BASIC PSYCHOPHARMACOLOGY

FOR COUNSELORS AND

PSYCHOTHERAPISTS
This page intentionally left blank
 Second Edition

BASIC PSYCHOPHARMACOLOGY
FOR COUNSELORS AND
PSYCHOTHERAPISTS
Richard S. Sinacola, Ph.D.
The Chicago School of Professional Psychology—Los Angeles

Timothy Peters-Strickland M.D.

Covance, Inc—Princeton

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Library of Congress Cataloging-in-Publication Data

Sinacola, Richard S.
Basic psychopharmacology for counselors and psychotherapists / Richard S. Sinacola,
Timothy Peters-Strickland.—2nd ed.
p. cm.
Includes bibliographical references and index.
ISBN-13: 978-0-13-707980-3
ISBN-10: 0-13-707980-X
1. Psychopharmacology. I. Peters-Strickland, Timothy. II. Title.
RM315.S56 2012
615'.78—dc22 2011000217

10 9 8 7 6 5 4 3 2 1

ISBN-10: 0-13-707980-X
ISBN-13: 978-0-13-707980-3
To my students, past and present, who always inspire me to do better.
R. S. Sinacola

To my loving family:
Howard, Alexia, and Alyssa
T. Peters-Strickland
 PREFACE

Welcome to the second edition of Basic Psychopharmacology for Counselors and Psychotherapists.
With more psychotherapy patients taking psychotropic medications than ever before, counselors and
therapists need quick and accurate information. Finding this information is not easy because most
textbooks on psychotropic medications are written by physicians for physicians. In the few cases that
nonphysicians, usually biologically oriented Ph.D.’s, have attempted this endeavor, they have pro-
duced works that are more like physiological psychology texts, which are beyond the basic questions
and interests of the student, counselor, or psychotherapist.
The second edition of Basic Psychopharmacology for Counselors and Psychotherapists, like
the first edition, is designed to provide basic yet comprehensive information for the typical gradu-
ate student in a mental health training program, as well as the practicing clinician in the field. Most
graduate students have not taken undergraduate courses in physiological psychology, and their
knowledge of the brain and neuronal functions is minimal. This textbook presents these and other
topics in easy-to-understand language. In fact, the entire text continues to be written in a familiar
style that invites the otherwise intimidated professional to learn more. Medical jargon is kept to a
minimum and voluminous information on psychopathology is also omitted because we assume that
clinicians and graduate students are familiar with The Diagnostic and Statistical Manual of Mental
Disorders, 4th ed.-TR (DSM-IV) and the criteria used in diagnostic determinations.
In addition to offering up-to-date information on the latest medications currently available
for treating mental illness and other related conditions, this book will assist clinicians in working
more effectively with their patients on medication and with the professionals prescribing them.
The book is organized to address the most commonly presented types of pathology first.

WHAT’S NEW IN THE SECOND EDITION

• Updated information on the latest medications used to treat a variety of mental health concerns.
• Updated research on the newest medications, including novel applications of some of the
older, well-known medications.
• Updated tables in each chapter that reflect the latest medications and their properties.
• An updated comprehensive table of all psychopharmacology agents, located in the appendix.
• The addition of clinical case examples in each treatment-related chapter.
• The addition of a Glossary to familiarize the student or professional with psychopharma-
cology and biology terms used in the text.
• The addition of new diagnostic considerations and medications in Chapter 14, Treatment
of Comorbidity and Other Disorders.

CHAPTER OUTLINES FOR THE SECOND EDITION

• Chapter 1 gives students and their professors and practicing clinicians reasons why the
study of psychopharmacology is so important for the mental health professional.
• Chapter 2 provides a basic explanation of the functions of the brain and neurological sys-
tem, including the anatomy and function of neurons, the role of neurotransmitters and
other neurochemicals involved in emotions and behavior, and the electrical and chemical
communications between cells.
vi
 Preface vii

• Chapter 3 addresses issues related to psychopharmacology and pharmacokinetics, including

methods of administering drugs; absorption, distribution, and elimination of drugs; thera-
peutic dose and therapeutic index; tolerance, withdrawal, and discontinuance of drugs; syn-
ergism and potentiation; placebo effects; and prescription and pharmaceutical terms.
• Chapter 4 provides the therapist with tools and techniques for taking a thorough history of
the patient, including a patient history outline, a mental status outline, assessment and test-
ing instruments, and an outline for an initial patient interview.
• Chapters 5 through 12 address trade and generic medications and herbals used to treat com-
mon mental health conditions: unipolar depression; bipolar illness; anxiety and psychotic
disorders; ADHD and attention disorders; and cognitive, sleep, and personality disorders.
• Chapter 11 concentrates solely on sleep disorders. It was included because many clinicians
who deal with patients presenting with these concerns are unfamiliar with the medications
used to treat insomnia.
• Chapter 13 addresses chemical dependency and co-occurring conditions and the special
medications used to treat this population. This topic is not addressed in most other texts.
• Chapter 14 provides typical medication regimens used to treat patients with comorbid con-
ditions, including patients with chronic pain, eating disorders and obesity, impulse control
problems, sexual compulsivity, gambling, and other intrusive behaviors.
• Chapters 15 through 19 present cases across the developmental continuum, including chil-
dren and adolescents and early, middle, and older adults. Many of the cases are based on
actual patients. The cases are used to demonstrate both the diagnostic process and the ra-
tionale for choosing one medication over another.
• Complete, easy-to-read tables of medications appear throughout the text and are combined
into a master table in the Appendix.
This text serves as a basic introduction to psychopharmacology for the nonmedical
provider. Although information on dosage and use was accurate at the time of writing, the clini-
cian should not use this information as a guide for prescribing medications. All clinicians should
consult their respective codes of ethics and their home state’s scope of practice to ensure that dis-
cussing medications and their effects with patients is within the scope of their license to practice.
This book was designed to be a brief yet comprehensive overview of clinical psychophar-
macology. It can be read easily in a weekend and will serve as a handy reference guide for men-
tal health professionals from all disciplines. Combined, we have more than 42 years of clinical
experience—one of a us as a psychologist with a private practice and a professor teaching psy-
chopharmacology in a graduate setting, and the other as a psychiatrist treating patients from all
walks of life. We hope that the readers find this book informative as well as interesting.
We wish to acknowledge the editors and staff at Pearson for their help and encouragement
in completing this task.
We would also like to thank the following reviewers for their time and feedback in making
this book a worthwhile contribution to the field: Derek Chignell, Wheaton College; Sandra J.
Croswaite, Pierce College; Katherine M. Dooley, Mississippi State University; Steven P. Farmer,
University of North Texas, Dallas; and Lynn Gilman, Indiana University, Bloomington.
R. S. Sinacola, Ph.D.
Los Angeles, CA
T. Peters-Strickland, M.D.
Princeton, NJ
 ABOUT THE AUTHORS
Richard S. Sinacola, Ph.D., a licensed psychologist, is Associate Professor and former Chair of
Clinical Psychology at the Chicago School of Professional Psychology in Los Angeles and
maintains a private practice in Pasadena. He was the former Director of Psychology Programs
for Chapman University in Palm Desert, CA. He also was the former Chair of Counseling and
Addiction Studies at the University of Detroit Mercy. He has served on the editorial board of the
Michigan Journal of Counseling and Development, and he is the past secretary of the Michigan
Psychological Association. He lectures internationally on various mental health topics. He holds
degrees in psychology, counseling, and clinical social work from The University of Detroit and
Wayne State University.

Timothy Peters-Strickland, M.D., is a Medical Director in Neuroscience at Covance in

Princeton, N.J., and conducts clinical research in the mental health field. Dr. Peters-Strickland
has held an appointment as a clinical instructor with the University of Southern California. He is
a diplomate of the American Board of Psychiatry and Neurology with an added qualification in
Addiction Psychiatry. Dr. Peters-Strickland obtained his medical degree from the University of
Florida after obtaining a BA in Biochemistry from Florida State University. He completed his
psychiatric residency at the University of Southern California.

viii
 BRIEF CONTENTS

Chapter 1 Why Study Psychopharmacology: Reasons for the

Nonmedical Therapist to Read This Book 1
Chapter 2 Basic Neurobiology 4
Chapter 3 Psychopharmacology and Pharmacokinetics 13
Chapter 4 History Taking and Assessment Techniques 18
Chapter 5 Treatment of Unipolar Depression 23
Chapter 6 Treatment of Bipolar Disorder 36
Chapter 7 Treatment of Anxiety Disorders 48
Chapter 8 Treatment of Psychotic Disorders 58
Chapter 9 Treatment of ADHD and Disorders of Attention 68
Chapter 10 Treatment of Cognitive Disorders 74
Chapter 11 Treatment of Sleep Disorders 81
Chapter 12 Treatment of Personality Disorders 89
Chapter 13 Treatment of Chemical Dependency and Co-Occurring
Conditions 93
Chapter 14 Treatment of Comorbidity and Other Disorders 102
Chapter 15 Case Vignettes: Children 111
Chapter 16 Case Vignettes: Adolescents 115
Chapter 17 Case Vignettes: Early Adulthood 119
Chapter 18 Case Vignettes: Middle Adulthood 123
Chapter 19 Case Vignettes: Older Adulthood 129

Appendix 133
Glossary 149
Bibliography 152
Index 163

ix
 CONTENTS
Chapter 1 WHY STUDY PSYCHOPHARMACOLOGY: REASONS FOR
THE NONMEDICAL THERAPIST TO READ THIS BOOK 1
Chapter 2 BASIC NEUROBIOLOGY 4
Neurons 4
Neural Communication 5
Electrical Chemical Properties of Neural Transmission 6
Neurotransmitters of Emotion and Behavior 9

Chapter 3 PSYCHOPHARMACOLOGY AND

PHARMACOKINETICS 13
Routes of Drug Administration 13
Drug Absorption, Distribution, and Metabolism 14
Drug Absorption 14
Drug Distribution 14
Drug Metabolism 15
Other Pharmacokinetic Principles 15
Therapeutic Index and Dose 15
Tolerance and Withdrawal 16
Discontinuation Syndrome 16
Potentiation and Synergism 16
Placebo Response 16
Prescription and Pharmacy Terms 17

Chapter 4 HISTORY TAKING AND ASSESSMENT TECHNIQUES 18

Obtaining Patient History 18
Mental Status Examination 20
Patient Questionnaires and Assessment Instruments 21
Structuring the Initial Interview 22

Chapter 5 TREATMENT OF UNIPOLAR DEPRESSION 23

Biological Versus Environmental Depression 23
Causes of Biological Depression 24
Counseling and Psychotherapy 25
Medications for Depression 25
Herbal and Holistic Substances 29
Light Therapy for Seasonal Affective Disorder (SAD) 31
Importance of Exercise 31
x
 Contents xi

Electroconvulsive Therapy (ECT) 31

Procedural Steps for Patient Treatment 32
왘 Case Vignette 34

Chapter 6 TREATMENT OF BIPOLAR DISORDER 36

Prevalence and Types of Bipolar Illness 36
Causes of Bipolar Disorder 37
Counseling and Psychotherapy 38
Medications for Bipolar Disorder 39
Lithium 39
Anticonvulsants 41
Atypical Antipsychotic Medications 42
Typical Antipsychotic Medications 43
Other Medications 44
Electroconvulsive Therapy (ECT) 44
Treatment Resistance and Protocol 44
Mania Treatment Protocol 44
Depression Treatment Protocol 45
Treatment Protocol for Mixed Mood States 45
Patient and Family Education 46
Patient Education 46
Family Education 46
왘 Case Vignette 46

Chapter 7 TREATMENT OF ANXIETY DISORDERS 48

Symptoms and Causes of Anxiety Disorders 48
Panic Disorder With or Without Agoraphobia 50
Generalized Anxiety Disorder 53
Posttraumatic Stress Disorder 54
Obsessive-Compulsive Disorder 54
Social Anxiety Disorder 55
Adjustment Disorders and Other Phobic Conditions 56
Treatment Reminders and Cautions 56
왘 Case Vignette 57

Chapter 8 TREATMENT OF PSYCHOTIC DISORDERS 58

Schizophrenia Spectrum Disorders 58
Schizophrenia 59
Symptoms in Schizophrenia 60
Causes of Psychotic Disorders 61
xii Contents

Medications for Psychotic Behaviors 62

Atypical Antipsychotic Medications 63
Typical Antipsychotic Medications 64
Adverse Effects of Typical Antipsychotics 64
Treatment Protocol 65
Other Significant Issues to Consider 66
왘 Case Vignette 67

Chapter 9 TREATMENT OF ADHD AND DISORDERS

OF ATTENTION 68
Etiology of ADHD 69
Diagnostic Assessment of Attention Disorders 69
Psychological and Pharmacological Treatment 69
왘 Case Vignette 72

Chapter 10 TREATMENT OF COGNITIVE DISORDERS 74

Forms of Dementia 74
Alzheimer’s Disease 75
Medical and Behavioral Evaluation of Cognitive Disorders 76
Medications for Cognitive Disorders 76
Other Approaches to Cognitive Enhancement 77
Other Significant Issues to Consider 78
왘 Case Vignette 79

Chapter 11 TREATMENT OF SLEEP DISORDERS 81

Stages of Sleep 82
Sleep Disorders and Conditions 82
Behavioral Techniques for Treating Sleep Disorders 84
Pharmacology for Sleep Disorders 85
Holistic Treatments 87
왘 Case Vignette 88

Chapter 12 TREATMENT OF PERSONALITY DISORDERS 89

Use of Medications for Personality Disorders 89
Tailoring Medications to Symptom Clusters 90
Other Considerations 92
왘 Case Vignette 92

Chapter 13 TREATMENT OF CHEMICAL DEPENDENCY

AND CO-OCCURRING CONDITIONS 93
Co-Occurring Conditions 93
The Dopamine Hypothesis 94
 Contents xiii

Treatment Issues 95
Assessment Instruments and Strategies 95
Treatment Phases and Goals 96
Psychopharmacology for Dually Diagnosed Patients 96
Alcohol Dependence 96
Opioid Dependence 98
Cocaine Dependence 99
Other Types of Addiction 99
Summary and Treatment Reminders 100
왘 Case Vignette 100

Chapter 14 TREATMENT OF COMORBIDITY

AND OTHER DISORDERS 102
Medical and Psychiatric Comorbidity 102
Chronic Neuropathic Pain 104
Eating Disorders and Obesity 105
Anorexia Nervosa 105
Bulimia Nervosa 106
Binge-Eating Disorder 107
Obesity 107
Impulse Control Disorders 108
왘 Case Vignette 109

Chapter 15 CASE VIGNETTES: CHILDREN 111

Napoleon 111
Clinical History 111
Postcase Discussion and Diagnosis 112
Psychopharmacological Treatment 112
Christina 112
Clinical History 112
Postcase Discussion and Diagnosis 113
Psychopharmacological Treatment 113
Marky 113
Clinical History 113
Postcase Discussion and Diagnosis 114
Psychopharmacological Treatment 114

Chapter 16 CASE VIGNETTES: ADOLESCENTS 115

Johnny 115
Clinical History 115
xiv Contents

Postcase Discussion and Diagnosis 115

Psychopharmacological Treatment 116
Jennifer 116
Clinical History 116
Postcase Discussion and Diagnosis 117
Psychopharmacological Treatment 117
Violet 117
Clinical History 117
Postcase Discussion and Diagnosis 118
Psychopharmacological Treatment 118

Chapter 17 CASE VIGNETTES: EARLY ADULTHOOD 119

Stone 119
Clinical History 119
Postcase Discussion and Diagnosis 120
Psychopharmacological Treatment 120
Ava 120
Clinical History 120
Postcase Discussion and Diagnosis 121
Psychopharmacological Treatment 121
Candy 121
Clinical History 121
Postcase Discussion and Diagnosis 122
Psychopharmacological Treatment 122

Chapter 18 CASE VIGNETTES: MIDDLE ADULTHOOD 123

Chester 123
Clinical History 123
Postcase Discussion and Diagnosis 124
Psychopharmacological Treatment 124
Sally 124
Clinical History 124
Postcase Discussion and Diagnosis 125
Psychopharmacological Treatment 126
Tony 126
Clinical History 126
Postcase Discussion and Diagnosis 127
Psychopharmacological Treatment 127
 Contents xv

Chapter 19 CASE VIGNETTES: OLDER ADULTHOOD 129

Rose 129
Clinical History 129
Postcase Discussion and Diagnosis 130
Psychopharmacological Treatment 130
Anthony 130
Clinical History 130
Postcase Discussion and Diagnosis 131
Psychopharmacological Treatment 131
Margarita 131
Clinical History 131
Postcase Discussion and Diagnosis 132
Psychopharmacological Treatment 132

Appendix 133
Glossary 149
Bibliography 152
Index 163
This page intentionally left blank
1 WHY STUDY
PSYCHOPHARMACOLOGY
Reasons for the Nonmedical Therapist to
Read This Book

Over the years various counseling and psychotherapy models have emerged, flourished,
continued, or faded from use. Many of these theories or models offered the clinician op-
tions for maximizing the therapeutic progress of their client. Many of them emphasized
humanistic, psychoanalytic, or behavioral techniques that downplayed the role of medica-
tion in the treatment of many conditions. In fact, except for those patients with serious
psychopathology requiring inpatient hospitalization, most patients were not on medica-
tions. Most counselors and therapists were not concerned by this, as their work with the
nonpsychiatric population was stable and secure.
Today, a vast majority of the patients seen in private practice settings and in commu-
nity mental health agencies either have been, are, or will be on psychotropic medications.
Most therapists, however, have not received adequate education to keep pace with a
changing treatment arena. In fact, most nonmedical therapists—namely, psychologists,
social workers, professional counselors, and marriage and family therapists—have never
taken a course in psychopharmacology or have taken only a brief survey course and feel
ill prepared to handle patients and clients on psychotropic medications (Barlow &
Herbert, 1995; Sinacola, 1997).
Some therapists choose not to seek this information. They offer the argument that
they work with cancer patients and do not need to know the etiology or how to treat the
disease. This argument has some truth in it; however, it might not be a valid premise for
choosing to be naive on the topic. For example, it has been well documented that all ther-
apists need to be aware of the role physical illness plays in mental illness. If any ethical or
professional therapist or counselor feels that a physical condition might be a cause for a
patient’s mental condition, the therapist should immediately refer the patient to a physi-
cian for an evaluation. Amazingly, many do not! Although a physical condition may re-
solve quickly when it is physically treated, a mental illness often requires a combination
of psychotherapy and medication. As a mental health expert, the clinician is expected to
diagnose and treat various conditions and be aware of the best treatment for them. To limit
treatment options by excluding medications, which represent a large part of the available

1
2 Chapter 1 • Why Study Psychopharmacology

protocol, is a disservice to the patient. Therapists who claim that medication would interfere with
their approach are often lulled into a false sense of inclusiveness. They believe the only way to
treat a patient is with nonmedical therapy, and if the patient is not responding, they believe he or
she is resisting treatment.
For years, psychiatrists have been accused by nonmedical therapists of being pill push-
ers. These therapists often cite the refusal of psychiatrists to spend any real therapeutic time
with patients as evidence that the psychiatrists either lack therapeutic skills or view everything
as a medical issue. The truth here is that many nonmedical practitioners feel uncomfortable
talking to psychiatrists and other prescribers about medications. Many nonmedical practition-
ers choose to reduce every psychological concern to purely behavioral manifestations and are
reluctant to even consider the role of biology or neurology. This choice is not new, even among
nonmedical therapists. When advising clients, some social workers and even nurses have min-
imized the need for psychological testing because they do not perform these services. Many
were reluctant to refer clients to psychologists for psychological testing because they feared
that the psychologist might steal their client. Historically, psychologists and psychiatrists have
waged turf wars over the issue of who is really in charge. In many states both the physician and
the psychologist share hospital privileges. Additionally, some states and jurisdictions, such as
Louisiana, New Mexico, and Guam, allow properly trained psychologists to prescribe psy-
chotropic medications. For years, clinical nurse specialists and physician assistants have been
prescribing medications.
Many nonmedical therapists agree that knowledge of psychotropic medications is nec-
essary and attempt to gain this knowledge, yet they feel their knowledge is inadequate. They
shy away from discussing medications with clients and defer to the physician in the case.
These therapists may claim that they do not wish to practice medicine without a license.
Many therapists, such as licensed psychologists, are aware that their scope of practice in
many states allows them to discuss medication options with patients, but they are not neces-
sarily the person who may ultimately prescribe them. Still, these therapists claim ignorance
and defer any decisions. They may be unclear as to what role they should take with patients
regarding their medications.
An analogy may apply here. Consider the patient a consumer whose car is not function-
ing properly. She may not be sure what’s wrong with the car, so she takes it to a local repair
facility (mental health clinic). The mechanic (therapist) is well trained in how to listen to the
engine and determine the problem. He will then recommend a plan of repair (treatment). In
many cases he knows what the problem is and how to fix it, but he may not know why the
problem occurred or why the part failed. The engineer (the physician) may be able to offer an
explanation here. She knows what the part was designed to do, and why it physically failed.
She may also be able to fix the part if it is taken to the factory (hospital). If the car needs to
be redesigned, the engineer, not the mechanic, would attempt to do it. A therapist who has no
knowledge of psychotropic medications is like a mechanic who listens to the car and says,
“Yep, you have a problem all right, and I think it’s in the transmission. Maybe you want to see
an engineer.”
In reality, most good mechanics and dealerships employ engineers and structural techni-
cians who work together to repair cars. In the same way, therapists and physicians need to
work together in the best interests of the patient. Today, the model of the medical home calls
upon primary care doctors to work collaboratively with mental health therapists in the service
of the patient.
 Chapter 1 • Why Study Psychopharmacology 3

How do nonmedical therapists or counselors determine just what they need to know?
Consider the following quiz:
1. What is an SSRI?
If you said, “an antidepressant,” you get one point. But do you know that SSRI stands for
selective serotonin reuptake inhibitors? Do you know the primary neurotransmitter in-
volved in their action? Do you know the major side effects? Can you name the six major
drugs in this class by brand name? Would you recognize the chemical names if you saw
them in a medical record? If a client told you a doctor placed him on meds and he was hav-
ing side effects A, B, and C, would you know that the side effects came from the SSRI?
2. What is a neuroleptic?
If you said, “a medication for treating schizophrenia,” you get another point. But do you
know the primary neurotransmitter that is involved in their action? Do you know the side
effects? Do you know which medications are major tranquilizers and which are minor? Do
you know which medications are better for the negative symptoms of psychoticism?
3. What is a benzodiazepine?
If you said, “they are used to treat anxiety,” you once again get a point. But do you know
where they interact in the brain? Do you know what neurotransmitter or amino acid is in-
volved? Are they habit forming? Can someone overdose on them?
If you were able to answer all of the above questions correctly, you do not need to read this
book and could probably teach others about psychopharmacology. If you knew a few answers,
consider reading further and you will not be disappointed. If you knew none of the answers, def-
initely read on.
This book will help the nonmedical therapist to increase his or her knowledge of medica-
tions and their proper use. Without complicating the picture with excessive biological terms and
neurochemistry, it will give the counselor the necessary information to work safely with a patient
currently taking or considering medications. It will also offer helpful suggestions to therapists
working directly with psychiatrists and other prescribers.
 2 BASIC NEUROBIOLOGY

This chapter will provide basic information on the purpose and function of the brain’s
neurological system with regard to mental health functioning.
Topics to be addressed include the following:
• Neurons
• Neural communication
• Electrical and chemical properties of neural transmission
• Neurotransmitters of emotion and behavior
As a counselor or psychotherapist, you need to understand how the brain works to
control thinking, behavior, and overall health. Further knowledge in this area should assist
you in comprehending your client’s symptoms and disease process. The field of psy-
chopharmacology is evolving rapidly and will continue to change with advances in medical
research. New interventions to treat psychiatric illnesses should enhance the quality of life
for your mental health clients.
This chapter provides some basic information on which to build an understanding of
various medications, their mechanisms of action, and how they might be used in day-to-
day practice. This chapter describes the anatomy of nerve cells or neurons, how they fit to-
gether, and the ways they communicate.

NEURONS
Since the brain is the most complex organ in the body, the discussion here will be lim-
ited to neurons in the central nervous system and the effect of drugs on them. Within
the central nervous system, neurons transmit messages or communicate with each
other, and as you will learn later, drugs can affect this transmission. In order to under-
stand how the messages are transmitted, you must first understand how a neuron
is structured.

4
 Chapter 2 • Basic Neurobiology 5

Terminal
button

Synapse on soma

Soma (cell body)

Dendrites
Nucleus

Synapse on
dendrite Axon

FIGURE 2.1 The Structure of a Neuron

A neuron has four basic parts: the soma, dendrites, axon, and terminal buttons (see Figure 2.1).
• The soma, or cell body, contains the vital parts of the cell, including the nucleus, mito-
chondria, and other substances in the cytoplasm (the space inside the neuron). A mem-
brane defines the boundary of the cell.
• Dendrites are large and small branches of the neuron, similar to branches of a tree, which
receive messages from other neurons through multiple molecular receptors.
• The axon is a long slender tube that carries messages from the soma to its terminal buttons.
• Terminal buttons are found at the ends of the axon. They contain small sacs, or vesicles,
that hold chemical messengers, or neurotransmitters. Terminal buttons deliver neurotrans-
mitters to other neurons across a physical gap called a synapse. The neurotransmitters can
cross the synapse between a terminal button of one neuron and a dendrite of an other neu-
ron or between a terminal button of one neuron and the soma of an other neuron.

NEURAL COMMUNICATION
Within the central nervous system, neuron communication is facilitated either electrically or
chemically. This communication is facilitated electrically within the neuron and chemically be-
tween neurons.
All drugs and substances that can activate neurons in the brain or central nervous system
and thus affect communication between neurons are classified as either endogenous or exogenous.
Endogenous substances, such as endorphins, insulin, and adrenalin (also known as ephinephrine),
come from within the body. Exogenous substances, such as caffeine, vitamins, herbs, and medica-
tions, are produced outside the body and introduced into the body in some manner.
6 Chapter 2 • Basic Neurobiology

Presynaptic Postsynaptic
Presynaptic Postsynaptic
terminal button dendrite

Receptor
Electrical impulse sites Electrical impulse

Neurotransmitter

Chemical transmissions
FIGURE 2.2 Electrical and Chemical Communication Between Cells

Receptor sites on the postsynaptic membranes of dendrites are often the targets of medica-
tions that can activate adjacent cells. That action begins when a receptor is stimulated by a neu-
rotransmitter. Once stimulated, an electrical impulse travels along the axon toward the terminal
button. Because an electrical signal or impulse is unable to cross the synapse, the transmission of
the signal across the synapse depends on chemical messengers, or neurotransmitters. After the
electrical impulse reaches the terminal button, a neurotransmitter is released. It travels from the
presynaptic membrane of the terminal button across the synapse to the postsynaptic membrane
of another neuron’s dendrites, where it might interact. The postsynaptic membrane of the den-
drite contains numerous receptors that receive the chemical signal and, in turn, activate the post-
synaptic cell, allowing it to transmit again (see Figure 2.2).

ELECTRICAL AND CHEMICAL PROPERTIES OF NEURAL TRANSMISSION

The electrical properties of a neuron relate to the difference between intracellular (inside the cell)
ion concentrations and extracellular (outside the cell) ion concentrations; ions are electrically
charged particles. The most common ions found in the extracellular spaces are sodium (Na⫹) and
chloride (Cl⫺) ions. The most frequent intracellular ions are potassium (K⫹) and negatively
charged ions. The resting potential of a neuron is the unexcited or relaxed state in which the aver-
age electrical difference between the inside and outside of the cell is about 70 millivolts (mV). The
resting potential is usually referred to as ⫺70 mV (the outside is more negative than the inside).
Other electrical properties that affect a cell include depolarization and hyperpolarization.
When a cell is significantly stimulated or depolarized, it generates a message, an electrical im-
pulse, called an action potential. This action potential is produced when a neuron’s resting po-
tential becomes less negative or depolarized. After an action potential occurs, the cell briefly be-
comes more polarized or hyperpolarized before it returns to a relaxed state. A depolarized
membrane is more likely to transmit an electrical impulse; a hyperpolarized membrane is less
likely to transmit an electrical impulse.
When neural transmission occurs, the signal may be excitatory or inhibitory in nature.
Excitatory messages increase the likelihood that an electrical impulse will be sent; inhibitory mes-
sages decrease that likelihood. All neurons may receive both excitatory and inhibitory messages at
the same time. Whether a message is or is not transmitted depends on the relative number of exci-
tatory and inhibitory signals a neuron receives. For example, if the excitatory messengers outnum-
ber the inhibitory messengers, an action potential (message) will be initiated along the axon.
 Chapter 2 • Basic Neurobiology 7

All action potentials are the same size when they are generated, but not all behavioral re-
sponses are equal in magnitude. More significant, or stronger, environmental stimuli produce a
higher number of action potentials (a higher rate of firing of action potentials). The higher the
rate of firings of action potentials, the stronger we would expect the behavioral response. For ex-
ample, a loud sound may generate ten action potentials in a time period, whereas a soft sound
may generate only two action potentials during the same period. Thus, the behavioral response to
the loud sound is usually greater than the response to the soft sound.
When the action potential reaches the nerve terminal, neurotransmitters are released by
a process called exocytosis, the secretion of a substance by a cell (see Figure 2.3). At the end
of the axon, the action potential causes calcium ions (Ca⫹⫹) in the terminal button to release
the neurotransmitter into the synapse. The neurotransmitter then diffuses across the synapse to
interact with receptors on the postsynaptic membrane of the dendrites or soma. When recep-
tors are activated, ion channels, or little gateways, open on the postsynaptic membrane, caus-
ing either depolarization or hyperpolarization. An excitatory signal leads to the process occur-
ring again; an inhibitory effect decreases further signals. Remember that depolarization
excites and hyperpolarization inhibits. The action potential is technically over when some of

Neurotransmitter Action potential causes

docking of vesicles with
presynaptic membrane.

Electrical impulse
or action potential

Stage 1: Axon potential travels along Stage 2: Action potential causes vesicles
axon to terminal button. to fuse with presynaptic membrane.

Calcium ions bind to presynaptic

membrane causing vesicles
filled with neurotransmitter
to fuse with membrane.

Ca++

Stage 3: Action potential causes calcium ions to Stage 4: Neurotransmitter released into
release vesicles of neurotransmitter synapse.
into synapse.
FIGURE 2.3 The Four Stages of Exocytosis
8 Chapter 2 • Basic Neurobiology

Presynaptic Synaptic Postsynaptic

Presynaptic cleft
Postsynaptic
terminal button terminal button

Receptor
sites

Neurotransmitter

Reuptake pumps or transporters remove

the neurotransmitter from the synaptic cleft
via the terminal buttons. This terminates
the action potential.
FIGURE 2.4 The Process of Reuptake

the neurotransmitter is taken back into the terminal button in a process called reuptake (see
Figure 2.4).
A neurotransmitter and its individual receptor site together act like a key fitting into a lock
(see Figure 2.5). Receptors, located on the extracellular membrane, are specific types of protein
structures made of amino acids. The structures make each receptor unique. By a process known
as signal transduction, the first messenger or neurotransmitter binds to a receptor that transmits
the message by changing the electrical characteristics of the cell, by starting a biochemical action
within the cell, or both. (The second messager will be explained later.) In general, a neurotrans-
mitter may open an ion channel in either of two major ways. One direct way is through ligand-
gated ion channel receptors (neurotransmitters and drugs are generally referred to as ligands). An
ion channel opens when a ligand binds to the receptor site (see Figure 2.6). In turn, the influx of
particular ions leads to either depolarization or hyperpolarization. For example, the acetylcholine
receptor works in this manner. When two acetylcholine molecules occupy the two acetylcholine
sites on a single receptor, a sodium pump is opened, resulting in an influx of sodium (Na⫹) ions
that causes depolarization.
The second way a neurotransmitter opens an ion channel is by inducing chemical
changes within the cell. The majority of receptors that produce these effects are called G protein–
linked receptors because they bind guanine nucleotides. For example, dopamine, glutamate,

Postsynaptic
membrane

Receptor
sites

Neurotransmitters
dock at receptor sites
FIGURE 2.5 Receptor Sites
 Chapter 2 • Basic Neurobiology 9

Neurotransmitters Ions

Postsynaptic Membrane Molecule of neurotransmitter

activates ion channel

Influx of ions

Closed ion channel Open ion channel

FIGURE 2.6 Ion Channel Activation

gamma-aminobutyric acid (GABA), and serotonin all facilitate neurotransmission by utilizing

G protein–linked receptors.
After the first messenger or neurotransmitter interacts with the extracellular receptor, the
chemical effects of the G proteins activate a second messenger within the cell. The best-known
second messenger is cyclic adenosine monophosphate, or cyclic AMP. Thus, the neurotransmit-
ter or first messenger binding to the receptor causes a cascade of chemical reactions in the post-
synaptic neuron involving a second messenger. Cyclic AMP usually activates other molecules or
enzymes that in turn activate or inhibit other chemicals. The resulting substances are known as
protein kinases. The protein kinases facilitate a change in the physical shape of other proteins
that control the opening of an ion channel. The alteration in the physical shape of the protein per-
mits the channel to open, allowing an influx of ions into the postsynaptic neuron. This ion influx
causes either depolarization or hyperpolarization. The final results of this process vary but may
include making other neurotransmitters, sending further electrical charges, and so on. An in-
creasingly complex cascade of effects occurs that alters cellular function.

NEUROTRANSMITTERS OF EMOTION AND BEHAVIOR

Three main neurotransmitters involved in emotion and behavior are the catecholamines
(dopamine and norepinephrine) and one indolamine (serotonin). The category designation cate-
cholamine or monoamine is based upon chemical structure. Other neurotransmitters that might
be considered include three important amino acids: GABA, glycine, and glutamate. In addition,
certain chains of amino acids known as neuropeptides, including substance P and endorphins,
may play a role in emotion and behavior.
Dopamine and norepinephrine are closely related and synthesized from the same precursor
substance known as tyrosine (see Figure 2.7). Tyrosine is an amino acid that comes from diet.
Synthesized tyrosine can be purchased in a health food store; however, some believe tyrosine is
not effective unless it is obtained from food. Dietary sources of tyrosine include meat, poultry,
seafood, beans, tofu, and lentils. Tyrosine enters dopaminergic neurons by diffusion, where the
cytoplasmic enzyme tyrosine hydroxylase converts it to L-DOPA. L-DOPA is then converted by
DOPA decarboxylase into dopamine. Some of the dopamine may be further converted by
dopamine ␤-hydroxylase into norepinephrine.
10 Chapter 2 • Basic Neurobiology

H COOH
C C NH2

HO H H
Tyrosine
Tyrosine hydroxylase
H COOH
C C NH2

HO H H
OH L-DOPA

DOPA decarboxylase
H H
C C NH2

HO H H
OH Dopamine
dopamine–␤-hydroxylase
OH H
C C NH2

HO H H
OH Norepinephrine
FIGURE 2.7 Synthesis of Catecholamines

The noradrenergic (or norepinephrine) pathways in the brain seem to be involved in the
regulation of sleep-wake cycles, sustained attention, alertness, and biological responses to new
stimuli. Noradrenalin is also thought to mediate anxiety, fear, and stress responses. Thus, nora-
drenergic abnormalities or drops in norepinephrine levels are thought to play a large role in mood
and anxiety disorders.
Serotonin or 5-hydroxytryptamine (5-HTP) is synthesized from tryptophan in our diet (see
Figure 2.8). Once again, synthesized tryptophan supplements have not been shown to be an effective

COOH

CH2 CH NH2
Tryptophan
N
Tryptophan hydroxylase

COOH

HO CH2 CH NH2

N 5–hydroxytryptophan–(5-HTP)

5-HTP decarboxylase

HO CH2 CH2 NH2

N 5–hydroxytryptamine–(5-HT)
or serotonin
FIGURE 2.8 Synthesis of Indolamines.
 Chapter 2 • Basic Neurobiology 11

way of obtaining serotonin. Dietary sources of tryptophan include bananas, sunflower seeds, and
milk. Tryptophan is converted into 5-hydroxytryptophan by an enzyme called tryptophan hydroxy-
lase. Then 5-hydroxytryptophan decarboxylase acts on 5-hydroxytryptophan to produce serotonin or
5-hydroxytryptamine.
Scientists believe that serotonin plays a large role in brain functioning, including mood,
anxiety, arousal, irritability, tranquility, cognition, appetite, sleep-wake cycles, and obsessions.
Serotonergic abnormalities or drops in serotonin levels are associated with anxiety disorders,
mood disorders, and even psychotic disorders. Explanations of neural activity might seem quite
concrete and straightforward, but the systems are much more complex. Neurons have an extraor-
dinary number of diverse interconnections. Because behavior is complicated, no one neurotrans-
mitter should be considered in isolation; for example, an individual’s depression might be caused
by insufficient levels of serotonin, norepinephrine, dopamine, or, in some cases, all three. Most
brain functions result from multiple influences of several different neurotransmitters trying to
find their own delicate balance.
Drugs may alter behavior by interfering with or interrupting any of the processes that oc-
cur during neural communication. A drug that increases the availability or action of a neurotrans-
mitter is called an agonist. Agonists are agents that bind to receptors and act. For example, flu-
oxetine (Prozac) increases the action of serotonin on the postsynaptic membrane. Conversely, a
drug that decreases the availability or action of a neurotransmitter is called an antagonist. They
bind to receptors and block. For example, risperidone (Risperdal) blocks dopamine at the postsy-
naptic membrane. Keep these concepts in mind. They will be revisited in later chapters with re-
spect to specific diseases and medications.
In summary, a few neurotransmitters are particularly important for those in the mental
health field. The following gives you a general foundation for each one.

• Acetylcholine. In the central nervous system, acetylcholine is widely distributed and

thought to play a role in memory, learning, behavioral arousal, attention, mood, and rapid-eye move-
ment that occurs during sleep. In the peripheral nervous system, acetylcholine is found at synapses
where the nerve terminals meet skeletal muscles, causing excitation leading to muscle contractions.
• Epinephrine or adrenalin. This neurotransmitter is probably more active in the periph-
eral nervous system than the central nervous system. Epinephrine is secreted by small endocrine
glands above the kidneys known as the adrenal glands. In the peripheral nervous system, epi-
nephrine regulates our fight-or-flight response. Its role is described in Chapter 7, The Treatment
of Anxiety Disorders.
• Norepinephrine. Primarily, norepinephrine is an excitatory neurotransmitter in the cen-
tral nervous system. Norepinephrine cell bodies in the brain stem have axons projecting into the
limbic system (brain structures involved in emotions) and the frontal lobes. Wakefulness and
alertness are the two major functions of norepinephrine. The role of norepinephrine is discussed
later in Chapters 7 and 9.
• Dopamine. Another major neurotransmitter, dopamine is involved with behavioral
regulation, movement, learning, mood, and attention. Dopamine may have both excitatory
and inhibitory effects in the brain. It is belived that overactivity of dopamine or oversensitiv-
ity of dopamine receptors is responsible for the major symptoms in schizophrenia.
Amphetamines, cocaine, and other drugs of abuse directly activate dopamine receptors. The
resulting excitation helps account for the psychotic symptoms commonly seen when these
drugs are abused.
12 Chapter 2 • Basic Neurobiology

• Serotonin. Another major neurotransmitter in the central nervous system is sero-

tonin, which involves the inhibition of activity and behavior. Other areas where serotonin
plays a significant role include mood regulation, control of appetite, sleep and arousal, and
pain regulation. Serotonin and norepinephrine axons project into almost the same areas of the
brain and are thought to have opposing actions.
• Other neurotransmitters. By virtue of its inhibititory nature, GABA makes the brain
more stable by decreasing the neural transmission that prevents overexcitation. Benzodiazepines
and barbiturates are two good examples that act to increase GABA. (See Chapter 7 for more
about GABA.) Glycine is another inhibitory amino acid neurotransmitter that is present mostly
in the spinal cord. When glycine receptors are activated, the cell becomes hyperpolarized and
less likely to transmit a signal. Strychnine, a toxin that causes convulsions, acts by blocking these
glycine receptors, leading to overexcitation and possibly death. Glutamate, another amino acid
neurotransmitter, is definitely excitatory. More neurotransmission occurs because glutamate low-
ers the threshold for neural excitation. Glutamate is often found in Asian food in the form of
monosodium glutamate (MSG), which excites the taste buds on the tongue (for further reading
see Carlson, 2004).
3 PSYCHOPHARMACOLOGY
AND PHARMACOKINETICS

This chapter will address issues related to psychopharmacology and pharmacokinetics,

how drugs work and bring about chemical and behavioral changes in the body, and how
drugs are dispensed and prescribed. It will provide some basic information that is helpful
in understanding the patient.
Topics to be addressed include the following:
• Routes of drug administration
• Drug absorption, distribution, and metabolism
• Other pharmacokinetic principles
• Prescription and pharmacy terms.
When we talk about pharmacology and more specifically psychopharmacology, we
need to start with some basic concepts. In Chapter 2, Basic Neurobiology, we described
pharmacodynamics, which may be defined as the study of how drugs affect receptor sites,
send signals, and cause some neurochemical changes. On the other hand, pharmacokinetics
refers to the administration, absorption, distribution, metabolism, and elimination of a drug
inside the body.

ROUTES OF DRUG ADMINISTRATION

Medications may be introduced into the body by various methods including orally (by
mouth), subcutaneously (deep tissue injection), intramuscularly or IM (muscle injection),
intradermally (dermal injection), intranasally (nasal spray), inhalational (respiratory infu-
sion), sublingual (dissolution under the tongue), transdermally (skin absorption), and in-
travenously or IV (venous injection). The most common way that a drug is administered
is by mouth or orally. In recent times, a few medications have been delivered orally in the
form of a “soltab” or orally dissolving tablet. Many psychiatric drugs are introduced into
the body in this way. Examples of medications available as soltabs include olanzepine

13
14 Chapter 3 • Psychopharmacology and Pharmacokinetics

(Zyprexa Zydis), mirtazepine (Remeron Soltabs), risperidone (Risperdal M-tabs), and clon-
azepam (Klonopin Wafers).
In more acute settings such as a hospital or clinic, intramuscular injections are commonly
used to control behavior. Long-acting intramuscular injections such as haloperidol (Haldol
Decanoate), fluphenazine (Prolixin Decanoate), or risperidone (Risperdal Consta) are used for
more chronically mentally ill patients.

DRUG ABSORPTION, DISTRIBUTION, AND METABOLISM

Drug Absorption
When a drug is introduced orally, the rate of absorption is determined by the form of the drug.
For example, liquids are absorbed faster than capsules or tablets. Over the last few years, many
slow- or extended-release forms of medications have become available. They allow for fewer
doses per day and cause fewer side effects because of the slower rate of absorption. Oral admin-
istration has the slowest rate of absorption when compared to intramuscular, intravenous, and
other forms available. Absorption usually occurs in the stomach and duodenum (the first seg-
ment of the small intestines). Some medications need to be given with food for better absorption
(i.e., ziprasidone); some need to be given without food, which might interfere with absorption.
Some gastrointestinal diseases and their treatments may also interfere with drug absorption; for
example, antacids interfere with certain antibiotics.

Drug Distribution
After administration and absorption into the venous system, drugs are delivered throughout the
body by the circulatory system. The liver is the first organ that orally absorbed drugs encounter.
It will break down some of the drug into nonactive metabolites. This process in the liver is known
as the first-pass metabolism. After leaving the liver, the drug is delivered to its target organ. The
central nervous system is the target for psychotropic drugs. Other factors that affect drug absorp-
tion include protein binding, drug half-life, and lipid solubility.

PROTEIN BINDING. Some drugs bind tightly to plasma proteins such as albumin in the blood-
stream. This protein-binding phenomenon determines how much drug is available to act on the
brain. Drug protein binding also hinders a drug’s metabolism and excretion, which causes it to
remain in the circulatory system longer.

DRUG HALF-LIFE. The half-life of a drug is the average time required to eliminate one-half of
the drug’s concentration. For example, alprazolam (Xanax) has a half-life of 11 hours. Thus, the
concentration of alprazolam will be reduced by about 50% after 11 hours, by 75% after 22 hours,
and so on. In general, it takes approximately 5 half-lives for any drug to be eliminated com-
pletely from the body.

LIPID SOLUBILITY. The lipid or fat solubility of a drug determines how easily it crosses a cell
membrane, which is important for absorption and effectiveness at its target site. Drugs that are
more lipid soluble (lipophilic) cross membranes easily and are more likely to cross over the
blood-brain barrier. Some drugs do not cross this barrier and do not exert their effects on the cen-
tral nervous system.
 Chapter 3 • Psychopharmacology and Pharmacokinetics 15

Drug Metabolism
In ways that can get very complex, drugs are metabolized or broken down primarily in the liver
by the P450 family of enzymes. These enzymes are important because of the potential for drug
interactions when multiple drugs compete for the same pathways. The liver breaks down the
drug into other forms or metabolites that are later excreted in the urine. Geriatric patients have
decreased liver enzyme activity that requires drug dosages to be reduced to avoid toxicity. Other
medical conditions such as viral hepatitis or liver cirrhosis might also decrease a drug’s metabo-
lism. A few of the psychiatric medications, such as lithium, are not metabolized by the liver and
are excreted unchanged by the kidneys in urine. A patient with kidney dysfunction may not ex-
crete the drug normally, and the concentration may become elevated or toxic.

OTHER PHARMACOKINETIC PRINCIPLES

Therapeutic Index and Dose
The concept of therapeutic index is a pharmacokinetic principle that needs to be addressed.
When a certain drug concentration gives a desired response, it is referred to as a therapeutic
dose. When a drug concentration causes mild or severe side effects, it is referred to as a toxic
dose. The therapeutic index then is the ratio of the toxic dose to the therapeutic dose. Desirable
drugs have a high therapeutic index because the risk of toxicity at therapeutic doses is minimal.
On the other hand, drugs that have a low therapeutic index carry more risk because the thera-
peutic concentration is relatively close to its toxic level. For example, lithium is difficult to use
because the toxic level is only slightly higher than the typical therapeutic level (see Chapter 6
for further details).
When determining a drug’s therapeutic dose, it might be helpful to consider a dose-re-
sponse curve (see Figure 3.1). When a drug is introduced into the body, a slow titration upward
of the dose usually corresponds to an increasing response. This effect is true up to a certain point,

Range of maximum effect

Increasing response

Range of increasing
effect with
increasing dose

Threshold

Range of no effect
Increasing dose
FIGURE 3.1 Dose-Response Curve
16 Chapter 3 • Psychopharmacology and Pharmacokinetics

at which the response of the drug levels off despite significant increases in the drug dose. As you
might expect, increasing the drug’s dose at this point only increases the risk of side effects and
toxicity. Although most medications are introduced slowly into the body, some drugs may be ini-
tiated at high doses to obtain a certain desired response. We call this a loading dose of the med-
ication. After loading the patient, further dosage adjustments are seldom needed because we
have introduced the therapeutic dose into the body all at once.

Tolerance and Withdrawal

Two important concepts that need to be defined are tolerance and withdrawal. If a patient devel-
ops tolerance for a drug, he or she needs greater amounts of the drug over time to produce the de-
sired effect. Withdrawal from a drug is defined as a set of characteristic symptoms that emerge
when a drug is abruptly discontinued after heavy and prolonged use. Depending on the sub-
stance, withdrawal symptoms can be medically dangerous and require inpatient treatment.
Tolerance and withdrawal are relatively easy to understand when considering alcohol. Tolerance
to alcohol develops over time, causing a person to increase the amount he or she consumes to ob-
tain the desired effect. Withdrawal from alcohol develops when an alcoholic suddenly stops
drinking, thus throwing his or her body into a state of shock. This withdrawal causes an expected
array of symptoms such as tremors, agitation, insomnia, hallucinations, and even seizures.
Tolerance and withdrawal are terms commonly used when working in the field of chemical de-
pendency or addictions. In the DSM-IV, addiction is more specially defined as substance abuse
and dependence. Addiction is discussed in Chapter 13, Treatment of Chemical Dependency and
Co-Occurring Disorders.

Discontinuation Syndrome
A relatively new concept in the field of psychopharmacology is the discontinuation syndrome.
This syndrome is distinct from withdrawal because it is not medically dangerous although some
people claim that they are going through withdrawal. For example, patients who take paroxetine
(Paxil) or venlafaxine (Effexor XR) often report that when they miss a dose or stop taking the
medication, they feel malaise and other flulike symptoms.

Potentiation and Synergism

A therapist must understand the concepts of potentiation and synergism. Potentiation means that
one drug may enhance the effect of a second drug. For example, drug X added to drug Y may po-
tentially cause drug Y to be more sedating. One drug that potentiates another drug may increase
the sedation effect only 2-fold or so. Synergism refers to the fact that one drug may enhance the
effect of a second drug significantly more than expected. For example, drug X added to drug Y
may increase the sedation effect of drug Y 6-fold. Because of synergism, a patient should not
mix alcohol with benzodiazepines.

Placebo Response
A discussion about psychopharmacology and pharmacokinetics would not be complete with-
out mentioning the placebo response. During any patient interaction, a complex series of
events and communications occur in addition to any prescribed drug effects. Some patients re-
spond regardless of the specific therapeutic intervention just because of a helper’s “therapeutic
interaction” with them. Many patients have shown actual chemical changes in their brain when
 Chapter 3 • Psychopharmacology and Pharmacokinetics 17

they receive a placebo even when an actual drug is not present. The brain acts “as if” the drug
were present even though the medication is not. The power of the placebo response should
never be underestimated.

PRESCRIPTION AND PHARMACY TERMS

Therapists will encounter numerous Latin abbreviations when reviewing records, prescriptions,
and discussing issues with their prescribing professional (see Table 3.1). Although these abbrevi-
ations seem quite foreign at first, they become familiar with use over time.
It is always good practice to record a patient’s medication regime in his or her chart. This
information might be necessary when consulting with other professionals involved in the pa-
tient’s care. Chapter 4 describes history taking and assessment techniques in further detail.

TABLE 3.1 Latin Abbreviations

Abbreviation Meaning Latin

a.c. before food ante cibum
b.i.d. twice a day bis in die
cap. capsule capula
c with bar on top with cum
h. hour hora
hs at bedtime hora somni
p.c. after food post cibum
p.o. by mouth per os
p.r.n. as occasion requires pro re nata
q4h every 4 hours quaque 4 hora
q6h every 6 hours quaque 6 hora
qd every day quaque 1 die
q.i.d. four times a day quater in die
Rx prescription recipere
stat. immediately statim
tab. tablet tabella
t.i.d. three times a day ter in die
 4 HISTORY TAKING AND
ASSESSMENT TECHNIQUES

This chapter reminds the clinician that good history taking is essential to a good diagnosis,
and a good diagnosis is essential before any referral or recommendation for medication.
Topics to be addressed include the following:
• Obtaining patient history
• Mental status examination
• Patient questionnaires and assessment instruments
• Structuring the initial interview

OBTAINING PATIENT HISTORY

No mental health professional should underestimate the importance of good history tak-
ing. It is always important to inquire about a patient’s physical health before starting any
counseling relationship, especially when a patient presents with issues of depression,
anxiety, psychoticism, or other highly intrusive behavior. By getting all of the facts sur-
rounding a presenting issue, a therapist is assured that all relevant contributing factors
have been considered.
It is critical to take a thorough history from a patient and to use assessment in-
struments that address the issue the patient presents. Depending on the setting where
the history is taken, a few simple questions on the presenting problem, nature of con-
cern, history of the problem, relevant family history, physical findings, and history of
treatment might be sufficient. If time allows, however, a more detailed assessment
may be in order. The following outline provides a detailed history and assessment of
the patient.
Patient’s History Format
I. Identifying Information
Name, age, sex, race, grade, religion, marital status, occupation, and diagnosis
(if applicable)
18
 Chapter 4 • History Taking and Assessment Techniques 19

II. Presenting Problem

a. Chief complaint
b. How he/she was referred to you
c. Dates of treatment or assessment
d. How the person defines the problem
e. Duration, intensity of concern (history of presenting problem)
f. Any history of counseling/therapy
III. Personal/Family History
a. Grandparents, parents, or other relatives
b. Spouse, lover, and his/her relationship with them
c. Children, stepchildren, and the relationship
d. Siblings and the relationship
e. Friends and the relationship
f. Religion or other spiritual beliefs
g. Complete school history (elementary, high school, or college)
h. Present career status and beliefs about work
i. Physical health or chronic illnesses
j. Sexual history or concerns
k. Any cultural or environmental issues
IV. Summary of Psychometric Information
a. Summarize the results of any test instruments used. Be sure to mention the type of
test, norms, and all scores collected.
b. If you are interpreting test results administered by another professional, be sure to
state all observations as quotes and compare with your findings.
c. Accurately summarize reports from other sources such as family and friends. Give
reasons for using this source of information.
V. Diagnostic Assessment
a. Present a developed, logical summary of the status of the patient. This summary
should include a mental status exam, the clinician’s observations, and conclusions
about the patient’s level of functioning. Be sure to comment on the patient’s intel-
lect and maturity level.
b. Assess the patient’s coping abilities and comment on ego strengths and defense
mechanisms.
c. Give an example of the patient’s insight level and his/her strengths and weaknesses.
d. Make a complete diagnostic statement including an appropriate DSM-IV-TR, mul-
tiaxial diagnosis.
VI. Proposed Treatment Goals and Methods
a. Be sure that all goals and methods relate to the diagnostic assessment.
b. Define the goals and the objectives leading to them.
c. Differentiate between short- and long-term goals.
d. Describe the length and frequency of for planned sessions.
e. Describe the theoretical approach chosen.
f. Describe any special issues anticipated during treatment, for example, transference,
countertransference, or ethical issues.
g. List other resources or professionals to contact (psychiatrist, nurse, psychologist,
social services, etc.).
20 Chapter 4 • History Taking and Assessment Techniques

h. List referrals to make to other professionals or agencies.

i. Set a time to evaluate the treatment approach.
j. Describe the complete prognosis.
VII. Other Information
a. Describe special circumstances encountered.
b. List releases needed for consults.

