Professional Documents
Culture Documents
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
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.
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 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.
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.
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
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
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
page 75
CME LESSON 7
page 89
CME LESSON 8
page 105
CME LESSON 9
page 117
CME LESSON 10
page 135
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
Christine J. Choe, MD
Mark S. Gold, MD
Richard Idell, MD
Shawen M. Ilaria, BS
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.
Michael A. Shapiro, MD
Dr. Elliott has been on the Speakers Bureau for Eli Lilly and Company, Pfizer, Inc., and GlaxoSmithKline.
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.
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.
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.
L6
Lesson 9
Lesson 10
L7
L8
L9
L10
Utilize informatics
ACGME Competencies
Patient care
Medical knowledge
Professionalism
System-based practice
X
X
Professional standing
Cognitive expertise
Performance in practice
X
X
X
X
X
X
X
X
X
X
X
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.
Directions in Psychiatry (ISSN #0891-3870) is published quarterly with one special report issue (4 issues per year) for $300 per year by The
Hatherleigh Company, Ltd., 62545 State Highway 10, Hobart, NY 13788. POSTMASTER: Please send address changes to Directions in Psychiatry,
The Hatherleigh Company, Ltd., 62545 State Highway 10, Hobart, NY 13788.
Copyright 2013, THE HATHERLEIGH COMPANY, LTD. All rights reserved. No part of this publication may be reproduced in any form or by any means,
except as permitted under sections 107 or 108 of the United States Copyright Act, without the prior written permission of the publisher. 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.
They may not to be duplicated or distributed or otherwise repurposed in digital or physical form in whole or in part without the express consent of the publisher. For educational use and reprints, please contact 1-800-367-2550. Statements made in its publications by contributing authors do not reflect the opinion
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
75
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
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
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
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
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.
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.
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
81
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.
82
References
1. Heim C, Shugart M, Craighead WE, Nemeroff CB. Neurobiological and psychiatric consequences of child abuse and neglect. Dev Psychobiol. 2010;52(7):671690.
doi:10.1002/dev.20494.
2. Felitti VJ, Anda RF. The relationship of adverse childhood experiences to adult medical disease, psychiatric disorders and sexual behavior: implications for healthcare. In:
The Impact of Early Life Trauma on Health and Disease. Cambridge University Press; 2010. Available at: http://dx.doi.org/10.1017/CBO9780511777042.010.
3. Heim C, Nemeroff CB. The role of childhood trauma in the neurobiology of mood and anxiety disorders: preclinical and clinical studies. Biol Psychiatry. 2001;49(12):1023
1039. doi:10.1016/S0006-3223(01)01157-X.
4. Beatriz Currier M, B. Nemeroff C. Inflammation and Mood Disorders: Proinflammatory Cytokines and the Pathogenesis of Depression. Anti-Inflamm Anti-Allergy Agents
Med Chem Former Cu. 2010;9(3):212220.
5. Costello EJ, Angold A. Developmental psychopathology and public health: past, present, and future. Dev Psychopathol. 2000;12(4):599618.
6. McCloskey LA, Walker M. Posttraumatic stress in children exposed to family violence and single-event trauma. J Am Acad Child Adolesc Psychiatry. 2000;39(1):108115.
7.
Luecken LJ, Roubinov DS. Pathways to lifespan health following childhood parental death. Soc Pers Psychol Compass. 2012;6(3):243257. doi:10.1111/j.1751-9004.2011.00422.x.
8. Koola MM, Qualls C, Kelly DL, et al. Prevalence of childhood physical and sexual abuse in veterans with psychiatric diagnoses. J Nerv Ment Dis. 2013;201(4):348352.
doi:10.1097/NMD.0b013e318288e333.
9. Huot RL, Thrivikraman K, Meaney MJ, Plotsky PM. Development of adult ethanol preference and anxiety as a consequence of neonatal maternal separation in Long Evans
rats and reversal with antidepressant treatment. Psychopharmacology (Berl). 2001;158(4):366373. doi:10.1007/s002130100701.
10. Nemeroff CB, Goldschmidt-Clermont PJ. Heartache and heartbreakthe link between depression and cardiovascular disease. Nat Rev Cardiol. 2012;9(9):526539.
doi:10.1038/nrcardio.2012.91.
11. Nemeroff CB, Vale WW. The neurobiology of depression: inroads to treatment and new drug discovery. J Clin Psychiatry. 2005;66 Suppl 7:513.
12. Bortolon C, Capdevielle D, Boulenger J-P, Gely-Nargeot M-C, Raffard S. Early maladaptive schemas predict positive symptomatology in schizophrenia: A cross-sectional
study. Psychiatry Res. 2013. doi:10.1016/j.psychres.2013.03.018.
13. Ackard DM, Neumark-Sztainer D. Multiple sexual victimizations among adolescent boys and girls: prevalence and associations with eating behaviors and psychological
health. J Child Sex Abuse. 2003;12(1):1737. doi:10.1300/J070v12n01_02.
14. Cohen LJ, Foster M, Nesci C, Tanis T, Halmi W, Galynker I. How do different types of childhood maltreatment relate to adult personality pathology? J Nerv Ment Dis.
2013;201(3):234243. doi:10.1097/NMD.0b013e3182848ac4.
15. Zlotnick C, Mattia J, Zimmerman M. Clinical features of survivors of sexual abuse with major depression. Child Abuse Negl. 2001;25(3):357367.
16. Dube SR, Anda RF, Felitti VJ, Chapman DP, Williamson DF, Giles WH. Childhood abuse, household dysfunction, and the risk of attempted suicide throughout the life
span: findings from the Adverse Childhood Experiences Study. JAMA J Am Med Assoc. 2001;286(24):30893096.
