Child and Adolescent Psychopathology E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 1991

Veröffentlichungsjahr: 2016

Beschreibung

A unique, multi-discipline, developmental approach to childhood psychopathology

Child and Adolescent Psychopathology is the only comprehensive text in the field to address genetic, neurobiological, and environmental factors within a developmental context. Based on cutting-edge research and aligned with the DSM-5, this book emphasizes how, when, and why disorders emerge among young people, and the ways in which symptom profiles change at different stages of development. This new third edition has been updated to include new chapters on OCD and trauma disorders consistent with DSM-5 classification, and includes new discussion on epigenetics and the neighborhood effects on the development of delinquency. Coverage includes extensive discussion of risk factors, from disturbed attachment relations and abuse/neglect, to head injury and teratogen exposure, followed by in-depth examination of behavior disorders and psychological disorders including Autism Spectrum, Schizophrenia Spectrum, and Eating Disorders.

Psychological disorders in children are increasingly being explored from a relational perspective, and continuous advances in neurobiology research are adding an additional dimension to our understanding of cause, effect, and appropriate intervention. This book provides detailed guidance toward all aspects of childhood psychopathology, with a multi-discipline approach and a unique developmental emphasis.

• Discover how psychopathology emerges throughout the stages of development
• Learn how both genetics and environmental factors influence risk and behaviors
• Understand the prevalence, risk factors, and progression of each disorder
• Gain deep insight from leading experts in neurobiology and developmental psychopathology

As the field of child psychology continues to evolve, behavioral and psychological disorders move beyond a list of symptoms to encompass the 'whole child'—biology, chemistry, environment, and culture are becoming increasingly relevant in understanding and treating these disorders, and must be considered from the earliest assessment stages. Child and Adolescent Psychopathology provides comprehensive information on childhood disorders from a developmental perspective.

Leseprobe

Table of Contents

Cover

Title Page

Copyright

Foreword

Preface

List of Contributors

PART I: THE DEVELOPMENTAL PSYCHOPATHOLOGY APPROACH TO UNDERSTANDING MENTAL ILLNESS

Chapter 1: Developmental Psychopathology as a Scientific Discipline: A 21st-Century Perspective

Relevance And Importance

Principles of DP

Summary

Chapter Contents

References

Chapter 2: Classifying Psychopathology: The DSM, Empirically Based Taxonomies, and the Research Domain Criteria

Historical Context

The

DSM

and Developmental Psychopathology

Empirically Derived Classification Systems

The Research Domain Criteria

Conclusions

References

Chapter 3: Genetic, Environmental, and Epigenetic Influences on Behavior

Historical Context

The Developmental Psychopathology Perspective

Terminological and Conceptual Issues

Psychiatric Genetics

Gene-Environment Interdependence

Epigenesis

Genetics of Comorbidity

Genetics of Continuity

Summary and Conclusions

References

PART II: VULNERABILITIES AND RISK FACTORS FOR PSYCHOPATHOLOGY

Chapter 4: Risk and Resilience in Child and Adolescent Psychopathology

Historical Context

Contemporary Terminological And Conceptual Issues

Unifying Concepts for Understanding Risk and Resilience: Current Perspectives on Stress, Coping, and Emotion Regulation

Risk and Resilience: Children of Depressed Parents

Conclusions

References

Chapter 5: Child Maltreatment and Risk for Psychopathology

Epidemiology of Abuse and Neglect

Maltreatment and Children's Risk For Psychopathology

Is the Association Between Maltreatment and Psychopathology Causal?

Etiological Formulations

Moderators of Child Maltreatment

Conclusions

References

Chapter 6: Impulsivity and Vulnerability to Psychopathology

Historical Context

Terminological and Conceptual Issues

Etiological Formulations

Genetics and Heritability

Impulsivity and Vulnerability to Psychopathology

Research Domain Criteria Framework

Synthesis and Future Directions

References

Chapter 7: High-Reactive Temperament, Behavioral Inhibition, and Vulnerability to Psychopathology

Historical Context

Diagnostic Issues

The Etiological Role of Temperaments

High- and Low-Risk Infants: Developmental Progression

Synthesis

References

Chapter 8: The Adaptive Calibration Model of Stress Responsivity: Concepts, Findings, and Implications for Developmental Psychopathology

Historical Context

Conditional Adaptation and Maladaptation

Functions of the Stress Response System

Environmental Information

Patterns of Responsivity

Adaptive Calibration and the Allostatic Load Model

Conclusion

References

Chapter 9: Exposure to Teratogens as a Risk Factor for Psychopathology

Introduction and Etiological Formulations

Historical Context

Terminological and Conceptual Issues

Mental Health Outcomes in FASD

Psychopathology Related to Other Prenatal Exposures

Conclusions

Risk and Protective Factors

Synthesis and Future Directions

References

Chapter 10: Brain Injury and Vulnerability to Psychopathology

Historical Context

Terminological and Conceptual Issues

Prevalence

Etiological Formulations

Developmental Considerations

Brain Injury and the Frontal Lobes

Clinical Considerations

Summary and Conclusions

References

Chapter 11: Emotion Dysregulation as a Vulnerability to Psychopathology

Historical Context

Terminological and Conceptual Issues

Emotion Dysregulation From a Clinical Perspective

Etiological Formulations

Heritability of Emotion Dysregulation

Summary and Conclusions

References

Chapter 12: Neighborhood Effects on the Development of Delinquency

Historical Context

Etiology

Developmental Progression

Sex Differences

Cultural Considerations

Summary and Conclusions

References

PART III: EXTERNALIZING DISORDERS

Chapter 13: Attention-Deficit/Hyperactivity Disorder

Historical Context

Terminological and Conceptual Issues

Diagnostic Issues and

DSM

Criteria

Prevalence

Risk Factors and Etiological Formulations

Developmental Progression

Comorbidity

Sex Differences

Cultural Considerations

Protective Factors

Theoretical Synthesis

Summary and Conclusions

References

Chapter 14: Oppositional Defiant Disorder, Conduct Disorder, and Juvenile Delinquency

