, body dysmoφhic disorder, or autism spectrum disorder.
J. If another medical condition (e.g., Parkinson’s disease, obesity, disfigurement from bums
or injury) is present, the fear, anxiety, or avoidance is clearly unrelated or is excessive.
Specify if:
Performance only: If the fear is restricted to speaking or performing in public

Clinical Features
Prevalence

Approximately 12 percent of the population meets the diagnostic criteria for social
phobia at some point in their lives (Kessler, Berglund, Demler, et al., 2005; Ruscio et al.,
2008).

Age of Onset
Social phobia has an early onset, usually in childhood or adolescence, and can persist
over many years, sometimes even into old age. Only about 50% of people with the
disorder seek treatment, usually after many years of symptoms Social phobia is more
common among women (about 60 percent of sufferers are women)

Nearly two-thirds of people with social phobia suffer from one or more additional anxiety
disorders at some point in their lives, and about 50 percent also suffer from a depressive
disorder at the same time Moreover, because of their distress and avoidance of social
situations, people with social phobia, on average, have lower employment rates and lower
socioeconomic status, and approximately one-third have severe impairment in one or
more domains of their life

Differential Diagnosis

1. Normative shyness.: Shyness is not by itself pathological when there is a

significant adverse impact on social, occupational, and other important areas of
functioning, a diagnosis of social anxiety disorder should be considered, and
when full diagnostic criteria for social anxiety disorder are met, the disorder
should be diagnosed
2. Agoraphobia: in agoraphobia fear and avoidance of social situation is because
there is no escape and help is not available. In social phobia fear is of negative
 scrutiny by people. In social phobia, when left alone people are calm which is not
the case in agoraphobia.
3. Panic Disorder: in social phobia concern is about fear of negative evaluation,
whereas in panic disorder the concern is about the panic attacks themselves.
4. Generalized anxiety disorder and depressive disorder: Social phobia has to be
distinguished from the former by establishing the situations in which anxiety
occurs, and from the latter from the history and mental state examination.
5. Specific phobias. Individuals with specific phobias may fear embarrassment or
humiliation (e.g., embarrassment about fainting when they have their blood
drawn), but they do not generally fear negative evaluation in other social
situations
6. Avoidant personality disorder: Individuals with avoidant personality disorder
have a broader avoidance pattern than those with social anxiety disorder.Social
phobia has to be distinguished from a personality characterized by lifelong
shyness and lack of self-confidence.

Case Study

Barry, a 22-year-old white male, was a student experiencing intense anxiety in

confronting social situations when he first presented for treatment. Barry had a 10-year
history of social phobia. His phobia significantly affected his college attendance,
academic performance and his social relationships. He would avoid people as he was
afraid that others would find him boring and foolish.He was often preoccupied with a
negative self-image; he would imagine himself in the middle of the class, with all his
peers laughing at him. He was extremely anxious whenever he was asked to make a
presentation or answer a question in class. Even though he often knew the answer, he
could never summon up the courage to speak for fear that his professors and peers would
evaluate him negatively and ridicule him. Whenever he had to confront any social
situation, his heart would start racing, his hands would tremble, and he would be unable
to speak. As a result, he almost always avoided such situations, preferring to be by
himself. Barry's mother passed away when he was seven years old. His father favored his
elder brother, who was very social and liked by all. His brother was admired by relatives
and friends, but little such attention was paid to Barry. In high school, Barry's classmates
teased him a lot for having "funny" facial expressions. Losing his mother at a young age
probably contributed to Barry's sense of threat. This fear intensified, and he continued to
avoid social situations.This fear intensified, and he continued to avoid social situations

Aetiology

Genetic factors
Genetic factors are suggested by the finding that social phobia is more common among
the relatives of people with social phobia than in the general population, and the risk is
greatest in first-degree relatives (about a fourfold increase in incidence), decreasing as the
degree of relatedness diminishes. The concordance rate of social phobia in monozygotic
twins (around 24%) is higher than that seen in dizygotic twins (around 15%) and
heritability has been estimated to be around 55%, with shared (familial) environment
making relatively little contribution.

Biological Causal Factors

The most important temperamental variable is behavioral inhibition, which shares
characteristics with both neuroticism and introversion (Bienvenu et al., 2007).
Behaviorally inhibited infants who are easily distressed by unfamiliar.stimuli and who are
shy and avoidant are more likely to become fearful during childhood and, by
adolescence, to show increased risk of developing social phobia (Hayward et al., 1998;
Kagan, 1997)

Conditioning

Most social phobias begin with a sudden episode of anxiety in circumstances similar to
those which become the stimulus for the phobia, and it is possible that the subsequent
development of phobic symptoms occurs partly through conditioning.

Cognitive factors

The principal cognitive factor in the etiology of social phobia is an undue concern that
other people will be critical of the person in social situations (often referred to as a fear of
negative evaluation). This concern is accompanied by several other ways of thinking,
including:
● excessively high standards for social performance
● negative beliefs about the self (e.g. ‘I’m boring’)
● excessive monitoring of one’s own performance in social situations
● intrusive negative images of the self as supposedly seen by others

Psychological factors

SOCIAL PHOBIA AS LEARNED BEHAVIOR

Social phobia often seems to originate from simple instances of direct or vicarious
classical conditioning such as experiencing or witnessing a perceived social defeat or
humiliation, or being or witnessing the target of anger or criticism. In two studies, 56 to
58 percent of people with social phobia recalled and identified direct traumatic
experiences as having been involved in the origin of their social phobias (Öst & Hugdahl,
1981; Townsley et al., 1995)

SOCIAL FEARS AND PHOBIA IN AN EVOLUTIONARY CONTEXT

It has been proposed that social fears and phobia evolved as a by-product of dominance
hierarchies that are a common social arrangement among animals such as primates
(Dimberg & Öhman, 1996; Öhman et al., 1985). Dominance hierarchies are established
through aggressive encounters between members of a social group, and a defeated
individual typically displays fear and submissive behavior but only rarely attempts to
escape the situation completely

Neural mechanisms
Functional neuroimaging studies have found that patients with social phobia have
increased amygdala responses to presentation of faces with expressions of negative
affect. The anticipation of public speaking in individuals with social phobia produced
activation limbic and associated regions, including the amygdala, hippocampus, and
insula, while activation of cortical regulatory areas such as the prefrontal cortex was
diminished.

LINK BETWEEN PANIC AND AGORAPHOBIA ( can write if asked about causes)

Panic disorder and agoraphobia are two distinct mental illnesses that frequently coexist. Panic
disorders characterised by panic attacks, which is often known as a "fight or flight" response, is
characterized by a sudden surge of severe anxiety accompanied by symptoms such as high heart
rate, trouble breathing, numbness or tingling, and/or dread of death.

