tmpC583 TMP

Directions in
Psychiatry
V O L U M E
CATEGORY 1
CME
3 3
I N
T H I S
2 0 1 3
N U M B E R
I S S U E
The Neurobiology of Child Abuse and Neglect . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .75

RICHARD IDELL, MD; AND CHARLES NEMEROFF, MD
This lesson presents structural and functional imaging studies documenting the consequences of early-life
stress (ELS). Study findings show that enduring disruption of the HPA axis, induced by childhood trauma, may
contribute to vulnerability to adult psychopathology. The authors present the implications of these findings
for our understanding of the physiopathology of mood and anxiety disorders and for the development of
novel treatments.
Antidepressant Medications in Preadolescent Children

with Unipolar Depression: A Review of the Evidence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .89
THOMAS N. BUTLER, MD; AND CHRISTINE J. CHOE, MD
This lesson will assist clinicians in their ability to practice evidence-based care while they conduct informed
discussions with patients and families. Clinicians will also review the evidence for individual antidepressant
agents and psychopharmacologic treatment strategies in children with depression.
Psychostimulants for Test-Taking and ADHD:

Assessing the Risks & the Benefits . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .105
SHAWEN M. ILARIA, BS; MICHAEL A. SHAPIRO, MD; AND MARK S. GOLD, MD
Psychostimulants are often used to treat ADHD in children, and even adults. However, there is a growing misuse of them to enhance academic performance. The authors review the use and misuse of psychostimulants and other treatment modalities, and consider the concepts of addiction, abuse, and other parental
concerns.
Internet and Videogame Addiction:

Clinical Implications for Assessment and Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .117
AVIV WEINSTEIN, PHD
Is there a biological basis for Internet addiction? Dr. Weinstein explores the recent evidence on the assessment, psychobiological basis, and treatment of videogame addiction and comorbidity with other psychiatric
disorders.
Community Resilience to Disasters for Mental Health Professionals . . . . . . . . . . . . . . . . . .135

ROSE L. PFEFFERBAUM, PHD, MPH; AND BETTY PFEFFERBAUM, MD, JD
We live in a world in which disasters occur much too frequently and threats are ongoing and widespread.
Disaster preparation is a must. Building community resilience is a vision and a strategy for disaster
management. This lesson introduces community resilience to disasters, distinguishes community resilience
from personal resilience, and explains the role of human agency in creating the potential for community
transformation.
A HATHERLEIGH
CME JOURNAL
w w w . D i r e c t i o n s I n P s y c h i a t r y . c o m
Directions in Psychiatry
Senior Content Advisor
Leah Dickstein, MD, MA
Professor Emerita,
University of Louisville, Psychiatriy & Behavioral Science,
Louisville, KY; and Lecturer ,Tufts University,
Medical Center, Psychiatry Dept., Boston, MA
Program Advisory Board

Barbaranne Branca, PhD
Michigan Head Pain & Neurological
Institute, Ann Arbor, MI
Robert L. DuPont, MD
Georgetown University, Washington, DC
Richard Elliott, MD
Mercer University School of Medicine,
Macon, GA
Joseph T. English, MD
St. Vincents Medical, Center of New York,
NY, NY
Deborah I. Frank, PhD, ARNP, MFT
Florida State University, College of Nursing,
Tallahassee, FL
Shervert Frazier, MD
PsychiatristinChief, Emeritus,
McLean Hospital, Belmont, MA
Wendy Packman, JD
Pacific Graduate School of Psychology,
San Francisco, CA
Mark S. Gold, MD
University of Florida, Gainesville, FL
Alison Heru, MD
University of Colorado, Denver, CO
George Papakostas, MD
Massachusetts General Hospital, Boston, MA
Robert M.A. Hirschfeld, MD

University of Texas, Galveston, TX
Gail Erlick Robinson, MD, DPsych, FRCPC

Toronto General Hospital, Toronto, Ontario
Jimmie C. Holland, MD
Memorial SloanKettering, Cancer Center,
NY, NY
Michael A. Schwartz, MD
University Hospitals of Cleveland,
Cleveland, OH
Hideo Hosaki, MD
Keio University, School of Medicine,
Tokyo, Japan
Peter C. Whybrow, MD
UCLA Department of Psychiatry and
Behavioral, Sciences, Los Angeles, CA
Philip Janicak, MD
Rush University, Chicago, IL.
Robert L. Williams, MD
Baylor College of Medicine, Houston, TX
Carl P. Malmquist, MD
University of Minnesota, Minneapolis, MN
Malkah T. Notman, MD,
The Cambridge Hospital, Cambridge, MA
Managing Editor
Stacy M. Powell
Founding Editor
Frederic Flach, MD, KCHS, DFLAPA
Accreditation Statement
w w w. D i r e c t i o n s i n p s y c h i a t r y. c o m
62545 State Highway 10, Hobart, NY 13788
The Hatherleigh Company, Ltd., designates this activity for a maximum of 40 AMA
PRA Category 1 Credits. Physicians should only claim credit commensurate with the
extent of their participation in the activity.
The Hatherleigh Company, Ltd., is accredited by the Accreditation Council for
Continuing Medical Education (ACCME) to provide continuing medical education
for physicians.
This activity has been planned and implemented in accordance with the Essential
Areas and Policies of the Accreditation Council for Continuing Medical Education
(ACCME) by The Hatherleigh Company, Ltd.
Directions in Psychiatry
Volume 33 Lessons 610
CME LESSON 6
The Neurobiology of Child Abuse and Neglect
page 75
Richard Idell, MD; and Charles B. Nemeroff, MD
CME LESSON 7

with Unipolar Depression: A Review of the Evidence
page 89
Thomas N. Butler, MD; and Christine J. Choe, MD
CME LESSON 8

Assessing the Risks & the Benefits
page 105
Shawen M. Ilaria, BS; Michael A. Shapiro, MD; and Mark S. Gold, MD
CME LESSON 9

Clinical Implications for Assessment and Treatment
page 117
Aviv Weinstein, PhD
CME LESSON 10
Community Resilience to Disasters

for Mental Health Professionals
Rose L. Pfefferbaum, PhD, MPH; and Betty Pfefferbaum, MD, JD
page 135
Conflict of Interest Faculty & Advisory Board Disclosures

The authors of the lessons in this CME program are paid an honorarium to produce original manuscripts on the invited topics.
The authors were selected for their expertise and, most often, on the strength of presentations made on those topics in previously
published papers or symposia. Relationships are disclosed below, if they exist, between the Directions in Psychiatry faculty and
their immediate family members, and commercial and/or pharmaceutical companies below. Disclosure of off-label medication
usage for indications that are not approved by the FDA will be disclosed on the title page of each lesson.
No commercial support was used in the development of the enclosed CME lessons.
Faculty Disclosures:
Medication usage mentioned in the lessons for indications that are not approved by the FDA are listed on the title page of each lesson if they exist.
Thomas N. Butler, MD
Dr. Butler has no conflicting interests to disclose.
Christine J. Choe, MD
Dr. Choe has no conflicting interests to disclose.
Mark S. Gold, MD
Dr. Gold has no conflicting interests to disclose.
Richard Idell, MD
Dr. Idell has no conflicting interests to disclose.
Shawen M. Ilaria, BS
Ms. Ilaria has no conflicting interests to disclose.
Charles Nemeroff, MD
Dr. Nemeroff has received research support/ grants from National Institutes of Health and Agency for Healthcare
Researchand Quality; has consulted for Xhale, Takeda, SK Pharma, Shire, Roche, Eli Lilly, Allergan, and Tashio and
Mitsubishi Tanabe; is a stockholder in Revaax and Xhale; has patents for a method and devices for transdermal
delivery of lithium (US 6,375,990B1) and a method of assessing antidepressant drug therapy via transport inhibition of monoamine neurotransmitters by ex vivo assay (US 7,148,027B2); is on scientific advisory boards of American Foundation for Suicide Prevention (AFSP), National Alliance for Research on Schizophrenia and Depression,
Xhale, Anxiety Disorders Association of America (ADAA), and Skyland Trail; is on the boards of directors of AFSP,
Gratitude America, and ADAA; has income sources of or equity of $10,000 or more in Reevax, American Psychiatric Publishing, and Xhale; and has received honoraria and royalties from and served as an expert witness for various companies and organizations.
Rose L. Pfefferbaum, PhD, MPH
Dr. Pfefferbaum has no conflicting interests to disclose.
Betty Pfefferbaum, MD, JD
Dr. Pfefferbaum has no conflicting interests to disclose.
Michael A. Shapiro, MD
Dr. Shapiro has no conflicting interests to disclose.
Aviv Weinstein, PhD
Dr. Weinstein has no conflicting interests to disclose.
Program Advisory Board Member Disclosures:

Leah J. Dickstein, MD, MA:
Dr. Dickstein has no conflicting interests to disclose.
Richard L. Elliott, MD, PhD:
Dr. Elliott has been on the Speakers Bureau for Eli Lilly and Company, Pfizer, Inc., and GlaxoSmithKline.
Deborah I. Frank, PhD, ARNP:
Dr. Frank has no conflicting interests to disclose.
Mark S. Gold, MD, PhD:
Dr. Gold has no conflicting interests to disclose.
Alison Heru, MD:
Dr. Heru has no conflicting interests to disclose.
Philip Janicak, MD:
Dr. Janicak has received grant funding from Neuronetics, Inc., Johnson & Johnson, Solvay Pharmaceuticals,
Sanofi Aventis, Otsuka Pharmaceutical Group, and Eli Lilly and Company; he is also a consultant for
Neuronetics, Inc.
George I. Papakostas, MD:
Dr. Papakostas has served as a consultant for the following: Aphios Corporation, Bristol-Myers Squibb Company,
Glaxo-SmithKline, Evotec Ltd., Inflabloc Pharmaceuticals, Jazz Pharmaceuticals, PAMLAB LLC, Pfizer, Inc., and
Wyeth, Inc. He has received honoraria from Bristol-Myers Squibb Company, Evotec Ltd., GlaxoSmithKline,
Inflabloc Pharmaceuticals, Jazz Pharmaceuticals, PAMLAB LLC, Pfizer, Inc., Titan Pharmaceuticals, and Wyeth,
Inc. Dr. Papakostas also has received research support from Bristol-Myers Squibb Company, PAMLAB LLC, and
Pfizer, Inc.
Hatherleigh Editorial Staff:

Andrew Flach, CEO:
Mr. Flach has no conflicting interests to disclose.
Stacy M. Powell, Managing Editor:
Ms. Powell has no conflicting interests to disclose.
Rick Gallub, Office Manager
Mr. Gallub has no conflicting interests to disclose.
Accreditation Standards: IOM; ACGME /ABMS Competencies

Directions in Psychiatry, Vol. 33: Part 2
In accordance with accreditation guidelines set forth by the ACCME, we encourage you to review the following areas of core
competency and desirable physician attributes endorsed by the Institute of Medicine (IOM); The Accreditation Council for
Graduate Medical Education (ACGME) / American Board of Medical Specialties (ABMS). Each CME lesson in this activity addresses at
least one or more of the following attributes in each of the three areas of competency as listed below.
Institute of Medicine Core Competencies:
Provide Patient-Centered Care: Identify, respect, and care about patients differences, values, preferences, and expressed needs; relieve pain and suffering; coordinate continuous care; listen to, clearly inform,
communicate with, and educate patients; share decision-making and management; and continuously advocate
disease prevention, wellness, and promotion of healthy lifestyles, including a focus on population health
Work in Interdisciplinary Teams: Cooperate, collaborate, communicate, and integrate care in
teams to ensure that care is continuous and reliable
Employ Evidence-Based Practice: Integrate best research with clinical expertise and patient values for optimum care, and participate in learning and research activities to the extent feasible
Apply Quality Improvement: Identify errors and hazards in care; understand and implement basic
safety design principles, such as standardization and simplification; continually understand and measure
quality of care in terms of structure, process, and outcomes in relation to patient and community needs;
and design and test interventions to change processes and systems of care, with the objective of improving quality
Utilize Informatics: Communicate, manage, knowledge, mitigate error, and support decision-making
using informationtechnology
ACGME Competencies:
Patient Care that is compassionate, appropriate, and effective for the treatment of health problems and
the promotion of health
Medical Knowledge about established and evolving biomedical, clinical, and cognate (e.g. epidemiological and social-behavioral) sciences and the application of this knowledge to patient care
Lesson 6
Lesson 7
Lesson 8
Practice-Based Learning and Improvement that involves investigation and evaluation of their
own patient care, appraisal and assimilation of scientific evidence, and improvements in patient care
Interpersonal and Communication Skills that result in effective information exchange and
teaming with patients, their families, and other health professionals
Professionalism, as manifested through a commitment to carrying out professional responsibilities, adherence to ethical principles, and sensitivity to a diverse patient population
Systems-Based Practice, as manifested by actions that demonstrate an awareness of and responsiveness to the larger context and system of health care and the ability to effectively call on system resources to
provide care that is of optimal value
ABMS Competencies:
Part I-Professional Standing: Medical specialists must hold a valid, unrestricted medical license in
at least one state or jurisdiction in the USA, its territories or Canada.
Part II-Lifelong Learning and Self-Assessment: Physicians participate in educational and
self-assessment programs that meet specialty-specific standards that are set by their member board.
Part III-Cognitive Expertise: They demonstrate, through formalized examination, that they have the
fundamental, practice-related and practice environment-related knowledge to provide quality care in their
specialty.
Part IV-Practice Performance Assessment: They are evaluated in their clinical practice
according to specialty-specific standards for patient care. They are asked to demonstrate that they can
assess the quality of care they provide compared to peers and national benchmarks and then apply the
best evidence or consensus recommendations to improve that care using follow-up assessments.
Directions in Psychiatry, Vol. 33: Part 2

Psychostimulants for Test-Taking and
ADHD: Assessing the Risks & the Benefits
IOM Core Competencies
L6
Lesson 9
Lesson 10
L7
Employ evidence-base practice
Apply quality improvement
Community Resilience to Disasters for

Mental Health Professionals
L8
L9
L10
Provide patient-centered care
Work in interdisciplinary teams

Utilize informatics
ACGME Competencies
Patient care
Medical knowledge
Practice-based learning and improvement
Interpersonal and communication skills
Professionalism
System-based practice
X
X
ABMS MOC Competencies
Professional standing
Commitment to lifelong learning
Cognitive expertise
Performance in practice
X
X
X
X
X
X
X
X
X
X
X
CME Information Page
Directions in Psychiatry, Vol. 33
Overall Learning Objective Target Audience Duration of CME Status

Overall Objective: The objective of this continuing medical education program is to present participants with an expanded psychiatric
skill set and raised awareness of clinically relevant issues in their profession. They will review key diagnostic criteria, cutting-edge treatment strategies, and practice points they can implement in the challenges of daily practice while providing evidenced-based care to
patients and clients with psychiatric symptoms and comorbid medical disorders. The expected outcomes include an increase in knowledge, competence, professionalism, and performance.
Target Audience: The primary target audience for this program includes, but is not limited to psychiatrists, psychiatric nurses, clinical psychologists, mental health counselors, and social workers. Clinicians who have caseloads composed significantly of individuals with psychiatric
disorders will find this program extremely useful.
Duration of CME Status: The program Directions in Psychiatry, Vol. 33 begins May 31, 2013, and the preliminary expiration date is
December 31, 2016. At that point, the Hatherleigh Medical Director and the editorial staff will review the CME material to determine
whether the program continues to be consistent with current accreditation guidelines and standards of care. A determination will be made as
to whether the program can be used to earn full CME credit after that date.
Conflict of Interest Disclosure Policy

The faculty of the CME lessons in this program are paid an honorarium to produce original manuscripts on the invited topic. Faculty
members were selected for their expertise and, most often, on the strength of their presentations from previously published papers or symposia.
Hatherleigh Medicial Education staff, contributing program faculty, and advisory board members, must disclose their relationships (also on
behalf of their immediate family members), if they exist, with commercial and/or pharmaceutical companies prior to Hatherleigh Medical
Educations distribution and publication of their contributions to Directions in Psychiatry and other Hatherleigh Medical Education CME
programs. Any aforementioned relationship that poses a potential conflict of interest will be resolved prior to publication/distribution of the
CME activity, and proper notification disclosed to program participants prior to the start of the activity.
Disclosure of any off-label medication usage for indications that are not currently approved by the Federal Drug Administration discussed within
the CME content will be disclosed at the beginning of each activity and/or on the title page of each CME lesson.
Accreditation Statement Hatherleighs CME Designation

The Hatherleigh Company, Ltd. designates this activity for a maximum of 40 AMA PRA Category 1 Credits. Physicians should only claim
credit commensurate with the extent of their participation in the activity.
The Hatherleigh Company, Ltd. is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide
continuing medical education for physicians.
This activity has been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education (ACCME) by The Hatherleigh Company, Ltd.
How the Program Works Needs Assessment Evaluation

Directions in Psychiatry lessons include 2-4 questions per lesson. The questions focus on bold-faced teaching points in the lessons. The answers
to those questions must be recorded on the supplied quiz response form, and only after all 78 questions have been answered on that form
should participants return it to Hatherleigh via fax or mail for scoring. On average, it will take up to 2 hours to complete an individual
Hatherleigh CME lesson (i.e., reading and studying the lesson and answering the CME questions). Participants must complete and return the
lesson-based learning assessment form, which is included with each program. Participants can return these forms with their quiz response
form. Upon successful completion (at least 75% correct) of the program, Hatherleigh will send the participant a certificate of achievement
worth 40 Category 1 credit hours and a score report.
The topics covered in detail throughout these lessons were derived from a learning needs assessment of participants in previous programs, who
are virtually all psychiatrists and other mental health clinicians. Their expressed needs were assessed by the Medical Director, the Program
Advisory Board members, and editorial staff in the development of this curriculum.
The Hatherleigh Company, Ltd. has published continuing medical education programs in psychiatry for over 30 years. Dr. Frederic Flach, the companys
founder, created this program to ensure the presence of a truly independent and highly professional perspective on issues of immediate clinical importranging from pharmacotherapy to psychotherapy, from technical information to ethical priorities. We look forward to hearing from all subscribers via e-mail at
support@hatherleigh.com. For more information about Directions in Psychiatry, visit our Web site at www.directionsinpsychiatry.com. For more information
about Hatherleigh, visit our Web site at www.hatherleigh.com, or call 1-800-367-2550.
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of the company or its employees. The Hatherleigh Company, Ltd. does not endorse any product, therapeutic method, and/or treatment mentioned herein.
The names of medications are typically followed by TM or symbols, but these symbols are not stated in this publication.
L003306
The Neurobiology of Child

Abuse and Neglect
Richard Idell, MD; and Charles B. Nemeroff, MD
No commercial support was used in the development of this CME lesson.
Key Words: Depression Abuse Neurobiology

learning objectives: Clinicians will review and become familiar with: (1) the lasting impact of adverse
childhood experience on the hypothalamic-pituitary-adrenal (HPA) axis and implications for the development
of adult psychiatric disorders, (2) the gene-environment (G X E) interactions contributing to the development of
depression and other psychiatric disorders, and (3) treatment recommendations and future directions for managing
patients with a history of child maltreatment.
Abstract: The authors present an overview of the hypothalamic-pituitary-adrenal (HPA) axis. The current literature
about how enduring disruption of the HPA axis, induced by childhood trauma, may contribute to vulnerability
to adult psychopathology is reviewed. Genetic studies are reviewed, specifically including investigation of geneenvironment interactions and epigenetic mechanisms contributing to increased vulnerability to mood and anxiety
disorders. Structural and functional imaging studies documenting the consequences of early-life stress (ELS) are
presented. The implications of these findings for our understanding of the physiopathology of mood and anxiety
disorders and for the development of novel treatments are described.
competency Areas: This lesson addresses the gap in learning in the area of neurobiology as it pertains to
patient care, and evidence based treatment. Many clinicians lack understanding of how enduring disruption
of the HPA axis, induced by childhood trauma, may contribute to vulnerability to adult psychopathology.
Depressed adults with a history of ELS may represent a unique treatment-resistant endophenotype which responds
preferentially to certain forms of psychotherapy or combination psychotherapy-antidepressant treatment. Upon
the conclusion of reading this lesson, readers will have a better understanding of treatment principles for depressed
individuals with a history of childhood trauma, and ongoing research designed to promote better identification and
treatment of depression.
75
L003306 : The Neurobiology of Child Abuse and Neglect
Introduction
Since the introduction of psychoanalysis in the early
part of the 20th century, clinicians and researchers have
sought to clarify the impact of childhood experience on
adult normal and abnormal behavior. Over recent years,
an ever-growing database has revealed that vulnerability
to adult psychopathology, particularly mood and anxiety disorders, is markedly increased by child abuse and
neglect; moreover, this phenomenon may be mediated
by persistent neurobiological changes produced by
early life stress (ELS).1 Through evaluation of the specific mechanisms by which childhood trauma increases
vulnerability to adult psychopathology, novel targeted
therapies may be developed for such patients. Child
maltreatment occurs at a staggering rate, with more
than three million cases of child maltreatment reported
annually in the United States (US), of which more than
one million are substantiated. Among the substantiated
cases, about 60% are classified as neglect, 20% as physical abuse, and 10% sexual abuse (Childrens Bureau,
Administration of Children, Youth and Families 2006).
Some studies suggest that more than 50% of depression
and nearly 60% of suicide attempts may be attributable
to ELS, particularly among women.2 It is of paramount
importance to note that many cases of child abuse may
be unreported, which broadens the public health scope
of the issue.
It is now clear that gene-environment (G X E)
interactions contribute to the development of most
major complex medical disorders including depression
and other major mental illnesses. Approximately 30% to
40% of the risk for the development of unipolar depression is believed to be heritable, with the remaining variability imparted by the environment. Current research
seeks to elucidate the genetic variations and life experiences that interact to produce distinct phenotypes of
affective disorders that may respond preferentially to one
or another of the available treatments. It has been established that early life stress, including physical and sexual
abuse3 has a profound impact on the developing brain.
The HPA axis, the major mammalian regulatory system
mediating the stress response, appears to undergo significant enduring change in response to ELS. It appears
that ongoing vulnerability to stress, partly as a consequence of this persistent HPA axis disturbance caused
by ELS, is a contributing factor in the development of
76
certain psychiatric disorders. In addition to activation