MENTAL STATUS EXAMINATION

It is wise to obtain a baseline measure of mental status from all patients. This information not
only gives a snapshot of how the patient is doing, but it gives a general sense of the patient in sev-
eral different realms, including cognitive capacity, intelligence, memory impairment, abstract
reasoning, and judgment. If done properly, a good mental status can help to predict a patient’s
behavior and provide valuable information for making a diagnosis. A full mental status should
include information from the following sources:
Mental Status Information
Attitude and Behavior
• Describe appearance, including hygiene, makeup, and dress.
• Describe mannerisms: lethargic, hyperactive, echopraxia, posture, etc.
• Describe attitude toward self and others.
• Describe affect: sad, flat, labile, etc.
Stream of Mental Activity
• Describe flow of speech: tangential, rapid, spontaneous, blocked, etc.
• Describe language deviations: clang associations or echolalia.
Emotional Reactions
• Describe displays: tearful, anxious, flat. Congruent with stated mood?
Mental Trend and Thought Content
• Describe major themes of conversation
• Describe evidence of auditory, visual, gustatory, tactile, olfactory, or visceral hallucinations
• Describe delusions, ideas of reference, paranoia, or grandiosity
• Describe somatizations, suicidal or homicidal ideation
• Describe history of substance abuse and list current medications.
Sensorium, Mental Grasp, and Capacity
Ask questions to determine the following:
• Oriented X 3 (person, place, and time)
• Memory: Immediate (recall of three items after five minutes); recent (events of last
evening); remote (name last nine Presidents)*
• Calculations: Serial 7s and 3s; digits forward and backward
• General intelligence and similarities: Abstract reasoning and proverbs
General Fund of Knowledge
• Ask questions of common knowledge and current events and of items that assess past
academic achievements.

*If patient is from another culture/country, he or she could list the last four heads of state.
 Chapter 4 • History Taking and Assessment Techniques 21

Judgment and Insight

• Ask questions to assess the patient’s common sense (ego strengths) and ability to live
independently.
A typical narrative description for the findings of the mental status exam would be worded
in the following fashion, depending on the particular questions asked of the patient and his or her
level of cooperation:
Mrs. Jane Doe is a 30-year-old, African-American female of average height and
weight. Her hygiene and dress were appropriate for the evaluation. She was oriented
X 3, and while her speech appeared normal, she began to stutter when she became
nervous. She denied hallucinations or other psychotic manifestations. Memory ap-
peared intact with good immediate, recent, and remote memory. She appeared to have
no educational or learning deficits. The patient appeared to have an above-average
level of intelligence. She denied suicidal/homicidal ideation and chemical depend-
ency. Judgment and insight appear sound and within normal limits.

PATIENT QUESTIONNAIRES AND ASSESSMENT INSTRUMENTS

For therapists, including those who are not psychologists, several patient checklists and question-
naires are available that can be used for patients who present with depression and/or anxiety.
These instruments are designed to be easy to use by both the clinician and the patient. While some
psychometric knowledge is helpful, most of these self-report format instruments are designed to
be administered by mental health professionals with at least a master’s degree and some relevant
clinical experience. Some assume that the clinician has special training in their use, and some may
require the practitioner to be a licensed psychologist. A test’s publisher may require professional
credentials before selling the instrument. The following list is by no means exhaustive, but it rep-
resents some popular tools used in the field today. To learn more about them, type in the name of
the test as a keyword on the Internet for publisher and research information.
Assessments for Depression
• The Beck Depression Inventory II: Twenty-one items, easy to score
• The Hamilton Depression Inventory: Available in a 17- or 21-item format; better for as-
sessing somatic, less cognitive-related depression
• The Geriatric Depression Inventory: Helpful to use with an older population
Assessments for Anxiety
• The Beck Anxiety Inventory: Brief, easy to score, and helpful in differentiating between
generalized anxiety and panic disorder
• The State-Trait Anxiety Inventory: Helpful in determining if the anxiety is one of an emo-
tional reaction “state” versus more of a personality “trait”

General Assessment of Personality Including Depression, Anxiety,

and Other Manifestations
• The Minnesota Multiphasic Personality Inventory (MMPI-2): Consists of 567 true/false
questions over 10 clinical scales including depression, somatization, anxiety, antisocial
tendencies, paranoia, mania, and psychoticism. It is also available in an adolescent version
(MMPI-A).
22 Chapter 4 • History Taking and Assessment Techniques

• The Million Clinical Multiaxial Inventory-III: A shorter test with 175 items; better for as-
sessing the presence of a personality disorder.
• The Personality Assessment Inventory: Consists of 344 items; shorter version, called the
PAS or Personality Assessment Screener, contains only 22 items and takes less than six
minutes to administer.

STRUCTURING THE INITIAL INTERVIEW

When a patient presents for counseling services and the therapist is aware that the patient may
need medication to treat a serious affective, anxiety, or thought disorder, it is very important to
gather as much information as possible. The following are information-gathering suggetions to
keep in mind.
1. Document the name of the patient’s primary care physician (PCP) and the date of his or
her last history and physical. Be sure to include any information on known diseases such as hy-
pertension, diabetes, cancer, stroke, thyroid conditions, and so on. If the patient does not have a
PCP, then he or she should be referred to one for a workup as soon as possible. Be sure to ask
the physician to assess for thyroid function, glucose tolerance, and electrolyte imbalances.
Typical tests would include complete blood count (CBC), thyroid function tests, a basic meta-
bolic panel, and urine toxicology.
2. Take a complete history of any treatment for the presenting problem. This history
should include the types of symptoms, that is, depression, panic, anxiety, and so on. Be sure to
include all professionals the patient has seen and any medications he or she has taken. Ask the
patient if the medications were helpful, effective, or intolerable. What side effects, if any, did the
patient experience and did they lead to noncompliance?
3. Prepare a complete mental status using other assessment instruments as appropriate to
confirm initial impressions. It would be appropriate for the therapist to formulate some initial
short-term goals for proceeding with this patient.
Good treatment starts with a good history and assessment. Taking a few extra moments
with the patient to address the issues mentioned above will assure both the patient and the thera-
pist that no stone was left unturned. Be sure to review the treatment plan with the patient to con-
firm that he or she is also in agreement. By knowing the patient’s history, the therapist can save
time later by not reexposing the patient to medication regimes that did not work or that interacted
with other medications the patient was taking for a medical condition. Pleading ignorance or
claiming not to be a physician is no protection from a malpractice claim. Always remember that
you are treating the whole patient.
5 TREATMENT OF UNIPOLAR
DEPRESSION

In this chapter we examine the medications and other treatment considerations for patients
with depression. Depression is the most common presenting concern in all treatment set-
tings. Assessing the nature and type of depression is key to suggesting proper medication.
Topics to be addressed include the following:
• Biological versus environmental depression
• Causes of biological depression
• Counseling and psychotherapy
• Medications for depression
• Herbal and holistic substances
• Light therapy for seasonal affective disorders (SAD)
• Importance of exercise
• Electroconvulsive therapy (ECT)
• Procedural steps for patient treatment
• Case vignette

BIOLOGICAL VERSUS ENVIRONMENTAL DEPRESSION

Depression is probably the most frequently presented issue in any mental health setting.
Researchers have estimated that at any one time, at least 3% of the population suffers from
chronic depression. More than 17% have had at least one episode in their lifetime, and an-
other 10% reported an episode in the last twelve months (Sutherland, Sutherland, &
Hoehns, 2003). It is interesting and sad that despite the recent advances in both psychother-
apy and medications for depression, only 30% of those with depression seek treatment for
the condition (Rakel, 1999). In addition, less than 20% of those who seek treatment take
antidepressants ( McIntyre, Muller, Mancini, & Silver, 2003).
Therapists have many issues to consider when treating depression. First, they must
determine the nature of the depression. Some forms of depression are biological or
endogenous; they are believed to stem from within the person. This form of depression is
23
24 Chapter 5 • Treatment of Unipolar Depression

likely to have a biological link or perhaps a family link to others who also have depression. In
fact, Rakel (1999) mentions that monozygotic twins have a 65% concordance rate, and dizygotic
twins have a 14% rate. Some forms of depression are more reactive or exogenous and are typi-
cally caused from forces outside of the body. In these cases, stress or grief may be the cause.
Therapists often find that both internal and external factors play a role in many patients’ depres-
sion (Barlow & Durand, 2005).
It is important for the therapist to determine the nature and source of a patient’s depression.
At times it may be rather clinical or endogenous in nature. Typically, major depression and the
depressive phases of bipolar conditions meet these criteria, but therapists are also aware that dys-
thymia, cyclothymia, and grief reactions have some biological components. Further, the clinician
must determine the role of other complicating factors such as substance use, psychotic features,
physical diseases, and medications that may cause depression.

CAUSES OF BIOLOGICAL DEPRESSION

For many patients presenting with depression, the cause can be related to another physical disor-
der that they may have. The following is a list of diseases and disorders that can cause or exacer-
bate depression:
Addison’s disease Cushing’s disease Mononucleosis
Alzheimer’s disease Diabetes mellitus Multiple sclerosis
Anemia Fibromyalgia Myocardial infarction
Asthma Hepatitis Pancreatitis
Brain tumor HIV/AIDSHuntington’s Parkinson’s disease
Cancer disease Porphyria
Cardiovascular Hyperthyroidism Postpartum hormonal
conditions Hypothyroidism changes
Chronic fatigue Influenza Premenstrual dysphoric
syndrome lupus disorder
Chronic infections Malnutrition Rheumatoid arthritis
Chronic pain syndrome Menopause Stroke
Colitis Mental retardation Syphilis
Congestive heart Metabolic Tuberculosis
failure abnormalities Uremia

In addition to the diseases and disorders mentioned above, many medications and other
substances have been known to cause or worsen a patient’s depression. The following is a list of
these medications and substances:
• Alcohol
• Antianxiety medications: diazepam, chlordiazepoxide, alprazolam, lorazepam, clon-
azepam, phenobarbital
• Antihypertensive medications: reserpine, propranolol, methyldopa, guanethidine sulfate,
clonidine, hydralazine, metoprolol, prazosin
 Chapter 5 • Treatment of Unipolar Depression 25

• Anti-inflammatory medications: indomethicin, butazolidin, rofecoxib (withdrawn from

U.S. market in 2004), celecoxib
• Antiparkinsonian medications: levodopa/carbidopa, amantadine
• Cold remedies: antihistamines, others containing alcohol
• Corticosteroids and other hormones: for example, estrogen, progesterone, cortisone ac-
etate, most oral contraceptives
• Drugs of abuse: marijuana, codeine, morphine, PCP, crystal methamphetamine, psyche-
delics, opium derivatives, synthetic pain killers
• Sedative-hypnotic medications: zolpidem, zaleplon, triazolam, flurazepam, temazepam,
meprobamate
If after careful history and assessment the therapist determines that the patient’s depression
appears to have little or no physical cause, a treatment plan is proposed to address the concern.
While it is a well-known fact that psychotherapy and counseling alone are very effective treat-
ments for depression, psychotherapy and medication together are most efficacious (Segal,
Kennedy, Cohen & Group, 2000). In cases of dysthymia (chronic-mild depression), psychother-
apy alone may be attempted. If little response is noticed, an antidepressant may be added. In
cases of a grief reaction with sleep disturbances, medications to improve sleep may be used with-
out an antidepressant. Only when the grief is prolonged, severe, and accompanied by suicidal
ideation should antidepressants be considered. Suicide assessment is very important to keep in
mind, as up to 80% of depressed patients also have suicidal ideation (Sonawalla & Fava, 2001).
The following is a list of treatment options for the patient with moderate to severe depression.
• Counseling and psychotherapy
• Medication, including pharmaceuticals and herbal remedies
• Light therapy for those with seasonally influenced depression
• Exercise
• Electroconvulsive therapy (ECT) and other treatments

COUNSELING AND PSYCHOTHERAPY

Psychotherapists often underestimate the effective nature of therapy. However, psychotherapy as
a medical treatment has been found to be more effective than bypass surgery, drug treatments for
arthritis, and even aspirin for heart attack (Lipsey & Wilson, 1993). Further, research on the per-
centage of improved patients at selected sessions has demonstrated that patients typically show
the greatest gains in the first 16–20 sessions (Howard, Kopta, Krause, & Orlinsky, 1986). While
nearly every form or approach of counseling or psychotherapy is helpful, some therapists believe
that solution-focused therapy or briefer forms of therapy offer quicker solutions. Still others be-
lieve that cognitive-behavioral approaches work better than other forms (Rakel, 1999).

MEDICATIONS FOR DEPRESSION

For the most part, antidepressants can be divided into four main categories: tricyclic antidepres-
sants (TCAs), selective serotonin reuptake inhibitors (SSRIs), monoamine oxidase inhibitors
(MAOIs), and heterocyclics or “others.”
The oldest antidepressants are the TCAs. Tricyclic antidepressants have been around for
more than forty years. They prevent the reuptake of neurotransmitter substance back into the
presynaptic cell. Although effective, TCAs are not “clean” medications, and, therefore, they affect
26 Chapter 5 • Treatment of Unipolar Depression

TABLE 5.1 Tricyclic Antidepressants (TCAs)

Neuro- Neuro-
Trade Generic Typical Dose Transmitter Transmitter Level of
Name Name (mg/day) 5-HT NE Sedation
Anafranil clomipramine 100–250 *** * Heavy
Ascendin amoxapine 150–400 * *** Moderate-heavy
Elavil amitriptyline 150–300 *** * Heavy
Ludiomil maprotiline 150–225 *** 0 Moderate
Norpramin desipramine 150–300 0 *** Light
Pamelor, Aventyl nortriptyline 75–125 ** *** Moderate-heavy
Sinequan, doxepin 150–300 ** *** Heavy
Adapin, Silenor
Surmontil trimipramine 100–300 ** ** Moderate
Tofranil imipramine 150–300 *** ** Light-moderate
Vivactil protriptyline 15–60 * *** Light

many nontarget organs and systems in the body. They have troublesome anticholinergic side effects
that include sedation, weight gain, difficulty urinating, dizziness, dry mouth, sexual dysfunction,
orthostatic hypotension, and blurred vision. Typically these medications are not safe for children or
the elderly. Due to their toxic cardiovascular nature, TCAs pose a serious risk of overdose for pa-
tients with significant suicidal ideation.
As was mentioned in Chapter 2, a patient’s depression may be caused by depletions in the
neurotransmitters serotonin (5-HT), norepinephrine (NE), dopamine (D) or all three. Table 5.1
lists TCAs with their trade and generic names, typical daily doses, neurotransmitter action, and
level of sedation.
In the early 1980s, a second-generation drug was introduced with the trade name Desyrel
and the generic name trazodone. This medication primarily affects serotonin but acts more as a
5-HT2 receptor antagonist. Trazodone is less likely to cause sexual side effects but may cause
priapism, a condition resulting in a prolonged, painful erection in men. Overall, it has fewer side
effects than older TCAs and is less of a suicidal risk, but the typical side effects of sedation and
dry mouth remain. Less expensive generic TCAs are available, making this medication more af-
fordable for many patients. Trazodone is often used as a general sedating medication without the
risk of addiction to sedative hypnotics for those who have trouble sleeping.
In the late 1980s, a new generation of drugs was born. Selective serotonin reuptake in-
hibitors, or SSRIs, block the reuptake of serotonin back into the presynaptic cell. This blocking
action allows more serotonin to exert its influence on the postsynaptic cell. Research has found
no statistical differences between the various SSRIs with relation to effectiveness, but some re-
search maintains that escitalopram and sertraline may be better tolerated, and, therefore, more
likely to be continued than others (Ciprani et al., 2009; Hansen et al., 2008). Table 5.2 lists
SSRIs, their trade and generic names, typical daily dose, and level of sedation.
The side effects for SSRIs are considerably less severe than for older TCAs. Typical side
effects include headache, nausea, diarrhea, dry mouth, anorexia, weight gain, restlessness, in-
somnia, tremor, sweating, yawning, dizziness, inhibited sexual desire, and inhibited orgasm for
some. (Hansen et al., 2008). As mentioned earlier, SSRIs are “cleaner” and interact with few
 Chapter 5 • Treatment of Unipolar Depression 27

TABLE 5.2 Selective Serotonin Reuptake Inhibitors (SSRIs)

Trade Name Generic Name Typical Dose (mg/day) Level of Sedation

Celexa citalopram 10–60 Light
Lexapro escitalopram 5–20 None
Luvox fluvoxamine 50–300 Light
Paxil, Paxil CR, Pexeva paroxetine 20–50/25–50 Moderate-heavy
Prozac, Sarafem fluoxetine 20–80 None
Prozac Weekly fluoxetine 90 (weekly) None
Zoloft sertraline 50–200 None

other medications the patient may be taking. They are considered safer medications for children,
seniors, and patients who may be at risk for a suicide overdose; however, recent FDA warnings
suggest that 2% to 3% of children and adolescents demonstrate an increase in suicidal thinking
and behavior (see the FDA website, www.fda.gov). Many clinicians believe that the benefits of
SSRIs outweigh their risks because without treatment, severely depressed children and
teenagers are at serious risk of suicide. While research has found that SSRIs and medications
like it (venlafaxine) increase the risk of gastrointestinal bleeding, newer research has found that
this may be to a lesser degree than once thought due to alcohol abuse among subjects (Opatrny,
Delaney, and Suissa, 2008).
If serotonin levels inside the central nervous system become too elevated from using SSRIs
or other medications, some patients may experience serotonin syndrome. Symptoms may include
agitation, confusion, insomnia, flushing, fever, shivering, muscle rigidity, hyperreflexia, incoor-
dination, diarrhea, and hypotension. Many of theses symptoms can be life threatening; therefore,
any patient started on medication for the first time should be closely monitored.
In the last few years, heterocyclic antidepressant medications have been introduced that
fall into the “other” category. These medications offer many possibilities (see Table 5.3).
Heterocyclic antidepressants have side effects similar to SSRIs, but they have less possibil-
ity of sexual dysfunction. Venlafaxine (Effexor/Effexor XR), a serotonin-norepinephrine reuptake
inhibitor (SNRI), is usually well tolerated and has been shown to be helpful in general depression,
generalized anxiety, and postpartum depression (Cohen, 1997). It has been known to increase
blood pressure at higher doses. Desvenlafaxine succinate is the succinate salt of the isolated major
active metabolite of venlafaxine, O-desmethylvenlafaxine. This drug, sold under the trade name
Pristiq, was approved by the FDA in 2008. Its potential advantages over other SNRIs include a
narrow dose range, requiring less adjustment and more effectiveness at lower dosing. Since the
drug is mainly excreted in urine, it has minimal effect on the CYP450 pathway in the liver, and,
therefore, it may be a preference for medically ill patients without renal impairment who may be
taking multiple medications (Lourenco & Kennedy, 2009). Duloxetine (Cymbalta), released in
2004, is similar to venlafaxine and desvenlafaxine in that it has a dual mechanism of action.
Duloxetine has the advantage of equally stimulating both serotonin and norepinephrine at all
doses. Venlafaxine is more serotonergic at lower doses.
Mirtazepine (Remeron) is helpful in restoring normal sleep patterns. It has also been found
to increase appetite, which is an undesirable side effect for overweight, depressed patients.
However, because of this side effect, mirtazepine may work wonders in depressed HIV or cancer
patients who are having trouble with weight loss. Like mirtazepine, nefazodone (Serzone) may
28

TABLE 5.3 Heterocclic Antidepressants

Typical Neuro- Neuro- Neuro-

Trade Dose Transmitter Transmitter Transmitter Level of
Name Generic Name (mg/day) 5-HT NE DA Sedation
Aplenzin bupropion 174–522 0 ** ** None
hydrobromide
Cymbalta duloxetine 20–60 *** *** 0 None
Desyrel, Oleptro trazodone 50–400 *** 0 0 Heavy
Effexor venlafaxine 50–300 *** *** *? None
Effexor XR venlafaxine XR 75–300 *** *** *? None
Pristiq desvenlafaxine 50–400 *** *** *? None
Remeron, mirtazepine 15–45 *** *** 0 Heavy
Remeron Soltab
Serzone1 nefazodone 100–500 *** * 0 Moderate
Wellbutrin bupropion 75–450 0 ** ** None
Wellbutrin SR bupropion SR 100–400 0 ** ** None
Wellbutrin XL bupropion XL 150–450 0 ** ** None
1
Serzone no longer available by prescription; the generic, nefazodone is available by prescription.
*
Minimal neurotransmission
**
Moderate neurotransmission
***
Significant neurotransmission
 Chapter 5 • Treatment of Unipolar Depression 29

help restore sleep patterns and cause sedation for many. Unfortunately, the medication has an
FDA “black-box” warning due to its increased risk of liver failure and must be used only with
caution especially for patients taking other medications that also use the CYP4503A4 pathway
for drug elimination in the liver. Patients who begin nefazodone therapy should have a baseline
liver function test and periodic tests for at least the first six months (Stewart, 2002).
Bupropion (Wellbutrin) is well tolerated but is rather uplifting and agitating for some.
While bupropion has not been associated with sexual dysfunction, it is not appropriate for pa-
tients with seizure or eating disorders, as it lowers the seizure threshold and reduces appetite.
The last major classification of antidepressants is known as monoamine oxidase in-
hibitors or MAOIs. These drugs work a bit differently than the others. They inhibit MAO, the
enzyme that breaks down neurotransmitters and renders them ineffective. MAOIs exert most
of their influence in the presynaptic cell. While the side effects of MAOIs closely resemble
those of TCAs, MAOIs are usually well tolerated. Patients taking MAOIs must adhere to
strict dietary restrictions, as ingestion of any food containing tyramine may cause a hyperten-
sive crisis. MAOIs have fallen out of use in this country but are still widely used in Europe.
Many prescribers use them as a last-resort drug for patients who do not respond well to other
medications. (see Table 5.4).
To be comprehensive, lithium must be mentioned as a possible treatment option for unipo-
lar depression, as well as for bipolar depression. This strategy is usually reserved for more diffi-
cult and treatment-resistant cases. Lithium will be explored further in Chapter 6.

HERBAL AND HOLISTIC SUBSTANCES

St. John’s wort is a plant that is said to have medicinal properties. Research, primarily con-
ducted in Europe, claims that St. John’s wort helps to control mild to moderate levels of de-
pression with virtually no side effects (Bloomfield, Nordfors, & McWilliams, 1996). Most
practicing clinicians believe that few patients are helped by St. John’s wort, and they are now
learning that it may interfere with or react to other medications patients may be taking. For ex-
ample, St. John’s wort potentiates blood thinners like warfarin (Coumadin) and lessens the ef-
fectiveness of other heart medications like digoxin (Lanoxin). It may also interfere with pro-
tease inhibitors taken by HIV/AIDS patients. The active ingredient in St. John’s wort is
hypericin. The Latin name of the plant is hypericum perforatum. Patients who are allergic to
plant derivatives should not take St. John’s wort because they might break out in a rash or be-
come seriously photophobic to it and experience severe burn when exposed to the sun. Patients
should take hypericum perforatum in its liquid form, which assures that they get a true dose.
Health food stores sell brands that may contain more inactive plant parts and less hypericum.
St. John’s wort should not be taken with other antidepressants because it may potentiate their
effects and cause serotonin syndrome.
Ginkgo biloba is a tree of Chinese origin. An extract from it is said to relieve mild depres-
sion and increase memory and concentration. While 60 mg/day of ginkgo biloba is typical for
depression and mild memory concerns, as much as 120 mg/day has been used with Alzheimer’s
patients. Since it is said to have blood-thinning properties, ginkgo biloba should be used with
caution by those taking blood-thinning medications. In our experience, it has not been as effec-
tive as antidepressants in the treatment of moderate to severe depression.
The hormone dehydroepiandrosterone or DHEA is normally secreted by the adrenal gland
and is a precursor to testosterone and estrogen. Typically, adolescents have high levels of this
substance, but the levels decrease with age. Some clinicians believe that when DHEA is taken
30

TABLE 5.4 Monoamine Oxidase Inhibitors (MAOIs)

Typical Neuro- Neuro- Neuro-

Trade Dose Transmitter Transmitter Transmitter Level of
Name Generic Name (mg/day) 5-HT NE DA Sedation
EMSAM selegiline transdermal 3 mg/24 hrs– ** ** ** None
system 12 mg/24
Marplan isocarboxazid 10–40 ** ** ** Light
Nardil phenelzine 30–90 ** ** ** Light
Parnate tranylcypromine 20–60 ** ** ** Light
*
Minimal neurotransmission
**
Moderate neurotransmission
***
Significant neurotransmission
 Chapter 5 • Treatment of Unipolar Depression 31

orally, it reduces mild to moderate depression, causes weight loss, increases large muscle mass,
and may increase sexual appetite. While these claims have yet to be fully proven, many practic-
ing endocrinologists believe DHEA may increase the risk of certain types of cancer. Side effects
are usually mild but may include oily skin, acne, irritability, and even psychosis.
S-adenosyl-L-methionine (SAM-e) is a substance that is endogenous to our body. It is
essential to many biological processes such as cell methylation. The body converts SAM-e
into the amino acid homocysteine, which accumulates and can cause depression, joint prob-
lems, and cancer. Homocysteine can be converted back into SAM-e by utilizing vitamins B6,
B12, and folic acid. Research conducted in Italy has shown that depressed patients have much
lower levels of SAM-e than nondepressed patients. Patients with poor diet typically make less
SAM-e. It is now available as a synthesized substance and has been shown to be as effective as
many prescription antidepressants for relieving depression. It is available as a prescription in
many European countries. SAM-e may also be helpful in relieving joint pain and for cleansing
the liver of other toxins. Researchers believe that SAM-e may increase the synthesis of sero-
tonin and dopamine and aid chemical communication between cells by potentiating the post-
synaptic membrane.
Animal research has also demonstrated that zinc and magnesium may possess antidepres-
sant properties and may serve as valuable agents in enhancing the activity of conventional anti-
depressants (Szewczyk et al., 2008).

LIGHT THERAPY FOR SEASONAL AFFECTIVE DISORDER (SAD)

Antidepressants have been shown to be helpful for patients with seasonal affective disorder; how-
ever, the use of light boxes is also effective. Therapists who treat patients living in colder, darker
climates and suffering from seasonal depression might consider suggesting the use of a light box
first unless the patient’s depression worsens and he or she becomes suicidal. Several commercially
produced lamps or boxes are available. They cost between $100 and $500. The light source should
produce at least 10,000 lux of full-spectrum light. Patients need to be directly exposed to the light
for 30–60 minutes/day and sit approximately 10–12 inches from most light sources. Bulbs sold in
hardware stores for use in overhead fixtures and in doorways may be esthetically pleasing, but
they offer little in the form of treatment. Most quality lamps can be found by searching the
Internet under seasonal affective disorders or full-spectrum lamps. In some cases, a letter from a
physician or psychologist is required for the patient to purchase the lamp directly.

IMPORTANCE OF EXERCISE
Therapists should always encourage depressed patients to exercise. Not only does exercise lead
to weight loss and increased levels of motivation, but it also helps to release important endor-
phins and neuromodulators like phenylethylamine (PEA). The presence of PEA is associated
with increased levels of endorphins and improvement in motivation, energy, and mood.

ELECTROCONVULSIVE THERAPY (ECT)

In some cases, patients with severe depression do not respond to antidepressants. If their depres-
sion worsens and includes suicidal ideation, they may be referred for ECT. Electroconvulsive
therapy is given when the patient is anesthetized and paralyzed. Electrodes are placed on the
scalp, usually on the nonspeech-dominant hemisphere to avoid later damage to verbal memories.
32 Chapter 5 • Treatment of Unipolar Depression

Electricity is then administered, resulting in a seizure. No movement is noted because the patient
is paralyzed or immobilized. Most patients receive three sessions per week for up to four weeks,
or until improvement is noted. While excessive use of ECT may cause brain damage and mem-
ory loss, some researchers have noted that naloxone (Narcan), a drug that blocks opioid recep-
tors, may reduce some of the adverse cognitive side effects of ECT (Prudic, et al., 1999). Some
clinicians, especially those who treat elderly and medically ill patients, believe that the risks as-
sociated with ECT are equivalent or even preferable to those associated with many medications
used to treat depression (Kelly & Zisselman, 2000).
For patients who may not be good candidates for ECT, new research into the use of tran-
scranial magnetic stimulation or TMS to the prefrontal cortex, stimulation of the vagus nerve,
and stimulation of other areas of the brain through deep brain stimulation may offer some relief
(Triggs, et al., 1999; Klein et al., 2003).

PROCEDURAL STEPS FOR PATIENT TREATMENT

When a decision is made to use medication to treat a patient’s depression, the therapist should
follow a treatment protocol or procedural steps to decide on the appropriate medications and how
to use them.
Step 1 Most prescribing professionals start with the easier medications first. These include the
SSRIs such as fluoxetine (Prozac), citalopram (Celexa), sertraline (Zoloft), and so on.
These medications have fewer side effects and interact with fewer other medications. In
many cases, the patient is started on a low dose and titrated up. The patient must end up
on a therapeutic dose of the medication to truly determine if the medication is helpful.
Research suggests that too many patients are maintained on too small a dose of antide-
pressants, which are no better than no dose at all (Leon et al., 2003). (This is a common
problem when primary care physicians write prescriptions.) If the patient has a satisfac-
tory response and all symptoms appear to remit, the therapist should continue with psy-
chotherapy and not increase the medication. The clinician may need to wait at least four
to five weeks to determine the level of response.
Step 2 In some cases the patient has only a partial response to SSRIs, even when the dose is in-
creased. Since SSRIs affect only the neurotransmitter serotonin, the patient’s depression
may be related to norepinephrine and/or dopamine. In such cases, additional medications
aimed at the other neurotransmitters might need to be added or substituted. It is not un-
usual for such patients to be taking an SSRI like fluoxetine or an SNRI like venlafaxine
(Effexor) with bupropion (Wellbutrin). Polypharmacy is more complicated and should
not be attempted by the patient’s primary care physician. In addition, antidepressants can
be augmented or boosted by adding a low dose of lithium for one or two weeks, or by
adding a stimulant like methylphenidate (Ritalin). Buspirone (Buspar), a nonbenzodi-
azepine anxiety medication with antidepressant qualities, and folic acid may also boost
the antidepressant response.
Step 3 If the patient appears to have psychotic features in addition to his or her depression, an
appropriate neuroleptic or antipsychotic medication might need to be added to the
regime. In rare cases, the patient may also have racing thoughts that interfere with his or
her ability to relax. In these cases, neuroleptics may also be added to calm the thoughts
and allow the patient to sleep better (Baune, 2009; Nelson, et al., 2008). Refer to
Chapter 8 for further information on these medications.
 Chapter 5 • Treatment of Unipolar Depression 33

Step 4 If the therapist and the prescriber have tried several drugs with no response, they should
check with the patient to determine if he or she is using alcohol or other substances, tak-
ing the medication as directed, not taking the medication at all, and/or taking an unre-
ported dietary supplement.
Step 5 The therapist should keep in mind that certain medications are contraindicated for cer-
tain types of patients. For patients with poor appetite or eating disorders, do not use
bupropion as it may decrease appetite. For overweight patients, use mirtazepine
(Remeron) and TCAs with caution, as they have been shown to cause an increase in
weight and appetite. Patients with a history of seizure should not take bupropion be-
cause it lowers the seizure threshold. Nefazodone must be used with extra caution be-
cause it may cause liver failure in some patients. It is important to remember that
MAOIs do not mix with other antidepressants and can cause a hypertensive crisis. It is
imperative to wait at least two weeks after using an MAOI before starting another anti-
depressant because of potential drug interactions; the prescriber must wait two weeks
after stopping another medication before trying MAOIs. There is one exception; the
prescriber should wait five weeks after discontinuing fluoxetine before MAOIs are
used. We call this the “washout period.”

Effective therapy includes patient education. As mentioned earlier, patients with dysthymia or
minor depression typically are not placed on medication unless they are experiencing sleep diffi-
culties, or the depression is seriously affecting their ability to function, which is true for patients
who are experiencing serious complications to grief. For patients who are suffering from major
depressive episodes and who are found to be good candidates for pharmacology, the therapist
should inform them of the following five facts where appropriate:

1. Antidepressant medications take time to work. Typically a patient waits between one
and four weeks before an antidepressant begins to work. Advise the patient to be patient! Some
medications, like venlafaxine and desvenlafaxine (Effexor/Pristiq) may begin to work within a
couple of days, but this is the exception, not the rule.
2. Inform the patient about the types of side effects to expect from the medication he or
she is taking. It is easy to remember the major side effects with antidepressants, as they all start
with the letter S. The side effects include sedation, seizure, sexual symptoms, and stomach-
related symptoms. In most cases, these side effects are minimal, and most of them disappear
within a few days. Try not to spend too much time taking about side effects because the patient
may begin to fear the medication and refuse to take it. The following is a list of typical side
effects and how best to resolve them.
• Dry mouth: increase water consumption, chew gum, and use hard candy (avoid TCAs)
• Inability to reach orgasm: reduce dose of SSRI; switch to bupropion (Wellbutrin); add
low dose mirtazepine (Remeron), bupropion, buspirone (Buspar), nefazodone (Serzone),
or cyproheptadine; also, consider switching to duloxetine (Cymbalta)
• Forgetfulness: add bupropion, ginkgo biloba, or stimulant
• Insomnia: check for serotonin syndrome; add sedative-hypnotic, trazodone or nefa-
zodone
• Sedation: avoid TCAs, paroxetine (Paxil), and nefazodone; use fluoxetine (Prozac),
venlafaxine, or bupropion
• Weight gain: avoid TCAs or mirtazepine, consider bupropion or other SSRIs
• Stomach upset: take with food, avoid SSRIs if GI upset is severe
34 Chapter 5 • Treatment of Unipolar Depression

• Headache: treat with acetaminophen (Tylenol) or aspirin if severe

• Hand tremors: reduce dose, add low-dose benzodiazepine

3. Remind the patient that he or she should never stop the medications abruptly. This may
cause the patient to experience a type of withdrawal known as discontinuation syndrome, which
is accompanied by severe flulike symptoms. If the patient is concerned about the medications, he
or she needs to discuss the problem with the therapist and the prescribing professional. If a deci-
sion is made to stop a medication, it should be done gradually and under medical supervision.
Watch for an increase in depression or suicidal ideation.
4. Pregnant patients should probably not take antidepressants (or any other medication) if
they can help it. The clinician should consider antidepressant only if the patient is severely de-
pressed and cannot function without them. Typically, antidepressants are most dangerous in the
first trimester. Teratogenicity data and practice experience have indicated that SSRIs and bupro-
pion are generally safer than other antidepressants. Lithium and antipsychotic medication should
be avoided or used only under strict medical supervision. Breast-feeding mothers should consult
their physician before they proceed (Howland, 2009).
5. Typically, antidepressants relieve symptoms of depression and associated anxiety.
Many patients today are concerned about taking drugs and resist the therapist’s recommenda-
tions. When working with a severely depressed patient for whom psychotherapy alone has not
helped, the therapist must help the patient to see that medication may be a very effective part of
treatment. The therapist may find it helpful to use the analogy of vitamins for the person who is
malnourished. Antidepressants allow the brain and neurotransmitters to work better, leading to
improved emotional functioning.

CASE VIGNETTE
Chapter Five
CLINICAL HISTORY
Justin is a 22-year-old Hispanic male who works full-time in an auto parts warehouse and attends community college
part-time in the evening. He recently sought counseling for depression at the urging of his new girlfriend. He claims
that he has always had a problem with depression, even as a youngster, but attributed it to the chaotic household he
grew up in. His parents divorced when he was very young due in part to his dad’s heavy drinking. Justin claims he does
not remember his father very much. His mother told him his father moved back to Guatemala when Justin was just
three. Justin has one older sister, who is a nurse. While she often looks and acts as if she is depressed, she claims she
is not, nor has she sought treatment of any kind. Justin’s mother however, has been placed on antidepressants by her
PCP at various times.
Justin admits that he used alcohol in his teen years to self-medicate his depression. His alcohol use became
problematic in the last two years and this lead to a break-up with his fiancée Marta four months ago. He decided
shortly after that to refrain from using alcohol when he met his current girlfriend Elena at a work-related event. He
has noticed that his depressive symptoms worsened when he didn’t have something to “soothe it.” He is most
bothered by poor sleeping and difficulty concentrating at work. While he is very happy about meeting Elena, his
depression has escalated recently, leading to thoughts of suicide on at least two occasions.

POSTCASE DISCUSSION AND DIAGNOSIS

Justin is suffering with Major Depressive Disorder that appears to be rather chronic and severe in nature (296.33). He
reports problems with poor sleeping, namely, terminal insomnia. He further presents with concentration concerns, feelings
 Chapter 5 • Treatment of Unipolar Depression 35

of sadness, and suicidal ideation. There also appears to be positive family history for mood disorders. While he reports
past issues with alcohol, there appears to be no reason for detox at this time. Since gaining sobriety, he has noticed an
increase in depressive symptoms, indicating a need to treat depression as a causal factor for his drinking. A complete
physical was conducted with his PCP and all blood work and other findings were within normal limits.

PHARMACOLOGICAL TREATMENT
Justin was started on 5 mg q.d. of Lexapro by his family doctor. He was watched closely by his physician and therapist
for any signs of mood changes or an increase in suicidal thinking. Within two weeks he reported an improvement in
both mood and outlook. While Marta also noticed a big change, Jason reported that his early morning awakening,
while better, has not fully improved. His dose was increased to 10 mg q.d. Within a month, he reported that he was able
to sleep through the night without awakening. At one visit with his therapist, Jason complained that although he was
happy with his overall level of improvement, he had noticed that it was much more difficult to have an orgasm when he
was with Marta. Upon consultation with his doctor, a low dose of nefazadone was added each day. The doctor did not
use Wellbutrin because of his past alcohol abuse. Three weeks later, Justin reported that he was doing well, with no
problems “in the sex department.”
 6 TREATMENT OF BIPOLAR
DISORDER

This chapter reviews the types and causes of bipolar illness, as well as current informa-
tion on treatment options for this population. Polypharmacy and family education will
also be discussed.
Topics to be addressed include the following:
• Prevalence and types of bipolar illness
• Causes of bipolar disorder
• Counseling and psychotherapy
• Medications for bipolar disorders
• Electroconvulsive therapy (ect)
• Treatment resistance and protocol
• Patient and family education
• Case vignette

PREVALENCE AND TYPES OF BIPOLAR ILLNESS

Bipolar illness is a disorder of mood regulation characterized by cycling between extreme
highs or mania and extreme lows or depression. Although effective treatments are available,
three out of four patients fail on maintenance treatment within five years (Moller & Nasrallah,
2003). The lifetime prevalence of bipolar disorder is approximately 1% of the general popu-
lation when a strict DSM-IV definition is used (Malhi, Mitchell, & Salim, 2003). When the
broader term bipolar spectrum disorders is used, Grunze, Schlosser, and Walden (2000) report
that the lifetime prevalence increases to 3% to 6%. Bipolar disorder usually begins with an in-
dex depressive episode about 50% of the time. The average age of onset of the first depressive
episode is 18.7 years, and the first manic episode is 24.5 years. Unfortunately, obtaining the
correct bipolar diagnosis is typically delayed until the patient reaches age 33.5 years.
In contrast to unipolar depression, bipolar disorder is thought to originate endogenously
but may be triggered by exogenous or environmental stimuli. Monozygotic twins have a 40%
to 70% concordance rate, whereas dizygotic twins or first-degree relatives have only a 5% to
36
 Chapter 6 • Treatment of Bipolar Disorder 37

10% chance of inheriting the illness (Craddock & Jones, 1999). The mainstay of treatment is, there-
fore, derived from a biological perspective, that is, medications. Psychosocial stressors may trigger
the patient to cycle or may cause a more severe cycle. Although some environmental factors influ-
ence the disorder, it is commonly known that a genetic predisposition or vulnerability is necessary.
There are many different types of bipolar spectrum disorders. Bipolar Disorder Type I is a
well-defined symptom cluster that may present as manic features, depressive features, or mixed
mood states. Bipolar Disorder Type II is similar but limited to hypomanic states only. In addition,
cyclothymia is considered to be the milder form of the classic disease that is characterized by cy-
cles between hypomania and low-level depression. Another useful term to know is rapid cycling,
which is defined as the occurrence of four or more episodes of mania or depression in a 12-
month period. The most common cause of rapid cycling is the uncritical use of antidepressant
medications (Grunze, Schlosser & Walden, 2000).
When compared to unipolar depression, bipolar depression is associated with higher rates
of suicide and psychosis. Primarily during the depressive cycle, approximately 10% to 20% of
bipolar patients complete suicide (Goodwin, 2002). According to Bowden (2001), psychotic
symptoms occur in the context of bipolar Type I disorder about 50% to 90% of the time.
Comorbidity commonly occurs in bipolar patients, with anxiety disorders and substance abuse
problems being the most prevalent. Cormorbidity is covered more extensively in Chapter 13,
Chemical Dependency and Co-occuring Conditions.

CAUSES OF BIPOLAR DISORDER

When evaluating a bipolar patient, the psychiatric symptoms are only one component of a larger
dynamic functioning person. While an exact cause of bipolar conditions is not well understood,
it is theorized that the cause may be related to neurotransmitter dysregulation or possibly abnor-
mal permeability of the postsynaptic membrane. The clinician needs to exclude medical issues
that might cause or contribute to a patient’s cycling mood disorder. The following is a list of dis-
eases and disorders that have been associated with or are known to exacerbate mania:
Brain tumors
Carcinoid syndrome
CNS syphilis
CNS trauma
Ddelirium (multiple etiologies)
Eencephalitis (herpes and other viruses)
Huntington’s disease
Influenza
Hyperthyroidism
Metabolic changes (electrolyte abnormalities)
Metastatic cancer
Multiple sclerosis
Parkinson’s disease
Pellagra (deficiency of nicotinic acid)
Postpartum metabolic changes
38 Chapter 6 • Treatment of Bipolar Disorder

Renal failure and hemodialysis

Stroke
Temporal lobe epilepsy
Vitamin B12 deficiency
Wilson’s disease
Furthermore, many medications and other substances have been known to cause or worsen
a patient’s mania. These substances are often overlooked when a patient presents to medical
providers. The following is a list of these medications and substances:
Antidepressants (pharmaceuticals and herbals)
Antihypertensive medications: captopril, hydralazine
Baclofen
Bromides
Bromocryptine
Cimetidine
Corticosteroids and other hormones: prednisone, testosterone
Cyclosporine
Disulfiram
Drugs of abuse: amphetamines, cocaine, ephedra, hallucinogens, PCP
Isoniazid
Levodopa
Opiates and opioids
Procarbazine
Procyclidine
Psychostimulants: dextroamphetamine, methylphenidate
Yohimbine

COUNSELING AND PSYCHOTHERAPY

After a thorough clinical assessment and medical evaluation, the therapist prepares an appropriate
treatment plan for the patient. In addition to pharmacotherapy and possible hospitalization, the pa-
tient will most likely need psychotherapy when he or she has stabilized on medications. Remember
that mild forms of unipolar depression may be treated with psychotherapy alone. However, phar-
macotherapy is the cornerstone of treatment, with psychotherapy playing a lesser role with bipolar
mood disorder. Suicide assessment is still an important part of any evaluation. Bipolar patients have
a higher risk of suicide because of their erratic and chaotic mood swings and behaviors.
One of the first steps a counselor or psychotherapist should address is basic family educa-
tion regarding the illness. Most families have little understanding of the symptoms, behavioral
management, causes, or treatments needed for the identified patient. Many educational resources
are available through organizations such as the National Institute of Mental Health (NIMH),
National Alliance on Mental Illness (NAMI), or Depression and Bipolar Support Alliance (for-
merly National Depressive and Manic Depressive Association). Family therapy should focus on
 Chapter 6 • Treatment of Bipolar Disorder 39

establishing a safe environment, constructive communication, and solving problems together.

The patient might benefit from individual psychotherapy to help him or her understand the ill-
ness, accept the diagnosis, and learn to manage the chronic nature of the disorder.
Psychotherapists know that various forms of psychotherapy may be appropriate, including psy-
chodynamic, cognitive behavioral, or solution focused.

MEDICATIONS FOR BIPOLAR DISORDER

Psychopharmacology for bipolar disorder involves a class of medications known as mood stabi-
lizers. The list of mood stabilizers consists of three broad categories, including lithium, anticon-
vulsants, and atypical antipsychotics. The choice of treatment options depends on whether the
patient is in the manic, depressed, or mixed phase of the illness. These options will be discussed
in more detail in the following sections.

Lithium
Lithium has been the gold standard for treating bipolar disorder since the early 1970s. Lithium is
indicated for treatment of acute mania and as maintenance therapy to prevent subsequent cy-
cling. Furthermore, both manic and depressive phases of the bipolar cycle may be treated with
lithium. Research by Sondergard, Lopez, Andersen, and Kessing (2008) has demonstrated that
lithium may be superior to many other bipolar medications in the prevention of suicide.
Although lithium’s mechanism of action is still unknown, Schatzberg, Cole, and DeBattista
(1997) have found that there are multiple biochemical effects, including the following:
• Increases synthesis of serotonin
• Enhances release of serotonin
• Increases rate of synthesis/excretion of norepinephrine in depressed patients
• Decreases rate of synthesis/excretion of norepinephrine in manic patients
• Blocks postsynaptic dopamine receptors’ supersensitivity
• Has direct or indirect effect on G proteins that mediates balance of neurotransmitters
• Inhibitis enzymes in the phosphoinositide (PI) second-messenger system that may affect
receptor activity of many neurotransmitters
Since lithium acts as a salt in the body, lithium concentration is determined by the patient’s
body fluid status. Lithium is not metabolized in the liver and is excreted unchanged by the kid-
neys. Thus, when dehydration occurs, the kidneys may reabsorb more lithium, which might lead
to toxicity. Because of the pharmacokinetics of lithium, the therapeutic level is close to the toxic
level, thus, this medication has a low therapeutic index (refer to Chapter 3 for more explanation).
The most common side effects of lithium include increased thirst, increased urination,
rash, tremor, dry mouth, increased appetite with weight gain, nausea, bloating, diarrhea, edema,
and thyroid dysfunction. The side effects of the drug may be diminished by using divided doses
throughout the day rather than one daily dose. In rare cases, lithium toxicity may cause renal in-
sufficiency or failure. Although this effect sounds terrible, lithium may be used with success
when it is monitored appropriately by the prescribing professional.
Lithium is usually started at 300 mg/day and increased to a therapeutic dose of 600–1200
mg/day (see Table 6.1). Laboratory testing is usually done before initiating therapy and subsequently
at regular intervals (about every six months) when the patient is stable. Therapeutic levels of lithium
are usually in the range of 0.7–0.9 mEq/L while the toxic rage is typically 1.5 mEq/L or above.
40

TABLE 6.1 Mood Stabilizers

Typical Dose
Trade Name Generic Name (Mg/Day) Proposed Mechanism of Action
Abilify, Abilify Discmelt aripiprazole 15–30 Partial agonism at dopamine type 2 and serotonin type 1A,
serotonin type 2A antagonism
Clozaril, Fazaclo clozapine 300–600 Low dopamine type 2 antagonism, high dopamine type 1 and
type 4 antagonism, high serotonin type 2 antagonism
Depakote, Depakote ER, valproate or valproic acid 500–2000 Inhibition of sodium and/or calcium channels, increases
Depakene, Stavzor GABA, releases glutamate
Fanapt iloperidone 12–24 Dopamine type 2 and serotonin type 2 antagonism
Gabitril tiagabine 8–16 Increases GABA
Geodon ziprasidone 80–160 Dopamine type 2 and serotonin type 2 antagonism
Invega, Invega Sustenna Paliperidone 6–12 Dopamine type 2 and serotonin type 2 antagonism
Klonopin, Klonopin Wafer clonazepam 2–6 Increases GABA
Lamictal. Lamictal XR, lamotrigine 200–400 Inhibition of sodium channels, presynaptic modulation of
Lamictal ODT, Lamictal CD glutamate release
Lithobid, lithium carbonate or 600–1200 Enhances serotonin, increases or decreases norepinephrine, blocks
Eskalith CR lithium citrate dopamine receptors’ supersensitivity, alters second messengers
Neurontin, Gabarone gabapentin 300–3600 Enhances GABA
Risperdal, Risperdal M-tab, risperidone 2–6 Dopamine type 2 and serotonin type 2 antagonism
Risperdal Consta
Saphris asenapine 10–20 Dopamine type 2 and serotonin type 2 antagonism
Seroquel, Seroquel XR quetiapine 400–600 Dopamine type 2 and serotonin type 2 antagonism
Symbyax olanzepine/fluoxetine 3/25–12/50 Inhibition of serotonin reuptake/dopamine type 2 and serotonin
type 2 antagonism
Tegretol, Tegretol XR, carbamazepine 600–1200 Inhibition of sodium channels
Carbatrol, Equetro
Trileptal oxcarbazepine 600–1200 Inhibition of sodium channels, modulation of calcium channels
Topamax topiramate 100–500 Increases GABA, blocks glutamate receptors
Verelan PM, Covera-HS, verapamil 200–400 Calcium channel blocker
Ispotin SR, Calan SR
Zonegran zonisamide 200–400 Inhibition of sodium and/or calcium channels, facilitates
dopaminergic and serotonergic neurotransmission
Zyprexa, Zyprexa Zydis, olanzepine 10–30 Dopamine type 2 and serotonin type 2 antagonism
Zyprexa Relprevv
 Chapter 6 • Treatment of Bipolar Disorder 41

Signs of lithium toxicity include ataxia, poor coordination, slurred speech, poor attention
span, severe tremors, severe nausea/vomiting, lethargy, arrhythmias, hypotension, seizure, coma,
and death. Lithium use in pregnancy has been contraindicated because of an association with
congenital heart malformation. More recently, the risk is rated as only moderate (Viguera,
Cohen, Baldessarini, & Nonacs, 2002).

Anticonvulsants
In addition to lithium, there is another class of mood stabilizers known as anticonvulsants or an-
tiseizure medications. Researchers believe that some of the anticonvulsants increase the concen-
tration of GABA, the inhibitory neurotransmitter. By increasing inhibition, electrical activity is
diminished and less neurotransmission occurs.

VALPROATE. The best known medication in the anticonvulsant group is valproic acid or val-
proate (Depakote). Unlike lithium, valproate may be more useful in patients with rapid cycling,
atypical features, or mixed mood states. Valproate has been approved by FDA for treatment of
acute mania and as an adjunctive therapy with other agents. The most common side effects of
valproate include nausea, diarrhea, hair loss, rash, weight gain, and tremor. Laboratory testing is
required with valproate to evaluate the serum concentration, complete blood count, and liver
function tests. Although the therapeutic index is wider when compared to lithium, valproate
serum concentrations of 150 micrograms/ml or greater lead only to more side effects, without
any improved clinical response. Valproate is not used during pregnancy because of the high risk
of neural tube defects, for example, spina bifida and anencephaly.

CARBAMAZEPINE. Another anticonvulsant that has widespread use as a mood stabilizer is carba-
mazepine (Tegretol). Although this medication has been extensively studied, it does not have FDA
approval for use as a mood stabilizer. The most common side effects of carbamazepine include rash,
fatigue, nausea, dizziness, and sedation. As with lithium and valproate, carbamazepine requires lab-
oratory monitoring because of the possibility of agranulocytosis (decreased white blood cell count)
and aplastic anemia (decreased production of all blood cells); however, both of these effects are rare.
Drug interactions with carbamazepine may be more problematic, and the prescribing professional
should be aware of the pitfalls. As with valproate, the use of carbamazeprine in pregnancy carries a
high risk of multiple fetal anomalies.

LAMOTRIGINE. Lamotrigine (Lamictal) is a newer generation of anticonvulsants that obtained

FDA approval in 2003 for maintenance treatment of bipolar disorder. This medication appears to
be superior to the other mood stabilizers for bipolar depression (Chang et al., 2008; Geddes,
Calabrese & Goodwin, 2009). The most important side effect to remember about lamotrigine is
the potential for a toxic rash (Stevens-Johnson syndrome). Other common side effects include
headache, dizziness, and sedation. The risk of this medication in pregnancy is virtually unknown;
however, some research suggests that it may be a safer alternative for pregnant women with bipo-
lar illness than lithium or other anticonvulsants (Newport et al., 2008).

GABAPENTIN. Gabapentin (Neurontin) is also used in the treatment of bipolar disorder, prima-
rily as an adjunctive treatment. This drug has been used clinically and has some research basis
but has not been approved by the FDA for use in bipolar disorder. The most common side effects
of gabapentin include sedation, tremors, nausea, dizziness, and weight gain. The use of
gabapentin during pregnancy is not recommended.
42 Chapter 6 • Treatment of Bipolar Disorder

TOPIRAMATE. Topiramate (Topamax) might be another useful alternative, but like gabapentin,
it does not have the FDA indication. This drug may have one major advantage over the others: It
does not cause weight gain. While not an advantage in terms of efficacy, weight loss is an impor-
tant factor for patients on so many medications shown to alter blood glucose and increase weight
and blood pressure (Chengappa et al., 2007). The most common side effects of topiramate in-
clude weight loss, sedation, cognitive dulling, fatigue, headache, and paresthesias (numbness in
extremities). The use of topiramate during pregnancy is not recommended.

OTHER ANTICONVULSANT MEDICATIONS. A few other anticonvulsant mood stabilizers

worth mentioning include tiagabine (Gabitril) and zonisamide (Zonegran). They are similar to
the other medications mentioned that are being researched for use in bipolar disorder.
Oxcarbazepine (Trileptal) is a medication similar to carbamazepine but does not carry the risk of
agranulocytosis or aplastic anemia. Further investigation of oxcarbazepine is needed to fully
confirm or deny its usefulness in bipolar disorder. Clonazepam (Klonopin) is another anticonvul-
sant medication, which happens to be a benzodiazepine. It is used primarily as an adjunctive
treatment in patients who do not have a history of chemical dependency.