In phobic disorders, the most important element is a persistent, irrational fear of a specifi c object
or situation that the person goes out of his or her way to avoid. Agoraphobia is defined as an
exaggerated fear of being in situations or places from which escape might be difficult, or in which
help, if needed, might be unavailable. In severe cases of agoraphobia, the person becomes entirely
housebound—unable to venture outside for fear of experiencing intense anxiety or a panic attack.
As a result, many persons who suffer agoraphobia also have a panic disorder.

Agoraphobia is a complexity of panic and many causal factors of agoraphobia are in connection
with factors of panic disorder.
AGORAPHOBIA

Agoraphobia was thought to be a fear of the agora, which is Greek meaning "open gathering
place." The most typically feared and avoided situations in agoraphobia include streets and
crowded areas such as shopping malls, movie theatres, and supermarkets.

People suffering from agoraphobia are also afraid of their own physiological sensations, therefore
they avoid activities that cause arousal, such as exercising, viewing scary movies, consuming
coffee, and even participating in sexual activity.

Agoraphobia can also develop without panic: It is the combination of two words: agora- fear of
open space ( uncertainty, fear for safety, unable to escape in , feeling trapped, not getting help in
fearful situations) and the physiological symptom of anxiety- panic like symptoms.

Diagnostic criteria:
A. Marked fear or anxiety about two (or more) of the following five situations:
1. Using public transportation (e.g., automobiles, buses, trains, ships, planes).
2. Being in open spaces (e.g., parking lots, marketplaces, bridges).
3. Being in enclosed places (e.g., shops, theatres, cinemas).
4. Standing in line or being in a crowd.
5. Being outside of the home alone.- issues of safety

B. The individual. fears or avoids these situations because of thoughts that escape might be
difficult or help might not be available in the event of developing panic-like symptoms or
other incapacitating or embarrassing symptoms (e.g., fear of falling in the elderly; fear of
incontinence). (agoraphobic situation might be generalized to other similar situations)

C. The agoraphobic situations almost always provoke fear or anxiety.

D. The agoraphobic situations are actively avoided, require the presence of a companion, or
are endured with intense fear or anxiety.

E. The fear or anxiety is out of proportion to the actual danger posed by the agoraphobic
situations and to the sociocultural context.

F. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.

G. The fear, anxiety, or avoidance causes clinically significant distress or impairment in

social, occupational, or other important areas of functioning.

H. If another medical condition (e.g., inflammatory bowel disease, Parkinson’s disease) is

present, the fear, anxiety, or avoidance is clearly excessive.
 I. The fear, anxiety, or avoidance is not better explained by the symptoms of another mental
disorder— specific phobia, situational- type, social anxiety disorder, obsessive-
compulsive disorder, body dysmorphic disorder, traumatic, posttraumatic stress
disorder, or and in separation anxiety disorder.

Note: Agoraphobia is diagnosed irrespective of the presence of panic disorder. If an

individual’s presentation meets criteria for panic disorder and agoraphobia, both diagnoses
should be assigned.

CLINICAL FEATURES
Patients diagnosed with Agoraphobia report considerable impairment and disability in terms of
role functioning & work productivity.

It’s severity is a strong determinant of the degree of disability, irrespective of the presence of
comorbid conditions.

More than one-third of individuals with agoraphobia are completely homebound and unable to
work.

Circumstances of onset.

Typical situation of the first episode include travelling in public transport or while visiting
crowded areas.
People report making efforts to escape when entering same or similar surroundings due to
increasing anxiety.
There is difficulty discovering any serious immediate stress that accounts for the first panic
attack. Some describe a background of serious problems, while others tend to report symptoms
soon after a physical illness or childbirth.

Panic attacks are recurrent and are experienced in a growing number of places.

Habit of avoidance is developed with or without the occurrence of preceding panic attacks.

Increased dependency is observed on partners and other family members especially when
engaging in activities that provoke anxiety.

Growing demands and dependency lead to relationship difficulties and over involvement
from partners.

Anticipatory fear of panic attacks within a period of 30 days of experiencing one is reported by
patients of agoraphobia..
 ONSET and COURSE
Panic disorder with or without agoraphobia typically begins in the 20s to the 40s, but it
sometimes begin in the late teen years. First onset in childhood is rare. The overall mean age at
onset for agoraphobia is 17 years. The course of agoraphobia is typically persistent and chronic.
Complete remission is rare unless the agoraphobia is treated. Decrease in rate of full remission
leads to increasing relapse and chronicity rates.

A range of other disorders, in particular other anxiety disorders, depressive disorders, substance
use disorders, and personality disorders, may complicate the course of agoraphobia.

Differential diagnosis:

Specific phobia, situational type: If the fear, anxiety, or avoidance is limited to one of the
agoraphobic situations.

Separation anxiety disorder: Thoughts in SAD are about detachment from significant others and
the home environment whereas in agoraphobia the focus is on panic-like symptoms or other
incapacitating or embarrassing symptoms in the feared situations.

Social anxiety disorder (social phobia): The situational clusters that trigger fear, anxiety, or
avoidance and the cognitive ideation are different in both disorders.

Panic disorder: Upon meeting criteria of panic disorder, agoraphobia is not diagnosed if the
avoidance behaviours associated with the panic attacks do not extend to avoidance of two or more
agoraphobic situations.

Acute stress disorder and posttraumatic stress disorder : If fear, anxiety, or avoidance is related
only to situations that remind the individual of a traumatic event, such a diagnosis is accepted.

Major depressive disorder: Avoidance behaviour differs in both disorders. In MDD, apathy, loss
of energy, low self-esteem, and anhedonia play a role while in agora, fear of panic-like or other
incapacitating or embarrassing symptoms are focused upon.

Comorbidity
Agoraphobia and panic disorder have high comorbidity rates other mental disorder ( 80%) It
frequently co-occurs with depression ( 50 to 70%) and other anxiety disorders (e.g., GAD,
specific phobias, panic disorder, social anxiety disorder). PTSD, and alcohol use disorder.

Prevalence:
Approximately 4.7 percent of the adult population has had panic disorder with or without
agoraphobia at some time in their lives, with panic disorder without agoraphobia being
more common.
 Panic disorder is about twice as prevalent and much more frequently in women than in men,the
percentage of women with severe agoraphobia 80 to 90 percent. Socilization processes account
for the gender differences.

It runs a chronic course and usually lasts for 5 years if symptoms have been met for a complete 1
year. Rates of recovery are greater in cases with followed with increasing recurrences.

Case study
Dave is a 41-year-old male who was referred by his primary care physician after presenting to the
ER with difficulty breathing. Dave’s physician was unable to find a medical explanation for his
symptoms, which left Dave feeling confused, stressed, and angry. Over the last 6 months, Dave
has had several instances where he felt an intense fear that would reach a peak within a few
minutes. During these instances, he would also experience sweating, heart palpitations, chest pain
and discomfort, and shortness of breath. At times, Dave worried that might die. As a result, Dave
has persistent worry about having another attack. In addition, he has begun to avoid unfamiliar
places and people where it may be difficult to get help in the event of another panic attack. The
panic and associated avoidance are significantly impacted Dave’s life as he turned down social
invitations, making excuses to stay at home whenever possible, and relying on his wife to drive
their children to their various activities. Although she was understanding at first, Dave’s wife
has grown frustrated with what she perceives as his irrational fear of panic attacks.