of the HPA axis, elevated levels of pro-inflammatory
cytokines, disruption of serotonin and dopamine
neurotransmission, prolonged glutamatergic activation, and reduced hippocampal neurogenesis have all
been reported consequences of ELS.4 The impact of
dysregulation of the HPA axis and the role of inflammation and stress in the pathogenesis of depression and
other disorders are summarized in this report.
Epidemiology
Many epidemiological studies have contributed to the
current estimate of trauma exposure in children to be
25%45%.5,6 A national sampling service produced a
random sample comprised of 1,442 US subjects stratified by geography. Of these, 935 (64.8%) returned
substantially completed surveys. Sixty-six men and
152 women (14.2% and 32.3%, respectively) reported
childhood sexual abuse experiences, and 22.2% males
and 19.5% females met the criteria for physical abuse.
Based on anecdotal accounts and clinical experience,
emotional abuse and neglect may be even more prevalent albeit more difficult to quantify. Parental loss due
to separation and death represents another traumatic
experience that has been linked with increased psychopathology in adulthood.7 Although retrospective studies
are limited in that memory is fallible, it is clear that early
life trauma is an unfortunately frequent and clinically
significant occurrence.
Psychiatric inpatients have a higher rate of ELS than
the general population. Taking a thorough trauma history is of clinical importance in both men and women,
as evinced by a recent retrospective study that evaluated
the prevalence of childhood (18 years) physical and
sexual abuse among veterans admitted to a psychiatric
inpatient service. This study consisted of a retrospective
chart review of 603 patients admitted to a psychiatric
inpatient unit during a period of one year at the Atlanta
Veterans Affairs Medical Center. The prevalence of
reported childhood physical or sexual abuse in this
inpatient clinical population was 19.4% (117/603). The
prevalence of reported physical abuse was 22.6% (19/84)
in women and 12.0% (62/519) in men; the prevalence
of sexual abuse was 33.3% (28/84) in women and 7.7%
(40/519) in men. A higher percentage of patients with
depressive disorders reported sexual abuse than did those
with many other diagnoses. A larger number of patients

with posttraumatic stress disorder (PTSD) reported physical and sexual abuse. The men with substance-induced
mood disorder (p = 0.01) were more likely to report
physical abuse compared with the men without substance-induced mood disorders.8 These findings mirror
results of laboratory studies using maternal separation in
rats in the first two weeks of life as a model of maternal
neglect, a form of ELS. The early separation resulted in
elevated neuroendocrine and autonomic responses to
stress, depression-like behavior (e.g., decreased preference for sucrose), anxiety (e.g., increased startle), and
increased alcohol preference.9
Clinical Consequences
Early life trauma is associated with increased risk of
psychopathology and medical disorders in childhood
and adulthood.3,10 A strong link between childhood
trauma and mood and anxiety disorders has been established, including: bipolar disorder, unipolar depression,
generalized anxiety disorder, panic disorder, phobias
and PTSD.3,11 Early life trauma is also associated with
increased rates of schizophrenia, eating disorders, and
personality disorders.12,13,14 In addition to increasing the
risk for psychopathology, ELS may increase the duration
and severity of depressive episodes. In a study with 235
outpatients seeking treatment for major depression,
childhood sexual abuse was linked to a longer duration of the index depressive episode.15 More recently,
a study of French and Norwegian bipolar disorder
patients revealed a markedly decreased age of onset
and increased depression severity in those exposed
to child abuse and neglect. A clear dose-response
relationship has been established between childhood
sexual and emotional abuse and emotional neglect and
the severity and course of a bipolar disorder, namely,
earlier age at onset, increased suicide attempts, caused
more rapid cycling, and increased the number of depressive episodes (Etain et al. 2013). A recent commentary
summarizes recent literature regarding the neurobiological consequences of abuse and neglect (Nemeroff and
Seligman 2013).
Traumatized children exhibit an earlier onset of
major depression compared with controls, as well as
higher levels of comorbidity. Widom, DuMont, and
Czaja (2007) performed a prospective longitudinal study

of major depression and comorbidity in 676 children
with substantiated abuse and neglect experienced before
the age of 11 years and a control group of 520 children.
Childhood trauma was associated with an increased risk
of current major depression in young adulthood (odds
ratio [OR] = 1.51). Those children who were physically
abused or experienced multiple types of abuse were at
increased risk for lifetime major depression with ORs
of 1.59 and 1.75, respectively. Childhood neglect
also increased the risk for current major depression
(OR = 1.59).
ELS appears to confer an increased risk for suicidality later in life. The adverse childhood experiences (ACE)
study by the Centers for Disease Control (CDC; Dube
et al. 2001) reported an increased risk of suicide attempts
in adults that experience childhood trauma. The patient
population consisting of 17,337 male and female
adult primary care patients in San Diego were studied
between 1995 and 1997. In patients with no ACEs, the
prevalence of attempted suicide was 1.1%. The lifetime
prevalence of having at least one suicide attempt in
those with reported adverse childhood events was
3.8%. Adverse childhood experiences in any category
(e.g., sexual abuse, physical abuse, etc.) increased the
risk of attempted suicide two to fivefold. The ACE score
was positively correlated with attempted suicide and
exhibited a strong, graded relationship. Compared with
those patients with no ACEs, the adjusted odds ratio of
ever attempting suicide among persons with seven or
more adverse experiences was 31:1.16
A national longitudinal study of adolescent health
revealed that developmental timing of first exposure to
maltreatment influences risk for depression and suicidal
ideation (n = 15,701).17 Among maltreated respondents,
exposure during early childhood (ages 05 years), particularly preschool (ages 35 years), was most strongly
associated with depression. Respondents exposed to
physical abuse during preschool had a 77% increase in
depression and those first exposed to sexual abuse during
early childhood had a 146% increase in suicidal ideation
compared to respondents maltreated as adolescents. This
finding supports the notion that abuse during specific
critical periods of development variably affects susceptibility to depression and suicidality later in life, depending in part on the victims age at maltreatment.
77
Medical Consequences of
Abuse and Neglect
In addition to its effects on vulnerability to several psychiatric disorders and suicide risk described above, ELS
has also been shown to increase risk for several chronic
medical conditions. Another finding of the aforementioned ACE study was that individuals with ELS
exhibited a greater incidence of ischemic heart disease
(IHD). Chronic disruption of the HPA axis, immune
dysfunction, and sensitization of the autonomic nervous
system as a consequence of ELS may contribute to this
increased risk of cardiovascular disease. Because both
depression and ELS are associated with an increased risk
for IHD, it is unclear whether the effects of ELS on cardiovascular disease (CVD) are mediated via depression or
by ELS independently.
ELS has been shown in previous studies to lead to
persistent alterations in immune function18 including
increased concentrations of C-reactive protein, fibrinogen, and white blood cell count, all markers of inflammation shown to be associated with cardiovascular
disease. Studies of the autonomic nervous system have
shown ELS victims exhibit increased blood pressure
and heart rate in response to stress. Additionally, ELS
in rodents has been shown to modify neural, immune,
and endocrine communication between the brain and
gut using a maternal separation paradigm.19 Visceral
sensation perception was found to be increased, consistent with the documented association between irritable
bowel syndrome and ELS. The aforementioned ACE
study showed an association between ELS and increased
rates of hospitalization of adults with autoimmune disease. Increased pro-inflammatory cytokines may be partially responsible for the association between ELS and
autoimmune disorders.4
The HPA Axis and Stress

Multiple studies have documented that ELS affects the
developing brain, leading to vulnerability in adulthood
to stress, depression, and anxiety. In laboratory animal
studies, maternal separation has been found to impact
several central nervous system (CNS) neurotransmitter
systems, including corticotropin-releasing hormone (CRH)
containing circuits. The 41-amino acid peptide CRH is
the main CNS coordinator of the stress response, including the behavioral, autonomic, immune, and endocrine
78
components.3 The hypothalamic (HPA) paraventricular

nucleus (PVN) CRH cell bodies in the medial parvocellular region form the CNS component of the HPA
axis. CRH originating in the PVN is released from nerve
terminals in the median eminence into the hypothalamo-hypophyseal portal circulation upon exposure to
stress, and it binds to CRH receptors in corticotrophs of
the anterior pituitary gland, stimulating the production
and release of adrenocorticotropin (ACTH), proopiomelanocortin-derivatives, and -endorphin. ACTH then
stimulates the production and release of glucocorticoids
(cortisol in humans) from the adrenal cortex into the
systemic circulation. Glucocorticoids provide negative
feedback to the hypothalamus, hippocampus, and anterior pituitary to regulate HPA axis activity; the feedback
effect is mediated by two types of receptors, the glucocorticoid and mineralocorticoid receptors.
CRH also acts as a bona fide CNS transmitter with
neurons expressing this peptide and its receptors widely
distributed throughout the brain, including cortical,
limbic, and brain-stem areas. Two well-characterized
CRH receptors, CRH-R1 and CRH-R2, are distributed
in the CNS. CRH-R1 deficient mice show a reduction
in the hormonal stress response and anxiety-like behaviors.20 CRH-R2 deficient mice show exaggerated anxiety
behaviors and are hypersensitive to stress.21 This suggests
that CRH-R1 activation promotes the stress response
and CRH-R2 activation attenuates this response. Several other neurotransmitter systems interact with CRH
in enhancing (norepinephrine) or buffering (-aminobutyric acid [GABA], oxytocin, neuropeptide Y) stress
responses.22 Unfortunately, despite preclinical evidence
of anxiolytic and antidepressant properties, CRH-R
antagonists have not been shown to be effective in the
treatment of depression or anxiety disorders,23 a subject
that was recently reviewed by Brothers et al. (2012).
Epigenetic mechanisms have been reported that
partly explain the development of glucocorticoid resistance associated with a hyperactive stress response characteristic of ELS and depression. Studies by Meaney and
associates (2004-2007) have demonstrated the existence
of direct epigenetic effects of variations in maternal care
on a neuron-specific promoter region of the glucocorticoid receptor gene.24 Specifically, adequate maternal
care limits cytosine methylation of the promoter region
of the GR gene, whereas poor early maternal care leads
to cytosine methylation and glucocorticoid resistance.
Such early gene modification results in life-long effects

on stress reactivity. Increased susceptibility to stress
appears to lead to increased vulnerability to mood and
anxiety disorders.
HPA axis alterations in depression may also result
from chronic corticotropin releasing factor (CRF) hypersecretion. Depressed patients frequently exhibit elevated
cerebrospinal fluid (CSF) CRF concentrations.25 Postmortem studies of individuals depressed at the time of
death or those who committed suicide have revealed
a decreased density of CRF receptors in the frontal
cortex, decreased expression of CRF1 receptor mRNA,
and increased CRF concentrations in a variety of cortical brain areas and the locus coeruleus compared with
control subjects.26 Successful treatment of depression
reduces elevated CSF CRF concentrations.27 Persistently
elevated CSF CRF in symptomatically improved
depressed patients is the harbinger of early relapse of
depression. Preclinical studies show that CRF administered directly into the CNS produces many signs and
symptoms of depression including decreased appetite,
weight loss, decreased sexual behavior, disrupted sleep,
and altered locomotor activity.28 Individuals with early
life stress histories exhibit: (a) increased CSF CRF concentration, (b) sensitization of the neuroendocrine stress
response, (c) glucocorticoid resistance, (d) activation of
the immune system, and (e) reduced hippocampal volume. Many of these abnormalities are similar to what
has previously been reported in depression. Given that
these findings are evident in individuals with a history of
ELS without depression, ELS, and not depression, may
be responsible for many of the aforementioned HPA axis
changes in depressed patients.1
As previously noted, stress may increase levels of
pro-inflammatory cytokines that activate the HPA
axis, and in turn affect dopamine, serotonin, and glutamate neurotransmitter systems. In response to stress,
proinflammatory cytokines IL-1, IL-6, and TNF-alpha
increase CRF production contributory to hyperactivity
of the HPA axis. IFN-alpha, IFN-gamma, and TNF-alpha up-regulate the human serotonin transporter,
(SERT), and this up-regulation may result in decreased
synaptic serotonin availability. Laboratory animal
studies have demonstrated that IFN-alpha administration decreases CSF dopamine concentrations. These
results are consistent with human studies that revealed
decreased CSF levels of homovanillic acid (the major
dopamine metabolite) in depressed patients. Pro-inflammatory cytokines have also been reported to produce
prolonged glutamatergic activation that may contribute
to depression.4
Clinical Studies
Two previous cross-sectional studies with differing
results have examined HPA and autonomic nervous system reactivity among ELS-exposed patients. In the first
study, adult women with a history of childhood abuse
and current major depression exhibited significantly
higher ACTH levels and cortisol responses in response
to stress compared to abused women without current
depression, non-abused women with current depression,
and non-abused, non-depressed control women.29 In the
second study, seventy-one adolescents were exposed to
the Trier Social Stress Test, a standard laboratory stressor.
Salivary cortisol was assessed at baseline, immediately
before the challenge, after the challenge, and during an
extended recovery period. In this study, the opposite
effect was found: adolescents with a history of ELS and
currently experienced moderate-to-severe depression
exhibited blunted cortisol stress responses, while those
with a history of ELS but only minimal to no current
depressive symptoms exhibited higher and more prolonged cortisol responses.30 The differences in findings
could reflect the intrinsic study differences, for example,
a study by Harkness et al.30 consisted of an adolescent
population, whereas the Heim et al. study consisted of
adult females. Given that depression appears to be a
heterogeneous syndrome, variations of endophenotype
in terms of HPA axis reactivity may be related to severity of depression, variations in the HPA system across
the lifespan, or timing of ELS during critical periods of
development.
A recent study sought to explore the divergent pattern of cortisol reactivity seen in adulthood in subjects
with a history of child maltreatment.31 ELS-exposed
older adults with recurrent psychological distress in
adulthood had blunted cortisol responses compared to
non-ELS-exposed adults, as well as decreased overall
cortisol output compared to ELS-exposed adults with a
history of no or minimal ongoing psychological distress.
In contrast, those ELS-exposed adults with minimal psychological distress during adulthood had elevated levels
of cortisol at baseline and prolonged responses to stress.
79
This study indicates that the variability in the magnitude of ongoing psychosocial stressors may contribute to
differential patterns in HPA axis reactivity observed in
clinical studies.
Imaging Studies: Structural

and Functional Imaging
Structural Magnetic Resonance Imaging
(MRI):
Advances in brain imaging have facilitated the identification of brain regions and associated circuits involved in
the pathogenesis of depression. MRI studies have shown
altered volumes of several brain regions in patients with
depression, most notably a reduction in hippocampal
and caudate nucleus size and an increase in pituitary volume. However, many of the reported changes in brain
structure may be more a consequence of ELS than major
depressive disorder.32 Patients with ELS often report sexual dysfunction in adulthood. A recent study revealed
that exposure to childhood sexual abuse was specifically associated with pronounced cortical thinning
in the genital representation field of the primary
somatosensory cortex. In contrast, emotional abuse
was associated with cortical thinning in regions relevant
to self-awareness and self-evaluation. These findings
indicate that neural plasticity during development
appears to result in cortical adaptation that may shield
a child from the sensory processing of ELS by altering
cortical representation fields in a regionally specific
manner. Such plastic reorganization may be protective
for the child living under abusive conditions, but it may
underlie the development of behavioral problems, such
as sexual dysfunction, later in life.33
Functional Magnetic Resonance Imaging

(FMRI):
Functional imaging studies have focused on clarifying
the impact of ELS on connectivity between the frontal
cortex and limbic circuitry. Dysregulation of the HPA
axis may alter amygdala-ventromedial prefrontal cortex
(vmPFC) circuitry, a circuit implicated in the regulation
of emotion.34 A recent study prospectively investigated
the roles of ELS and childhood basal cortisol concentrations in the development of adolescent resting-state
functional connectivity (rs-FC) in the amygdala-PFC
80
circuit, assessed by functional connectivity magnetic resonance imaging (fcMRI).35 In females only, greater ELS
predicted increased childhood cortisol levels, which
predicted decreased amygdala-vmPFC rs-FC 14 years
later. For females, adolescent amygdala-vmPFC functional connectivity was inversely correlated with concurrent anxiety symptoms but positively associated with
depressive symptoms, suggesting differing pathways
from childhood HPA axis activity to adolescent amygdala-vmPFC functional connectivity to anxiety and
depression. These data highlight that, for females, the
effects of ELS on early HPA axis function and emotional
processing circuitry may be detected much later in life.
Genetics and Epigenetics

Recent studies have revealed a number of single nucleotide polymorphisms (SNPs) of candidate genes which may
affect vulnerability for the development of depression or
anxiety disorders after ELS. Some of the genes that confer risk to mental illness after childhood maltreatment
will be reviewed including SLC6A4, FK506 binding
protein (FKBP5), CRHR-1, and BDNF).
One of the most studied gene variants to show a
quantifiable G X E interaction in the etiology of depression is the SLC6A4 (also known as 5-HTT) serotonin
transporter gene. In a seminal study, allelic variation
amongst a repeat length polymorphism in the promoter
region of SLC6A4 was shown to affect susceptibility to
depression as a result of ELS.36 Adults carrying one or
two copies of the relatively low-expressing short (S) allele
of the serotonin transporter linked polymorphic region
(5-HTTLPR) exhibit elevated depression symptoms,
with increased incidence of depression and suicidality
after experiencing ELS. Prior studies laid the groundwork for this landmark study. In 2002, it was reported
that S-carriers exhibit elevated amygdala reactivity to
threatening stimuli; this was assessed by functional
MRI.37 This interaction of the S-allele and vulnerability
to depression has not been universally supported by all
reports; however, a recent meta-analysis has confirmed
a positive relationship between the short allele of the
5HTTLPR genotype, stressful life events, and risk for
depression.38
A recent study suggests that stress response variations in depressed patients determined by differences
in FK506 binding protein 51 expression, may allow
identification of specific subgroups of depression.39 The

FK506 binding protein 51 or FKBP5 has emerged as
a key element in the stress response.40 FKBP5 is a heat
shock protein 90 (HSP90) co-chaperone, which modifies steroid receptor hormone sensitivity and interacts
with the glucocorticoid receptor (GR), the progesterone
receptor (PR), and the androgen receptor (AR).41 Individuals carrying the FKBP5 risk alleles associated with a
higher induction of FKBP5 mRNA upon GR activation
show a more prolonged cortisol response to psychological stressors,42 indicative of GR resistance. This altered
stress responsiveness appears to be linked to the development of certain major psychiatric disorders. A number of studies have shown association of these FKBP5
polymorphisms with an increased susceptibility to major
depression,43 bipolar disorder,44 and posttraumatic stress
disorder (PTSD)45 as well as an increased suicide risk,46
especially when there was exposure to early trauma.
Treatment
A recent review, briefly discusses four adult and four
adolescent treatment studies of depression.47 All studies
concluded that a history of ELS predicted a poor
treatment response to antidepressants, psychotherapy, or a combination of the two. The findings were
expanded upon by Nanni et al. (2012) in an updated
review of available meta-analyses. One meta-analysis of
16 epidemiological studies (23,544 participants) suggested that childhood maltreatment was associated
with an elevated risk of developing recurrent and
persistent depressive episodes. Another meta-analysis
of 10 clinical trials (3,098 participants) revealed that
childhood maltreatment was associated with lack of
response or remission during treatment for depression. Nemeroff and associates48 reanalyzed data from a
large multicenter treatment trial of chronically depressed
patients, comparing the efficacy of an antidepressant,
nefazodone (Serzone), psychotherapy (cognitive-behavioral analysis system of psychotherapy) and a combination of these, by subdividing the patients according
to a history of childhood trauma. The likelihood of
achieving remission in depressed patients with an
early life adverse event was twice as high with psychotherapy compared to antidepressant treatment
only, and remission was three times as high for those
with parental loss, emphasizing the importance of
trauma processing. Combination treatment with

both psychotherapy and antidepressant treatment
was no better than psychotherapy alone in induction
of remission in depressed patients with ELS. This discrepancy in treatment response in subjects with a history
of ELS suggests a novel endophenotype of major depressive disorder, opening the door to the development of
targeted psychopharmacologic and psychotherapeutic
modalities to those with a history of ELS.
Patients with early life trauma and depression often
present a multitude of psychological symptoms that render treatment challenging. Psychologically these patients
are characterized by being mistrustful, having volatile
relationships, social isolation, low self-image, insecure
attachment, cognitive distortion, and emotional lability
with poor impulse control.49 Psychotherapy addressing a
number of domains, such as emotional regulation, cognitive reframing, careful exploration of past traumatic
events, attachment, and interpersonal relationships in a
safe and trusting therapeutic environment may be part
of a multimodal treatment for patients with ELS. However, no clear psychotherapeutic approach to depression
in patients with ELS has been established. Given the
poor response shown in previous studies to antidepressant treatment, the development of new drug therapies
is imperative.
Antidepressants and ELS:

New Pharmacologic Targets
and Potential Biomarkers of
Treatment Response
Maternal separation induces depressive-and anxiety like
behavior in rats. Escitalopram (Lexapro), an SSRI antidepressant, reverses the depressive-like features and ameliorates the cognitive deficits induced in this stress model
(Couto et al. 2012). Depressive behavior was assessed
in the forced swimming test (FST) and memory performance in the Morris water maze (MWM). Chronic
treatment with escitalopram improved hippocampal
dependent memory. The study suggests that the benefits
of antidepressant treatment might extend beyond relief
of depressive symptomatology alone into the realm of
functional ability or cognitive function of patients with
a history of ELS. However, clinical studies are necessary
to confirm these laboratory studies.
81
Recent brain imaging studies have analyzed the

effect of ELS. One region in particular, the infralimbic
medial prefrontal cortex, a region of the ventromedial
prefrontal cortex (vmPFC), is implicated in processing
emotion context and has been shown to manifest early
changes that appear to increase susceptibility to the
development of major depression.50 Deep brain stimulation of the (vmPFC) region can prolong remission of
depression in treatment-resistant patients, indicating a
role for this brain region in depressive states.51 Previous
studies indicate that abnormal BDNF-Ntrk2 signaling
in the ILmPFC may occur early as a consequence of
ELS, indicating this abnormal signaling as a molecular
marker of depression developing well before depression-like behaviors manifest. Targeting this pathway
prophylactically, particularly in depression-susceptible
individuals, may be of therapeutic benefit; this abnormal
signaling resulting from ELS was shown to be prevented
with fluoxetine treatment.50 This finding supports the
idea that, in the future, preventative medicine may be
implemented by psychiatrists on a pharmacologic basis
through genotyping. Thus, victims of ELS with a particular genetic polymorphism may be potentially treated
prior to the onset of symptoms to prophylactically
prevent depressive episodes. This study warrants further
duplication and clinical studies.
As previously described, hyperactivity of the HPA
axis and hypersecretion of CRH may be involved in the
evolution of mood and anxiety disorders in adulthood,
and recent clinical studies have focused on targeting this
HPA axis dysregulation. New therapeutic targets include
inhibition of CRH release, antagonism at CRH1 receptors, antagonism at vasopressin V1b receptors, inhibition
of cortisol synthesis, antiglucocorticoid treatment with
dehydroepiandrosterone, and treatment with glucocorticoid receptor antagonists. Although preclinical data
support the idea that CRH1 receptor antagonists possess
antidepressant efficacy, no randomized controlled trials
have demonstrated their clinical efficacy in depressed

patients. The antidepressant effects of the antiglucocorticoid neuroactive steroid dehydroepiandrosterone, the
cortisol synthesis inhibitor metopirone (Metyrapone),
and the glucocorticoid receptor antagonist mifepristone
(Mifeprex) in depression have been demonstrated in
some small, double-blind, placebo-controlled studies.
However, three Phase III trials failed to significantly separate mifepristone from placebo in depression, though
patients with higher plasma concentrations did exhibit
clear efficacy. Thus, it is unclear at present to what extent
new, clinically effective antidepressant therapies can be
developed to target dysregulation of the HPA axis.52
Summary
In summary, depressed patients with a history of
childhood trauma may have a distinct depressive
endophenotype, which is characterized by specific
neurobiological alterations and risk alleles that may
be more responsive to different treatment strategies
than depressed patients without childhood adversity.
As noted above, certain risk alleles confer vulnerability to HPA axis dysregulation secondary to ELS. This
dysregulation of the HPA axis, possibly mediated via
cytokine-mediated mechanisms, appears to affect monoamine metabolism, including serotonin and dopamine.
These alterations appear to manifest in alterations in
connectivity between the frontal cortex and limbic
circuits, changing the perception of stressful life events
leading to mood and anxiety disorders. Certain molecular biomarkers described above may eventually lead
to laboratory markers of depressive symptomatology,
and genotyping may lead to identification of patients
who can benefit from prophylactic treatment of mood
disorders. Laboratory animal studies have documented
SSRI mediated amelioration of depressive and cognitive
symptoms of depression in stress models.
About the Faculty