17. Dunn EC, McLaughlin KA, Slopen N, Rosand J, Smoller JW. Developmental timing of child maltreatment and symptoms and symptoms of depression and suicidal
ideation in young adulthood: results from the national longitudinal study of adolescent health. Depress Anxiety. 2013. doi:10.1002/da.22102.
18. Danese A MT. ELevated inflammation levels in depressed adults with a history of childhood maltreatment. Arch Gen Psychiatry. 2008;65(4):409415. doi:10.1001/
archpsyc.65.4.409.
19. OMahony SM, Marchesi JR, Scully P, et al. Early Life Stress Alters Behavior, Immunity, and Microbiota in Rats: Implications for Irritable Bowel Syndrome and Psychiatric
Illnesses. Biol Psychiatry. 2009;65(3):263267. doi:10.1016/j.biopsych.2008.06.026.
20. Smith GW, Aubry JM, Dellu F, et al. Corticotropin releasing factor receptor 1-deficient mice display decreased anxiety, impaired stress response, and aberrant neuroendocrine
development. Neuron. 1998;20(6):10931102.
21. Bale TL, Picetti R, Contarino A, Koob GF, Vale WW, Lee K-F. Mice deficient for both corticotropin-releasing factor receptor 1 (CRFR1) and CRFR2 have an impaired
stress response and display sexually dichotomous anxiety-like behavior. J Neurosci Off J Soc Neurosci. 2002;22(1):193199.
22. Kaufman J, Plotsky PM, Nemeroff CB, Charney DS. Effects of early adverse experiences on brain structure and function: clinical implications. Biol Psychiatry.
2000;48(8):778790.
23. Binneman B, Feltner D, Kolluri S, Shi Y, Qiu R, Stiger T. A 6-week randomized, placebo-controlled trial of CP-316,311 (a selective CRH1 antagonist) in the treatment of
major depression. Am J Psychiatry. 2008;165(5):617620. doi:10.1176/appi.ajp.2008.07071199.
24. Weaver ICG, Cervoni N, Champagne FA, et al. Epigenetic programming by maternal behavior. Nat Neurosci. 2004;7(8):847854. doi:10.1038/nn1276.
25. Nemeroff CB, Widerlv E, Bissette G, et al. Elevated concentrations of CSF corticotropin-releasing factor-like immunoreactivity in depressed patients. Science.
1984;226(4680):13421344.
26. Merali Z, Du L, Hrdina P, et al. Dysregulation in the suicide brain: mRNA expression of corticotropin-releasing hormone receptors and GABA(A) receptor subunits in
frontal cortical brain region. J Neurosci Off J Soc Neurosci. 2004;24(6):14781485. doi:10.1523/JNEUROSCI.4734-03.2004.
27. Nemeroff CB, Bissette G, Akil H, Fink M. Neuropeptide concentrations in the cerebrospinal fluid of depressed patients treated with electroconvulsive therapy.
Corticotrophin-releasing factor, beta-endorphin and somatostatin. Br J Psychiatry J Ment Sci. 1991;158:5963.
28. Heinrichs SC, Menzaghi F, Merlo Pich E, Britton KT, Koob GF. The role of CRF in behavioral aspects of stress. Ann N Y Acad Sci. 1995;771:92104.
29. Heim C ND. PItuitary-adrenal and autonomic responses to stress in women after sexual and physical abuse in childhood. JAMA. 2000;284(5):592597. doi:10.1001/
jama.284.5.592.
83
30. Harkness KL, Stewart JG, Wynne-Edwards KE. Cortisol reactivity to social stress in adolescents: Role of depression severity and child maltreatment. Psychoneuroendocrinology.
2011;36(2):173181. doi:10.1016/j.psyneuen.2010.07.006.
31. Goldman-Mellor S, Hamer M, Steptoe A. Early-life stress and recurrent psychological distress over the lifecourse predict divergent cortisol reactivity patterns in adulthood.
Psychoneuroendocrinology. 2012;37(11):17551768. doi:10.1016/j.psyneuen.2012.03.010.
32. Vythilingam M, Heim C, Newport J, et al. Childhood trauma associated with smaller hippocampal volume in women with major depression. Am J Psychiatry.
2002;159(12):20722080.
33. Heim CM, Mayberg HS, Mletzko T, Nemeroff CB, Pruessner JC. Decreased Cortical Representation of Genital Somatosensory Field After Childhood Sexual Abuse. Am J
Psychiatry. 2013;170(6):616623. doi:10.1176/appi.ajp.2013.12070950.
34. Lupien SJ, Parent S, Evans AC, et al. Larger amygdala but no change in hippocampal volume in 10-year-old children exposed to maternal depressive symptomatology since
birth. Proc Natl Acad Sci U S A. 2011;108(34):1432414329. doi:10.1073/pnas.1105371108.
35. Burghy CA, Stodola DE, Ruttle PL, et al. Developmental pathways to amygdala-prefrontal function and internalizing symptoms in adolescence. Nat Neurosci.
2012;15(12):17361741. doi:10.1038/nn.3257.
36. Caspi A, Sugden K, Moffitt TE, et al. Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene. Science. 2003;301(5631):386389.
doi:10.1126/science.1083968.
37. Hariri AR, Mattay VS, Tessitore A, et al. Serotonin transporter genetic variation and the response of the human amygdala. Science. 2002;297(5580):400403. doi:10.1126/
science.1071829.
38. Karg K BM. The serotonin transporter promoter variant (5-httlpr), stress, and depression meta-analysis revisited: Evidence of genetic moderation. Arch Gen Psychiatry.