Atypical Antipsychotic Medications

In addition to lithium and the anticonvulsants, the final category of mood stabilizers is the atypi-
cal antipsychotic medications.

OLANZEPINE (ZYPREXA). The first antipsychotic mediation to receive FDA approval for acute
mania was olanzepine. When a patient presents with mania and psychosis, olanzepine is the drug
of choice, because it functions both as a mood stabilizer and an antipsychotic. Olanzepine has re-
ceived FDA approval for acute monotherapy treatment, maintenance monotherapy treatment,
and combination treatment for bipolar disorder. The medication also comes in an alternative
form, Zyprexa Zydis (orally disintegrating tablet), which is used in hospital settings where com-
pliance is called into question. The most common side effects of olanzepine include sedation,
weight gain, constipation, dry mouth, dizziness, orthostatic hypotension, and weakness. When a
patient takes olanzepine, laboratory monitoring of glucose, lipids, and liver functions is recom-
mended because of the likelihood of the drug causing diabetes, hypercholesterolemia, and liver
dysfunction. The use of olanzepine in pregnancy is not recommended.

SYMBYAX. Another medication approved by the FDA, specifically for the depressive phase of
bipolar disorder, is known as Symbyax. This medication is a combination of fluoxetine (Prozac) and
olanzepine. More information about the individual medications can be found in Chapters 5 and 8.

RISPERIDONE. This antipsychotic medication that has mood stabilizing properties is risperi-
done (Risperdal). It has been approved by the FDA as monotherapy or adjunctive therapy for
treatment of acute manic or mixed episodes. As with Zyprexa Zydis, Risperdal has an orally dis-
integrating tablet called Risperdal M-tab. The most common side effects include restlessness, in-
somnia, constipation, and dizziness. Recommendations for laboratory monitoring are basically
the same as with olanzepine. Risperidone use during pregnancy carries significant risk and is not
recommended. Paliperidone (Invega) is the major metabolite of risperidone. One advantage of
this newer formulation is that approximately 59% is eliminated through the kidneys as an un-
changed drug. The cytochrome P450 enzyme system, therefore, plays a minimum role in drug
 Chapter 6 • Treatment of Bipolar Disorder 43

elimination. (Fowler, Bettinger, & Argo, 2008). Neither paliperidone or the injectable version
(Sustenna) are currently FDA approved for the treatment of bipolar illness.

QUETIAPINE. Quetiapine (Seroquel) is an antipsychotic medication that may be useful with

acute mania. It is currently approved by the FDA for acute mania, either as monotherapy or ad-
junctive therapy. Quetiapine’s side effects include sedation, dizziness, constipation, and dry
mouth. As with the other atypical antipsychotic medications, laboratory monitoring of blood
sugar and lipids is recommended when using quetiapine. It is not recommended during pregnancy.

ZIPRASIDONE. Ziprasidone (Geodon) is another option available for acute mania, with or with-
out psychosis. Compared with the other atypical agents, ziprasidone is more likely to cause QT
prolongation on EKG, which is associated with a potentially fatal arrhythmia. The most common
side effects include somnolence, dizziness, rash, anxiety, and nausea. Laboratory monitoring of
glucose, lipids, and liver functions is recommended. Ziprasidone use during pregnancy is not rec-
ommended unless the potential benefit to the mother outweighs the potential risk to the fetus.

ARIPIPRAZOLE. The newest atypical antipsychotic available is aripiprazole (Abilify). This

medication is also clinically effective as a mood stabilizer. In late 2004, the FDA-approved
Abilify for use in acute manic or mixed episodes. The most common side effects of aripiprazole
include headache, nausea, insomnia, and somnolence. Laboratory monitoring is again necessary.
As with other newer medications, aripiprazole is not recommended during pregnancy.

CLOZAPINE. The last atypical antipsychotic medication that is worth noting is clozapine
(Clozaril). Although this medication is only approved for treatment-resistant schizophrenia, cloza-
pine has been used for the last decade to manage severe mania in some circumstances. This drug is
used only in select cases, because it may have very severe side effects, including agranulocytosis
and seizures. Clozapine requires weekly monitoring of the white blood cell (WBC) count for the
first six months, then every other week while the patient remains on the drug. Other common side
effects include weight gain, sedation, headache, orthostatic hypotension, constipation, salivation,
tachycardia (increased heart rate), and myocarditis (inflammation of the heart). Clozapine is defi-
nitely an effective medication but requires more intense monitoring by the prescribing professional.
Interestingly, clozapine is not known to be teratogenic and may be used in pregnancy if the benefits
outweigh the risks. Clozapine comes in an orally disintegrating tablet form known as Fazaclo.

OTHER. Iloperidone and asenapine are newer atypicals that have action similar to the others;
however, they are not currently FDA approved for the treatment of bipolar illness.

Typical Antipsychotic Medications

As opposed to atypical antipsychotic medications, a multitude of other typical antipsychotic medica-
tions are used adjunctively with other mood stabilizers. Haloperidol (Haldol), fluphenazine
(Prolixin), trifluoperazine (Stelazine), thioridazine (Mellaril), and chlorpromazine (Thorazine) are a
few of the best known agents. These medications are used primarily for acute agitation while the pa-
tient is hospitalized. Haloperidol and some of the other medications may be given intramuscularly or
by mouth, depending on the acuity of the situation. Although this class may cause major side effects,
including extrapyramidal symptoms, typical antipsychotics are used for behavioral management
only in the short term (less than one week). More information about these medications may be found
in Chapter 8, Treatment of Psychotic Disorders.
44 Chapter 6 • Treatment of Bipolar Disorder

Other Medications
In addition to the medications already discussed, some other options are worth mentioning.
Verapamil is a calcium channel blocker that is primarily used in the treatment of hypertension,
angina, and supraventricular arrhythmias. A small number of open trials suggest that the drug
has antimanic properties. One randomized, double-blind, placebo-controlled study did not show
any antimanic effect (Bowden, 2001).
Benzodiazepines are useful medications that may be used adjunctively with other mood
stabilizers. For example, lorazepam (Ativan) is commonly given to manic patients early in
their treatment to decrease agitation, which helps with behavioral management, until the pri-
mary mood stabilizer becomes effective. Finally, some researchers believe that omega-3 fatty
acids may be helpful when taken in combination with lithium as compared to lithium alone.
Although omega-3 fatty acids may have other health benefits, their use in bipolar disorder is
still being debated.

ELECTROCONVULSIVE THERAPY (ECT)

In some severe manic patients, who are unresponsive to medications, a course of electroconvulsive
therapy (ECT) is appropriate. During the depressed phase of the illness with suicidality present, ECT
may be an option for a rapid response. As with any treatment option, the benefits of ECT must be
weighed against the risks before proceeding. See the discussion in Chapter 5 for more information.

TREATMENT RESISTANCE AND PROTOCOL

Mania Treatment Protocol
As with depression, making decisions on medication for bipolar disorder requires a logical ap-
proach, depending on the phase of the bipolar cycle.
Step 1 The first place to start is with FDA-approved medications for treatment of acute
mania. For example, lithium or valproate would be first-line agents. If psychotic
symptoms are present, olanzepine or another atypical antipsychotic might also be
appropriate. The acutely manic patient is typically hospitalized during this phase of
treatment. As noted earlier, a therapeutic dose or level of a particular medication is
necessary. These medications need 5–15 days in a patient’s system before a re-
sponse may be evaluated.
Step 2 If the first drug trial fails or the patient is unable to tolerate the side effects, an alterna-
tive is chosen. For example, if the patient started with lithium first, he or she may then
be switched to valproate, or vice versa.
Step 3 If monotherapy fails, the next step would be a two-drug combination. Lithium plus an anti-
convulsant, two anticonvulsants, or either of the previous with an atypical antipsychotic
would be reasonable choices. If the patient fails to respond or only partially responds, a dif-
ferent two-drug combination therapy would be indicated. Most experts recommend contin-
uing the various two-drug combinations until all are exhausted or the patient responds.
Step 4 If the two-drug combinations fail, the next step would be a three-drug combination. The
most common formula would include one drug from each of the main categories:
lithium, an anticonvulsant, and an atypical antipsychotic. For the patient who gets to
this level of difficulty, ECT or clozapine would also be appropriate options to consider.
 Chapter 6 • Treatment of Bipolar Disorder 45

Remember that benzodiazepines and typical antipsychotics are used as adjunctive ther-
apies throughout each step that is presented here.
Step 5 If the patient is not responding to the treatment plan, the clinician should take a step
back and reassess the diagnosis, comorbid medical conditions, compliance issues,
and/or substance abuse issues. Clinicians must stay alert to changes in the patient’s ill-
ness and must reassess the situation at every step along the way.

Depression Treatment Protocol

In addition to the mania protocol, the depressive phase of bipolar disorder requires the prescriber
to consider some alternative issues.
Step 1 The primary medication to treat bipolar disorder, regardless of phase, is a mood stabi-
lizer. When a patient is in the depressive phase, the mood stabilizer should be optimized
first, usually by increasing the dosage. For example, lithium therapy should be in-
creased to obtain a serum concentration of 0.7–0.9 mEq/L.
Step 2 The addition of an antidepressant such as an SSRI or bupropion would be the next
choice. Remember that each medication must be given at an adequate dose and for an ap-
propriate amount of time to see if the patient will respond. Another option would be to
add lamotrigine rather than to add an antidepressant. As mentioned earlier, lamotrigine
has a specific niche for bipolar depression. The prescriber must be cautious when using
lamotrigine with valproate because of the significantly elevated risk for the toxic rash.
Step 3 If the patient fails to respond to the previous steps, a combination of two antidepressants
would be used with the mood stabilizer. For example, venlafaxine or nefazodone are
other antidepressants that might be added to an SSRI or bupropion. Lamotrigine may be
added once again to another antidepressant at this stage to obtain a response.
Step 4 The next choice in this process would include adding an atypical antipsychotic medica-
tion or a monoamine oxidase inhibitor (MAOI). Further steps beyond this include using
ECT, thyroid hormones, typical antipsychotics, tricyclic antidepressants, hormones,
omega-3 fatty acids, psychostimulants, and so on.

Treatment Protocol for Mixed Mood States

Although there may be some similarities with the mania protocol, the treatment of mixed mood
states needs to be further explained.
Step 1 Atypical forms of bipolar disorder respond preferentially to anticonvulsants or atypical
antipsychotics rather than to lithium. For example, valproate or olanzepine would be
first-line treatments. As noted in the other protocols, the prescriber may need to opti-
mize the dose in order to achieve the maximum response.
Step 2 If monotherapy with one medication fails, then monotherapy with the other agent
would be appropriate. For example, valproate would be given if olanzepine was unsuc-
cessful, or vice versa.
Step 3 As noted in the mania protocol, two-drug combinations would reasonably be followed
by three-drug combinations, and so on. The most important factor to consider is keep-
ing a logical approach to this complex behavioral disorder. In other words, keep the
treatment plan simple.
46 Chapter 6 • Treatment of Bipolar Disorder

PATIENT AND FAMILY EDUCATION

Patient Education
The counselor or psychotherapist must assess the patient’s level of understanding of his or her
illness and try to fill in the gaps when necessary. The first step in this process is basic patient ed-
ucation about the natural history, symptoms, comorbidities, and various treatments of bipolar
disorder. The best way for the patient to learn about his or her own illness is by reading and by
talking to others who have the same problems. Support groups give patients an opportunity to
learn from others and to help normalize their experiences. Compliance with medications is an
enormous problem with bipolar patients, because they often miss the euphoric mania. In fact,
lithium is known to be less effective the more it is started and stopped for whatever reasons.
Comorbid alcohol or drug abuse is also common with bipolar patients and should be as-
sessed routinely. Controlling excessive alcohol use in bipolar patients may provide a more prom-
ising treatment outcome with less novelty seeking, suicidality, aggressivity, and impulsivity.
Further, the use of medications like topiramate may reduce alcohol cravings in patients who
drink regularly (Frye & Salloum, 2006). It is also not uncommon for a patient to minimize his or
her use of “recreational” methamphetamine, which may be complicating the patient’s response
or lack thereof to the medications. Patients often “forget” to inform the prescriber about drinking
one or two martinis before or during dinner, which is likely contributing to the patient’s sympto-
matology. The clinician should keep in mind that these patients have little concept of balance in
their life, because they live between the extremes.

Family Education
As noted previously, family education is very important because the patient’s life has a context
that needs to be understood by family members. Remember that the manic phase of the illness,
primarily the euphoria, feels really great to the patient. The clinician can help the family to un-
derstand that the patient may not want to lose this feeling. Family members may be helpful in
monitoring the patient’s compliance with medications and appointments. Any competent clini-
cian would enlist the patient’s family to assess symptomatology, compliance issues, and be in-
volved in implementing the treatment plan. Moreover, the family is the clinician’s eyes and ears
while the patient is at home.
The psychotherapist can be helpful by referring family members for their own individual
treatment when they are having difficulty coping with the patient’s behaviors. Although the most
experienced clinician may be overwhelmed at times by the patient’s bipolar illness, keep in mind
that the family assists the patient on a daily basis to manage the symptoms.

CASE VIGNETTE
Chapter Six
CLINICAL HISTORY
Trisha is a 28 year old, unemployed white female. She is no stranger to therapy, having seen counselors for most of her
teen and adult years. Her friends would describe her as a “wild woman” who takes no crap from anyone. She has held
various part-time jobs for the last few years because she usually gets angry at her boss or coworkers and quits. While
she has had a string of boyfriends over the years, she has been seeing one man for the last year or so. He too is unem-
 Chapter 6 • Treatment of Bipolar Disorder 47

ployed and has both an alcohol and meth problem. She describes the relationship as “addictive and dysfunctional, yet
exciting and hot.” Trisha is back in treatment at the urging of her parents, who describe her behavior as erratic and un-
predictable. They also claim that she has periods where she “sleeps little and parties lots.” There were also several oc-
casions in the last five years when she was so depressed she didn’t eat or want to leave the house. Her father also ad-
mits to periods of depression, and Trisha’s grandfather was diagnosed with manic depression, resulting in numerous
hospitalizations in the 1950s and 60s. Trisha’s only brother died in a car accident several years ago. He was drunk at the
time, but she claims he had a long history of depression. Recently Trisha was arrested for disorderly conduct at a
friend’s party. She had not slept for nearly 24 hours and was drunk and combative. When she was first approached by
police, she solicited them for sex. They report that she was rather hyperverbal and hyperactive. They later had to inves-
tigate a complaint from local store owners for bad checks she wrote in excess of $7,000.

POSTCASE DISCUSSION AND DIAGNOSIS

Trisha has Bipolar I Disorder, Most Recent Episode Manic (296.4). She appeared to have boundless energy with little
need to rest and was engaging in dangerous, promiscuous and irresponsible behavior. She also meets criteria for recent
episodes of major depression. According to Trisha and her parents, she uses alcohol only when she is feeling “high on
life” or when she is so depressed she can’t get out of bed. There is also a positive family history for both unipolar and
bipolar depression.

PHARMACOLOGICAL TREATMENT
Upon consultation with a psychiatrist, Trisha was placed on valproate and titrated to a dose of 750 mg q.d. In addition, her
psychiatrist added quetiapine 300 mg qhs to assist with sleeping and restlessness at night. Trisha’s mood has stabilized and
she has been attending therapy twice weekly and group once weekly. She has also been able to return to a part-time job as
a waitress and is no longer dating her boyfriend, who was recently arrested for meth use. She hopes to attend college in the
next year if she is able to save enough money for her own apartment. She has gained much insight into her illness and now
helps other young women in a local support group.
 7 TREATMENT OF ANXIETY DISORDERS

This chapter explores the symptoms associated with anxiety conditions, the general con-
cept of anxiety, and its role in behavior. A biological explanation for panic states is
explored, along with the various treatment options and cautions.
Topics to be addressed include the following:
• Symptoms and causes of anxiety disorders
• Panic disorder with or without agoraphobia
• Generalized anxiety disorder
• Posttraumatic stress disorder
• Obsessive-compulsive disorder
• Social anxiety disorder
• Adjustment disorders and other phobic conditions
• Treatment reminders and cautions
• Case Vignette

SYMPTOMS AND CAUSES OF ANXIETY DISORDERS

Second only to depression and alcohol abuse, anxiety disorders are commonly presented
in both mental health and medical-surgical settings. A well-known fact is that anxious
patients overuse medical services (Lindesay, 1991). The pathophysiology of most anxiety
disorders is rather complex and most likely linked to abnormal regulation of neurotrans-
mitters such as serotonin, GABA, and glutamate. Additionally, a strong comorbidity
exists among anxiety disorders, and while they often have similar symptoms, the manifes-
tation or presentation might be different. Since the symptoms of most anxiety disorders
are similar, the pharmacological treatment is the same (Bourin & Lambert, 2002).
Anxiety disorders typically include the following symptoms in various
forms and intensity: trembling, general nervousness or tension, shortness of breath,

48
 Chapter 7 • Treatment of Anxiety Disorders 49

diarrhea, hot flashes, feelings of depersonalization, worry, agitation, initial insomnia, poor
concentration, tingling, sweating, rapid heartbeat (tachycardia), frequent urination, and
dizziness. In assessing these symptoms, the therapist needs to determine the intensity, dura-
tion, and quality of these symptoms. This information helps the therapist make the proper
diagnosis and treatment.
Anxiety symptoms may result from many other physical conditions, so it is important to
rule out any of the following conditions:
Adrenal tumor Hypoglycemia
Alcoholism or other substance Hyperthyroidism
abuse Mitral valve prolapse
Angina Parathyroid disease
Cardiac arrhythmia or other Postconcussion syndrome
cardiovascular problem
Premenstrual syndrome (PMS)
Chronic sinus conditions
Seizure disorders
Cushing’s disease
Delirium

It is also important to remember that many substances or drugs may cause or exacerbate
anxiety. These include amphetamines and other stimulants, diet medications and other appetite
suppressants, certain asthma medications, decongestants, cocaine, caffeine, and steroids.
Withdrawal from antidepressants, anxiolytics, and other substances of abuse may cause anxi-
ety also.
Once a medical or substance etiology has been ruled out, the therapist needs to determine
the type and nature of the anxiety and a likely diagnosis. Anxiety disorders are now categorized
as follows:

Panic disorder or PD (with or without agoraphobia)

Agoraphobia with or without panic disorder
Generalized anxiety disorder or GAD
Posttraumatic stress disorder or PTSD
Obsessive-compulsive disorder or OCD
Social anxiety disorder
Adjustment disorder with anxious mood
Simple phobias

Treatment and choice of medication depends on the type and severity of the anxiety
disorder. Research has consistently demonstrated that anxiety disorders respond well to psy-
chotherapy and that relaxation, cognitive therapy, and cognitive behavioral therapy work
best (Bourin and Lambert, 2002; Cukor, Spitalnick, Difede, Rizzo, & Rothbaum, 2009;
Gorman, 2002). Further, Gorman maintains that the combination of therapy and medication
offers the best prognosis for resistance to relapse of symptoms. With this in mind, we
address each disorder mentioned above with the most efficacious approach based on
research and our experience.
50 Chapter 7 • Treatment of Anxiety Disorders

PANIC DISORDER WITH OR WITHOUT AGORAPHOBIA

Many patients present to a therapist with complaints of anxiety and believe that they have panic
disorder. Patients often confuse periods of uncomfortable anxiety with actual panic attacks.
However, for those patients who experience four or more intense attacks within one month, panic
disorder is a seriously debilitating condition.
What is happening in the panic-disordered patient? The patient experiences anxiety when
the brain perceives a threat. As part of the fight-or-flight response, the limbic system goes on red
alert. The body responds to a series of physiological reactions: the limbic system sends signals to
the hypothalamus and the locus ceruleus; they in turn send signals to the pituitary, the thyroid,
and the adrenal cortex. As a result, various hormones such as cortisol and adrenaline are pro-
duced, readying the body for attack, but with panic disorder, it is a false alarm with no actual
threat. Panic disorder often runs in families, and the cause appears to be biological in nature. A
dysregulation of the limbic system, serotonin depletion, excessive glutamate, and insufficient
amounts of GABA may all be to blame. Panic can be induced in patients with panic disorder by
injecting them with either lactic acid (a byproduct of muscular activity) or cholecystokinin
(CCK), a peptide produced by cells in the duodenum and in the brain. When large amounts of
cortisol and adrenaline are produced, the patient is in a constant or chronic state of arousal. The
effects of stress on the body cause these hormones to suppress immune functions and increase
blood pressure. These chronic conditions have been linked to other medical illnesses, cardiac
problems, and cancer.
On the surface of about 40% of nerve cells in the brain, including the locus ceruleus, are
tiny gateways or receptor sites called chloride ion channels. Chloride ions, which have a nega-
tive charge, are found in the fluid surrounding each cell. The ion channel can be activated or
opened when stimulated by the naturally occurring neurotransmitter GABA. As the channel
opens, the chloride ions are drawn in. When the cell is infused with negative ions, the cell hyper-
polarizes or relaxes. This causes a calming effect of the locus ceruleus. Benzodiazepines also
bind at the chloride ion channels, causing a calming effect. This effect is also true for alcohol.
(See Figure 7.1.)
The treatment for panic disorder involves three stages: (1) stop the panic, (2) regulate the
limbic system with drugs that increase serotonin, and (3) provide appropriate psychotherapy to
educate the patient and reduce anticipatory anxiety or self-defeating behaviors.
Stage 1 In this stage the therapist sees that the patient is experiencing intense anxiety
and needs immediate relief. Many patients with panic disorder use or abuse
alcohol, which binds with the chloride ion channel to control their symptoms.
Unfortunately, as tolerance develops, more alcohol is required, resulting in addic-
tion for many patients.
Benzodiazepines are the drugs of choice for quick relief of panic symptoms.
Alprazolam (Xanax), lorazepam (Ativan), and oxazepam (Serax) offer the fastest relief
because of their short half-lives (see Table 7.1). For many patients with panic disorder,
the treatment ends here.
Primary care physicians often provide benzodiazepines to patients with panic dis-
order and forget to follow up with them. These patients assume that since they are no
longer panicking, they must be okay. Although the patients are no longer in a state of
anxiety or having panic attacks, the use of benzodiazepines for panic disorder has only
relieved the symptoms, but the cause remains.
 Chapter 7 • Treatment of Anxiety Disorders 51

Cl- Cl- Cl- Cl- Cl- Cl- Cl-

Benzodiazepine GABA
receptor receptor

+ + +
Phase 1: Choride ion channel closed (patient anxious)

Cl- Cl- Cl-

GABA
molecules

Cl- + Cl- + Cl- +

Phase 2: GABA binds to receptors: Channel begins to open

Benzodiazepine
molecules

-
Cl- Cl- Cl- Cl Cl-

Phase 3: Benzodiazepine binds to receptors: Channel fully

opens (patient relaxed)

FIGURE 7.1 Three Phases of the Chloride Ion Channel

52 Chapter 7 • Treatment of Anxiety Disorders

TABLE 7.1 Various Medications Used in Anxiety Disorders

Typical
Trade Generic Dose Medication
Name Name (mg/day) Class Uses

Ambien, zolpidem 5–10 Sedative-hypnotic Sleep aid

Ambien
CR, Edluar,
Zolpimist
Ativan lorazepam 1–6 Benzodiazepine PD, seizure, anxiety NOS
Buspar buspirone 5–40 Nonbenzodiazepine GAD, depression, anxiety NOS
Catapres clonidine 0.1–0.3 Central alpha agonist Hypertension, social anxiety
disorder
Centrax prazepam 20–60 Benzodiazepine PD, anxiety NOS
Dalmane flurazepam 15–30 Sedative-hypnotic Sleep aid
Doral quazepam 7.5–15 Sedative hypnotic Sleep aid
Halcion triazolam 0.25–0.50 Sedative-hypnotic Sleep aid
Inderal propranolol 20–80 Nonselective Hypertension, social anxiety
beta-blocker disorder
Klonopin clonazepam 0.5–4 Benzodiazepine PD, seizure, sleep aid, mood
stabilizer
Librium chlordiazepoxide 15–100 Benzodiazepine Anxiety NOS, muscle relaxation
Lunesta eszopiclone 1–3 Sedative-hypnotic Sleep aid
Prosom estazolam 2–4 Sedative-hypnotic Sleep aid
Restoril temazepam 15–30 Sedative-hypnotic Sleep aid
Rozerem ramelteon 8 GABA agonist Sleep aid
Serax oxazepam 30–120 Benzodiazepine Anxiety NOS
Sonata zaleplon 5–10 Sedative-hypnotic Sleep aid
Tranxene clorazepate 15–60 Benzodiazepine Anxiety NOS
Valium diazepam 5–40 Benzodiazepine Seizure, anxiety NOS, muscle
relaxation
Visken pindolol 10–60 Nonselective Hypertension, Akathisia, Sexual
beta-blocker Dysfunction
Xanax alprazolam 0.25–4 Benzodiazepine PD, anxiety NOS

Generalized panic disorder (GAD), Panic disorder (PD), Not otherwise specified (NOS)

Stage 2 In this stage the therapist initiates antidepressant therapy. Once panic has been con-
trolled with benzodiazepines, the use of various antidepressants increases serotonin and
helps regulate the limbic system. While some of the older tricyclics like imipramine,
nortriptyline, and amitriptyline are used, the newer SSRIs offer better relief with fewer
side effects. MAOIs do work as well, but dietary restrictions result in poor compliance
for panic patients (see Chapter 5).
Stage 3 In this stage the therapist provides cognitive behavioral treatment for patients with
panic disorder. These patients must learn to manage their anxiety without developing
 Chapter 7 • Treatment of Anxiety Disorders 53

avoidance behaviors that are caused by experiencing panic attacks in places such as
shopping malls. This anticipatory anxiety is actually more debilitating than the panic it-
self. For patients with panic disorder and agoraphobia, or agoraphobia without panic
disorder, the use of in vivo or real-life techniques is helpful. Encouraging patients to
take walks outside of the home with the therapist and/or other treatment staff reduces
isolation and discourages additional phobias from developing (Sinacola, 1998). For
many patients with panic disorder, fears tend to compound the longer they go untreated.
It is best to address fears early in therapy. As expected, many patients are reluctant at
first and may complain of increased levels of arousal until new relaxation and other
therapeutic methods are understood and practiced.

With panic disorder it is very important for the therapist to address all three stages. Once
the therapist determines that a patient truly has the condition, benzodiazepines should be started.
The therapist should inquire about any history of substance abuse because these patients often
enjoy the “high” they get from benzodiazepines and may abuse them. It is worth noting here that
the longer acting benzodiazepines like clonazepam (Klonopin) are less likely to be abused than
alprazolam (Xanax) or lorazepam (Ativan). The prescriber must include an appropriate antide-
pressant along with the benzodiazepine. The benzodiazepine first controls the panic, and within
one or two weeks the antidepressant begins to work. Then the benzodiazepine should be gradu-
ally withdrawn. It is crucial not to withdraw the benzodiazepine too quickly, as the panic may
return. Typically, withdrawing the benzodiazepines over 2 or 3 weeks is effective unless the
patient has been taking the medication for a long time and the dose is high. The antidepressant
should maintain patients if they are not abusing alcohol or other drugs. Psychotherapy may be
attempted at any time during this process once the patient is calm enough to focus and concen-
trate in the session.

GENERALIZED ANXIETY DISORDER

Many practicing clinicians believe that generalized anxiety disorder or GAD is a behavioral con-
dition and should not be treated with medication. Further, some researchers believe that GAD is
more closely related to depression than to anxiety (Sheehan, 1999). Sheehan also found that peo-
ple with GAD utilized medical services more than those without the diagnosis.
Most patients with GAD respond well to a combination of medication and psychotherapy
(Sheehan, 2002). Cognitive therapy is helpful as a form of psychoeducation that allows patients
to see patterns in their perceptions of issues and the behaviors or actions that follow. While ben-
zodiazepines have been used to treat GAD in the past, this use is not the best approach because
it does not teach patients to manage their condition.
Typically, the best medications for GAD include venlafaxine/desvenlafaxine (Effexor/
Pristiq), buspirone (Buspar), and most of the SSRIs such as fluoxetine (Prozac) and paroxetine
(Paxil). When patients also present with pain symptoms, research has demonstrated the efficacy
of using venlafaxine and duloxetine (Cymbalta) to control both the anxiety and pain brought on
by chronic tension (Beesdo et al., 2009; Khan & Macaluso, 2009). Buspirone is a nonbenzodi-
azepine antianxiety drug with properties more similar to an antidepressant. As mentioned in
Chapter 5, buspirone may alleviate depression for the anxious patient with co-occurring mood
concerns. Unlike benzodiazepines, buspirone and the other antidepressants may take three to
four weeks before they take effect. Patients need to be informed of this fact and they must be
patient. Patients also need to be told that these medications should be taken as directed and not
54 Chapter 7 • Treatment of Anxiety Disorders

only as needed. If the patient is concerned about sedation, fluoxetine, venlafaxine, sertraline
(Zoloft), citalopram (Celexa), and escitalopram (Lexapro) may be better choices. If the patient
has serious trouble relaxing, buspirone or paroxetine may be better because they have a more
relaxing and calming effect.
For many patients with GAD, initial insomnia is a problem. Sleep aids may be helpful for
the short term, but many of them, such as the newer drugs zolpidem (Ambien) and zaleplon
(Sonata), may be habit forming in the long term. It is probably better to begin the antidepressant
therapy and wait a week or two to see if sleep improves. If the patient is persistent, the clinician
could recommend a low dose of a sedative-hypnotic. For example, 5–10 mg of zolpidem at bed-
time for only one week reduces the likelihood of dependence. If the patient is concerned about
taking prescription sleep aids, the clinician could recommend over-the-counter diphenhy-
dramine (Benadryl) at 25–50 mg before bedtime. For patients with severe agitation and racing
thoughts at bedtime, gabapentin (Neurontin) may enhance sleep. Research has also demon-
strated that adding an atypical antipsychotic such as quetiapine may not only enhance the effec-
tiveness of SSRIs, but also reduce racing thoughts at bedtime (Baune, 2008; see Chapters 5 and 6
and Table 7.1).

POSTTRAUMATIC STRESS DISORDER

Historically, benzodiazepines and neuroleptics have been used to treat patients with posttrau-
matic stress disorder (PTSD), especially when they demonstrate psychotic behaviors (Albucher
& Liberzon, 2002). Today, considering reported overall efficacy and side-effect profiles, clini-
cians have found much success with SSRIs. In some cases, mood stabilizers like lamotrigine
(Lamictal) and atypical neuroleptics (i.e., risperidone, quetiapine, aripiprazole or olanzepine)
might be needed if the patient becomes agitated, combative, or psychotic (Berger et al., 2009).
Recent research has examined the role of various medications in the prevention of PTSD
symptoms by interfering with how memories are chemically stored in the brain. Medications like
propranolol appear to interfere with how emotional memories are stored and may prove to be an
effective prophylactic for those recently traumatized or as an adjunct to current medications
(Chamberlain, Muller, Blackwell, Robbins, & Sahakian, 2006; Henry, Fishman, & Youngner,
2007; Nugent et al., 2010). Some question the ethics of altering memory or experience, but agree
that for severe cases, the benefits outweigh the risks (Bell, 2008). Prazosin, an adrenergic-
inhibiting agent, may also be a promising medication when trauma-related nightmares and sleep
disturbances are prominent symptoms (Berger et al., 2009; Reardon & Factor, 2008).
Psychotherapy is a very important part of the treatment for PTSD. Patients may need to
slowly expose themselves to the event or events that contributed to the condition. Various behav-
ioral therapies and imagery rescripting and rehearsal have been found to be effective (Cukor et
al., 2009). Like bipolar patients, PTSD patients typically abuse substances in an attempt to dull
the pain and anxiety. Detoxification may be needed first to ensure successful use of psychotropic
medications. While any antidepressant would be helpful, SSRIs like paroxetine and sertraline
have been approved for such use.

OBSESSIVE-COMPULSIVE DISORDER
Obsessive-compulsive disorder (OCD) is more of a worldwide health problem than once
thought. Approximately 3% of the general population suffers from OCD, with typical onset
in patients in their twenties (Jenike, 2001). Psychotherapy alone has not been shown to be
 Chapter 7 • Treatment of Anxiety Disorders 55

very effective; behavioral and cognitive behavioral treatments along with medication offer
the best possibilities.
The cause of OCD remains unknown, but a familial link might exist, since patients with
OCD typically have a close relative who has OCD or OCD co-occurring with a tic disorder. The
most likely cause of OCD is dysfunction in one or more of several segregated corticostriatal
pathways. According to Jenike (2001), OCD seems to involve subtle structural abnormalities in
the caudate nucleus, as well as functional dysregulation of neural circuits of the orbital frontal
cortex, cingulate cortex, and the caudate nucleus. Some reseachers believe that childhood infec-
tions may contribute to the development of OCD (Insel, 1992). In any case, serotonergic systems
have been implicated.
The treatment of choice for OCD involves the use of SSRIs. While the tricyclic
clomipramine (Anafranil) has been used, sedation and anticholinergic side effects are trouble-
some and have been shown to lead to problems with compliance (Choi, 2009). SSRIs affect sero-
tonin levels and typically relieve symptoms. It is important to remember that the doses used for
depression and other anxiety disorders might not be high enough for the OCD patient. Therefore,
a dose of 60–80 mg of fluoxetine (Prozac) or 200–300 mg of fluvoxamine (Luvox) may be
needed for OCD relief. Escitalopram (Lexapro) may be a bit more effective due to its lower side
effect profile and demonstrated effectiveness when compared to similar SSRIs (Montgomery &
Moller, 2009; see Chapter 5 and Table 7.1).
In some cases the obsessions are severely intrusive, and the patient may complain of racing
thoughts and insomnia. Low-dose, atypical neuroleptics such as risperidone (Risperdal) could be
added along with a sleep aid if needed. While most atypicals are helpful as adjuncts to SSRIs in
reducing symptoms in patients with severe OCD, quetiapine may not be as effective in reducing
OCD symptoms as the others; however, it may still be helpful in reducing agitation and racing
thoughts before bedtime (Kordon et al., 2008).
In cases of severe treatment-resistant OCD in children and teens, memantine (Namenda),
an NMDA receptor agonist, may be an effective augmenting agent when added to a standard
SSRI regimen (Hezel, Beattie, & Stewart, 2009).

SOCIAL ANXIETY DISORDER

Social anxiety disorder or social phobia is a common presenting issue in private practices and
public clinics. In such cases the therapist needs to determine that the patient has never had a his-
tory of panic disorder. Many professionals believe that social anxiety should be treated with psy-
chotherapy alone and medications should not be used; however, several medications have been
found to be useful (Davidson, 2003). Many patients with social anxiety have found that alcohol
relieves their symptoms, but they demonstrate obvious alcohol dysfunction in social situations.
This dysfunction may lead to social or occupational problems, or worse, alcohol dependence.
Typically, primary care physicians offer benzodiazepines to socially phobic patients. While these
drugs may lessen patients’ fears a bit, they do not afford patients an opportunity to understand
their fears and subsequent behaviors.
The use of SSRIs and MAOIs offers the best results for social anxiety patients. Tricyclics, ben-
zodiazepines, and buspirone (Buspar) offer little benefit in the long run. In some cases, when the
patient reports only situational anxiety, for example, when he or she has to speak publicly, the use of
beta-blockers like propranolol (Inderal) or clonidine (Catapres), an alpha agonist, might prove helpful.
In these cases the patient may take the medication an hour before the speech and notice less sweating,
heart palpitations, and general anxiety without the need to take medication on an ongoing basis.
56 Chapter 7 • Treatment of Anxiety Disorders

Psychotherapy, especially behaviorally based treatments, helps the patient to see the con-
nection between environments and the fears they produce. Cognitive rehearsal and role playing
may assist the patient to achieve a more lasting recovery.

ADJUSTMENT DISORDERS AND OTHER PHOBIC CONDITIONS

When a patient presents with anxiety and sleep disturbance related to a stressful event, the clini-
cian must rule out PTSD, GAD, or another long-standing anxiety disorder. If the patient appears
to have no history of an anxiety disorder and he or she seems to be aware of the stressor that
might be responsible, counseling and psychotherapy are recommended. In most cases the symp-
toms remit within six months. A sleep aid could be used for a short period of time if the patient
complains of ongoing problems with insomnia. If the patient appears to have significant anxiety,
a low-dose SSRI could be used for four to six months. If the patient is agitated and cannot relax
enough to work or concentrate, sedating antidepressants like paroxetine (Paxil), trazodone
(Desyrel), or amitriptyline (Elavil) could be used. If there are concerns related to a recent loss,
such as the death of a loved one, referral to a grief counselor or other professional experienced in
loss may be appropriate.
For patients who present with simple phobias, such as fear of cats, spiders, or elevators, a
therapist competent in behavioral techniques might be the answer. Typically, various exposure
techniques are preferred rather than medication for phobias.

TREATMENT REMINDERS AND CAUTIONS

For all patients with anxiety disorders, the therapist should advise them to eliminate or reduce
the use of caffeine. In fact, patients may wish to evaluate their general diet and watch for exces-
sive amounts of sugar or stimulants such as sodas, candy, and cigarettes.
For most anxiety disorders, the four “Bs” are used. These include benzodiazepines such as
diazepam (Valium), alprazolam (Xanax), lorazepam (Ativan), and clonazepam (Klonopin);
barbiturates such as pentobarbital (Nembutal) and secobarbital (Seconal), which may potentiate
GABA, but are very sedating and habit forming; buspirone (Buspar) for GAD; and beta-blockers
for specific forms of social anxiety.
Side effects for anxiety medications vary according to the type used. Benzodiazepines
are usually well tolerated and the side effects are minimal, but the symptoms of benzodi-
azepine intoxication include slurred speech, severe sedation, dizziness, cognitive slowing,
gait abnormalities, and an exaggerated sense of “high.” Since some patients enjoy this feel-
ing, therapists must watch for tolerance and abuse. Benzodiazepines should be given cau-
tiously to seniors because an excess may lead to falls and broken bones. Failure to assess
the patient for a more serious depressive disorder or a psychotic disorder can result in a
worsening of the condition when treated with benzodiazepines alone. The therapist should
warn the patient that sudden withdrawal from benzodiazepines may cause an increase in
anxiety and insomnia. Benzodiazepines should never be taken with alcohol, which will
potentiate its effects. Discontinuing the medication should be done gradually, under med-
ical supervision, and only after the patient has discussed other options with the therapist
and the prescribing professional.
The side effects for buspirone are usually mild and similar to those for antidepressants.
They include drowsiness, dry mouth, nausea, headache, dizziness, and insomnia. As with the
benzodiazepines, the patient must watch for dizziness, especially if operating heavy machinery.
 Chapter 7 • Treatment of Anxiety Disorders 57

Sleep aids should be used judiciously, that is, only when necessary and only for one to
two weeks maximum if taken daily. In some cases patients may take sleep aids for long peri-
ods if they use them only for intermittent insomnia. Side effects are minimal, but include, of
course, drowsiness, amnesia, dizziness, falling, lethargy, disorientation, cognitive slowing, and
possible depression.
In conclusion, since clinicians prescribing medication for anxiety disorders must make a
quick and accurate assessment of the condition, they need to have confidence that patients will
comply with treatment. Clinicians should obtain information about the duration and intensity of
the condition, as well as history of substance abuse and previous treatment attempts.

CASE VIGNETTE
Chapter Seven
CLINICAL HISTORY
Beth is a 23-year-old Asian-American graduate student. She is currently in treatment with a psychologist for anxiety.
While she claims that her cognitive behavioral therapy has helped her control her worry and anxiety, she has noticed
that her symptoms have worsened this year with all of the pressures of school. In addition to worry, her mind races at
night when she tries to sleep and she claims it may often take her 2–3 hours to finally fall asleep. She describes her-
self as a “type A” person who is rather “anal” about doing well. She worries nonstop about grades, but also worries
nonstop about her health, money, her parents’ health, and world affairs. She is very insightful about her condition and
agrees the worry is excessive and unwanted. She admits that there is really no basis for the worry, as she has a full
scholarship, she and her parents are in good health, and she currently has a 3.9 GPA. She claims that she has always
been rather tense, but it didn’t get to the point that she sought treatment until her senior year in college. She was
worried about getting accepted to grad school and “obsessed” over getting straight A’s. She sought the help of a
psychologist at the university counseling service and was placed on Paxil in addition to therapy. For the most part,
her symptoms disappeared, but she remembers feeling tired during the day.

POSTCASE DISCUSSION AND DIAGNOSIS

Beth appears to have a rather classic case of Generalized Anxiety Disorder (300.02). Her worry is rather chronic, base-
less, and interferes with sleep and concentration. After additional history, it appears that both her mother and sister
have had problems with anxiety and her sister currently takes Celexa to address the issue. Beth denies that she has
ever had a panic attack and she feels comfortable in most social situations. She has refrained from dating because
she fears that a boyfriend would distract her from her studies and she hopes to be accepted into a Ph.D. program
when she completes the M.A.

PSYCHOPHARMACOLOGICAL TREATMENT
In addition to psychotherapy, Beth was placed on Pristiq 50 mg every morning. While paroxetine was helpful in the
past, she did not like the sedation during the day. Since she also complains of muscle tension in her neck, Pristiq and
medicines like it help to reduce pain symptoms. In a follow-up session with her psychiatrist two weeks after starting
the medication, she reported sleeping better and stated that her level of worry was drastically reduced. She still
obsesses over grades, but expects to get into the doctoral program with her current GPA.
 8 TREATMENT OF PSYCHOTIC
DISORDERS

In this chapter we explore the various schizophrenia spectrum disorders, their prevalence,
causes, and treatment. The role of both typical and atypical antipsychotics is explored,
with advantages and disadvantages presented.
Topics to be addressed include the following:
• Schizophrenia spectrum disorders
• Causes of psychotic disorders
• Medication for psychotic behaviors
• Treatment protocol
• Other significant issues to consider
• Case vignette

SCHIZOPHRENIA SPECTRUM DISORDERS

Schizophrenia and the other psychotic disorders affect more than 1% percent of the
world’s population and cost society a tremendous amount of financial and medical re-
sources (Sadock & Sadock, 2000). These authors also report that there are various schizo-
phrenia spectrum disorders, including schizoid personality disorder, schizotypal personality
disorder, schizoaffective disorder, delusional disorder, and psychotic disorder NOS,
which are reported to be less prevalent but still significant. Although hard data are scarce,
Baethge (2002) reports the prevalence of schizoaffective disorder to be about 0.5%, one-
half the prevalence of schizophrenia. Patients with schizophrenia need treatment in the
earlier stages; this will help prevent relapse because of the higher morbidity and mortality
associated with the earlier phases (Tandon & Jibson, 2003). In fact, Lambert, Conus,
Lambert, & McGorry (2003) report that during the untreated phase and first-year treat-
ment period, 10% to 15% of first-episode psychotic patients attempt suicide. Overall, the
disorder is associated with an increased risk of mortality due to lifestyle and chronic ill-
ness associated with the disorder (Seeman, 2007).

58
 Chapter 8 • Treatment of Psychotic Disorders 59

Schizophrenia
Schizophrenia is first and foremost a brain disease with numerous abnormalities in structure,
function, and neurochemistry. With regards to brain structure, the most common finding is an
enlargement of the lateral ventricles, followed by a decreased volume of gray and white mat-
ter. The medial temporal structures, including the hippocampus and amygdala, have been
noted to be smaller in size when compared to normal brains. When looking at brain function-
ing, the clinician notes a relative decrease in cerebral blood flow and metabolism in the
frontal lobes.
Studies of the most common neurochemical abnormalities in patients with schizophrenia
have focused on the dopamine hypothesis, in which too much dopamine is causing the psy-
chotic symptoms (Di Forti, Lappin, & Murray, 2007). This is referred to as a
hyperdopaminergic hypothesis. As you may know, the conventional or typical antipsychotics
(i.e., haloperidol or chlorpromazine) reduce the symptoms of schizophrenia by blocking post-
synaptic dopamine D 2 receptors. The newer atypical antipsychotics (i.e., risperidone or
olanzepine) have potent serotonergic 5-HT2 and dopaminergic D2 antagonism. Other neuro-
transmitter systems that may be involved in schizophrenia include glutamate, acetylcholine,
serotonin, norepinephrine, and other neuromodulators, such as substance P and neurotensin.
These neuromodulators are localized with other neurochemicals and may influence their ac-
tion. As noted in Chapter 2, their influence could facilitate, inhibit, or alter the patterns of
firing (Buchanan et al., 2007).
As you may recall, schizophrenia and other schizophrenia spectrum disorders occur more
commonly in families of patients with schizophrenia. Most researchers agree that monozygotic
twins have a 40% to 50% concordance rate for schizophrenia, whereas dizygotic twins have only
about a 10% concordance rate. This latter rate is consistent for the rate of occurrence of schizo-
phrenia in other first-degree relatives (Pinel, 2009).
In addition to the genetic theories of schizophrenia, immune and viral hypotheses have
also been put forward. In fact, some researchers believe that schizophrenia is more common
in urban areas and in lower socioeconomic groups. This social-drift phenomenon refers to
the fact that vulnerable patients have a tendency to lose their social and occupational status
and drift toward pockets of poverty and inner city areas. The prevalence of schizophrenia may
have a rising north-to-south gradient in the Northern Hemisphere, whereas it may have a ris-
ing south-to-north gradient in the Southern Hemisphere. The illness may be endemic in a
few areas, such as colder climates with patients born in the winter months ( Kendell &
Adams, 1991).
When considering the viral hypotheses, researchers suggest that a retrovirus could insert it-
self in the genome and alter the patient’s genetic code; this altered code could be passed down
through generations. Other mechanisms that might result in schizophrenia include a viral infec-
tion in early life that creates a vulnerability toward the disease, a viral infection leading to
secondary scar tissue formation, a virus triggering an autoimmune response, and so on. Some
studies have reported that pregnant women exposed to the influenza virus during their second
trimester are more likely to give birth to a child who is at increased risk for schizophrenia. The
theory is that a viral infection may interfere with normal brain development during the active
migration of neuronal cells (Sadock & Sadock, 2000).
Some researchers used to think that poor parenting could cause schizophrenia. In the
1950s, Harry Stack Sullivan (1953) focused on patients’ disturbance that affected their capacity
60 Chapter 8 • Treatment of Psychotic Disorders

to relate to others, and this capacity is thought to reflect dysfunction in the mother-infant dyad.
In the stress-diathesis model, various internal or external stressors can convert vulnerability for
schizophrenia into symptoms.
Another concept worthy of mention is that of expressed emotion (EE). Several family fac-
tors, including criticism, emotionally overinvolved attitudes and behaviors, and negative-affective
style, may precipitate the illness or aggravate its course. Schizophrenic patients living with fam-
ilies with high EE have a higher rate of relapse than those living in families with low EE. The
chaotic and stressful family interactions might not be the cause of the dysfunction in schizo-
phrenia, but rather the cause might be the complex collection of problems the patient brings to
the family setting (Sadock & Sadock, 2000).

Symptoms in Schizophrenia
There are four different types of symptoms seen in schizophrenia and other psychotic illnesses:
positive, negative, cognitive, and mood. Although there is a classic presentation, each patient has
a unique relative contribution from each of the four categories.

POSITIVE SYMPTOMS. These symptoms involve a break from reality in the areas of percep-
tion, behavior, thought content, and thought processes. Hallucinations, delusions, loose associa-
tions, and grossly disorganized behavior are examples of positive symptoms. These symptoms
may require acute psychiatric hospitalizations.

NEGATIVE SYMPTOMS. Unlike positive symptoms, negative symptoms represent something

that is deficient and may include apathy, blunted affect, amotivation, anhedonia, poverty of
speech, poverty of thought content, asociality, ambivalence, poor hygiene, and so on. Although
these symptoms cause the majority of functional disability associated with schizophrenia, nega-
tive symptoms rarely lead to hospitalization.

COGNITIVE AND MOOD SYMPTOMS. Symptoms of the third type are the cognitive
symptoms. Schizophrenia is characterized by a broad impairment in cognition and neuropsycho-
logical functions, which correlate with functional impairment. A growing body of research
suggests that some of these neurocognitive deficits may be associated with alterations in blood
levels of neurosteroids such as DHEA (Ritsner & Strous, 2010).
Symptoms of the fourth type are mood symptoms. Some patients exhibit depression, agi-
tation, anxiety, insomnia, irritability, and mood lability.
When a patient is diagnosed with a psychotic illness, it is important to evaluate him or her
properly for confounding factors such as substance abuse, medical illness, other psychiatric dis-
orders, developmental disorders, and so on. The psychotic disorders include schizophrenia,
schizophreniform disorder, schizoaffective disorder, delusional disorder, brief psychotic disor-
der, shared psychotic disorder, psychotic disorder due to a general medical condition, substance-
induced psychotic disorder, and psychotic disorder NOS. When looking at schizophrenia more
closely, there are five distinct subtypes defined by the predominant symptomatology: paranoid
type, disorganized type, catatonic type, undifferentiated type, and residual type. Besides the
psychotic disorders, other diagnoses may have secondary psychotic symptoms. For example,
psychotic depression, postpartum depression, and bipolar disorder might possibly present with psy-
chosis, depending on the level of severity. Later in this chapter, we will discuss treatment issues,
which are similar among the various diagnoses.
 Chapter 8 • Treatment of Psychotic Disorders 61

CAUSES OF PSYCHOTIC DISORDERS

As with other psychiatric diagnoses, the etiology of a psychotic illness may be related to a phys-
ical rather than a functional disorder. The following is a list of common diseases that may cause
or exacerbate psychosis:
Addison’s disease (adrenal insufficiency) Hypothyroidism (myxedema)
Brain tumors Metabolic abnormalities
CNS infections Multiple sclerosis
Cushing’s disease (hyperadrenalism) Porphyria
Delirium Postoperative states
Dementia (Alzheimer’s, Parkinson’s, etc.) Pregnancy/postpartum hormonal changes
Encephalitis (herpes, AIDS, neurosyphilis, etc.) Stroke
Systemic lupus erythematosus Traumatic brain injury
Epilepsy Uremia
Huntington’s disease Vitamin deficiency (B12, folate, or zinc)
Hyperthyroidism (thyrotoxicosis) Wilson’s disease
In addition to the medical diagnoses, many medications and other substances may cause or
exacerbate psychosis. The following is a list of these psychoactive substances:
Alcohol (intoxication or withdrawal)
Anticholinergic medications: benztropine, trihexyphenidyl, etc.
Antihistamines (diphenhydramine)
Anti-Parkinson medications: bromocriptine, amantadine, levodopa
Appetite suppressants (phentermine)
Barbiturates (intoxication or withdrawal)
Benzodiazepines (intoxication or withdrawal)
Beta-blockers: propranolol, metoprolol, atenolol
Corticosteroids and other hormones: prednisone, methylprednisolone androgens
Digoxin
Drugs of abuse: marijuana, amphetamines, PCP, psychedelics, cocaine, heroin/morphine,
ephedra and other herbal stimulants
Environmental toxins: volatile hydrocarbons, organophosphates, and heavy metals
Narcotic medications: morphine, hydrocodone, etc.
Psychostimulant medications: dextroamphetamine, methylphenidate
Tricyclic antidepressants (TCAs)
After making a thorough assessment, establishing a differential diagnosis, and eliminating
other causes for the psychosis, the therapist would plan an appropriate treatment protocol. While
the mainstay of treatment for psychosis is pharmacotherapy, psychotherapy may still play an
appropriate role. Although social skills training for patients with schizophrenia may help improve
communication skills, little evidence suggests that the behaviors learned generalize to improve
62 Chapter 8 • Treatment of Psychotic Disorders

social competence. However, broad-based training, such as the UCLA Social and Independent
Living Skills, does enhance knowledge in specific areas studied (Huxley, Rendall, & Sederer,
2000). Researchers believe that the more specific training does generalize to improve social
functioning. As expected, family therapy generally improves symptoms, decreases relapse, and
improves social and occupational functioning. Individual sessions to educate the patient about
medication improve compliance. In addition, researchers overwhelmingly believe that a combi-
nation of family therapy and social skills training administered simultaneously works best.

MEDICATIONS FOR PSYCHOTIC BEHAVIORS

Although a wide range of treatment options is available for treating psychotic behaviors, expert
consensus guidelines recommend starting with the atypical antipsychotics. According to Kane,
Leucht, Carpenter, & Docherty (2003), risperidone (Risperdal) is the treatment of choice for a
first-episode psychotic patient with positive symptoms, negative symptoms, or a combination of
both. Aripiprazole (Abilify), olanzepine (Zyprexa), ziprasidone (Geodon), and quetiapine
(Seroquel) are additional choices but are secondary to risperidone. Paliperidone (Invega), the
major metabolite of risperidone, has been shown to be as effective as risperidone, but has the
same dose-related extrapyramidal symptoms (EPS). Its primary elimination through the kidneys
may make it a drug of choice for patients demonstrating liver abnormalities (Marino &
Caballero, 2008). You should note that all these are newer atypical antipsychotic medications,
not the older typical (i.e., conventional) antipsychotics. Clozapine (Clozaril) was rated an excel-
lent choice for second-line treatment after adequate trials of at least two of the atypical agents.
See Table 8.1 for more information.