Richard Idell, MD: Dr. Idell is PGY-IV Fellow, Child and Adolescent Psychiatry, Jackson Behavioral Health Hospital,
University of Miami, Jackson Health System, Miami, Florida.
Charles B. Nemeroff, MD: Dr. Nemeroff is the Leonard M. Miller Professor and Chairman, Department of Psychiatry and
Behavioral Sciences; Director Center on Aging; Chief of Psychiatry, Jackson Memorial Hospital; Chief of Psychiatry, University of
Miami Hospital, Leonard M. Miller School of Medicine, University of Miami, Florida.
82
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Neuropsychopharmacology. 2011;36(10):19821991. doi:10.1038/npp.2011.81.
46. Brent D, Melhem N, Ferrell R, et al. Association of FKBP5 Polymorphisms With Suicidal Events in the Treatment of Resistant Depression in Adolescents (TORDIA) Study.
Am J Psychiatry. 2009;167(2):190197. doi:10.1176/appi.ajp.2009.09040576.
47. Uher R. Genes, environment, and individual differences in responding to treatment for depression. Harv Rev Psychiatry. 2011;19(3):109124. doi:10.3109/10673229.20
11.586551.
48. Nemeroff CB, Heim CM, Thase ME, et al. Differential responses to psychotherapy versus pharmacotherapy in patients with chronic forms of major depression and
childhood trauma. Proc Natl Acad Sci U S A. 2003;100(24):1429314296. doi:10.1073/pnas.2336126100.
49. Saveanu RV, Nemeroff CB. Etiology of Depression: Genetic and Environmental Factors. Psychiatr Clin North Am. 2012;35(1):5171. doi:10.1016/j.psc.2011.12.001.
50. Barreto RA, Walker FR, Dunkley PR, Day TA, Smith DW. Fluoxetine prevents development of an early stress-related molecular signature in the rat infralimbic medial
prefrontal cortex. Implications for depression? BMC Neurosci. 2012;13:125. doi:10.1186/1471-2202-13-125.
51. Kennedy SH, Giacobbe P, Rizvi SJ, et al. Deep brain stimulation for treatment-resistant depression: follow-up after 3 to 6 years. Am J Psychiatry. 2011;168(5):502510.
doi:10.1176/appi.ajp.2010.10081187.
52. Schle C, Baghai TC, Eser D, Rupprecht R. Hypothalamic-pituitary-adrenocortical system dysregulation and new treatment strategies in depression. Expert Rev Neurother.
2009;9(7):10051019. doi:10.1586/ern.09.52.
84
L003306
Multiple-Choice Questions
21. What is the lifetime prevalence of having at least one suicide attempt in individuals with reported
adverse childhood events?
A. 1%
B. 1.5%
C. 2.2%
D. 3.8%
22. Childhood maltreatment is associated with:

A. An elevated risk of developing recurrent and persistent depressive episodes
B. Lack of response or remission during treatment for subsequent depression after ELS
C. Poor treatment response to antidepressants, psychotherapy, or a combination of the two
D. All of the above
23. A recent brain imaging study has shown that exposure to childhood sexual abuse specifically showed:
A. Pronounced cortical thinning in the genital representation field of the primary somatosensory cortex
B. Pronounced cortical thickening in the genital representation field of the primary somatosensory cortex
C. Pronounced cortical thinning in the genital representation field of the primary somatomotor cortex
D. Pronounced cortical thickening in the genital representation field of the primary somatomotor cortex
24. Depressed patients with a history of childhood trauma may have a distinct depressive endophenotype
characterized by:
A. Specific neurobiological alterations and risk alleles that may be responsive to different treatment strategies
than depressed patients without childhood adversity
B. A better response to antidepressant medications
C. A lower rate of suicide completion
D. Decreased susceptibility to depressed mood due to ongoing life stress
85
Best Practices in CME

By Richard Idell, MD; and Charles B. Nemeroff, MD
ID#: L003306
This valuable take-home reference translates evidence-based continuing medical education research and
theory, acquired from reading the associated CME lesson, into a step-wise approach that reviews key
learning points for easy assimilation into your armamentarium of knowledge and daily practice.
Brief Lesson Overview:

This lesson reviews the lasting impact of adverse childhood experience on the hypothalamic-pituitary-adrenal
(HPA) axis and implications in the development of adult psychiatric disorders.
Step 1: Psychotherapy Treatment

Psychotherapy should be utilized that addresses a number of domains, such as
emotional regulation, cognitive reframing, careful exploration of past traumatic
events, attachment, and interpersonal relationships in a safe and trusting therapeutic
environment.
Step 2: Genotyping
With advances in genotyping, at-risk individuals who have suffered child maltreatment may potentially be treated prophylactically with antidepressants.
Step 3: Pharmacotherapy
Pharmacotherapy may restore baseline
state stress responsiveness and reverse
epigenetic modifications that lead to increased emotional perception of stressful
experience due to changes in connectivity
between the frontal cortex and the limbic
system.
Step 4: HPA Axis

Ongoing social stress appears to potentiate
HPA axis reactivity.
Step 5: Identifying At-risk Individuals

Certain polymorphisms of identified genes
may identify individuals at risk for mood
and anxiety disorders due to ELS.
Step 6: Pathogenesis of Mental Illness

The HPA axis and monoamine neurotransmitter systems are systems influenced by
ELS and involved in the pathogenesis of
mental illness. The search for novel pharmacologic treatments of depression in
patients with early life stress is ongoing.
Advances in neuroimaging and genotyping
may lead to new therapeutic options in the
treatment of mental illness, which appear
to be on the horizon.
The information presented herein is based upon the content in the associated CMElesson. If you have comments or feedback about this page,
please send your feedback via email to: editorial@hatherleighpress.com and reference the ID number under the title to which you are referring.
We will review your commentary which may be used for publication.
The material in this journal is not a substitute for seeking the attention of a licensed health or medical clinician. These materials were created for professional education
purposes only and are not the express opinion of The Hatherleigh Company, Ltd.
Notes
L003307
Antidepressant Medications in
Preadolescent Children with
Unipolar Depression:
A Review of the Evidence
Thomas N. Butler, MD; Christine J. Choe, MD
The authors have no financial relationships to disclose.
No commercial was used in the development of this CME lesson.
Medications listed within this lesson, with the exception of fluoxetine, have not been approved
by the FDA in the treatment of depression in children under 12 years old.
Key Words: Antidepressants Depression Children

Learning Objectives: This lesson provides a brief overview on recent developments in research on antidepressant
medications in preadolescent children with unipolar depression. The lesson will assists clinicians in their ability to practice
evidence-based care while they conduct informed discussions with patients and families. Clinicians will also review the evidence
for individual antidepressant agents and psychopharmacologic treatment strategies in children with depression.
Abstract: The use of antidepressant medications in the pediatric population has increased dramatically in the United
States in the last few decades, primarily from growth in the use of selective serotonin reuptake inhibitors (SSRIs). There has
been a concurrent proliferation of randomized controlled trials (RCTs) of antidepressants for major depression in youth, which
has provided much needed efficacy and safety data. Among preadolescents, some perplexing findings have also emerged; for
example, only fluoxetine (Prozac) has shown efficacy for depression in randomized controlled trials. Fluoxetine is also the only
antidepressant with FDA approval and established dosing guidelines. RCTs have also yielded important safety information in
young children. An overview of the empirical evidence for antidepressant medications in preadolescent children with unipolar
depression is provided, with a focus on efficacy, dosing, and safety information.
Competency Areas: This lesson addresses learning gaps in the areas of knowledge, competence and performance. In
the area of knowledge, this lesson provides an overview of the empirical evidence for the efficacy and safety of antidepressant
medications in preadolescent children with depression. Equivocal and potentially confusing aspects of the existing research
is also discussed. Regarding competence, this lesson aims to help clinicians improve in their ability to determine and discuss
appropriate treatment options with their patients and monitor for efficacy and safety during treatment. Lastly, in performance,
clinicians may be able to improve the clinical outcomes for their preadolescent patients with depression.
89
L003307 : Antidepressant Medications in Preadolescent Children with Unipolar Depression: A Review of the Evidence
Introduction
The use of antidepressants in the pediatric population
has increased dramatically in the United States since the
late 1980s.1,2,3 Olfson1 found that the rate of antidepressant use among children and adolescents tripled between
1987 and 1996, based on nationally-representative
surveys. Another study in a large, insured population
of children and adolescents found a doubling in antidepressant use between 1994 and 2003, from 9.4 to 21.3
per 1000.2 Much of this growth can be attributed to an
increase in use of selective serotonin reuptake inhibitors
(SSRIs).2 Some concerns have been raised about possible
over-diagnosis and inadequate use of non-medication
therapies.4 Overall, however, the rate of children with
psychiatric disorders who are being treated with psychotropic medications continues to be low5if they receive
any treatment at all.6 Racial disparities in the treatment
of depression have also been found. Caucasians are
twice as likely to receive antidepressant treatment than
African-American youths.3 These and other findings
indicate that many depressed children and adolescents
continue to get inadequate treatment.
There has been a concurrent proliferation of trials
of antidepressant medications in youth, primarily due
to legislation that provided incentives and increased
requirements for pharmaceutical companies to include
children and adolescents in medication studies.7,8 The
Food and Drug Administration (FDA) Modernization
Act of 1997 extended exclusivity rights for an additional
6 months to companies that studied medications in children. The Best Pharmaceuticals for Children Act (BPCA)
of 2002 awarded grants for safety and efficacy trials of
medications deemed a priority for the pediatric population,9 and the Pediatric Research Equity Act (PREA) of
2003 gave the FDA the authority to require the study of
medications for conditions relevant to children. There
have been over 400 pediatric labeling changes as a result
of these pieces of legislation.9
The increased availability of antidepressant trials
in the pediatric population is certainly a positive development in terms of the safe and effective treatment of
preadolescent children, as young children have unique
pharmacokinetic and pharmacodynamic profiles that
can only be explained with direct study. For example,
children have higher rates of behavioral activation
90
and vomiting and less sedation than adolescents.10

Data from RCTs also revealed the increased risk of suicidal thoughts and behaviors in those 24 years of age and
below;11 that has led to labeling changes by the FDA.11
Some authors have noted the seemingly lower efficacy of antidepressant medications for depression in
pre-adolescent children compared with adolescents and
adults.12,13 When trial data is stratified by age, fluoxetine (Prozac) is the only antidepressant that has
demonstrated efficacy in children under 12 years of
age.12 The lack of statistically significant findings in preadolescent children may not reflect a true lack of efficacy,
as trial design and chronicity of illness have been shown
to be major factors in determining whether or not a trial
is positive.12 Bridge12 found that the negative findings
for second-generation antidepressants other than fluoxetine can be correlated with high placebo rates among
children.12 The high placebo rates were in turn directly
correlated with a number of study sites, and this could
potentially result in poorer consistency in the screening
of subjects and execution of study procedures.14,15 Other
potential causes of the high placebo rate among children
are unclear. Unlike in adults, expectancy of improvement and non-specific effects (e.g., regular contact with
care providers) were not significant factors in youths in
an analysis of placebo-controlled and comparator trials.16
Bridge also found that longer duration of illness (which
indicates greater chronicity of illness) also correlated
with positive findings of efficacy.12 Emslie suggests that
pediatric trials should use careful screening to ensure that
the depression is of adequate severity to warrant the use
of medications and to minimize placebo and non-specific responses.17 He also notes that even negative trials
provide direct safety information for these medications
in young children. A review of pharmacokinetic studies
of antidepressants in children and adolescents also suggested that inappropriate dosing may have contributed to
many of the negative trials.18 Further studies in depressed
children and adolescents are needed, as demonstrated by
the widespread off-label prescribing of antidepressants
in youth, particularly for children younger than 13 years
of age.19 Few trials beyond the acute phase of treatment
or focusing on augmentation or adjunctive strategies
have been conducted in youth.
Clearly, the data on the pharmacologic treatment of
depression in preadolescent children is incomplete and
may have been affected by study features that were not

ideal for young subjects. This lesson reviews the available evidence and will also emphasize dosages used in
the studies and safety information in preadolescent children. The focus will be on findings among preadolescent
children; however, where no randomized data exists in
that population, adolescent studies will be reviewed.
Review of Specific
Antidepressant Medications
Pharmacologic treatment of depression in children
should be initiated only after a careful evaluation and
as part of a comprehensive treatment plan that includes
psychological, social, and family interventions.20 The
combination of psychological-social interventions and
medications is generally considered more intensive than
either modality alone,21 but there is a need for further
study in this area.22 Once the decision has been made
to use medications, the overall elements of pharmacologic treatment are much the same as in adolescents and
adults, consisting of acute, continuation, and maintenance phases of treatment. A step-wise algorithm for
treatment during the acute phase has been published.23
Continuation and maintenance treatment studies will
be included when available, but few trials have been
conducted in youth during those phases of treatment.
Therefore, the focus of the present lesson will be on trials conducted during the acute phase.
Selective Serotonin Reuptake Inhibitors

(SSRIs):
Fluoxetine
Fluoxetine (Prozac) is an SSRI distinguished by a long
half-life of four to six days, which delays attainment of
steady state but also minimizes rapid drops in serum
levels with missed doses or discontinuation effects when
stopped abruptly. The recommended starting dose for
children is 10 mg/day, with a target dose of 20 mg to 40
mg/day, and a maximum dose of 60 mg/day.24 However,
in patients of school age or younger, a starting dose of 5
mg, with an initial target dose of 10 mg is reasonable.
Fluoxetine is currently the only antidepressant
with FDA approval for major depressive disorder
in children under 12. Data to support its efficacy
in preadolescent children comes from pooled results

from two randomized controlled trials. The first study
included 96 children and adolescents randomized
to 20 mg of fluoxetine or a placebo over eight weeks,
with response defined by CGI-1 scores of 1 or 2, and
the second was a multi-site replication of the first study
conducted with 219 patients.25,26 Response rates were
significantly higher for fluoxetine compared to the
placebo (41% vs. 20%; P<0.1) in the combined population, and risk differences in response were similar for
preadolescent children (21%; 95% CI, 4%37%) and
adolescents (20%; 95% CI, 7%33%; P = 0.002).12 A
third RCT included adolescents only, and it randomized
participants to cognitive behavioral therapy (CBT) with
fluoxetine, fluoxetine alone, CBT alone, or a placebo.21
Response rates of the two arms containing fluoxetine
were statistically greater than those of CBT alone or
placebo. Final mean dosing was 33.3 mg daily in this
study. Fluoxetine was also shown in two RCTs (with a
total of 142 participants) to be effective for the prevention of recurrence and relapse of depression in children
and adolescents who had responded during the acute
phase.27,28 In summary, fluoxetine is the only antidepressant with demonstrated efficacy in children
under 12 and should be considered as a first-line
treatment for children with depression. 23
Escitalopram
Escitalopram (Lexapro) is an SSRI that is the active
S-enantiomer of the racemic citalopram, with twice the
potency of citalopram to inhibit the serotonin transporter.29 The starting dose in children and adolescents is
5 to 10 mg/d, which can be increased after one week to
a target dosage of 10 to 20 mg/d, and can be increased
further to a maximum dosage of 30 mg/d.
Escitalopram has an FDA indication for the treatment of adolescents with depression, but it has not been
approved in preadolescent children. Two RCTs of escitalopram have been conducted in the pediatric population. The first study compared escitalopram at 10 or 20
mg with a placebo in 264 patients aged 6 to 17 years.30
The overall response rates were 62.8% for escitalopram
and 52.3% for placebo, which was not a statistically significant difference (P = .14; defined by a CGI-I of 1 or
2). A post hoc analysis by age group showed significant
effects of medication on all outcome measures among
91
adolescents only. The second trial did not include children, but modest efficacy was found among adolescents,
with response rates of 64.3% for escitalopram and
52.9% for placebo (P = .03).31 Dosing in these studies
started at 10 mg daily and was subsequently increased to
2040 mg daily. The mean final doses in the two studies
were 11.9 mg and 13.2 mg daily, respectively.
Citalopram
Citalopram (Celexa) is an SSRI that, like escitalopram,
shows minimal CYP inhibition. It does carry a risk of
qTC prolongation at high doses and is therefore not recommended at doses greater than 40 mg/day. Citalopram
should also be avoided in patients who are taking other
qTC-prolonging drugs or who may have comorbid
conditions that put them at risk of developing irregular
heart rhythms.32 The recommended dosing strategy is to
start with 10 mg/day, with an initial target dose of 20
mg/day to a maximum of 40 mg/day.
Citalopram has one published RCT in children and
adolescents, but it was not powered sufficiently to detect
treatment differences by age group.33 In this trial of 174
patients aged 7 to 17 years, remission rates at week eight
(defined by CDRS-R scores of 28 or less), were found to
be modestly but significantly higher in the citalopram
group (36%) than in the placebo group (24%; P<.05).
Another randomized trial of citalopram in adolescents
only allowed patients to receive concurrent psychotherapy. Although there was no significant difference in
overall response rates between citalopram and the placebo, citalopram was significantly more effective among
those who had not received psychotherapy. Response
rates were 52% with citalopram and 45% with placebo
(P<.019; response defined as 50% reduction in Montgomery-Asberg Depression Scale [MADRS] score).34 Citalopram was started at 1020 mg daily and increased to
a maximum of 40 mg daily in these studies. Mean final
doses were 23.3 mg and 26 mg daily, respectively. Citalopram currently has not been approved by the FDA
for any indication in the pediatric population.
Sertraline
Sertraline (Zoloft) is an SSRI with moderate CYP interactions. It can be started at 25 mg/day in children and
adolescents and then increased after one week to 50 mg/
day. Doses can be increased further to 100 to 150 mg/
92
day for inadequate responses, with a maximum dosage

of 200 mg/day.
Two RCTs of sertraline of identical design were
conducted on 376 youths aged 6 to 17.35 No significant
difference between medication and placebo was found
when the trials were analyzed individually, but pooled
results showed a modest but significantly higher
response rate in the sertraline group than in the placebo
group (response rates: SERT 63% vs. PBO 53%, P <
0.05, defined by CGI-I <= 2). A non-significant trend
of greater improvement in CDRS-R score among
adolescents compared with children was noted. Initial
sertraline dosing started at 25 mg daily and was titrated
up to a maximum of 200 mg daily. Mean final dosing
was 131 mg daily. Sertraline was also found to be
effective as a maintenance treatment in an RCT of 22
adolescents who had responded to open-label acute
treatment.36 Sertraline has not been approved for use
in pediatric patients except for those with obsessivecompulsive disorder (OCD).
Paroxetine
Paroxetine (Paxil) is an SSRI that is a potent inhibitor of
CYP2D6 and CYP2B6. It also has a short half-life that
shows considerable variation in the pediatric population,
and can result in a discontinuation syndrome than is
more severe than with other SSRIs. The starting dose is
typically 10 mg/day, with a target dose of 2040 mg/day
and a maximum dose of 50 mg/day.
Only one of three RCTs of paroxetine in the pediatric population has been positive, with no positive
data on the two studies that included preadolescent
children.37-39 The positive pediatric study included 275
adolescents randomized to paroxetine at 20 to 40 mg/
day or a placebo over eight weeks.37 The response rate
was 65.6% among patients in the paroxetine group and
48.3% in the placebo group (P = .02). Patients taking
paroxetine also showed favorable results on several
secondary measures. Paroxetine was initiated at 20 mg
daily with the option of increasing up 40 mg daily in
divided doses. The mean final dose was 28.0 mg daily.
Paroxetine has not been approved for use in the pediatric population, and it is generally not recommended for
use in children under 12 due to a high discontinuation
rate.
Fluvoxamine
Fluvoxamine (Luvox) is an SSRI that is generally not
used to treat depression. No randomized trials of fluvoxamine in youth with depression have been published.
Fluvoxamine does have an FDA indication for treatment
of OCD in patients 817 years of age.
Table 1: Suggested Antidepressant Dosing
in Preadolescent Children
Medication
Initial dose
Target
dose
20 40 mg
daily
Maximum
dose
60 mg daily
Fluoxetine *
10 mg daily
Escitalopram
**
5 10 mg
daily
10 20 mg
daily
30 mg daily
Citalopram
10 mg daily
20 40 mg
daily
40 mg daily
Sertraline
25 mg daily
50 150 mg 200 mg daily

daily
Paroxetine
10 mg daily
20 50 mg
daily
(may divide
dose BID)
Venlafaxine SR
37.5 mg daily 37.5 225

mg daily
Duloxetine
30 mg daily
60 120 mg 120 mg daily

daily
Mirtazapine
7.5 15 mg
QHS
15 45 mg
QHS
45 mg QHS
Bupropion IR
100 mg daily
200 300
mg daily
(TID dosing
for 300 mg)
150 mg/
dose,
up to 450
mg daily
Bupropion SR
150 mg daily
300 mg daily
(BID dosing
for 300 mg)
200 mg/
dose,
up to 400
mg daily
Bupropion XL
150 mg daily
300 mg daily
450 mg daily
50 mg daily
(may divide
dose BID)
225 mg daily
* Fluoxetine is FDA approved for depression in children 8-17 years of age.