Causal factors

Biological causal factors

Genetic factors:
According to family and twin studies, panic disorder has a moderate heritable component (Maron
et al., 2010; Norrholm & Ressler, 2009). In a large twin study, López-Solà and colleagues (2014)
estimated that 30 to 34 percent of the variance in liability to panic symptoms is due to genetic
factors. As noted earlier, this genetic vulnerability is manifested at a psychological level at
least in part by the important personality trait called neuroticism (which is in turn related
to the temperamental construct of behavioral inhibition). A study suggests overlap in the
genetic vulnerability for panic disorder, generalized anxiety disorder, and agoraphobia (Hettema,
Prescott, et al., 2005).

Panic and the brain:

it is recognized that it is increased activity in the amygdala that plays a central role in panic
attacks than does activity in the locus coeruleus.

Stimulation of the central nucleus of the amygdala is known to stimulate the locus coeruleus as
well as the other autonomic, neuroendocrine, and behavioral responses that occur during a panic
attack. amygdala is the central area involved in what has been called a “fear network,with
connections not only to lower areas in the brain like the locus coeruleus but also to higher brain
areas like the prefrontal cortex. According to this view, panic attacks occur when the fear
network is activated, either by cortical inputs or by inputs from lower brain areas.

Fear network
↓
Prefrontal cortex ← Amygdala → locus coeruleus

Biochemical Abnormalities:

Klein (1981) and others (Sheehan, 1982, 1983) argued that panic attacks are alarm reactions
caused by biochemical dysfunctions. At present, two primary neurotransmitter systems are most
implicated in panic attacks: the noradrenergic and the serotonergic system s (Graeff & Del-
Ben, 2008; Neumeister et al., 2004). Noradrenergic activity in certain brain areas can stimulate
cardiovascular symptoms associated with panic (Gorman et al., 2000). Increased serotonergic
activity also decreases noradrenergic activity.
The inhibitory neurotransmitter GABA has also been implicated in the anticipatory anxiety that
many people with panic disorder have about experiencing another attack. GABA is known to
inhibit anxiety and has been shown to be abnormally low in certain parts of the cortex in people
with panic disorder

Cognitive Factors

Cognitive hypothesis

The cognitive hypothesis proposes that the anxiety attack develops because the person is
unreasonably afraid of some aspect of the situation or of certain physical symptoms that are
experienced in the situation ( Although such fears are expressed by people with established
agoraphobia, it is not known whether they were present before the onset.

Cognition
↓
Catastrophising Trigger
↓
1. Mind (I'm going to die, I'm going out of control)
2. Body (heart rate, hyperventilation)
3. Behaviour (trying to escape)

Anxiety sensitivity and perceived control:

 People who have high levels of anxiety sensitivity—a trait-like belief that certain bodily
symptoms may have harmful consequences—are more prone to developing panic attacks and
perhaps panic disorder (McNally, 2002; Pagura et al., 2009).

Several important studies have shown that simply having a sense of perceived control—for
instance, over the amount of carbon-dioxide–altered air that is inhaled (a panic provocation
procedure known frequently to bring on anxiety and panic)—reduces anxiety and even blocks
panic (e.g., Sanderson et al.,1989). . In addition, if a person with panic disorder is accompanied
by a “safe” person when undergoing a panic provocation procedure, that person is likely to show
reduced distress, lowered physiological arousal, and reduced likelihood of panic relative to
someone who came alone

Theories of spread and maintenance

Learning theories:

Conditioning could account for the association of anxiety with increasing numbers of situations,
and avoidance learning could account for the subsequent avoidance of these situations. Although
this explanation is plausible and is consistent with observations of learning in animals, there is no
direct evidence to support it.

Personality:
Agoraphobic patients are often described as dependent, and prone to avoiding rather than
confronting problems. This dependency could have arisen from overprotection in childhood,
which is reported more often by agoraphobic individuals than by controls. However, despite such
retrospective reports, it is not certain that the dependency was present before the onset of the
agoraphobia.

Family influences:
Agoraphobia could be maintained by family problems, and clinical observation suggests that
symptoms are sometimes prolonged by overprotective attitudes of other family members, but this
feature is not found in all cases.

STRESS RELATED DISORDERS

When we experience or perceive challenges to our physical or emotional well-being that
exceed our coping resources and abilities, the psychological condition that results is typically
referred to as stress. Stress is fundamentally an interactive and dynamic construct because it
reflects the interaction between the organism and the environment over time. Stress can occur
not only in negative situations (such as taking an examination) but also in positive situations
(such as a wedding). Both kinds of stress can tax a person’s resources and coping skills, although
bad stress (distress) typically has the potential to do more damage. Stress can also occur in
more than one form—not just as a simple catastrophe but also as a continuous force that
exceeds a person’s ability to manage it.

CARDIOVASCULAR DISEASE

Behavioural medicine: It is a field concerned with psychological factors as predisposing factors

to physical illness. Areas of behavioural medicine research include anxiety, arthritis, asthma,
cancer, cardiovascular disease (heart disease, hypertension, stroke), diabetes etc.

Stressor: Stressors are the external demands on the organism that create stress.

Coping: Efforts to deal with stress are called coping strategies. They serve to reduce the impact
of stressful events, thus attenuating the emotional and somatic responses and making it more
possible to maintain normal performance at the time. There are 2 types of coping mechanisms:

1. Problem-solving strategies: They can be used to make adverse circumstances less

stressful
2. Emotion-reducing strategies: They alleviate the emotional response to the stressors.

Hans Selye’s GAS model

The term ‘stress’ was coined by Hans Selye in his General Adaptation Syndrome Model
(GAS), proposed that stress responses can be characterised as having 3 distinct phases over time.

1. Alarm Phase: The alarm reaction stage refers to the initial symptoms the body
experiences when under stress. You may be familiar with the “fight-or-flight” response,
which is a physiological response to stress. This natural reaction prepares you to either
flee or protect yourself in dangerous situations. The stress response causes the release of
2 stress-related hormones (cortisol and epinephrine) which together produce a series
of changes within the body that mobilise the body’s resources for coping with short
term immediate threats.Your heart rate increases, your adrenal gland releases cortisol,
and you receive a boost of adrenaline (epinephrine), which increases energy. This fight-
or-flight response occurs in the alarm reaction stage.
2. Resistance Stage: Some stressful situations continue for extended periods of time. If you
don’t resolve the stress and your body remains on high alert, it eventually adapts
and learns how to live with a higher stress level. In this stage, the body goes through
changes in an attempt to cope with stress like increased heart rate, irregular blood
sugar, and immune system suppression. The body continues to secrete cortisol &
epinephrine and your blood pressure remains elevated. If the resistance stage continues
for too long of a period without pauses to offset the effects of stress, this can lead to the
exhaustion stage.
3. Exhaustion Stage: This stage is the result of prolonged or chronic stress. Struggling
with stress for long periods can drain your physical, emotional, and mental resources
to the point where the body no longer has strength to fight stress. The physical effects
of this stage also weaken your immune system and put you at risk for stress-related
illnesses due to the long term-effects of epinephrine and cortisol.
Yerkes-Dodson Law: It states that there is an empirical relationship between stress and
performance, and an optimal level of stress corresponding to an optimal level of performance.