2011;68(5):444454. doi:10.1001/archgenpsychiatry.2010.189.
39. Menke A, Klengel T, Rubel J, et al. Genetic variation in FKBP5 associated with the extent of stress hormone dysregulation in major depression. Genes Brain Behav.
2013;12(3):289296. doi:10.1111/gbb.12026.
40. Binder EB. The role of FKBP5, a co-chaperone of the glucocorticoid receptor in the pathogenesis and therapy of affective and anxiety disorders. Psychoneuroendocrinology.
2009;34, Supplement 1:S186S195. doi:10.1016/j.psyneuen.2009.05.021.
41. Storer CL, Dickey CA, Galigniana MD, Rein T, Cox MB. FKBP51 and FKBP52 in signaling and disease. Trends Endocrinol Metab. 2011;22(12):481490. doi:10.1016/j.
tem.2011.08.001.
42. Ising M, Depping A-M, Siebertz A, et al. Polymorphisms in the FKBP5 gene region modulate recovery from psychosocial stress in healthy controls. Eur J Neurosci.
2008;28(2):389398. doi:10.1111/j.1460-9568.2008.06332.x.
43. Lavebratt C, berg E, Sjholm LK, Forsell Y. Variations in FKBP5 and BDNF genes are suggestively associated with depression in a Swedish population-based cohort. J
Affect Disord. 2010;125(13):249255. doi:10.1016/j.jad.2010.02.113.
44. Willour VL, Chen H, Toolan J, et al. Family-based association of FKBP5 in bipolar disorder. Mol Psychiatry. 2008;14(3):261268. doi:10.1038/sj.mp.4002141.
45. Appel K, Schwahn C, Mahler J, et al. Moderation of Adult Depression by a Polymorphism in the FKBP5 Gene and Childhood Physical Abuse in the General Population.
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%
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
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.
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.
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.
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
L003307 : Antidepressant Medications in Preadolescent Children with Unipolar Depression: A Review of the Evidence
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.
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
L003307 : Antidepressant Medications in Preadolescent Children with Unipolar Depression: A Review of the Evidence
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
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.
L003307 : Antidepressant Medications in Preadolescent Children with Unipolar Depression: A Review of the Evidence
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
Paroxetine
10 mg daily
20 50 mg
daily
(may divide
dose BID)
Venlafaxine SR
Duloxetine
30 mg 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
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
L003307 : Antidepressant Medications in Preadolescent Children with Unipolar Depression: A Review of the Evidence
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
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.
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
L003307 : Antidepressant Medications in Preadolescent Children with Unipolar Depression: A Review of the Evidence
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
L003307 : Antidepressant Medications in Preadolescent Children with Unipolar Depression: A Review of the Evidence
96
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.
L003307 : Antidepressant Medications in Preadolescent Children with Unipolar Depression: A Review of the Evidence
97
L003307 : Antidepressant Medications in Preadolescent Children with Unipolar Depression: A Review of the Evidence
References
1.
Olfson M, Marcus SC, Weissman MM, Jensen PS. National trends in the use of psychotropic medications by children. Journal of the American Academy of Child and
Adolescent Psychiatry. 2002;41(5):514-521.
2.
Hunkeler EM, Fireman B, Lee J, et al. Trends in use of antidepressants, lithium, and anticonvulsants in Kaiser Permanente-insured youths, 1994-2003. Journal of Child and
Adolescent Psychopharmacology. 2005;15(1):26-37.
3.
Zito JM, Safer DJ. Services and prevention: pharmacoepidemiology of antidepressant use. Biological Psychiatry. 2001;49(12):1121-1127.
4.
Correll CU, Kratochvil CJ, March JS. Developments in pediatric psychopharmacology: focus on stimulants, antidepressants, and antipsychotics. The Journal of Clinical
Psychiatry. 2011;72(5):655-670.
5.
Merikangas KR, He JP, Rapoport J, Vitiello B, Olfson M. Medication use in US youth with mental disorders. JAMA Pediatrics. 2013;167(2):141-148.
6.
Merikangas KR, He JP, Brody D, Fisher PW, Bourdon K, Koretz DS. Prevalence and treatment of mental disorders among US children in the 2001-2004 NHANES.
Pediatrics. 2010;125(1):75-81.
7.
Vernon JA, Shortenhaus SH, Mayer MH, Allen AJ, Golec JH. Measuring the patient health, societal and economic benefits of US pediatric therapeutics legislation.
Paediatric Drugs. 2012;14(5):283-294.
8.
Christensen ML. Best pharmaceuticals for children act and pediatric research equity act: time for permanent status. JPPT : The Official Journal of PPAG. 2012;17(2):140-141.
99
L003307 : Antidepressant Medications in Preadolescent Children with Unipolar Depression: A Review of the Evidence
31. Emslie GJ, Ventura D, Korotzer A, Tourkodimitris S. Escitalopram in the treatment of adolescent depression: a randomized placebo-controlled multisite trial. Journal of
the American Academy of Child and Adolescent Psychiatry. 2009;48(7):721-729.
32. Vitiello B, Rohde P, Silva S, et al. Functioning and quality of life in the Treatment for Adolescents with Depression Study (TADS). Journal of the American Academy of
Child and Adolescent Psychiatry. 2006;45(12):1419-1426.
33. Wagner KD, Robb AS, Findling RL, Jin J, Gutierrez MM, Heydorn WE. A randomized, placebo-controlled trial of citalopram for the treatment of major depression in
children and adolescents. The American Journal of Psychiatry. 2004;161(6):1079-1083.