** Escitalopram is FDA approved for depression in adolescents 12 years and up.
Other than for fluoxetine, these dosing recommendations are not FDA approved.
venlafaxine and its extended-release version are short,

which can cause more severe discontinuation symptoms.
The initial dosage for immediate-release venlafaxine
is 75 mg/d in divided doses; for extended-release, the
dosage is 37.5 to 75.0 mg/d. Dosages can be increased
by 75 mg/d every 4
7 days, to a target dosage of
150 to 225 mg/d, with maximum dosages of 225 to
400 mg/d.
Venlafaxine may be more efficacious for Major
Depressive Disorder (MDD) than SSRIs in adults,40 but
this finding has not been replicated in youth.41,42 Two
multicenter RCTs of similar design studied extended-release venlafaxine in a total of 367 children and
adolescents.42 Individually, neither study showed statistical significance in the primary outcome measure
(reduction in CDRS-R score from baseline). A post hoc
analysis of pooled data continued to show no significant
effects among children, but a significant difference in
CDRS-R score was found in adolescents (change scores:
-24.4 vs. -20 for venlafaxine and placebo, respectively;
P = 0.022). Dosing of venlafaxine was based on weight,
starting at 37.5 mg daily and increased up to 112.5 mg
daily in those weighing 2539 kg, up to 150 mg daily
in those weighing 4049 kg, and up to 225 mg daily
for those greater than or equal to 50 kg. The mean final
dose of these studies overall was 97.1 mg daily. In the
Treatment of Resistant Depression in Adolescents (TORDIA) trial, 334 adolescents who had not responded to
an eight-week trial of an SSRI were switched to either
venlafaxine or to another SSRI.41 No significant difference was found in response rates between the two
groups, although the venlafaxine group experienced a
higher incidence of side effects. Venlafaxine was started
at 37.5 mg daily and increased up to 225 mg daily for
all subjects, with a mean final dose of 205.4 mg daily.
Venlafaxine has not been approved for use in children or
adolescents.
Duloxetine
Serotonin Norepinephrine
Reuptake Inhibitors (SNRIs):
Venlafaxine
Venlafaxine (Effexor) is a serotonin norepinephrine
reuptake inhibitor (SNRI) that also weakly blocks the
reuptake of dopamine at high doses. The half-lives of
Duloxetine (Cymbalta) is a newer SNRI that is often used

to treat adults with comorbid pain disorders. Few studies
have been conducted among youth. Duloxetine was generally well tolerated in one open-label study of patients
aged 7to 17 with depression.43 Dosing begins at 20 mg
daily and can be increased to a target dose of 4060,
with a maximum of 60 mg/day. Two placebo-controlled
93
trials compared duloxetine, fluoxetine, and a placebo in

800 patients aged 7to 17 and found that neither duloxetine nor the active control differed significantly from
placebo.44 Dosing in these studies started at 3060 mg
daily and was increased to 60120 mg daily after 10
weeks. Duloxetine has not been approved for use in the
pediatric population.
Mirtazapine
Mirtazapine (Remeron) is an atypical antidepressant
that may directly enhance central noradrenergic and
serotonergic activity. In adults with depression, mirtazapine has shown greater efficacy than both SSRIs
and venlafaxine at two weeks and at the end of acute
phase treatment, with comparable tolerability.45 It can
be started at 7.5 to 15 mg nightly and can be increased
by 15 mg every one to two weeks to target dosages of 15
to 45 mg/d.
One open trial in 24 adolescents with MDD showed
efficacy on all rating scales and good tolerability; 46
however, placebo-controlled trials have not demonstrated
efficacy in youth. Two RCTs comparing mirtazapine to
placebo in a total of 259 children and adolescents with
MDD showed no difference in response rates between
the two groups.47 The mean daily dosing in the open
trial was 32.9 mg; in the RCTs, it was 1545 mg daily.
Currently, mirtazapine has not been approved for use
with the pediatric population.
Bupropion
Bupropion (Wellbutrin) is an antidepressant that is
thought to work by inhibiting neuronal uptake of norepinephrine and dopamine. It is sometimes prescribed
for attention-deficit hyperactivity disorder (ADHD). In
adults, the immediate-release and sustained-release
forms are started at 100 to 150 mg/d, and they are
increased three days later to a target dosage of 300 mg/d,
with a total maximum dosage of 400 to 450 mg/d. The
extended release form is started at 150 mg/d for three
days and is increased to a target dosage of 300 mg/d.
The maximum daily dosage is 450 mg.
No RCTs have been conducted for bupropion
in youth with MDD. An open study of bupropion
SR included 24 adolescents with ADHD and either
MDD or dysthymic disorder; it showed a response rate
of 88% defined by a CGI I score of 1 or 2.48 Dosing
started at less than 2 mg/kg or 100 mg in the morning
94
and could not exceed 150 mg twice daily. Final mean

doses were 2.2 mg/kg in the morning and 1.7 mg/kg in
the afternoon. Bupropion has not been approved for use
in the pediatric population. Bupropion has no approved
indications in children and adolescents.
Tricyclic Antidepressants:
Tricyclic antidepressants, including amitriptyline
(Elavil, Tryptanol), imipramine (Tofranil), nortriptyline
(Pamelor, Aventyl), clomipramine (Anafranil), and desipramine (Norpramin, Pertofrane), are rarely prescribed
for youth due to largely equivocal results, high risk of
mortality with overdose, and increased risk of side
effects. In a Cochrane review of 14 RCTs of tricyclics
in 590 youths with depression, no overall difference
was found in response compared to the placebo.49
Further analysis showed no improvement in depressive symptoms in children and only a small improvement in adolescents. Tricyclics also caused significantly
more vertigo, orthostatic hypotension, tremor, and dry
mouth than placebo.
Monoamine Oxidase Inhibitors (MAOIs):

Monoamine oxidase inhibitors (MAOIs), including
phenylzine (Nardil), tranylcypromine (Parnate), isocarboxazid (Marplan), and selegiline (Anipryl, Eldepryl),
are not commonly prescribed for youth due to a narrow
therapeutic index and the challenge of adhering to a
tyramine-free diet.50 The selegiline patch has been
demonstrated to be safe at the dose of 6 mg/24 hours
without the need of a special diet.50 A RCT examining
the selegiline patch in adolescents with MDD showed
no difference in response compared to placebo.51
Studies on Augmentation
and Switching Strategies
Approximately 40% of children and adolescents may
have an inadequate response to monotherapy with
an antidepressant medication. In cases of treatment
failure, in addition to adjustments in psychological and
social interventions, one of two pharmacologic strategies
can be employedaugmentation with a second agent
or switching to an alternate medication. Augmentation
is generally recommended for partial responders (i.e.,
approximately 50% reduction in symptoms), while
switching to a different medication should be considered
in cases of minimal to no response.23
Unfortunately, augmentation studies in depressed

children and adolescents are scarce. One case series of
10 adolescents with inadequate responses to fluoxetine
showed improvement with the addition of quetiapine.52
Among adults, augmentation of an antidepressant with
agents such as stimulants, lithium, thyroid hormone,
atypical antipsychotics, or another antidepressant has
shown some efficacy.53 The previously mentioned
TORDIA study examined switching strategies in
adolescents with MDD. A total of 334 adolescents
who failed eight weeks of treatment with an SSRI were
randomized to switch to either another SSRI or to
venlafaxine (two arms also included CBT in addition
to each medication). There was no significant difference
in response rates between SSRI and venlafaxine (47%
[95% CI 40%55%], versus 48% [95% CI 41%56%]
respectively).41 Venlafaxine was associated with a slightly
higher incidence of increased blood pressure and pulse
and more frequent occurrence of skin problems. In
summation, in the absence of a proven benefit and
with an increased risk of side effects from switching
to venlafaxine rather than an alternate SSRI,
switching to an alternate SSRI before venlafaxine is
generally recommended.
Adverse Effects
Adverse Effects in the General Population:
Potential side effects of the various antidepressant classes
in the general population have been reviewed in detail
elsewhere and will be mentioned only briefly here.
Common side effects of SSRIs in children are similar to
those in adults and include headache, dizziness, nausea,
diarrhea, somnolence or insomnia, tremors, sweating,
rash, jitteriness, increased anxiety, vivid dreams, and
sexual dysfunction. Rare side effects of SSRIs include a
prolonged QT interval on electrocardiogram, increased
bleeding, seizures, hyponatremia, psychosis, mania, and
serotonin syndrome. SNRIs can have similar side effects
to SSRIs but also include noradrenergic effects, including increased heart rate and blood pressure, sweating,
dizziness, loss of appetite, dry mouth, and jitteriness. In
adults, mirtazapine has an overall comparable tolerability to SSRIs and SNRIs, but it may be more likely to
cause weight gain, increased appetite, and somnolence
than SSRIs, as well as less nausea, vomiting, and sexual

side effects. 45
Discontinuation syndromes can occur with abrupt
withdrawal of antidepressants of any class, although
agents with short half-lives carry the greatest risk and
can induce more severe symptoms. Drug interactions
should always be considered in any patient taking
multiple medications. Most SSRIs, duloxetine, and
bupropion have moderate to potent inhibitory effects
on the activity of various CYP enzymes. SSRIs are
contraindicated for concomitant use with MAOIs (cardiotoxicity, serotonin syndrome), pimozide ([Orap]; bradycardia, somnolence, cardiotoxicity), and thioridazine
(cardiotoxicity). Bupropion is contraindicated in the
presence of eating disorders, a high risk of seizures, or
with MAOIs. Venlafaxine, duloxetine, and mirtazapine
are all contraindicated for concurrent use with MAOIs.
Duloxetine is also contraindicated in the presence of
uncontrolled narrow-angle glaucoma.
Adverse Effect in Children

and Adolescents:
Safer pooled data from RCTs of SSRIs in order to
examine effects of age on reported adverse events.10
Somnolence as a side effect of SSRIs was rare in children (average -0.4%), more common in adolescents
(average 6.3%), and most common in adults (average
8.9%). Safer (2006) also found that preadolescent
children had a two- to three-fold greater prevalence
of SSRI-induced vomiting and behavioral activation, which included restlessness, hyperkinesis,
hyperactivity, and agitation.10 The average rates of
behavioral activation among children were 10.7% for
those on medication and 3.4% for placebo. For adolescents, the averages were 2.1% on medication and 1.9%
on placebo. SSRI-induced activation frequently resolves
upon discontinuation of the medication;54 however,
SSRI-induced activation has also been associated with
an increased risk of suicidal thoughts and behaviors.11
Another concern is that activation may, in at least some
instances, represent hypomanic and manic reactions
to antidepressants. This is particularly concerning, as
possible long-term effects of antidepressants on a young
persons course of illness, particularly those with latent
bipolar disorder, are unknown.55
The TORDIA trial, a RCT comparing venlafaxine and SSRIs in adolescents, found a higher
95
incidence of increases in blood pressure and pulse as

well as skin rashes with venlafaxine.41 In a six-month
open-label trial of venlafaxine conducted by a pharmaceutical company, children and adolescents were
observed to have smaller than expected increases in
weight and height, with a greater effect in children
under 12 than in adolescents.56 A meta-analysis of suicidality events among second-generation antidepressants
in various conditions found that only venlafaxine as an
individual agent showed an increased risk of suicidal
events.11 The authors of the study note that this finding
may represent factors, such as inadequately powered
studies, variation in the recording and reporting of
events, or a true difference in suicide risk. Similar to
SSRIs, somnolence from venlafaxine may be uncommon
in preadolescent children. In a set of two identically
designed RCTs of extended-release venlafaxine in generalized anxiety disorder, young children had significantly
lower rates of somnolence than adolescents (children:
4% on venlafaxine, 4% on placebo; adolescents: 11% on
venlafaxine, 0% on placebo).57 Small but statistically
significant increases in pulse and blood pressure as
well as smaller than expected increases in weight and
height were also seen for children and adolescents
taking active mediation.
Suicidal Thoughts and Behaviors:

The FDA issued a black box warning in 2004 for all
antidepressants indicating that their use in the pediatric
population was associated with an increased risk of suicidal thinking and behavior. A subsequent meta-analysis
of 24 placebo-controlled trials, which included 4,582
pediatric patients treated with antidepressants, showed
the overall relative risk for suicidal thinking and behaviors to be 1.95 (95% CI, 1.282.98), with a relative
risk of 1.66 (95% Cl, 1.022.68) for SSRIs used for
depression.11 The risk difference between treatment
with antidepressants and placebo was 0.02 (95% CI,
0.010.03), and there were no completed suicides in
any of the studies. A more recent meta-analysis looking specifically at 13 studies of 2910 youth specifically
with depression and treated with antidepressants found
absolute rates of suicidality of 3% (95% CI, 2%4%)
in those treated with antidepressants and 2% (95%
CI, 1%2%) in those treated with a placebo.12 In this
96
analysis, the number needed to treat (NNT) was 10, and

the number needed to harm (NNH) was 112.
Despite the increased risk of suicidal thinking
and behaviors associated with antidepressant use,
epidemiological data have not demonstrated a
relationship between antidepressant prescribing rates
in youth and completed suicides.58 Studies following
the black box warning in fact showed decreased
antidepressant use in youth with a concurrent increase
in suicides.59 These trends suggest that depression is
inherently a risk factor for suicide, and, by treating it, the
risk of suicide attributed to the underlying depression
decreases. Thus, the small but real risk of suicidality as an
adverse effect of antidepressant use needs to be balanced
with the risks of inadequately treated depression.
Conclusion
The recent proliferation of antidepressant trials in the
pediatric population has provided evidence of the
efficacy of fluoxetine in preadolescent children with
depression and has yielded data on the dosing and safety
of fluoxetine and other agents in this population. Currently, randomized controlled trials of antidepressants
that include pre-adolescent children have been limited
to monotherapy during the acute phase of treatment.
Data on non-SSRIs, augmentation, switching strategies, and the continuation and maintenance phases in
children and adolescents are scarce. For children with
depression who need treatment with medications, fluoxetine is a reasonable initial agent for monotherapy,
unless individual patient factors indicate otherwise.
Other SSRIs are reasonable choices for second-line treatment despite negative trials in depressed young children,
as the negative findings likely reflect trial design rather
than true lack of efficacy. It is difficult to make recommendations on non-SSRI and non-SNRI medications,
as very few randomized studies have been conducted on
these agents in the pediatric population. The available
data on second-generation antidepressants support
their overall safety in children. However, consideration
should be paid to the unique profile of adverse effects
found in children, which includes increased suicidality
and activation effects.
About the Faculty

Thomas N. Butler, MD: Dr. Butler is a Psychiatry Resident, Department of Psychiatry, University of Texas Southwestern
Medical Center, Dallas, TX.
Christine J. Choe, MD: Dr. Choe is Assistant Professor, Department of Psychiatry, Division of Child and Adolescent Psychiatry,
University of Texas Southwestern Medical Center, Dallas, TX.
97
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trials. JAMA : the journal of the American Medical Association. Aug 27 2003;290(8):1033-1041.
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41. Brent D, Emslie G, Clarke G, et al. Switching to another SSRI or to venlafaxine with or without cognitive behavioral therapy for adolescents with SSRI-resistant
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43. Prakash A, Lobo E, Kratochvil CJ, et al. An open-label safety and pharmacokinetics study of duloxetine in pediatric patients with major depression. Journal of Child and
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44. Shamseddeen W, Asarnow JR, Clarke G, et al. Impact of physical and sexual abuse on treatment response in the Treatment of Resistant Depression in Adolescent Study
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48. Daviss WB, Bentivoglio P, Racusin R, Brown KM, Bostic JQ, Wiley L. Bupropion sustained release in adolescents with comorbid attention-deficit/hyperactivity disorder
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100
L003307
25. The only antidepressant that has demonstrated statistically significant efficacy in depressed children
under 12 is:
A. Sertraline
B. Citalopram
C. Fluoxetine
D. Bupropion
26. According to the lesson, all of the following adverse effects of antidepressants have been found to be
more common in preadolescent children than in adolescents, except:
A. Sedation
B. Behavioral activation
C. Vomiting
D. Less than expected weight gain
27. Which one of the following statements is true?

A. Escitalopram has been FDA-approved for the treatment of depression in children and adolescents
B. TORDIA was a study of treatment-resistant depression in children and adolescents.
C. Preadolescent children have not been included in any randomized controlled trials of venlafaxine.
D. Tricyclic antidepressants have generally not been found to be effective for depression in randomized
controlled trials of preadolescent children.
28. Which one of the following statements is true?

A. Approximately 80% of depressed children and adolescents will have an adequate response to an initial trial
of an antidepressant medication.
B. In cases where a depressed pediatric patient has not responded to antidepressant monotherapy, the general
recommendation is to switch to an SNRI rather than to an alternate SSRI.
C. RCTs have shown that augmentation with various agents, including bupropion, antipsychotics, and
stimulants, are not effective in children and adolescents who have had an inadequate response to
antidepressant monotherapy.
D. One RCT of the selegine patch in depressed adolescents did not show efficacy but supported its safety and
tolerability in adolescents.
101

By Thomas N. Butler, MD; Christine J. Choe, MD
ID#: L003307

This lesson provides a brief overview on recent developments in research on antidepressant
medications in preadolescent children with unipolar depression. Clinicians will review the
evidence for individual antidepressant agents and psychopharmacologic treatment strategies
in children with depression.
Key Point 1: Background
There has been a proliferation of randomized controlled trials (RCTs) of antidepressants in the pediatric population over the
past few decades, primarily as a result of
legislation that promoted the inclusion of
children and adolescents in medications
studies.
Key Point 2: Needs Assessment
RCTs that include preadolescent children

are necessary because young children have
unique efficacy and safety profiles.
Key Point 3: Efficacy Findings
Fluoxetine is the only antidepressant that

has demonstrated efficacy in RCTs among
preadolescent children.
Negative trials of many secondgeneration antidepressants in children have
been linked to factors in study design and
may not reflect a true lack of efficacy.
Key Point 4: Adverse Effects of Anti

depressants in Pediatric Population
population, and specifically in preadolescent

children. For example, children have higher
rates of behavioral activation and vomiting
and less sedation than adolescents. The increased risk of suicidal thoughts and behaviors in young patients was also confirmed
through randomized trials.
Key Point 5: T
reatment-Resistant
Depression
In adolescents who have failed to respond

to monotherapy with an SSRI, there may
be no additional benefit and a higher risk
of side effects from switching to venlafaxine
rather than an alternate SSRI. No comparable trials of treatment-resistant depression
have been conducted in young children.
Key Point 6: Need for Research
Research in monotherapy with non-SSRIs

and augmentation strategies in the pediatric population have been scarce. Extrapolation from adult data is frequently necessary
in these areas.
RCTs have yielded information on adverse

effects of antidepressants in the pediatric
Notes
L003308
Psychostimulants
for Test-Taking and ADHD:
Shawen M. Ilaria, BS; Michael A. Shapiro, MD; and Mark S. Gold, MD
The authors declare that there are no competing interests.
The authors would like to thank Paula J. Edge, a gifted editor, for her assistance in preparing this manuscript for publication.
KEY WORDS: ADHD Psychostimulant Performance Enhancement

LEARNING OBJECTIVES: In this lesson, clinicians will: (1) review the definition of attention-deficit hyperactivity
disorder (ADHD); (2) review psychostimulants and other treatment modalities; (3) consider the increasing misuse of
psychostimulants; (4) compare the concepts of addiction, abuse, and other parental concerns; and (5) consider the implications
of psychostimulants as academic performance-enhancing drugs.
ABSTRACT: Attention-deficit/hyperactivity disorder (ADHD) is an increasingly popular topic, and more children than ever
are garnering the diagnosis in this country. The major treatment modalities for ADHD include behavioral modification and
psychostimulants. The use of psychostimulants is a controversial and fascinating topic, as it has very different implications
for children, adolescents, and adults, and can affect a person regardless of whether he or she has ADHD. The stigmas of
psychostimulant use are varied: Parents are chided for overmedicating their hyperactive children, and adolescents and young
adults are accused of using psychostimulants as academic performance-enhancing drugs. In this lesson, the authors strive to
spark a conversation on the use of psychostimulants, especially in the academic setting. The authors also review ADHD and
basic psychostimulant pharmacology.
COMPETENCY AREAS: This lesson addresses the need for an updated medical knowledge base that will allow the use of
evidence-based practices to provide quality patient-centered care for children, adolescents, and adults with ADHD.
105
L003308 : Psychostimulants for Test-Taking and ADHD: Assessing the Risks & the Benefits
Introduction
Attention-deficit/hyperactivity disorder (ADHD) and
attention-deficit disorder (ADD) are now household
terms. Although the term ADD was replaced by ADHD
in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) in 1994,1 the original
acronym is still used, mainly by nonclinicians. With
the increase in public awareness, this disorder has taken
on a looser definition. A person with a distractible or
energetic personality variant might identify with having
ADHD without ever having a diagnosis. Whether or
not the term is used freely, those truly deserving of the
diagnosis are hard to forget.