TABLE 8.1 Atypical Antipsychotic Medications

Typical Dose Autonomic

Trade Name Generic Name (mg/day) Sedation Effects EPS
Abilify, Abilify Discmelt aripiprazole 10–30 * * *
Clozaril, Fazaclo clozapine 400–600 *** *** None
Fanapt iloperidone 12–24 * ** *
Geodon ziprasidone 80–160 * ** *
Invega paliperidone 3–12 * ** *
Invega Sustenna paliperidone 78 mg–156 mg/ * ** *
month
Risperdal Consta risperidone 25–50 mg/2 weeks * * *
Risperdal, Risperdal M-tab risperidone 3–6 * ** *
Saphris asenapine 5—20 * * *
Seroquel, Seroquel XR quetiapine 300–600 *** *** *
Symbyax olanzepine/fluoxetine 3/25–12/50 ** ** *
Zyprexa Relprevv olanzepine 150 mg/2 wk– ** ** *
405 mg/ 4 wk
Zyprexa, Zyprexa Zydis olanzepine 10–20 ** ** *
*Minimal, ** Moderate, ***Significant
 Chapter 8 • Treatment of Psychotic Disorders 63

TABLE 8.2 Typical or Conventional Antipsychotic Medications

Typical Dose Autonomic

Trade Name Generic Name (mg/day) Sedation Effects EPS
Haldol haloperidol 2–20 * * ***
Haldol Decanoate haloperidol decanoate 100–300 mg/ month * * **
Loxitane loxapine 20–100 ** * **
Mellaril thioridazine 200–600 *** *** **
Moban molindone 20–100 ** * **
Navane thiothixene 5–30 * * ***
Orap pimozide 1–10 * * ***
Prolixin fluphenazine 2–20 * * ***
Prolixin Decanoate fluphenazine decanoate 25–50 mg/ 2 wks * * **
Serentil mesoridazine 50–400 *** *** *
Stelazine trifluoperazine 5–30 * * ***
Thorazine chlorpromazine 200–600 *** *** **
Trilafon perphenazine 8–64 ** * **

*Minimal, ** Moderate, ***Significant

For multiepisode, psychotic patients, risperidone was again the treatment of choice regard-
less of predominating symptomatology. In addition to the other choices noted previously,
Risperdal Consta, the only long-acting atypical antipsychotic, is considered an excellent second-
line choice. Other less desirable choices include a long-acting, intramuscular, conventional neu-
roleptic (such as Haldol or Prolixin Decanoate); an oral, high-potency neuroleptic, for example,
haloperidol (Haldol); fluphenazine (Prolixin); trifluoperazine (Stelazine); or thiothixene
(Navane). The oral, lower potency, conventional antipsychotic agents, such as chlorpromazine
(Thorazine) and thioridazine (Mellaril), were less desirable to the experts when the literature was
reviewed (Kane, et al., 2003; see Table 8.2). Although acute treatment of agitation is not the
focus here, three atypical antipsychotics that have an intramuscular formulation should be men-
tioned. Ziprasidone (Geodon IM), olanzepine (Zyprexa IM), and aripiprazole (Abilify IM) are
available in injectable forms for use in emergency departments and acute psychiatric hospitals.
Long-acting injectable medications are typically well tolerated, but in some patients the injection
site swells, forming lumpy, painful modules. Current research suggests that the deltoid muscle
may prove to be an alternative location for such injections (Saxena, et al., 2008).

Atypical Antipsychotic Medications

The atypical antipsychotics have little or no EPS (dystonia, Parkinsonism, akathisia, and tardive
dyskinesia). Also, a broader spectrum of efficacy is thought to be associated with the newer agents.
Benefits of the atypical antipsychotics agents versus the typical agents include the following:
• Minimal EPS
• Efficacy for positive symptoms (at least as effective as conventional agents)
• Improved efficacy for negative symptoms
• Improved cognition
• Improved mood
64 Chapter 8 • Treatment of Psychotic Disorders

Although the atypical agents have similar efficacy, the side effect profiles have been found
to be quite different. Tandon & Jibson (2003) report risperidone (Risperdal) shows a clear dose-
related increase in EPS and prolactin level, especially at doses greater than 6 mg daily. Prolactin
is a hormone secreted by the pituitary gland that increases when dopamine is blocked or sup-
pressed. Increased prolactin concentrations may lead to breast enlargement, galactorrhea (exces-
sive production of breast milk), irregular menses, and so on. Patients who receive increasing
doses of olanzepine (Zyprexa) likely exhibit akathisia, Parkinsonism, modest prolactin elevation,
and weight gain. One study concluded that using aripiprazole as adjunctive therapy with
olanzepine may mitigate weight gain and adverse effects on lipid metabolism (Henderson et al.,
2009). Asenapine (Saphris) while most similar to clozapine, is less likely to cause weight gain
and prolactin elevation, but its effects on QTc prolongation are comparable to quetiapine
(Bishara & Taylor, 2009).
The use of ziprasidone (Geodon) shows a trend toward an increasing level of anticholiner-
gic effects at higher doses (Daniel, et al. 1999), but may be less likely to elevate prolactin levels
or cause weight gain (Rosa et al., 2008).
Quetiapine (Seroquel), while still likely to cause weight gain, may be an alternative for pa-
tients who must switch medications due to serious weight gain and cholesterol levels; however,
overall efficacy may be compromised (Deberdt et al., 2008). Quetiapine has been found helpful
as a sedating agent, but because it has developed a reputation as a drug of abuse, some have re-
considered using it with those who have a history of substance abuse. Street names like “quell”
and “Suzie Q” have been associated with quetiapine, but research establishing a clear addictive
relationship is still inconclusive (Sansone & Sansone, 2010).
Clozapine (Clozaril) results in the most weight gain and sedation of all the agents. Keep in
mind that clozapine requires weekly blood monitoring and more intense supervision (see
Chapter 6).

Typical Antipsychotic Medications

The typical neuroleptics have similar efficacy with respect to positive symptoms, but they may
worsen negative symptoms because of their side effect profiles. Extrapyramidal symptoms have
a tremendous negative impact on treatment. Acute dystonic reactions are uncomfortable, fright-
ening, and lead to poor compliance. Bradykinesia, cogwheel rigidity, and stiffness, which are
parkinsonian side effects, contribute to the negative symptoms of the illness (i.e., reduced facial
expression, affective responses, gestures, and vocal intonation) with which the patient is already
struggling. Akathisia is a common subacute side effect related to these medications and may be
experienced as restlessness, anxiety, agitation, or insomnia. Tardive dyskinesia is the major
chronic extrapyramidal symptom that should be avoided if at all possible. The typical agents also
have a negative impact on cognition, which further impairs the patient’s ability to think and func-
tion independently. EPS is commonly treated with anti-Parkinson or anticholinergic medications
that may also interfere with cognition (see Table 8.3). All of these side effects contribute to dis-
continuing therapy and long-term compliance issues.

Adverse Effects of Typical Antipsychotics

Adverse drug reactions may be seen with any prescribed or over-the-counter medication. As
noted in Table 8.2, typical antipsychotics vary with their ability to cause side effects including
sedation, autonomic effects, and EPSs. Autonomic side effects refer to the adverse effect of med-
ications on the autonomic nervous system and include dizziness, hypotension, and flushing.
 Chapter 8 • Treatment of Psychotic Disorders 65

TABLE 8.3 Antiparkinsonian and Anticholinergic Medications

Typical Dose
Trade Name Generic Name (mg/day) Chemical Class
Artane trihexyphenidyl 5–15 anticholinergic
Ativan lorazepam 1–3 benzodiazepine

Benadryl diphenhydramine 25–50 antihistamine

Cogentin benztropine 2–6 anticholinergic

Inderal, nonselective
propranolol 40–80
Inderal LA beta-blocker
Klonopin clonazepam 1–3 benzodiazepine
Symmetrel amantadine 100–300 dopamine agonist
Valium diazepam 5–10 benzodiazepine

The typical or conventional antipsychotics are known for their EPS effects, which include
acute dystonia, parkinsonism, akathisia, and tardive dyskinesia. An acute dystonic reaction may
occur immediately following a dose of medication and involves intermittent and/or sustained
spasms of the muscles of the trunk, head, and neck. Dystonias usually occur within hours to days
of the medication and typically are very frightening to the patient.
Parkinsonism, the second form of EPS, may include rigidity, bradykinesia, shuffling gait,
and tremor. Patients who take dopamine receptor blockers may look like they have idiopathic
Parkinson’s disease. This side effect usually occurs within days to weeks of starting the antipsy-
chotic medications.
The most common extrapyramidal side effect is akathisia, which translates to “inability to sit
still.” Akathisia usually presents itself clinically as feelings of inner restlessness, inability to keep
the legs still, constant shifting of weight from one foot to the other, walking in place, frequent shift-
ing of body positions in a chair, and so on. Like Parkinsonism side effects, akathisia typically oc-
curs after days to weeks of treatment. Acute dystonia, parkinsonism, and akathisia occur early in
treatment with the typical antipsychotics and remit soon after the drug is discontinued.
The last type of EPSs is tardive dyskinesia (TD). It is an involuntary movement disorder that
may occur after the patient has been on the medication for months to years. Patients with TD may
have abnormal movements including lip smacking, sucking or puckering, facial grimacing, blinking,
tremors, trunk movements, and so on. Approximately 10% to 20% of patients who are treated with
dopamine receptor antagonists for more than a year are at risk for developing tardive dyskinesia.
Certain populations such as elderly females and patients with mood disorders are at greater risk.
Drugs like lithium may offer some protection from TD; however, experts caution against adding
lithium unless a mood stabilizer is clearly needed (Van Harten, Hoek, Matroos, & Van Os 2007 ).

TREATMENT PROTOCOL
The following general steps simplify the treatment information, which may be a bit overwhelm-
ing and confusing.
Step 1 Most prescribing professionals start with risperidone/paliperidone (Risperdal/Invega)
or a similar atypical agent for the patient’s psychotic illness.
66 Chapter 8 • Treatment of Psychotic Disorders

Step 2 If the patient is unable to tolerate risperidone because of side effects or does not re-
spond, the next logical choices would be olanzepine (Zyprexa), quetiapine (Seroquel),
ziprasidone (Geodon), aripiprazole (Abilify), iloperidone (Fanapt), and asenapine
(Saphris). Preferably, the clinician should try two or more of the atypical agents before
moving on to the next steps.
Step 3 This step varies and depends on the art of medicine. Some clinicians would recommend
a trial of clozapine (Clozaril) while others would use a typical antipsychotic medication
like haloperidol (Haldol) or thiothixene (Navane).
Step 4 Another option the clinician could try is to add a third agent in the atypical antipsy-
chotic class. Remember that the long-acting typical antipsychotics (e.g., Haldol
Decanoate or Prolixin Decanoate) are also available for patients who have compliance
issues. In addition, the newer atypical agents have long-acting injectable forms includ-
ing Risperdal Consta, Invega Sustenna, and Zyprexa Relprevv.

OTHER SIGNIFICANT ISSUES TO CONSIDER

In addition to choosing the most appropriate medication, other issues must be considered. An
adequate dose of the antipsychotic, which is approximately the dose recommended in the pack-
age labeling, must be prescribed. For example, the optimal dose of risperidone is 4–6 mg daily,
whereas the dose for olanzapine is 15–30 mg daily. Each drug has a different dose because of dif-
ferent potencies, but they are all equally efficacious at therapeutic doses. For chronic patients, the
dose may be higher than for first-episode patients.
Information on therapeutic drug monitoring with the antipsychotics is limited. Clozapine
is the only agent for which researchers have considered the plasma level most clinically useful.
Some experts believe that plasma levels of other neuroleptics can be useful to aid in dosage ad-
justment, especially when there is an inadequate response or problematic side effects.
Research indicates a relationship between certain patient characteristics and necessary
dose adjustments. First, smoking can reduce the plasma levels of some antipsychotics drugs (van
der Weide, Steijns, & van Weelden, 2003). A mounting body evidence suggests that the effects of
genetic polymorphisms involve cytochrome P450 liver enzymes and the metabolism of psy-
chotropic drugs. Ethnicity, sex, age, and other medical conditions may be factors in determining
the best dose for the patient. For example, geriatric patients and Asian patients who tend to be
more sensitive to antipsychotic medications require lower dosages because of their slower meta-
bolic processes in the liver.
Since the patient’s response to these medications is delayed, an adequate treatment trial is
important. Expert consensus guidelines recommend waiting a minimum of three weeks and a
maximum of six weeks before making a major change in the treatment regimen (Kane et al.,
2003). Some prescribers wait longer than six weeks if the patient is showing a partial response,
especially during the second or subsequent trials.
When switching from one atypical agent to another, most prescribers recommend cross-
titration as opposed to overlap and taper. Cross-titration refers to tapering the dose of the first
agent while gradually increasing the dose of the second antipsychotic. In contrast, overlap and
taper refer to continuing the same dose of the first drug while gradually increasing the second
drug to a therapeutic level and then tapering the first.
As with the antidepressants, the antipsychotic medications may also be augmented if the
patient has a partial response. A combination of an atypical antipsychotic and a mood stabilizer
has been used clinically despite the lack of empirical evidence in the literature. Some prescribers
 Chapter 8 • Treatment of Psychotic Disorders 67

use combinations of two atypical antipsychotics agents or one atypical agent and one conven-
tional antipsychotic. Again, there is a lack of data to support these practices. The various combi-
nations of medications usually lead to an increased number of side effects, as well as excessive
cost. Symbyax is an example of a combination drug that consists of fluoxetine (Prozac) and
olanzepine (Zyprexa) in varying doses. This may be useful in patients with schizophrenia and de-
pression or the depressive phase of bipolar disorder.
Clozapine (Clozaril) is indicated for treatment-refractory schizophrenia. Most clinicians de-
fine treatment refractory as failing to respond to one or more conventional antipsychotics and two
atypical antipsychotics. In addition, approximately 30% to 50% of treatment-refractory patients
respond to clozapine. In some instances, ECT may be considered after other options have been ex-
hausted. Remember that the primary goals of treatment are rapid and complete control of acute
psychotic symptoms, avoidance of functional deterioration, and prevention of relapse.

CASE VIGNETTE
Chapter Eight

CLINICAL HISTORY
Christopher is a 20-year-old college junior who has just returned from the summer break. He lives in a fraternity on cam-
pus and they just had their welcome back beer bash. When the party was over, his two roommates noticed that he was
acting strange. At first they just thought he was drunk and ignored his behavior, but around 3:00 AM he started to be-
come paranoid and combative with others in the house. There were reports from observers that he was convinced that
his frat brothers were “in a conspiracy with aliens to steal intelligence secrets from the university.” It escalated to a
point that he barricaded himself in his room and campus security was called. He was taken to a secure psychiatric
facility. After examination, it was determined that he was not under the influence of drugs and actually had very little
alcohol in his system. He was kept in the facility for 72 hours for further evaluation.

POSTCASE DISCUSSION AND DIAGNOSIS

Christopher’s father provided history to the social worker at the facility. As it turns out, his mother was diagnosed with
Schizoaffective Disorder several years before Christopher’s birth and was placed on medication after a stay in the
hospital. His older brother was once diagnosed as Schizotypal when he was a student in college. He now works as a
video game engineer. His maternal grandmother also was diagnosed with a “psychiatric illness” and was hospitalized at
various times in her life. There is no psychiatric illness on the father’s side of the family. After an examination by his
attending psychiatrist, the diagnosis was first-episode Paranoid Schizophrenia (295.30).

PSYCHOPHARMACOLOGICAL TREATMENT
Christopher was rather agitated when he arrived at the facility and was given a Zyprexa injection. When he was calmer
and had an opportunity to adjust to the unit, he was interviewed by several of the treatment staff. This included a so-
cial worker, a psychologist, and his attending psychiatrist. His paranoid ideations continued, and he refused to sit in the
day room as he was convinced that the TV monitor was beaming messages to the very aliens trying to steal intelligence
information. He told staff he could hear their voices even when the monitor was turned off. When staff attempted to
work with him and get him to interact with others, he became aggressive and stayed in his room. He was placed on
3 mg qd of risperidone. Over a period of three days, he became less combative and much of the hallucinations dimin-
ished. His dose was increased to 6 mg per day and he was monitored closely by the staff. His progress continued and
he was discharged two weeks later with a referral for outpatient treatment and medication management.
 9 TREATMENT OF ADHD AND
DISORDERS OF ATTENTION

This chapter explores the nature and causes of ADHD and other disorders of attention.
Special consideration is given to diagnosis and matching the right behavioral and pharma-
cological treatment to the needs of patients and their families.
Topics to be addressed include the following:

• Etiology of ADHD
• Diagnostic assessment of attention disorders
• Psychological and pharmacological treatment
• Case vignette

Attention deficit disorders are the most common disorders presenting in childhood.
Researchers estimate that approximately 3% to 7% of all school-age children have atten-
tion deficit disorders (Kratochvil, Vaughan, Harrington & Burke, 2003; Spencer,
Biederman, Wilens & Faraone, 2002). ADHD is diagnosed 2 or 3 times more often in
boys than in girls, and is commonly comorbid with other mental health concerns such as
conduct/antisocial personality, substance abuse, anxiety disorders, and mood disorders in-
cluding pediatric mania (Nevels et al., 2010; Strange, 2008). Further, it is estimated that as
much as 70% of these youth will demonstrate ADD or ADHD symptoms into their adult
years (Aviram, Rhum & Levin, 2001; McCann & Roy-Byrne, 2000). While the symptoms
for adults with these disorders are almost identical to the symptoms seen in children,
adults tend to display less hyperactivity and more internalized restlessness.
Treatment of ADHD can be complicated because many children who meet diagnos-
tic criteria for the disorder may also have comorbid oppositional and conduct disorders
(Wilson & Levin, 2001). Wilson and Levin also estimated that approximately 50% of
youth treated for substance abuse meet diagnostic criteria for ADHD. Some clinicians are
concerned that treating ADHD with stimulants may increase the risk for substance abuse,
including possibly abusing the stimulant, but research suggests that treating ADHD early
may in fact reduce this risk (Aviram et al. 2001; Wilson & Levin, 2001). Animal studies
have indicated that stimulants such as methylphenidate are far less likely to be abused
68
 Chapter 9 • Treatment of ADHD and Disorders of Attention 69

than other stimulants such as cocaine (Kollins, 2003). Further, Kollins found that an ADHD pa-
tient is less likely to abuse methylphenidate and other therapeutic stimulants than those without
the diagnosis. Long-acting preparations may be more beneficial because of their higher potential
for increased compliance and lower potential for abuse (Bright, 2008; Nair & Moss, 2009).
Bright further maintains that mixed amphetamine salts are more likely to be abused than
methylphenidate (40% vs. 15%, respectively). Nair & Moss further state that, despite concern
about diversion of the drug, recent data suggest that there may be benefits in preventing sub-
stance abuse disorders in patients with adult ADHD.

ETIOLOGY OF ADHD
Molecular genetics and neuroimaging studies confirm that disorders of attention like ADHD are
heterogeneous neurobiological disorders, mainly of the dopaminergic and noradrenergic path-
ways (Adler & Chua, 2002). These researchers further found as much as a 50% concordance rate
with other first-degree relatives. Subsequent studies have further demonstrated frontal lobe dys-
function in the pathophysiology of ADHD and a dysregulation of the neurotransmitters
dopamine and norepinephrine in the frontal lobes, the basil ganglia, the amygdala, and possibly
the reticular formation (Zimmerman, 2003). Functional MRI scans have consistently shown ir-
regular neurotransmitter activity in the frontal striatal networks and in the anterior cingulate
gyrus (Weiss & Murray, 2003). These areas of the brain also act like filters, assisting the patient
in screening out irrelevant information. Drugs used in the treatment of attention disorders
stimulate these brain centers, allowing them to work faster and more efficiently. This stimulation
assists the patient with both attention and retention of information.

DIAGNOSTIC ASSESSMENT OF ATTENTION DISORDERS

While attention disorder symptoms for adults and children are essentially similar, adults may
exhibit less hyperactivity and report more restlessness and agitation. As stated in the DSM-IV
diagnostic criteria, considering a childhood history of ADD or ADHD is necessary for the adult
diagnosis. A strong family history is usually found. Another important item to remember is the
DSM-IV criterion that requires the patient to demonstrate symptoms and behaviors in more than
one setting. Various testing and evaluation instruments can assist in making the diagnosis. Many
professionals use the Conner’s Rating Scales—Revised, the Conner’s Adult ADHD Rating Scales,
the Attention Deficit/Hyperactivity Disorder Test, or the ADHD Problem Checklist. Once again, to
determine if the patient truly has this disorder, the clinician should review all of the DSM criteria
and rule out another Axis I or Axis II condition or learning disability and perhaps the existence of
a physical condition, such as a thyroid abnormality, that could contribute to these symptoms.

PSYCHOLOGICAL AND PHARMACOLOGICAL TREATMENT

Only a few controlled studies have considered the efficacy of psychological treatments for ADHD.
Most available studies have emphasized the need for social-skills training, time-management tech-
niques, vocational and career appraisal, and life coaching in addition to addressing poor self-esteem
and other stereotypes experienced by these patients (Bemporad, 2001; Weiss & Murray, 2003).
These authors and others stress the need for daily coping strategies, including meal planning, con-
flict resolution, and parenting skills. Good patient education is also necessary to help patients and
their families understand the condition and to formulate realistic expectations (Barkley, 2002).
70 Chapter 9 • Treatment of ADHD and Disorders of Attention

The best treatment approach for attention disorders involves both a psychological and pharma-
cological approach (Meijer, Faber, van den Ban, & Tobi, 2009). The use of stimulants and other an-
tidepressants that potentiate levels of dopamine and norepinephrine show the greatest promise. In
fact, the pharmacologic treatment of ADHD remains one of the most promising of any disorder in
the DSM-IV-TR, with a response rate of 70%–90% in most cases (Strange, 2008). Table 9.1 lists the
psychostimulants used in the treatment of ADHD. These are the same stimulants mentioned in
Chapter 5 for augmentation of antidepressants. These medications tend to be dose dependent; that is,
higher doses typically correspond to better response rates. Typical side effects include hypertension,
insomnia, headaches, weight loss, and growth retardation in children. Growth retardation varies from
patient to patient and may be mitigated by brief drug holidays, or if pronounced, a treatment interrup-
tion (Findling, Childress, Krishnan, & McGough, 2008). In some cases, research on growth suppres-
sion is lacking, with insufficient follow-up on patients’ final heights (Goldman, 2010). Insomnia is
usually controlled by using stimulants with shorter half-lives that wear off before bedtime.
As clinicians know, the potential for abuse with stimulants is high, and they may need to
determine the risk of using these substances with patients who have a history of abuse. Also, pa-
tients who are taking MAOIs; lithium; neuroleptics such as haloperidol (Haldol) and chlorpro-
mazine (Thorazine); certain antidepressants, such as amitriptyline (Elavil), nortriptyline
(Pamelor), and imipramine (Tofranil); and certain analgesics should refrain from using stimu-
lants unless they are monitored closely.

TABLE 9.1 Psychostimulant Medications

Child/Adult Typical
Trade Name Generic Name Dose (mg/day) Level of Insomnia
Adderall, amphetamine/mixed 5–30/5–60 **
Adderall-XR salts /***
Cylert pemoline 37.5–112.5 **
Dexedrine dextroamphetamine 5–10/5–60 *
Dextrostat
Dexedrine Spansules **
Desoxyn methamphetamine 5–25/5–30 *
Focalin1 dexmethylphenidate 5–30/5–40 *
Focalin XR2 5–40 ***
Ritalin1 methylphenidate 10–30/10–40 *
Ritalin-SR **
Methylin-ER **
Metadate-ER2 **
Daytrana Transdermal 12.5 –37.5 cm2 ***
System
Concerta3 18–54 ***
Vyvanse lisdexamfetamine 30–70 ***
1
Effective for 2–6 hours
2
Effective for 6–8 hours
3
Once per day dosing
* Mild ** Moderate *** Significant
 Chapter 9 • Treatment of ADHD and Disorders of Attention 71

If the patient is a child who needs to be able to focus during school, after school, and for
evening homework, the clinician should consider the longer acting stimulants such as Adderall
XR (a brand of amphetamine salts) and Concerta (a brand of methylphenidate). If the child has
problems with sleeping, the clinician should consider stimulants with shorter half-lives such as
standard dextroamphetamine (Dexedrine) or methylphenidate (Ritalin). The longer acting stimu-
lants such as Metadate ER and Ritalin SR (i.e., types of methylphenidate) have a polymer, mul-
tiparticulate bead system that allows for breakdown and delivery over several hours. Concerta is
a bit more ambitious. It has an outer capsule that delivers an immediate dose and an inner core
that is released over 12 hours by gastrointestinal pressure through a laser-drilled hole in the
membrane. Once empty, the capsule is passed in the stool. Methylphenidate is also available in a
transdermal patch (Daytrana). A transdermal patch eliminates the need for multiple dosing
throughout the day and may be helpful for children who show an exaggerated gag reflex when
taking oral medications.
Lisdexamfetamine (Vyvanse) is a prodrug psychostimulant of dextroamphetamine avail-
able in doses of 30, 50, and 70 mg. The use of a prodrug may greatly reduce the potential for
abuse because it depends on first-pass hepatic metabolism. The current formulation is designed
to be activated in the liver, and, therefore, any alteration of the original form had decreased phar-
macological activity. While research on the long-term use of stimulants is lacking in adults, lis-
dexamfetamine appears generally well tolerated and effective for long-term use in children with
ADHD (Findling, Childress, Krishnan, & McGough, 2008). Further, it does not appear to be a
significant contributor to insomnia in adults with ADHD (Adler et al., 2009).
Any patient with ADHD should see a physician for a complete physical. Patients with
glaucoma, hypertension, and tic disorders should be evaluated and counseled by their primary
care physician before starting stimulants.
In addition to the psychostimulants, antidepressants and alpha-adrenergic agonists are
used in the treatment of ADHD (see Table 9.2). The response from antidepressants and alpha 2-
agonists is usually not as robust as stimulants, however. Alpha 2-agonists such as clonidine
(Catapres) and guanfacine (Tenex and Intuniv) may enhance prefrontal cortical regulation of at-
tention and impulse control. With optimal prefrontal cortical regulation, the locus coeruleus fires
to relevant, but not irrelevant, information, thus improving overall attention (Strange, 2008).

TABLE 9.2 Typical Antidepressants and Alpha-Adrenergic Agonists Used in the

Treatment of ADHD

Trade Name Generic Name Typical Dose (mg/day)

Catapres clonidine 0.2–0.9
Effexor, venlafaxine 50–300
Effexor XR venlafaxine /75–300
Intuniv guanfacine extended release 1–4
Norpramin desipramine 150–300
Pamelor nortriptyline 75–125
Strattera atomoxetine 40–100
Tenex guanfacine 1–9
Wellbutrin, bupropion 75–450
Wellbutrin SR bupropion /100–400
Wellbutrin XL bupropion /150–450
72 Chapter 9 • Treatment of ADHD and Disorders of Attention

Since the use of alpha 2-agonists may lower blood pressure, regular monitoring and cardiac eval-
uation is advised. These medications may be a good alternative for patients who cannot tolerate
stimulants or the problems with insomnia they may cause. As mentioned in Chapter 5, antide-
pressants need to be prescribed cautiously for children and adolescents because of the FDA
warning about an increase in suicidal thinking and behaviors. For more complete information on
medication side effects, see Chapter 5 or the Appendix.
Many experts who treat patients with ADHD have found that a combination of psychother-
apy, stimulants, and antidepressants offer a complete and direct treatment approach to the condi-
tion. While stimulants work for most patients, in some cases antidepressants offer symptom
relief. Atomoxetine (Strattera) is a stimulating antidepressant that increases levels of norepineph-
rine. While it has been shown to be effective in both children and adults, it may be slightly more
effective in younger children (6–7 years) than older children (8–12 years), but younger children
may report greater rates of GI upset and somnolence (Kratochvil, Milton, Vaughan, & Greenhill,
2008). Antidepressants with stimulating qualities often are prescribed alone for the condition.
Bupropion (Wellbutrin) is most often the antidepressant of choice because it does not interfere
with most stimulants and offers enriched levels of dopamine and norepinephrine. Some research
may suggest that males and females may respond to bupropion differently. Males appear to
respond to bupropion regardless of ADHD type. Females with combined, but not inattentive
type, responded better than those with other ADHD types (Wilens et al., 2005). Though not FDA
approved, tricyclics like desipramine have been shown to be efficacious, but side effects and
cardiotoxicity may preclude their use with some patients.
Medications are typically given by titrating doses upward until complete symptomatic
relief is obtained. It is not uncommon for parents to request drug holidays for children in the non-
school, summer months. This practice often helps allow growing periods for the child since
many stimulants can stunt growth.
Many parents today are concerned about placing their child on drugs, especially stimu-
lants. They will often cite newspaper articles and pieces from popular magazines suggesting that
behavioral therapy alone is sufficient. Some parents believe that diet alone will improve their
child’s symptoms. While sugary snacks certainly do not help children with ADHD, the connection
between sweets and behavior is not conclusive. In most cases, children and adults with moderate-
to-severe cases of ADHD do not respond adequately to dietary changes, behavioral interventions,
and environmental changes alone. The clinician should educate the parents and the patient about
the benefits of medications. The proof will be apparent in the child’s behavior and academic per-
formance. Nothing else, aside from counseling, is better for raising self-esteem and assuring a
healthy sense of independence.

CASE VIGNETTE
Chapter Nine
CLINICAL HISTORY
Jacob is an eight-year-old African-American boy who lives with his mother and younger sister. His parents are sep-
arated and he sees his father on twice per month visits. While Jacob has always been a very active child who loves
sports and anything relating to video games and wrestling, even his father has noticed that his behavior has gotten
to be a bit out of control. He has noticed that Jacob can be a bit hard to discipline and doesn’t seem to listen when
he is directly spoken to. In consultation with his teacher and principal, and after speaking with the school counselor,
 Chapter 9 • Treatment of ADHD and Disorders of Attention 73

who has spoken with Jacob about several of his detentions after class, it was determined to refer him to the school
psychologist for learning disabilities evaluation.
While Jacob is essentially a happy child, he often disrupts his second-grade class with excessive talking and
walking about the room. While he returns to his seat when asked, he often interrupts the teacher to ask to use the rest-
room or sharpen his pencil. He also blurts out answers and won’t let others answer questions without interrupting
them. The teacher has also noticed that he can’t seem to wait his turn in both board games and in games on the play-
ground. She is concerned about his grades and he appears to be having trouble with retention of information from one
subject to another. Reading comprehension is especially difficult for him.
Various evaluation questionnaires were given to Jacob, his teacher, the principal of his school, and his parents. It
is clear that these behaviors appear to be problematic in several settings. In fact, Jacob failed a spelling quiz because he
forgot to study for it. He also forgot to take home a permission slip for a field trip to the zoo and was not allowed to go.
He frequently loses books, backpacks, and sporting equipment. His coach said he may not be able to stay on the team if
he forgets to attend another practice after school.

POSTCASE DISCUSSION AND DIAGNOSIS

After examining the questionnaires completed by Jacob, his parents, his teacher, and his principal, he was referred to
the school psychologist for a battery of tests. The results confirm that Jacob appears to have significant evidence for
Attention Deficit/Hyperactivity Disorder, Predominantly Hyperactive-Impulsive Type (314.01). Jacob’s father also had
this condition when he was younger, but did not continue to have symptoms into his adult years. There is no history of
other mental illness or substance use in his family, and his sister appears to be without a learning difficulty.

PSYCHOPHARMACOLOGICAL TREATMENT
Jacob was evaluated by his pediatrician and after reading the psychologist’s report, agreed with the diagnosis and
placed Jacob on 18 mg of Concerta each morning. . Within a few weeks Jacob’s grades improved and he was better
able to attend to school tasks and homework. While he was tolerating the medication well, there were reports of some
insomnia. He was switched to methylphenidate 15 mg every morning and again at 3:00 PM. This dose appeared to work
well without excessive stimulation at bedtime.
 10 TREATMENT OF COGNITIVE
DISORDERS

This chapter presents a discussion of the various forms and causes of dementia and how best
to treat them and reduce the negative aspects caused by these conditions. The advantages
and disadvantages of various medications for cognitive decline are explored and discussed.
Topics to be addressed include the following:
• Forms of dementia
• Alzheimer’s disease
• Medical and behavioral evaluation
• Medications for cognitive disorders
• Other approaches to cognitive enhancement
• Other significant issues to consider
• Case vignette
The cognitive disorders consist of delirium and dementia although this chapter
focuses mainly on dementia. Delirium is an acute confusional state that is basically a med-
ical emergency; the patient needs acute medical treatment to find the etiology of the confu-
sion and treat it accordingly. For the most part, delirium would not be part of a patient’s clin-
ical presentation to your treatment settings. On the other hand, dementia is becoming more
of an issue as our population ages. Alzheimer’s disease (AD), the most common type of de-
mentia, affects more than 15 million people worldwide; the United States has about 4 mil-
lion people with the disease (Grossberg, 2003). In fact, Brookmeyer, Gray, & Kawas (1998)
have suggested the prevalence of AD in the United States will rise to approximately 9.3 mil-
lion over the next fifty years. Grossberg further reports this would translate to about 1 in 45
Americans with AD. It is also estimated that 34 million persons worldwide will suffer with
some form of dementia by 2025 (Toda, Kaneko, & Kogen, 2010).

FORMS OF DEMENTIA
Dementia has many different forms that include memory disturbance as their central fea-
ture. The three most common forms are Alzheimer’s disease, dementia with Lewy bodies,
and vascular dementia.
74
 Chapter 10 • Treatment of Cognitive Disorders 75

Alzheimer’s disease accounts for approximately 55%–60% of all irreversible demen-

tias, and to date, no single factor causing AD has been identified (Toda, Kaneko, & Kogen,
2010). It will be discussed as the prototype for our purposes although other less common di-
agnoses may be treated in a similar fashion. In addition to the memory problems,
Alzheimer’s disease is characterized by either aphasia, apraxia, and/or agnosia. Toda,
Kaneko, & Kogan (2010) further state that neuropathologically AD is identified by amyloid
plaque, neurofibrillary tangles, and synaptic loss. A loss of acetylcholine, a critical neuro-
transmitter, is also noted.
Dementia with Lewy bodies (DLB) is the second most common type of dementia, account-
ing for about 20% to 25%; it is characterized by memory dysfunction with visual hallucinations,
Parkinsonism, and/or fluctuating alertness levels. Dementia with Lewy bodies and another cause
of dementia, Parkinson’s disease, probably have similar neuropathology. Vascular dementia is
the third most common type, but accounts for less than 20% of all cases. Classically, vascular de-
mentia was thought to be the second most common type, leading DLB, and was previously
known as multi-infarct dementia (MID). The less common forms of dementia include the follow-
ing: frontotemporal dementia (i.e., Pick’s disease), corticobasal degeneration, progressive
supranuclear palsy, Creutzfeldt-Jakob disease, neurosyphilis, normal-pressure hydrocephalus,
and HIV-associated dementia (Boeve, Silber, & Ferman, 2002).
Overall, these disorders are a significant public health concern because of their economic
burden. Grossberg (2003) reports the estimated annual cost of AD in the United States to be in
the range of $67 billion. Of the total costs, direct patient care accounts for 31%, lost productivity
due to illness or premature mortality accounts for 20%, and unpaid caregiver cost accounts for
the remaining 49%. As the number of patients and the cost to society increases, we will all be
facing this issue at some point, either professionally or personally.

ALZHEIMER’S DISEASE
Alzheimer’s disease is characterized by gradual onset and is marked by progressive decline
in cognition; motor function declines in the later stages. Research indicates that several
neurotransmission pathways may be involved, including cholinergic, glutamatergic,
serotonergic, and dopaminergic. Currently, loss of cholinergic neurons appears to be the
most important abnormality. In the mid-1970s, researchers discovered a deficit in brain
presynaptic cholinergic systems in postmortem brain tissue in patients with AD (Davies &
Maloney, 1976). This discovery has led to a major finding: Acetylcholinesterase inhibitors,
which increase intrasynaptic acetylcholine levels, produce moderate symptomatic improve-
ment in AD.
Inflammatory processes may also play a role in the disease progression. Senile plaques
consisting of beta-amyloid are the most widely studied neuropathologic change in AD. These
plaques do not affect the whole nervous system uniformly, but only certain vulnerable cortical
and subcortical areas; the sensory and motor regions of the brain tend to remain unaffected.
Chronic neuroinflammation may be responsible for the degeneration of cholinergic neurons via
a chain of inflammatory processes initiated by beta-amyloid.
Sometimes a faulty gene may cause the problem, as in the familial form of AD. On
the other hand, the more common form of the disease is known as sporadic AD. The genes
that contribute to AD appear in all cells, but their expression varies in different areas of the
brain and in different individuals. Obviously, the neuroanatomy and neurochemistry are
very complex and beyond the scope of this chapter. We just want to give you some hint of
these issues.
76 Chapter 10 • Treatment of Cognitive Disorders

MEDICAL AND BEHAVIORAL EVALUATION OF COGNITIVE DISORDERS

As part of the medical evaluation of the cognitive disorders, an inventory of currently prescribed
and over-the-counter medications needs to be reviewed and analyzed as potential causes.
Behavioral toxicity associated with pharmacotherapy is the most common etiology of reversible
delirium. Appropriate laboratory evaluation, including serum electrolytes, blood urea nitrogen
(BUN) levels, serum B12 level, and thyroid-function tests should be done. Vitamin B12 defi-
ciency and hypothyroidism may present as reversible causes of a cognitive disorder if detected in
the earlier stages. A diagnostic neuroimaging procedure (CT or MRI of the brain) is commonly
used to rule out tumors, subdural hematomas, and normal-pressure hydrocephalus. The clinician
should obtain a past psychiatric history from the patient or family because patients with major
mental illness can also develop dementia in later life (e.g., schizophrenia complicated by AD).
While the medical aspects of cognitive disorders are important, the clinician also needs to look
at behavioral factors that precipitate or contribute to some of the dysfunction. Patients with dementia
who have poor short-term memory and disorientation may appear quite compensated as long as they
remain in a familiar environment that does not require new learning. Furthermore, when these
patients are moved to a hospital, nursing home, or other unfamiliar setting, they may become disori-
ented and disorganized, leading to physical aggression and acting out. Once the patient adapts to the
new environment, behavioral problems may resolve spontaneously over a month or so. If aphasia is
part of the dementia, patients have difficulty expressing themselves. This difficulty may present as
grabbing or aggressive behaviors when a patient is in pain or needs to go to the restroom. Patients
who are apraxic may be unable to carry out their routine activities of daily living, which leads to ag-
itation and/or low frustration tolerance. In addition, family and staff visits are not always welcomed
by the patient. If any particular behavior patterns arise, hospital or nursing home staff may need to
observe interactions and determine the triggers of these behavioral problems (Goldberg, 2002).

MEDICATIONS FOR COGNITIVE DISORDERS

Only a few approved medications are available for treatment of Alzheimer’s disease (see
Table 10.1). These drugs improve cognitive function only modestly; however, they are best
conceptualized as drugs that “stabilize” cognition, activities of daily living, and behavioral
function. Basically, the cholinesterase inhibitors slow the clinical deterioration in AD, but
they do not cure it. In the early 1990s, tacrine (Cognex) was the first cholinesterase inhibitor
demonstrated to be effective in the treatment of AD. Unfortunately, liver toxicity has signifi-
cantly limited its use in treatment.

TABLE 10.1 Medications for Cognitive Disorders

Trade Name Generic Name Typical Dose (mg/day) Chemical Class

Aricept donepezil 5–10 cholinesterase inhibitor
Cognex tacrine 40–160 cholinesterase inhibitor
Exelon rivastigmine 6–12 cholinesterase inhibitor
Exelon Patch rivastigmine transdermal 4.6–9.5 mg/24 hours cholinesterase inhibitor
system
Namenda memantine 10–20 NMDA receptor antagonist
Reminyl galantamine 16–24 cholinesterase inhibitor
 Chapter 10 • Treatment of Cognitive Disorders 77

Second-generation cholinesterase inhibitors, such as donepezil (Aricept), have been shown

to be as effective as tacrine without the hepatic toxicity. Donepezil has shown positive effects on
cognition and overall functioning in AD patients with mild-to-moderate disease (Rogers &
Friedhoff, 1996). This medication is easy to use because it is given once daily and has only two
therapeutic doses, 5 mg or 10 mg. As with all the cholinesterase inhibitors, the most common side
effects are gastrointestinal symptoms including nausea, vomiting, and diarrhea. Donepezil also ap-
pears to extend its benefit into more advanced stages of AD than initially thought. Some research
maintains that donepezil may also be better tolerated than other AD medications due to a lower risk
for GI upset when compared to rivastigmine and galantamine (Lockhart, Mitchell, & Kelly, 2009).
Feldman, et al. (2001) demonstrated significant benefits using cholinesterase inhibitors in moderate
to severe AD with continued good tolerability as far as side effects are concerned.
Rivastigmine (Exelon) is another medication used in treatment of AD. In addition to inhibit-
ing acetylcholinesterase, rivastigmine inhibits butyrylcholinesterase. The clinical significance of
this latter effect remains to be determined, but butyrylcholinesterase appears to regulate brain
acetylcholine levels in animal studies (Blazer, Steffens, & Busse, 2004). Gastrointestinal effects
of rivastigimine occur in up to 40% of patients, more than with donepezil. Some evidence sug-
gests that rivastigmine may be effective with behavioral problems that are particularly prominent
in dementia with Lewy bodies and in patients experiencing a more aggressive course of dementia,
in particular, patients with hallucinations (Cummings et al., 2010). The transdermal rivastigmine
patch (Exelon Patch), approved in 2007, provides the option of a continuous medication delivery
method that is less likely to cause the GI upset associated with oral medications because of fluctu-
ating drug plasma levels (Darreh-Shori & Jelic, 2010; Wentrup, Oertel, & Dodel, 2008).
The final cholinesterase inhibitor is galantamine (Reminyl), which also modulates the
nicotinic acetylcholine receptor responsiveness at an allosteric binding site (Blazer et al. 2004).
Because a prominent nicotinic cholinergic deficit exists in AD, this additional benefit may be
clinically useful. The dosage titration with galantamine is more cumbersome; the maximum dose
is 24 mg/day. The side-effect profile looks similar to donepezil if galantamine is slowly increased
to a therapeutic dose.
Another class of medications being used are the N-methyl-D-aspartate (NMDA) receptor
antagonists. According to the glutamate excitotoxicity hypothesis, beta-amyloid indirectly stimu-
lates the production of excessive glutamate; glutamate in turn overstimulates the NMDA receptors.
This process results in neuronal death because of the chronic excitation. To reduce the negative
effect of glutamate, experts theorize that intervening as early as possible in the process of AD
would help the patient most. Glutamate is thought to play a more prominent role in the early
stages of AD rather than the late stages. A medication called memantine (Namenda) was approved
in late 2003 for use in AD. The most common side effects of memantine include agitation, urinary
incontinence, urinary tract infection, and insomnia. Tariot, Farlow, Grossberg, Graham, &
McDonald (2004) have reported that memantine, when used in combination with cholinesterase
inhibitors, may be useful in patients with more moderate to severe AD. In fact, the use of
cholinesterase inhibitors may delay nursing home admissions in cognitively impaired patients.
This effect was significantly enhanced with the addition of memantine (Lopez et al., 2009).

OTHER APPROACHES TO COGNITIVE ENHANCEMENT

Vitamin E and other antioxidants have been used to slow the progression of aging and dementia
(Sano, et. al., 1997). Vitamin E may slow the deterioration associated with AD, but not necessar-
ily in the cognitive domain. Some studies found that antioxidants were more effective than
78 Chapter 10 • Treatment of Cognitive Disorders

placebo in delaying deterioration to functional endpoints such as nursing home placement or sub-
stantial loss of ability to perform activities of daily living. The dose of Vitamin E recommended in
the studies was 1,000 IU given twice daily.
Another medication to consider is selegiline (Eldepryl), which is a selective inhibitor of
monoamine oxidase. This medication is used most commonly in Parkinson’s disease but may
also be used for depression given that it is an MAOI. The doses of selegiline used in the studies
were 10–40 mg daily. As with Vitamin E, treatment with selegiline slows functional deteriora-
tion but has little effect on cognitive decline.
Extracts of the leaf of the ginkgo biloba tree have been used in traditional Chinese medica-
tions and may have antioxidant, anti-inflammatory, and stimulant properties. A standardized ex-
tract of ginkgo biloba has been studied; the results show a small but statistically significant effect
on cognitive functioning (Le Bars, et al., 1997). The improvement was approximately one-half of
the effect seen with the cholinesterase inhibitors. Currently, ginko biloba is being studied further
to evaluate its effectiveness and usefulness.
Studies in postmenopausal women suggest that estrogen replacement therapy decreases
the risk of AD for this population. Evidence is still conflicted as to whether conjugated estrogens
or more naturally occurring forms are neuroprotective. Keep in mind that treatment with estro-
gens may also increase the risk of heart disease and breast cancer (Warren, 2004).
Research suggests that nonsteroidal anti-inflammatory drugs (NSAIDS) might decrease
the risk of AD in some patients. By decreasing the inflammation caused by the plaques contain-
ing beta-amyloid, the neurons have less damage and cell death; however, there appears to be lit-
tle benefit to patients already suffering from AD symptoms (Wentrup, Oertel, & Dodel, 2008).
Unfortunately, the potent anti-inflammatory steroid prednisone failed to show any positive effect
on cognition or disease progression (Aisen 2002). Trials using naproxen (Naprosyn) and rofe-
coxib (Vioxx) have also been negative. Rofecoxib has been withdrawn from worldwide markets
because of the increased risk of heart attack and stroke. Some clinicians have suggested that cer-
tain types of NSAIDS and aspirin may decrease beta-amyloid production, while other types do
not. At this point in time, the use of NSAIDS and aspirin does not seem promising in the treat-
ment of AD; however, they may be helpful in prevention.
Agents that lower cholesterol may be useful in preventing AD. Lipid-lowering agents,
such as various statin drugs, are associated with a decrease in central nervous system amyloid
deposition in animal models (Sano, 2003). Atorvastatin (Lipitor), simvastatin (Zocor), and
pravastatin (Pravachol) are common examples of statins. Clinical trials are currently underway to
evaluate their usefulness in the treatment of AD.

OTHER SIGNIFICANT ISSUES TO CONSIDER

Behavioral complications of dementia include physical agitation, verbal aggression, physical ag-
gression, depression, and psychosis. Research suggests as many as 50% of all AD patients may
present with aggressive and agitated symptoms (Amann et al., 2009). An organized way to ap-
proach patients with behavioral problems is to define some target symptoms, which will dictate
the treatment protocol. For example, an atypical antipsychotic agent would be considered a start-
ing point for an AD patient presenting with agitation, aggression, or psychotic symptoms.
Risperidone (Risperdal) has been effective in this situation, with dosages up to 2 mg with mini-
mal side effects. However, the use of atypical antipsychotic medications in the elderly has been
associated with an increase in cerebrovascular events (stroke and transient ischemic attacks) and
even death. Their use should be considered only when behavioral redirection has not worked and
 Chapter 10 • Treatment of Cognitive Disorders 79

when their benefits outweigh their risks (Herrmann & Gauthier, 2008). Typical antipsychotic
medications, such as haloperidol (Haldol) or chlorpromazine (Thorazine), should be avoided if
possible because they present a high risk of tardive dyskinesia (TD) in the elderly (see Chapter 8
for more information on TD).
Another option for a patient with agitation would be mood stabilizers. Carbamazepine
(Tegretol) and valproate (Depakote) have both been used in low-to-moderate doses with overall
decrease in agitation; however, pharmacokinetic interactions with secondary enzyme induction
limit the use of this drug. Lamotigine (Lamictal), gabapentin (Neurontin), or topiramate
(Topamax) may be safer choices (Amann et al., 2009).
If an AD patient primarily has depressive and anxiety symptoms, an SSRI would be an ex-
cellent choice. Some research suggests that dual inhibition of cholinesterase and serotonin reup-
take would greatly improve the effect of AD medications and perhaps mitigate the dose-related
side effects of most AD medications (Toda, Kaneko, & Kogen, 2010). The information regarding
antidepressant medications discussed in previous chapters will be applicable here. Note that cau-
tion should be used in medicating elderly patients given the high prevalence of polypharmacy
and multiple medical diagnoses.
Except for Alzheimer’s disease, the data on the treatment of other dementia syndromes are
sparse. Vascular dementia, for example, occurs rarely in isolation. More commonly, a combina-
tion of two neuropathological processes may occur together, referred to as a mixed dementia.
These types of dementias may respond to the treatment options suggested for Alzheimer’s dis-
ease alone.

CASE VIGNETTE
Chapter Ten

CLINICAL HISTORY
Eleanor is a 77-year-old white female resident of a skilled nursing facility. Recently her daughter requested an evalua-
tion from the staff psychologist because she noticed that her mother’s Alzheimer’s symptoms appeared to be getting
worse. Eleanor was admitted to the facility six months ago with moderately severe cognitive and physical decline and
had to be placed in a skilled facility since she could no longer manage herself at home. Her daughter is a single mother
of four teens and works too many hours to care for her mother in her home. She had attempted to care for her until
Eleanor left the stove on, resulting in a minor kitchen fire. Eleanor has no history of mental illness, but began to show
signs of cognitive decline in her late fifties. The symptoms became much more pronounced after her husband’s death
five years ago.
Recently her daughter and other members of the nursing staff noticed that Eleanor has become rather rest-
less and combative. When she gets confused over her surroundings, she wanders through the halls attempting to
open fire doors. When nurses attempt to redirect her back to her room, she swears at them and even struck one of
them in the face. Her PCP authorized the use of restraints one day after she managed to wander out the front door
and was found standing in the middle of the street trying to take a dog away from a woman who was walking it. She
yelled at the woman, telling her that she needed the dog to protect her from people who were stealing her clothing
in the nursing home.

POSTCASE DISCUSSION AND DIAGNOSIS

Eleanor has Dementia of the Alzheimer’s Type with Behavioral Disturbance (294.11). Her condition has worsened in the
last few months. She seldom recognizes her daughter when she visits and now has become rather combative with
80 Chapter 10 • Treatment of Cognitive Disorders

staff. She often becomes both extremely confused and inconsolable when she is agitated. Staff members have re-
ported that it is difficult to feed her because she often gets angry and throws food on the floor. She will no longer bathe
without constant redirection from staff, and they are willing only to assist with sponge baths because she is too much
to handle in the shower room.

PSYCHOPHARMACOLOGICAL TREATMENT
Upon evaluation and consultation with the geriatric psychologist and the facility social worker, Eleanor’s physician ad-
justed her medication regimen. In addition to the 10 mg per day of Aricept and 10 mg per day of Namenda she was already
taking, 2 mg of risperidone was added. After one week with partial improvement of symptoms, trazodone 50 mg qhs was
added for continued sleep difficulties. Within a week, staff reported that Eleanor was much less agitated and combative.
She had no further paranoid delusions, and restraints were no longer needed. While her daughter noticed no changes in
her cognitive abilities, she was much more pleasant to visit and would occasionally walk with her in the garden without
the need for staff present.
11 TREATMENT OF SLEEP DISORDERS

This chapter thoroughly explores sleep disturbances, primary sleep disorders, and para-
somnias. Various treatment issues and options are presented and discussed.
Topics to be addressed include the following:
• Stages of sleep
• Sleep disorders and conditions
• Behavioral techniques for treating sleep disorders
• Pharmacology for sleep disorders
• Holistic treatments
• Case vignette
Sleep disturbances are a frequently cited problem by mental health patients. While
many of these patients also have comorbid physical conditions that interfere with the
quality of their sleep, many have other Axis I and/or Axis II conditions that cause sleep
disturbances secondary to mental health conditions. Some patients experience sleep dis-
turbances related to substance use or abuse. Research has established that those with
sleep disorders are at increased risk for developing hypertension and suffering cardiovas-
cular morbidity and mortality (Richert & Baran, 2003). The most common sleep com-
plaints made by mental health patients involve initial insomnia (difficulty falling asleep)
or intermittent awakening throughout the night (middle insomnia). Some patients may
fall asleep normally but awaken very early in the morning, with difficulty falling back to
sleep (terminal insomnia). A national survey of more than 1000 adults studied by re-
searchers found that 43% reported middle-of-the-night awakening, of which 26% could
not return to sleep and 34% complained of daytime fatigue. A similar study found that as
many as 56% had difficulty with initial insomnia, and 67% experienced intermittent
awakening (Scharf, 2001). While insomnia is a rather common disorder and can affect
nearly everyone at various times of their lives, it becomes chronic for about 10% of the
population (Hardeland, 2009).

81
82 Chapter 11 • Treatment of Sleep Disorders

STAGES OF SLEEP
There are five distinct stages of sleep. Stages 1 and 2, the theta stages, are rather light stages of
sleep. If patients’ names are called out during these stages, they would probably awaken without
feeling groggy. People spend about 50% of sleep time in stages 1 and 2.
Stages 3 and 4 are called the delta stages of sleep, which are characterized by slow-wave
patterns and very deep, restorative sleep. Here, shaking the patient is necessary to awaken him or
her, and the patient would be groggy. People spend about 20% of their sleep time in these stages.
Stage 5 is the rapid-eye movement or REM stage. It occupies about 25% of the night and
is characterized by both theta- and delta-type activity that resembles the wave patterns seen while
awake. Most dreams occur during this stage. If patients are sleep deprived, they demonstrate ad-
ditional time spent in stages 3, 4, and REM during their next sleep period, which is called the
rebound phenomenon (Carlson, 2004). Serotonin is necessary to maintain adequate sleep, espe-
cially in stages 1–4. Norepinephrine is necessary for REM sleep, so not surprisingly, depressed
patients with lower levels of serotonin and norepinephrine experience problems with the quality
of their sleep.
When discussing sleep concerns with a patient, the clinician needs to determine if the pa-
tient has a primary sleep disturbance, that is, a sleep disorder that is not caused by a medical, psy-
chiatric, or substance abuse –related issue. In such cases, the clinician must collect adequate his-
tory information to assure that no other complicating conditions or factors exist. The clinician
should inquire about such issues as daytime sleepiness, memory/concentration concerns, depres-
sion, an increase in accidents, and impaired job functioning. Referral to a neurologist or sleep
specialist may be in order to determine the cause.