34. von Knorring AL, Olsson GI, Thomsen PH, Lemming OM, Hulten A. A randomized, double-blind, placebo-controlled study of citalopram in adolescents with major
depressive disorder. Journal of clinical psychopharmacology. Jun 2006;26(3):311-315.
35. Wagner KD, Ambrosini P, Rynn M, et al. Efficacy of sertraline in the treatment of children and adolescents with major depressive disorder: two randomized controlled
trials. JAMA : the journal of the American Medical Association. Aug 27 2003;290(8):1033-1041.
36. Cheung A, Kusumakar V, Kutcher S, et al. Maintenance study for adolescent depression. Journal of Child and Adolescent Psychopharmacology. 2008;18(4):389-394.
37. Keller MB, Ryan ND, Strober M, et al. Efficacy of paroxetine in the treatment of adolescent major depression: a randomized, controlled trial. Journal of the American
Academy of Child and Adolescent Psychiatry. 2001;40(7):762-772.
38. Berard R, Fong R, Carpenter DJ, Thomason C, Wilkinson C. An international, multicenter, placebo-controlled trial of paroxetine in adolescents with major depressive
disorder. Journal of Child and Adolescent Psychopharmacology. 2006;16(1-2):59-75.
39. Emslie GJ, Wagner KD, Kutcher S, et al. Paroxetine treatment in children and adolescents with major depressive disorder: a randomized, multicenter, double-blind,
placebo-controlled trial. Journal of the American Academy of Child and Adolescent Psychiatry. 2006;45(6):709-719.
40. Papakostas GI, Thase ME, Fava M, Nelson JC, Shelton RC. Are antidepressant drugs that combine serotonergic and noradrenergic mechanisms of action more
effective than the selective serotonin reuptake inhibitors in treating major depressive disorder? A meta-analysis of studies of newer agents. Biological Psychiatry.
2007;62(11):1217-1227.
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
depression: the TORDIA randomized controlled trial. JAMA : the journal of the American Medical Association. Feb 27 2008;299(8):901-913.
42. Emslie GJ, Findling RL, Yeung PP, Kunz NR, Li Y. Venlafaxine ER for the treatment of pediatric subjects with depression: results of two placebo-controlled trials. Journal
of the American Academy of Child and Adolescent Psychiatry. Apr 2007;46(4):479-488.
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
Adolescent Psychopharmacology. Feb 2012;22(1):48-55.
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
(TORDIA). Journal of the American Academy of Child and Adolescent Psychiatry. 2011;50(3):293-301.
45. Watanabe N, Furukawa TA, Shimodera S, et al. Brief behavioral therapy for refractory insomnia in residual depression: an assessor-blind, randomized controlled trial. The
Journal of Clinical Psychiatry. 2011;72(12):1651-1658.
46. Haapasalo-Pesu KM, Vuola T, Lahelma L, Marttunen M. Mirtazapine in the treatment of adolescents with major depression: an open-label, multicenter pilot study.
Journal of Child and Adolescent Psychopharmacology. 2004;14(2):175-184.
47. Cheung AH, Emslie GJ, Mayes TL. Review of the efficacy and safety of antidepressants in youth depression. Journal of Child Psychology and Psychiatry, and Allied
Disciplines. 2005;46(7):735-754.
48. Daviss WB, Bentivoglio P, Racusin R, Brown KM, Bostic JQ, Wiley L. Bupropion sustained release in adolescents with comorbid attention-deficit/hyperactivity disorder
and depression. Journal of the American Academy of Child and Adolescent Psychiatry. 2001;40(3):307-314.
49. Hazell P, Mirzaie M. Tricyclic drugs for depression in children and adolescents. The Cochrane Database of Systematic Reviews. 2013;6:CD002317.
50. Everett AV. Pharmacologic treatment of adolescent depression. Current Opinion in Pediatrics. 2002;14(2):213-218.
51. Yu ZJ, Kratochvil CJ, Weller RA, Mooreville M, Weller EB. From TADS and SOFTADS to TORDIA and beyond: whats new in the treatment of adolescent depression?
Current Psychiatry Reports. 2010;12(2):88-95.
52. Pathak S, Johns ES, Kowatch RA. Adjunctive quetiapine for treatment-resistant adolescent major depressive disorder: a case series. Journal of Child and Adolescent
Psychopharmacology. 2005;15(4):696-702.
53. Fleurence R, Williamson R, Jing Y, et al. A systematic review of augmentation strategies for patients with major depressive disorder. Psychopharmacology Bulletin.
2009;42(3):57-90.
54. Riddle MA, King RA, Hardin MT, et al. Behavioral Side Effects of Fluoxetine in Children and Adolescents. Journal of Child and Adolescent Psychopharmacology.
1991;1(3):193-198.
55. Goldsmith M, Singh M, Chang K. Antidepressants and psychostimulants in pediatric populations: is there an association with mania? Paediatric Drugs. 2011;13(4):225-243.
56. Pfizer medication guide EX. http://labeling.pfizer.com/showlabeling.aspx?ID=100 (Accessed 8/8/13).
57. Rynn MA, Riddle MA, Yeung PP, Kunz NR. Efficacy and safety of extended-release venlafaxine in the treatment of generalized anxiety disorder in children and
adolescents: two placebo-controlled trials. The American Journal of Psychiatry. 2007;164(2):290-300.
58. Henry A, Kisicki MD, Varley C. Efficacy and safety of antidepressant drug treatment in children and adolescents. Molecular Psychiatry. 2012;17(12):1186-1193.
59. Cheung A, Sacks D, Dewa CS, Pong J, Levitt A. Pediatric prescribing practices and the FDA Black-box warning on antidepressants. JDBP. 2008;29(3):213-215.