Generally, practitioners present this relationship as an inverted U-shaped curve. Research

supports that if arousal is too much or too little, performance also tends to suffer. Optimal
arousal depends on the complexity and difficulty of the task to be performed. This law holds that
simple tasks are best performed when arousal levels are relatively high and complex tasks are
best performed when arousal levels are low.

CARDIOVASCULAR SYSTEM

● Cardiovascular system consists of the heart, blood vessels, and complex control
mechanisms for regulating their function.
● Strokes are temporary blockages of blood vessels leading to the brain or a rupture of
blood vessels in the brain that results in temporary or permanent brain damage and loss of
functioning
● Cardiovascular problems receiving the most attention are hypertension and coronary
heart disease.

HYPERTENSION

Blood pressure increases when the blood vessels leading to organs and peripheral areas
constrict (become narrower), forcing increasing amounts of blood to muscles in central parts of
the body. Because so many blood vessels have constricted, the heart muscles must work much
harder to force the blood to all parts of the body, which causes the increased pressure -
producing wear and tear. Risk factor for stroke and kidney diseases.

● The overwhelming majority (close to 90%) have no specific verifiable physical cause
and are considered essential hypertension.
 ● Normal blood pressure in a young adult is about 120 over 80.
● Blood pressure is defined as high by the World Health Organization if it exceeds 160/95,
although measures of 140/90 or higher are cause for concern and more usually used to
define hypertension.
● · The first value is called the systolic blood pressure, the pressure when the heart is
pumping blood.
● · The second value is the diastolic blood pressure, the pressure between beats when
the heart is at rest.
● · Elevations in diastolic pressure seem to be more worrisome in terms of risk of
disease.
● · It has been called the “silent killer” because there are few—if any—symptoms and
most people don’t know they have it
● · Symptoms of hypertension include chest discomfort, headache, and dizziness.

Prevalence of Hypertension

● According to a comprehensive survey, 27.6% of individuals between the ages of 35 and

64 suffer from hypertension in North America, with a corresponding and shocking
figure of 44.2% in six European countries.
● A more recent survey examined hypertension rates by county in the United States, and
found a staggering median prevalence of 38% for men and 40% for women.
● Furthermore, among people with hypertension and other cardiovascular concerns,
minority groups have poorer management of these conditions compared with white
Americans.
● African Americans have hypertensive vascular diseases at a rate 5 to 10 times greater
than whites. This makes hypertension a principal disorder of concern within the African
American population.
● Saab and colleagues demonstrated in a classic study that during laboratory stress tests
African Americans without high blood pressure show greater vascular responsiveness,
including heightened blood pressure. Thus, African Americans in general may be at
greater risk to develop hypertension.
● Interestingly, other research has suggested that African Americans’ risk for hypertension
may be augmented by chronic experiences of stereotype threat (i.e., situations in which
an individual fears that she will confirm negative beliefs about her demographic group),
which increase blood pressure both during and after the experience.
● Differential Diagnosis: In addition to essential hypertension, renal, vascular, and
endocrine disorders are the most common causes of hypertension. Renal artery stenosis,
adrenal adenomas (Cushing syndrome), and pituitary adenomas (Cushing disease) result
in hypertension, with characteristic findings on neuroendocrine testing and clinical
examination; in these illnesses, hypertension responds to correction of the lesion.
● Course & Prognosis: Although hypertension is often clinically silent for decades, it
may eventually lead to stroke, cardiac disease, or renal failure.

CORONARY HEART DISEASE

● Coronary heart disease (CHD), quite simply, is a blockage of the arteries supplying
blood to the heart muscle.
● Chest pain resulting from partial obstruction of the arteries is called angina pectoris or,
just angina.
● The symptoms of angina pectoris are periodic chest pains, usually located behind
the sternum and frequently radiating into the back and sometimes the left shoulder
and arm
● The major cause of these severe attacks of pain is an insufficient supply of oxygen to
the heart, called ischemia, which in turn is due to coronary atherosclerosis.
● Atherosclerosis occurs when a fatty substance or plaque builds up inside the arteries
and causes an obstruction.
● Some episodes of ischemia do not cause pain, so these are called episodes of silent
ischemia. Both angina and episodes of silent ischemia are precipitated by physical
exertion or emotional stress and are commonly relieved by rest or medication.
● Angina and silent ischemia rarely result in serious physical damage to the heart,
because blood flow to the heart is reduced but not cut off. If, however, the narrowing of
one or more coronary arteries progresses to the point of producing a total blockage, a
myocardial infarction, or heart attack, is likely to occur
● Heart attack, is a much more serious disorder leads to the death of heart tissue when a
specific artery becomes clogged with plaque. Arteries can constrict or become blocked
for a variety of reasons other than plaque.
● It is caused by an insufficient supply of oxygen to the heart.
● Severe stress, as in learning that a family member suddenly died, can lead on rare
occasions to a condition called myocardial stunning, which is basically heart failure.

Epidemiology

● Approximately one-third of all adults older than 35 years of age ultimately die of
cardiovascular disease, most often of complications of CAD. In the United States, the
incidence of CAD is more than 5 million cases per year, and more than 600,000
persons per year have a first MI. One-fifth of survivors of an acute infarction die
within 1 year.
● Public health education campaigns and more effective treatments have reduced CAD
mortality, but not its incidence.
● Established risk factors for coronary disease include family history, male sex,
hypertension, hyperlipidemia, diabetes, sedentary lifestyle, obesity, and smoking.
Premenopausal women have reduced risk compared to men, but the incidence of
clinically significant disease rises after menopause to match that of men.
● A variety of additional metabolic, nutritional, and inflammatory factors have been
identified as risk factors for incident coronary disease. Psychological factors have
increasingly been recognized to contribute to the risk of incident coronary disease and for
disease progression. Notably, depression is independently associated with an almost
doubled risk of the development of CAD.

Course & Prognosis

● One-third of patients experiencing their first MI die within 1 hour of the onset of
symptoms. Evolving trends in coronary care have reduced the short-term mortality of
patients with acute coronary syndrome who survive long enough to be hospitalized.
 ● In survivors, recurrent cardiac events occur with an incidence of 10 to 20 percent per
year, and the 1-year mortality after MI is 20 percent.