I remember meeting Jack in a clinic during

medical school; he was six years old and
absolutely overwhelming. Within seconds
of escaping from the exam room, he had
found the break room, opened the staff
refrigerator, and retrieved a half-full can
of soda. A pressured string of questions
led to Can I have some? as I successfully
wrestled it away. I gave Jack a pen and paper
and immediately recognized my mistake.
He scribbled with such determination that
no piece of paper could be large enough to
keep his pen from contacting surrounding
surfaces. It was like the DSM-IV entry of
ADHD came to life as a wild caricature of
itself. I couldnt imagine Jack riding a bus to
school without disastrous effects, much less
doing schoolwork or taking a test.
In general, parents are increasingly concerned with

the implications of ADHD. Parents of children who
cant sit still in class may rush to the psychiatrist for a
diagnosis; others are skeptical of its increasing prevalence
and prescriptions written for psychostimulants. Indeed,
treating ADHD with psychostimulants is a controversial topic. Parents of children diagnosed with ADHD
often ask if psychostimulants will change their childs
personality or make them zombies. Others might say
that parents are simply medicating their child rather
than using discipline and structure. Another increasing
concern is the use of psychostimulants by those without
a diagnosis of ADHD, such as college students during
106
finals week or students cramming for exams in medical

school. Although these uses are impossible to measure,
they are nonetheless an increasing concern.
ADHD in Childhood
and Adolescence
As defined in the DSM-IV, ADHD manifests in
childhood and has symptoms of inattention (Inattentive Type), hyperactivity-impulsivity (Hyperactive/
Impulsive Type), or both (Combined Type). These
symptoms must occur for at least 6 months and
cause significant impairment in multiple settings,
such as home, school, work, or social situations. The
DSM has consistently portrayed ADHD as a disorder of
childhood; the DSM-IV indicated that symptoms must
be present before the age of 7 years2 while DSM-5 has
changed the cutoff age to before the age of 12 years.3
ADHD is a common disorder, and the number of
individuals carrying the diagnosis is growing. ADHD
is the most common neurobehavioral disorder of child
hood, with an estimated 8.7% of children in the United
States (US) aged 815 years meeting DSM-IV criteria
for ADHD, with a male-to-female ratio of nearly 2:1 in
children;3 however, less than half receive an actual diagnosis or treatment.4 Approximately 60%85% of children diagnosed with ADHD continue to meet criteria
for the disorder in adolescence.5 Teens with ADHD are
more likely to fail a grade than teens without ADHD.5
Possibly more serious than the obvious academic difficulties, teens diagnosed with ADHD are more likely to
have car accidents, smoke cigarettes, drink alcohol, use
drugs, or be suspended from school.5
ADHD in Adulthood
Physicians used to assure parents of ADHD children,
Dont worry, he will grow out of it when he hits puberty.
Unfortunately, that is a fallacy; we now know that many
children with ADHD become adults with ADHD.6
Although there is no adult-onset ADHD,6 the symptomology evolves and changes over time and, therefore,
may not be recognized as ADHD. Additionally, some
adults with ADHD were merely children who were
never brought to the attention of a clinician, diagnosed,
or treated. The number of adults living with ADHD
is even more difficult to quantify, with one telephone

survey estimating 2.9% prevalence of narrow ADHD
(symptoms occurring often) and 16.4% broad ADHD
(screening prevalence for further assessment by a clinician).7 Another study estimated adult ADHD prevalence
at 3.4% in surveys spanning 10 countries including the
US, often co-occurring with other psychiatric disorders.8
Several studies have estimated the proportion of children with ADHD who continue to have symptoms into
adulthood. This ranges from as low as 10% to as high
as 50%.5 The male-to-female ratio becomes more equal
in adulthood at approximately 1.5:1, with females more
likely than males to present primarly with the inattentive subtype.3
Symptoms of ADHD are subtler in adults, and
can sometimes mimic or be part of antisocial behaviors.5 Additionally, most teens and adults experience
occasional problems with inattention, impulsivity,
distractibility, and restlessness.9 However, the level of
functional impairment these symptoms cause is variable
and extremely subjective. This makes it more difficult
to screen for true ADHD in adults who were not previously diagnosed as children.
Similar to children and adolescents, adults with
ADHD often have relationship difficulties in their occupations and their personal lives. In adulthood, this can
lead to a higher divorce rate, higher risk of traffic accidents, and higher crime rate and arrest rate. Inattention
can appear in the workplace setting as trouble completing tasks, keeping appointments, or even maintaining
a stable job. Impulsivity can lead to overspending or
unplanned pregnancy, and novelty-seeking and risky
behavior such as gambling. Adults with a childhood history of ADHD are also more likely to develop comorbid
psychiatric pathology as adults, and have higher rates of
substance-use disorders.9
For adults, optimal management of ADHD requires
a comprehensive evaluation and treatment approach.
Some type of psychosocial therapy or cognitive behavioral therapy (CBT), paired with pharmacotherapy, can
improve quality of life while maximizing the benefits of
symptom reduction.
The future of research in ADHD appears aimed
at the genetic signature of the disorder10,11 and how
the brain is different in those with ADHD and those
without.12 Cocchi et al. found results that suggested the

frontal, temporal, and occipital cortices were abnormally
connected locally, as well as with the rest of the brain, in
adults with ADHD.13
Pharmacotherapy for ADHD

When treatment options for ADHD are considered,
every childs situation may be different, and a conversation with the child and parents should always take place.
Considerations such as duration of coverage, timing of
coverage and how that might determine administration at
school, ability to swallow pills, and comorbid psychiatric
or behavioral issues, can affect best treatment options.14
Clinical practice guidelines suggest a stimulant as
the first-line agent for treating ADHD in school-aged
children, aged 6 or older.15 Evidence supports that stimulants are safe and effective, and behavioral therapy alone
has limited efficacy.16 Stimulants are often categorized by
duration of action. Short-acting stimulants have been
studied extensively and are effective and safe.17 Examples
include methylphenidate (Ritalin), dexmethylphenidate
(Focalin), dextroamphetamine (Dexedrine), and amphetamine mixed salts (Adderall).18 Used alone, they are
administered 23 times per day to achieve a lasting effect.
Chewable or oral solution formulations are available for
children who cannot swallow pills. Recently, long-acting
stimulant formulations have become increasingly used
due to the ease of once-daily dosing. Such formulations
include single-pulse sustained release (Ritalin SR), sustained-release bead preparations (Dexedrine, Ritalin LA,
Adderall XR, Focalin XR), osmotic release (Concerta),
patch (Daytrana), and the prodrug lisdexamfetamine
(Vyvanse).18 Long-acting stimulants can be dosed once
per day, avoiding administration at school, but can be
more expensive. The sustained-release bead preparations (can be opened and sprinkled on food), the
patch, the prodrug (can be opened and mixed with
water), and the new long-acting oral-suspension
methylphenidate hydrochloride (Quillivant XR)19 are
all options for children who cannot swallow pills. It
is not uncommon to combine a long-acting stimulant in
the morning with a short-acting stimulant boost in the
afternoon when needed.
Nonstimulants may be less efficacious than stimulants, but are good alternatives to discuss with parents
107
and children. Atomoxetine (Strattera) is a selective norepinephrine reuptake inhibitor. It can be dosed once
or twice daily and has a lower potential for abuse than
stimulants, but may have an increased risk of suicidal
ideation. Alpha-2-adrenergic agonists approved for
treating ADHD include extended-release guanfacine
(Intuniv) and extended-release clonidine (Kapvay).
These medications may also treat coexisting conditions
such as tic and sleep disorders.18
The risk of treatment with stimulants also needs to
be considered. The most commonly reported side effects
of stimulant treatment are appetite suppression and
sleep disturbance.5 Less commonly reported side effects
include mood disturbance, gastrointestinal (GI) disturbance, and headache. Stimulants can also increase blood
pressure and heart rate, the clinical significance of which
is still under debate. Early studies indicated that patients
with underlying heart defects may be at risk for sudden
death. Patients should be screened for a family history
of early cardiac death or arrhythmias or a personal history of structural abnormalities, chest pain, palpitations,
shortness of breath, or fainting episodes. In such cases,
a baseline electrocardiogram (ECG) or cardiology evaluation may be appropriate. There were also early concerns
that stimulants may precipitate or worsen tics or tic
disorders such as Tourette syndrome. However, recent
randomized controlled trials show that the proportion
of patients who complained of worsening tics were the
same in patients treated with a stimulant compared to
placebo.5
Psychostimulant Misuse
Healthcare providers are challenged by the increasing
misuse and diversion of psychostimulants. There are
many reasons that this medication commonly switches
hands, one certainly being that individuals with or without ADHD report improved attention and concentration with psychostimulant use.
To better understand the prevalence of psychostimulant misuse, we examined an extensive systematic
review of the literature, published in 2008, which
identified 21 studies representing 113,104 subjects. The
review reported rates of past-year nonprescribed stimulant use ranging from 5% to 9% in grade-school and
high schoolage children and 5% to 35% in college-age
108
individuals. Lifetime rates of diversion ranged from 16%

to 29% of students with stimulant prescriptions asked to
give, sell, or trade their medications. Reported reasons
for use, misuse, and diversion of stimulants include to
concentrate, improve alertness, get high, or experiment.20 In a study of 55 college students who reported
past-year use of prescribed stimulants for ADHD,
40% endorsed at least one item of misuse. The most
frequently endorsed misuse items were used too much
(36%), self-reported misuse (19%), and intentionally
used with alcohol or other drugs (19%).21
Although misuse is prevalent, these behaviors may be
attributed to comorbid substance use behaviors. Those
who were prescribed stimulant medication and reported
misuse were also more likely to report cigarette smoking,
binge drinking, illicit use of cocaine, and screen positive
on the Drug Abuse Screening Test (DAST-10) criteria.
Diversion of prescribed stimulants was common (36%)
and occurred more frequently among stimulant misusers
(57%).21
Addiction, Abuse, and Other

Parental Concerns
Addiction to psychostimulants is a concern that parents
may have when considering this treatment option for
their children. Stimulants are a Class II Schedule drug
under the Controlled Substances Act. Other substances
in this class include cocaine, opium, morphine, and
methadone.22 Class II Schedule drugs are usually prescribed without refills on a monthly basis.
Table 1:
Schedule II Drugs
(A) The drug or other substance has a high potential for
abuse.
(B) The drug or other substance has a currently accepted
medical use in treatment in the United States or a
currently accepted medical use with severe restrictions.
(C) Abuse of the drug or other substances may lead to
severe psychological or physical dependence. 23
Despite this readily available information, psychostimulants are safe when used properly. Oral doses of
methylphenidate do not induce euphoric effects; abuse
to achieve euphoria typically requires administering

the medication through other routes, such as snorting,
inhaling, or intravenously.24 Thus, there is greater risk
for abuse with immediate-release stimulant formulations that can be crushed.5 Another study showed that
although methylphenidate has shown the potential for
substance abuse in the laboratory setting, there is virtually no evidence to date that the drug possesses significant abuse potential in patients who are likely to take
the drug for clinical purposes.25
Parents worry that starting their children on psychostimulants will increase the risk of drug abuse later in
life. In fact, children with ADHD, whether or not they
are treated, are at a much greater risk of drug abuse than
children without ADHD. Children with ADHD also
start smoking at an earlier age, are drawn into deviant
peer relationships, and are vulnerable to undesirable
social influences associated with drug abuse. For many
years, treatment with psychostimulants has been thought
to reduce the risk of drug and alcohol abuse later in life.
However, this was balanced with the concern for giving
children and adolescents prone to drug abuse, stimulant
medications that could be abused themselves. However, a recent meta-analysis indicated that treatment of
ADHD with stimulants neither protects nor increases
the risk for later substance use disorders.26
Intentional abuse or misuse of psychostimulants
has serious consequences. One study queried the American Association of Poison Control Centers National
Poison Data System for the years 19982005 for all
cases involving people aged 13 to 19 years, for intentional abuse or misuse of medications used for ADHD
treatment. During that time period, estimated prescriptions for teenagers and preteenagers increased 133%
for amphetamine products, 52% for methylphenidate
products, and 80% for both together. Calls related to
teenage abusers of prescription ADHD medications
rose 76%, which is faster than calls for abusers of
other substances generally and for teen substance
abuse. The annual rate of total and teen exposures
was unchanged. This suggests an increasing problem
with teen psychostimulant abuse.27
Parents often confuse appropriate lifelong use of a
medication with addiction, as they might perceive their
child is dependent on a medication. This concern
especially reflects the ongoing stigma of mental illness.

Indefinite use of medications for asthma, diabetes, or
heart disease is accepted as necessary, but lifelong medications for mental health disorders are questioned. The
opinion exists that taking these medications represents
a lack of coping, motivation, or, especially in children,
discipline. A popular entry in a Psychology Today blog
suggests that the French emphasis on self-control and
strict discipline is the reason why less than 0.5% of
children in France are diagnosed with and treated for
ADHD.28
Although successful treatment may be less obvious
to detect (as in blood glucose levels in diabetes or pulmonary function tests in asthma), the consequences of
nontreatment on behavior, psychiatric disorders, and
substance use disorders are significant. Children and
adolescents with ADHD who remain untreated have
more difficulties in school, have a higher rate of traffic
violations,29 and may struggle with interactions with
their teachers and peers. Parents could be encouraged to
view successes in small ways: fewer notes sent home from
teachers, more chores completed, less frustration with
homework, and fewer disruptive behaviors at home.
Parents may be surprised to learn it is possible to have
a quiet family dinner at home without their children
getting up from the table before the meal is finished.
Academic Performance
Enhancement
Many studies highlight the misuse of stimulants, especially in colleges and universities. These data are often
collected by surveys of students who are willing to share
their habits and behaviors with a stranger. Most of us,
however, collect our working data from one-on-one
patient encounters, and the perspective of a recent college graduate speaks to the current status of psychostimulants in the academic setting:
In the authors experience, it would not be surprising to learn that an individual was acquiring
Adderall or Ritalin while enduring premed courses, writing a research paper, or leading up to finals week. The source of these medications wasnt
a drug dealer staked out on campus or an underground black market. It was usually someone the
109
user knew, perhaps a friend with ADHD who did

not always take his or her medications, or who
diverted a few doses each month to sell for extra
money. Stories were told of physicians who would
write prescriptions for psychostimulants after just
one visit, and friends suggested them to each other.
Many opinions existed of psychostimulants as academic performance enhancers. For each student
who compared it to an athlete doping up, there
was another who likened it to drinking coffee.
Some found it unfair, and others would do anything to graduate top of the class. Opinions were
mixed, but misuse of psychostimulants was fact.
We know that students perceive psychostimulants as
enhancing their academic performance. In one study, 14
of 27 students misused their ADHD medication exclusively for academic reasons. The remaining 13 misused
for academic and nonacademic reasons. No student misused ADHD medication solely for nonacademic reasons.
Enhancing the ability to study more effectively outside
class was students primary motive for misuse, and students felt that using psychostimulants was helpful.30
However, this may be more of a psychological or
placebo effect. One review found that, overall, stimulant
drugs do not improve the academic performance of
non-ADHD-diagnosed students.31 Although objective
measurements failed to show an improvement with the
use of stimulants, healthy individuals perceived their
performance was improved by taking the medication.
These variables all factor in to a complicated picture.
The simple and harmonious conclusion might be that
stimulants are only part of the picture when it comes
to academic success; effective study habits (regardless
of stimulant use) are the most influential determinants
of academic success in a student with ADHD.32 This
hypothesis does not lend itself to a randomized, controlled study, and more information is needed, especially
on how stimulants affect those without ADHD.
Summary
The goal of treatment is to provide ADHD-diagnosed
patients with a plan that enables success in school, work,
and social interactions. Open communication between
provider, patients, and families fosters the highest quality of care, especially when dealing with a disorder that
can be complicated and controversial. A comprehensive
assessment and determination of nature, longevity,
frequency, and severity of symptoms is the first step in
determining what treatment, if any, is warranted. The
way in which we approach prescribing psychostimulants
will determine how they are used in the future. Will
psychostimulants continue to be the first-line treatment
for ADHD? Or, will they be prescribed more liberally to
those without ADHD and become a mainstay of cosmetic psychiatry? With further research efforts and the
changing demographic of the psychostimulant user, these
answers are still forthcoming. Additionally, in July 2013
the U.S. Food and Drug Administration (FDA) approved
the Neuropsychiatric EEG-Based Assessment Aid (NEBA)
System to diagnose ADHD in children ages 617.33 The
1520 minute test analyzes the ratio of certain brain wave
frequencies that have been shown to be increased in children with ADHD compared to those without ADHD.
This may be a very promising aid, as this marks one of
the first radiographic tools to help diagnose a psychiatric
condition. This test, as part of a comprehensive evaluation, may help clinicians more accurately determine if
ADHD is the cause of a behavioral problem, which also
may lead to more accurate prescribing of psychostimulants to the correct target population.
About the Faculty

Shawen M. Ilaria, BS: Ms. Ilaria is a fourth-year medical student at the University of Florida, College of Medicine, Gainesville, FL.
Michael A. Shapiro, MD: Dr. Shapiro is an Assistant Professor in the Division of Child & Adolescent Psychiatry, Department of
Psychiatry, University of Florida, Gainesville, FL.
Mark S. Gold, MD: Dr. Gold is a Distinguished Professor, Eminent Scholar and Chairman of Psychiatry at the College of
Medicine, University of Florida, Gainesville, FL.
110
References
1. APA. Attention-Deficit/Hyperactivity Disorder. In: Diagnostic and Statistical Manual of Mental Disorders - 4th edition (DSM-IV). Washington, D. C.: American Psychiatric
Association; 1994.
2. APA. Attention-Deficit/Hyperactivity Disorder. In: Diagnostic and Statistical Manual of Mental Disorders - 4th edition text revision (DSM-IV-TR). Washington, D. C.:
American Psychiatric Association; 2000.
3.
APA. Attention-Deficit/Hyperactivity Disorder. In: (DSM-5). Arlington, VA: American Psychiatric Association; 2013:59-66.
4.
Froehlich TE, Lanphear BP, Epstein JN, Barbaresi WJ, Katusic SK, Kahn RS. Prevalence, recognition, and treatment of attention-deficit/hyperactivity disorder in a national
sample of US children. Arch Pediatr Adolesc Med. 2007;161:857-64.
5.
Dulcan MK. Dulcans Textbook of Child and Adolescent Psychiatry. Washington, D. C.: American Psychiatric Publishing, Inc.; 2010.
6.
Resnick RJ. Attention deficit hyperactivity disorder in teens and adults: they dont all outgrow it. J Clin Psychol. 2005;61:529-33.
7.
Faraone SV, Biederman J. What is the prevalence of adult ADHD? Results of a population screen of 966 adults. J Atten Disord. 2005;9:384-91.
8.
Fayyad J, De Graaf R, Kessler R, et al. Cross-national prevalence and correlates of adult attention-deficit hyperactivity disorder. Br J Psychiatry. 2007;190:402-9.
9.
Biederman J, Monuteaux MC, Mick E, et al. Young adult outcome of attention deficit hyperactivity disorder: a controlled 10-year follow-up study. Psychol Med.
2006;36:167-79.
10. Akutagava-Martins GC, Salatino-Oliveira A, Kieling CC, Rohde LA, Hutz MH. Genetics of attention-deficit/hyperactivity disorder: current findings and future directions.
Expert Rev Neurother. 2013;13:435-45.
11. Hawi Z, Matthews N, Wagner J, et al. DNA variation in the SNAP25 gene confers risk to ADHD and is associated with reduced expression in prefrontal cortex. PLoS One.
2013;8:e60274.
12. Weyandt L, Swentosky A, Gudmundsdottir BG. Neuroimaging and ADHD: fMRI, PET, DTI findings, and methodological limitations. Dev Neuropsychol. 2013;38:211-25.
13. Cocchi L, Bramati IE, Zalesky A, et al. Altered functional brain connectivity in a non-clinical sample of young adults with attention-deficit/hyperactivity disorder. J Neurosci.
2012;32:17753-61.
14. Pliszka S. Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry.
2007;46:894-921.
15. Wolraich M, Brown L, Brown RT, et al. ADHD: clinical practice guideline for the diagnosis, evaluation, and treatment of attention-deficit/hyperactivity disorder in children
and adolescents. Pediatrics. 2011;128:1007-22.
16. Brown RT, Amler RW, Freeman WS, et al. Treatment of attention-deficit/hyperactivity disorder: overview of the evidence. Pediatrics. 2005;115:e749-57.
17. Daughton JM, Kratochvil CJ. Review of ADHD pharmacotherapies: advantages, disadvantages, and clinical pearls. J Am Acad Child Adolesc Psychiatry. 2009;48:240-8.
18. Drugs for treatment of ADHD. Treat Guidel Med Lett. 2011;9:23-8; quiz 2 p following 8.
19. Pfizer. Press Release: The First Once-Daily, Extended-Release Liquid Medication for the Treatment of ADHD is Now Available in Pharmacies. In. http://www.pfizer.com/
news/press-release/press-release-detail/pfizer_announces_availability_quillivant_xr_methylphenidate_hydrochloride_cii_extended: Pfizer Pharmaceuticals; 2013.
20. Wilens TE, Adler LA, Adams J, et al. Misuse and diversion of stimulants prescribed for ADHD: a systematic review of the literature. J Am Acad Child Adolesc Psychiatry.
2008;47:21-31.
21. Sepulveda DR, Thomas LM, McCabe SE, Cranford JA, Boyd CJ, Teter CJ. Misuse of prescribed stimulant medication for ADHD and associated patterns of substance use:
preliminary analysis among college students. J Pharm Pract. 2011;24:551-60.
22. Controlled Substances by CSA Schedule Department of Justice, 2013. (Accessed July 15, 2013, at http://www.deadiversion.usdoj.gov/schedules/orangebook/e_cs_sched.
pdf.)
23. Title 21, Chapter 13, Subchapter 1, Part B, 812 - Schedules of controlled substances. Cornell University Law School - Legal Information Institute (LII), 2013. (Accessed
July 1, 2013, at http://www.law.cornell.edu/uscode/text/21/812.)
24. Swanson JM, Volkow ND. Serum and brain concentrations of methylphenidate: implications for use and abuse. Neurosci Biobehav Rev. 2003;27:615-21.
25. Kollins SH. Comparing the abuse potential of methylphenidate versus other stimulants: a review of available evidence and relevance to the ADHD patient. J Clin Psychiatry.
2003;64 Suppl 11:14-8.
26. Humphreys KL, Eng T, Lee SS. Stimulant Medication and Substance Use Outcomes: A Meta-analysis. JAMA Psychiatry. 2013;70:740-9.
27. Setlik J, Bond GR, Ho M. Adolescent prescription ADHD medication abuse is rising along with prescriptions for these medications. Pediatrics. 2009;124:875-80.
28. Wedge M. Why French Kids Dont Have ADHD. In: Suffer the Children. Online Blog: Psychology Today; 2013.
29. Voeller KK. Attention-deficit hyperactivity disorder (ADHD). J Child Neurol. 2004;19:798-814.
30. Rabiner DL, Anastopoulos AD, Costello EJ, Hoyle RH, McCabe SE, Swartzwelder HS. The misuse and diversion of prescribed ADHD medications by college students.
J Atten Disord. 2009;13:144-53.
31. Ilieva I, Boland J, Farah MJ. Objective and subjective cognitive enhancing effects of mixed amphetamine salts in healthy people. Neuropharmacology. 2013;64:496-505.
32. Advokat C, Scheithauer M. Attention-deficit hyperactivity disorder (ADHD) stimulant medications as cognitive enhancers. Front Neurosci. 2013;7:82.
33. First ADHD brain wave test approved by FDA. CBS News, 2013. (Accessed Aug 1, 2013, at http://www.cbsnews.com/8301-204_162-57593832/first-adhd-brain-wavetest-approved-by-fda/
111
L003308
29. Regarding DSM-IV Criteria for ADHD, at least how many months of symptoms of inattention and
hyperactivity-impulsivity must be present?
A. 3 months
B. 9 months
C. 6 months
D. 12 months
30. In the DSM-IV, all of the following types of ADHD are identified, except:
A. Combined Type
B. Predominantly Inattentive Type
C. Predominantly Impulsive Type
D. Predominantly Hyperactive-Impulsive Type
31. Which of the following is the only long-acting liquid formulation psychostimulant for ADHD?
A. Dexmethylphenidate
B. Methylphenidate hydrochloride
C. Lisdexamfetamine
D. Guanfacine
32. From 1998 to 2005, calls related to teenaged victims of prescription ADHD medications abuse rose
by what percentage?
A. 24%
B. 52%
C. 76%
D. 90%
113