100
L003307 : Antidepressant Medications in Preadolescent Children with Unipolar Depression: A Review of the Evidence
L003307
Multiple-Choice Questions
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
101
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.
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 5: T
reatment-Resistant
Depression
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
L003308
Psychostimulants
for Test-Taking and ADHD:
Assessing the Risks & the Benefits
Shawen M. Ilaria, BS; Michael A. Shapiro, MD; and Mark S. Gold, MD
The authors declare that there are no competing interests.
No commercial support was used in the development of this CME lesson.
The authors would like to thank Paula J. Edge, a gifted editor, for her assistance in preparing this manuscript for publication.
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.
106
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
L003308 : Psychostimulants for Test-Taking and ADHD: Assessing the Risks & the Benefits
107
L003308 : Psychostimulants for Test-Taking and ADHD: Assessing the Risks & the Benefits
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
Despite this readily available information, psychostimulants are safe when used properly. Oral doses of
methylphenidate do not induce euphoric effects; abuse
L003308 : Psychostimulants for Test-Taking and ADHD: Assessing the Risks & the Benefits
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
L003308 : Psychostimulants for Test-Taking and ADHD: Assessing the Risks & the Benefits
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.
110
L003308 : Psychostimulants for Test-Taking and ADHD: Assessing the Risks & the Benefits
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 : Psychostimulants for Test-Taking and ADHD: Assessing the Risks & the Benefits
L003308
Multiple-Choice Questions
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
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.
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
L003309
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
L003309 : Internet and Videogame Addiction: Clinical Implications for Assessment and Treatment
Youngs Internet
Addiction Scale (IAD)
Country
US
Validation study
Widyanto et al.
(2004)4
Bernardi and Pallanti
(2009)5
Jelenchick et al.
(2012)6
UK
Taiwan
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
L003309 : Internet and Videogame Addiction: Clinical Implications for Assessment and Treatment
120
L003309 : Internet and Videogame Addiction: Clinical Implications for Assessment and Treatment
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
Impaired executive
control
China
Cognitive bias to
cues
China
Abnormal activity
at the resting state
South Korea
and China
Abnormal gray
matter density
Europe,
China, and
South Korea
Abnormal white
matter density
China
US, Taiwan,
and
South Korea
Reduced dopamine
activity
South Korea
Videogameinduced dopamine
release
UK and
Israel
Koepp et al.
(1988)76
Weinstein (2010)77
121
L003309 : Internet and Videogame Addiction: Clinical Implications for Assessment and Treatment
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
122
L003309 : Internet and Videogame Addiction: Clinical Implications for Assessment and Treatment
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
L003309 : Internet and Videogame Addiction: Clinical Implications for Assessment and Treatment
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)
L003309 : Internet and Videogame Addiction: Clinical Implications for Assessment and Treatment
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
South Korea
and US
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.
125
L003309 : Internet and Videogame Addiction: Clinical Implications for Assessment and Treatment
References
1.
DellOsso B, Altamura C, Allen A, Marazziti D, et al. Epidemiological and clinical updates on impulse control disorders: a critical review, Eur Arch Psychiat Clin Neurosciences.
2006;256:464475.
Jelenchick LA, Becker T, Moreno MA. Assessing the psychometric properties of the Internet Addiction Test (IAT) in US college students. Psychiat Res. 2012;196(23):296301.
7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th Ed. Washington, DC: American Psychiatric Association, 1994.
8. Canan F, Ataoglu A, Ozcetin A, et al. The association between Internet addiction and dissociation among Turkish college students Comp Psychiat. 2012;53(5):422426.
9. Yen CF, Ko CH, Yen JY, et al. Multi-dimensional discriminative factors for Internet addiction among adolescents regarding gender and age. Psychiat Clinl Neurosci.
2009;63(3):357364.
10. Beranuy FM, Chamarro LA, Graner JC, et al. Validation of two brief scales for Internet addiction and mobile phone problem use. Psicothema. 2009;21(3):4805 [Article
in Spanish].
11. Meerkerk GJ, Van Den Eijnden RJ, Vermulst AA, et al. The Compulsive Internet Use Scale (CIUS): some psychometric properties. Cyberpsychol Behav. 2009;12(1):16.
12. Khazaal Y, Chatton A, Horn A, et al. French validation of the compulsive Internet use scale (CIUS). Psychiat Quarterly. 2012;83(4):397405.
13. Demetrovics Z, Szeredi B, Rzsa S. The three-factor model of Internet addiction: the development of the Problematic Internet Use Questionnaire. Behav Res Methods.
2008;40(2):563574.
14. Widyanto L, Griffiths MD, Brunsden VA. Psychometric comparison of the Internet Addiction Test, the Internet-Related Problem Scale, and self-diagnosis. Cyberpsychol
Behav Soc Net. 2011;14(3):141149.
15. Beard KW. Internet addiction: a review of current assessment techniques and potential assessment questions. Cyberpsychol Behav. 2005;8(1):714.
16. Petersen KU, Weymann N, Schelb Y, et al. Pathological Internet use--epidemiology, diagnostics, co-occurring disorders and treatment. Fortschritte der Neurologie Psychiatrie.
2009;77(5):263271 [Article in German].
17. Greenfield DN. Psychological characteristics of compulsive internet use: a preliminary analysis. Cyberpsychol Behav. 1999;2(5):403412.
18. Shaw M, Black DW. Internet addiction: definition, assessment, epidemiology and clinical management. CNS Drugs. 2008;22(5):353365.
19. Fortson BL, Scotti JR, Chen YC, et al. Internet use, abuse, and dependence among students at a southeastern regional university. J Am Coll Health. 2007:56(2):137144.