Differential Diagnosis

● Shortness of breath occurs in primary lung disease, CHF without significant coronary
disease, and psychiatric disorders including anxiety and somatic symptom disorders.
● Chest pain occurs in peptic ulcer disease, gastroesophageal reflux disease, hiatal hernia,
functional heartburn; and pneumonia.
● Palpitations occur in cases of CAD but also in mitral valve prolapse, in patients with
arrhythmias due to other causes, in hyperthyroidism, and in many patients with somatic
symptom preoccupation, panic, and anxiety disorders.

When we experience or perceive challenges to our physical or emotional well-being that

exceed our coping resources and abilities, the psychological condition that results is typically
referred to as stress. The relationship between stress and psychopathology is considered so
important that the role of stress is recognized in diagnostic formulations. This is evident in the
5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM 5) which
introduced a new diagnostic category called trauma- and stressor related disorders. It includes
Reactive Attachment Disorder (RAD), Disinhibited Social Engagement Disorder (DSED),
Post-Traumatic Stress Disorder (PTSD), Acute Stress Disorder (ASD), and Adjustment
Disorders (AD). These disorders are generally categorized by exposure to a deeply traumatic/
stressful event as a necessary diagnostic prerequisite and involve patterns of psychological
and behavioral disturbances that occur in response to identifiable stressors. The key
differences among them lie not only in the severity of the disturbances but also in the nature of
the stressors and the time frame during which the disorders occur.

PTSD
Posttraumatic Stress Disorder is primarily characterised by intense, prolonged, and sometimes
delayed reactions to an intensely stressful event for instance a natural calamity, an accident,
acts of terrorism, war, or rape, or who have been faced with threats of death, sexual violence, or
grave injury. This traumatic event is considered to cause a pathological memory acting at the
centre of the characteristic clinical symptoms associated with the disorder. Re-experiencing
aspects of the stressful event, hyperarousal, avoidance of reminders, and negative
cognitions and mood are four essential features of a post-traumatic stress reaction.

CLINICAL PICTURE
The diagnostic criteria in DSM-V for adults, adolescents, and children older than 6 years is as
follows:

A. Exposure to actual or threatened death, serious injury, or sexual violence in one

 (or more) of the following ways:
1. Directly experiencing the traumatic event(s).
2. Witnessing, in person, the event(s) as it occurred to others.
3. Learning that the traumatic event(s) occurred to a close family member or
close friend.
4. Experiencing repeated or extreme exposure to aversive details of the
traumatic event(s)

B. Presence of one (or more) of the following intrusion symptoms associated with the
traumatic event(s), beginning after the traumatic event(s) occurred:
1. Recurrent, involuntary, and intrusive distressing memories of the traumatic
event(s).
2. Recurrent distressing dreams in which the content and/or affect of the dream
are related to the traumatic event(s).
3. Dissociative reactions (e.g., flashbacks) in which the individual feels or acts as
if the traumatic event(s) were recurring.
4. Intense or prolonged psychological distress at exposure to internal or external
cues that symbolize or resemble an aspect of the traumatic event(s).
5. Marked physiological reactions to internal or external cues that symbolize or
resemble an aspect of the traumatic event(s).

C. Persistent avoidance of stimuli associated with the traumatic event(s), beginning

after the traumatic event(s) occurred, as evidenced by one or both of the following:
1. Avoidance of or efforts to avoid distressing memories, thoughts, or feelings about
or closely associated with the traumatic event(s).
2. Avoidance of or efforts to avoid external reminders that arouse distressing memories,
thoughts, or feelings about or closely associated with the traumatic event(s).

D. Negative alterations in cognitions and mood associated with the traumatic

event(s), beginning or worsening after the traumatic event(s) occurred, as evidenced by
two (or more) of the following:
1. Inability to remember an important aspect of the traumatic event(s) (typically due to
dissociative amnesia and not to other factors such as head injury, alcohol, or drugs).
2. Persistent and exaggerated negative beliefs or expectations about oneself, others, or the
world
3. Persistent, distorted cognitions about the cause or consequences of the traumatic event(s)
that lead the individual to blame himself/herself or others.
4. Persistent negative emotional state
5. Markedly diminished interest or participation in significant activities.
6. Feelings of detachment or estrangement from others.
7. Persistent inability to experience positive emotions

E. Marked alterations in arousal and reactivity associated with the traumatic

event(s), beginning or worsening after the traumatic event(s) occurred, as evidenced by
two (or more) of the following:
1. Irritable behavior and angry outbursts (with little or no provocation) typically
expressed as verbal or physical aggression toward people or objects.
2. Reckless or self-destructive behavior.
3. Hypervigilance.
4. Exaggerated startle response.
5. Problems with concentration.
6. Sleep disturbance

F. Duration of the disturbance (Criteria B, C, D, and E) is more than 1 month.

G. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
H. The disturbance is not attributable to the physiological effects of a substance (e.g.,
medication, alcohol) or another medical condition.

Specify whether: With dissociative symptoms: The individual’s symptoms meet the criteria for
post-traumatic stress disorder, and in addition, in response to the stressor, the individual
experiences persistent or recurrent symptoms of Depersonalization or Derealization
Specify if: With delayed expression: If the full diagnostic criteria are not met until at least
6 months after the event (although the onset and expression of some symptoms may be
immediate).

CASE STUDY
T, a 42-year old male and an earthquake survivor, had been experiencing PTSD symptoms
for over 8 years. He made a conscious effort to avoid thoughts and visuals associated with his
memories of the event- especially those related to the injuries and deaths that he witnessed. In
an attempt to keep himself distracted, he started investing more and more of his time in work
and other hobbies, filling up all his days with some activity or the other to minimize chances of
his mind straying to his mental account of the event. T also tried to actively avoid people
who had undergone the same experience, and would divert the flow of the conversation in a
different direction when the topic of the event came up. Despite his best efforts, intrusive
thoughts and images about the trauma would continue to bother him whenever he was not
preoccupied and found that the harder he tried to resist the thoughts, the stronger and more
recurrent they would become. He also experienced frequent and increasingly distressing
nightmares which would significantly deteriorate the quality of his sleep as he would
constantly wake up violently. These behavioural issues permeated into his interpersonal space
as it would disturb his sleeping wife, causing them to start sleeping in different bedrooms. He
was afraid that these recurring memories of the event may cause his emotions to spiral out of
control, rendering him helpless and unable to cope. He was extremely concerned that the
accompanying fear and panic associated with the trauma would be a chronically crippling
feeling he would have to live with forever. As his emotional and behavioural symptoms
worsened, they began to adversely impair his psychological, social, and occupational
functioning.