By Shawen M. Ilaria, BS; Michael A. Shapiro, MD; and Mark S. Gold, MD
ID#: L003308

The information in this lesson will be helpful to medical students, general practitioners, pediatricians, and
family physicians who may not have an updated knowledge base on ADHD. Knowing the signs, symptoms,
and behaviors can only increase identification and treatment of this difficult and lifelong disorder.
Key Point 1: Diagnosis

The diagnosis and treatment of ADHD, particularly in adults, is difficult and at times
controversial.
ADHD is difficult to diagnose in adulthood; some children continue to have
symptoms, and some adults were never diagnosed as children.
Key Point 2: Symptomology

Symptoms of ADHD are either inattentive,
hyperactive/impulsive, or both, have onset
during childhood, and cause functional impairment.
Key Point 4: Prognosis in Adults

Adults with ADHD are more likely to get
divorced, have car accidents, have difficulty
maintaining employment, and abuse drugs
and alcohol than those without ADHD.
Key Point 5: Psychostimulant Misuse

Stimulants are controlled substances that
are effective for ADHD, but can be abused,
misused, or diverted.
Stimulants are sometimes misused as
academic performance enhancers, but
the evidence of this effect is limited.
Key Point 3: Prognosis in Children

Children and adolescents with ADHD are
more likely to have academic difficulties,
smoke cigarettes, be in car accidents, and
use drugs and alcohol than children without ADHD.
Notes
L003309

Clinical Implications for
Assessment and Treatment
Aviv Weinstein, PhD
The author declares no conflicts of interest.
Off-label use of escitalopram and bupropion is discussed in the treatment section of this lesson.
These medications are not FDA approved for treatment of the disorder indicated.
Dr. Weinstein is supported by grants from the National Institute for Psychobiology in Israel and the Israeli anti-drug authority.
Key Words: Videogame Addiction Problematic Internet Use Behavioral Addiction

Learning Objectives: Clinicians will review recent evidence on assessment, psychobiological basis, and treatment of
videogame addiction. They will interpret diagnostic information including comorbidity with other psychiatric disorders and
treatment studies. Readers will review instruments for assessing videogame addiction as well as data on the neuropsychological
and biological basis of this disorder.
Lesson Abstract: Problematic Internet addiction (PIU) or excessive Internet use is characterized by excessive or
poorly controlled preoccupations, urges, or behaviors regarding computer use and Internet access that lead to impairment or
distress. There is no consensus on the diagnosis of Internet addiction, although it has been proposed for inclusion in the next
version of the Diagnostic and Statistical Manual of Mental Disorder (DSM-V). Surveys in the United States and Europe have
indicated prevalence of between 1.5% and 8.2%, with varying diagnosis methods being used across countries. Cross-sectional
studies on samples of patients report high comorbidity of Internet addiction with psychiatric disorders, especially affective
disorders (including depression), anxiety disorders (e.g., generalized anxiety disorder, social anxiety disorder), and attentiondeficit hyperactivity disorder (ADHD). Videogame addiction particularly for Massively Multiplayer Online Role-Playing Games
(MMORPGs) has been associated with social and emotional escapism from the real self into the virtual reality. Internet and
videogame addiction was also shown to be associated with deficits in decision making, executive function, and cognitive bias to
Internet-related stimuli. There is emerging evidence that the psychobiological mechanisms underlying Internet and videogame
addiction resemble those of addiction to substances abuse. The published treatment studies for Internet and videogame
addiction are based on interventions and strategies used in the treatment of substance use disorders. Limitations include
problems in diagnosis, lack of randomization and blinding techniques, lack of adequate control, and insufficient information
about treatment procedures. Thus, it is premature to recommend any evidence-based treatment of Internet and videogame
addiction, although preliminary results of psychological and pharmacological interventions seem promising.
COMPETENCY AREAs: This lesson addresses the gap in learning in the area of knowledge, diagnosis, treatment, and
practice-based learning and improvement. Many clinicians lack understanding about how to adequately identify Internet and
videogame addiction which often goes underreported by adolescents and their family. There are few pharmacological and
cognitive-behavioral treatment studies for internet and videogame addiction. Upon the conclusion of reading this lesson, readers
will have a better understanding of internet and videogame addiction, its treatment and how to assess and manage this disorder.
117
L003309 : Internet and Videogame Addiction: Clinical Implications for Assessment and Treatment
Introduction
History of Internet and Videogame
Addiction and Its Treatment:
Problematic Internet use, or addiction, is characterized by excessive or poorly controlled preoccupations,
urges, or behaviors regarding Internet use that lead
to impairment or distress. There appear to be at least
three subtypes: excessive gaming-gambling, sexual
preoccupations (cybersex), and e-mail/text messaging.
There is considerable controversy with respect to diagnosis of Internet addiction and whether it ought to
be included as a diagnosis entity in the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition of
the American Psychiatric Association. There are three
different models proposed for Internet addiction.1 Some
researchers have considered impulse-control disorders
as part of the obsessive-compulsive disorder spectrum
model. This model is supported by brain-imaging and
pharmacological treatment studies with SSRIs (although
other treatments and brain-imaging studies may challenge it). Secondly, the DSM-V task force has decided
to create a separate category of compulsive Internet
usage disorder from the non-specified impulse-control
disorder (ICD-NOS). Thirdly, some psychiatrists have
argued that Internet addiction should be included in
the behavioral addiction spectrum since it shows the
features of excessive use despite adverse consequences,
withdrawal phenomena, and tolerance that characterize
many substance use disorders; however, there are little
data to bear out these claims. It is not clear whether
Internet addiction usually represents a manifestation
of an underlying disorder or is truly a discrete disease
entity. The frequent appearance of Internet addiction
in the context of numerous comorbid conditions raises
complex questions of causality. The growing research
suggests that some individuals with Internet addiction
are at significant risk and merit professional care and
treatment. Carefully controlled studies are required to
settle these controversies. This lesson will concentrate
on the assessment, cognitive and psychobiological basis,
and treatment of Internet and videogame addiction.
118
Diagnosis and Assessment

Criteria
The diagnosis of Internet addiction and dependence
remains problematic. It does not appear in any official
diagnostic system, including DSM-IV, and there are no
widely accepted diagnostic criteria. Four components
have been suggested as essential to the diagnosis:2 (1)
excessive Internet use, often associated with a loss of
sense of time or a neglect of basic drives (i.e., lack
of motivation to do other things like schoolwork,
socialize with people outside the web); (2) withdrawal, including feelings of anger, tension, and/
or depression when the computer is inaccessible;
(3) tolerance, including the excessive need for better
equipment, more software, or more hours of use;
and (4) adverse consequences, including arguments,
lying, poor school or vocational achievement, social
isolation, and fatigue. A recent systematic analysis of
the various diagnostic instruments found that previous
studies utilized inconsistent criteria to define Internet
addicts, applied recruiting methods that may cause
serious sampling bias, and examined data using primarily exploratory rather than confirmatory data analysis
techniques to investigate the degree of association rather
than causal relationships among variables.3 Thus, prevalence data on pathological Internet use are limited by
methodological difficulties concerning the diagnosis and
the heterogeneity of diagnostic instruments. This makes
it difficult to compare prevalence rates across countries.
The questionnaires for diagnosis of Internet
addiction have used items from substance dependence questionnaires, as well as new items related
to Internet addiction. The most commonly used
questionnaire is Youngs Internet Addiction Scale
(IAD) (cut off point score 70 and above), which has
been validated in the United Kingdom (UK)4 and the
United States (US)5,6 and other countries. The Internet
Addiction Scale (IAS), a self-report instrument based on
the seven substance dependence criteria of the Diagnostic and Statistical Manual of Mental Disorders7 and
two additional criteria recommended by Griffiths was
validated in Turkey.8 The Chen Internet Addiction Scale
(CIAS) has been widely used in Taiwan.9 The Questionnaire of Experiences Related to Internet has been validated
in Spain.10 The Compulsive Internet Use Scale (CIUS)
is used in Holland11 and France;12 and the Problematic
Internet Use Questionnaire (PIUQ) in Hungary.13 The

Internet Addiction Test (IAT) and the Internet-Related
Problem Scale (IRPS) were correlated positively in a UK
study.14 The assessment methods have been reviewed,
and it was concluded that these instruments are based
on different theoretical underpinnings and do not agree
on the underlying dimensions that make up problematic
Internet use.15 Another criticism is that some items do
not relate to addiction. There are also general concerns
related to using self-reports, getting dishonest answers,
participants not understanding various questions, or misinterpretation of various test items. Additionally, there
is also a problem of selection bias with the participant
pool obtained from web sites or undergraduate courses
and no adequate control group. The use of a web page
may influence how people responded and the number of
valid responses obtained. A person may show addictive
behaviors toward one application but not others.
Table 1: Q
uestionnaire Assessing Internet
and Videogame Addiction
Questionnaire
Youngs Internet
Addiction Scale (IAD)
Country
US
Validation study
Widyanto et al.
(2004)4
Bernardi and Pallanti
(2009)5
Jelenchick et al.
(2012)6
The Internet Addiction

Scale (IAS)
UK
Canan et al. (2012)
The Chen Internet

Addiction Scale (CIAS)
Taiwan
Yen et al. (2009)9
The Questionnaire of
Experiences Related
to Internet
Spain
Beranuy et al.
(2009)10
Holland
The Compulsive Internet
and
Use Scale (CIUS)
France
Meerkerk et al.
(2009)11
Khazaal et al.
(2012)12
The Problematic
Internet Use
Questionnaire (PIUQ)
Demetrovics et al.
(2008)13
Hungary
Prevalence Rates
A review on international prevalence rates for Internet
addiction using questionnaires such as the IAT has
shown a range from 1.5 % to 8.2 %.16 In the US, an
online survey found that 6% met the criteria for Internet addiction.17 A recent telephone survey of the general
US population reported an estimate of 0.30.7%.18 A
study of Southern US university students found that
about 25% met the criteria for Internet dependence.19
While a more recent study found that 4% of students
had a problematic or addicted range on the IAT.20 A
quality review evaluated 18 studies of US college student
PIU and found prevalence rates ranging from 0% to
26.3%.21 The wide range of conceptual approaches may
have impacted the reported prevalence rates. A major
cross-sectional survey in Europe investigated the prevalence of pathological Internet use (PIU) and maladaptive
Internet use (MIU) among adolescents in 11 European
countries in relation to demographic, social factors, and
Internet accessibility.22 A total of 11,956 adolescents
were recruited from randomly selected schools within
the 11 study sites. Measurements used the Young Diagnostic Questionnaire for Internet Addiction (IAD). The
overall prevalence of PIU was 4.4%; it was higher among
males than females and differed between countries.
Psychiatric Comorbidity
Cross-sectional studies report high comorbidity of
Internet addiction with psychiatric disorders, such
as affective disorders, anxiety disorders (including
generalized anxiety disorder, social anxiety disorder),
and attention-deficit hyperactivity disorder (ADHD).
German Internet-dependent students had a 78% rate
of comorbid depressive mood disorder and higher
rates of impulsivity and depression23 and anxiety
disorder.24 The association between Internet use and
depression was also found in the UK.25
In the US, adolescents presented comorbidity with
hypomania, dysthymia, obsessive-compulsive personality disorder, borderline personality disorder, and avoidant personality disorder.5 A combination of alexithymia,
dissociative experiences, low self-esteem, and impulse
dysregulation were suggested as risk factors for Internet
addiction in a sample of Italian adolescents.26 An association between problematic Internet use and hyperactivity,
119
conduct problems, and comprehensive psychosocial

maladjustment was found in Greek adolescents.27 In the
Far East, Internet addiction was associated with depressive symptoms in South Korean adolescents,28 along with
high levels of depression and suicidal ideation.29,30 Adolescents with Internet addiction had higher ADHD
symptoms, depression, social phobia, and hostility
in Taiwan.31 Internet addiction and impulsivity were
associated with adult ADHD, and the association
between attention deficit and Internet addiction was
more significant among female Taiwanese college
students.32 Internet addiction was also associated with
harmful use of alcohol among Taiwanese students.33
Furthermore, online gamers in Taiwan tended to have
more severe depressive, social phobic, and Internet
addiction symptoms.34 Female online gamers had fewer
weekly online gaming hours and shorter previous online
gaming history, but they tended to have more severe
somatic, pain, and social phobic symptoms.
A review on studies correlating problematic Internet use and mental disorders found that the majority
of research was conducted in Asia and comprised of
cross-sectional designs. Only one prospective study was
identified.35 Of the 20 studies that met the inclusion
and exclusion criteria of the review, 75% reported significant correlations of PIU with depression, 57% with
anxiety, 100% with symptoms of ADHD, 60% with
obsessive-compulsive symptoms, and 66% with hostility/aggression. Limitations included heterogeneity in
the definition and diagnosis of PIU. More studies with
prospective designs in Western countries are critically
needed.
120
Social, Physical, and

Emotional Factors Associated
with Videogame Addiction:
Creating a Virtual Ideal Self
and Escapism on the Internet
There is growing interest in players of Massively Multiplayer Online Role-Playing Games (MMORPGs). A
sample of 448 participating adult French gamers who
were mainly young adult university graduates living
alone in urban areas showed high rates of Internet addiction and Internet tolerance and more social, financial,
marital, family and/or professional difficulties since they
started online gaming.36 Furthermore, these gamers
self-reported higher rates of irritability, daytime sleepiness, sleep deprivation due to play, low mood, and emotional changes since online gaming onset. Five distinct
motivations to play were identified in gamers in Switzerland: achievement, socializing, immersion, relaxing,
and escaping.37 Addictive MMORPG use was predicted
by achievement, escapism and socializing motives.
Gender was also a significant predictor of problematic
involvement in MMORPGs, and addictive MMORPG
use positively correlated with the weekly time devoted
to playing MMORPGs. For certain individuals who are
characterized by a tendency to act rashly in emotional
contexts and motivated toward immersion in a virtual
world, MMORPGs can become problematic and engender tangible negative consequences in daily life.38 Finally,
among MMORPG players in Singapore, depression
mediated the relationship between actual-ideal self-discrepancy and escapism. It is plausible that pathological
gaming behaviors may be over-regulated coping strategies allowing users approach the ideal self and avoid the
actual self.39
Table 2: Social, Emotional, Cognitive and

Psychobiological Characteristics of
Internet and Videogame Addiction
Characteristic
Country
Study
Social and
emotional escapism
France,
Switzerland,
and
Singapore
Achab et al.
(2011)36
Zanetta et al.
(2011)37
Billieux et al.
(2011)38
Lin et al. (2011)39
Deficit in decision
making
China and
Taiwan
Sun et al. (2009)40

Ko et al. (2010)41
Impaired executive
control
China
Dong et al. (2011)42
Cognitive bias to
cues
China
Zhou et al. (2012)43
Abnormal activity
at the resting state
South Korea
and China
Park et al. (2010)61

Liu et al. (2010)62
Liu et al. (2010)63
Abnormal gray
matter density
Europe,
China, and
South Korea
Kuhn et al. (2011)64

Zhou et al. (2011)65
Han et al. (2012)66
Yuan et al. (2011)68
Abnormal white
matter density
China
Lin et al. (2012)67

Yuan et al. (2011)68
Activation of cueinduced brain

circuits of craving
US, Taiwan,
and
South Korea
Hoeft et al. (2008)69

Ko et al. (2009)70
Han et al. (2010)71
Ko et al. (2011)72
Ko et al. (2013)73
Reduced dopamine
activity
South Korea
Kim et al. (2011)74

Hou et al. (2012)75
Videogameinduced dopamine
release
UK and
Israel
Koepp et al.
(1988)76
Weinstein (2010)77
Cognitive Factors Associated

with Problematic Internet and
Videogame Use
Deficits in Decision-making:
Deficits in decision-making among Internet addicted
individuals demonstrate that they may have difficulty suppressing their excessive online behaviors in
real life. A study using the Iowa Gambling Task found
that Internet addicted individuals have deficits in the
decision-making function; this manifests as a strategy
learning lag rather than an inability to learn from task
contingencies. They showed better performance on a
go/no-go task, suggesting some dissociation between
mechanisms of decision making and those of pre-potent response inhibition.40 A recent study investigated
the neurocognitive correlates of Internet addiction and
described the characteristics of decision making (IOWA
gambling task), potential to take risks (BART), and
personality of college students with Internet addiction.41
Internet-addicted students on the gambling task showed
better decision making and performance on the BART
indicating that they were not more likely to engage in
risk-taking behaviors. In the Iowa test, their higher performance on the Iowa gambling test differentiated the
Internet addiction group from the substance use and
pathologic gambling groups, which have been shown to
be deficient in decision making.
Executive Control Ability:

Executive control ability of male students with Internet
Addiction Disorder (IAD) was investigated in China by
recording event-related brain potentials (ERP) during
a color-word Stroop task in 17 IAD and 17 male control university students.42 IAD students showed longer
reaction time and more response errors in incongruent
conditions than the control group. Participants with
IAD showed reduced medial frontal negativity (MFN)
deflection in incongruent conditions than the control
group. Both of the behavioral performance and ERP
results indicated that people with IAD showed impaired
executive control ability unlike the control group.
121
Cognitive Bias and Executive Function:
Psychobiological Mechanisms
Cognitive bias and executive function involving mental flexibility and response inhibition in IAD were also
investigated using the cue-related the go/no-go switching task.43 The Internet game addiction (IGA) group
showed cognitive biases towards information related to
Internet gaming, and the length of the addiction (number of years) was correlated positively with the severity
of the cognitive bias. These biases and poor executive
functioning skills (lower mental flexibility and response
inhibition) might be responsible, in part, for Internet
game addiction.
Kuss and Griffiths61 discuss consistent findings demonstrating the resemblance between the neural mechanisms
underlying drug and alcohol abuse and videogame
addictions. Studies of the resting state61 in Positron
Emission Tomography (PET), and in functional Magnetic Resonance (fMRI)62,63 demonstrated an association of excessive Internet game use with abnormal
neurobiological mechanisms in the orbitofrontal
cortex, striatum, and sensory regions, which are
implicated in impulse control, reward processing,
and somatic representation of previous experiences.
Structural studies with fMRI showed changes in
gray matter volume in frequent videogame players.
The brains gray matter is a major component of the
central nervous system that is made up of neuronal cell
bodies, and it is involved in motor control, perception,
memory, emotions, and speech. In Internet-addicted
individuals, long-term changes were found in the striatum64 in the cingulate cortex, insula, and lingual gyrus,65
the thalamus, inferior temporal gyri, right middle occipital gyrus, and left inferior occipital gyrus.66
Furthermore, changes in white matter density
were reported in videogame addicted individuals.
The brains white matter is another component of the
central nervous system that consists mostly of glial cells
and myelinated axons, which transmit signals from the
cerebellum to other brain centers. White matter changes
were shown in Internet-addicted adolescents throughout
the brain, including the orbitofrontal cortex, corpus
callosum, cingulum, inferior fronto-occipital fasciculus,
corona radiation, and internal and external capsules.67
These findings suggest widespread reductions of major
white matter pathways and these abnormal white matter structures were also linked to anxiety and Internet
addiction.
Finally, a single study investigated the effects of
Internet addiction on the microstructural integrity of
major neuronal fiber pathways.68 An optimized voxel-based morphometry (VBM) technique (used to measure white matter fractional anisotropy [FA] changes with
the diffusion tensor imaging [DTI] method) linked these
brain structural measures to the duration of Internet
Physical and Mental