20. Christakis DA, Moreno MM, Jelenchick L, et al. Problematic internet usage in US college students: a pilot study. BMC Med. 2011;9:77.
21. Moreno MA, Jelenchick L, Cox E, et al. Problematic internet use among US youth: a systematic review. Arch Ped Adolesc Med. 2011;165(9):797805
22. Durkee T, Kaess M, Carli V, et al. Prevalence of pathological internet use among adolescents in Europe: demographic and social factors. Addiction. 2012;107(12):22102222.
23. te Wildt BT, Putzig I, Zedler M, et al. Internet dependency as a symptom of depressive mood disorders. Psychiat Prax. 2007;34 Suppl 3:S31822 [Article in German].
24. Kratzer S, Hegerl U. Is Internet Addiction a disorder of its own?a study on subjects with excessive internet use. Psychiat Prax. 2008;35(2):8083 [Article in German].
25. Morrison CM, Gore H. The relationship between excessive Internet use and depression: a questionnaire-based study of 1,319 young people and adults. Psychopathology.
2010;43(2):121126.
26. De Berardis D, DAlbenzio A, Gambi F, et al. Alexithymia and its relationships with dissociative experiences and Internet addiction in a nonclinical sample. Cyberpsychol
Behavr. 2009;12(1):6769.
27. Kormas G, Critselis E, Janikian M, et al. Risk factors and psychosocial characteristics of potential problematic and problematic internet use among adolescents: a crosssectional study. BMC Public Health. 2011;11:595.
28. Ha JH, Kim SY, Bae SC, et al. Depression and Internet addiction in adolescents. Psychopathology. 2007;40(6):424430.
29. Kim K, Ryu E, Chon MY, et al. Internet addiction in Korean adolescents and its relation to depression and suicidal ideation: a questionnaire survey. Internat J Nurs Stud.
2006;43(2):185192.
30. Park JW, Park KH, Lee IJ, et al. Standardization study of internet addiction improvement motivation scale. Psychiat Invest. 2012;9(4):373378.
31. Yen JY, Ko CH, Yen CF, et al. The comorbid psychiatric symptoms of Internet addiction: attention deficit and hyperactivity disorder (ADHD), depression, social phobia,
and hostility. J Adolesc Health. 2007;41(1):9398.
32. Yen JY, Yen CF, Chen CS, et al. The association between adult ADHD symptoms and internet addiction among college students: the gender difference. Cyberpsychol Behav.
2009;12(2):187191.
33. Yen JY, Ko CH, Yen CF, et al. The association between harmful alcohol use and Internet addiction among college students: comparison of personality. Psychiat Clin Neurosci.
2009;63(2):218224.
34. Wei HT, Chen MH, Huang PC, et al. The association between online gaming, social phobia, and depression: an internet survey. BMC Psychiat. 2012;12:92.
35. Carli V, Durkee T, Wasserman D, et al. M. The association between pathological internet use and comorbid psychopathology: a systematic review. Psychopathology.
2013;46(1):113. doi:10.1159/000337971.
127
L003309 : Internet and Videogame Addiction: Clinical Implications for Assessment and Treatment
36. Achab S, Nicolier M, Mauny F, et al. Massively multiplayer online role-playing games: comparing characteristics of addict vs non-addict online recruited gamers in a French
adult population. BMC Psychiat. 2011;11:144.
37. Zanetta Dauriat F, Zermatten A, et al. Motivations to play specifically predict excessive involvement in massively multiplayer online role-playing games: evidence from an
online survey. European Addiction Res. 2011;17(4):1859.
38. Billieux J, Chanal J, Khazaal Y, et al. Psychological predictors of problematic involvement in massively multiplayer online role-playing games: illustration in a sample of male
cybercaf players. Psychopathology. 2011;44(3):16571.
39. Lin MP, Ko HC, Wu JY. Prevalence and psychosocial risk factors associated with internet addiction in a nationally representative sample of college students in Taiwan.
Cyberpsychol Behav Soc Netw. 2011;14(12):7416.
40. Sun DL, Chen ZJ, Ma N, et al. Decision-making and prepotent response inhibition functions in excessive internet users. CNS Spectrum. 2009;14(2):7581.
41. Ko CH, Hsiao S, Liu GC, et al. The characteristics of decision making, potential to take risks, and personality of college students with Internet addiction. Psychiat Res.
2010;170(12):121125.
42. Dong G, Zhou H, Zhao X. Male Internet addicts show impaired executive control ability: evidence from a color-word Stroop task. Neurosci. Lett. 2011; 499(2):1148.
43. Zhou Z, Yuan G, Yao J. Cognitive biases toward Internet game-related pictures and executive deficits in individuals with an Internet game addiction. PLoS One.
2012;7(11):e48961.
44. Loftus GA, Loftus EF. Mind at Play: The Psychology of Video Games. New York: Basic Books; 1983.
45. Griffiths M, Wood RTA. Risk factors in adolescence: the case of gambling, videogame playing and the internet. J Gambling Studies. 2000;16(2/3):199225.