SLEEP DISORDERS AND CONDITIONS

Patients who present with co-occurring mental illness and sleep disturbances report either initial
and/or terminal insomnia. Initial insomnia is usually indicative of an anxiety disorder such as
generalized anxiety disorder, or an adjustment disorder with anxious mood. These patients have
great difficulty falling asleep, but once they are asleep, they usually stay asleep throughout the
night. Some patients present with middle insomnia (intermittent awakening); they fall asleep, but
wake up periodically during the night. In addition, some have “early morning awakening” or ter-
minal insomnia. These patients can usually fall asleep easily, but awaken around 3 or 4 A.M., and
cannot get back to sleep. Most of these patients are likely to have a disorder with an affective
component, such as major depression, schizoaffective disorder, dysthymia, or an adjustment dis-
order with depressed or mixed features.
Sometimes a patient presents what appears to be a sleep-related disorder in addition to the
types of poor sleeping patterns that are observed in the depressed or anxious patient. A primary
care physician or neurologist should evaluate the patient for the presence of other dyssomnias or
primary sleep disorders. The following list describes a few that may affect the patient:
1. Obstructive Sleep Apnea (OSA). This condition is troublesome for many patients. A
milder form is called upper airway resistance syndrome. These conditions are much more
common in overweight, middle-aged men, or patients with certain types of oropharyngeal and
facial anatomies. The patient is unable to keep airways open during sleep, and the airway nar-
rows or collapses, leading to gasping or awakening throughout the night. Medications are usually
not used here, and instead options include the continuous positive airway pressure machine or
CPAP. This device splints the airway open and prevents airway narrowing during sleep. Surgery
 Chapter 11 • Treatment of Sleep Disorders 83

is an option for some, but it is rather drastic and effective in only about 50%of cases (Richert &
Baran, 2003). Various mouth appliances have been designed to reposition the mandible, tongue,
or both when sleeping. They have mixed, less promising results and are usually attempted only
by those with mild OSA.
2. Sleep Bruxism. Sleep-related teeth grinding is a parasomnia much more common
among children, but it can be seen in adults during times of stress. In many cases psychotherapy
and/or anxiety-reducing medications may improve this condition. A dentist may be consulted,
and a mouth guard could be used to reduce the possibility of tooth damage or chronic headaches.
3. Sleepwalking and Night Terrors. These conditions are also typically seen in about
10% of children. Since patients usually outgrow these conditions, the use of medications such
as benzodiazepines is not recommended for children or those patients with a history of sub-
stance dependence.
4. Narcolepsy. This condition consists of uncontrolled attacks of short-duration, restful
sleep. The attacks are usually triggered by strong emotions such as laughter or anger. Since this
condition may cause excessive daytime sleepiness, patients should receive counseling to assist
with the stigma of the disorder and the perception that they are lazy or unmotivated. Short naps
during the day, as well as consistent sleep/wake times are suggested.
Narcolepsy is typically treated with various psychostimulants such as methylphenidate
(Ritalin) and pemoline (Cylert). However, pemoline is rarely used due to hepatic concerns.
Modafinil (Provigil) and the newer armodafinil (Nuvigil) are also used. Historically, stimulants
have been used to reduce daytime sleepiness and sleep attacks, along with antidepressants to in-
crease sleep quality. Modafinil and armodafinil are not considered stimulants per se, and research
on modafinil suggests it may be less effective for narcoleptic patients, especially if they have been
successfully treated with stimulants in the past (Brooks & Kushida, 2002). Armodafinil, also used
for narcolepsy, was found to be especially helpful for shift workers who need to remain alert dur-
ing the night, but are seeking a medication that will not affect their daytime sleeping patterns
(Czeisler, Walsh, Wesnes, Arora, & Roth, 2009). The clinician needs to watch for signs of toler-
ance or dependency with all stimulants used in the treatment of narcolepsy
Gamma-hydroxybutyrate (GHB) or sodium oxybate is also known by the trade name
Xyrem. Xyrem was approved by the FDA in 2002 for excessive daytime sleepiness and cata-
plexy in patients with narcolepsy. It is a CNS depressant that received the street name date-rape
drug along with Rohypnol because both are abused as party drugs and are often slipped into an
alcoholic beverage in the hope that someone taking the drug would be mentally impaired and
willing to participate in sexual relations. Many patients often have impaired memory upon awak-
ening. When taken for sleep disorders including narcolepsy, GHB increases the quality of both
REM and non-REM sleep cycles. Side effects of GHB include excessive grogginess and mental
confusion before the drug wears off.
5. Restless Leg Syndrome (RLS) and Periodic Leg Movement Disorder (PLMD). These
conditions often occur together, but they are distinct entities. Restless leg syndrome usually oc-
curs in the evening and throughout the night. Patients complain of feeling restless or jittery and
may not be able to relax. They often report that this feeling starts deep within their legs, and they
often move or tap their feet to gain relief. Periodic leg movement disorder, which was previously
known as nocturnal myoclonus, can cause sleep fragmentation and daytime sleepiness. With
this disorder, the legs often jerk every few seconds, and this movement can increase in intensity
to a point where sleep is seriously disturbed. Some researchers have also pointed out that RLS
can be caused or exacerbated by various drugs including several common antidepressants, so it is
84 Chapter 11 • Treatment of Sleep Disorders

vitally important for evaluating physicians to inquire about medications taken for mood condi-
tions (Hoque & Chesson, 2010).
Treatment for both disorders involves either the use of benzodiazepines such as clon-
azepam (Klonopin) or the use of dopaminergic agents such as levodopa/carbidopa (Sinemet) or
pramipexole (Mirapex). Ropinirole (Requip) is another alternative used in the treatment of RLS.
Pregabalin (Lyrica) has not received FDA approval yet but is used off-label for limb movement
concerns. In severe cases, opioids may be considered. Research has shown that some patients
with PLMD have iron, vitamin B12, and folate deficiencies, so complete blood counts with dif-
ferential should be ordered and evaluated (Richert & Baran, 2003).
In all cases of serious sleep disturbances, the clinician should order a complete sleep study
or nocturnal polysomnogram (NPSG). This study is conducted at night in a sleep laboratory
under the supervision of a neurologist or a sleep specialist. It involves recording multiple neuro-
physiologic and respiratory parameters during a patient’s typical sleep period (often at night).
Data are recorded from several places on the body including the following:
electroencephalogram (EEG) or brain-wave activity
electrocardiogram (EKG) and pulse
facial muscle movement
leg muscle movement
respiratory effort (chest and abdominal wall excursion)
oxygen saturation and carbon dioxide output
With the NPSG information, the clinician can more easily pinpoint the causes of various sleep
disturbances and institute the appropriate treatment plan.
Before prescribing professionals consider medication, they should also determine if the
sleep problem is chronic or brief in nature. Having occasional sleepless nights might be due to
transient stress, poor sleeping environments, or lifestyle incompatibilities. Patients should be in-
structed in ways to improve their environments and make necessary lifestyle changes to reduce the
frequency and intensity of these episodes. Most professionals would probably agree that occa-
sional sleeplessness could be addressed with counseling or therapy sessions. If the patient is con-
cerned about taking a prescription sleep medication, the clinician can suggest over-the-counter
sleep aids such as Nidol, Sominex, Tylenol PM, or even Benadryl (brand of diphenhydramine).

BEHAVIORAL TECHNIQUES FOR TREATING SLEEP DISORDERS

Behavioral approaches such as relaxation training and biofeedback may be helpful in teaching
patients ways to manage their sleep disturbances. While these techniques typically take longer to
learn and do not offer immediate relief, they have been shown to have lasting effects that patients
can employ long after medications have been discontinued (Doghramji, 2003). Many profession-
als use these behavioral techniques along with various medications for both immediate and last-
ing relief. Research suggests that patients may not be aware that options like cognitive behavioral
therapy and relaxation training are effective and may work well alone or in conjunction with
medications (Neubauer, 2009). All patients with sleep disturbances should consider these sleep-
hygiene tips:
1. Reduce or eliminate the use of nicotine, alcohol, caffeine, or other stimulating substances,
except those suggested by a health care provider.
2. Try to maintain a regular sleep-wake cycle, that is, sleep and rise at the same time each day.
 Chapter 11 • Treatment of Sleep Disorders 85

3. Avoid napping during the day unless advised to do so.

4. Use the bed only for sleeping and sex, not for thinking, working, reading, or watching TV.
5. Try to relax and unwind an hour before going to bed.
6. Try not to go to bed hungry; a light snack is permissible an hour before bed.
7. If you cannot sleep, don’t lie there staring at the clock. Get up, read, watch TV, or engage
in a nonstimulating activity in another room until you are tired.
8. Often moderate exercise during the day, or light exercise, such as walking an hour or so be-
fore bed, helps you to feel tired and sleep better.
9. A warm bath before bed helps to relax sore muscles and induce sleep.
10. Make a list two hours before bed of all activities you need to accomplish the next day. This
prevents dwelling on them while you are trying to relax and sleep.
11. Counseling or psychotherapy helps identify issues and reduce stress associated with sleep
disturbances. Professionals can assist patients with coping skills and relaxation training.
12. Adjust temperature and noise and light levels in the room before you retire.

PHARMACOLOGY FOR SLEEP DISORDERS

Sedative-hypnotics are indicated in the treatment of most sleep disturbances. If the sleep disturbance
is intermittent or temporary, these agents can be used safely in the short run without much concern
for tolerance and dependence. If the patient appears to have a chronic problem, however, a careful
examination must be made by the professional to evaluate the efficacy of using these medications in
the long term, especially with patients who have a history of substance abuse or affective disorders.
Except where indicated, patients should not use these medications, especially the benzodiazepines,
for more than two to three weeks. Adequate evaluation and diagnosis should indicate the best course
of action, which may include a sleep study, physical examination, and psychotherapy if helpful.
Benzodiazepines such as alprazolam, triazolam, lorazepam, or diazepam should be used
sparingly and only by patients without a history of substance abuse. These medications have
been known to increase the risk of cognitive impairment and of slip/fall accidents in the elderly.
Newer medications have emerged in recent years that are safer overall and offer the prescriber al-
ternatives. See Table 11.1 for a list of medications used in the treatment of sleep disturbances.
In determining the best type of medication to use, half-life and onset of action are key points
to consider. Sedating antidepressants such as mirtazapine, nefazodone, or trazodone may be help-
ful, especially when the patient has an affective disorder (see Chapter 5). These medications
should be used primarily before bedtime to avoid daytime sleepiness. Trazodone Contramid (an
investigational formulation), an extended-release version of trazodone, has been found to improve
the quality of sleep for both depressed and nondepressed patients. It allows for the ease of once
per day dosing but may increase daytime dizziness and sleepiness (Sheehan et al., 2009). The
older tricyclic antidepressants can also be used, but most of these medications increase anticholin-
ergic side effects such as weight gain, daytime drowsiness, dizziness, and orthostatic hypotension
Benzodiazepine receptor agonists or BRAs have emerged in recent years as the mainstay
of sleep medications for the average patient. They are less likely to be abused when compared to
standard benzodiazepines. Zaleplon (Sonata) has a rapid onset, but may wear off before the pa-
tient has had adequate sleep. Zolpidem (Ambien and Ambien CR) is available as an immediate-
release or sustained-release formulas, allowing for the medication to be released throughout
the night. The CR version is less likely to cause the patient to awaken again during the night.
A sublingual formulation (Edluar) that has been shown to significantly reduce sleep onset time
in patients currently taking zolpidem tablets (Staner et al., 2010). Zolpimist, a zolpidem oral
86 Chapter 11 • Treatment of Sleep Disorders

TABLE 11.1 Medications Used in Treating Sleep Disturbances

Trade Name Generic Name Typical Dose Onset Of Action

Ambien, Edluar, Zolpimist zolpidem 5–10 Rapid
Benzodiazepines
Dalmane flurazepam 15–30 Rapid
Doral quazepam 7.5–15 Rapid
Halcion triazolam 0.125–0.25 Rapid
Prosom estazolam 2–4 Rapid
Restoril temazepam 15–30 Intermediate
Imidazopyridine
Nuvigil armodafinil 150–250 Intermediate
Other
Benadryl diphenhydramine 25–50 Intermediate
Desyrel, Oleptro trazodone 50–150 Intermediate
Lunesta eszopiclone 2–3 Rapid
Rozerem ramelteon 8 Rapid
Silenor doxepin 3–6 Intermediate
Xyrem gamma-hydroxybutyrate/ 4.5–9 g/night Rapid
sodium oxybate
Provigil modafinil 200–400 Intermediate
Pyrazolopyrimidine
Requip ropinirole 2–4 Rapid
Sonata zaleplon 10–20 Rapid

spray, is also available. Eszopiclone was approved by the FDA early in 2005 as a new treat-
ment for insomnia. This novel nonbenzodiazepine sleep aid marketed under the trade name of
Lunesta is indicated for patients with both initial insomnia and those who have trouble sleep-
ing through the night. Doses of 1–2 mg before bedtime are indicated for patients who have
trouble falling asleep, while higher doses of 2–3 mg are indicated for those with sleep mainte-
nance difficulty. The FDA approved eszopiclone for both short- and long-term treatment of in-
somnia because it may pose less of an abuse and tolerance risk. These drugs have been labeled
to indicate the possibility of rare, but troubling side effects that may include allergic reaction,
facial swelling, sleep driving, and night-time bouts of eating with no memory of the events
(Zammit, 2009).
Barbiturates such as amobarbital (Amytal), phenobarbital (Nembutal), and secobarbital
(Seconal) cause sedation and have been used to treat insomnia; however, they are not used much
today because they have a narrow therapeutic index, a high potential for abuse, and may interfere
with normal sleep cycles.
Melatonin is an endogenous chemical produced in the pineal glad. The levels of mela-
tonin fall with age and may be further depleted if the patient regularly uses aspirin or ibupro-
fen. Various studies have demonstrated that taking 0.5–3 mg/day of melatonin may reduce the
effects of insomnia due to jet lag and shift changes, but side effects include daytime drowsi-
ness, cognitive slowing, and possibly an increase in depression over time (Oxenkrug &
Requintina, 2003).
 Chapter 11 • Treatment of Sleep Disorders 87

Newer drugs such as a sustained-release formula of melatonin (Circadin) and a melatonin

receptor agonist ramelteon (Rozerem) have been developed in recent years. Sustained-release
formulas of melatonin and ramelteon have been shown to be efficacious in treating insomnia, es-
pecially phase shifts, jet lag, and sleep onset latency (Hardeland, 2009). Some research has sug-
gested that ramelteon may be an effective alternative to antidepressants in the treatment of
Generalized Anxiety Disorder (GAD); Gross, Nourse, & Wasser, 2009). Since these medications
are not benzodiazepines and carry no known risk of dependency, they may be a safer choice for
those with substance abuse concerns. Little research has been conducted about the safety of
long-term use of these sustained-release melatonin agonists and synthetic melatoninergic ago-
nists. Researchers caution against their use in children, adolescents, and in any patient who has
hepatic impairment, autoimmune disorders, or Parkinson’s disease or any patients taking drugs
like fluvoxamine, which utilizes the cytochrome P450 pathway in the liver, possibly increasing
circulating levels of melatonin and ramelteon (Hardeland, 2009; Neubauer, 2009). Sleep re-
searchers at Henry Ford Hospital Sleep Disorders Center in Detroit have conducted a 1-year
open-label study in the use of ramelteon. They concluded that it was well tolerated by patients
and improved their sleep onset. The researchers expressed some concern about its effect on en-
docrine functioning, however, noting a mild, transient increase in prolactin levels in women.
They noted no changes in other endocrine functions (Richardson & Wang-Weigand, 2009;
Richardson, Zammit, Wang-Weigand, & Zhang, 2009).
Diphenhydramine (Benadryl) or other antihistamine hypnotics may be used to reduce
problematic intermittent insomnia. A diphenhydramine dose of 25–50 mg/day is recommended,
but like most sleep medications, it should not be taken long term, as rebound insomnia may
occur. Anticholinergic side effects are of course probable with these medications.

HOLISTIC TREATMENTS
Various holistic remedies have mixed results. These remedies may include substances like kava,
which has been used by the peoples of the South Pacific for thousands of years. Its action is sim-
ilar to a sedative-hypnotic because it appears to bind at the GABA receptors. Animal studies
have shown that kava acts much like a benzodiazepine (Jullien, 2001). More recently, the FDA,
scientists, and others promoting holistic health have stated that kava may increase the risk of
liver damage with prolonged use.
Valerian or valerian root has historically been used as a mild sedative, anxiolytic, and anti-
depressant. Its action is not well understood, but since GABA itself is a component of valerian,
scientists and holistic advocates believe that valerian is a source of naturally occurring GABA.
However, since GABA crosses the blood-brain barrier poorly, valerian is an unlikely source of
GABA that would affect the central nervous system. Since valerian causes sedation, it should be
used with caution by those taking other sedating medications. Valerian contains quercitin, a sub-
stance that inhibits the liver cytochrome enzymatic pathway CYP1A2. This inhibiting action
could result in other significant drug interactions (Jullien, 2001; Tyler, 1993).
As with all sedative-hypnotic treatments, the clinician must take great caution to cor-
rectly identify the type and nature of a patient’s sleep difficulties. If medications are used, pa-
tients must be educated about typical side effects. Clinicians must use sedating medications
with caution when prescribing them for elderly patients who often become disoriented during
the night and might fall and injure themselves. Patients with a history of substance abuse
should be carefully screened for their potential to abuse stimulants and to use benzodi-
azepines excessively.
88 Chapter 11 • Treatment of Sleep Disorders

CASE VIGNETTE
Chapter Eleven
CLINICAL HISTORY
Lotus is a 36-year-old Asian-American female who recently started a new executive position with an advertising firm.
While she loves her new job and the field of advertising, she admits that the new schedule is grueling and she often
doesn’t get home until quite late. She has noticed that it is difficult for her to relax before getting to bed and her mind
often wanders to the many tasks she needs to complete when she returns to work in the morning. These “racing
thoughts” result in significant initial insomnia, causing her to be alert for nearly an hour or more before she is able to fall
asleep. When questioned about these symptoms, she claims that she has never seen a therapist before, doesn’t consider
herself to be anxious or depressed, and has never had a problem with sleeping in the past. There are no worries of money
or health-related issues, and she claims to enjoy her job and the people she works with. She even does not find these
thoughts unpleasant, as she uses the time to plan her next day. She admits they are just a bit intrusive and she really
needs to wind down and get more rest.

POSTCASE DISCUSSION AND DIAGNOSIS

While Lotus may have a case of Adjustment Disorder related to starting her new position, it is more likely that she is
just attempting to do well in her new duties and is a bit overly diligent. A complete physical, including a sleep study, is
suggested to rule out other physical causes. She agreed to limit or eliminate the use of any stimulants in her diet and
to follow sleep hygiene suggestions given to her by her family physician’s assistant (PA). Since there is no history of
mental illness in her family, and she denies feeling depressed or anxious, there is no reason to suggest a more serious
mental illness. While Asian-Americans often minimize their mental health symptoms, she is a third-generation female
who does not present with physical symptoms often seen in first-generation patients with depression or anxiety.

PSYCHOPHARMACOLOGICAL TREATMENT
Since Lotus has no positive history for substance abuse, benzodiazepines could be safely used in the short term;
however, it was decided that a benzodiazepine receptor agonist would be a safer choice. She was given 5 mg qhs of
zolpidem rather than the e extended-release formulation since her insomnia was limited to the first hour or so and
did not reoccur throughout the night. In a follow-up appointment with her PA she reported that her sleep had improved
dramatically, and she had more energy during the day. Her sleep study was unremarkable and her H&P results were
within normal limits. She agreed to follow up with a mental health professional should the symptoms return or
worsen in the future. Her PA agreed to prescribe the drug only for the next three weeks and if the symptoms persist
to reassess her condition to avoid any problems with potential drug tolerance or dependency.
12 TREATMENT OF PERSONALITY
DISORDERS

While there are technically no FDA-approved medications for treating personality disor-
ders, this chapter explores some common helpful medications or combinations of medica-
tions used in day-to-day practice for symptom reduction and control.
Topics to be addressed include the following:
• Use of medications for personality disorders
• Tailoring medications to symptom clusters
• Other considerations
• Case vignette

USE OF MEDICATIONS FOR PERSONALITY DISORDERS

Historically, psychotherapy has been the mainstay of treatment for Axis II syndromes, as
opposed to pharmacotherapy, which has been the primary therapeutic method for the major-
ity of Axis I disorders. Medication treatment for personality disorders is a fairly new phe-
nomenon in the field of psychopharmacology. Reich (2002) reports that epidemiological
studies have consistently estimated that 10% of the population of the United States has a
personality disorder. Other researchers have noted a prevalence rate for these disorders in the
general population of up to 23% (Sadock & Sadock, 2000). Clinicians once believed that the
use of medications in the treatment of personality disorders would be counterproductive be-
cause it would interfere with the psychotherapy. Today, both psychotherapy and psy-
chopharmacological treatments are important considerations and used together.
Most types of psychotherapy have been used in the treatment of personality disor-
ders. Each school of thought provides some understanding of behavior and method of in-
tervention; however, the different schools are not mutually exclusive because they tend to
overlap and complement one another. Numerous forms of psychotherapy have been tried,
including dynamic, behavioral, cognitive, supportive, and dialectical. As a rule, the best
way to approach these patients is to use combinations of various orientations. The empha-
sis should be on teamwork (i.e., doing something with the patient, not to the patient).
89
90 Chapter 12 • Treatment of Personality Disorders

For many years there was an assumption that Axis I disorders arose from “biological” pre-
dispositions and Axis II disorders from “environmental” issues. Research evidence suggests that
personality disorders are a biopsychosocial entity caused by complex interactions of psychoso-
cial and biological factors (New, Triebwassar, & Goodman, 2009). For example, Livesley (2000)
notes that twin studies indicate that personality disorder traits are genetically linked about 40%
to 60% of the time. The variance is accounted for by specific environmental factors. When re-
viewing available information on twin studies, adoption studies, twins reared apart, and molecu-
lar genetics, researchers found significant evidence that antisocial and aggressive behaviors have
genetic influences. Keep in mind that genetic processes need an environment in which to become
expressed. Environmental stressors may turn genetic influences on and off across the life span
(Raine, 2002). New et al. further state that genetic vulnerability appears to place individuals at
increased risks for the development of various personality disorders. According to Kaylor
(1999), impulsive and violent behavior may stem from brain dysfunction or damage secondary to
head trauma, toxic chemical substances, trace elements in hair, focal lesions of the temporal
lobe, low-serotonin levels, or other serotonergic dysfunction. Even neuroimaging studies have
demonstrated measurable differences in key frontal regions during the memory retention period
of a visuospatial working memory test with schizotypal personality disorder when compared to
normal controls (Koenigsberg et al., 2005). These complicated interactions between nature and
nurture will continue to be the focus of attention for many years to come.
Before considering pharmacotherapy for personality disorders, the clinician must obtain a
comprehensive assessment (see Chapter 4 for details). Obtaining a complete psychiatric and med-
ication history is not only important, but crucial. The focus is on targeting symptoms and their re-
sponse to the pharmacotherapy, rather than treating the diagnosis. With the patient’s permission, an
interview with family members would be helpful in making a personality disorder diagnosis. An
assessment of substance abuse or dependence is important and may mimic diagnostic symptoms of
a personality disorder. Comorbidity also exists with respect to chemical dependency and personal-
ity disorders in a subset of the population. Family history is also valuable and may suggest the
existence of biological vulnerabilities for mood disorders, drug and alcohol abuse, and perhaps
personality disorders. Furthermore, endocrine, neurological, rheumatological, and metabolic
disturbances may present as psychiatric illnesses, including personality or character disorders.
Medications prescribed for these medical conditions may have cognitive, behavioral, or affective
consequences. Laboratory evaluation, appropriate neuroimaging studies, and an electroencephalo-
gram (EEG) may be necessary in the evaluation to rule out confusing medical symptomatology.

TAILORING MEDICATIONS TO SYMPTOM CLUSTERS

First of all, clinicians need to know that the FDA has not approved any medications for use in per-
sonality disorders. With the exception of avoidant personality disorder, there are no specific drugs
for specific disorders. Then what are clinicians doing? They are basically treating comorbid Axis
I diagnoses and personality disorder traits. Their goal is to find medications that can appropriately
treat the individual array of symptoms with which a patient presents. Although combinations of
various classes of medications may be useful, clinicians should be cautious of polypharmacy.
Most experts define three different symptom clusters for personality disorders, which
prove to be useful. The clusters are as follows:
1. The paranoid, eccentric, thought disorder, dissociative cluster
2. The impulsive, depressive, angry, labile cluster
3. The anxious, inhibited, avoidant behavior cluster
 Chapter 12 • Treatment of Personality Disorders 91

This theoretical construct helps clinicians determine pharmacological treatment options.

The three categories generally correspond to the DSM-IV-TR Personality Disorder Clusters A, B,
and C. Each cluster will be considered and some recommendations for treatment will be made.
1. The paranoid, eccentric, thought disorder, dissociative cluster involves psychotic
symptoms and a thought disorder that are theoretically at the mild end of the spectrum.
Schizotypal personality disorder is a good example of this category. The treatment of choice
would be an atypical antipsychotic medication because of the mild psychotic symptoms. As
noted in Chapter 8, risperidone (Risperdal) is probably the best place to start; lower dosages
are preferred. Reich (2002) recommends using about one-quarter to one-half of the usual
dose that clinicians would use for other schizophrenia-related disorders. If the first antipsy-
chotic fails, the clinician should then try a second atypical agent like olanzepine (Zyprexa) or
quetiapine (Seroquel). Typical antipsychotics are not recommended because of the risk of tar-
dive dyskinesia.
2. The impulsive, depressive, angry, labile cluster corresponds to Cluster B in the DSM-
IV-TR. Impulsivity, aggression, mood lability, self-destructiveness, and suicidality are the main
symptoms in this group. Many patients in this cluster also report various somatic complaints.
Research has demonstrated the effectiveness and tolerability of duloxetine for borderline per-
sonality disorder patients who may also present with excessive impulsivity and somatic preoc-
cupation (Bellino, Paradiso, Bozzatello, & Bogetto, 2010). Although these symptoms are most
commonly found in borderline personality disorder, they may occur in other forms in the other
Cluster B diagnoses. For example, impulsivity and aggression in antisocial personality may
present as lying, stealing, and destruction of property. Patients with these symptoms have a
major disregard for social norms. In histrionic personality, low frustration tolerance would cor-
relate with this impulsivity and aggressiveness; narcissistic rage expressed in response to criti-
cism would be a good example in that disorder.
With respect to medications, an SSRI antidepressant would be the most logical place to
start; however, recent research suggests that mood stabilizers such as topiramate, lamotrigine,
and valproate, along with atypical antipsychotics like aripiprazole and olanzepine, would be bet-
ter choices for mood control than SSRIs (Lieb, Vollim, Rucker, Timmer, & Stoffers, 2010).
SSRIs, when used, should be titrated upward as tolerated to high doses, which are the doses used
in obsessive-compulsive disorder. If one SSRI fails, try another. If the patient has a partial re-
sponse to an SSRI, the clinician might consider augmenting with other medications such as atyp-
ical antipsychotics. Some clinicians may use gabapentin (Neurontin) for anxiety, impulsivity,
and sedation in these types of patients. They may use naltrexone (Revia), an opiate antagonist,
known to reduce self-harming behaviors when present. As noted previously, combinations of
medications may be the most useful.
3. The anxious, inhibited, avoidant behavior cluster may be manifested by shyness, dimin-
ished ability to function or use opportunities, rejection sensitivity, avoidant behaviors, and anxi-
ety. Initially, an SSRI would be the treatment of choice. A second SSRI should be tried if the first
one fails. With these patients, the clinician could consider a long-acting benzodiazepine such as
clonazepam (Klonopin) as an adjunctive treatment option. Other considerations for treatment
would be atypical antipsychotics, buspirone (Buspar), gabapentin, and perhaps beta-blockers.
Some clinicians still use MAOIs to help reduce isolative behaviors and rejection sensitivity.
However, their use has declined since the introduction of medications with safer side effect pro-
files. If patients have a history of substance abuse, remember to avoid benzodiazepines due to
their addictive nature.
92 Chapter 12 • Treatment of Personality Disorders

OTHER CONSIDERATIONS
The duration of medication treatment with personality disorders is debatable. Treatment trials should
last for at least four to six weeks to determine the drug’s effectiveness (i.e., adequate trial). Although
no patient should be on a medication longer than necessary, the clinician should be mindful that
character issues are long term and chronic. If a drug or combination of drugs improves the patient
symptomatically and has an acceptable level of side effects, long-term treatment can be justified.
Personality traits and disorders are best conceptualized on a continuum. Hopefully, future re-
search will illuminate the role of biological, psychological, and social factors in each personality
disorder. Clinicians may then focus on primary prevention rather than treating the chronic sequelae
of these illnesses.

CASE VIGNETTE
Chapter Twelve
CLINICAL HISTORY
Cindy is a 21-year-old white female. She has been recently released from a short hospital stay for self-mutilating behav-
ior and threatening suicide. While she managed to finish high school, she has attended more than six different colleges.
Her classes start off okay, but then she accuses her professors of not caring about her, and claims that her roommates
seem to hate her. If she meets and dates a young man, she quickly accuses him of cheating on her and she threatens to
kill herself to punish him. When questioned about her symptoms, she claims to be depressed and empty, yet her level of
anger reaches the point where she screams at others until she cries uncontrollably accusing everyone of abandoning her
in her hour of need. She attempted to get help at the university counseling center, but when she was placed in a therapy
group she dominated it and wouldn’t let others talk. When she was confronted by the other group members, she told
them all to “go to hell” and she walked out of the center never to return. She refused to call her psychologist back be-
cause she needed to punish her for not running after her when she left the session. Recently, she sought out another pri-
vate therapist, but when the therapist refused to allow her to call her cell phone whenever she felt angry or upset, she
“fired” the therapist and self-mutilated to feel better. History provided by her parents confirms that Cindy has been ex-
hibiting these behaviors for several years with little treatment success from her past therapists and psychiatrists.

POSTCASE DISCUSSION AND DIAGNOSIS

Cindy clearly has problems with Borderline Personality Disorder (301.83). She reports chronic feelings of emptiness and
anger. She also has a long history of arguing with her parents and siblings, claiming they do not understand or love her.
When it gets especially bad, she will stop talking to them for months on end. She has a history of self-mutilation and
suicidal ideation.

PSYCHOPHARMACOLOGICAL TREATMENT
While there are no FDA-approved medications for personality disorders per se, her psychiatrists have tried spot treatments
with various drugs without success. The main reason for this appeared to be poor compliance on the part of the patient.
Cindy agreed to see a new psychiatrist upon discharge from the hospital. At the urging of her family, she agreed to follow
her doctor’s medication orders and attend a DBT group conducted by a local therapist. She was prescribed Lamictal 25 mg
qd for the first week and increased 25 mg each week until she was taking 200 mg per day. After 8 weeks of Lamictal ther-
apy, her psychiatrist added 50 mg of naltrexone to control her urges to cut herself.
Upon follow-up with Cindy one month later, she reported less labile behavior, no cutting behaviors, and much
less depression. She was able to maintain herself at school and was attending the DBT group with regularity. While
she still had many personality issues to address in treatment, her behavior was much calmer and less labile.
13 TREATMENT OF CHEMICAL
DEPENDENCY AND CO-OCCURRING
CONDITIONS

This chapter looks at treatment considerations for people with co-occurring substance abuse
conditions. The dopamine hypothesis and relevant treatment issues are explored with help-
ful diagnostic instruments and pharmacological suggestions for each substance of concern.
Topics to be addressed include the following:
• Co-occurring conditions
• The dopamine hypothesis
• Treatment issues
• Assessment instruments and strategies
• Treatment phases and goals
• Psychopharmacology for dually diagnosed patients
• Summary and treatment reminders
• Case vignette

CO-OCCURRING CONDITIONS
In many patients presenting with various Axis I conditions, clinicians also observe the use
and abuse of various substances. These substances may include alcohol and various other
illegal drugs but may also include prescription medications. The use of a substance, even
to alter mood or the patient’s physical state, is not necessarily problematic unless patients
experience detrimental effects on their social and occupational functioning. Clinicians
should try to examine the nature and intensity of drug use to determine if patients are
compulsive in their use patterns and appear to have little control over the conditions and
amounts used. Here the clinician is concerned with the following issues:
1. Loss of control (cannot stop or limit drug use)
2. Tolerance, or the need to use more and more of the substance to avoid withdrawal or
to maintain a desired state
3. Impairment in functioning such as failure to work or keep other life obligations
93
94 Chapter 13 • Treatment of Chemical Dependency and Co-Occurring Conditions

The clinician needs to evaluate these issues even if the patient meets full criteria for a singular di-
agnosis of substance abuse or dependence per the DSM-IV-TR.
Research into the use patterns of patients with co-occurring conditions indicates that sub-
stance abuse is a problem for about 61% of those with bipolar disorder, 47% of those with schiz-
ophrenia, 39% of those with personality disorders, 33% of those with obsessive-compulsive dis-
order, and 32% of those with an affective disorder (Reiger et al., 1990). Additionally, about 50%
of bipolar patients seriously abuse alcohol at various points in their lifetime (Azorin et al., 2010).
It is not surprising then to learn that the majority of patients who have been treated for a sub-
stance abuse condition also meet criteria for another Axis I and/or Axis II diagnosis.
Although attempting to determine which condition came first may be nearly impossible, the
clinician who can obtain a good history from the patient or the family may be able to accomplish
this task. Current longitudinal research has suggested that chronic drinking may in fact lead to ma-
jor depression because the drinking behaviors were observed long before reports of a mood disor-
der (Fergusson et al., 2009). The clinician should consider these questions: In the absence of a fam-
ily or personal history of mental illness, did the patient develop depression after years of abusing
alcohol or drugs? After years of struggling with anxiety and panic, did the patient notice that drink-
ing had a calmative effect and reduced the number of panic attacks? Did the ADHD teenager start
abusing caffeine and speed once he noticed that it allowed him to relax and concentrate?
In patients with an existing Axis I and/or Axis II disorder, a co-occurring or dually occur-
ring substance abuse and mental illness disorder exists when the use of a substance exceeds so-
cial use. For these patients, treatment for chemical dependency or detoxification (detox) may be
needed. Determining the type and scope of treatment is based largely on the nature and intensity
of the presenting problems and the particular treatment philosophy employed in the treatment
setting. Researchers have long wondered how to improve patient compliance in substance abuse
treatment and increase sobriety. Some believe that increasing patients’ positive perceptions of
treatment and their level of alliance with their treating clinician are associated with more days of
abstinence (Ernst, Pettinati, Weiss, Donovan, & Longabaugh, 2008).
Some researchers believe that chemical addiction is not simply a direct effect of the drug on
the brain, but rather a pathological relationship that a person has with the drug (Schneider & Irons,
2001). Milkman & Sunderwirth (1987) found that drugs and behaviors can have addictive effects on
the brain. When people pursue gratification, they experience three basic types of neurochemical re-
sponses: arousal, satiation, or an increase in preoccupation of the desired object (fantasy). Arousal is
accompanied by an increase in dopamine and norepinephrine, satiation with GABA, and fantasy
with serotonin. Typically, people seeking arousal use drugs that increase arousal (cocaine or amphet-
amines), or they engage in high-risk behaviors such as gambling; both activities increase dopamine
and norepinephrine. A sedation and/or satiation response could be achieved with excessive food
consumption, television watching, video games, or drugs like benzodiazepines or alcohol. Fantasy is
often the core issue in sexual addiction. Researchers believe that when a person is addicted, the ad-
diction is in fact to a set of behaviors involving a drug or an activity. The behavioral activities them-
selves can produce chemical changes in the brain similar to those produced by any exogenous drug.

THE DOPAMINE HYPOTHESIS

Most drugs of abuse, including cigarettes, increase the concentration of dopamine in the nucleus
accumbens and the mesolimbic system (the brain’s reward centers). Overstimulation exhausts the
dopamine system and causes the brain to reduce both the amount of dopamine available and the re-
ceptor sites they bind with. Most abusers start out seeking the high that comes from drug use; later
 Chapter 13 • Treatment of Chemical Dependency and Co-Occurring Conditions 95

they use drugs to avoid withdrawal. In withdrawal they experience dysphoria and depression be-
cause of an increase in dopamine-3 receptor sites that are craving or looking for dopamine. Much
of the psychopharmacology used in the treatment of patients with co-occurring conditions attempts
to address depression, anxiety, and craving to increase the patient’s chances of a sustained recovery.

TREATMENT ISSUES
While most treatment centers (and the general public) adhere to a zero-tolerance model that em-
phasizes total abstinence, some researchers believe that the patient could learn harm-reduction
techniques leading to nonsymptomatic, responsible use (Marlatt & Witkiewitz, 2002). These re-
searchers cite empirical studies that demonstrate that harm-reduction approaches to alcohol are
at least as effective as abstinence-based treatment approaches in reducing alcohol consumption
and alcohol-related consequences.
As mentioned earlier, treatment centers tend to have their own unique philosophies about
detox and recovery. Some centers adhere to the traditional moral model, often utilizing some
type of 12-step approach. Others employ more of a rational-recovery viewpoint, assuming that
patients may not buy into a spiritual or religious reason for their use or recovery. Still other cen-
ters consider the disease model that assumes complete abstinence with no return to nonproblem-
atic or social use of any kind.
A good treatment center takes all modalities into consideration. It does not assume that the
patient is self-medicating an Axis I or II condition or that all of the patient’s behaviors are caused
by drug use. Neither does the center assume that all patients have chemically addicted brains and
can never use a drug again. The center treats both co-occurring issues together and watches to
see if after treatment a singular condition reemerges to be treated more aggressively.

ASSESSMENT INSTRUMENTS AND STRATEGIES

Many instruments can be used to assess client readiness for recovery and levels of resistance.
The Michigan Alcohol Screening Test (MAST) is a short, 24-item questionnaire in a yes/no for-
mat that detects the presence and extent of drinking. A shorter, 13-item version is also available.
The Substance Abuse Subtle Screening Inventory (SASSI-3) is a 67-item instrument that meas-
ures issues like openness, chemical dependency predisposition, and defensiveness. The
Substance Abuse Life Circumstance Evaluation (SALCE) contains 98 items and may be helpful
in identifying triggers for relapse, for example, the patient’s levels of stress. The MacAndrew
Alcoholism Scale of the MMPI-2 is helpful in identifying the potential for drug or alcohol abuse
in a patient. The Substance Abuse Problem Checklist consists of 377 items and examines prob-
lematic areas such as treatment motivation, health problems, personality issues, social relation-
ships, job problems, leisure issues, legal issues, and spirituality. This checklist is helpful in as-
sessing patients who have co-occurring personality disorders and social concerns.
For many clinicians who do not work in chemical dependency settings, substance abuse
screening is often determined simply from historical information. In this case, using the CAGE
questionnaire is helpful:
1. Have you ever felt that you should Cut down on your drinking (or drug use)?
2. Have people Annoyed you by criticizing your drinking (or drug use)?
3. Have you ever felt bad or Guilty about your drinking (or drug use)?
4. Have you ever had a drink (or used drugs) first thing in the morning (an Eye opener) to
steady your nerves or get rid of a hangover?
96 Chapter 13 • Treatment of Chemical Dependency and Co-Occurring Conditions

TREATMENT PHASES AND GOALS

In most treatment centers, treatment is achieved in a series of steps or phases of treatment. A typ-
ical first phase involves a complete assessment of the patient and his or her situation. Here the cli-
nician obtains the nature and patterns of drug use, as well as related emotions. A detailed history
is taken, including the types of drugs abused, dates of use, attempts at treatment, relevant legal or
medical problems, and the extent of financial hardships caused by the patient’s condition. In deter-
mining the nature of drug use, the clinician needs to inquire about the intensity and frequency of
the patient’s use of drugs. Patients who use drugs on a steady basis may exhibit more antisocial
tendencies; patients who are more like binge users are more likely to use drugs for self-medication
or social lubrication reasons. The clinician will find it helpful to interview spouses, partners, and
other family members to learn how they view the patient and his or her level of functioning.
In the second phase of treatment, the clinician attempts to determine the special needs of
the dually diagnosed patient. The following questions guide this effort.
1. Does the patient need medically supervised detox?
2. Does the patient need psychotropic medication or a psychiatric evaluation?
3. Does the patient need inpatient observation based on the patient’s behaviors or threats?
4. What is the patient’s level of resistance?
5. What is the patient’s potential for relapse?
6. What, if any, are the environmental issues that affect treatment (i.e., childcare, work, fi-
nances, spousal abuse, codependency, enabling issues, etc.)?
In the third phase of treatment, the clincian examines the need for using various medica-
tions in the treatment of the patient with co-occurring concerns. The clinician should carefully
weigh the use of psychotropic medications. In most cases only antidepressants and appropriate
antipsychotics should be considered. The use of pain medications and/or anxiolytics should be
avoided, except during the initial stages of detox and only when the clinician determines that
their use outweighs their risks (Sattar & Bhatia, 2003).

PSYCHOPHARMACOLOGY FOR DUALLY DIAGNOSED PATIENTS

This section describes medications and various other substances used in the treatment of dually di-
agnosed patients for alchohol, opioid, and cocaine dependence and other addictions. Table 13.1
lists the medications used to treat chemical dependency.

Alcohol Dependence
To date, only four agents are approved by the FDA for the treatment of alcohol abuse: disulfiram,
acamprosate (Campral), oral and once-monthly injectable naltrexone (Vivitrol). This section will
examine these four, as well as the novel uses of other medications used in the treatment of vari-
ous Axis I and Axis II conditions that now appear to show real promise in the treatment of sub-
stance abuse conditions.
1. Disulfiram (Antabuse) is used as a form of aversion therapy because it causes a very un-
pleasant chemical reaction when patients who use it drink alcohol. Typically, the enzyme acetalde-
hyde dehydrogenase converts acetaldehyde to harmless acetate, but disulfiram interferes with this
process and allows toxic acetaldehyde to accumulate when alcohol is consumed, causing nausea,
sweating, and rapid pulse. While not life-threatening to most patients, this medication is not indi-
cated for those who have serious health concerns or for cardiovascular patients. The typical dose is
 Chapter 13 • Treatment of Chemical Dependency and Co-Occurring Conditions 97

TABLE 13.1 Medications Used for Chemical Dependency

Trade Name Generic Name Typical Dose (mg/day) Type of Addiction

Antabuse disulfiram 125–500 Alcohol

Campral acamprosate 2000 Alcohol
Chantix varenicline 0.5–2 Nicotine
Dolophine methadone 20–200 Opioid
Kemstro/Lioresal baclofen 10–80 Alcohol
LAAM l-alpha-acetyl-methadol 20–80 (3X/WK) Opioid
Norpramin desipramine 150–300 Cocaine
Parlodel bromocryptine 2.5–15 Cocaine
Revex nalmefene 20–80 Alcohol
Revia naltrexone 50 Alcohol
Ritalin methylphenidate 15–60 Cocaine
Sanorex/Mazanor mazindol 1–3 Cocaine
Suboxone buprenorphine/naloxone 2–16 Opioid
Subutex buprenorphine 2–16 Opioid
Symmetrel amantadine 100–400 Cocaine
Topamax topiramate 25–300 Alcohol
Vivitrol naltrexone 380 mg/4 weeks Alcohol
Wellbutrin SR/Zyban bupropion 150–300 Nicotine
N/A ibogain 10–60 Cocaine

125–250 mg/day, but doses of up to 500 mg/day may be considered. The clinician should know that
this medication can stay in a patient’s system for several days after discontinuance, so drug holi-
days may still lead to chemical reactions in patients who “fall off the wagon.” For this reason, disul-
firam is most helpful for binge drinkers trying to maintain sobriety. While most patients tolerate
this medication without difficulty, some complain of mild gastrointestinal upset. The clinician
might suggest taking the medication with food to avoid these side effects.
Some treatment centers request that the medication be given by a family member to assure
compliance. When the medication is obtained from the pharmacy, the pharmacist will give the pa-
tient some other instructions. For example, if disulfiram is used with any alcohol-containing product
such as aftershave, mouthwash, or rubbing alcohol, unpleasant rashes or other side effects can result.
2. Naltrexone (Revia) mimics the action of naturally occurring opiate neurotransmitters in
the brain by acting as an opioid receptor antagonist. In animal studies, when opiate antagonists
are administered, the animals consumed less alcohol. In human studies, patients reduced their
levels of drinking and reported prolonged abstinence. The typical daily dose of naltrexone is
50 mg/day. Side effects may include sedation, nausea, and liver dysfunction. This medication is
not indicated for patients with compromised liver functioning because higher doses of naltrexone
have been associated with liver toxicity. This medication is best suited to patients who are early
in recovery and who are steady users. An extended-release injectable is now available (380 mg
given IM) and appears to demonstrate clinical efficacy by reducing drinking behaviors by about
49% in studies with chronic steady drinkers and by an overall increase in reported quality of life
(Lee et al., 2010; Pettinati, Gastfriend, Dong, Kranzler, & O’Malley, 2008).
98 Chapter 13 • Treatment of Chemical Dependency and Co-Occurring Conditions

3. Nalmefene (Revex), at the writing of this text, was not indicated for use with chemi-
cally dependent patients. However, the drug is FDA-approved for complete or partial reversal of
opioid drug effects (used primarily in the field of anesthesia) and for management of known or
suspected opioid overdose ( as in an emergency department). As with naltrexone, endogenous
opioid brain circuits are blocked, thus blocking the dopamine-mediated euphoria. Nalmefene is
a mu-opioid antagonist with fewer side effects and a longer half-life than naltrexone.
4. Acamprosate (Campral) was approved by the FDA in 2004 for use in patients with alco-
hol dependence. It has been used in Europe for many years. Although the mechanism of action is
unknown, researchers believe that acamprosate may facilitate the calming action of GABA at its
receptors, while inhibiting glutamate (an excitatory neurotransmitter). In fact, it may restore the
normal activity of glutamatergic neurotransmission altered by chronic alcohol exposure (Mason
& Heyser, 2010). Acamprosate may also reduce the hyperexcitability associated with alcohol
withdrawal and craving. The typical dose is approximately 2000 mg/day.
Other promising medications not approved by the FDA are currently being investigated as
treatments for conditions like alcoholism. Topiramate (Topamax) has been shown not only to re-
duce craving and withdrawal symptoms, but also to increase days of abstinence and overall qual-
ity of life for alcohol recovery patients (Johnson, 2007; Kenna, Lomastro, Schiesl, Leggio, &
Swift, 2009). Some research has shown it to be superior compared to naltrexone in terms of treat-
ment outcome and AA attendance (Baltieri, Daro, Ribeiro, & de Andrade, 2008). In addition to
topiramate, the muscle relaxant baclofen may also be helpful with some patients (Garbutt, 2009).
The use of benzodiazepines is typically reserved for detox settings and is not recom-
mended for maintenance because of the possibility of developing dependence. Some clinicians
find that SSRIs, such as fluoxetine (Prozac) or sertraline (Zoloft), are helpful and may reduce al-
cohol use, but only in patients with a co-occurring affective disorder. Some research suggests
that ondansetron (Zofran), which is used to reduce nausea for cancer patients in chemotherapy
and for bulimia nervosa patients, may help reduce the craving for both alcohol and methamphet-
amine (Psychopharmacology Update, 2003). While some clinicians have used trazodone for
sleep disturbance after alcohol detox, researchers caution that, despite a short-term improvement
of sleep quality, trazodone may lead to increased drinking behaviors when it is discontinued
(Friedmann et al., 2008).

Opioid Dependence
1. Methadone (Dolophine) is a synthetic opiate that is taken orally (liquid). It produces a
minimal high and sedation and has few side effects at therapeutic doses. While controversial,
methadone maintenance programs have helped many heroin users return to work and maintain
family obligations. Typical methadone doses range from 20 to 200 mg/day, depending on the
severity of the addiction.
2. L-alpha-acetyl-methadol or long-acting analog methadone (LAAM) has properties that
are similar to methadone, but it has been shown to be superior to methadone in reducing intra-
venous drug use. Since it has a slower onset of action and a longer half-life, it can be adminis-
tered only three times per week, rather than daily, as for methadone. Typical doses of LAAM
start at 20 mg three times per week and may go up to 80 mg three times per week. This medica-
tion may not be indicated for cardiac patients per FDA warnings.
3. Naloxone (Narcan) is used to reverse the effects of an opioid overdose. While medications
like naloxone act as antagonists and shorten the withdrawal period, they also intensify withdrawal.
 Chapter 13 • Treatment of Chemical Dependency and Co-Occurring Conditions 99

A procedure called ultrarapid detox uses naloxone in combination with clonidine or other seda-
tives for a 24-hour detoxification.
4. Buprenorphine (Subutex) is a mixed, opioid agonist–antagonist used as an analgesic. In
treatment centers, it is given sublingually at 2–4 mg/day and can be increased to 16 mg/day if
needed. Advantages of buprenorphine include a milder withdrawal upon discontinuance and less
potential for abuse because the agonist effects are diminished at higher doses. This medication is
also available as a mixed compound with buprenorphine called Suboxone (buprenorphine/nalox-
one), which has been shown to be more effective than clonidine as a medically supervised with-
drawal therapy. Also, because the naloxone part of the medication exerts no clinically significant
effect, the opioid agonist effects of buprenorphine predominate. This combination of drugs is
much less likely to be abused (Orman & Keating, 2009). It may also show promise as an emer-
gency treatment in cases of heroin overdose (Welsh, Sherman, & Tobin, 2008).

Cocaine Dependence
1. Tricyclic antidepressants like desipramine (Norpramin) have shown some promise in
reducing cravings and improving abstinence associated with cocaine abuse, even when depres-
sion is not present.
2. Bromocriptine (Parlodel), amantadine (Symmetrel), and mazindol (Sanorex/Mazanor)
are dopamine agonists given to reduce craving and discomfort in the early stages of cocaine
withdrawal.
3. Ibogain is derived from the root of the African iboga shrub. This botanical substance is
an indole alkaloid that helps to mask cocaine and opioid withdrawal, but it is a potent hallucino-
gen with potential for abuse. Ibogain was shown to reduce stimulant use in lab animals. It may
have some promise as a treatment for stimulant abuse as well (Jullien, 2001). Typical doses range
from 10 to 60 mg/day.
4. Methylphenidate (Ritalin) has been shown to reduce cocaine relapse, especially in patients
with ADHD. Typical doses range from 15 to 60 mg/day (see Chapter 9 for details regarding its use).
Methylphenidate and disulfiram show promise as potential treatments, but the effectiveness is opti-
mized depending on genetic polymorphisms in patients ( Haile, Kosten, & Kosten, 2009).
5. Buprenorphine (Subutex) is a mixed, opioid agonist–antagonist used as an analgesic. In
treatment centers, it is given sublingually at 2–4 mg/day and can be increased to 16 mg/day if
needed. Advantages of buprenorphine include a milder withdrawal upon discontinuance and less
potential for abuse because the agonist effects are diminished at higher doses.

Other Types of Addiction

Bupropion (Wellbutrin SR/Zyban) has been approved by the FDA for the treatment of nicotine
addiction. It has been shown to be more effective than nicotine replacement gums or patches in
reducing relapse in smokers (Williams & Hughes, 2003). This result was found to be especially
true when a co-occurring depression was present. Nicotine dependence has a high comorbidity,
not only with depression but also with conduct disorder and ADHD. The newer drug varenicline
(Chantix) has been shown to be twice as effective as sustained-release bupropion, mainly be-
cause it actually binds with neuronal nicotinic acetylcholine receptors; thus, nicotine is blocked
and cannot activate receptors. It further binds with moderate affinity to the 5HT3 receptor (a
pleasure receptor), resulting in a reduction of nicotine as a reinforcer (Tobin, 2007). Tobin cautions
100 Chapter 13 • Treatment of Chemical Dependency and Co-Occurring Conditions

about using this medication with patients presenting with mood disorders even though it is not
metabolized by the cytrochrome P450 system typically utilized by some antidepressants.
Changes in mood and behavior have been reported in patients and should be noted when the
medication is taken for the first time.
Because SSRIs often reduce sexual appetite, they may offer some hope to people with sex-
ual addiction and compulsivity. Sexual addiction disorders often coexist with chemical depend-
ency and frequently trigger relapse (Schneider & Irons, 2001). This research also mentions that
as many as 70% of cocaine addicts are also sexually addicted, and as many as 76% of metham-
phetamine users consider themselves to be “sexually obsessed.”

SUMMARY AND TREATMENT REMINDERS

In the fourth or final phase of treatment, the clinician assesses the patient’s progress and the need
for more attention to either the substance abuse issue or the mental health issue. Clinicians must
keep in mind that when treating the primary mental health diagnosis with medications, they must
not compromise the patient’s chemical dependency issues (i.e., treating an anxiety disorder with
benzodiazepines in a patient with a history of alcohol dependence). In this situation, the clinician
is likely to see abuse of the benzodiazepines. Another common example is the anxious patient
who is trying to remain substance-free and presents with a chief complaint of initial insomnia.
The patient’s physician gives the patient a sedative-hypnotic as a sleep aid only to learn months
later that the patient has become dependent on them.
Clinicians also need to be sensitive with respect to patients whom they refer to Alcoholics
Anonymous (AA) and Narcotics Anonymous (NA) groups. Most of these groups have little tol-
erance for people with co-occurring conditions and are likely to hassle them for taking “other
drugs” for their condition. The clinician needs to inquire about the group’s composition and send
patients only to groups that are sensitive to the medication issues.
Preventing a patient’s relapse is the key to continued success, and reducing stress is the key
to preventing relapse. “Booster” sessions and stress-reduction groups are excellent ideas. While
relapse tends to happen in about 50% of all cases, clinicians should have a clear plan for resum-
ing treatment without a heavy emphasis on failure so that patients can rework their program
without shame and to strive for full recovery.