CLINICAL FEATURES
ONSET, COURSE AND PROGNOSIS: It can occur at any age, even in childhood. In most
cases, the onset of symptoms begins immediately after the traumatic event, usually within 3
months. Symptom duration varies by proximity, duration, and intensity of trauma, along
with comorbidity with other disorders.
A large percentage of people will recover on their own, although the average duration of
symptoms in people not receiving treatment may go up to 64 months. On the other hand, in those
receiving treatment, the duration may be as less as 36 months. About one-third of cases of PTSD
remit within 3 months, but about 40% of patients have a chronic course and may not recover
for many years (Santiago et al., 2013).
Long-term outcome depends on initial symptom severity and the experience of further
traumatic events. Good prognosis is dependent on rapid engagement of treatment, early and
ongoing social support, avoidance of retraumatization, positive premorbid function, and an
absence of other psychiatric disorders or substance abuse.

DIFFERENTIAL DIAGNOSIS
● Acute Stress Disorder: ASD can be differentiated from PTSD based on its symptom
duration which is restricted to 3 days to 1 month following exposure to trauma and
PTSD is diagnosed only after 1 month of symptomatology has elapsed.
● Adjustment Disorders: They are distinguished in terms of the stressor which can be of
any type or severity rather than the ones listed under Criterion A for PTSD. A
diagnosis for AD may also be made when the response to a stressor that meets PTSD
Criterion A does not meet all other PTSD criteria.
● OCD: Recurrent intrusive thoughts meet the definition of an obsession and are
unrelated to a traumatic event. Compulsions are also usually present, while other
PTSD symptoms are typically absent.
● Other Anxiety Disorders: Anxiety disorders are not associated with a specific
traumatic event.
 ● Dissociative Disorders: do not necessarily meet full PTSD criteria
● Depressive Disorder: Many symptoms of PTSD may be absent in depressive disorders,
especially from Criterion B or C of PTSD.
● Psychotic Disorders: Flashbacks in PTSD are distinguished from illusions,
hallucinations, and other perceptual disturbances characteristic of psychotic
disorders such as schizophrenia and substance/medication-induced disorders.

Comorbidity
Individuals with PTSD are 80% more likely to have symptoms that meet diagnostic criteria for
at least one other mental disorder (e.g., depressive, bipolar, anxiety, or substance use
disorders). Comorbid substance use disorder and conduct disorder are more common among
males than among females. Most young children with PTSD also have at least one other
diagnosis, with oppositional defiant disorder and separation anxiety disorder
predominating. Finally, there is considerable comorbidity between PTSD and major
neurocognitive disorder.

Prevalence
Estimates of PTSD in the general population have mainly been obtained from the USA, where
lifetime rates (using older diagnostic criteria) have been between 6% and 9%. Rates in high-
risk groups (for example, soldiers exposed to combat) can be much higher, up to 40%
(Sareen, 2014). Also higher in areas prone to natural calamities. Lifetime PTSD rates are
higher among females than males (10.4% versus 5%), likely due to their higher occurrence
of exposure to traumatic experiences such as rape, domestic abuse, and other forms of
interpersonal violence. Prevalence rates vary slightly across cultural groups- compared with
U.S. non-Latino whites, higher rates of PTSD have been reported among U.S. Latinos, African
Americans, and American Indians, and lower rates have been reported among Asian
Americans.

AETIOLOGY
THE STRESSOR: The necessary cause of PTSD is an exceptionally stressful event. DSM-
5 describes such events as involving actual or threatened death or serious injury or a threat to
the physical integrity of the person or others.
Epidemiological research has revealed the following findings (Ehlers, 2009):
● The majority of people will experience at least one traumatic event in their lifetime.
● Intentional acts of interpersonal violence, in particular combat and sexual assault, are
more likely to lead to PTSD than accidents or disasters.
● Men tend to experience more traumatic events in general than women, but women
experience more events that are likely to lead to PTSD (e.g. childhood sexual abuse, rape,
and domestic violence).
● Women are also more likely to develop PTSD in response to a traumatic event than men.
This enhanced risk is not explained fully by differences in the type of traumatic event.
While the nature, intensity, and exposure to the trauma significantly impacts the
development of PTSD, other factors also come into play:

GENETIC FACTORS: A family history of anxiety suggests a generalized biological

vulnerability for PTSD. Studies of twins suggest that differences in susceptibility to PTSD are
in part genetic. True et al. (1993) studied monozygotic and dizygotic male twins and found that
genetic variation accounted for about one- third of the variance in susceptibility to self-
reported PTSD. The genetic liability to PTSD is partly explained by a genetic effect on
personality, which modifies the propensity of individuals to engage in risky behaviours.
Nevertheless, as with other disorders, there is little or no evidence that genes directly cause
PTSD. Rather, the stress-diathesis model (stressors cause certain vulnerabilities to precipitate
into mental disorders) comes into play again since genetic factors predispose individuals to be
easily stressed and anxious, which then may make it more likely that a traumatic experience
will result in PTSD.

RECIPROCAL GENE–ENVIRONMENT INTERACTIONS: Breslau, Davis, and

Andreski (1995) demonstrated that characteristics such as a tendency to be anxious, as well as
factors such as minimal education, predict exposure to traumatic events in the first place
and therefore an increased risk for PTSD. Higher intelligence has also been found to predict
decreased exposure to these types of traumatic events. That is, personality and other
characteristics, some of them at least partially heritable, may predispose people to the
experience of trauma by making it likely that they will be in (risky) situations where
trauma is likely to occur (Norrholm & Ressler, 2009).

NEUROBIOLOGICAL CORRELATES: It seems clear that PTSD involves a number of

neurobiological systems. Research has focused on monoamine neurotransmitters and
corticotropin-releasing factor (CRF) which indicates heightened activity in the
hypothalamic– pituitary– adrenal (HPA) axis, both of which are involved in mediating
defensive responses to stressful events. Chronic arousal associated with HPA axis and some
other symptoms of PTSD may be directly related to changes in brain function and structure.
Studies have implicated changes in the hippocampus, important in memory formation, and
the amygdala, which plays a role in non- conscious emotional processing. These findings
suggest that hippocampal dysfunction prevents adequate memory processing, while
increased activity of the amygdala increases arousal and facilitates the automatic encoding
and partial recall of traumatic memories.