46. Griffiths MD, Meredith A. Videogame Addiction and its Treatment. J Contemp Psychother. 2009;39:247253.
47. Spence SA. Nintendo hallucinations: a new phenomenological entity. Irish J Psychol Med. 1993;10:9899.
48. Schink JC. Nintendo enuresis. Am J Diseases Child. 1991;145:1094.
49. Corkery JC. Nintendo power. Am J Diseases Child.1990;144;959.
50. McCowan TC. Space Invaders wrist. New Eng J Med. 1981;304:1368.
51. Miller DLG. Nintendo neck. Can Med Assoc J. 1991;145:1202.
52. Reinstein, L. de Quervains stenosing tenosynovitis in a video games player. Arch Physical Med Rehab. 1983;64:434435.
53. Brasington, R. Nintendinitis. New Engl J Med. 1990;322:14731474.
54. Casanova J, Casanova J. Nintendinitis. J Hand Surg. 1991;16:181.
55. Siegal IM. Nintendonitis. Orthopedics. 1991;14:745.
56. Cleary AG, Mckendrick H, Sills JA. Hand-arm vibration syndrome may be associated with prolonged use of vibrating computer games. Brit Med J. 2002;324:301.
57. Mirman MJ, Bonian VG. Mouse elbow: a new repetitive stress injury. J Am Osteopathic Assoc. 1992;92:701.
58. Friedland RP, St. John JN. Video-game palsy: distalulnar neuropathy in a video game enthusiast. New Engl J Med. 1984;311:5859.
59. Chuang YC. Massively multiplayer online role-playing game-induced seizures: a neglected health problem in Internet addiction. Cyberpsychol Behav. 2006;9(4):4516
60. Kuss DJ, Griffiths MD. Online social networking and addictiona review of the psychological literature. Int J Environ Res Pub Health. 2011;8(9):3528552.
61. Park HS, Kim SH, Bang SA, et al. Altered regional cerebral glucose metabolism in internet game overusers: a 18F-fluorodeoxyglucose positron emission tomography study.
CNS Spectr. 2010;15(3):159166.
62. Dong G, Huang J, Du X. Alterations in regional homogeneity of resting-state brain activity in internet gaming addicts. Behav Brain Funct. 2012;8:41.
63. Liu J, Gao XP, Osunde I, et al. Increased regional homogeneity in internet addiction disorder a resting state functional magnetic resonance imaging study. Chin Med J
(Engl). 2010;123(14):19048.
64. Kuhn S, Romanowski A, Schilling C, et al. The IMAGEN Consortium. The neural basis of video gaming, Transl Psychiatry. 2011;e53.
65. Zhou Y, Lin FC, Du YS, et al. Gray matter abnormalities in internet addiction: a voxel-based morphometry study. Eur J Radiol. 2011;79(1):925.
66. Han DH, Lyoo IK, Renshaw PF. Differential regional gray matter volumes in patients with on-line game addiction and professional gamers. J. Psychiatr. Res.
2012;46:507515.
67. Lin F, Zhou Y, Du Y, et al. Abnormal white matter integrity in adolescents with internet addiction disorder: a tract-based spatial statistics study. PLoS ONE. 2012;7(1):e30253.
68. Yuan K, Qin W, Wang G, et al. Microstructure abnormalities in adolescents with Internet Addiction Disorder. PloS One. 2011;6:e20708.
69. Hoeft F, Watson CL, Kesler SR, et al. Gender differences in the mesocorticolimbic system during computer game-play. J Psychiat Res. 2008;42(4):253258.
70. Ko CH, Liu GC, Hsiao S, et al. Brain activities associated with gaming urge of online gaming addiction. J Psychiatr Res. 2009;43(7):73947.
71. Han DH, Kim YS, Lee YS, et al. Changes in cue-induced, prefrontal cortex activity with video-game play. Cyberpsychol Behav Soc Netw. 2010;13(6):65561.
72. Ko CH, Liu GC, Yen JY, et al. Brain correlates of craving for online gaming under cue exposure in subjects with Internet gaming addiction and in remitted subjects. Addict
Biol. 2013;18(3):55969.
73. Ko CH, Liu GC, Yen JY, et al. The brain activations for both cue-induced gaming urge and smoking craving among subjects comorbid with Internet gaming addiction and
nicotine dependence. J Psychiatr Res. 2013;47(4):486493.
74. Kim SH, Baik SH, Park CS, et al. Reduced striatal dopamine D2 receptors in people with Internet addiction. Neuroreport. 2011;22(8):40711.
75. Hou H, Jia S, Hu S, et al. Reduced striatal dopamine transporters in people with internet addiction disorder. J Biomed Biotechnol. 2012;854524.
128
L003309 : Internet and Videogame Addiction: Clinical Implications for Assessment and Treatment
76. Koepp MJ, Gunn RN, Lawrence AD, et al. Evidence for striatal dopamine release during a video game. Nature. 1998;393:266268.
77. Weinstein A. Computer and video game addiction. Am J Drug Alc Abuse. 2010;36(5):268276.
78. Kalke J, Raschke P. Learning by doing: initiated abstinence, a school-based programme for the prevention of addiction. Results of an evaluation study. European Addiction
Res. 2004;10(2):8894.
79. Shek DT, Tang VM, Lo CY. Evaluation of an Internet addiction treatment program for Chinese adolescents in Hong Kong. Adolescence. 2009;44(174):35973.
80. Young KS. Cognitive behavior therapy with Internet addicts: treatment outcomes and implications. Cyberpsychol Behav. 2007;10(5):671679.
81. Du YS, Jiang W, Vance A. Longer term effect of randomized, controlled group cognitive behavioural therapy for Internet addiction in adolescent students in Shanghai.
Australia and New Zealand J Psychiat. 2010;44(2);12934.
82. Han D, Lee Y, Na C, et al. The effect of methylphenidate on Internet video game play in children with attention-deficit/hyperactivity disorder. Comp Psychiat.
2009;50(3):251256.
83. DellOsso B, Altamura AC, Hadley SJ, et al. An open-label trial of escitalopram in the treatment of impulsive-compulsive internet usage disorder. European
Neuropsychopharmacol. 2007;16:S82S83.