CASE VIGNETTE
Chapter Thirteen
CLINICAL HISTORY
Reggie is a 42-year-old African-American male recently referred for outpatient psychotherapy by his PCP. While he is in
relatively good health, he admitted to his doctor that he has been drinking alcohol excessively again over the last three
months. Reggie had a problem with alcohol when he was in his twenties, but with the help of AA and his first male
partner, was able to cease drinking for the last 19 years. Reggie admits that it has not always been easy for him to ab-
stain, but he is committed to trying again. He has attended AA meetings, but has not been able to maintain complete
sobriety. On average, he has 1 or 2 drinks nearly every evening. His partner Bob has a zero-tolerance policy for Reggie’s
drinking and has moved in with a friend rather than deal with Reggie’s promises to stop. Reggie is worried that Bob may
not come back. Reggie does not want to end up like his father, who drank himself to death at the age of 56. His father
 Chapter 13 • Treatment of Chemical Dependency and Co-Occurring Conditions 101

and mother divorced when Reggie was only 15. Reggie’s only sister had a serious addition to benzodiazepines and
spent 28 days in a rehab center. She is clean now, but also abuses alcohol on occasion.

POSTCASE DISCUSSION AND DIAGNOSIS

Reggie has Alcohol Dependence in sustained partial remission (305.00) He clearly shows signs of dependence and abuse as
he continues to use alcohol despite the effect it is having on his relationship. He admits that coworkers have commented on
his being late to work and that they have noticed alcohol on his breath. He has now taken to chewing gum to mask his alco-
holic breath and working longer hours to justify his lateness in the morning.

PSYCHOPHARMACOLOGICAL TREATMENT
At the urging of his family doctor and friends, Reggie has agreed to attend 90 meetings in 90 days. He now attends
only gay AA meetings, so he can feel more comfortable sharing aspects of his relationship with Bob without strange
looks or criticism. Reggie also agreed to try Campral at the suggestion of his doctor. Reggie typically dislikes taking
any medications, so his dose was started low (1000 mg qd). His dose was slowly raised to 2000 per day, and he re-
ported that he was tolerating it without side effects. While Reggie did not immediately crease drinking, by the end of
the first week he reported a tremendous drop in both the interest of alcohol and the enjoyment of drinking while
engaging in drinking. He thought at first that he was losing interest in drinking whiskey, so he switched to beer. He
later lost interest in beer and reported several days without alcohol. In a follow-up appointment with his PCP after six
weeks on the medication, he reported he celebrated 30 days sober and was on his way to the meeting to get his
30-day chip. While he admits he has a long road to a sustained recovery, he believes that Campral has helped him
take the first serious steps and, with Bob’s forgiveness, he is taking one day at a time.
 14 TREATMENT OF COMORBIDITY
AND OTHER DISORDERS

This chapter examines the often complex role of comorbid conditions. All clinicians deal
with patients who present with issues such as chronic pain, eating disorders and obesity,
and, of course, disorders of impulse control, but few suggestions for treatment are pre-
sented in most psychopharmacology texts. Helpful pharmacological considerations are
presented here with a rationale for reducing symptoms.
Topics to be addressed include the following:
• Medical and psychiatric cormorbidity
• Chronic neuropathic pain
• Eating disorders and obesity
• Impulse control disorders
• Case vignette
Psychiatric disorders exist in real life, not in an isolated system, but rather within the con-
text of other serious medical and psychiatric diagnoses. Besides looking at the various medical
and psychiatric comorbidities, in this chapter we consider other important psychiatric issues in-
cluding chronic pain, eating disorders, obesity, and impulse control disorders. Frequently, these
diseases co-occur with multiple other medical illnesses. The common features that bind these
topics together are the complexity and sometimes the resistant nature of their treatment.
According to Kroenke (2003), unexplained or multiple somatic symptoms are the leading
cause of outpatient medical visits and also the predominant reason patients with common men-
tal disorders, such as anxiety and depression, initially present themselves in primary care.

MEDICAL AND PSYCHIATRIC COMORBIDITY

The complicated interaction between the mind and body may lead to disease processes
that are more difficult to treat than individual illnesses themselves. According to Blazer,
Steffens, & Busse (2004), depression has been shown to be a risk factor for declines in
physical functioning; likewise, declines in physical functioning have been shown to be a
102
 Chapter 14 • Treatment of Comorbidity and Other Disorders 103

risk factor for depression. Attention to psychiatric symptoms among medically ill patients has
emerged in general medical settings over the last ten years or so. Kroenke (2003) reports that pa-
tients have at least a twofold greater risk of experiencing a depressive or anxiety disorder if they
have a concomitant disease including cardiovascular disease, neurological disease, cancer, dia-
betes, HIV, and many other physical disorders. Psychiatric comorbidities are important factors
that may increase the length of acute medical/surgical inpatient stays, the frequency of medical
complications, and the overall mortality (Sadock & Sadock, 2000). Larsen & Christenfeld
(2009) suggest that the high comorbidity between cardiovascular disease and psychiatric disor-
ders may be attributable to a general state of inflexibility (cognitive, emotional, or physiologi-
cal), leading to rumination, worry, obsessions, low heart rate variability and vagal tone, and ex-
tended sympathetic arousal.
Depression often co-occurs with a variety of psychiatric and substance abuse/dependence
disorders. In co-occurrence, the presence of both illnesses is frequently unrecognized and, unfor-
tunately, leads to serious and unnecessary negative consequences for patients and families.
According to Kupfer & Frank (2003), concurrent depression is present in 13% of patients with
panic disorder. With respect to eating disorders, 50% to 75% of patients suffering from anorexia
nervosa or bulimia nervosa have a lifetime history of major depressive disorder. These high lev-
els of comorbid diagnoses with depression are also true for substance abuse disorders (see
Chapter 13). When Axis II disorders are considered, dysfunctional personality traits have a neg-
ative effect on the outcome of treatment of Axis I disorders (Reich, 2003).
When looking at concurrent medical disease, Lesperance, Frasure-Smith, & Talajic
(1996) demonstrated that 40% to 65% of patients who have experienced a myocardial infarc-
tion suffer from depression. The point prevalence of major depression in patients with coro-
nary artery disease is estimated at 17% to 22%; this prevalence is roughly twice that in primary
care patients and three to four times the point prevalence in the population at large (Sadock &
Sadock, 2000). In general practice, cancer patients suffer from depression about 25% of the
time according to many experts. In patients with neurological diseases (e.g., stroke), re-
searchers suggest that depression occurs in about 25% of cases. . Morbidity and mortality con-
tinue to increase in connection with the number of medical and/or psychiatric diagnoses
(Kupfer & Frank, 2003).
Even in the medical-psychiatric comorbidity context, the treatment of the particular psy-
chiatric diagnosis is very similar to the treatment of the psychiatric problem alone. For example,
depression either alone or in the context of a comorbid medical condition should be treated sim-
ilarly. However, the clinician should use the lowest possible medication dose to treat the disorder,
especially when treating multiple conditions with many different pharmacotherapies.
Communication between the various prescribers treating the patient’s co-occurring conditions is
of utmost importance.
The field of psychosomatic medicine is a rapidly evolving and increasingly important
area of study. For example, psycho-oncology is a recognized field in which mental health pro-
fessionals provide consultative services to support cancer patients and their families at all stages
of disease, including cancer survivorship (Breitbart & Alici, 2009). Psychoneuroimmunology is
another emerging interdisciplinary science that examines the impact of behavior and psycho-
logical states on immunity. Biobehavioral factors that show robust associations with markers of
inflammation include variables such as diet, smoking, coffee consumption, alcohol consump-
tion, exercise, and sleep disruption (O’Connor & Irwin, 2010). Other current fields of study
related to comorbidity include psychocardiology, psychoneuroendocrinology, and functional
gastrointestinal disorders.
104 Chapter 14 • Treatment of Comorbidity and Other Disorders

CHRONIC NEUROPATHIC PAIN

According to the International Association for the Study of Pain, pain is an unpleasant sensory
and emotional experience associated with actual or potential tissue damage (Merskey, 1979).
The emotional dimension of pain was even noted by Freud in the 1890s (Strachey, 1953). Since
pain is neither a purely physiological state nor a purely psychological one, treatment demands a
comprehensive, integrated, multidisciplinary plan, as well as clear communication of all findings
to the patient. More recently, neuropathic pain has been redefined as “pain arising as a direct
consequence of a lesion or disease affecting the somtosensory system” (Treede et al., 2008,
p. 1630). Keep in mind that neuropathic pain can adversely affect patients’ overall quality of life,
including physical and emotional functioning, and it is associated with substantial societal costs
(O’Connor, 2009). The clinician must keep in mind that there is no typical pain patient; individu-
alized treatment is absolutely necessary. Although there are many types of peripheral and central
neuropathic pain, postherpetic neuralgia and diabetic peripheral neuropathy are the most com-
mon types studied.
Evidence-based guidelines for the pharmacological treatment of chronic neuropathic pain
have been published. First-line treatments include tricyclic antidepressants, dual reuptake in-
hibitors of serotonin and norepinephrine, calcium channel alpha2-delta ligands (such as
gabapentin and pregabalin), and topical lidocaine. Opioid analgesics and tramadol are recom-
mended as second-line treatments that can be considered for initial use in certain clinical circum-
stances. Although some of these treatment options are not psychopharmacologic, they are in-
cluded for completeness (Dworkin et. al., 2010).
Although many chronic pain patients resist psychiatric help, a formal psychiatric consul-
tation is important to clarify the medical diagnoses, screen for psychiatric diagnoses, and iden-
tify emotional influences that underlie or exacerbate primary pain. Chronic pain may be a pre-
senting symptom of many of the following psychiatric diagnoses: major depression,
generalized anxiety disorder, panic disorder, posttraumatic stress disorder, and substance
abuse. Other less common psychiatric diagnoses that may be present in the context of chronic
pain include delusional disorders, chronic psychosis, somatoform disorders, and malingering.
Over 75% of depressed patients report chronic pain issues (Delgado, 2006). Sansone &
Sansone (2008) indicate that patients with pain have a substantially increased risk for depres-
sion, from 2 to 5 times that of the general population. Furthermore, emotional influences that
may affect the experience of pain include unresolved grief; sexual or developmental conflicts;
sexual, physical, or emotional abuse; anger at physicians; and even symbolic identification
with a loved one (Mufson, 1999).
Chronic pain conditions such as fibromyalgia are especially difficult to treat. Fibromyalgia
is different than most other rheumatologic disorders in that it is not due to tissue damage or in-
flammation per se (Spaeth & Briley, 2009). In addition to widespread pain, patients also experi-
ence fatigue, cognitive, and sleep disturbances. Many of these patients also present with depres-
sion and, increasingly often, with anxiety (Arnold, Crofford, Martin, Young, & Sharma, 2007).
Most researchers agree that no one medication best addresses the pain and accompanying mood
concerns, but antidepressants are becoming increasing effective with this group of patients.
While the older TCAs have been shown to be effective, the newer dual-action (serotonin/norepi-
nephrine) inhibitors have been shown to be as effective, without the typical anti-cholinergic side
effects (McCleane, 2008; Spaeth & Briley, 2009). In fact, medications like duloxetine and mil-
nacipran may soon become the new standard for chronic pain treatment whether it is associated
with depression or not (Delgado, 2006). Dual-action medications like venlafaxine, duloxetine,
 Chapter 14 • Treatment of Comorbidity and Other Disorders 105

and milnacipran may be more efficacious because norepinephrine and serotonin are two key neu-
rotransmitters in the pain modulation pathway from the basil ganglia. Medications that combine
serotonergic and noradrenergic reuptake inhibition may have stronger analgesic effects than
agents that inhibit reuptake of either neurotransmitter alone (Mease, 2009). In addition to antide-
pressants, pregabalin (Lyrica), a calcium channel alpha2-delta ligand, and tramadol (an opioid)
are used for pain management in patients with fibromyalgia and neuropathic pain.
From the psychiatric perspective, the treatment of chronic pain and its emotional compo-
nents relies on medications and various forms of psychotherapy. Antidepressants are probably
the most prescribed group of medications because of their effect on improving mood and de-
creasing anxiety. Tricyclic antidepressents are still widely used in this context, not only for the
reasons already mentioned (see Chapter 5), but also for their noradrenergic effects that decrease
neuropathic pain. Many pain physicians use amitriptyline (Elavil) in a 25 mg dose at bedtime to
help decrease pain, improve sleep, and possibly improve mood. As a class, the SNRIs (serotonin-
norepinephrine reuptake inhibitors), such as venlafaxine/desvenlafaxine (Effexor/Pristiq) and
duloxetine (Cymbalta), may be more effective than SSRIs in decreasing the somatic symptoms
associated with depression and anxiety syndromes (Grothe, Scheckner, & Albano, 2004).
Finally, Bischofs, Zelenka, & Sommer (2004) report that topiramate (Topamax), an anticonvul-
sant mood stabilizer, decreases neuropathic pain and improves mood lability.
Psychotherapeutic options for chronic pain patients include individual, marital, and family
therapy to address the underlying dynamic factors. Cognitive behavioral therapy, hypnosis, and
biofeedback are probably the most useful and most practical ways to approach these complicated
and challenging patients.

EATING DISORDERS AND OBESITY

The eating disorders are a complex group of illnesses that are heavily underpinned by psy-
chopathology and are associated with significant medical consequences. These disorders prima-
rily affect young women. Patients who suffer from anorexia nervosa and bulimia nervosa place
extraordinary emphasis on weight, shape, and the pursuit of thinness. Most recently, binge-
eating disorder, which is characterized by episodes of uncontrollable eating, has emerged as a di-
agnostic entity. Patients with eating disorders tend to have high rates of psychiatric comorbidity
and medical complications (Pederson, Roerig, & Mitchell, 2003). Interestingly, recent data indi-
cate the majority of people with eating disorders are classified under “eating disorder not other-
wise specified” (EDNOS) category, similar to other psychiatric diagnoses including personality
disorders, dissociative disorders, and somatoform disorders (Thomas et al., 2009). Furthermore,
obesity is discussed because of the prominent nature it plays in one’s self-concept, as well as so-
cietal views of beauty and attractiveness.

Anorexia Nervosa
Anorexia nervosa is characterized by patients’ refusal to maintain a normal body weight, along
with their intense fear of gaining weight despite being underweight. According to Pederson,
Roerig, & Mitchell (2003), the disorder can lead to serious medical consequences including os-
teoporosis, cardiac arrhythmias, and congestive heart failure. The estimates of comorbidity rates
in eating disorder patients indicate that 50% to 75% of patients have comorbid depression, ap-
proximately 25% of patients have obsessive-compulsive disorder, and 42% to 75% of patients
have a personality disorder (APA website, 2004).
106 Chapter 14 • Treatment of Comorbidity and Other Disorders

Anorexia nervosa has two distinct phases of the illness: the acute, underweight phase (usu-
ally inpatient) and the maintenance, weight-restored phase (usually outpatient). The two phases
basically represent different biological entities in that the treatment options differ. In the acute
phase of treatment with patients close to emaciation, the treatment plan largely focuses on inpa-
tient care, medically supervised refeeding programs, dietary counseling, and individual, group,
and family therapies. Medications play a more significant role in the maintenance, weight-re-
stored phase of treatment. Although anorexia nervosa was defined as a diagnostic entity over a
century ago, the absolute etiology underlying the disorder remains elusive (Mitchell Pederson
et.al, 2003; Mitchell, de Zwaan, & Roerig, 2003).
A large variety of compounds have been explored in treating anorexia nervosa including
antidepressants, antipsychotics, antihistamines, narcotic antagonists, lithium, and zinc, to name
a few. To date, there are, however, no FDA-approved medications for anorexia nervosa
(Jackson, Cates, & Lorenz 2010). Controlled medication trials in patients with anorexia nervosa
are few in number; thus, optimal treatment has yet to be defined. Research has predominately
focused on two drug groups: antidepressants and antipsychotics. Trials of TCAs and fluoxetine
(Prozac) have not been shown to offer much benefit for the acute treatment phase. However, a
controlled outpatient maintenance trial suggests that patients randomized to fluoxetine gained
more weight, had decreased core eating-disorder symptoms, and displayed more improvement
in mood symptoms compared with the placebo group at the one-year endpoint (Kaye, Nagata,
& Weltzin, 2001). Both in terms of stimulating weight gain and in reducing delusional thoughts
about food, weight, and shape, pilot studies and case reports have described successful use of
atypical antipsychotics such as olanzepine (Zyprexa) and risperidone (Risperdal) in anorexia
nervosa patients.
A summary of research conducted on the use of medication for anorexia nervosa before
September 2009 appears to conclude that while atypical antipsychotics have been used with this
treatment group, only mild evidence of improvement in depression, anxiety, and core eating-dis-
ordered psychopathology was found. As a whole, there is insufficient evidence to confirm that
atypical antipsychotics enhance weight gain (McKnight & Park, 2010).

Bulimia Nervosa
In contrast to anorexia nervosa, which is relatively rare, bulimia nervosa is more prevalent and
affects about 1% to 3% of adolescent and young adult females. Bulimia nervosa patients place
great emphasis on body weight and shape, but unlike anorexia nervosa patients, they usually fall
within a normal weight range. This disorder is characterized by binge-eating episodes and asso-
ciated inappropriate compensatory behaviors aimed at preventing weight gain. Medical conse-
quences of bulimia nervosa include dental complications (permanent loss of tooth enamel, in-
creased frequency of caries, and parotid gland swelling), amenorrhea, electrolyte abnormalities,
esophageal tears, gastric rupture, and cardiac arrhythmias. The last three medical conditions may
be fatal. As with anorexia nervosa, bulimia nervosa patients have high rates of comorbid psy-
chopathology: about 50% have a lifetime diagnosis of depression, about 25% have a lifetime di-
agnosis of substance abuse or dependence, and about 40% have a personality disorder (Agras,
2001). The cause of bulimia is uncertain, but mounting evidence suggests that genetic factors
play an important role (Bulik, Devlin, & Bacanu, 2003). Disturbances in serotonergic systems
may play a role in causing bulimia because of the involvement of serotonin in the regulation of
food intake. Cultural attitudes toward standards of physical attractiveness are also believed to be
contributing causes (Mehler, 2003).
 Chapter 14 • Treatment of Comorbidity and Other Disorders 107

Bulimia nervosa has been more extensively studied than anorexia. Pharmacotherapy with
antidepressants results in significant reductions in target eating behaviors such as binge eating
and vomiting and associated mood or anxiety disorders. The only FDA-approved treatment for
bulimia nervosa is fluoxetine (Prozac) in the dosage range of 60–80 mg/day. Furthermore, stud-
ies have consistently shown that cognitive behavioral therapy (CBT) is the first-line treatment of
choice when it is available. Although CBT alone is superior to medication treatment alone, most
experts would consider the use of CBT plus an antidepressant to be more effective than either
treatment alone (Mitchell, Peterson, Myers, & Wonderlich, 2001). Other medications studied
that may be useful in treating bulimia include odansetron (Zofran), a 5-HT3 antagonist, and top-
iramate (Topamax), an anticonvulsant mood stabilizer. Topiramate appears to have efficacy in
bulimia nervosa as demonstrated by two placebo-controlled studies (McElroy et al., 2009).
Further studies involving nonantidepressants are needed to establish efficacy.

Binge-Eating Disorder
Finally, binge-eating disorder (BED) is characterized by binge-eating patterns similar to bulimic
patients without compensatory weight-loss behaviors such as purging episodes or overexercis-
ing. The estimated prevalence of BED is 1.5% to 2% in the general population. When looking at
obese populations such as those seeking weight-loss assistance programs, the prevalence of BED
increases to 8% to 19% (Devlin, 2002). In bariatric surgery programs, Wadden, Sarwer, and
Womble (2001) report that approximately 25% of the individuals may have BED.
Treatment efforts for BED have included TCAs, SSRIs, anticonvulsants, and antiobesity
medications. Unlike the information available for bulimia nervosa, pharmacological data for treat-
ment of BED are much more preliminary. Cognitive behavioral therapy appears to be more effica-
cious than SSRIs in about half of the controlled trials. More recently, research has focused on top-
iramate (Topamax) and sibutramine (Meridia) as future possibilities for decreasing the
psychopathology and promoting weight loss (Pederson et al. 2003). Sibutramine (Meridia) is an
SNRI like venlafaxine (Effexor) and duloxetine (Cymbalta). According to Tziomalos, Krassas, &
Tzotzas (2009), three placebo-controlled studies have shown sibutramine to reduce body weight
and the frequency of binge-eating episodes more than placebo. Topiramate has shown positive re-
sults in three placebo-controlled trials while zonisamide (Zonegran) indicated positive results in
one small controlled study in binge-eating disorder with obesity (McElroy et al., 2009).

Obesity
Obesity is another prevalent disease that affects over 60 million Americans today. Approximately
64% of adult Americans are categorized as being overweight (body mass index [BMI] of 25–29.9
kg/m2) or obese (BMI more than 30 kg/m2). Obesity is associated with increased mortality and
comorbidities such as hypertension, hyperglycemia, dyslipidemia, coronary artery disease, and
certain cancers. The suggested goal for weight loss is to achieve a 10% weight reduction in six
months through lifestyle changes. If lifestyle changes alone are not effective, then pharmacother-
apy may be indicated (American Obesity Association website, 2004).
Over the last few years, fenfluramine (Pondimin), dexfenfluramine (Redux), and phenyl-
propanolamine (an ingredient in over-the-counter nasal decongestants and weight-control
drugs) have been withdrawn by the FDA because of severe adverse effects. The only medica-
tions approved by the FDA as anorectics are the following: phentermine (Adipex-P/Ionamin),
sibutramine (Meridia), and orlistat (Xenical). According to Campbell & Mathys (2001), phen-
termine has been shown to cause 5% to 15% weight loss if given daily or intermittently. The
108 Chapter 14 • Treatment of Comorbidity and Other Disorders

limiting factor with this medication is that it is approved only for short-term use, and tolerance
often develops.
Sibutramine acts as an SNRI and increases both norepinephrine and serotonin levels.
However, it should not be prescribed with most antidepressants because of the risk of increased
norepinephrine and serotonin levels. In patients with cardiovascular disease, sibutramine is con-
traindicated due to the possibility of hypertension and tachycardia. Orlistat (Xenical) works as a
reversible inhibitor of lipases in the gastrointestinal tract; these inactivated enzymes are unavail-
able to hydrolyze dietary fat, and thus the fats are not absorbed. Orlistat has an advantage over
the other medications in that it is not absorbed systemically, and it may have cholesterol-lowering
effects in some patients. Unfortunately, orlistat is less desirable in some patients due to the high
incidence of gastrointestinal side effects, and it must be given three times daily with meals. As
the only medications currently approved for long-term treatment of obesity, sibutramine and orli-
stat should be prescribed only in combination with lifestyle changes (Rao, 2010).
Other antiobesity drugs are being studied, including, but not limited to, nutrients, neuropep-
tides, mazindol (Sanorex/Mazanor), antidepressants, anticonvulsants, growth hormone fragments,
and so on. Due to the brevity of the discussion here, other treatments options have not been ex-
plored but include dietary therapy, physical activity, behavioral therapy, combination therapy, and
even bariatric surgery. The five A’s behavioral counseling paradigm (ask, advise, assess, assist,
and arrange) can be used as the basis for a systematic, practical approach to the management of
obesity that incorporates evidence for managing common obesity-related behaviors (Rao, 2010).

IMPULSE CONTROL DISORDERS

The impulse control disorders are characterized by the failure to resist an impulse, drive, or
temptation to perform some act that is harmful to the patient or others. In most cases, the patient
senses increasing tension or arousal prior to the act and experiences pleasure, gratification, or re-
lief during or following the act. These disorders include kleptomania, pathological gambling, tri-
chotillomania, pyromania, intermittent-explosive disorder, and the residual not otherwise speci-
fied category. Potential diagnoses such as compulsive buying and self-mutilation are appropriate
examples of this NOS category. Some researchers have proposed that these disorders of impulses
be more specifically called obsessive-compulsive spectrum disorders (OCSD), which include
body dysmorphic disorder, hypochondriasis, onychophagia (nail biting), psychogenic excoria-
tion (repetitive, compulsive scratching), compulsive buying, problematic Internet use, eating dis-
orders, dissociative disorders, and some neurological disorders (e.g., Tourette’s disorder).
Cognitive behavioral strategies have generally shown evidence for first-line treatment
across OCSD, with some variability in degree of benefit (Ravindran, da Silva, Ravindran,
Richter, & Rector, 2009). In addition, successful psychopharmacological interventions have
been described throughout the literature. When treating kleptomania, various serotonergic anti-
depressants including fluvoxamine (Luvox), fluoxetine (Prozac), clomipramine (Anafranil),
amitriptyline (Elavil), imipramine (Tofranil), nortriptyline (Pamelor), and trazodone (Desyrel)
have been used with some success (Sadock & Sadock, 2000). Mood stabilizers such as lithium,
valproate (Depakote), and topiramate (Topamax) have been successful in some case studies
(Dannon, 2003). As mentioned in Chapter 13, opioid-receptor antagonists such as naltrexone
(Revia) have been used with the impulse control disorders, resulting in positive outcomes for
some, especially for pathological gambling (Leung & Cottler, 2008). Pathological gambling and
trichotillomania have been treated similarly to kleptomania with the SSRIs, mood stabilizers,
and opioid antagonists offering some success. In addition, Leung & Cottler indicate that newer
 Chapter 14 • Treatment of Comorbidity and Other Disorders 109

treatments such as N-acetyl cysteine and modafinil have produced significant improvement for
pathological gamblers. According to Ravindran et al., 2009 SSRIs have shown benefit as first-
line, short-term treatments for body dysmorphic disorder, hypochondriasis, onychophagia, and
psychogenic excoriation, with some benefits in trichotillomania, pathological gambling, and
compulsive buying. Atypical antipsychotics such as risperidone (Risperdal) or olanzepine
(Zyprexa) have also been attempted in some cases with a positive response. Ravindran et al.,
2009 further mentions that several atypical antipsychotics have shown promise in disorders with
a high degree of impulsivity, such as trichotillomania and pathological gambling, and to a lesser
extent kleptomania and psychogenic excoriation.
For intermittent-explosive disorder, research evidence suggests that mood stabilizers, atyp-
ical antipsychotics, beta-blockers, alpha-2 agonists, phenytoin (Dilantin), and serotonergic anti-
depressants may be useful (Olvera, 2002).
Problematic Internet Use (PIU) appears to be a growing concern in forensic psychiatry.
Problems range from inappropriate personal use of the Internet in the workplace and excessive
use of online games, pornography, and gambling, to cyberbullying among children and adoles-
cents. SSRIs are recommended treatment for PIU unless there is a manic or hypomanic compo-
nent (Recupero, 2008).
Although we have focused only on medical-psychiatric comorbidity, chronic neuropathic
pain, eating disorders, obesity, and impulse control disorders, medications may be used with
some effectiveness for many other psychiatric diagnoses. Most of these areas of study are based
on small case reports or anecdotal evidence from busy clinicians. In conclusion, more random-
ized controlled trials are needed to evaluate individual and combination treatments for short-term
and long-term use.

CASE VIGNETTE
Chapter Fourteen
CLINICAL HISTORY
Ray is a 32-year-old white male seeing a clinical social worker for the first time for an “anger problem.” He was re-
cently arrested for assault after a road rage incident in Los Angeles. It happened at 6:20 in the evening. Ray was in a
hurry to get home and catch the Lakers game during the play-offs. He encountered someone driving a bit too slow in
the fast lane of the freeway. He couldn’t get around him because of heavy traffic in the other lanes. He used his horn
and flashed his lights to no avail. The longer he sat behind this car the angrier Ray became. Finally he noticed his exit
was coming up so he moved from the fast lane to the right lane, just as the person in front of him did the same.
Unfortunately, the car exited at the same exit and was once again traveling slowly in front of Ray. At the first traffic
light they came upon, Ray pulled up along side of the car and yelled several obscenities at the driver. The driver very
calmly gave Ray the finger and started to drive away. Ray sped up and whipped his car in front of the other driver,
nearly causing the driver to rear-end him. Ray jumped out of the car, walked over to the other driver’s side window and
struck the driver twice in the face. Unfortunately for Ray, a CHiP (California Hwy. Patrol) motorcycle cop witnessed the
whole event.

POSTCASE DISCUSSION AND DIAGNOSIS

Ray has no clinical diagnosis per se. He does not meet criteria for Intermittent Explosive Disorder or a mood disorder. He
denies use of alcohol or other substances. While he has no history of domestic violence, he did get into more than one
110 Chapter 14 • Treatment of Comorbidity and Other Disorders

physical altercation with former boyfriends of his current wife of six years. He had one other arrest for assault ten years
ago over a parking spot at a crowded shopping mall.
When questioned about his behavior, Ray admits he shouldn’t react to people so harshly, but claims that road
rage and “stupid drivers” are his pet peeve. Construction sites and lane closing are sure to set him off. He admits that he
has always been a “hot head” and is worried now that he will have a police record.

PSYCHOPHARMACOLOGICAL TREATMENT
In addition to anger management, his clinical social worker arranged for a medication consultation with a local psy-
chiatrist. Ray agreed to try taking a low-dose SSRI to see if it helped him curb his anger. He was started on 10 mg of
citalopram (Celexa) every morning. In a follow-up visit with his therapist two weeks later, he reported feeling less tense
while driving and less likely to anticipate problems when he encountered a construction site on the freeway. In fact, his
wife reported that when they pulled into the grocery store parking lot last week, he didn’t seem to mind that someone
else got to the last spot before he did. Normally he would have raced to the spot and yelled to the other driver to inform
him that the spot was taken. He once got out of the car and waited for the other car to drive away before taking the
spot. His wife is so happy that he appears to have become a new “chilled-out” man. Ray is also happy with his
progress, noting that he is also less argumentative with others in the workplace.
15 CASE VIGNETTES
Children

NAPOLEON
Clinical History
Napoleon is a 9-year-old Hispanic male with a four-year history of behavior problems
consisting of hyperactivity, impulsivity, and incorrigibility. He presented to a community
mental health clinic for evaluation and treatment. His mother reported that her son had al-
ways been extremely moody and had difficulty sitting still, paying attention in school, and
following rules. The mother was getting to the point where she could not manage him
anymore, and she may need to look into placement options because his behavior is uncon-
trollable. During the clinical interview, further details about Napoleon were obtained,
including his extremely irritable moods, elevated or euphoric moods, grandiose ideas
about the future, severe bouts of depression, distractibility, frequent use of profanity, and
sexually inappropriate comments toward females. Napoleon’s self-esteem seemed to cor-
relate with his moods, as did his school performance. Napoleon also reported that when he
was sad, he heard the voice of the devil who told him that he was no good and should die.
On the other hand when his mood was “really good,” Napoleon heard God’s voice telling
him that he was special.
Napoleon’s mother reported that he had always been fairly healthy except for the
use of an inhaler at times for his asthma. When asked about psychiatric family history, his
mother reported that she had some mood swings when she was younger and was hospital-
ized on two occasions. Although she had taken medications, she was unable to recall the
names of the medications or the diagnosis for which she had been treated. Napoleon’s ma-
ternal grandfather was an alcoholic and went on intermittent binges.
Napoleon’s mother recalled that her son had taken medications such as Ritalin and
Dexedrine in the past, but they reduced his appetite without any therapeutic benefit.
Napoleon has been disruptive in school and was frequently sent home for his bad behavior.
However, he has gone weeks or months at a time without any behavioral problems in school.

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Postcase Discussion and Diagnosis

Napoleon appears to have some symptoms consistent with ADHD as well as bipolar disorder.
When his mother was questioned in more detail, further symptoms emerged, including periods
of increased energy and hyperactivity, a decreased need for sleep, grandiose thoughts with hy-
perreligiosity, increased verbal output (nonpressured speech), and being easily distractible.
Following these elevated moods, Napoleon would experience depressed periods characterized
by hypersomnia, poor appetite, intermittent voices (mood congruent), low energy, sense of
hopelessness, and anhedonia. Given the family’s history of bipolar spectrum disorders (the
mother’s moodiness and the grandfather’s binge drinking), Napoleon appears to have bipolar
disorder NOS (296.80) and needs immediate treatment. Since suicidality is not present, treat-
ment can be initiated in the outpatient setting with his mother’s consent and support. Inpatient
treatment may be necessary if Napoleon becomes a danger to himself, a danger to others, and/or
unmanageable at home for his mother.

Psychopharmacological Treatment
After an appropriate medical and psychiatric evaluation, Napoleon was started on lithium 150 mg
twice daily with a plan to increase as tolerated to a dose of 600–900 mg/day. Lithium was chosen
for its tolerability and effectiveness. When starting any psychotropic medication in children, par-
ents must watch the child closely and monitor his or her moods on a daily basis. Prior to starting
the lithium, appropriate laboratory testing was done and will be followed per typical protocols.
When Napoleon returned for a follow-up visit ten days later, he was feeling OK taking
lithium at 600 mg/day. His mother reported that he had been doing much better. He was less im-
pulsive and irritable, his sleeping patterns improved, and his moods were more level or even.
Napoleon and his mother agreed to proceed with outpatient medication management and to en-
gage in psychotherapy to address the school and social problems his mood disorder had caused.
After approximately one year of treatment, Napoleon was doing well in school with minimal be-
havioral issues.

CHRISTINA
Clinical History
Christina is a 12-year-old African American female who has been in foster care for the last two
years because her mother died from HIV/AIDS. She resides with her foster parents (also her
legal guardians) and two other foster children who are two and three years younger than she. At
the strong encouragement of the Child Protective Services social worker, Christina was brought
in for a psychiatric evaluation because she was sleeping all the time. Christina reluctantly ad-
mited that she liked to sleep too much and did not like to talk about her emotions. When asked
about her mother, she was very distant and aloof but admited to missing her sometimes. Christina
would not discuss the process of losing her mother or the disease that overcame her mother. In
passing, the social worker reported that Christina was not doing as well in school lately and had
been missing an excessive number of school days because she refused to get up for the bus.
Christina denied ever seeing a therapist previously or taking any psychiatric medications.
Christina’s mother contracted HIV from her father who was an intravenous heroin user. He
died from HIV/AIDS during Christina’s first year of life. Other psychiatric family history was
basically unknown. According to the social worker, Christina has no other family involvement
 Chapter 15 • Case Vignettes: Children 113

or support. Her developmental history was basically normal although her language was some-
what delayed.

Postcase Discussion and Diagnosis

Christina’s symptoms were further explored and revealed the following: experiencing depressed
mood, feeling listless, feeling hopeless or helpless, having intermittent thoughts of wanting to
die in order to join her mother, having poor appetite with a ten-pound-weight loss over the past
month, feeling tired, having difficulty concentrating in school, and showing increased isolative
behaviors. Christina was diagnosed with major depression, single episode, moderate (296.22),
and needs immediate treatment. Given her thoughts of death, Christina needs to be carefully
evaluated for suicidality. Psychotherapy is strongly recommended to address the enormous
changes and losses that she has experienced in her short life. Although the issue of HIV transmis-
sion from mother to child should have already been addressed, the clinician needs to investigate
and recommend an appropriate workup if necessary.

Psychopharmacological Treatment
Christina was started on fluoxetine (Prozac) 5 mg/day after consent was obtained from her foster
parents. After two weeks, she was reevaluated and the fluoxetine was increased to 10 mg/day.
After four weeks in treatment, she returned to the clinic with much less depression and isolation.
She had also started psychotherapy to confront issues in her life. After taking the medication for
ten weeks, Christina’s depression had completely remitted and her therapy was progressing
appropriately. She was beginning to process the loss of her mother and to look at how it had
affected her own young life.

MARKY
Clinical History
Marky is an 8-year-old white male who presented to the psychiatrist’s office with both of his par-
ents although they are divorced. He was being brought in for evaluation at the recommendation
of his third-grade teacher because he was disruptive in the classroom. His mother, who is the
primary caretaker, reported he is always on the go and has trouble sitting still to do essentially
anything. Marky’s mother reported, “Everything in his room is in disarray.” His father admited
that their son may be a little hyper but sees him as basically just a normal kid. The parents pre-
sented a letter from Marky’s teacher that raised the following issues: difficulty attending to tasks,
hyperactive in and out of the classroom, difficulty awaiting his turn, highly impulsive, difficulty
following through with tasks, often procrastinates, frequently forgets, constantly daydreams,
fights frequently, talks excessively, and so on. Marky has made average grades in school but has
the potential to perform much better, according to his teachers. Marky and his parents denied any
significant depression, psychotic symptoms, obsessions, compulsions, or suicidality. Marky did
admit to some anxiety and tends to worry mostly about the future.
Marky has always been in excellent health and tends to excel athletically. The parents
denied any psychiatric family history of mental disorders or substance abuse. When giving the
history, the father acknowledged that he also had trouble focusing in school when he was
Marky’s age. For this reason he tends to see Marky just as a normal child. Marky has never used
any psychotropic medications in the past.
114 Chapter 15 • Case Vignettes: Children

Postcase Discussion and Diagnosis

Marky clearly meets criteria for ADHD, combined type (314.01). After having the parents,
teacher, and a family friend complete the Connors Rating Scale, the diagnosis was undisputed.
The patient has features of hyperactivity, impulsivity, and inattention. The patient was also seen
by his pediatrician, who felt that Marky was healthy and developing normally.

Psychopharmacological Treatment
Marky and his parents agreed to a trial of Adderall XR (brand of amphetamine) starting at 5 mg
every morning; the medication will be titrated up as tolerated every three to five days until Marky
has a clinical response or has limiting side effects. A clinical response may be reported by the
parents or child or objectively observed by a significant decrease in his Connors Rating Scale.
The extended-release (XR) form of the medication was chosen because the medication is given
as a single dose only in the morning, which helps improve compliance. Psychoeducation and
therapy are necessary not only for the patient, but also for the family to ensure the best prognosis.
After being on Adderall XR 20 mg/day for a few days, Marky was functioning much bet-
ter in school with improved self-confidence in his own abilities. His parents and teachers have
noticed significant clinical improvements in his overall attitude, functioning, and demeanor.
Marky had experienced no side effects to date from the psychostimulant. Objective measure-
ments from the Connors Rating Scale showed Marky with lower scores, which correlate with a
therapeutic response.
16 CASE VIGNETTES
Adolescents

JOHNNY
Clinical History
Johnny is a 16-year-old white male with no previous history of mental or physical illness. He
recently presented to his family physician with complaints of depressed mood, loss of energy,
poor motivation, and middle insomnia. His parents also mentioned that he had isolated him-
self from friends and dropped out of soccer. The history and physical showed no significant
findings, but Johnny had lost seven pounds since his last physical about a year ago and ap-
peared to be rather apathetic about personal hygiene. Johnny denied drug use, and while not
presently suicidal, he did appear to have significant passive-death themes in this conversation.
Johnny’s parents appeared to have a good relationship, and they appeared to have no
concerns about Johnny’s sister, who is two years older than he. His sister had a brief period
of depression last year, but it remitted without the need for further treatment. His mother,
age 41, had several bouts of depression earlier in her life that resulted in a few years of psy-
chotherapy and a course of antidepressant medication (imipramine) for several years. She
claimed to have had no real depression over the last ten years. Johnny’s father, age 45,
reported that he occasionally is blue, but he had never felt the need to see a therapist or take
medication. He does, however, drink two or more beers each evening when he gets home
from work. He claimed that the beer calmed him and helped him sleep. Johnny’s maternal
grandfather committed suicide when Johnny’s mother was three years old.
To date, Johnny has taken no medication and has talked with the school counselor on
only three occasions about his depression and slumping grades. The counselor then referred
him to his family physician for an assessment and gave him the name of a therapist in the area.

Postcase Discussion and Diagnosis

Johnny appears to have major depressive disorder (296.22). His score of 29 on the Beck
Depression Inventory further confirms the presence of depression. He complains of poor

115
116 Chapter 16 • Case Vignettes: Adolescents

motivation, death themes, tearful bouts, isolative behaviors, and trouble staying asleep at night.
At this time, it is not certain if he will have subsequent bouts of depression, but based on the fam-
ily’s history, it is likely. While Johnny poses no immediate suicide risk, a timely evaluation by a
mental health professional is needed. Psychotherapy and medication are indicated. Johnny will
see a local counselor at least twice a week for individual sessions and have an immediate medica-
tion and psychiatric evaluation with a psychiatrist.

Psychopharmacological Treatment
After the evaluation was completed, Johnny was placed on citalopram (Celexa) 10 mg/day for
the first week and 20 mg/day starting with the second week. This particular medication was se-
lected because of its low overdose profile, low sedation, and its efficacy for facilitating sleep.
Johnny will be watched closely by his parents and counselor for any changes in suicidal thoughts
or behaviors. Follow-up sessions with the psychiatrist were scheduled in three-week intervals.
Upon follow-up with the counselor and the psychiatrist, Johnny reported that his depres-
sion was 80% better and that his grades had returned to normal. He no longer had trouble sleep-
ing, nor was he plagued by thoughts of death and depression. He had decided to continue to talk
with the counselor as needed since it helps him think more clearly and positively.

JENNIFER
Clinical History
Jennifer is a 17-year-old Hispanic female who presented with anger, agitation, and antisocial ten-
dencies. She lived with her parents until her father was sent to jail for an auto theft. Her mother,
who was unable to support herself and her three children on a farm worker’s salary, moved in
with her sister and her five children. Jennifer had been in and out of school until she dropped out
last year. She has about a sixth-grade achievement level. Her grades have always been poor,
especially in reading and math. Jennifer claimed that she spent most of the fifth and sixth grades
in the hallway because of her poor behavior. She just cannot seem to listen and sit still long
enough for things to stick. Her parents and teachers thought of her as just a headstrong tomboy
who had to have the last word.
Jennifer’s aunt had taken a strong interest in her behavior and believed that Jennifer should
be able to have a decent educational experience. She had talked with Jennifer often and believed
that she was “hyper and indifferent” to her current situation. Jennifer has spent much too much
time with some neighborhood boys who have formed a type of gang with other young boys who
have dropped out of the local high school. The neighborhood boys would rather skip school than
attend and their grades were also poor. Jennifer’s parents wanted to see her succeed in school but
were more concerned that she would ruin her social reputation by hanging out with “bad boys.”
They never really noticed her hyper behaviors before and just thought she had a lot of youthful
energy. They feared she might become like many girls who hang out with such boys and end up
dropping out of school, getting into legal trouble, or getting pregnant.
Reviews of Jennifer’s academic records showed poor performance and behavior patterns.
She spent at least an hour a day in the hallway or in the principal’s office when she last attended
school last year. While Jennifer had little insight into her behavior, she was aware that school was
not one of her favorite places and that she was not doing well there. She maintained that school
was stupid and for geeks. Although she tended to hang out with a rather antisocial crowd, she ap-
peared to be concerned about her family and her other childhood friends. She appeared to have
 Chapter 16 • Case Vignettes: Adolescents 117

some sense of conscience, as she would not go with boys who planned vandalism or petty
crimes. She was also very sensitive to other teens who had trouble learning in school and was
often found talking with them in the cafeteria.

Postcase Discussion and Diagnosis

After extensive conversations with her former teachers, counselor, school psychologist, and so-
cial worker and a thorough workup from her family physician and her current psychologist, the
team determined that Jennifer demonstrated enough clinical criteria for a diagnosis of ADHD of
the hyperactive type. She was beginning to notice less hyperactivity and more restlessness with
her life and her friends. Her self-esteem was rather low because she realized that her educational
skills were poor and her job prospects weak. With her psychologist’s help, Jennifer was willing
to work toward progress and improvement.

Psychopharmacologic Treatment
In addition to her weekly counseling sessions, Jennifer was sent to a psychiatrist who special-
izes in adult and childhood ADHD. She was initially started on a trial of atomoxetine (Strattera)
but showed little response after one month. She was then switched to bupropion (Wellbutrin
XL) 300 mg/day and methylphenidate (Ritalin) 15 mg b.i.d. Her psychiatrist was not concerned
about stimulant abuse since Jennifer used no known substances. She responded well to this
regime, as evidenced by self-reports and weekly reports from her psychologist. Subsequent
psychological evaluations revealed that Jennifer had better concentration, attention, and reten-
tion of learned material.
In a series of follow-up sessions she demonstrated more calmness, less anger and agitation,
and a willingness to enroll in a GED program. Her career and vocational tests indicated a strong
interest and the ability to assist others in a counseling or teaching capacity. Jennifer hopes to be-
come a teen counselor working with ADHD youth.

VIOLET
Clinical History
Violet is a 15-year-old female in the ninth grade. She came with her parents to a local mental
health center, complaining of intense anxiety and social shyness. The visit was prompted by a
rather traumatic school dance. Violet came home early with her friend, Lisa, at Violet’s insis-
tence. Violet reported that she was feeling more and more uncomfortable at the dance, and when
she mentioned her feelings to Lisa, her friend told her “lighten up” and stop obsessing about
everything. Violet became quite upset and started to cry. Others at the dance gathered around her
until school personnel escorted Violet and Lisa from the building. Violet’s parents were called
and the two girls were taken home.
Violet is the older of two children. She has an 11-year-old brother who has no apparent
mental health concerns. Her parents appeared to be happy and well adjusted with no history of
mental illness: however, her mother reported that she was rather anxious herself in high school
and college. Violet’s mother took nortriptyline (Pamelor) for several years but reported no anxi-
ety problems now.
Both parents claimed that Violet had always been a shy, quiet, and very sensitive little girl.
She was always uncomfortable around strangers and other students. In fact, she had a difficult
118 Chapter 16 • Case Vignettes: Adolescents

time adjusting to both kindergarten and first grade. Although she is a very pretty girl, Violet
avoided social contact with other students, and quickly excused herself when approached by
them. Recently, while Violet was visiting at Lisa’s home, a few more friends showed up and sug-
gested calling some boys over. Violet became more and more anxious until she excused herself
and retreated to Lisa’s bedroom. Lisa called Violet’s mom who came to take her home.
Violet is aware that her fears and behaviors are ruining her life. She reported that she felt
very inadequate in social situations. Violet is afraid that she will do or say something that will
bring attention to her, and others will laugh at her. She also reported feeling very uncomfortable
in the girl’s shower room at school. Violet will not shower or dress unless the other students have
gone. She once became so concerned that others were watching her that she had trouble breath-
ing and felt dizzy.
After a complete physical by her family doctor and an evaluation by the therapist in the
clinic, no physical causes for Violet’s anxiety were found. She functioned quite well at home and
in the presence of people she knew well. School performance was good except when she had to
raise her hand or give speeches in front of the class. She appeared to have no other phobias, his-
tory of depression, and no history of trauma or abuse.

Postcase Discussion and Diagnosis

Violet appears to have social phobia (300.23). She has always been rather shy and anxious in
social situations, but recently her symptoms have worsened. She purposely avoids social situa-
tions and the possibilities of social invitations. She once dropped a class because the teacher said
the students would have to work in groups. She fears that if her anxieties continue, she will not
be able to finish high school or attend college.

Psychopharmacological Treatment
In addition to cognitive behavioral therapy and social skills training classes, her therapist and
parents decided that Violet should try medication. She was first given paroxetine (Paxil) 20 mg/day.
She responded very well but reported feeling rather drugged during the day. Her yawning was so
pronounced that her teachers excused her from class to sleep in the student lounge. She was then
instructed to take the medication before bed, which helped, but sedation and dizziness continued
to be a problem. She was then switched to venlafaxine (Effexor XR) and showed less sedation
and balance issues.
A follow-up found that Violet was much happier and certainly more social. Once the med-
ication reduced her fears, Violet opened up to the therapist and really worked hard on finding
ways to reduce her fears and increase her strengths. The social skills classes increased her self-
esteem and allowed her to address her need that everyone must like her.
In a true in vivo test, she attended a school dance recently and actually accepted a boy’s in-
vitation to dance. She was quite smitten with him and is now wearing his school ring.
17 CASE VIGNETTES
Early Adulthood

STONE
Clinical History
Stone is a 23-year-old white male college student who presented to the Campus Health
Center with concerns about failing health. Upon further questioning, the patient reported
concerns about microwaves, X-rays, and other electromagnetic forces interfering with his
decision-making capacity. Although he was initially guarded, Stone confided that he
stopped watching television one year ago and stopped listening to the radio six months
ago because he felt like “the government” was trying to control his mind. At times, the
patient referred to hearing his “mother and father” in his head but refused to elaborate
when questioned.
Stone had been attending college for the past four years and had approximately one
more year to finish his bachelor’s degree in chemistry. Stone remorsefully admited to
drinking and smoking “too much weed” that led to his withdrawal from about half of his
classes during his first and second years of college. Stone denied any current use of drugs,
but he did admit to having some alcohol about once a month with friends. Further assess-
ment of his alcohol history revealed two positive answers out of a possible four on the
CAGE questionnaire. Stone reported that he did not date much and preferred to be alone.
He casually mentioned having some friends but was reluctant to give any names or reveal
anything specific. Despite his initial complaint of failing health, his review of systems was
basically negative.
Stone denied any significant medical history except for surgery on a broken arm
when he was about 15 years old. When questioned about psychiatric family history, Stone
admited that his maternal grandfather had a “nervous breakdown” and was institutional-
ized most of his adult life. Stone admited that his grandfather used to hallucinate and act
weird. Stone was unsure of the diagnosis. Stone reported that his father drinks too much
alcohol and has had one DUI in the past. Stone denied any particular stressors lately
except for the pressure he was getting from his parents to finish college and get a job.

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120 Chapter 17 • Case Vignettes: Early Adulthood

Postcase Discussion and Diagnosis

According to Stone’s history, he appears to have a diagnosis of schizophrenia, paranoid type
(295.30), alcohol abuse (305.00), and cannabis abuse (305.20). Additional information about
Stone revealed few relationships, increasing isolation over the last few years, increasing paranoid
delusions, and intermittent auditory hallucinations. His school performance was average but ap-
peared to be declining overall when compared to his high school years. He was ambivalent about
discussing his concerns with others because he feared his health would deteriorate. Stone’s use
of alcohol and marijuana complicated his presentation but was probably an independent phe-
nomenon. If his substance abuse continues or progresses, his psychotic disorder will likely
worsen. Stone’s family history most likely indicated his maternal grandfather had either schizo-
phrenia or some other psychotic illness. Although Stone desired to process his thoughts and feel-
ings in therapy, he was not an appropriate candidate given his subacute psychotic symptoms. At
some later point in time, therapy may be appropriate. Before considering medication, Stone was
referred for an appropriate medical and neurological examination.

Psychopharmacological Treatment
Stone was started on aripiprazole (Abilify) 10 mg/day because he felt safe taking a neuromodula-
tor, rather than some of the other atypical neuroleptics. Given his chemistry background, he was
suspicious of being prescribed anything he felt was a tranquilizer. After four weeks on the medica-
tion, Stone reported very little change in his symptomatology. He appeared to be tolerating the
medication well without any side effects. At eight weeks, Stone appeared much more relaxed and
focused on completing school rather than being obsessed with his “failing health.” When asked
about his health at this point, Stone denied having any problems and was even listening to the
radio in his car again. Furthermore, at twelve weeks of aripiprazole 10 mg/day, he reported having
a potential girlfriend in his chemistry class. Since his psychosis was responding to the medication,
psychotherapy should be initiated with the focus on psychoeducation, relapse prevention, and
avoidance of substances.

AVA
Clinical History
Ava is a 27-year-old Hispanic-Asian homemaker and mother of a 3-year-old daughter. She was
accompanied to the clinic by her husband of six years with a complaint of unusual behaviors.
Ava had been taking walks in the middle of the night when she was unable to sleep, had become
fearful of her husband for no apparent reason, and was consuming and hiding alcohol at various
places in their home. Her husband reported that Ava did not usually drink alcohol whatsoever
because of their religious beliefs. Upon further questioning, Ava revealed that she was six weeks
pregnant and the father of the baby was not her husband. Both Ava and her husband were unwill-
ing to reveal much information about the pregnancy except to say that they would remain mar-
ried and raise the child as their own.
When asked about historical information, Ava said that she had a “strange episode” about
seven years earlier when she impulsively took a vacation with a college friend. After drinking
excessively for one month, Ava returned to school to learn that she had failed her semester
classes. She did not seek any mental health treatment and thought her behavior was just related
to “growing up.”
 Chapter 17 • Case Vignettes: Early Adulthood 121

With the exception of alcohol, Ava had no history of other drug use. She had never taken
any previous psychiatric medications. The psychiatric family history was negative for mood dis-
orders, psychotic disorders, anxiety disorders, and substance-use disorders. During the interview,
Ava acknowledged other symptoms, including increased energy, moodiness (dysphoria, elation,
and irritability), racing thoughts, hearing the voice of God, feeling like she is “God’s chosen
one,” and cleaning excessively at home.
Ava saw her primary care physician who felt she was in good health. The physician
advised her not to drink alcohol while she is pregnant because of fetal-alcohol concerns and
referred her for follow up with her OB/GYN. Ava currently takes a prenatal vitamin only.

Postcase Discussion and Diagnosis

Ava appears to have a diagnosis of bipolar disorder, manic, severe with psychotic features
(296.34) and alcohol abuse (305.00). Her symptoms that support this diagnosis include hyperreli-
giosity, grandiose delusions, mild paranoia, racing thoughts, decreased need for sleep, increased
goal-directed activities, auditory hallucinations, impulsivity, possible hypersexuality, and poor
judgment. Her intermittent alcohol consumption may be a form of self-medication to control her
mania. Based on Ava’s history, she probably had at least one manic episode previously that went
undiagnosed and untreated. In addition to referring Ava for medication evaluation and treatment,
the clinician needs to provide psychotherapeutic support to her and her husband and ensure the
safety of her daughter. Ava’s husband agreed to enlist support of relatives to provide childcare and
support for Ava until she gets back to her old self.