Health Hazards
For more than 20 years, the medical profession has
voiced a number of concerns about videogame playing.
Back in the early 1980s, rheumatologists described cases
of Pac-Man Elbow and Space Invaders Revenge in
which players suffered skin, joint, and muscle problems
from repeated button hitting and joystick pushing
on the game machines.44 Early research by Loftus and
Loftus indicated that two-thirds of (arcade) videogame
players examined complained of blisters, calluses, sore
tendons and numbness of fingers, hands, and elbows as
a direct result of their playing. There have been a whole
host of case studies in the medical literature reporting
some of the adverse effects of playing videogames.45,46
These have included auditory hallucinations,47 enuresis,48 encoprisis49 wrist pain50 neck and elbow pain51
tenosynovitis (also called nintendinitis),52-55 hand-arm
vibration syndrome,56 repetitive strain injuriesc,57 and
peripheral neuropathy.58 Recently, a study described 10
patients who experienced epileptic seizures while playing
the newest genre of electronic MMORPGs.59 Patients
were predominantly young male adults, and most of the
events were generalized tonic-clonic seizures, myoclonic
seizures, and absences. The author suggested that while
the prevalence of MMORPG-induced seizures remains
unknown, there should be an awareness of this special
form of reflex seizures in order to provide an appropriate
health warning to MMORPG players.
122
addiction. Decreased gray matter volume in the bilateral dorsolateral prefrontal cortex, the supplementary
motor area, the orbitofrontal cortex, the cerebellum and
the anterior cingulate were found in Internet addicted
subjects. Using diffusion tensor imaging (DTI) analysis
enhanced FA values were found in the internal capsule
and reduced FA value in the white matter within the
parahippocampal gyrus.
Functional brain imaging studies showed that exposure to gaming cues activated regions that were previously shown to be associated with drug addiction,69,70-73
including the orbitofrontal, nucleus accumbens, anterior
cingulate, medial frontal, and dorsolateral prefrontal
cortices and the caudate nucleus.
Furthermore, similar to drug-dependent individuals, reduced levels of dopamine D2 receptor availability
in the striatum were shown in addicted subjects in a
brain imaging study using with the radiolabeled ligand
[11C] raclopride in Positron Emission Tomography (PET).
The reduced levels of dopamine D2 receptor availability contributes to the hypothesis of deficient dopamine
reward mechanisms in Internet addiction.74 Dopamine
deficiency at the pre-synaptic level measured striatal
dopamine transporter (DAT) occupancy by (99m)
Tc-TRODAT-1 in single photon emission computed
tomography (SPECT) in individuals with IAD. DAT
occupancy of the striatum was significantly decreased
and the volume, weight and whole brain were greatly
reduced in individuals with IAD compared with control
subjects.75 Moreover, these results suggest that IAD
is associated with dysfunctions in the dopaminergic
brain systems and they also support the claim that
IAD may share similar neurobiological abnormalities
with other addictive disorders. Finally, previous studies showed significant dopamine-release in the ventral
striatum following videogame play in healthy control
participants, which may explain why these games are
highly addictive.76,77
Treatment
Psychological Treatment:
Cognitive Behavior Therapy
Treatment for Internet addiction is based on interventions and strategies used in the treatment of substance
use disorders. Psychosocial approaches are the mainstay of treatment, with very little use of pharmacological treatment. Due to the lack of methodologically adequate research, it is currently impossible
to recommend any evidence-based treatment of
Internet addiction.16 There is preliminary evidence for
success of an initiated abstinence program in 1215
year old pupils in Austria, Germany, and Italy78 and
in a counseling program in Hong Kong.79 Preliminary
results from a study of 114 patients receiving cognitive
behavior therapy indicated that most clients were able
to manage their presenting complaints by the eighth
session, and symptom management was sustained at
six-month follow-up.80 Cognitive behavioral approaches
and psychosocial support may be helpful. Marital and
family therapy may help in selected cases, and online
self-help books and CD/DVDs are available. Finally, a
self-imposed ban on computer use and Internet access
may be necessary in some cases.18
A treatment study group using cognitive behavioral
therapy (CBT) for Internet addiction in adolescents
has been reported.81 A total of 56 patients, aged 1217
years, who met Beards diagnostic criteria for Internet
addiction, were divided randomly into an active treatment group and a clinical control group. Participants
in the active treatment group were treated with an
eight-session multimodal school-based group CBT,
while participants in the clinical control group received
no intervention. Internet use, time management,
emotional, cognitive, and behavioral measures were
assessed for both groups at baseline immediately after
the intervention and at six-month follow-up by investigators blind to the participants group status. Results
showed that Internet use decreased in both groups while
only the multimodal school-based group CBT showed
improved time management skills and better emotional,
cognitive, and behavioral symptoms. The authors
123
suggested that multimodal school-based group CBT is

effective for adolescents with Internet addiction, particularly in improving emotional state, regulation ability,
and behavioral and self-management style.
Pharmacological Treatment:
Given that there is comorbidity between Internet
addiction and other psychiatric disorders such as obsessive-compulsive disorder (OCD) and ADHD, several
studies have used pharmacological agents designed to
address the common mechanism. Others have identified
the comorbidity with ADHD as the rationale for using
methylphenidate in children with Internet video game
addiction together with ADHD.82 A pharmacological open-label treatment study using extended release
methylphenidate (mean dose 30.5 +/-13.3 mg/d, range
18-54 mg/d) in 62 Korean children with Internet video
game addiction and comorbid ADHD found that after
eight weeks of treatment, measures of Internet use and
Internet use duration were significantly reduced. This
improvement was positively correlated with improvement in measures of attention. These findings led the
investigators to suggest that Internet video game playing
might be a form of self-medication for children with
ADHD. Another study identified the comorbidity of
impulsive-compulsive Internet use with OCD to examine whether SSRIs such as escitalopram (Lexapro) can be
useful for treatment of Internet addiction.83 A pharmacological open-label treatment study using escitalopram
(dose 10mg/day) with impulsive-compulsive Internet
users showed significant decrease in the number of hours
spent on the Internet during the first phase of treatment
(weeks 110) but not later.
Relatively few studies have investigated the effects of
pharmacological treatment on videogame cue reactivity.
It was investigated whether bupropion (Wellbutrin), a
dopamine and norepinephrine inhibitor medication
used for treatment of nicotine and substance dependence, may be useful for treatment of Internet videogame addiction in patients with Internet video game
addiction (IAG).84 Eleven subjects who met criteria for
IAG playing StarCraft and eight healthy comparison
124
subjects who had experienced playing StarCraft underwent six weeks of bupropion sustained release (SR)
treatment and measurement of Internet game cue-induced brain activity using fMRI. Internet videogame
addiction subjects showed higher brain activation in
left occipital lobe cuneus, left dorsolateral prefrontal
cortex, and left parahippocampal gyrus in response to
game cues than healthy control subjects. After a sixweek period of bupropion SR, craving for Internet video
game play, total game play time, and cue-induced brain
activity in dorsolateral prefrontal cortex were decreased
in the Internet videogame addiction players. It was suggested that bupropion SR may change craving and brain
activity in ways that are similar to those observed in
individuals with substance abuse or dependence. These
results are similar to the attenuation that occurs in nicotine-dependent users.85
A following study86 has evaluated the effects of
bupropion treatment on the severity of excessive online
videogame play as well as depressive symptoms. Fifty
male individuals with comorbid EOP and MDD were
randomly assigned to bupropion and education for Internet use (EDU) or placebo and EDU groups. The current
study consisted in a 12-week prospective, randomized,
double-blind clinical trial, including an eight-week
active treatment phase and a four-week post treatment
follow-up period. Results showed that during the active
treatment period, Young Internet Addiction Scale (YIAS)
scores and the mean time of online game playing in
the bupropion group were greatly reduced compared
with those of the placebo group. The Beck Depression
Inventory (BDI) scores in the bupropion group were
also greatly reduced compared with those of the placebo
group. During the four-week post-treatment follow-up
period, bupropion-associated reductions in online game
play persisted, while depressive symptoms recurred. The
authors suggested that bupropion may improve depressive mood and reduce the severity of excessive online
videogame play in patients with comorbid major depressive disorder and online game addiction. (For review of
existing pharmacological treatment see Camardese, De
Risio, Di Nicola, Pizi, & Janiri, 2012.87)
Table 3: P
sychological and Pharmacological
Treatment Studies of Internet and
Videogame Addiction
Treatment Type
Country
Cognitive behavior
treatment
Austria,
Germany,
Italy, US,
Hong-Kong,
and China
Kalke and Raschke

(2004).78
Shek et al. (2009)80
Young (2007)79
Du et al. (2010)81
South Korea
and US
Han et al. (2009),82

methylphenidate
DellOsso et al.
(2007).83 an
open-label trial of
escitalopram
Han et al. (2010),84
bupropion
sustained release
Han and Renshaw
(2012),86 bupropion
Pharmacological
treatment
Study
Evaluation of Treatment
An evaluation of treatment of Internet addiction according to the 2010 Consolidating Standards of Reporting
Trials (CONSORT) statement was reported.88 Several
key limitations were highlighted, including: (a) inconsistencies in the definition and diagnosis of Internet
addiction; (b) a lack of randomization and blinding
techniques; (c) a lack of adequate controls or other comparison groups; and (d) insufficient information concerning recruitment dates, sample characteristics, and
treatment effect sizes. It was concluded that improvements in future studies design and reporting would be
of significant benefit to both researchers and clinicians
and to the overall positioning of Internet addiction in
the behavioral addiction field.
Finally, a meta-analysis of pharmacological and
psychological treatment of Internet addiction89 was
conducted based on 16 studies, covered a total of 670
participants, and used a random effects model. Effect size
estimates suggest that psychological and pharmacological
interventions were highly effective for improving Internet addiction, time spent online, depression, and anxiety
in pre- to post-treatment in the overall sample. Studies
including individual treatments, a higher number of
female participants, older patients, or a North-American
sample had a larger effect sizes for some outcome variables. Most effect sizes were high, robust, unrelated to
study quality or design, and maintained over follow-up.
Conclusions
Internet addiction, i.e., excessive use of the Internet with
resulting adverse consequences, does not appear in any
official diagnostic system, including DSM-IV. Conceptually, the diagnosis is a compulsive-impulsive spectrum
disorder that involves online and/or offline computer
usage. At least three subtypes have been identified:
excessive gaming, sexual preoccupations, and e-mail/
text messaging. All of the variants share the following
four components: (1) excessive use, often associated
with a loss of sense of time or a neglect of basic drives;
(2) withdrawal, including feelings of anger, tension,
and/or depression when the computer is inaccessible;
(3) tolerance, including the need for better computer
equipment, more software, or more hours of use; and (4)
adverse consequences, including arguments, lying, poor
achievement, social isolation, and fatigue. Little data are
available to resolve this question, and the pathophysiological mechanisms underlying Internet and videogame
addiction are still under investigation. There is relatively little evidence for the efficacy of psychological
and pharmacological treatment of Internet addiction.
The few published treatment studies for Internet addiction are based on interventions and strategies used in
the treatment of substance use disorders. Limitations
include problems in diagnosis, lack of randomization
and blinding techniques, lack of adequate control, and
insufficient information on treatment procedures. Thus,
it is premature to recommend any evidence-based treatment of Internet addiction, although preliminary results
of psychological and pharmacological interventions
seem promising.
About the Faculty

Aviv Weinstein, PhD: Dr. Weinstein is a Senior Lecturer, Department of Behavioral Science, University of Ariel, Ariel, Israel.
125
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129
L003309
33. According to the lesson, all of the following statements are believed to be true regarding Internet and
videogame addiction, except:
A. Excessive Internet use is often associated with a sense of time loss or neglect of basic drives.
B. Excessive Internet use is often associated with withdrawal, including feelings of anger, tension, and/or
depression when the computer is inaccessible.
C. Excessive Internet use is often associated with tolerance, including the need for better computer equipment,
more software, or more hours of use.
D. Excessive Internet use is often associated with adverse consequences, including binge eating, compulsive
shopping, violence, and hallucinations.
34. Which one of the following instruments is most commonly used worldwide to assess Internet and
videogame addiction?
A. Youngs Internet Addiction Scale (IAD)
B. The Chen Internet Addiction Scale (CIAS)
C. The Problematic Internet Use Questionnaire (PIUQ)
D. The Questionnaire of Experiences Related to Internet (QERI)
35. Which of the following psychiatric disorders has been frequently described as related to Internet
addiction?
A. Depression
B. Anxiety
C. Attention-deficit and attention-deficit hyperactivity disorder
D. All of the above
36. Internet addiction has been postulated to be associated with all of the following, except:
A. Abnormal white matter density
B. Increased dopamine transporter occupancy
C. Deficit in decision making
D. Good response to pharmacological and cognitive behavioral treatments
131

By Aviv Weinstein, PhD
ID#: L003309

This lesson reviews the evidence on assessment, psychobiological basis, and treatment of videogame
addiction. Readers will review instruments for assessing videogame addiction as well as data on the
neuropsychological and biological basis of this disorder.
Step 1: Diagnosis
Diagnose the disorder using valid instruments such as: Youngs Internet Addiction
Scale (IAD), the Internet Addiction Scale
(IAS), the Chen Internet Addiction Scale
(CIAS), the Problematic Internet Use Questionnaire (PIUQ), and the Questionnaire of
Experiences Related to Internet (QERI).
Step 2: Assessment
Assess psychiatric comorbidity with disorders (e.g., ADHD, ADD, Depression, Anxiety) as well as physical and cognitive effects
of the disorder.
Step 3: Identification
Identify social, physical and emotional circumstances
Step 4: Psychological Treatment

Discuss psychological treatment such as
CBT.
Step 5: Pharmacological Treatment

Consider pharmacological treatments.
Step 6: Pharmacological Treatment

Integrate the clinical picture-assessment,
phenomenology and treatment.
Notes
L003310
Community Resilience to Disasters

for Mental Health Professionals
Rose L. Pfefferbaum, PhD, MPH; and Betty Pfefferbaum, MD, JD
The authors declare that there are no competing interests.
Acknowledgments
This work was supported in part by the Terrorism and Disaster Center (TDC), located at the University of Missouri, Columbia, Missouri,
and at the University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma. TDC is a partner in the National Child Traumatic
Stress Network (NCTSN), which is funded by the Substance Abuse and Mental Health Services Administration (SAMHSA),
U.S. Department of Health and Human Services (DHHS). The findings, conclusions, opinions, and contents of this lesson are those
of the authors and do not represent the official position of NCTSN, SAMHSA, or DHHS.
Key Words: Community Community Resilience Disaster Mental Health Disasters

learning objectives: Upon completion of this lesson, readers will be able to: (1) define and describe community,
disasters, and community resilience; (2) discuss community resilience attributes, properties, adaptive capacities, and features
in the context of disasters; and (3) describe activities especially appropriate for mental health professionals for increasing
community resilience to disasters.
Abstract: In a world in which disasters occur much too frequently and threats are ongoing and widespread, attention is
now focused on building disaster-resilient communities. Community resilience has become a vision and a strategy for disaster
management, which includes disaster prevention and mitigation, preparedness, response, and recovery. This lesson introduces
community resilience to disasters, distinguishes community resilience from personal resilience, and explains the role of human
agency in creating the potential for community transformation. Aspects of community resilience (the attributes, properties,
and adaptive capacities that help define and characterize it) are discussed along with the features of resilient communities.
Barriers to, and general strategies for, building community resilience are summarized. The authors suggest three broad
recommendations, which are especially appropriate for mental health professionals: (1) advocate mental health as integral to
a holistic wellness approach to disaster management, (2) integrate disaster preparedness and community resilience into mental
health practice, and (3) participate in local disaster management efforts.
competency Areas: This lesson addresses a gap in learning among clinicians regarding disease prevention, wellness,
promotion of healthy lifestyles, and population health related to disasters. Many clinicians lack knowledge of disasters and the
importance of building community resilience to disasters. After studying this lesson, readers will have a better understanding of
community resilience in the context of disasters and will be aware of steps they can take to improve community resilience.
135
L003310 : Community Resilience to Disasters for Mental Health Professionals
Introduction
Disaster
Recent disasters and widespread threats have focused

attention on the importance of building disaster-resilient communities. Community resilience has become a
vision and a strategy for disaster management. After this
lesson sets the stage for understanding community resilience by providing definitions, the lesson distinguishes
community resilience from personal resilience and
elaborates on the characteristics and essential elements
of community resilience before presenting suggestions
that can assist mental health specialists in fostering community resilience to disasters as part of their professional
roles. Learning objectives address: (1) definitions and
descriptions of community, disasters, and community
resilience; (2) attributes, properties, adaptive capacities,
and features associated with community resilience; and
(3) activities especially appropriate for mental health
professionals for increasing community resilience to
disasters.
Disasters are extreme events resulting from endogenous

or exogenous forces of natural or deliberate or accidental
human origin that overwhelm the resources of a community or region. Disasters include earthquakes, floods,
and hurricanes; airplane crashes, industrial accidents,
and major power outages; terrorist attacks; epidemics;
and other mass casualty events. Often sudden and unexpected, disasters are experienced collectively and individually. They cause injury and death, create distress and
emotional problems, destroy resources, induce chaos
and confusion, interrupt routines, disrupt commerce
and government, and undermine the very substance and
functioning of communities.
One type of disaster is terrorism, which involves
the illegal or threatened use of force to coerce societies or governments by inducing fear and mistrust
in their populations in order to disable political and
social structures. Usually motivated by ideology and/
or politics, terrorism is primarily a psychological assault
that erodes our sense of safety and sense of security, two
of the most basic human needs.6p24 Terrorism, thus, is
of particular importance to mental health professionals.
Terrorists target the community in its broadest sense,
not just the geographic area or even the residents themselves, but that which connects and serves community
members: their culture, values, and mores; their sense of
relatedness and belonging; and their public and private
systems for addressing problems and providing goods
and services. Although only those most directly affected
by an incident or those who have close relationships
with victims and survivors are likely to experience true
psychiatric morbidity, the psychological effects of terrorism on the population at largeincluding emotional,
behavioral, and cognitive changes as well as psychiatric
disordersare a primary concern.6 Personal reactions
include mistrust, anger, a sense of vulnerability, feelings
of isolation, a sense of lost control over ones environment, and a fractured worldview.7,8
Definitions:
For clinicians to understand what community resilience
is and the role of mental health professionals in advancing it, several terms must be defined. In particular, community, disaster, and resilience are defined and described
here.
Community
The concept of community has been widely discussed
in the health and social science literatures. Traditionally,
a community has been viewed as people, organizations,
structures, and systems in close geographic proximity
and with physical, though often imprecise, boundaries.
Communities involve relatedness, relationships, interactions, and a sense of belonging among individuals and
groups that, while potentially highly diverse, share some
aspects of circumstance, history, culture, values, norms,
interests, laws, and risk.1-5 More recent definitions
extend the concept of community beyond geography to
include, for example, virtual communities (e.g., online
communities) as well as entities linked by common
beliefs, interest, or purpose (e.g., faith-based or professional communities).
136
Resilience
Mental health professionals generally are aware of the
meaning and implications of personal resilience. The
term resilience may be applied to individuals as well as
materials, networks, ecosystems, families, organizations,
and communities, any of which is potentially relevant in
relation to disasters. Resilience is defined differently in

the lexicon of various disciplines (e.g., computer science,
ecology, economics, engineering, geography, health,
physical science, psychology, sociology) depending on
the context and purpose. For this lesson, the term
resilience is used to describe the process of successfully adapting to, and recovering from, adversity.
Although some definitions characterize resilience as
an attribute (e.g., ability, capacity) or an outcome, the
process definition used here distinguishes resilience from
the attributes that characterize a resilient entity and from
the outcome of adaptation and recovery.
Resilience emerges in response to adversity, rather
than being the absence of adversity. Resilience permits
successful progress in spite of, in the midst of, and in
response to adversity.9 An entity may be resilient regarding some adversities and not others, and it may respond
differently to a given stressor at various times and differently to various stressors.
Understanding
Community Resilience
Understanding community resilience requires appreciating the distinction between personal and community
resilience, which is often missed. The differences, along
with the role of human agency in community resilience
and the potential for growth, are summarized below.
Characteristics and essential elements of community
resilience have been referred to as attributes, properties,
and adaptive capacities by various authorities seeking
to identify constituent components and to characterize
community resilience. In addition to community resilience attributes, properties, and adaptive capacities,
features of resilient communities are described below.
Community Resilience as
Distinguished from Personal Resilience:
It is a mistake to assume that community resilience is
simply a collection of personally resilient individuals.
Community resilience derives from collective activity
in which community members are resilient together,
not merely in similar ways.10p43 Rather than an aggregate of individuals acting independently on their
own behalf, community resilience involves interrelationships and joint efforts that foster response and
recovery for the whole. These relationships and efforts

are supported in resilient communities by physical and
social conditions, structures, and systems through which
resilience emerges in reaction to threat and adversity.10-12
Systems aiding in creating resilient communities include
health, mental health, and public health infrastructures
that identify, study, prevent, address, and resolve threats
and potential threats to the health of individuals and
communities.
Resilient communities address the needs of their
members by supporting personal resilience. Nonetheless, much as the personal resilience of community members does not ensure that a community will
be resilient, community resilience does not ensure
that individual members will be personally resilient.
The conditions, structures, and systems that contribute
to community resilience can strengthen the personal
resilience of some, perhaps many, community members
by attending to functional and behavioral problems at
the individual level.11 Some members of resilient communities may not adapt well to various adversities. This
is particularly true in the case of disasters, which, by
their nature, tax community resources. Thus, although
a community may recover successfully from a disaster,
some individual members may not.
Human Agency and

the Potential for Growth:
The process of adaptation and change that characterizes community resilience is grounded in human
agency, the capacity for people to make choices and
take deliberate, meaningful action. Effective communication helps community members to interpret their
environment and act together to remedy the effects of
a disaster. Community resilience requires proactive and
reactive efforts that may create the potential to grow
from a crisis.10-12 Transformation of the environment can
be initiated by individual and collective decisions and
activities to mitigate future adversities.
Community Resilience Attributes:

The literature on community competence and capacity
suggests seven factors that contribute to healthy communities.2,13-17 These factors have been refined through key
informant interviews and community surveys to address
context, culminating in eight attributes of community
137
resilience: (1) Connectedness, Commitment, and

Shared Values; (2) Participation; (3) Support and Nurturance; (4) Structure, Roles, and Responsibilities; (5)
Resources; (6) Critical Reflection and Skill Building; (7)

Communication; and (8) Disaster Management.12 These
attributes are described below and displayed in Table 1.
Table 1: Community Resilience Attributes, Properties, Adaptive Capacities, and Features

Attributes12
Properties18
Adaptive Capacities19
Features22
Connectedness, Commitment, and

Shared Values
Robustness
Economic Development
Community engagement
Participation
Redundancy
Social Capital
Partnerships for emergency

management
Support and Nurturance
Resourcefulness Information and

Communication
Structure, Roles, and Responsibilities Rapidity
Community Competence
Sustained local leadership
Education regarding risks
Resources
Optimal community health
Critical Reflection and Skill Building
Integration of disaster preparedness

and wellness activities
Communication
Rapid restoration post disaster
Disaster Management
Individual preparedness
Attention to vulnerable populations
Financial resilience of families and
businesses
Efficient use of resources for
recovery
Connectedness, Commitment,
and Shared Values
Relatedness and connection to a place and others with
shared history, laws, interests, and values help to form
the foundation of community. Relationships of mutual
concern and benefit and the perception that ones personal well-being is improved by membership in the
community enhance the sense of belonging and commitment to community goals and foster cooperation and
consensus building. A communitys ability to address the
138
many needs that arise during and after disasters may

be improved by equitable treatment and historical and
ongoing support for diverse members.12
Participation
A sense of belonging, feelings of ownership, and identification with a community can be intensified by participation in community organizations and activities, thus
potentially increasing personal contribution and commitment to community well-being. When communities
encourage participation, members are more likely to
become actively invested in community life and engaged

in civic roles. Extending opportunities for involvement
to diverse members of the community in ways that
consider the members interests and demographics may
improve a communitys ability to identify and address
concerns that arise during and after disasters.12
Support and Nurturance

Personal and community resilience can be advanced by
attention to the needs of individual members regardless of socioeconomic status, ethnicity, education, and
background. Supportive and nurturing communities
listen to and help members to meet basic human needs,
overcome challenges, and achieve goals. These communities empower individuals and groups, promote their
well-being, and instill hope. Communities that effectively mobilize and equitably allocate resources may be
better able to provide support and nurturance. Resilient
communities provide support by assessing and assisting
vulnerable members before, during, and after disasters.
The personal, social, and economic losses that accompany collective trauma require ongoing support.12
Structure, Roles, and Responsibilities