PSYCHOLOGICAL FACTORS:
● Generalized Psychological Vulnerability: described in the context of early
experiences with unpredictable events. Family instability is one factor that may instil
a sense that the world is an uncontrollable, potentially dangerous place (Chorpita &
Barlow, 1998; Suárez et al., 2009), so it is not surprising that individuals from unstable
families are at increased risk for developing PTSD if they experience trauma.
 ● Fear conditioning: Some patients with PTSD experience vivid memories of the
traumatic events in response to sensory cues, such as smells and sounds related to
the stressful situation. They can thus develop a conditioned or learned alarm reaction
to stimuli that remind them of the trauma.
● Cognitive theories: suggest that PTSD arises when the normal processing of
emotionally charged information is overwhelmed, so that memories persist in an
unprocessed form in which they can intrude into conscious awareness. Patients with
PTSD tend to have incomplete and disorganized recall of the traumatic events.
Individual differences in response to the same traumatic events are explained as being
because of differences in the appraisal of the trauma and of its effects. Similarly,
differences in the appraisal of the early symptoms may explain why these symptoms
persist for longer in some individuals.
● Psychodynamic theories: emphasise the role of emotional development in
determining individual variations in the response to stressful events. It is supported by
the fact that factors such as positive self- esteem, trust, and secure attachment
increase resilience and decrease the risk of experiencing PTSD following trauma.
● Maintaining factors: symptoms of PTSD may be maintained in part by negative
appraisals of the early symptoms. Other suggested maintenance factors include
avoidance of reminders of the traumatic situation (which prevents deconditioning and
cognitive reappraisal), suppression of intrusive memories (which is known to make
them more likely to recur).

SOCIAL FACTORS: Results from a number of studies show that if you have a strong and
supportive group of people around you, it is much less likely you will develop PTSD after a
trauma. The broader and deeper the network of social support, the less the chance of
developing PTSD. Similarly, positive coping strategies involving active problem solving can
be protective.

OBSESSIVE-COMPULSIVE AND RELATED DISORDERS

Obsessive and Compulsive and related disorders include:
1. Obsessive-Compulsive Disorder (OCD),
2. Body Dysmorphic Disorder,
3. Hoarding Disorder,
4. Trichotillomania (hair-pulling disorder),
5. Excoriation (skin-picking) Disorder,
6. Substance/Medication-Induced Obsessive-Compulsive and Related disorder,
7. Obsessive-Compulsive and Related Disorder Due to Another Medical Condition,
8. Other Specified Obsessive-Compulsive and Related Disorder and Unspecified Obsessive-
Compulsive and Related Disorder (E.G., Body-Focused Repetitive Behaviour Disorder,
Obsessional Jealousy).

Obsessive Compulsive Disorder

In DSM-5, obsessive-compulsive disorder was removed from the category of anxiety disorders
and placed into a new category, ‘obsessive compulsive and related disorders.’ The primary
reason for moving OCD into the new category was that anxiety is not generally used as a
primary indicator of OCD severity. It was also noted that anxiety occurs in a wide range of
disorders, so the presence of some anxiety symptoms is not valid for regarding OCD as an
anxiety disorder.

OCD is defined by the occurrence of both obsessive thoughts and compulsive behaviors
performed in an attempt to neutralize such thoughts. It is characterized by obsessional
thinking, compulsive behaviour and varying degrees of anxiety, depression, and
depersonalization.

The Diagnostic Criteria for Obsessive Compulsive Disorders is:

A. Presence of obsession, compulsion, or both:

Obsessions are defined by (1) and (2)

1. Recurrent or persistent thoughts, urges, or images which are at some point

during the disturbance, experienced as intrusive and unwanted, and that in
most individuals cause marked anxiety or distress.

2. The individual tries to suppress these thoughts, urges, or images, or to

neutralise them with some other thought or action (i.e., by performing a
compulsion).

Compulsions are defined by (1) and (2)

1. Repetitive behaviors (e.g., handwashing, ordering, checking) or mental acts

(e.g., praying, counting, repeating words silently) that the individual feels
driven to perform in response to an obsession or according to rules that
must be applied rigidly.

2. The behaviours or mental acts are aimed at preventing or reducing anxiety

or distress, or preventing some dreaded event or situation; however, these
behaviours or mental acts are not connected in a realistic way with what
they are designed to neutralize or prevent, or are clearly excessive.

B. The obsessions or compulsions are time-consuming (e.g., take more than 1 hour per day)
or cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning.
 C. The obsessive-compulsive symptoms are not attributable to the physiological effects
of a substance (e.g., a drug of abuse, a medication) or another medical condition.

D. The disturbance is not better explained by the symptoms of another mental disorder

Specify if:

With good or fair insight: The individual recognizes that obsessive-compulsive disorder beliefs
are definitely or probably not true or that they may or may not be true.

With poor insight: The individual thinks obsessive-compulsive disorder beliefs are probably
true.

With absent insight/delusional beliefs: The individual is completely convinced that obsessive-
compulsive disorder beliefs are absolutely true.

Specify if

Tic-related: The individual has a current or past history of a tic disorder

Clinical Features

Types of Obsessions and Compulsions

Many obsessive thoughts involve contamination fears, fears of harming oneself or others,
and pathological doubt. Other fairly common themes are concerns about need for symmetry
(e.g., having magazines on a table arranged in a way that is “exactly right”), sexual obsessions,
and obsessions concerning religion or aggression.

There are five primary types of compulsive rituals: cleaning (hand washing and showering),
checking, repeating, ordering or arranging, and counting, and many people exhibit multiple
kinds of rituals. For a smaller number of people, the compulsions are to perform various
everyday acts (such as eating or dressing) extremely slowly (primary obsessional slowness), and
for others the compulsions are to have things exactly symmetrical or “evened up”.

Age of Onset

According to the data from the United States, the mean age at onset of OCD is 19.5 years and
25% cases start by the age of 14 years. Males have an earlier age at onset than females: nearly
25% of males have onset before age 10 years. The onset of symptoms is typically gradual;
however, acute onset has also been reported. Onset age after 35 years is rare, but does occur.

Development and Course

If OCD is untreated, the course is usually chronic, often with waxing and waning symptoms.
Some individuals have an episodic course, and a minority have a deteriorating course. Without
treatment, remission rates in adults are low. However, 40% of individuals with onset of OCD
in childhood or adolescence may experience remission by early adulthood. The course of OCD
is often complicated by the co-occurrence of other disorders.

Prevalence
The 12-month prevalence of OCD in the United States is 1.2%, with a similar prevalence
internationally (1.1%-1.8%). Females are affected at a slightly higher rate than males in
adulthood, although males are more commonly affected in childhood.