Psychopharmacological Treatment
After an appropriate evaluation and review of all options available, Ava and her husband chose to
start lithium 300 mg b.i.d. initially, with dosage adjustments over the next few weeks. Because of
her psychosis, antipsychotics were discussed, but Ava and her husband decided to wait for now
and see how she responds to the lithium. After two weeks of lithium, Ava was sleeping about
seven hours per night, had less racing thoughts, and was abstinent from alcohol. Her husband re-
ported a significant improvement from his perspective saying, “my wife is coming back.” The
lithium was increased to 300 mg t.i.d. at that time; the lithium level subsequently was 0.8 mEq/l,
which was therapeutic. In consultation with her OB/GYN, an ultrasound was done to check for
cardiac abnormalities in the fetus because of the lithium exposure. Results were negative, indi-
cating that the fetus was unaffected. Given Ava’s alcohol abuse, the possibility of fetal-alcohol
effects needs to be assessed after delivery.

CANDY
Clinical History
Candy is a 25-year-old white female who presented for an evaluation at the insistence of her pri-
mary care physician because of weight loss. Candy reported that she felt overweight, fat, and dis-
gusted with her appearance. She claimed, “My thighs, stomach, and butt are just too fat. . . . I
have to lose more weight.” Candy acknowledged some depression but tended to minimize it, say-
ing she was fine. She denied any sleep disturbance, energy changes, hopelessness, helplessness,
concentration problems, suicidality, and so on. She reported having a normal appetite but was
very careful to eat only “healthy foods.” When asked about stressors, she admited to some
122 Chapter 17 • Case Vignettes: Early Adulthood

trouble in her marriage but did not elaborate. Candy works as an attorney. She reported that she
gets angry at clients and even judges when “things” don’t go her way. She exercises daily for ap-
proximately one hour, focusing on aerobics and cardiovascular fitness. Her stats are as follows:
height, 5⬘8⬙, weight, 98 pounds, and BMI 14.9 kg/m2. According to standard measurements, her
BMI is in the 2nd percentile. She mentioned in passing that her doctor was concerned because
she has not had a menstrual period for the last two years.
Candy went on to report that she had been obsessed with her weight since her teenage
years. She remembered constantly struggling with her parents over control issues such as cloth-
ing, school performance, friends, dating, and so on. She denied any significant past medical or
psychiatric history, as well as any alcohol or drug abuse. Her psychiatric family history revealed
some depression in her mother and maternal grandmother. Candy also stated, “Nobody in my
family is fat and I’m not going to be either.” In passing, she reluctantly admited to sexual abuse
in the past but refused to discuss details.

Postcase Discussion and Diagnosis

Candy presents with a diagnosis of anorexia nervosa (307.1) and may have a secondary diagno-
sis of depressive disorder. She is excessively focused on body image and has an intense fear of
gaining weight despite being underweight. She appears to be in the acute phase of the illness al-
though she has not experienced any medical consequences to date other than her amenorrhea. It
is difficult to assess whether Candy has experienced depressive episodes in the past because of
her vague history. She does not meet criteria for a specific diagnosis of mood or anxiety disorder
at this time. Candy does need appropriate laboratory evaluation to check for electrolyte abnor-
malities, which could be medically dangerous. An appropriate trial of psychotherapy should be
initiated as well as evaluating her need for inpatient hospitalization.

Psychopharmacological Treatment
Although most data would not suggest treating the acute phase with medications, Candy agreed
to a trial of fluoxetine (Prozac) 10 mg/day for one week, then 20 mg/day. She understood that the
medication may help her mood as well as decrease her core eating-disorder symptoms. The
fluoxetine was increased over the next four weeks to 60 mg/day, which she tolerated well with-
out side effects. After approximately six weeks on the fluoxetine, Candy appeared to be less
depressed and less obsessed with her weight. Over the subsequent six weeks, her weight
increased to 104 pounds, and she appeared to be unconcerned about it. The combination of psy-
chotherapy and medication management has provided Candy with the best possible prognosis.
Ongoing psychotherapy, medications, and psychoeducation will be required to maintain her
emotional health.
18 CASE VIGNETTES
Middle Adulthood

CHESTER
Clinical History
Chester is a 42-year-old white male seeking an evaluation at a university-based treat-
ment center. He decided to consult the experts because he had tried so many other treat-
ments in the past with mixed results. He presented with a history of panic attacks dating
back to high school. His first attack came during his senior year when he was not
accepted to Princeton University. This rejection was a terrible blow to his self-esteem
because his father attended Princeton and expected that both Chester and his brother
would also attend. His brother was then in his junior year and planning to attend law
school when finished.
After Chester’s first attack in high school, he and his parents consulted their
doctor and a cardiologist who found no reason for the attacks and no heart-related is-
sues. Chester was told to reduce his stress and return if the attacks continued. They did
not return and Chester was accepted to Harvard, an acceptable alternative. In his fresh-
man year, Chester experienced another attack while he was sleeping. He consulted the
university health services, which once again found no medical reason for the attacks,
and they explained to him that the attacks may be a stress-related condition. An ap-
pointment was made for him at the university counseling service, but he did not keep
the appointment.
Chester made it through college by using alcohol to self-medicate. He was able to
hide most of his drinking from his family and friends until he graduated and met Judy. He
and Judy fell in love and married within six months. His drinking became harder to hide,
and Judy confronted him after he fell at a neighbor’s party where he was very drunk and
rather loud. Chester confided in her about his panic and fears, and how he needs the alco-
hol to function at home and at work. With Judy’s help, he decided to attend AA and seek
counseling from a mental health professional.

123
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Chester slowly refrained from drinking but felt increasingly more anxious until he had
three panic attacks in one week. He was placed on alprazolam (Xanax) by a consulting psychia-
trist. He found the medication very helpful and was able to learn how to identify, label, and mod-
ify his thoughts in counseling with the use of cognitive therapy. He attended therapy weekly for
nearly two years, but stopped when he and the therapist felt they had progressed far enough. He
continued to take the medication and remained symptom-free for over 14 years.
When he was 36 years old, his primary care physician believed that Chester was over his
emotional concerns. His physician felt Chester should stop taking the alprazolam. Over the
years, Chester had increased his dose from 0.5 mg/day to over 3 mg/day. He still attended AA
meetings from time to time but never touched alcohol again. By the second week of his step
down from alprazolam, Chester experienced a panic attack while driving home from work. His
medication was increased back to 3 mg/day of alprazolam and has remained at this dose for the
past six years. He attempted to return to therapy, but found the principles of therapy were not
helping him much this time around. Chester changed therapists, but the next therapist was less
versed than the first, adding to his sense of failure.
About a month ago Chester’s 17-year-old son was accepted to Princeton. Although happy
for his son, Chester became very depressed and while shopping with his wife in a grocery store,
he experienced an intense panic attack. He is tired of partially effective approaches and desires a
more comprehensive form of treatment.

Postcase Discussion and Diagnosis

Chester has a long history of panic disorder without agoraphobia (300.01), with secondary, alco-
hol and sedative-hypnotic abuse. While he used alcohol to self-medicate early in his life, he
abused the benzodiazepine alprazolam later in his life. Both drugs offered some level of immedi-
ate relief but did not provide a permanent solution to his concerns.

Psychopharmacologic Treatment
Since Chester has such a long and chronic history of panic disorder, it is very likely that he will
continue to experience panic, especially if he attempts to reduce his dose of alprazolam. Since
cognitively based psychotherapy helped him before, he should try it again. Antidepressants, es-
pecially SSRIs, are very helpful in reducing or eliminating panic. Chester will be placed on an
SSRI such as fluoxetine (Prozac), sertraline (Zoloft), or citalopram (Celexa), and he will be
reevaluated every two weeks to determine drug effectiveness. Concurrently, the alprazolam will
be very slowly tapered off in increments of 0.25 mg/week. Good patient education will be
needed to help Chester understand that he will not have additional panic attacks once the antide-
pressant medication takes effect.
In a five-month follow-up visit, Chester was symptom-free and attending counseling twice
per month. He continues to take the SSRI but no longer uses benzodiazepines or alcohol for symp-
tom relief. He also attends a group for others with panic disorder called Agoraphobics in Motion.

SALLY
Clinical History
Sally is a 47-year-old white female, who worked as a loan officer in a bank, was married for
nearly twenty years when her husband Jack asked her for a divorce. While she loved Jack, she
admitted that they had fallen out of love many years ago. They had a very civil divorce when
 Chapter 18 • Case Vignettes: Middle Adulthood 125

their only daughter Amy was a senior in high school. Amy appeared to be the only person in
the home who was upset about the divorce, and Sally was there to be supportive. Amy is now
in her junior year at a university more than 1500 miles away. While Amy comes home for
major holidays, she spends little time with Sally or with her father, who lives in an apartment
in a nearby town. While this tends to upset Sally more than Jack, Sally is trying to understand
that college kids would rather spend more time with their old high school friends than with
their parents.
After the divorce, Sally started to spend more time with her own parents. They were well
into their seventies. While she loved her father, she was closer to her mother. Sally too was an
only child, and she often stopped by her parent’s home just to check in on them. One Sunday
morning Sally received a call from her mother; her father had a heart attack. He was pro-
nounced dead before he arrived at the emergency room. Sally and her mother were devastated,
but Sally tried to be strong for her mother. Her mother moved in with Sally, and Sally started to
care for her. Sally started spending less and less time with others. She never went out with
friends or coworkers, in fact, the only time Sally left the house was to go to work or take her
mother on errands.
Sally began to notice that she was isolating more and was growing more depressed. Her
sleep was problematic since her father died and it was not getting better. Sally tried to treat the
initial insomnia with over-the-counter sleep aids, but they offered only temporary assistance. She
would also experience terminal insomnia two to three times per week. Sally was also growing
more concerned that she seldom saw or heard from her daughter. She once took a trip to see Amy
at the university, but Amy was away on an extended field trip.
When Sally returned from her trip to see Amy, she found that her mother had a very seri-
ous cold. When her mother’s breathing became labored, Sally took her to a local urgent-care cen-
ter and her mother was immediately hospitalized with pneumonia. Her condition continued to
decline until she was placed on a respirator. Four days later Sally’s mother died. Sally was over-
whelmed with grief. She phoned her daughter, who came home but only stayed until the day of
the funeral. Amy claimed that she needed to return to school to prepare for her LSAT exam.
Sally was tearful nearly twenty-four hours a day. She barely slept, and the sleep remedies
offered no relief. She attempted to see her minister, but he referred her to a grief group. She at-
tended meetings for several weeks but found that the grief of others made her worse. Sally at-
tempted to return to work but could not concentrate or do her job well. After more than six
months, her grief and loss was still very much with her. She felt that she may need to consult a
mental health professional for the first time in her life.

Postcase Discussion and Diagnosis

While Sally clearly exhibited all clinical criteria for a major depressive episode, which should be
considered in her treatment approach, she most certainly demonstrated a complicated bereave-
ment. Sally often dreamed of her mother, and once she thought that she heard her mother calling
out to her and asking for assistance because she had fallen down the basement steps. Sally raced
down the stairs in the middle of the night, only to find that her cat was locked outside and wanted
to come in for the night. Sally feels she cannot continue to live in the house because it has too
many reminders of her mother. She has basically sealed off the guest room where her mother
slept and is afraid to touch her mother’s things.
When Sally’s father died, she did not have an opportunity to grieve. She had to be strong
for her mother and daughter. Sally wanted to be comforted but could not find comfort in her own
126 Chapter 18 • Case Vignettes: Middle Adulthood

daughter. Sally had few close friends to confide in, but her bond with her mother was close.
When her mother died, the only bond Sally ever really had was broken and lost. She realized that
the bond with Amy was weak and unreliable. Sally panicked thinking about her own vulnerabil-
ities. Who would care for her when she got sick? Who would grieve for her? Did she fail as a
mother? Why did her daughter distance herself?

Psychopharmacologic Treatment
Sally was evaluated at a comprehensive health and mental care facility. After a complete physi-
cal, change-of-life issues were assessed by her gynecologist. Her gynecologist suggested
appropriate hormone replacement and referred Sally to a counselor who specialized in grief
therapy. Since Sally’s depressive symptoms have been severe for so long, she was referred to a
physician for medication. She was placed on Wellbutrin XL (brand of bupropion), 150 mg/day.
While this medication did offer some relief from depression, Sally reported feeling rather
agitated during the day, and her sleep disturbances continued. She was switched to sertraline
(Zoloft), which improved her sleep but increased her irritable bowel symptoms. Finally, Sally
was placed on trazodone (Desyrel), which offered the antidepressant action with sedation
around the time for sleep.
Upon follow-up three months later, Sally reported feeling much less depressed. Her sleep
had returned to normal without disturbing dreams. She felt that she was able to “move on” now
and let her mother rest. She continues to take the medication and see the counselor when needed.
Sally approached her daughter on her last trip home. Her daughter did not realize just how far
they had drifted apart, and Sally vowed to try harder to bridge the gap between them.

TONY
Clinical History
Tony is a 50-year-old Asian male with a long history of severe depression. He is the oldest of
three siblings who were raised in the suburbs of Philadelphia. His parents owned a dry cleaning
and tailoring business; each family member worked there as well. Tony’s family were devout
Catholics and expected each child to attend a Catholic school. Tony’s parents hoped that he
would get a scholarship to Notre Dame or Georgetown University. Tony was a good student and
did in fact earn a scholarship to Georgetown.
Tony first noticed his depression at age fourteen. He was afraid that he was different from
other boys because he found other boys attractive. He never mentioned his fear to his parents be-
cause the family never really talked about problems in the home. Tony did not want to disrespect
his family by talking to an outsider about his concerns, so he kept it to himself. During his years
at Georgetown, the depression became quite severe, and Tony had to inform his family about it.
As often seen in Asian families, they were disappointed in him for having a mental illness. Tony
never told them he was gay.
At the insistence of a professor, Tony entered therapy and started taking nortriptyline for
his depression. He showed enough improvement to finish his degree and move to Detroit to start
a new job in engineering. Tony functioned fairly well for about six years, until he decided to stop
the medication due to weight gain and other side effects. He experienced a serious depressive
episode that led to a fairly lengthy hospitalization. Tony was reintroduced to nortriptyline, but
this time it would not work. He was finally placed on trazodone (Desyrel) and clonazepam
(Klonopin) because of his agitation and related anxiety. When he was released, he attended day
 Chapter 18 • Case Vignettes: Middle Adulthood 127

hospital for several weeks. Although Tony was functioning fairly well, he believed that he was
only 65 percent better.
The next eight years demonstrated Tony’s need for additional medications and increases
in medications already in use. He was introduced to various SSRIs as they arrived on the treat-
ment scene, but each offered only moderate effectiveness. Numerous consultations with
experts at both Wayne State University and the University of Michigan lead to various
polypharmacologic approaches. Tony demonstrated only moderated levels of improvement
with lithium augmentation and stimulant boosters. He refused to try MAOIs because of their
dietary restrictions.
Tony was able to return to work, but he took so much sick time that he was transferred to a
less stressful department. The transfer resulted in a pay cut that Tony viewed as a demotion.
After years of psychotherapy, Tony finally felt comfortable with his sexual orientation and
decided to tell his family. While his sisters were supportive, his parents were not. They never
missed an opportunity to tell him about “change therapies” and the “evils” of a gay lifestyle.
Tony stopped returning to Philadelphia to see them. Over time, the rejections had somewhat of a
“kindling effect,” that is, these stressors were setting off subsequent bouts of depression that
were becoming more severe.
Feeling more comfortable with his gay identity, Tony was able to venture out a bit and
meet others. He met another man, and they started to date. This man was very understanding
about Tony’s chronic depression and tried to help Tony with some of his issues. Since this friend
had a very accepting family, Tony quickly felt welcomed and accepted by them, but he continued
to obsess over the loss of his own family.
Over the next few years, Tony and his partner, Bob, set up housekeeping, but Tony’s
numerous hospitalizations and leaves from work led him to apply for permanent disability.
Tony was granted disability, but unfortunately he spent his time lying around the house sleep-
ing. He isolated and refused to speak to anyone other than Bob. Except for his sisters, Tony
had no contact with his family, who viewed his gayness and his mental illness as a major
stigma (not unusual in an Asian family). Both Tony and Bob felt there must be more effective
forms of treatment.

Postcase Discussion and Diagnosis

Tony is suffering from major depression with a rather chronic history (296.32). While he has
never been actively suicidal, his chronic depressive episodes have left him feeling that life is not
worth living. He does not abuse alcohol or other drugs, and there are no psychotic manifestations
to his illness. While his homosexuality was rather ego dystonic at first, Tony appears to have
made a healthy adjustment to it in the last few years. The family stressors continue, but Tony is
happy with the relationship he has with his sisters and Bob’s family.

Psychopharmacologic Treatment
Tony had been through a trial of every known TCA, SSRI, and heterocyclic. Various stimulant
and lithium boosters were not very helpful. A recent augmentation with olanzepine (Zyprexa)
showed little change. Even though Tony was opposed to the use of MAOIs, their use was reeval-
uated with him. With his psychologist’s help, Tony was educated about possible MAOI use and
informed of the possible benefits. He reluctantly agreed to try them, and after the appropriate
discontinuance period from the other medications, he was started on phenelzine (Nardil), 30 mg/day.
Initially his depression worsened after the discontinuance of the other medications, but by the
128 Chapter 18 • Case Vignettes: Middle Adulthood

third week on phenelzine, Tony was beginning to improve. His dose was increased to 60
mg/day, and by the sixth week of treatment, he was reporting less daytime sleeping, no tearful
bouts, and a much improved affect. Bob reported that Tony was helping him in the yard, asking
to see their friends, and joining him for family visits.
The final evaluation came three months after the phenelzine was started. Tony reported no
measurable depression. He is not working as an engineer, but he is working three half-days per
week in a bookstore and loves his job. He reported that he and Bob are getting along well. Tony
is planning a trip home at Christmas to see his parents; he believes that he is ready to see them
and to confront their issues with his depression and sexual identity.
19 CASE VIGNETTES
Older Adulthood

ROSE
Clinical History
Rose is an 82-year-old white female who presented for a psychiatric evaluation with a re-
ferral from her primary care physician. According to Rose, “My doctor was concerned
about my memory, but I think it is fine.” Rose lives alone in a mobile home with her two
cats. She reported that she had no family to help her because they are all deceased. Rose
was accompanied to the appointment by a long-time friend who drives her to the store and
other appointments. Rose admited to feeling sad but denied feeling depressed on a consis-
tent basis. She worried about the future now that she was getting old but knew that she
would be taken care of one way or another. She stated, “My memory is not as good as it
used to be, but I get by okay.” She does not drink anymore but used to enjoy an occasional
martini with friends. Rose reported some difficulty sleeping but denied any energy distur-
bance, appetite disturbance, difficulty concentrating, hopeless feelings, helpless feelings,
or thoughts of death.
According to her friend, Rose is having significant difficulty with her memory. For ex-
ample, twice within the past two weeks she had forgotten to turn off the stove after preparing
a meal. Rose frequently lost her mail, bills, and social security checks, but generally they
were just misplaced. In the past six months, Rose’s electricity had been shut off once and her
water had been shut off twice because of nonpayment. When asked about her finances, Rose
reported that everything is fine. She was unable to provide further details even when directly
asked. Her friend stated that Rose was forgetting to feed her animals and at times she even
forgot to eat. Information from Rose’s primary care physician revealed an 18-month history
of cognitive decline as well as various medical diagnoses including hypertension, osteoarthri-
tis, and a previous history of myocardial infarction. She is currently taking an antihyperten-
sive medication, as well as an arthritis medication, which has remained unchanged for the last
seven years. Her primary care physician also noted that Rose was more forgetful, called him
by the wrong name at times, and no longer knew the names of her medications.

129
130 Chapter 19 • Case Vignettes: Older Adulthood

While her mental status was essentially unremarkable, Rose tended to avoid current events
and did not know the names of the president or vice president. She tended to minimize her
deficits saying, “. . . those politicians are no good anyway.”

Postcase Discussion and Diagnosis

Rose appears to have dementia of the Alzheimer’s type (294.10). Her mini-mental status exam
(MMSE) is 15/30 (-5 orientation, -2 attention, -2 recall, -2 naming, -2 command, -1 writing sen-
tence, -1 copy). Rose has additional symptoms including aphasia, apraxia, agnosia, and problems
with executive functioning. She has also been evaluated recently by a neurologist who ordered an
MRI of the brain that showed moderate atrophy. The neurologist agreed with the dementia diag-
nosis and did not feel any further workup was necessary. In addition, Rose, who was quite dis-
tressed at hearing the diagnosis, needed a referral for psychotherapy to address these issues. Her
primary care physician indicated that Rose uses atenolol, 50 mg/day for her hypertension, and
Tylenol, 2 pills/day (over-the-counter) for her arthritis.

Psychopharmacological Treatment
Rose was started on donepezil (Aricept), 5 mg/day for the first four weeks, then 10 mg/day there-
after. She appeared to tolerate the medication well except for mild sedation. When the dosing
was changed from the morning to the evening, the sedation side effect resolved. Her medications
were reviewed and no significant drug interactions between the atenolol, Tylenol, and donepezil
were found. Rose was able to continue living in her current environment, but four hours daily of
home care assistance were added. This care will help ensure compliance with her medication,
adequacy of meals, cleanliness of her home, and so on. Rose allowed her long-time friend and
her accountant to take over her finances and pay the monthly expenses.
Rose initially attended psychotherapy sessions weekly, but sessions were tapered to
monthly by the end of six months. The individual psychotherapy appeared to help Rose adjust to
the enormous changes that were occurring in her life. After six months of treatment with
donepezil, her MMSE was 14/30. Following one year of treatment, Rose was still living at home,
had eight hours of home care daily, and had a MMSE of 15/30. Since she is still living independ-
ently with the same basic MMSE score, the medication to minimize her cognitive decline has
definitely been efficacious.

ANTHONY
Clinical History
Anthony is a 65-year-old African-American male who presented for psychiatric evaluation with
his daughter. Anthony revealed that he lost his wife suddenly fifteen months ago after a fatal my-
ocardial infarction. He reported, “We were married for forty years. . . . I don’t know what to do
now.” His daughter reported that nothing had been the same since her mother died. She further
mentioned, “My dad has been isolating himself to the point of being a recluse.” The patient
admited that the isolation was true, along with other symptoms including early and middle in-
somnia, decreased appetite with a 25-pound-weight loss over the past year, decreased energy,
poor concentration, and increased forgetfulness. When questioned about suicide, Anthony re-
ported thoughts of wanting to join his wife, but he had no acute suicide plan or intent. He drank
one glass of red wine daily for the last twenty years without any history of abuse. Because he and
 Chapter 19 • Case Vignettes: Older Adulthood 131

his wife used to do almost everything together, Anthony was feeling very lonely and had much
survivor’s guilt.
Anthony, whose only medication is one aspirin and a multivitamin daily, had been evalu-
ated by his internist and given a good bill of health. He denied any personal history of depression
or emotional problems or any in his family. He reported that his daughter and extended family
were supportive, but life was just not the same without his wife. Anthony had used spiritual re-
sources that had been somewhat helpful at times, but he seemed to fall back again into the
mourning process.
In addition, Anthony reported increasing forgetfulness and memory dysfunction over the
past year. There was no pattern or consistency to his cognitive dysfunction. According to him,
“Some days I can remember recent things . . . some days I can remember past things.”
Furthermore, his daughter reported that he had stopped his morning walks and had dropped out
of his bowling league.

Postcase Discussion and Diagnosis

Anthony clearly has the diagnosis of major depression, single episode, moderate (296.22). Upon
further interview, the patient had significantly worsened over the past three months, since the
first anniversary of his wife’s death. His depressive episode has been further characterized by an-
hedonia, isolation, distractibility, hopelessness, helplessness, and worthlessness. In order to eval-
uate the memory complaints, a MMSE was completed during his initial visit with the score being
27/30 (-1 orientation, -1 attention, -1 recall). His effort on this examination was poor due to his
level of depression. He was referred for psychotherapy to help facilitate the grieving process,
which was most likely the root of his clinical depression.

Psychopharmacological Treatment
Anthony was started on sertraline (Zoloft), 25 mg/day for the first week. then 50 mg/day there-
after. He had requested this medication after seeing an advertisement on TV. After taking the
medication for two weeks, it was unclear whether he was benefiting or not. He reported having
no side effects. At that time, the sertraline was increased to 75 mg/day for the third week, then
100 mg/day thereafter. During his next visit, he reported a moderate response to the sertraline
100 mg/day after taking it for two weeks. The only side effect he reported was mild loosening of
his bowel movements, which were tolerable. Anthony engaged in psychotherapy with full remis-
sion of his grief and depression and even invited his daughter to a few sessions. At three months
in treatment, his MMSE was 30/30, revealing that he was cognitively intact. The initial cognitive
dysfunction was due to his depression rather than to a dementing process. Again, the combina-
tion of psychotherapy and medication management was helpful in restoring Anthony’s previous
level of functioning.

MARGARITA
Clinical History
Margarita is a 70-year-old Hispanic-American female who was referred by her primary care
physician and managed-care plan for ongoing evaluation and treatment. She stated her chief
complaint insisting, “I need my medication, doctor. . . . I can’t go without it or I’ll get sick again.”
The patient gave a long psychiatric history with multiple psychiatric hospitalizations dating back
132 Chapter 19 • Case Vignettes: Older Adulthood

to her twenties. She now reported that a man was bothering her, making sexual advances to her, and
frequently attempting to have “brain sex” with her. Upon further questioning, she reported hearing
his voice at night through the walls in her single-family home. She got rather upset, angry, and
paranoid that this was happening to her and frequently called the police for help. She stated, “The
police don’t even try to help me anymore. . . . They say that he is not real.” Margarita went on to re-
port “strange sensations” on her skin when she was out in public (e.g., grocery store or bank) and
related these sensations to men looking at her amorously. She has siblings and other relatives but re-
fuses contact with them saying they are “cursed.” The patient also reported a history of depression
and moodiness with one previous suicide attempt by overdosing about fifteen years ago.
Margarita is currently taking chlorpromazine (Thorazine), 500 mg/day, diazepam
(Valium), 30 mg/day, imipramine (Tofranil), 100 mg/day, and chloral hydrate (Notec) 500 mg/day.
She also takes antihypertensive medication, an oral agent for her diabetes, and an inhaler for her
emphysema. She reported that she had been on this psychiatric medication regimen for years
with marginal functioning. She had a history of alcohol abuse when she was in her thirties and
forties and reported that the alcohol helped decrease her mood swings. Her psychiatric family
history revealed that her paternal grandmother was institutionalized in a sanitarium, and her ma-
ternal aunt had depression with multiple suicide attempts. The family had no history of substance
abuse. Margarita’s social history revealed that she was different from her peers even in her teens.
She attempted college but dropped out because she could not concentrate and focus on her work.
Although she had never been employed, she had been financially supported by a trust fund from
her father who was a wealthy businessman in Mexico.

Postcase Discussion and Diagnosis

Margarita has the diagnosis of schizoaffective disorder, bipolar type (295.70). Observation of her
during the interview revealed mild to moderate tardive dyskinesia of the face and upper extremi-
ties, resulting from years of exposure to the typical neuroleptics. She appeared very isolated and
lonely, which was most likely the result of her chronic psychiatric disability. Although Margarita
never had a clear manic episode, she had experienced mixed mood states that were indicative of
the bipolar type of the diagnosis. Medication changes could be extremely helpful in decreasing
her psychotic mood symptoms.

Psychopharmacological Treatment
After developing some trust with the patient over a few weeks time, her psychiatrist adjusted her
medications to an alternative regimen that should be more helpful. The chlorpromazine 500
mg/day was replaced gradually by risperidone (Risperdal) 3–4 mg/day for her psychotic symp-
toms, which seemed to be the most bothersome at this time. Subsequently, the diazepam and
chloral hydrate were tapered slowly over a period of six to eight weeks. Topiramate (Topamax)
was a logical alternative to replace these two medications, given Margarita’s mood instability, in-
somnia, and anxiety. After these changes were implemented, the imipramine was reevaluated
and tapered to reduce her polypharmacy regimen. She should not be given benzodiazepines be-
cause of her history of alcohol abuse.
After six months of treatment, Margarita was taking risperidone 3 mg/day and topiramate
200 mg/day without any significant side effects. She still had some unusual thoughts and con-
cerns, but she was functioning much better on a daily basis with an improved quality of life. The
tardive dyskinesia was still present at the same level, but it should not worsen with this atypical
antipsychotic drug regimen.
 APPENDIX
Table of Psychotropic Medications
Abbreviations used in the table include the following:
DA (dopamine), EPS (extra pyramidal symptoms),
GABA (gamma-aminobutyric acid), H (histamine),
5 HT (serotonin), M (muscarinic), NE (norepinephrine),
NMS (neuroleptic malignant syndrome),
WBC (white blood count)

133
134

Generic Name Trade/Brand Mechanism

(Drug Class) Name of Action Typical Dose (MG/Day) Most Common Side Effects

acamprosate Campral GABA receptor 2000–3000 Diarrhea, dyspepsia, headache, nausea, vomiting,
(antialcohol) modifier rash
alprazolam Xanax, Xanax Increases GABA 0.25–4 Poor coordination, dizziness, sedation, weakness,
(antianxiety) XR memory dysfunction, depression, lethargy
amantadine Symmetrel DA agonist 100–300 Nausea, dizziness, insomnia, dry mouth,
(antiparkinsonian) constipation, confusion, fatigue, anxiety
amitriptyline Elavil 5-HT reuptake 150–300 Sedation, weight gain, dry mouth, blurry vision,
(antidepressant) inhibition, NE constipation, urinary retention, sexual dysfunction,
reuptake inhibition ortho static hypotension, dizziness
amoxapine Ascendin NE reuptake 150–400 Sedation, weight gain, dry mouth, blurry vision,
(antidepressant) inhibition, 5-HT constipation, urinary retention, sexual dysfunction,
reuptake inhibition orthostatic hypotension, dizziness
amphetamine Adderall, NE and DA 5–60 Insomnia, anorexia, weight loss, irritability,
(psychostimulant) Adderall XR reuptake inhibition, tachycardia, agitation, abdominal pain, headache,
promotes NE and dry mouth, increased psychosis, asthenia, fever,
DA release infection, growth retardation (children)
aripiprazole Abilify, Abilify D2 partial agonist, 10–30 (9.75 mg injection) Nausea, vomiting, headache, insomnia,
(antip-sychotic) Discmelt, 5-HT1A partial somnolence, dizziness, akathisia, abnormal vision,
Ability agonist, 5-HT2A orthostatic hypotension, NMS, TD, hyperglycemia,
Injection antagonism, alpha- leukopenia, tremor, constipation, lethargy
1 antagonism
armodafanil Nuvigil DA reuptake 150–250 Headache, nausca, dizziness, insomnia, anxiety, dry
(antinar-colepsy) inhibition mouth, diarrhea, rash
asenapine Saphris 5-HT 10–20 Akathisia, oral hypoesthesia, somnolence,
(antipsychotic) 1A/1B/2A/2B/2C dizziness, EPS, increased weight, NMS, TD,
5/6/7 antagonism, orthostatic hypotension, leukopenia, QT-interval
D1-4 antagonism, prolongation, hyperprolactinemia, insomnia,
alpha-1/2 constipation, headache, cognitive and motor
antagomnism, H1-2 impairment, hyperglycemia
antagonism
atomoxetine Strattera NE reuptake 40–100 Aggression, irritability, somnolence, vomiting,
(anti-ADHD) inhibition dyspepsia, nausea, fatigue, decreased appetite
 Generic Name Trade/Brand Mechanism
(Drug Class) Name of Action Typical Dose (MG/Day) Most Common Side Effects

baclofen Kemstro, CNS depressant 10–80 Dizziness, weakness, fatigue, confusion, head-
(antialcohol) Lioresal (muscle relaxer) ache, insomnia, hypotension, nausea, constipation,
urinary frequency,
benztropine Cogentin Anticholinergic 2–6 Tachycardia, nausea, constipation, confusion, dry
(anticholinergic) mouth, urinary retention, blurry vision
bromocriptine Parlodel DA agonist 2.5–15 Dizziness, nausea, vomiting, dry mouth, poor
(antiparkinsonian) appetite, abdominal pain, diarrhea, dyspepsia,
constipation
buprenorphine Subutex Partial agonist at 2–16 Nausea, vomiting, constipation, liver dysfunction,
(antiopioid) muopioid receptor, respiratory depression
antagonist at
kappa-opioid
receptor
buprenorphine, Suboxone Mixed opioid 2–16/0.5–4 Nausea, vomiting, constipation, liver dysfunction,
naloxone agonist- respiratory depression, acute withdrawal
(antiopioid) antagonist/opioid syndrome
antagonist
bupropion Wellbutrin, NE reuptake 75–450/100–400/ Insomnia, dizziness, headache, dry mouth, nausea,
(antidepressant) Wellbutrin SR inhibition, DA 150–450 decreased appetite, constipation,
(Zyban), reuptake inhibition agitation/nervousness, seizure
Wellbutrin
XL, Aplenzin
buspirone Buspar 5-HT1A agonist, 5–40 Dizziness, insomnia, nervousness, dry mouth,
(antianxiety) moderate D2 drowsiness, nausea, headache, fatigue
agonist
carbamazepine Tegretol, Inhibition of 600–1200 Nausea, vomiting, diplopia, dizziness, poor
(mood stabilizer) Tegretol XR, sodium channels coordination, drowsiness, anemia, rash, liver
Carbatrol, dysfunction, fatigue, low WBCs
Equetro
chloral hydrate Noctec CNS depressant 500–1000 Drowsiness, dizziness, rash, confusion, restlessness,
(sedative- amnesia, irritability
hypnotic)
chlordiazepoxide Librium Increases GABA 15–40 Poor coordination, dizziness, sedation, weakness,
(antianxiety) memory dysfunction, depression, lethargy

(continued)
135
136
Generic Name Trade/Brand Mechanism
(Drug Class) Name of Action Typical Dose (MG/Day) Most Common Side Effects
chlordiazepoxide/ Limbitrol Increases GABA, 30–60/75–150 Poor coordination, dizziness, sedation, weakness,
amitriptyline 5-HT reuptake memory dysfunction, depression, lethargy, weight gain,
(antianxiety) inhibition, NE dry mouth, blurry vision, constipation, urinary retention,
reuptake inhibition sexual dysfunction, orthostatic hypotension
chlorpromazine Thorazine D2 antagonism 200–600 Sedation, weight gain, dry mouth, dizziness, poor
(antipsychotic) coordination, EPS, photosensitivity, lethargy, blurry
vision, constipation, seizures, tachycardia, weakness,
NMS, gynecomastia, leukopenia, hyperglycemia,
hyperlipidemia, QT-interval prolongation
citalopram Celexa 5-HT reuptake 10–60 Nausea, diarrhea, dry mouth, anorexia, weight gain,
(antidepressant) inhibition sexual dysfunction, tremor, restlessness,
anxiety/nervousness, insomnia, dizziness, headache
clomipramine Anafranil 5-HT reuptake 100–250 Sedation, weight gain, dry mouth, blurry vision,
(antidepressant) inhibition, NE constipation, urinary retention, sexual dysfunction,
reuptake inhibition orthostatic hypotension, dizziness
clonazepam Klonopin, Increases GABA 0.5–4 Poor coordination, dizziness, sedation, weakness,
(antianxiety, mood Klonopin memory dysfunction, depression, lethargy
stabilizer) wafers
clonidine Catapres, Central alpha 0.1–0.3 Drowsiness, dizziness, constipation, sedation,
(anti-ADHD, Catapres agonist weakness, fatigue, agitation, nausea, vomiting,
antianxiety) patch sexual dysfunction, myalgias, arthralgias,
hypotension
clorazepate Tranxene Increases GABA 15–60 Poor coordination, dizziness, sedation, weakness,
(antianxiety) memory dysfunction, depression, lethargy
clozapine Clozaril, D4 antagonism, 400–600 Agranulocytosis, eosinophilia, seizures, myocarditis,
(antipsychotic) Fazaclo alpha 2 dizziness, tachycardia, tremor, hyperglycemia,
antagonism, H1 fever, weight gain, sedation, salivation, sweating,
antagonism, 5-HT constipation, headache, orthostatic hypotension,
antagonism hyperglycemia, hyperlipidemia, QT-interval
prolongation
desipramine Norpramin NE reuptake 150–300 Sedation, weight gain, dry mouth, blurry vision,
(antidepressant) inhibition constipation, urinary retention, sexual dysfunction,
orthostatic hypotension, dizziness
desvenlafaxine Pristiq NE reuptake 50–100 Nausea, dizziness, insomnia, hyperhidrosis,
(anti-depressant inhibition, 5-HT constipation, somnolence, decreased appetite,
reuptake inhibition anxiety, sexual dysfunction, vomiting
 dexmethylphenidate Focalin, NE reuptake 5–40 Insomnia, anorexia, weight loss, irritability,
(psychostimulant) Focalin XR inhibition, DA tachycardia, agitation, abdominal pain, headache,
reuptake inhibition, dry mouth, increased psychosis, asthenia, fever,
promotes NE and infection, growth retardation (children)
DA release
dextroamphetamine Dexedrine, NE reuptake 5–60 Insomnia, anorexia, weight loss, irritability,
(psychostimulant) Dexedrine inhibition, DA tachycardia, agitation, abdominal pain, headache,
Spansules, reuptake inhibition, dry mouth, increased psychosis, asthenia, fever,
Dextrostat promotes NE and infection, growth retardation (children)
DA release
diazepam Valium Increases GABA 5–40 Poor coordination, dizziness, sedation, weakness,
(antianxiety) memory dysfunction, depression, lethargy
diphenhydramine Benadryl Antihistamine 25–50 Sedation, dry mouth, dizziness, nausea,
(antiparkinsonian) nervousness, headache
disulfiram Antabuse Acetaldehyde 250–500 Drowsiness, fatigue, headache, sexual dysfunction,
(antialcohol) dehydrogenase rash, psychotic-like reactions, liver dysfunction
antagonist
donepezil Aricept Cholinesterase 5–10 Nausea, vomiting, insomnia, diarrhea, muscle
(antidementia) inhibitor cramps, fatigue, anorexia,
doxepin Sinequan, NE reuptake 150–300 Sedation, weight gain, dry mouth, blurry vision,
(antidepressant) Adapin inhibition, 5-HT constipation, urinary retention, sexual dysfunction,
reuptake inhibition dizziness, orthostatic hypotension
doxepin (sedative- Silenor NE reuptake 3–6 Sedation, weight gain, dry mouth, blurry vision,
hypnotic) inhibition, 5-HT constipation, urinary retention, sexual dysfunction,
reuptake inhibition dizziness, orthostatic hypotension
droperidol Inapsine D2 antagonism 2.5–15 Sedation, weight gain, dry mouth, dizziness, poor
(antipsychotic) coordination, EPS, NMS, lethargy, blurry vision,
seizures, constipation, tachycardia, weakness,
gynecomastia, leukopenia, hyperglycemia,
hyperlipidemia, QT-interval prolongation
duloxetine Cymbalta NE reuptake 20–60 Nausea, hypertension, anorexia, dizziness,
(antidepressant) inhibition, 5-HT somnolence, insomnia, dry mouth, nervousness,
reuptake inhibition sexual dysfunction, sweating
escitalopram Lexapro 5-HT reuptake 5–20 Nausea, diarrhea, dry mouth, anorexia, weight
(antidepressant) inhibition gain, sexual dysfunction, tremor, restlessness,
anxiety/nervousness, insomnia, dizziness,
137

headache
(continued)
138 Generic Name Trade/Brand Mechanism
(Drug Class) Name of Action Typical Dose (MG/Day) Most Common Side Effects
estazolam Prosom Increases GABA 2–4 Sedation, dizziness, falling, lethargy, disorientation,
(sedative-hypnotic) amnesia
eszopiclone Lunesta Selective 2–3 Daytime drowsiness, dizziness, falls, amnesia,
(sedative-hypnotic) modulation of unpleasant taste
GABA receptor
complex
fluoxetine Prozac, 5-HT reuptake 20–80/90 (weekly) Nausea, diarrhea, dry mouth, anorexia, weight
(antidepressant) Sarafem, inhibition gain, sexual dysfunction, tremor, restlessness,
Prozac anxiety/nervousness, insomnia, dizziness,
Weekly headache
fluoxetine, Symbyax Inhibition of 5-HT 6–12/25–50 see fluoxetine and olanzepine
olanzepine reuptake/DA and 5-
(antidepressant HT2 antagonism
antipsychotic)
fluphenazine Prolixin, D2 antagonism 2–20/25–50 every Sedation, weight gain, dry mouth, dizziness, poor
(antipsychotic) Prolixin 2 weeks coordination, EPS, NMS, lethargy, blurry vision,
decanoate seizures, constipation, tachycardia, weakness,
gynecomastia, leukopenia, hyperglycemia,
hyperlipidemia, QT-interval prolongation
flurazepam Dalmane Increases GABA 15–30 Sedation, dizziness, falling, lethargy, disorientation,
(sedative-hypnotic) amnesia
fluvoxamine Luvox 5-HT reuptake 50–300 Nausea, diarrhea, dry mouth, anorexia, weight
(antidepressant) inhibition gain, sexual dysfunction, tremor, restlessness,
anxiety/nervousness, insomnia, dizziness,
headache
gabapentin Neurontin Enhances GABA 300–3600 Dizziness, somnolence, edema, weight gain,
(mood stabilizer) diplopia, headache, agitation, nausea, tremors
galantamine Reminyl Cholinesterase 16–24 Nausea, vomiting, asthenia, sweating, dizziness,
(antidementia) inhibitor headache, diarrhea, anorexia, insomnia
guanfacine Tenex Central alpha-2A 0.5–3 Drowsiness, dizziness, constipation, sedation,
(anti-ADHD) agonist weakness, fatigue, agitation, nausea, vomiting,
sexual dysfunction, myalgias, arthralgias,
hypotension
guanfacine Intuniv Central alpha-2A 1–4 Somnolence, sedation, abdominal pain, dizziness,
extended release agonist hypotention/decreased blood pressure, dry mouth,
(anti-ADHD) constipation, headache, fatigue
 halazepam Paxipam Increases GABA 60–160 Poor coordination, dizziness, sedation, weakness,
(antianxiety) memory dysfunction, depression, lethargy
haloperidol Haldol, D2 antagonism 2–20/100–300 every Sedation, weight gain, dry mouth, dizziness, poor
(antipsychotic) Haldol month coordination, EPS, NMS, lethargy, blurry vision,
Decanoate seizures, constipation, tachycardia, weakness,
gynecomastia, leukopenia, hyperglycemia,
hyperlipidemia, QT-interval prolongation
hydroxyzine Vistaril, Antihistamine 50–150 Confusion, irritability, dry mouth, constipation,
(antianxiety) Atarax dizziness, blurry vision, sedation
iloperidone Fanapt 5-HT2A 12-24 Dizziness, dry mouth, fatigue, nasal congestion,
(antipsychotic) antagonism, D2 orthostatic hypotension, somnolence, tachycardia,
and D3 increased weight, nausea, leukopenia,
antagonism,alpha-1 hyperglycemia, hyperlipidemia, QT-interval
and alpha-2 prolongation, NMS, EPS
antagonism
imipramine Tofranil 5-HT reuptake 150–300 Sedation, weight gain, dry mouth, blurry vision,
(antidepressant) inhibition, NE constipation, urinary retention, sexual dysfunction,
reuptake inhibition orthostatic hypotension, dizziness
isocarboxazid Marplan 5-HT reuptake 10–40 Nausea, insomnia, drowsiness, dry mouth,
(antidepressant) inhibition, NE increased appetite, dizziness, headache, irritability,
reuptake inhibition, nervousness, weakness, sexual dysfunction, muscle
DA reuptake twitching/cramps, constipation, weight gain,
inhibition hypertensive crisis
L-alpha-acetyl- LAAM, Synthetic opioid 20–80 three times weekly Feelings of unreality, hallucinations, hives, itching,
methadol Orlaam agonist rash, sweating, restlessness, nausea, vomiting,
(methadone dizziness, sedation, muscle twitching, depression,
maintenance) QT-interval prolongation, Torsades de pointes,
cardiac arrest
lamotrigine (mood Lamictal, Inhibition of sodium 200–400 Nausea, vomiting, dizziness, diplopia, poor
stabilizer) Lamictal XR, channels, coordination, somnolence, headache, toxic rash
Lamictal ODT presynaptic
modulation of
glutamate release
lisdexamfetamine Vyvanse Prodrug of 30–70 Decreased appetite, dizziness, dry mouth,
(anti-ADHD) dextroamphetamine irritability, insomnia, upper abdominal pain,
nausea, vomiting, decreased weight, diarrhea,
fatigue, irritablility, feeling jittery, anorexia,
139

headache, anxiety, insomnia, tics

(continued)
140

Generic Name Trade/Brand Mechanism

(Drug Class) Name of Action Typical Dose (MG/Day) Most Common Side Effects
lithium carbonate Lithobid, Enhances 5-HT, 600–1200 Anorexia, dry mouth, nausea, vomiting, diarrhea,
or lithium citrate Eskalith CR increases or drowsiness, muscle weakness, decreased
(mood stabilizer) decreases NE, coordination, fatigue, lethargy, tremor,
blocks DA arrhythmias, polyuria, polydipsia, renal
supersensitivity, dysfunction, thyroid dysfunction, alopecia, rash,
alters second edema, increased appetite, weight gain
messengers
lorazepam Ativan Increases GABA 1–6 Poor coordination, dizziness, sedation, weakness,
(antianxiety) memory dysfunction, depression, lethargy
loxapine Loxitane D2 antagonism 20–100 Sedation, weight gain, dry mouth, dizziness, poor
(antipsychotic) coordination, EPS, photosensitivity, lethargy, blurry
vision, constipation, seizures, tachycardia,
weakness, NMS, gynecomastia, leukopenia,
hyperglycemia, hyperlipidemia, QT-interval
prolongation
maprotiline Ludiomil 5-HT reuptake 150–225 Sedation, weight gain, dry mouth, blurry vision,
(antidepressant) inhibition constipation, urinary retention, sexual dysfunction,
orthostatic hypotension, dizziness
mazindol Sanorex, NE reuptake 1–3 Constipation, dizziness, dry mouth, headache,
(anticocaine) Mazanor inhibition, DA irritability, nausea, vomiting, restlessness,
reuptake inhibition, abdominal cramps, insomnia
promotes NE and
DA release
memantine Namenda NMDA antagonists 10–20 Fatigue, pain, dizziness, hypertension, nausea,
(antidementia) insomnia, flulike symptoms, edema, anxiety,
anorexia, arthralgias, diarrhea, poor coordination,
agitation, urinary incontinence, urinary tract
infection
mesoridazine Serentil D2 antagonism 50–400 Sedation, weight gain, dry mouth, dizziness, poor
(antipsychotic) coordination, EPS, photosensitivity, lethargy, blurry
vision, constipation, seizures, tachycardia,
weakness, NMS, gynecomastia, leukopenia,
hyperglycemia, hyperlipidemia, QT-interval
prolongation
 methamphetamine Desoxyn NE reuptake 5–30 Insomnia, anorexia, weight loss, irritability,
(psychostimulant) inhibition, DA tachycardia, agitation, abdominal pain, headache,
reuptake inhibition, dry mouth, hypertension, increased psychosis,
promotes NE and twitching
DA release
methadone Dolophine Synthetic opioid 20–100 Feelings of unreality, hallucinations, hives, itching,
(methadone agonist rash, sweating, restlessness, nausea, vomiting,
maintenance) dizziness, sedation, muscle twitching, depression
methylphenidate Ritalin, Ritalin NE reuptake 10–50 Insomnia, anorexia, weight loss, irritability,
(psychostimulant) SR, Ritalin LA, inhibition, DA tachycardia, agitation, abdominal pain, headache,
Metadate CD, reuptake inhibition, dry mouth, increased psychosis, asthenia, fever,
Metadate ER, promotes NE and infection, growth retardation (children), tics,
Methylin, DA release crying, nausea, vomiting, nasal congestion
Concerta
methylphenidate Daytrana NE reuptake 12.5–37.5 cm2 Application site reactions, insomnia, anorexia,
transdermal system inhibition, DA weight loss, irritability, tachycardia, agitation,
(anti-ADHD) reuptake inhibition, abdominal pain, headache, dry mouth, increased
promotes NE and psychosis, asthenia, fever, infection, growth
DA release retardation (children), tics, crying, nausea,
vomiting, nasal congestion
milnacipran Savella NE reuptake 100–200 Serotonin syndrome, heart rate increased, seizures,
(antifibromyalgia) inhibition, 5-HT hepatotoxicity, discontinuation syndrome,
reuptake inhibition abnormal bleeding, nausea, constipation,
headache, dizziness, insomnia, hot flush,
hyperhidrosis, vomiting, palpitations, dry mouth.
mirtazepine Remeron, Central presynaptic 15–45 Sedation, weight gain, increased appetite, dry
(antidepressant) Remeron alpha-2 mouth, constipation, dizziness, asthenia
Soltabs autoreceptor
antagonist, H1
antagonist,
moderate alpha-1
antagonist,
moderate
muscarinic
antagonist
modafinil Provigil DA reuptake 100–200 Headache, nausea, nervousness, rhinitis, diarrhea,
(antinarcolepsy) inhibition back pain, insomnia, dizziness, dyspepsia
141

(continued)
142 Generic Name Trade/Brand Mechanism
(Drug Class) Name of Action Typical Dose (MG/Day) Most Common Side Effects
molindone Moban D2 antagonism 20–100 Sedation, weight gain, dry mouth, dizziness, poor
(antipsychotic) coordination, EPS, photosensitivity, lethargy, blurry
vision, constipation, seizures, tachycardia, weakness,
NMS, gynecomastia, leukopenia, hyperglycemia,
hyperlipidemia, QT-interval prolongation
nalmefene Revex Opioid antagonist 20–80 Liver dysfunction, constipation, irritability,
(antialcohol) increased thirst, dizziness, rash, chills, anorexia
naloxone Narcan Opioid antagonist 0.4–2 Acute withdrawal syndrome, agitation,
(antiopioid) hallucinations, flushing, dyspnea, hypotension,
hypertension, arrhythmias
naltrexone Revia Opioid antagonist 50 Liver dysfunction, constipation, irritability,
(antialcohol) increased thirst, dizziness, rash, chills, anorexia,
nausea, fatigue, anxiety, insomnia
naltrexone Vivitrol Opioid antagonist 380 mg/4 wks Injection site reactions, eosinophilic pneumonia,
(antialcohol) nausea, headache, asthenia, dizziness, insomnia,
pharyngitis, diarrhea, vomiting
nefazodone Serzone 5-HT2A antagonist 100–500 Dizziness, blurry vision, headache, dry mouth,
(antidepressant) nausea, constipation, agitation, increased appetite,
drowsiness, weakness, liver toxicity
nortriptyline Pamelor, NE reuptake 75–125 Sedation, weight gain, dry mouth, blurry vision,
(antidepressant) Aventyl inhibition, 5-HT constipation, urinary retention, sexual dysfunction,
reuptake inhibition orthostatic hypotension, dizziness
olanzepine Zyprexa, 5-HT2A and 5- 10–20 (5-10 mg IM) Weight gain, increased appetite, constipation,
(antipsychotic) Zyprexa Zydis, HT2C antagonism, agitation, dizziness, dry mouth, sedation, abnormal
Zyprexa IM D1–D4 antagonism, gait, back pain, speech disorder, amnesia, tremor,
M1–M5 weakness, leukopenia, hyperglycemia,
antagonism, H1 hyperlipidemia, EPS, NMS, cognitive and motor
antagonism, alpha-1 impairment, seizures, hyperprolactinemia,
antagonism orthostatic hypotension
olanzepine Zyprexa 5-HT2A and 5-HT2C 150 mg/2 wks–405 mg/ See olanzepine + injection site reactions
(antipsy-chotic) Relprevv antagonism, D1–D4 4 wks
antagonism, M1–M5
antagonism, H1
antagonism, alpha-1
antagonism
ondansetron Zofran 5-HT3 antagonist 8–24 Diarrhea, headache, constipation, rash, dizziness,
(anticraving) dry mouth, drowsiness
 orlistat Xenical Reversible lipase 360 Oily spotting or stool, flatus, fecal urgency,
(antiobesity) inhibitor in GI tract increased defecation, fecal incontinence
oxazepam Serax Increases GABA 30–120 Poor coordination, dizziness, sedation, weakness,
(antianxiety) memory dysfunction, depression, lethargy
oxcarbazepine Trileptal Inhibition of sodium 600–1500 Dizziness, somnolence, diplopia, nausea, vomiting,
(mood stabilizer) channels, headache, ataxia, abnormal vision, abdominal
modulation of pain, tremor
calcium channels
paliperidone Invega D2 antagonism, 3–12 EPS, tachycardia, akathisia, somnolence, dyspepsia,
(antipsychotic) 5-HT2 antagonism, constipation, increased weight, naso-pharyngitis,
alpha-1 and alpha-2 headache, leukopenia, hyperglycemia,
antagonism, H1 hyperlipidemia, QT-interval prolongation, NMS
antagonism
paliperidone Invega D2 antagonism, 5- 39–234 See paliperidone + injection site reactions
palmitate Sustenna HT2 antagonism,
(antipsychotic) alpha-1 and alpha-2
antagonism, H1
antagonism
paroxetine Paxil, Paxil 5-HT reuptake 20–50/25–75 Nausea, diarrhea, dry mouth, anorexia, weight
(antidepressant) CR inhibition gain, sexual dysfunction, tremor, restlessness,
anxiety/nervousness, insomnia, dizziness,
headache
pemoline Cylert DA mechanisms 37.5–112.5 Liver dysfunction, agitation, seizures, insomnia,
(psychostimulant) (??) anorexia, weight loss
perphenazine Trilafon D2 antagonism 8–64 Sedation, weight gain, dry mouth, dizziness, poor
(antipsychotic) coordination, EPS, photosensitivity, lethargy, blurry
vision, constipation, seizures, tachycardia,
weakness, NMS, gynecomastia, leukopenia,
hyperglycemia, hyperlipidemia, QT-interval
prolongation
perphenazine/ Triavil D2 antagonism, 5–6–16/75–200 Sedation, weight gain, dry mouth, dizziness, poor
amitriptyline 5-HT reuptake coordination, EPS, photosensitivity, lethargy, blurry
(antianxiety) inhibition, NE vision, constipation, seizures, tachycardia,
reuptake inhibition weakness, NMS, gynecomastia, urinary retention,
sexual dysfunction, leukopenia, hyperglycemia,
hyperlipidemia, QT-interval prolongation
143