84. Han DH, Hwang JW, Renshaw PF. Bupropion sustained release treatment decreases craving for video games and cue-induced brain activity in patients with Internet video
game addiction. Exp Clin Psychopharmacol. 2010;18(4):297304.
85. Weinstein A, Greif J, Yemini Z, et al. Attenuation of cue-induced smoking urges and brain reward activity in successfully treated smokers with bupropion. J Psychopharmacol.
2010;24:829838.
86. Han, D.H., Renshaw, P.F. Bupropion in the treatment of problematic online game play in patients with major depressive disorder. J Psychopharmacol. 2012;26(5):689696.
87. Camardese G, De Risio L, Di Nicola M, et al. A role for pharmacotherapy in the treatment of internet addiction. Clin Neuropharmacol. 2012;35(6):283289.
88. King DL, Delfabbro PH, Griffiths MD, et al. Assessing clinical trials of Internet addiction treatment: a systematic review and CONSORT evaluation. Clinical Psychology
Review. 2011;31(7):11101116.
89. Winkler A, Drsing B, Rief W, et al. Treatment of internet addiction: a meta-analysis. Clin Psychol Rev. 2013;33(2):317329.
129
L003309 : Internet and Videogame Addiction: Clinical Implications for Assessment and Treatment
L003309
Multiple-Choice Questions
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
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.
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
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
L003310
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
Introduction
Disaster
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
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
137
Properties18
Adaptive Capacities19
Features22
Robustness
Economic Development
Community engagement
Participation
Redundancy
Social Capital
Community Competence
Resources
Communication
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
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
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
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
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
Social Capital
140
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
142
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
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.
143
References
1.
2.
Cottrell LS Jr. The competent community. In: Kaplan BH, Wilson RN, Leighton AH, eds. Further Explorations in Social Psychiatry. New York: Basic Books, Inc.;
1976:195-209.
3.
Institute of Medicine of the National Academies. The Future of the Publics Health in the 21st Century. Washington, DC: The National Academies Press; 2003. http://www.
nap.edu/catalog.php?record_id=10548. Accessed September 1, 2013.
4.
5.
Kulig JC. Community resiliency: The potential for community health nursing theory development. Public Health Nurs. 2000;17(5):374-385.
6.
Institute of Medicine of the National Academies. Preparing for the Psychological Consequences of Terrorism: A Public Health Strategy. Washington, DC: The National Academies
Press; 2003. http://www.nap.edu/catalog.php?record_id=10717. Accessed September 1, 2013.
7.
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.
1997;185(8):519-522.
8.
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.
9.
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.
13. Gibbon M, Labonte R, Laverack G. Evaluating community capacity. Health Soc Care Community. 2002;10(6):485-491.
14. Goeppinger J, Baglioni AJ Jr. Community competence: A positive approach to needs assessment. Am J Community Psychol. 1985;13(5):507-523.
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
capacity to provide a basis for measurement. Health Educ Behav. 1998;25(3):258-278.
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
and enhance the seismic resilience of communities. Earthquake Spectra. 2003;19(4):733-752.
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:
Program on Information Resources Policy; 2005. http://www.pirp.harvard.edu/pubs_pdf/longsta/longsta-p05-3.pdf. Accessed September 1, 2013.
22. Chandra A, Acosta JD. Building Resilient Communities: An Online Training: Users Guide and Audio Transcript. Santa Monica, CA: RAND Corporation; 2013. http://
www.rand.org/pubs/tools/TL109.html. Accessed September 1, 2013.
23. Pfefferbaum RL, Klomp RW. Community resilience, disasters, and the publics health. In: Murphy FG, ed. Community Engagement, Organization, and Development for
Public Health Practice. New York: Springer Publishing Company; 2013:275-298.
24. Pfefferbaum B, Reissman D, Gurwitch R, Steinberg A, Montgomery J. Executive Summary: Community Resilience Mini-summit: Developing Community Resilience for
Children and Families. Los Angeles: National Child Traumatic Stress Network; March 24-25, 2004.
25. Friedman MJ. Every crisis is an opportunity. CNS Spectrums. 2005;10(2):96-98.
26. Pfefferbaum B, Flynn BW, Schonfeld D, Brown LM, Jacobs GA, Dodgen D, Donato D, Kaul RE, Stone B, Norwood AE, Reissman DB, Herrmann J, Hobfoll SE, Jones
RT, Ruzek JI, Ursano RJ, Taylor RJ, Lindley D. The integration of mental and behavioral health into disaster preparedness, response, and recovery. Disaster Med Public
Health Prep. 2012;6(1):60-66.
27. Auf der Heide E. Disaster Response: Principles of Preparation and Coordination. St. Louis: CV Mosby; 1989 (original). http://www.coe-dmha.org/Media/Disaster_Response_
Principals.pdf. Accessed September 1, 2013.
28. American Psychiatric Association. Disaster Psychiatry. http://www.psychiatry. org/practice/professional-interests/disaster-psychiatry. Accessed September 1, 2013.
29. Centers for Disease Control and Prevention. Coping with a Disaster or Traumatic Event. http://emergency.cdc.gov/mentalhealth. Accessed September 1, 2013.
30. Substance Abuse and Mental Health Services Administration. http://www.samhsa.gov. Accessed September 1, 2013.
31. Medical Reserve Corps. http://www.medicalreservecorps.gov. Accessed September 1, 2013.
32. American Red Cross. http://www.redcross.org. Accessed September 1, 2013.
33. American Psychological Association. Disaster Response Network. http://www.apa.org/practice/programs/drn. Accessed September 1, 2013.
145
L003310
Multiple-Choice Questions
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.
147
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.
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.
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