Differential Diagnosis

1. Anxiety Disorders: Recurrent thoughts, behaviours, and requests for reoccurrence in

anxiety disorders are usually about real-life concerns, whereas obsessions of OCD
usually include content that is odd, irrational or seemingly of a magical nature.
2. Major Depressive Disorder: MDD is characterised by rumination that is often mood
congruent and not necessarily experienced as intrusive or distressing; ruminations are
not linked to compulsions, as in OCD.
3. Other Obsessive Compulsive and Related Disorders: Other disorders are more
specific to their compulsions. Body Dysmorphic Disorders are limited to concerns about
physical experiences and trichotillomania is limited to hair pulling.
4. Tics (in tic disorder) and stereotyped movements: A tic is a sudden, rapid, recurrent,
nonrhythmic motor movement or vocalization (e.g., eye blinking, throat clearing). A
stereotyped movement is a repetitive, seemingly driven, non-functional motor behaviour
(e.g., head banging, body rocking, self-biting). On the other hand, compulsions are
usually preceded by obsessions, tics are often preceded by premonitory sensory urges.
In cases of both symptoms- both diagnoses may be warranted
5. Psychotic Disorders: Some individuals with OCD have poor insight or even delusional
OCD beliefs. However, they have obsessions and compulsions (distinguishing their
condition from delusional disorder) and do not have other features of schizophrenia or
schizoaffective disorder (e.g., hallucinations or formal thought disorder).
6. Other compulsive-like behaviours: Certain behaviours are sometimes described as
''compulsive," including sexual behaviour (in the case of paraphilias), gambling (i.e.,
gambling disorder), and substance use (e.g., alcohol use disorder). However, these
behaviours differ from the compulsions of OCD in that the person usually derives
pleasure from the activity and may wish to resist it only because of its deleterious
consequences.
7. Obsessive-compulsive personality disorder: Obsessive-compulsive personality disorder
involves an enduring and pervasive maladaptive pattern of excessive perfectionism
and rigid control. If an individual manifests symptom of both OCD and obsessive-
compulsive personality disorder, both diagnoses can be given.

Comorbidities
OCD frequently co-occurs with other anxiety disorders, most commonly social phobia, panic
disorder, GAD, and PTSD (Kessler, Chiu, Demler, et al., 2005; Mathews, 2009). Moreover,
approximately 25 to 50 percent of people with OCD experience major depression at some time
in their lives and as many as 80 percent experience significant depressive symptoms (Steketee
& Barlow, 2002; Torres et al., 2006), often at least partly in response to having OCD.

Case Study (Butcher, Hooley, and Mineka)

Mark was a 28-year-old single male who suffered from severe obsessive thoughts and images
about causing harm to others such as running over pedestrians while he was driving. He
also had severe obsessions that he would commit a crime such as robbing a store of a large
amount of money or poisoning family members or friends.

These obsessions were accompanied by lengthy and excessive checking rituals. For example,
one day when he drove, he began obsessing that he had caused an accident and hit a pedestrian at
an intersection, and he felt compelled to spend several hours driving and walking around all
parts of that intersection to find evidence of the accident.

At first, the obsessions were focused on the possibility that he would be implicated in some
crime that he had not committed; later, they evolved to the point where he was afraid that he
might actually commit a crime and confess to it. The checking rituals and avoidance of all
places where such confessions might occur eventually led to his having to give up his career
and his own apartment and move back in with his family.

At the time he presented for treatment, Mark’s obsessions about harming others and confessing
to crimes (whether or not he had committed them) were so severe that he had virtually
confined himself to his room at his parents’ house. Indeed, he could leave his room only if he
had a tape recorder with him so that he would have a record of any crimes he confessed to
out loud because he did not trust his own memory. He also could not speak at all on the
phone for fear of confessing some crime that he had (or had not) committed. He also could
not go into a store alone or into public bathrooms, where he feared he might write a
confession on the wall and be caught and punished.

Aetiology/Clinical Dynamics/Causal Picture of OCD

1. Psychological Factors:

1.1. OCD as Learned Behaviour: Learning view of obsessive-compulsive disorder is

derived from Mowrer’s two-process theory of avoidance learning (1947).
According to this theory, neutral stimuli become associated with frightening
thoughts or experiences through classical conditioning and come to elicit
anxiety. For example, touching a doorknob or shaking hands might become
associated with the “scary” idea of contamination. Once having made this
association, the person may discover that the anxiety produced by shaking hands or
touching a doorknob can be reduced by hand washing. Washing his or her hands
extensively reduces the anxiety, and so the washing response is reinforced, which
makes it more likely to occur again in the future when other situations evoke
 anxiety about contamination (Rachman & Shafran, 1998). Once learned, such
avoidance responses are extremely resistant to extinction (Mineka & Zinbarg,
2006). Moreover, any stressors that raise anxiety levels can lead to a heightened
frequency of avoidance responses in animals or compulsive rituals in humans
(Cromer et al., 2007).

1.2. OCD and Preparedness: The preparedness concept considers the

evolutionarily adaptive nature of fear and anxiety for our early ancestors and can
help us to understand the occurrence and persistence of OCD (De Silva,
Rachman, & Seligman, 1977; Rapoport, 1989). Peoples’ preoccupation with dirt,
contamination, and other potentially dangerous situations has led to the
conclusion that the features may have evolutionary roots. Additionally, some
theorists have argued that the displacement activities that many species of animals
engage in under situations of conflict or high arousal resemble the compulsive
rituals seen in obsessive-compulsive disorder (Craske, 1999; Mineka & Zinbarg,
1996; Rapoport, 1989; Winslow & Insel, 1991).

1.3 Cognitive Biases and Distortions: People with OCD have an attentional bias toward
disturbing material relevant to their obsessive concerns, much as occurs in the other
anxiety disorders. They also have difficulty blocking out negative, irrelevant input or
distracting information, so they may attempt to suppress negative thoughts stimulated by
this information which may paradoxically increase their frequency.

Moreover, those with OCD have low confidence in their memory ability (especially for
situations they feel responsible for), which may contribute to their repeating their
ritualistic behaviours over and over again (Cougle et al., 2007; Dar et al., 2000).

An additional factor contributing to their repetitive behaviour is that people with OCD have
deficits in their ability to inhibit both motor responses (Morein-Zamir et al., 2010) and
irrelevant information (Bannon et al., 2008).

2. Biological Causal Factors

2.1 Genetic Factors: Evidence from twin studies reveals a moderately high
concordance rate for OCD for monozygotic twins and a lower rate for dizygotic
twins. However, it may be at least partially a “neurotic” predisposition (Hanna, 2000;
van Grootheest et al., 2007). Consistent with twin studies, most family studies have found
higher rates of OCD in first-degree relatives of OCD clients.

2.2 OCD and the Brain: Findings from studies using PET scans have shown that people
with OCD have abnormally high levels of activity in two parts of the frontal cortex (the
orbital frontal cortex and the cingulate cortex/gyrus), which are also linked to the limbic
area.

People with OCD also have abnormally high levels of activity in the subcortical caudate
nucleus, which is part of the basal ganglia. These primitive brain circuits are involved
in executing primitive patterns of behaviour such as those involved in sex,
aggression, and hygiene concerns.

Dysregulation in the cortico–basal–ganglionic–thalamic circuit, causes inappropriate

behavioural responses, including repeated sets of behaviours stemming from
territorial and social concerns and from hygiene concerns.

2.3 Neurotransmitter Abnormalities: Current evidence suggests that increased

serotonin activity and increased sensitivity of some brain structures to serotonin are
involved in OCD symptoms. Other neurotransmitter systems like dopaminergic, GABA,
and glutamate systems also seem to be involved, although their role is not yet well
understood.