(continued)
144 Generic Name Trade/Brand Mechanism
(Drug Class) Name of Action Typical Dose (MG/Day) Most Common Side Effects
phenelzine Nardil 5-HT reuptake 30–90 Nausea, insomnia, drowsiness, dry mouth,
(antidepressant) inhibition, NE increased appetite, dizziness, headache, irritability,
reuptake inhibition, nervousness, weakness, sexual dysfunction, muscle
DA reuptake twitching/cramps, constipation, weight gain,
inhibition hypertensive crisis
phentermine Adipex-P, NE reuptake 37.5–75 Insomnia, anorexia, weight loss, irritability,
(antiobesity) Ionamin inhibition, DA tachycardia, agitation, abdominal pain, headache,
reuptake inhibition, dry mouth, increased psychosis, asthenia, fever,
promotes NE and infection, growth retardation (children)
DA release
pimozide Orap D2 antagonism 1–10 Sedation, weight gain, dry mouth, dizziness, poor
(antipsychotic) coordination, EPS, lethargy, NMS, blurry vision,
seizures, constipation, tachycardia, weakness,
gynecomastia
pindolol (anti- Visken Nonselective beta- 10–60 Anxiety, lethargy, bradycardia, hyperhidrosis, visual
anxiety) blocker disturbance, claudication, cold extremities,
hypotension, syncope, tachycardia, weight gain,
diarrhea, vomiting, wheezing, impotence, excess
urination, burning eyes
pramipexole Mirapex DA agonist 1.5–4.5 Nausea, dizziness, somnolence, insomnia,
(antiparkinsonian) constipation, confusion, asthenia, hallucinations,
edema, sedation, headache
prazepam Centrax Increases GABA 20–60 Poor coordination, dizziness, sedation, weakness,
(antianxiety) memory dysfunction, depression, lethargy
pregabalin Lyrica Voltage-gated 150–450 Dizziness, somnolence, dry mouth, edema, blurred
(antipain) calcium channels vision, weight gain, thinking abnormal, asthenia,
(increases GABA ataxia, nausea, tremor, headache, vertigo
transport)
propranolol Inderal, Nonselective beta- 20–80 Bradycardia, rash, hypotension, dizziness,
(antianxiety, Inderal LA blocker depression, weakness, bronchospasm, fatigue,
antiparkinsonian) sexual dysfunction, insomnia, alopecia
protriptyline Vivactil NE reuptake 15–60 Sedation, weight gain, dry mouth, blurry vision,
(antidepressant) inhibition, 5-HT constipation, urinary retention, sexual dysfunction,
reuptake inhibition orthostatic hypotension, dizziness
quazepam Doral Increases GABA 7.5–15 Sedation, dizziness, falling, lethargy, disorientation,
(sedative-hypnotic) amnesia
 quetiapine Seroquel, 5-HT1A and 5-HT2 300–600 Sedation, dizziness, dry mouth, asthenia,
(antipsychotic) Seroquel XR antagonism, D1 constipation, headache, liver dysfunction, weight
and D2 gain, dyspepsia, orthostatic hypotension, EPS,
antagonism, H1 NMS, leukopenia, hyperglycemia, hyperlipidemia
antagonism,
alpha-1 and alpha-2
antagonism
ramelteon Rozerem Melatonin receptor 8 Somnolence, dizziness, fatigue, nausea, headache
(sedative-hypnotic) agonist
risperidone Risperdal, D2 antagonism, 3–6 Somnolence, EPS, weight gain, anxiety,
(antipsychotic) Risperdal M- 5-HT2 antagonism, restlessness, insomnia, dizziness, constipation,
tab alpha-1 and alpha-2 nausea, rhinitis, rash, tachycardia, sexual
antagonism, H1 dysfunction, NMS, leukopenia, hyperglycemia,
antagonism hyperlipidemia, QT-interval prolongation, TD,
hyperprolactinemia, orthostatic hypotension,
cognitive and motor impairment, seizures,
dysphagia, priapism
risperidone Risperdal D2 antagonism, 25–50 mg/2 wks See risperidone + injection site reactions
(antipsychotic) Consta 5-HT2 antagonism,
alpha-1 and alpha-2
antagonism, H1
antagonism
rivastigmine Exelon Cholinesterase 6–12 Nausea, vomiting, asthenia, sweating, dizziness,
(antidementia) inhibitor headache, diarrhea, anorexia, insomnia
rivastigmine Exelon Patch Cholinesterase 4.6–9.5 mg/24 hrs Application site reactions, nausea, vomiting,
transdermal system inhibitor asthenia, sweating, dizziness, headache, diarrhea,
(antidementia) anorexia, insomnia
ropinirole Requip Dopamine agonist 0.75–3 Excessive drowsiness, syncope, bradycardia,
hypotension, hallucinations, fatigue, nausea,
headache, vomiting, dyspepsia, constipation,
increased sweating, asthenia, confusion abdominal
pain, abnormal vision, leg edema
selegiline Eldepryl 5-HT reuptake 10–20 Nausea, hallucinations, insomnia, dizziness,
(antidepressant) inhibition, NE confusion, poor balance, agitation, syncope,
reuptake inhibition, hypertensive crisis (higher doses)
DA reuptake
inhibition
145

(continued)
146 Generic Name Trade/Brand Mechanism
(Drug Class) Name of Action Typical Dose (MG/Day) Most Common Side Effects
selegiline EMSAM 5-HT reuptake 6–12 mg/24 hrs Application site reactions, nausea, hallucinations,
transdermal system inhibition, NE insomnia, dizziness, confusion, poor balance,
(antidepressant) reuptake inhibition, agitation, syncope, hypertensive crisis (higher
DA reuptake doses), diarrhea, constipation
inhibition
sertraline Zoloft 5-HT reuptake 50–200 Nausea, diarrhea, dry mouth, anorexia, weight
(antidepressant) inhibition gain, sexual dysfunction, tremor, restlessness,
anxiety/nervousness, insomnia, dizziness,
headache
sibutramine Meridia NE reuptake 10–15 Headache, back pain, constipation, anorexia, dry
(antiobesity) inhibition, 5-HT mouth, dizziness, insomnia, nervousness, rhinitis,
reuptake inhibition, pharyngitis
DA reuptake
inhibition
sodium Xyrem CNS depressant 4.5–9.0 gm/night Seizure, respiratory depression, confusion,
oxybate/gamma- headache, nausea, dizziness, nasopharyngitis,
hydroxy-butyrate somnolence, vomiting, urinary incontinence
(anti-narcolepsy)
tacrine Cognex Cholinesterase 40–160 Abdominal pain, anxiety, agitation, poor
(antidementia) inhibitor coordination, constipation, depression, diarrhea,
dizziness, fatigue, flushing, headache, insomnia,
dyspepsia, liver dysfunction, muscle pain, anorexia,
nausea, rash, sedation
temazepam Restoril Increases GABA 15–30 Sedation, dizziness, falling, lethargy, disorientation,
(sedative-hypnotic) amnesia
thioridazine (anti- Mellaril D2 antagonism 200–600 Sedation, weight gain, dry mouth, dizziness, poor
psychotic) coordination, EPS, photosensitivity, lethargy, blurry
vision, constipation, seizures, tachycardia,
weakness, NMS, gynecomastia, leukopenia,
hyperglycemia, hyperlipidemia, QT-interval
prolongation
thiothixene Navane D2 antagonism 5–30 Sedation, weight gain, dry mouth, dizziness, poor
(antipsychotic) coordination, EPS, NMS, lethargy, blurry vision,
seizures, constipation, tachycardia, weakness,
gynecomastia, leukopenia, hyperglycemia,
hyperlipidemia, QT-interval prolongation
 tiagabine (mood Gabitril Increases GABA 8–16 Dizziness, asthenia, somnolence, nausea,
stabilizer) nervousness, abdominal pain, decreased
concentration, tremor, poor coordination
topiramate (mood Topamax Increases GABA, 100–500 Somnolence, fatigue, dizziness, decreased weight,
stabilizer) blocks glutamate poor coordination, speech problems, memory
receptors dysfunction, abnormal vision, paresthesias,
nervousness, confusion, cognitive dulling,
headache
tranylcypromine Parnate 5-HT reuptake 20–60 Nausea, insomnia, drowsiness, dry mouth,
(antidepressant) inhibition, NE increased appetite, dizziness, headache, irritability,
reuptake inhibition, nervousness, weakness, sexual dysfunction, muscle
DA reuptake twitching/cramps, constipation, weight gain,
inhibition hypertensive crisis
trazodone Desyrel, 5-HT2A and 5-HT2C 50–400 Somnolence/sedation, blurred vision, dizziness,
(antidepressant) Oleptro antagonism, constipation, priapism, headache, dry mouth,
alpha-1 nausea, fatigue
antagonism
triazolam (sedative- Halcion Increases GABA 0.25–0.5 Sedation, dizziness, falling, lethargy, disorientation,
hypnotic) amnesia
trifluoperazine Stelazine D2 antagonism 5–30 Sedation, weight gain, dry mouth, dizziness, poor
(antipsychotic) coordination, EPS, NMS, lethargy, blurry vision,
seizures, constipation, tachycardia, weakness,
gynecomastia, leukopenia, hyperglycemia,
hyperlipidemia, QT-interval prolongation
trihexyphenidyl Artane Anticholinergic 5–15 Tachycardia, nausea, constipation, confusion, dry
(anticholinergic) mouth, urinary retention, blurry vision
trimipramine Surmontil NE reuptake 150–300 Sedation, weight gain, dry mouth, blurry vision,
(antidepressant) inhibition, 5-HT constipation, urinary retention, sexual dysfunction,
reuptake inhibition orthostatic hypotension, dizziness
valproate or Depakote, Inhibition of sodium 500–2000 Nausea, vomiting, diarrhea, weight gain,
valproic acid (mood Depakote ER and/or calcium abdominal pain, flatulence, edema, rash,
stabilizer) channels, increases drowsiness, tiredness, liver dysfunction, alopecia
GABA, reduces
glutamate
varenicline Chantix Nicotinic 0.5–2 Angioedema, serious skin reaction, nausea,
(antismoking) acetylcholine abnormal dreams, constipation, flatulence,
receptor agonist vomiting, headache, agitation/hostility, suicide
147

ideation
(continued)
148

Generic Name Trade/Brand Mechanism

(Drug Class) Name of Action Typical Dose (MG/Day) Most Common Side Effects
venlafaxine Effexor, NE reuptake 50–300/75–300 Nausea, hypertension, anorexia, dizziness,
(antidepressant) Effexor XR inhibition, 5-HT somnolence, insomnia, dry mouth, nervousness,
reuptake inhibition sexual dysfunction, sweating
verapamil (mood Verelan PM, Calcium channel 200–400 Constipation, nausea, headache, infection,
stabilizer) Covera-HS, antagonist dizziness, edema, liver dysfunction, arrhythmias,
Isoptin SR rash, hypotension, fatigue
zaleplon (sedative- Sonata Selective 5–10 Daytime drowsiness, dizziness, falls, amnesia
hypnotic) modulation of
GABA receptor
complex
ziprasidone Geodon D2 antagonism, 80–160 Nausea, agitation, rash, EKG abnormality, asthenia,
(antipsychotic) 5-HT2 antagonism, orthostatic hypotension, anorexia, arthralgias,
H1 antagonism, anxiety, tremor, rhinitis, abnormal vision, EPS, NMS,
alpha-1 leukopenia, hyperglycemia, hyperlipidemia, QT-
antagonism interval prolongation
zolpidem (sedative- Ambien, Selective 5–10 Daytime drowsiness, dizziness, falls, amnesia
hypnotic) Edluar, modulation of
Zolpimist GABA receptor
complex
zonisamide (mood Zonegran Inhibition of sodium 200–400 Somnolence, anorexia, weight loss, dizziness,
stabilizer) and/or calcium headache, nausea, agitation, mental slowing
channels, facilitates
DA and 5-HT
neurotransmission
 GLOSSARY
acetaldehyde dehydrogenase. An enzyme that converts bradykinesia. A decrease in movement and spontaneity.
acetaldehyde to harmless acetate. bruxism. A condition in which the patient grinds his/her
acetylcholine. In the central nervous system, a neuro- teeth during sleep.
transmitter thought to play a role in memory, learning, be- chloride ion channels. Tiny gateways or receptor sites
havioral arousal, attention, mood and rapid-eye movement found on the surface of cells. These are opened or activated
activity during sleep. In the peripheral nervous system, by various neurotransmitters.
acetylcholine is found at synapses where the nerve termi-
nals meet skeletal muscles, causing excitation leading to cholinergic. Relating to nerve cells that utilize acetyl-
muscle contraction. choline as their neurotransmitter.

acetylcholinesterase inhibitors. Medications that in- cross-titration. Gradual decrease or tapering of a drug
crease intra-synaptic acetylcholine levels and produce mod- dose while gradually increasing the dose of a second drug
erate symptomatic improvement in Alzheimer’s disease. or agent.
action potential. Produced in a neuron when the rest- dehydroepiandrosterone (DHEA). A steroid secreted by
ing potential becomes less negative or depolarized. It is the adrenal gland and the testes that is a precursor to testos-
mediated by voltage-dependent ion channels that trans- terone and estrogen.
mit the essential cellular information for that neuron’s dendrites. The branchlike part of the neuron that collects
function. chemical messages via its molecular receptor sites from
adequate dose. The dose recommended in the package nearby cells. The surface of the dendrite is also referred to
labeling of a medication, indicating what is typically as the “postsynaptic membrane.”
prescribed. depolarization. Results from an increase in the permeabil-
adequate treatment trial. A time period of a minimum of ity of a cell’s membrane, resulting in an action potential.
four weeks and a maximum of six weeks before making a depression treatment protocol. Procedural steps used in
major change in the treatment regimen because the pa- the treatment of depressive illness.
tients’ response to medication may be delayed. discontinuation syndrome. Various symptoms experi-
agonist. A drug that increases the action of a neurotrans- enced after the discontinuation of medication. These are
mitter at its receptor site. not typically dangerous although they may mimic with-
akathisia. A common subacute side effect that may be drawal symptoms.
experienced as inner restlessness, anxiety, agitation. Dopamine. A biogenic amine neurotransmitter involved
antagonist. A drug that prevents an action of a neuro- in behavioral regulation, movement, learning, mood, atten-
transmitter at its receptor site. tion, and the reward cycle of addiction.
anticonvulsants (anti-seizure medication). A variety of dopaminergic. Pertaining to the action or function of
medication used for treatment of epileptic seizures and dopamine.
used in the treatment of bipolar disorder and other psychi- endogenous substances. Substances that come from
atric conditions. within the body, such as endorphins, insulin, and adrenalin.
atypical antipsychotic medication. Second-generation electrocardiogram (ECG or EKG). A record of the
antipsychotic drugs used to treat psychiatric conditions. heart’s integrated action currents often obtained in a rou-
axon. A cylindrical, tubelike tail of a neuron that transmits tine physical or cardiac workup.
information from the soma to its terminal buttons and ulti- electroconvulsive therapy (ECT). A series of treatments
mately to other neurons or cells. involving the application of electrical current to the brain
barbiturates. Medications such as Nembutal and Seconal of an anesthetized patient. This induces a seizure to bring
used in the treatment of anxiety that are very sedating and about an improvement in mood/psychotic states.
habit forming. electroencephalogram (EEG). A record of brain wave
benzodiazepines. Sedative-hypnotic medications used in activity, which is analyzed during a nocturnal polysomno-
the treatment of anxiety and other psychiatric conditions. gram or neurologic exam.

149
150 Glossary

epinephrine (adrenalin). A neurotransmitter, primarily mood stabilizers. A variety of psychiatric medications

of the peripheral nervous system, that regulates the fight- used to treat mood disorders characterized by intense and
or-flight response. sustained mood shifts. Lithium and anticonvulsant medica-
exocytosis. The process by which neurotransmitters are tions are examples of mood stabilizers.
released from a cell. neuron. The morphologic and functional unit in the nerv-
exogenous substances. Substances that are produced ous system involved in the transmission of chemical mes-
outside the body and introduced into the body in some sages to facilitate a thought, action, or behavior. It consists
manner. of four basic parts: the soma, dendrites, axon, and terminal
buttons.
extrapyramidal symptoms (EPS). Side effects typically
found with many medications, including neuroleptics. nocturnal polysomnogram (NPSG). A sleep study, which
These may include bradykinesia, parkinsonism, akathisia, is conducted at night in a sleep laboratory under the super-
and/or tardive dyskinesia. vision of a neurologist or a sleep specialist. This test is also
referred to as a polysomnograph (PSG) and is used to diag-
first-pass metabolism. In the body, the set of reactions in nose sleep disorders.
which orally absorbed medications first encounter the liver,
where some of the drug is metabolized and then delivered nonsteroidal anti-inflammatory drugs (NSAIDs).
to the target organ. Medications typically used to decrease inflammation and
pain that may decrease the risk of Alzheimer’s disease in
ginkgo biloba. A tree extract said to relieve mild depres- some patients.
sion and increase memory and concentration.
noradrenergic. Pertaining to the action or function of
glutamatergic. Pertaining to the action or function of norepinephrine.
glutamate.
norepinephrine. A biogenic amine neurotransmitter, which
half-life. The average time required to eliminate one-half is primarily excitatory in the central nervous system. It is in-
of a drug’s concentration from the body. volved in attention, arousal, mood, and sleep regulation.
hyperdopaminergic hypothesis. The concept that too obstructive sleep apnea (OSA). A condition character-
much dopamine may be causing psychotic symptoms. ized by obstructed airways during sleep, resulting in loud
hyperpolarization. A process that occurs after an action snoring, gasping, awakening throughout the night, and
potential when the cell briefly becomes more polarized, or periods when breathing stops (apnea).
hyperpolarized, as it returns to a relaxed state. overlap and taper. The practice of continuing the same
ion. An atom with either a positive or negative electrical dose of one drug while gradually increasing a second drug
charge. to a therapeutic level and then tapering the first.
lipid solubility. A characteristic of a drug that determines pharmacodynamics. The process of how drugs affect re-
how easily it may cross a cell membrane. Drugs that are ceptors sites, send signals, and cause neurochemical
said to be “lipophilic” are more likely to cross the blood- changes, i.e., what the drug does to the body.
brain barrier. pharmacokinetics. The process of drug administration,
loading dose. The practice of introducing a drug into the absorption, distribution, metabolism, and elimination, i.e.,
body at high doses in order to obtain a certain desired re- what the body does to the drug.
sponse, as opposed to starting with a low dose and gradu- placebo response. A demonstrated physical response
ally increasing. when a placebo is taken.
mania treatment protocol. Procedural steps used in the potentiation. A process that occurs when one drug en-
treatment of the manic phase of bipolar illness. hances the effect of another drug, For example, stimulants
mixed dementia. Dementia that may be caused by a com- and antidepressants.
bination of two neuropathological processes, which may protein binding. A process in which drugs bind to pro-
occur together. For example, Alzheimer’s disease and vas- teins in the bloodstream, which may reduce the amount of
cular dementia occurring together would be referred to as a a drug that is actually available to act at a target site based
mixed dementia. on the size of the bound protein substance. A substance
monoamine oxidase inhibitors (MAOIs). Medications that has high protein binding is not available in the blood-
that inhibit the enzyme that breaks down certain neuro- stream to act on its target. Some substances like albumin
transmitter substances and renders them ineffective. that have large molecular weight may bind to a drug and
 Glossary 151

interfere with the action of the drug at the target; i.e., they synapse. A physical gap or space between the terminal
may interfere with the transport of the drug through small buttons (presynaptic cell), and the dendrites of the next
capillary junctions. neuron (postsynaptic cell). The synapse can be between a
protein kinases. A secondary messenger activated within terminal button and a dendrite or between the terminal but-
the postsynaptic membrane by a neurotransmitter to alter ton and the soma.
neuronal functions. synergism. A process that occurs when one drug signifi-
psychostimulants. Stimulating medications (i.e., amphet- cantly enhances the effect of another drug, for example, al-
amines and methylphenidate) used primarily for enhancing cohol and sedatives.
the efficacy of antidepressants and in the treatment of ADHD. tardive dyskinesia. A potentially chronic side effect of
rebound phenomenon. The observation that after sleep antipsychotic medications. Symptoms may include invol-
deprivation patients spend additional time in stages 3, 4, untary abnormal movements of the tongue, lips, neck,
and REM in their next sleep period. limbs, and/or trunk.
resting potential. The electrical potential of the neuron in terminal button. Found at the ends of the branches of the
the unexcited or relaxed state. The average electrical differ- axon, this structure contains stored sacs of neurotransmit-
ence between the inside and the outside of the cell is about ters substance.
70 millivolts (mV). Typically referred to as –70 mV (the therapeutic dose. The concentration or dose of a drug
outside is more negative than the inside). required to achieve the desired response.
reuptake. A process that signals the end of the action po- therapeutic index. The difference between a drug’s thera-
tential; some of the neurotransmitter substance is taken peutic level and its toxic level.
back into the terminal button after exocytosis. tolerance. Condition in which a patient needs to acquire
S-adenosyl-L-methionine (Sam-E). A naturally occur- and use greater amounts of a drug to achieve the original
ring endogenous substance produced by the body and syn- desired effect.
thesized from food and essential B vitamins. Lower levels toxic rash. Associated with Stevens-Johnson syndrome, a
have been found in depressed patients. It is available as a potentially life-threatening skin rash that may require med-
synthesized dietary supplement that may increase sero- ical attention.
tonin and norepinephrine levels.
treatment refractory. Applied to an illness when a
satiation. A sensation of fullness that can be achieved patient fails to respond to three or more psychotropic
with excessive food consumption, television watching, medications.
video gaming, or drugs like benzodiazepines or alcohol.
tricyclic antidepressants (TCAs). First-generation anti-
selective serotonin reuptake inhibitors (SSRIs). depressant medications that prevent the reuptake of neuro-
Medications that block the reuptake of serotonin back into transmitter substances back into the presynaptic cell.
the presynaptic cell. typical antipsychotic medications. First-generation an-
serotonergic. Pertaining to the action or function of tipsychotic drugs used to treat psychosis and agitated mood
serotonin. states (mania, agitation, and schizophrenia).
serotonin. A neurotransmitter in the central nervous sys- ultrarapid detox. A detoxification procedure conducted
tem involved in the inhibition of obsessive thinking and under anesthesia that utilizes naloxone in combination with
compulsive behaviors, mood regulation, eating and sleep- other sedatives for an intense 24 hour detoxification.
ing patterns, and pain regulation. upper airway resistance syndrome. A milder form of
signal transduction. The process by which a neurotrans- obstructive sleep apnea. The patient is unable to keep air-
mitter binds to a receptor site, changing electrical and ways open during sleep, and the airway narrows or col-
chemical characteristics within the cell. lapses, leading to gasping or awakening throughout the
soma. The physical cell body that contains the vital parts night.
of the cell, including the nucleus, mitochondria, and other vascular dementia. Dementia occurring from disease
substances in the cytoplasm (the space inside the neuron). related to the brain’s vascular system.
St. John’s wort. A plant found to have medicinal proper- withdrawal. Characteristic symptoms that emerge when a
ties that may help to control mild to moderate levels of drug is abruptly discontinued after heavy and prolonged
depression. use, for example, alcohol.
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 INDEX
Note: Information presented in tables and figures is presented by t and f respectively.

A Ambien. see Zolpidem

Abbreviation, 17t Ambien CR. see Zolpidem
Abilify. see Aripiprazole Amitriptyline, 26t
Abilify Discmelt. see Aripiprazole Amoxapine, 26t
Absorption, 13, 14 AMP. see Cyclic AMP
a.c., 17t Amphetamines
Acamprosate, and alcohol abuse, 96, 97t, 98 in ADHD, 70t, 71
Acetylcholine, 11 and bipolar disorder, 38
and Alzheimer’s disease, 75 Anafranil. see Clomipramine
Acetylcholine receptor, 8 Anemia, and depression, 24
Action potential, 6–7 Angina, and anxiety, 49
Adapin. see Doxepin Anorexia nervosa, 105–106
Adderall. see Amphetamine Antabuse. see Disulfiram
Addiction. see Chemical dependency Antacids, 14
Addison’s disease Antagonists, defined, 11
and depression, 24 Antibiotics, 14
and psychotic disorders, 61 Anticonvulsants, for bipolar disorder, 41–42
ADHD, 68–72 Antidepressants
assessment of, 69 and bipolar disorder, 38
etiology of, 69 heterocyclic, 27–29, 28t
treatment of, 69–72, 70t, 71t pregnancy and, 34
ADHD Problem Checklist, 69 tricyclic, 25–26, 26t
Adjustment disorders, 56 Antipsychotics
Administration, routes of, 13–14 for schizophrenia, 59
Adolescents, case studies, 115–118 Anxiety disorders
Adrenalin. see Epinephrine assessment for, 21
Adrenal tumor, and anxiety, 49 comorbidity, 48
Adults, case studies, 119–128 medications for, 52t
Agonists, defined, 11 OCD, 54–55
Alcohol panic disorder (with or without agoraphobia), 50–53
and bipolar disorder, 46 pathophysiology of, 48
dependence, 96–98 social, 55–56
and depression, 24 symptoms of, 48–49
tolerance to, 16 types of, 49
withdrawal from, 16 Aplenzin. see Bupropion
Alprazolam, 52t Aricept. see Donepezil, in cognitive disorders
Alzheimer’s disease, 75 Aripiprazole
and depression, 24 in bipolar disorder, 40t, 43
as economic burden, 75 in psychotic disorders, 62, 62t, 63
and ginkgo biloba, 29, 78 Armodafinil
medications for, 76–77, 76t for narcolepsy, 83
Amantadine in sleep disturbances, 86t
and cocaine dependence, 97t, 99 Artane. see Trihexyphenidyl
in psychotic disorder, 65t Ascendin. see Amoxapine

163
164 Index

Asenapine, 40t psychotherapy for, 38–39

in psychotic disorders, 62t types of, 37
Assessment, 21–22 vs. unipolar depression, 36–37
Asthma, and depression, 24 Brain tumors
Ativan. see Lorazepam and bipolar disorder, 37
Atomoxetine, in ADHD, 71t, 72 and depression, 24
Attention deficit disorder. see ADHD Bromides, and bipolar disorder, 38
Attention Deficit/Hyperactivity Disorder Test, 69 Bromocryptine
Atypical antipsychotics and bipolar disorder, 38
for bipolar disorder, 42–43 and cocaine dependence, 99
for psychotic disorder, 63–64 Bulimia nervosa, 106–107
Atypical antipsychotics, and schizophrenia, 59 Buprenorphine
Aventyl. see Nortriptyline and cocaine dependence, 97t, 99
Axon, 5, 5f and opiate dependence, 97t, 99
Bupropion, 28t
B in ADHD, 71t
Baclofen and depression, 29
and alcohol abuse, 97t, 98 Bupropion hydrobromide, 28t
and bipolar disorder, 38 Bupropion SR, 28t
Barbiturates, 86 Bupropion XL, 28t
Beck Anxiety Inventory, 21 Buspar. see Buspirone
Beck Depression Inventory II, 21 Buspirone, 52t
BED. see Binge-eating disorder (BED)
Behavioral approaches, for sleep C
disorders, 84–85 Calan SR. see Verapamil
Behavioral toxicity, 76 Campral. see Acamprosate, and alcohol abuse
Benadryl. see Diphenhydramine Cancer, and depression, 24
Benzodiazepine receptor agonists, 85 cap., 17t
Benzodiazepines Captopril, and bipolar disorder, 38
for bipolar disorder, 44 Carbamazepine, for bipolar disorder, 40t, 41
for panic disorder, 50, 52, 53 Carbatrol. see Carbamazepine
for PLMD, 84 Carcinoid syndrome, and bipolar disorder, 37
for RLS, 84 Cardiac arrhythmia, and anxiety, 49
Benztropine Cardiovascular conditions, and depression, 24
in psychotic disorder, 65t Case studies
b.i.d., 17t of adolescents, 115–118
Binge-eating disorder (BED), 107 of adults, 119–128
Bipolar Disorder Type I, 37 of children, 111–114
Bipolar Disorder Type II, 37 of elderly, 129–132
Bipolar illness, 36–47 Catapres. see Clonidine
anticonvulsants for, 41–42 CBT. see Cognitive behavioral therapy (CBT)
causes of, 37–38 CCK. see Cholecystokinin (CCK)
counseling for, 38–39 Celexa. see Citalopram
depressive phase treatment in, 45 Centrax. see Prazepam
electroconvulsive therapy for, 44 Chantix. see Varenicline, for nicotine abuse
family education and, 46 Chemical dependency, 93–100
manic phase treatment in, 44–45 assessment for, 95
medications for, 39–44, 40t co-occurring conditions, 93–94
mixed-mood states in, 45 medications for, 96–100, 97t
patient education and, 46 treatment issues, 95
prevalence of, 36–37 treatment phases, 96
 Index 165

Children, case studies, 111–114 c with bar on top, 17t

Chlordiazepoxide, 52t Cyclic AMP, 9
Chloride ion channels, 50, 51f Cyclosporine
Chlorpromazine, 63t and bipolar disorder, 38
Cholecystokinin (CCK), 50 Cylert. see Pemoline
Cholinesterase inhibitors, for cognitive disorders, 77 Cymbalta. see Duloxetine
Chronic fatigue syndrome, 24 CYP1A2, 87
Chronic infections, and depression, 24 Cytochrome P450, 87
Chronic pain, 104–105
and depression, 24 D
Chronic sinus conditions, and anxiety, 49 Dalmane. see Flurazepam
Cimetidine, and bipolar disorder, 38 Daytrana Transdermal System. see Methylphenidate
Citalopram, 27t Delirium
Clomipramine, 26t and bipolar disorder, 37
Clonazepam, 52t Dehydroepiandrosterone (DHEA), 29, 31
in bipolar disorder, 40t, 42 Delirium, and anxiety, 49
for personality disorders, 91 Dementia. see Cognitive disorders
in psychotic disorder, 65t Dementia with Lewy bodies (DLB), 75
Clonidine, 52t Dendrites, 5, 5f
in ADHD, 71, 71t Depakene. see Valproate
Clorazepate, 52t Depakote. see Valproate
Clozapine Depakote ER. see Valproate
in bipolar disorder, 40t, 43 Depression
in psychotic disorders, 62, 62t assessment for, 21
in schizophrenia, 67 biological vs. environmental, 23–24
Clozaril. see Clozapine comorbidities, 102–103
CNS syphilis, and bipolar disorder, 37 counseling for, 25
CNS trauma, and bipolar disorder, 37 dieseases causing, 24
Cocaine, and bipolar disorder, 38 electroconvulsive therapy for, 31–32
Cocaine dependence, 99 exercise and, 31
Cogentin. see Benztropine herbal remedies for, 29, 31
Cognex. see Tacrine, in cognitive disorders light therapy for, 31
Cognitive behavioral therapy (CBT), 107 magnetic stimulation and, 32
Cognitive disorders, 74–79 medications for, 25–29, 26t, 27t, 28t, 30t
evaluation of, 76 prevalance, 23
forms of, 74–75 psychotherapy for, 25
issues to consider for, 78–79 and side effects, 33–34
medications for, 76–77, 76t and suicidal ideation, 25
Cognitive symptoms, of schizophrenia, 60 and suicide, 25
Colitis, and depression, 24 treatment steps and, 32–34
Comorbidity, 102–109 Desipramine, 26t
Concerta. see Methylphenidate in ADHD, 71t
Congestive heart failure, 24 and cocaine dependence, 97t, 99
Conner’s Adult ADHD Rating Scales, 69 Desoxyn. see Methylphenidate
Conner’s Rating Scales—Revised, 69 Desvenlafaxine, 28t
Corticosteroids, and bipolar disorder, 38 Desvenlafaxine succinate, 27
Coumadin. see Warfarin Desyrel. see Trazodone
Covera-HS. see Verapamil Dexedrine. see Dextroamphetamine
Cross-titration, 66 Dexedrine Spansules. see Dextroamphetamine
Cushing’s disease, and anxiety, 49 Dexmethylphenidate
Cushing’s disease, and depression, 24 in ADHD, 70t
166 Index

Dextroamphetamine ECT. see Electroconvulsive therapy (ECT)

in ADHD, 70t, 71 Edluar. see Zolpidem
and bipolar disorder, 38 EE. see Expressed emotion (EE)
Dextrostat. see Dextroamphetamine Encephalitis, and bipolar disorder, 37
DHEA. see Dehydroepiandrosterone (DHEA) Effexor. see Venlafaxine
Diabetes mellitus Effexor XR. see Venlafaxine XR
and depression, 24 Elavil. see Amitriptyline
Diazepam, 52t Elderly, case studies, 129–132
in psychotic disorder, 65t Electroconvulsive therapy (ECT)
Digoxin, 29 for bipolar illness, 44
Diphenhydramine for depression, 31–32
in psychotic disorder, 65t EMSAM. see Selegiline transdermal system
in sleep disturbances, 86t Endogenous depression, 23–24. see also Depression
Discontinuation syndrome, 16 Endogenous substances, 5
Distribution, of drugs, 14 Enzymes, P450, 15
Disulfiram Ephedra, and bipolar disorder, 38
for alcohol abuse, 96, 97, 97t Epinephrine, 11
and bipolar disorder, 38 Equetro. see Carbamazepine
Dizygotic twins, 36–37 Escitalopram, 27t
schizophrenia in, 59 for OCD, 55
DLB. see Dementia with Lewy bodies (DLB) Eskalith CR. see Lithium carbonate
Dolophine. see Methadone Estazolam, 52t
Donepezil, in cognitive disorders, 76t, 77 in sleep disturbances, 86t
Dopamine, 11 Eszopiclone, 52t
and schizophrenia, 59 for sleep disorders, 86
Dopamine agonists, and cocaine dependence, 99 in sleep disturbances, 86t
Dopamine hypothesis, 94–95 Exelon. see Rivastigmine, in cognitive disorders
Doral. see Quazepam Exelon Patch. see Rivastigmine transdermal system
Dosing, 15–16, 15f Exercise, for depression, 31
Doxepin, 26t Exocytosis, 7, 7f
in sleep disturbances, 86t Exogenous depression, 24. see also Depression
Drugs. see also specific drugs Exogenous substances, 5
absorption of, 14 Expressed emotion (EE), 60
distribution of, 14
dosing of, 15–16, 15f F
half-life of, 14 Family education, and bipolar illness, 46
metabolism of, 15 Fanapt. see Iloperidone
and potentiation, 16 Fat solubility. see Lipid solubility
and protein binding, 14 Fazaclo. see Clozapine
routes of administration, 13–14 Fibromyalgia, 104
and synergy, 16 and depression, 24
DSM-IV, 16 First-pass metabolism, 14. see also Liver
Duloxetine, 28t Five5-hydroxytryptamine (5-HTP). see Serotonin
and depression, 27 Fluoxetine, 27t, 40t
Dysthymia, 25 in psychotic disorders, 62t
Fluphenazine, 63t
E Fluphenazine decanoate, 63t
Eating disorders, 105–107 Flurazepam, 52t
anorexia nervosa, 105–106 in sleep disturbances, 86t
BED, 107 Fluvoxamine, 27t
bulimia nervosa, 106–107 for OCD, 55
 Index 167

Focalin. see Dexmethylphenidate Huntington’s disease

and bipolar disorder, 37
G and depression, 24
GABA. see Gamma-aminobutyric Hydralazine
acid (GABA) and bipolar disorder, 38
Gabapentin Hyperdopaminergic hypothesis, 59
for bipolar disorder, 40t, 41 Hypericum perforatum. see St. John’s wort
for personality disorders, 91 Hyperthyroidism
Gabarone. see Gabapentin and bipolar disorder, 37
Gabitril. see Tiagabine and depression, 24
GAD. see Generalized anxiety disorder (GAD) Hyperthyroidism, and anxiety, 49
Galantamine, in cognitive disorders, 76t, 77 Hypoglycemia, and anxiety, 49
Gamma-aminobutyric acid (GABA), 12 Hypothyroidism
for sleep disorders, 87 and depression, 24
Gamma-hydroxybutyrate (GHB)
for narcolepsy, 83 I
in sleep disturbances, 86t Ibogain, and cocaine dependence, 97t, 99
Generalized anxiety disorder (GAD), 53–54 Iloperidone, 40t
Geodon. see Ziprasidone in psychotic disorders, 62t
Geriatric Depression Inventory, 21 Imipramine, 26t
GHB. see Gamma-hydroxybutyrate (GHB) Impulse control disorders, 108–109
Ginkgo biloba, 29, 78 Inderal. see Propranolol
Glutamate, 12 Inderal LA. see Propranolol
for cognitive disorders, 77 Inflammation, and Alzheimer’s disease, 75
Glycine, 12 Influenza
G proteins, 8, 9 and bipolar disorder, 37
Guanfacine and depression, 24
in ADHD, 71, 71t Injections, intramuscular, 14
Guanfacine extended release Insomnia, 81. see also Sleep disorders
in ADHD, 71t initial, 82
middle, 82
H International Association for the Study of Pain, 104
h., 17t Interview, patient, 22
Halcion. see Triazolam Intramuscular injections, 14
Haldol. see Haloperidol Intuniv. see Guanfacine extended release
Haldol Decanoate. see Haloperidol decanoate Invega. see Paliperidone
Half-life of a drug, 14 Invega Sustenna. see Paliperidone
Hallucinogens Ion channel, 8, 9f
and bipolar disorder, 38 Isocarboxazid, 30t
Haloperidol, 14, 63t Isoniazid
Haloperidol decanoate, 63t and bipolar disorder, 38
Hamilton Depression Inventory, 21 Ispotin SR. see Verapamil
Henry Ford Hospital Sleep Disorders Center
in Detroit, 87 K
Hepatitis Kemstro. see Baclofen
and depression, 24 Klonopin. see Clonazepam
Heterocyclic antidepressants, 27–29, 28t Klonopin Wafer. see Clonazepam
HIV/AIDS
and depression, 24 L
Homocysteine, 31 LAAM. see L-alpha-acetyl-methadol,
hs, 17t and opiate dependence
168 Index

L-alpha-acetyl-methadol, and opiate dependence, 97t, 98 Mazanor. see Mazindol, and cocaine dependence
Lamictal. see Lamotrigine Mazindol, and cocaine dependence, 97t, 99
Lamictal CD. see Lamotrigine Medical comorbidities, 102–103
Lamictal ODT. see Lamotrigine Melatonin, for sleep disorders, 86–87
Lamictal XR. see Lamotrigine Mellaril. see Thioridazine
Lamotrigine Memantine
for bipolar disorder, 40t, 41 for cognitive disorders, 76t, 77
Lanoxin. see Digoxin for OCD, 55
L-DOPA, 9 Menopause
Levodopa and depression, 24
and bipolar disorder, 38 Mental health professionals, 21
Lexapro. see Escitalopram Mental retardation
Librium. see Chlordiazepoxide and depression, 24
Light therapy, for depression, 31 Mental status examination, 20–21
Lioresal. see Baclofen Mesoridazine, 63t
Lipid-lowering agents, 78 Metabolic abnormalities
Lipid solubility, 14 and depression, 24
Lisdexamfetamine Metabolic changes
in ADHD, 70t, 71 and bipolar disorder, 37
Lithium Metadate-ER. see Methylphenidate
for bipolar disorder, 39, 41 Metastatic cancer
metabolism of, 15 and bipolar disorder, 37
Lithium carbonate, 40t Methadone
Lithium citrate, 40t and opiate dependence, 97t, 98
Lithobid. see Lithium carbonate Methamphetamine
Liver in ADHD, 70t, 71
and drug distribution, 14 Methylin-ER. see Methylphenidate
and drug metabolism, 15 Methylphenidate
Loading dose, 16 in ADHD, 70t
Lorazepam, 52t and bipolar disorder, 38
in bipolar disorder, 44 and cocaine dependence, 97t, 99
in psychotic disorder, 65t Michigan Alcohol Screening Test (MAST), 95
Loxapine, 63t MID. see Multi-infarct dementia (MID)
Loxitane. see Loxapine Million Clinical Multiaxial Inventory-III, 22
Ludiomil. see Maprotiline Minnesota Multiphasic Personality Inventory (MMPI-2),
Lunesta. see Eszopiclone 21
Lupus Mirtazepine, 28t
and depression, 24 and depression, 27
Luvox. see Fluvoxamine Mitral valve prolapse, and anxiety, 49
Lyrica. see Pregabalin MMPI-2. see Minnesota Multiphasic Personality
Inventory (MMPI-2)
M Moban. see Molindone
MacAndrew Alcoholism Scale, 95 Modafinil
Magnesium, as antidepressant, 31 for narcolepsy, 83
Malnutrition in sleep disturbances, 86t
and depression, 24 Molindone, 63t
MAOI. see Monoamine oxidase inhibitors (MAOI) Monoamine oxidase inhibitors (MAOI), 29, 33
Maprotiline, 26t Mononucleosis
Marplan. see Isocarboxazid and depression, 24
MAST. see Michigan Alcohol Screening Test (MAST) Monosodium glutamate (MSG), 12
 Index 169

Monozygotic twins, 36 Obsessive-compulsive spectrum disorders

schizophrenia in, 59 (OCSD), 108
Mood stabilizers, for bipolar illness, 39–44, 40t Obstructive sleep apnea (OSA), 82–83
Mood symptoms, of schizophrenia, 60 OCD. see Obsessive-compulsive disorder (OCD)
MSG. see Monosodium glutamate (MSG) OCSD. see Obsessive-compulsive spectrum
Multi-infarct dementia (MID), 75 disorders (OCSD)
Multiple sclerosis Olanzepine
and bipolar disorder, 37 for bipolar disorder, 40t, 42
and depression, 24 in psychotic disorders, 62t
Myocardial infarction Oleptro. see Trazodone
and depression, 24 Opiates
and bipolar disorder, 38
N Opioids
Nalmefene, and alcohol abuse, 97t, 98 and bipolar disorder, 38
Naloxone, and opiate dependence, 97t, 98–99 dependence, 98–99
Naltrexone Orap. see Pimozide
and alcohol abuse, 97, 97t, 98 Oxazepam, 52t
for personality disorders, 91 Oxcarbazepine, for bipolar disorder, 40t, 42
Namenda. see Memantine
Narcolepsy, 83 P
Nardil. see Phenelzine Pain, 104–105
Navane. see Thiothixene emotional dimension, 104
Nefazodone, 28t evidence-based guidelines, 104
and depression, 27, 29, 33 Paliperidone, 40t
Neural communication, 5–9 in psychotic disorders, 62, 62t
electrical and chemical properties of, 6–9 Pamelor. see Nortriptyline
Neurons, 4–5, 5f Pancreatitis
resting potential of, 6 and depression, 24
Neurontin. see Gabapentin Panic disorder (with or without agoraphobia), 50–53
Neurotransmitters, 9–12 Parasomnia, 83
Night terrors, 83 Parathyroid disease, and anxiety, 49
N-methyl-D-aspartate (NMDA) receptor antagonists, 77 Parkinson’s disease
Nocturnal polysomnogram (NPSG), 84 and bipolar disorder, 37
Nonsteroidal anti-inflammatory drugs (NSAIDS), 78 and depression, 24
Noradrenergic pathways, 10 Parlodel. see Bromocryptine
Norepinephrine, 11 Parnate. see Tranylcypromine
Norepinephrine, for REM sleep, 82 Paroxetine, 27t
Norpramin. see Desipramine discontinuation syndrome, 16
Nortriptyline, 26t Patient education, and bipolar illness, 46
in ADHD, 71t Patient education, for ADHD, 69
NPSG. see Nocturnal polysomnogram (NPSG) Patient history, 18–20
NSAIDS. see Nonsteroidal anti-inflammatory drugs Paxil. see Paroxetine
(NSAIDS) Paxil CR. see Paroxetine
Nuvigil. see Armodafinil p.c., 17t
PEA. see Phenylethylamine (PEA)
O Pellagra
Obesity, 107–108 and bipolar disorder, 37
Obsessive-compulsive disorder (OCD), 54–55 Pemoline
cause of, 55 in ADHD, 70t
treatment of choice for, 55 for narcolepsy, 83
170 Index

P450 enzymes, 15 Propranolol, 52t

Periodic leg movement disorder (PLMD), 83–84 in psychotic disorder, 65t
Perphenazine, 63t Prosom. see Estazolam
Personality Assessment Inventory, 22 Protein binding, 14
Personality disorders, 89–92 Protriptyline, 26t
assessment of, 90 Provigil. see Modafinil
medications for, 89–91 Prozac. see Fluoxetine
symptom clusters for, 90–91 Psychiatric comorbidities, 102–103
Pexeva. see Paroxetine Psychoactive substances, 61
Pharmacodynamics, defined, 13 Psychosis, 58–67. see also Schizophrenia
Pharmacokinetics. see also Drugs causes of, 61–62
defined, 13 medications for, 62–65, 62t, 63t, 65t
Phenelzine, 30t treatment protocol, 65–66
Phenylethylamine (PEA), 31 Psychotherapy
Phobia, 56. see also Anxiety disorders for bipolar illness, 38–39
Pimozide, 63t for depression, 25
Pindolol, 52t for OCD, 54–55
Placebo response, 16–17 for PTSD, 54
PLMD. see Periodic leg movement disorder (PLMD) PTSD. see Posttraumatic stress disorder (PTSD)
PMS. see Premenstrual syndrome (PMS)
p.o., 17t Q
Polypharmacy, 32 qd, 17t
Porphyria q4h, 17t
and depression, 24 q6h, 17t
Postconcussion syndrome, and anxiety, 49 q.i.d., 17t
Postpartum hormonal changes Quazepam, 52t
and depression, 24 in sleep disturbances, 86t
Postpartum metabolic changes Questionnaires, 21–22
and bipolar disorder, 37 Quetiapine
Posttraumatic stress disorder (PTSD), 54 in bipolar disorder, 40t, 43
Potentiation, 16 in psychotic disorders, 62t
Prazepam, 52t
Prednisone R
and bipolar disorder, 38 Ramelteon, 52t
Pregabalin, 84 for GAD, 87
Pregnancy for sleep disorders, 87
antidepressants and, 34 in sleep disturbances, 86t
topiramate in, 42 Rapid cycling, 37
Premenstrual dysphoric disorder Rapid-eye movement (REM), 82
and depression, 24 Rebound phenomenon, 82
Premenstrual syndrome (PMS), 49 REM. see Rapid-eye movement (REM)
Priapism, 26 Remeron. see Mirtazepine
Pristiq. see Desvenlafaxine; Desvenlafaxine succinate Remeron Soltab. see Mirtazepine
p.r.n., 17t Reminyl. see Galantamine, in cognitive disorders
Procarbazine Renal failure
and bipolar disorder, 38 and bipolar disorder, 38
Procyclidine Requip. see Ropinirole
and bipolar disorder, 38 Restless leg syndrome (RLS), 83–84
Prolixin. see Fluphenazine Restoril. see Temazepam
Prolixin Decanoate. see Fluphenazine decanoate Revex. see Nalmefene, and alcohol abuse
 Index 171

Revia. see Naltrexone, and alcohol abuse Seroquel XR. see Quetiapine
Rheumatoid arthritis Serotonin, 10–11, 10f, 12
and depression, 24 Serotonin syndrome, 27
Risperdal. see Risperidone Sertraline, 27t
Risperdal Consta. see Risperidone Serzone. see Nefazodone
Risperdal M-tab. see Risperidone Signal transduction, 8
Risperidone Silenor. see Doxepin
for bipolar disorder, 40t, 42–43 Sinequan. see Doxepin
for OCD, 55 Sleep, stages of, 82
for personality disorders, 91 Sleep Bruxism, 83
in psychotic disorders, 62, 62t, 63 Sleep disorders, 81–87
Ritalin. see Methylphenidate behavioral approaches for, 84–85
Rivastigmine, in cognitive disorders, 76, 76t, 77 and conditions, 82–83
Rivastigmine transdermal system, 76t, 77 holistic remedies for, 87
RLS. see Restless leg syndrome (RLS) medications for, 85–87
Ropinirole Sleepwalking, 83
for RLS, 84 Social anxiety disorder, 55–56
in sleep disturbances, 86t Social-drift phenomenon, 59
Rozerem. see Ramelteon Social phobia. see Social anxiety disorder
Rx, 17t Soma, 5, 5f
Sonata. see Zaleplon
S SSRI. see Selective serotonin reuptake
SAD. see Seasonal affective disorder (SAD) inhibitors (SSRI)
S-adenosyl-L-methionine (SAM-e), 31 St. John’s wort, 29
SALCE. see Substance Abuse Life Circumstance stat., 17t
Evaluation (SALCE) State-Trait Anxiety Inventory, 21
SAM-e. see S-adenosyl-L-methionine (SAM-e) Stavzor. see Valproate
Sanorex. see Mazindol, and cocaine dependence Stelazine. see Trifluoperazine
Saphris. see Asenapine Strattera. see Atomoxetine
Sarafem. see Fluoxetine Stress-diathesis model, 60
SASSI-3. see Substance Abuse Subtle Screening Stroke
Inventory (SASSI-3) and bipolar disorder, 38
Schizophrenia, 58–60 and depression, 24
genetic theories of, 59 Strychnine, 12
neurochemical abnormalities with, 59 Suboxone. see Buprenorphine
prevalence of, 59 Substance abuse. see Chemical dependency
symptoms in, 60 Substance Abuse Life Circumstance Evaluation
Seasonal affective disorder (SAD), 31 (SALCE), 95
Seizure disorders, 49 Substance Abuse Problem Checklist, 95
Selective serotonin reuptake inhibitors (SSRI), 26–27, Substance Abuse Subtle Screening Inventory
27t, 32 (SASSI-3), 95
for GAD, 53 Subutex. see Buprenorphine
for OCD, 55 Sullivan, Harry Stack, 59–60
for PTSD, 54 Surmontil. see Trimipramine
Selegiline, for cognitive disorders, 78 Symbyax. see Fluoxetine; Olanzepine
Selegiline transdermal system, 30t Symmetrel. see Amantadine
Senile plaques, 75 Synapse, 5, 5f
Serax. see Oxazepam Synergism, 16
Serentil. see Mesoridazine Syphilis
Seroquel. see Quetiapine and depression, 24
172 Index

T Upper airway resistance syndrome, 82.

tab., 17t see also Obstructive sleep apnea (OSA)
Tacrine, in cognitive disorders, 76, 76t, 77 Uremia
TCA. see Tricyclic antidepressants (TCA) and depression, 24
Tegretol. see Carbamazepine
Tegretol XR. see Carbamazepine V
Temazepam, 52t Valerian
in sleep disturbances, 86t for sleep disorders, 87
Temporal lobe epilepsy Valium. see Diazepam
and bipolar disorder, 38 Valproate
Tenex. see Guanfacine for bipolar disorder, 40t, 41, 44, 45
Terminal buttons, 5, 5f Valproic acid. see Valproate
Testosterone Varenicline, for nicotine abuse, 97t,
and bipolar disorder, 38 99–100
Therapeutic dose. see Dosing Vascular dementia, 75
Therapeutic index, 15–16 Venlafaxine, 28t
Thioridazine, 63t in ADHD, 71t
Thiothixene, 63t and depression, 27
Thorazine. see Chlorpromazine discontinuation syndrome, 16
Tiagabine, for bipolar disorder, 40t, 42 Venlafaxine XR, 28t
t.i.d., 17t Verapamil, 40t
Tofranil. see Imipramine for bipolar disorder, 44
Tolerance, 16 Verelan PM. see Verapamil
Topamax. see Topiramate Viral hypotheses, for schizophrenia, 59
Topiramate Visken. see Pindolol
and alcohol abuse, 97t, 98 Vitamin B12 deficiency
for bipolar disorder, 40t, 42 and bipolar disorder, 38
Toxic dose, 15. see also Dosing Vitamin E, and cognitive disorder, 77, 78
Tranxene. see Clorazepate Vivactil. see Protriptyline
Tranylcypromine, 30t Vivitrol. see Naltrexone, and alcohol abuse
Trazodone Vyvanse. see Lisdexamfetamine
and depression, 26, 28t
and sleep disturbances, 86t W
Triazolam, 52t Warfarin, 29
in sleep disturbances, 86t Wellbutrin. see Bupropion
Tricyclic antidepressants (TCA), 25–26, 26t Wellbutrin SR. see Bupropion SR
Trifluoperazine, 63t Wellbutrin XL. see Bupropion XL
Trihexyphenidyl Wilson’s disease
in psychotic disorder, 65t and bipolar disorder, 38
Trilafon. see Perphenazine Withdrawal, 16
Trileptal. see Oxcarbazepine
Trimipramine, 26t X
Tuberculosis Xanax. see Alprazolam
and depression, 24 Xyrem. see Gamma-hydroxybutyrate
Typical antipsychotics
for psychotic disorder, 64–65 Y
Tyrosine, 9 Yohimbine
and bipolar disorder, 38
U
Unipolar depression, vs. bipolar depression, Z
36–37 Zaleplon, 52t
 Index 173

for sleep disorders, 85 for sleep disorders, 85–86

in sleep disturbances, 86t in sleep disturbances, 86t
Zinc, as antidepressant, 31 Zolpimist. see Zolpidem
Ziprasidone, 14 Zonegran. see Zonisamide
in bipolar disorder, 40t, 43 Zonisamide, for bipolar disorder, 40t, 42
in psychotic disorders, 62t Zyprexa. see Olanzepine
Zoloft. see Sertraline Zyprexa Relprevv. see Olanzepine
Zolpidem, 52t Zyprexa Zydis. see Olanzepine
in GAD, 54