Community structure, roles, and responsibilities can
enhance a communitys capacity for disaster prevention,
preparedness, response, and recovery. Resilient communities establish and apply community standards, rules,
and procedures objectively. Members learn, and teach
each other, to navigate the complex reciprocal links and
overlapping networks of individuals, groups, organizations, and agencies that exist within their community.
Individuals and groups identify and address common
concerns through relatively frequent and supportive
interactions. Formal and informal associations that set
priorities and resolve problems can provide solutions.
Response and recovery are facilitated by effective leadership; teamwork; clear organizational structures; well-defined roles, responsibilities, and lines of authority; and
established relationships with other communities and the
larger society that provide assistance and support after
a disaster. Resilient communities adopt an all-hazards
approach that seeks to protect against any type of hazard.
In a highly uncertain environment, structural elements
(e.g., health, mental health, and public health systems;
emergency management infrastructure) must be flexible
to manage unforeseen vulnerabilities and threats.12
Resources
A communitys resources include natural, physical, financial, human, and social assets of individual members as
well as those attached to the community itself. Natural
resources comprise land and raw materials. Physical
resources include existing infrastructure and machinery and tools used for production. Financial resources,
such as money and credit, facilitate exchange within
and across community boundaries, acquisition of other
resources, and the production and distribution of goods
and services. Human resources are a workforce, skills,
leadership, and member qualities (e.g., work ethic, hope,
the will to improve personal and community well-being).
Social resources comprise relationships, support systems,
and interpersonal networks within a community, along
with characteristics such as collaboration and cohesion.
Resources can complement or substitute for each other.
Resilient communities acquire, mobilize, allocate, invest
in, and use resources effectively on behalf of members
and to meet community goals. Investment in physical,
human, and social capital (e.g., improvements in health
facilities, job training, neighborhood development) likely
must continue to enable local systems and infrastructures
to endure and respond to a wide variety of potential
community hazards. Redundancy in essential resources
can help a community maintain critical functions in a
crisis. Community resources may be augmented in the
aftermath of a disaster by an infusion of resources from
other communities (e.g., through mutual aid agreements
in which emergency assistance is provided across jurisdictional boundaries) and from the larger society.12
Critical Reflection and Skill Building

Critical reflection about values, their history and experiences, and the experiences of others allow formal and
informal community leaders to establish meaningful
goals and objectives, make better decisions, and develop
and implement strategies for the benefit of the community and its members. Resilient communities establish
structures to collect, analyze, and use information; identify and address local issues, needs, and problems; recognize and frame collective experiences; and plan, manage,
and evaluate programs. These communities examine
their successes and failures, assess their performance,
learn from adversity, and support skill building of individuals and systems. Learning, adaptation, and growth
can improve capacity and foster disaster resilience.12
139
Communication
Community resilience depends upon timely, accurate,
and effective communication among community members and groups, between authorities and community
members, and with other communities and the larger
society. Constructive communication is based on shared
meanings and perceived to be open and honest. Opportunities to express needs and views should be provided
to all community members and groups which should be
encouraged to participate in community problem-solving. Effective communication and participation can
cultivate trust in leadership, foster disaster prevention
and preparedness, improve compliance with disaster
directives, promote effective response, enhance recovery,
and help resolve existing and emerging unmet needs as
well as those that arise as a result of disasters. To ensure
resources are mobilized and deployed in a timely manner
for disaster resilience, communication channels must be
sufficiently redundant.12
Disaster Management
Disaster managementincluding measures for preventing and mitigating, preparing for, responding to, and
recovering from disastersis indispensable for community resilience. Prevention and mitigation include
activities to avoid or control an event, to decrease risks
to people and property, and to lessen potential or actual
adverse effects. Mitigation efforts implemented before,
during, or after a disaster decrease the likelihood of
hazardous incidents and limit exposure to, or potential
loss from, them. Preparedness is an ongoing process
that identifies vulnerabilities, analyzes threats, determines resource requirements, and amasses resources for
response and recovery. Response addresses the direct,
short-term effects of a disaster by providing assistance
and through efforts to curtail further damage during
or immediately after a disaster; to support basic human
needs; and to preserve the social, economic, and political
structure of an affected community. As the relatively
short-term response phase evolves into a longer period
of recovery, survivors begin to rebuild their lives and
their community.12
1).18 Robustness is the strength or ability of elements,

resources, and systems to withstand stress without degradation or loss of function. Redundancy describes the
ability of an element, resource, or system to substitute
for another so that essential functioning is not disrupted
during a crisis. Resourcefulness is the ability to identify
problems, establish priorities, mobilize resources in
response to threats and disruptions, and use resources to
accomplish goals. Rapidity is the ability to meet priorities and achieve goals in a timely fashion in order to
contain losses and prevent future disruption.18
Adaptive Capacities:
Community resilience has been characterized as
emerging from four adaptive capacities (i.e., resilience
resources): (1) Economic Development, (2) Social Capital, (3) Information and Communication, and (4) Community Competence (See Table 1).19 Resilience depends
on these adaptive capacities, which have dynamic attributes of robustness, redundancy, and rapidity. When
these resilience resources are damaged or disrupted by
a disaster, resilience can fail.19 The adaptive capacities
of communities are supported by health, mental health,
and public health systems in that the systems create conditions needed for the health and wellness of community
members through programs and services for personal
and community prevention, preparedness, protection,
response, and recovery. The four adaptive capacities are
described below.
Economic Development
In terms of economic development, community resilience depends on the volume and diversity of economic
resources (e.g., raw materials, machinery, physical
infrastructure, labor force, service systems) and equity
in resource distribution. When poor and developing
communities are confronted with a disaster, they are at
greater risk of being destroyed. They also tend to be less
successful in mounting effective response and recovery
efforts than wealthier and better-developed communities. A communitys ability to distribute resources to
those most in need is related to community resilience.19
Community Resilience Properties:
Social Capital
Four properties characterize resilience of physical and

social systems, including communities: robustness,
redundancy, resourcefulness, and rapidity (See Table
Social capital is the collection of actual and potential

resources needed for a durable network of relationships.19,20 Social capital, an adaptive capacity that
140
contributes to community resilience, involves network

structures and linkages; social support; and community
roots, bonds, and commitments. Network structures and
linkages refer to overlapping, interorganizational systems
with reciprocal links, frequent supportive interactions,
and processes for cooperative decision-making.15,19
Social support entails social interactions that provide
assistance (received or delivered social support) and
those that are expected to provide assistance when it is
needed (perceived or expected social support). Community roots, bonds, and commitment are associated with
place attachment (i.e., an emotional connection to ones
community), a sense of togetherness including feelings
of belonging, and participation in local organizations
and grass-roots leadership.19
Information and Communication

A communication infrastructure, including the media,
is an important element of this adaptive capacity since
community resilience depends on information and
communication. A trusted source of accurate information is among the most important resilience assets for
individuals and groups.21 Another valuable element of
information and communication resources is communal
narratives, which convey and help to validate shared
understandings of a disaster.19
Community Competence
A competent community is one in which various community components cooperate effectively to identify
community needs and problems; attain a working
consensus on goals and priorities; concur about how to
implement these goals; and take effective, collaborative
action.2 Decision-making and collective action that
may derive from collective efficacy and empowerment
contribute to community competence. Mutual trust
and a willingness to work toward the common good are
required for collective efficacy.19
Features of Resilient Communities:

Identified features of resilient communities, based on
examples from past disasters, embody many of the attributes and adaptive capacities described above. Resilient
communities are characterized by engagement at the
community level, including neighborhood involvement
and a sense of cohesiveness. Interorganizational partnerships promote integrated pre-disaster planning and
exercises and ideally result in established agreements

that engender cooperation during response and recovery.
Sustained local leadership is buttressed by partnerships
with state and federal governments. Information and
education about risks are effective and culturally relevant. Access to quality health services leads to optimal
community health. Disaster preparedness is integrated
with wellness activities. Social functioning is restored
rapidly post disaster through, for example, the reopening
or rebuilding of schools, religious institutions, commercial establishments, community facilities, and other centers of social networking. Resilient communities have a
high degree of disaster preparedness and self-sufficiency
at the individual level. They enact targeted strategies to
empower and engage vulnerable populations. Families
and businesses are financially resourceful. Finally, resilient communities use resources efficiently for recovery.22
See Table 1.
Advancing Community Resilience

Many strategies have been proposed for building community resilience to disasters. Communities should
decrease risk and resource inequities, engage members
in mitigation, create organizational links, enhance and
protect social support, and plan for the unexpected.19
Communities are also encouraged to adopt a holistic
wellness approach, to promote a conscious awareness
of community resilience,12 and to foster community
development based on input and engagement of community members.23 Communities should develop and
practice disaster plans at the individual, family, business,
organization, and community level. For the most part,
these and other community resilience strategies focus
on systems and require concerted action among various
stakeholders within the community. These strategies
typically involve community-level interventions that
include multiple components applied across various
settings.
Building community resilience to disasters should
involve mental health professionals, because they have
special and essential expertise in addressing trauma at
individual and group levels. Mental health professionals should be involved in the following broad recommendations: advocate mental health as integral to a
holistic wellness approach to disaster management,
integrate disaster preparedness and community
141
resilience into mental health practice, and participate

in local disaster management efforts.
Advocate Mental Health as Integral to a

Holistic Wellness Approach to Disaster
Management:
Potential barriers to community resilience include some
that are specific to mental health including: limited
familiarity with mental health issues among non-mental healthcare professionals, the stigma associated with
mental illness and treatment, a schism between community health and mental health, and a limited evidence
base for disaster mental health services and for distinguishing universally appropriate and culture-specific
approaches.24 These barriers are best addressed by a
holistic wellness, rather than illness, perspective for
communities (as well as individuals). A holistic wellness approach requires societal support to maintain
and restore: healthy physical and mental functioning, effective coping and health-oriented behaviors,
and improved understanding of traumatic stress, and
promotion of mental and physical health.25
To integrate mental health into disaster management, mental health must be addressed in education and
training in emergency management. Mental health education and training must include more content related
to disasters and be incorporated into disaster services.
This integration must be supported by research and
policy.26 Integrating mental health into local emergency
management systems requires a clear understanding of
these systems, including their separate and overlapping
structures, roles, and responsibilities and knowledge of
available resources. Emergency management, mental
health, public health, and health systems all provide
essential support and nurturance for community members that may be augmented by informal resources
available outside established structures and traditional
markets. Mental health professionals should be among
those who design and implement effective emergency
management tactics at the local level. Mental health
service providers and professional associations can be
instrumental in promoting the incorporation of mental
health concerns into emergency management.
142
Integrate Disaster Preparedness and

Community Resilience into Practice:
A potential barrier to community resilience is apathy.
Public apathy toward disaster preparedness has been
linked to a lack of familiarity with, and underestimation of, disaster risks; a false sense of security including the belief that government will assume primary
responsibility for the safety and care of individual citizens; denial; fatalism; and social pressures to appear
brave. Government apathy toward preparedness can be
due to competing priorities at individual and communal
levels, overestimation of capacity, ambiguity of responsibility, and defeatism.27 If community resilience strategies
are grounded in community values and priorities, address
local social issues, and result in obvious benefits for individuals and the community, these strategies may be met
with less apathy than disaster preparedness. Community
resilience strategies, once undertaken, may reduce apathy, thus giving rise to additional resilience building.
Mental health professionals can help address apathy
and support the preparedness, resilience, and recovery
of their patients and communities by becoming knowledgeable about local vulnerabilities and threats, educated about basic disaster preparedness, and informed
about available resources. Information about disaster
mental health is available through the American Psychiatric Association,28 the Centers for Disease Control
and Prevention,29 and the Substance Abuse and Mental
Health Services Administration,30 among other sources.
Information about local vulnerabilities and threats and
about preparedness is available through local and state
emergency management and public health and mental
health authorities.
Practitioners should infuse their routine practice
with disaster resilience information and activities to
the greatest extent possible. This may involve making
preparedness and recovery materials available in waiting
rooms, on websites, and in newsletters; helping individuals to become aware of and assess their vulnerability
to hazards; and sharing information about sources of
emergency assistance. It also involves many aspects of
traditional practice, including, for example, teaching
patients to examine their strengths and challenges and
helping them to problem-solve, enhancing their communication skills, connecting them with personal and
community social supports, fostering their engagement
and participation in community activities and organizations, and increasing their awareness and use of
successful coping strategies. All of these contribute to
personal resilience and ultimately may benefit community resilience when individuals become aware of
and value the concept and appreciate the potential
for application at the community level.
Participate in Disaster
Management Efforts:
Mental health professionals play a pivotal role in disaster
management because of their ability to advance the psychological and social adjustment of populations affected
by mass trauma and to limit maladaptation over time.
Mental health professionals should involve themselves
in planning, designing, implementing, and evaluating
prevention and mitigation, preparedness, response,
and recovery efforts at the local, regional, and national
levels. Mental health professionals can become involved
in disaster management through national organizations
that support local response activities. Examples include
the Medical Reserve Corps,31 the American Red Cross,32
and the American Psychological Associations Disaster
Response Network.33
The Medical Reserve Corps (MRC) engages volunteers to strengthen public health, emergency response,
and community resilience. Community-based MRC
units supplement existing emergency and public health
resources by organizing and using volunteers who
donate time and expertise to prepare for, and respond
to, community emergencies. In addition to serving a
local area, MRC volunteers can support communities in
need across the nation.31
The American Red Cross relies extensively on volunteers in responding to approximately 70,000 crises every
year. Volunteers with various backgrounds, talents, and

skills constitute approximately 95% of the American
Red Cross workforce. The American Red Cross, working in partnership with other agencies and organizations
that deliver disaster services, provides shelter, food, and
health and mental health services to address immediate
emergency needs resulting from disasters.32
The American Psychological Association Disaster
Response Network (DRN) is made up of licensed psychologists with training in disaster response who provide
volunteer assistance to disaster survivors and relief workers. DRN volunteers work with known disaster response
organizations to make referrals to community resources,
provide information, advocate on behalf of survivors
and workers, listen, and help people solve problems.
DRN members also teach courses on disaster mental
health, participate in planning with various government
and non-government agencies, and educate the public
about traumatic stress.33
Conclusion
For effective disaster management and the health and
recovery of individuals and communities, mental health
professionals must become involved in local disaster
management efforts. These professionals can regularly
foster community resilience through their contributions
to the attributes, properties, adaptive capacities, and features of resilient communities. Mental health professionals should also engage in specific activities for which they
are particularly well-suited, including advocating mental
health as integral to a holistic wellness approach to disaster management, integrating disaster preparedness and
community resilience into mental health practice, and
participating in local disaster management efforts.
About the Faculty

Rose L. Pfefferbaum, PhD, MPH: Dr. Pfefferbaum is Faculty Emeritus, Phoenix Community College, Phoenix, AZ; she is also
Project Director for Community Resilience, Terrorism and Disaster Center, University of Missouri, Columbia, MO.
Betty Pfefferbaum, MD, JD: Dr. Pfefferbaum is George Lynn Cross Research Professor, Paul and Ruth Jonas Chair, Professor
and Chairman, Department of Psychiatry and Behavioral Sciences, University of Oklahoma Health Sciences Center, Oklahoma
City, OK.
143
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Difede J, Apfeldorf WJ, Cloitre M, Spielman LA, Perry SW. Acute psychiatric responses to the explosion at the World Trade Center: A case series. J Nerv Ment Dis.
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Ofman PS, Mastria MA, Steinberg J. Mental health response to terrorism: The World Trade Center bombing. J Ment Health Counseling. 1995;17(3):312-320.
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Pfefferbaum B, Pfefferbaum RL, Norris F. Community resilience and wellness for children exposed to Hurricane Katrina. In: Kilmer RP, Gil-Rivas V, Tedeschi RG, Calhoun
LG, eds. Helping Families and Communities Recover From Disaster: Lessons Learned From Hurricane Katrina and Its Aftermath. Washington, DC: American Psychological
Association; 2010:265-288.
10. Brown DD, Kulig JC. The concept of resiliency: Theoretical lessons from community research. Health Can Soc. 1996-1997;4(1):29-50.
11. Pfefferbaum B, Reissman DB, Pfefferbaum RL, Klomp RW, Gurwitch RH. Building resilience to mass trauma events. In: Doll LS, Bonzo SE, Sleet DA, Mercy JA, Haas
EN, eds. Handbook of Injury and Violence Prevention. New York: Springer; 2007:347-358.
12. Pfefferbaum RL, Reissman DB, Pfefferbaum B, Wyche KF, Norris FH, Klomp RW. Factors in the development of community resilience to disasters. In: Blumenfield M,
Ursano RJ, eds. Intervention and Resilience After Mass Trauma. New York: Cambridge University Press; 2008:49-68.
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15. Goodman RM, Speers MA, McLeroy K, Fawcett S, Kegler M, Parker E, Smith SR, Sterling TD, Wallerstein N. Identifying and defining the dimensions of community
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16. Labonte R, Laverack G. Capacity building in health promotion, Part 1: for whom? And for what purpose? Crit Public Health. 2001;11(2):111-127.
17. Labonte R, Laverack G. Capacity building in health promotion, Part 2: whose use? And with what measurement? Crit Public Health. 2001;11(2):129-138.
18. Bruneau M, Chang SE, Eguchi RT, Lee GC, ORourke TD, Reinhorn AM, Shinozuka M, Tierney K, Wallace WA, von Winterfeldt D. A framework to quantitatively assess
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19. Norris FH, Stevens SP, Pfefferbaum B, Wyche KF, Pfefferbaum RL. Community resilience as a metaphor, theory, set of capacities, and strategy for disaster readiness. Am J
Community Psychol. 2008;41(1/2):127-150.
20. Bourdieu P. The forms of capital. In: Richardson J, ed. Handbook of Theory and Research for the Sociology of Education. New York: Greenwood; 1986:241-258. http://www.
marxists.org/reference/subject/philosophy/works/fr/bourdieu-forms-capital.htm. Accessed September 1, 2013.
21. Longstaff PH. Security, Resilience, and Communication in Unpredictable Environments Such as Terrorism, Natural Disasters, and Complex Technology. Cambridge, MA:
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31. Medical Reserve Corps. http://www.medicalreservecorps.gov. Accessed September 1, 2013.
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145
L003310
37. Community resilience:
A. Derives from collective activity that supports response and recovery for the whole
B. Depends on effective disaster preparedness and recovery but has no real role in disaster response
C. Requires efficiency in resource utilization so it is undermined by redundancy of resources
D. Is likely to improve when community members assert their independence and disengage from community
activities
38. Which of the following statements is true of the relationship between personal and community
resilience?
A. There is no difference between personal and community resilience.
B. Community resilience ensures that community members will be personally resilient.
C. A community will be resilient if its members are personally resilient.
D. Resilient communities support the personal resilience of community members.
39. In the context of community resilience, human agency:

A. Prevents disasters
B. Requires proactive, but not reactive, efforts
C. Eliminates injuries and deaths due to disasters
D. Can lead to deliberate, meaningful collective action
40. Mental health professionals can promote community resilience by:

A. Helping to ensure that the mental health disciplines remain separate from disaster management
B. Reassuring patients that the government will assume the primary responsibility for their individual safety
and care
C. Infusing their routine practice with disaster resilience information and activities
D. All of the above
147

Community Resilience to Disasters for Mental Health Professionals
By Rose L. Pfefferbaum, PhD, MPH; and Betty Pfefferbaum, MD, JD
ID#: L003310

Mental health is essential to the health and recovery of individuals and communities faced with disasters.
Mental health professionals should engage in specific activities for which they are particularly well-suited,
including advocating mental health as integral to a holistic wellness approach to disaster management.
Step 1: Advocate
Advocate mental health as integral to a
holistic wellness approach to disaster management.
Step 2: Integrate
Help integrate mental health practitioners
into disaster management by becoming involved in planning, designing, implementing, and evaluating prevention and mitigation, preparedness, response, and recovery
efforts at local, regional, and national levels.
Step 3: Learn
Learn about basic disaster preparedness
for individuals, families, organizations, and
communities.
Step 5: Assist
Assist patients in developing personal and
family resilience skills by helping them to
problem-solve, enhancing their communication skills, connecting them with personal and community social supports, fostering their engagement and participation
in community activities and organizations,
and increasing their awareness and use of
successful coping strategies.
Step 6: Participate
Participate in local disaster management
efforts, including preparedness, response,
and recovery activities.
Step 4: Prepare
Make preparedness and recovery materials
available to patients in waiting rooms, on
websites, and in newsletters.
Notes

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Directions in

The Neurobiology of Child Abuse and Neglect . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .75

Antidepressant Medications in Preadolescent Children

Psychostimulants for Test-Taking and ADHD:

Internet and Videogame Addiction:

Community Resilience to Disasters for Mental Health Professionals . . . . . . . . . . . . . . . . . .135

Program Advisory Board

Robert M.A. Hirschfeld, MD

Gail Erlick Robinson, MD, DPsych, FRCPC

The Neurobiology of Child Abuse and Neglect

Richard Idell, MD; and Charles B. Nemeroff, MD

Antidepressant Medications in Preadolescent Children

Thomas N. Butler, MD; and Christine J. Choe, MD

Psychostimulants for Test-Taking and ADHD:

Shawen M. Ilaria, BS; Michael A. Shapiro, MD; and Mark S. Gold, MD

Internet and Videogame Addiction:

Aviv Weinstein, PhD

Community Resilience to Disasters

Conflict of Interest Faculty & Advisory Board Disclosures

Dr. Butler has no conflicting interests to disclose.

Dr. Choe has no conflicting interests to disclose.

Dr. Gold has no conflicting interests to disclose.

Dr. Idell has no conflicting interests to disclose.

Ms. Ilaria has no conflicting interests to disclose.

Rose L. Pfefferbaum, PhD, MPH

Dr. Pfefferbaum has no conflicting interests to disclose.

Betty Pfefferbaum, MD, JD

Dr. Pfefferbaum has no conflicting interests to disclose.

Dr. Shapiro has no conflicting interests to disclose.

Aviv Weinstein, PhD

Dr. Weinstein has no conflicting interests to disclose.

Program Advisory Board Member Disclosures:

Dr. Dickstein has no conflicting interests to disclose.

Richard L. Elliott, MD, PhD:

Deborah I. Frank, PhD, ARNP:

Dr. Frank has no conflicting interests to disclose.

Mark S. Gold, MD, PhD:

Dr. Gold has no conflicting interests to disclose.

Alison Heru, MD:

Dr. Heru has no conflicting interests to disclose.

Philip Janicak, MD:

George I. Papakostas, MD:

Hatherleigh Editorial Staff:

Mr. Flach has no conflicting interests to disclose.

Stacy M. Powell, Managing Editor:

Ms. Powell has no conflicting interests to disclose.

Rick Gallub, Office Manager

Mr. Gallub has no conflicting interests to disclose.

Accreditation Standards: IOM; ACGME /ABMS Competencies

Directions in Psychiatry, Vol. 33: Part 2

The Neurobiology of Child Abuse and Neglect

Antidepressant Medications in Preadolescent Children

IOM Core Competencies

Employ evidence-base practice

Apply quality improvement

Community Resilience to Disasters for

Provide patient-centered care

Work in interdisciplinary teams

Internet and Videogame Addiction:

Practice-based learning and improvement

Interpersonal and communication skills

ABMS MOC Competencies