Introduction

Terminological and Conceptual Issues

Comorbidity

Considering Development and Sex Differences

Prevalence and Age of Onset

Adolescent and Adult Outcomes of Childhood ODD and CD

Vulnerabilities to and Risk Factors for Conduct Problems

Neural Mechanisms

Theoretical Synthesis

Unresolved Questions and Future Directions

Validity of Diagnostic Subtypes of CD

References

Chapter 15: Substance Use Disorders

Introduction

Prevalence of Alcohol and Other Drug Use

DSM-5

Criteria and Diagnostic Issues

Historical Context and Etiological Formulations

Environmental Risk Factors and Genetic Vulnerabilities

Developmental Pathways to Abuse and Dependence

Effects of Adolescent Alcohol Use on Brain Development

Summary and Conclusions

References

PART IV: INTERNALIZING DISORDERS

Chapter 16: Anxiety Disorders

Historical Context

Diagnostic Issues and

DSM-5

Criteria

Prevalence

Etiology

Developmental Progression

Comorbidities

Cultural Considerations

Sex Differences

Research Domain Criteria

Summary and Conclusions

References

Chapter 17: Obsessive-Compulsive and Related Disorders

Introduction

Historical Context

DSM-5

Criteria and Diagnostic Issues

Prevalence

Developmental Progression

Sex Differences

Comorbidities

Cultural Considerations

Etiology

Neuropsychological Functioning

Research Domain Criteria

Summary and Conclusions

References

Chapter 18: Depressive Disorders

Introduction

Historical Context

Prevalence

Developmental Progression and Comorbidity

Sex Differences

Etiology

Cultural Considerations

Research Domain Criteria

Synthesis and Future Directions

References

Chapter 19: The Development of Borderline Personality and Self-Inflicted Injury

Introduction

Historical Context

Diagnostic, Terminological, and Conceptual Issues

Etiological Formulations

Familiality and Heritability

Genetics and Neurotransmitter Dysfunction

Contextual and Family Risk Factors

Summary and Conclusions

References

PART V: OTHER DISORDERS

Chapter 20: Trauma- and Stressor-Related Disorders in Infants, Children, and Adolescents

Historical Context

Etiology

Diagnostic Issues and

DSM-5

Criteria

Prevalence

Research Domain Criteria

Synthesis and Future Directions

References

Chapter 21: Bipolar Disorder

Historical Context

Episodes

Specific Bipolar Disorder Diagnoses

Problems With Diagnosis of Bipolar Disorder Among Youth

Prevalence

Etiology

Pathogenesis and Pathophysiology

Sex Differences

Comorbidities

Cultural Considerations

Research Domain Criteria

Theoretical Synthesis and Future Directions

References

Chapter 22: Autism Spectrum Disorder

Historical Context

Terminological and Conceptual Issues

Prevalence

Etiologic Formulations

Developmental Progression

Protective Factors

Synthesis and Future Directions

References

Chapter 23: Childhood-Onset Schizophrenia

Historical Context

Diagnostic Issues and

DSM-5

Criteria

Differential Diagnostic Issues

Prevalence

Sex Differences

Comorbidity

Overlap Between Autism and COS

Risk Factors

Insights into Pathophysiology

Theoretical Synthesis and Future Directions

Continuity Between COS and Adult-Onset Schizophrenia

References

Chapter 24: Eating Disorders

Historical Context

Diagnostic Issues and

DSM-5

Criteria

Prevalence

Risk Factors, Protective Factors, and Etiologic Formulations

Developmental Progression

Comorbidity

Sex Differences

Cultural Considerations

Synthesis and Future Directions

References

About the Authors

Theodore P. Beauchaine

Stephen P. Hinshaw

Author Index

Subject Index

End User License Agreement

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Guide

Table of Contents

Begin Reading

List of Illustrations

Chapter 2: Classifying Psychopathology: The DSM, Empirically Based Taxonomies, and the Research Domain Criteria

Figure 2.1 A simplified depiction of the hierarchical latent structure of psychopathology.

Chapter 3: Genetic, Environmental, and Epigenetic Influences on Behavior

Figure 3.1 The general latent structure of psychopathology, as determined by twin, adoption, and population-based studies.

Figure 3.2 The bifactor structure of psychopathology, including a superordinate general vulnerability factor (see Caspi et al., 2014; Lahey et al., 2011; Lahey et al., 2012).

Chapter 8: The Adaptive Calibration Model of Stress Responsivity: Concepts, Findings, and Implications for Developmental Psychopathology

Figure 8.1 Predicted curvilinear relation between developmental context and optimal levels of stress responsivity.

Chapter 13: Attention-Deficit/Hyperactivity Disorder

Figure 13.1 Patterns of comorbidity in the MTA study (A 14-month randomized clinical trial, 1999).

Chapter 19: The Development of Borderline Personality and Self-Inflicted Injury

Figure 19.1 Biosocial developmental model of BPD and SII.

Chapter 22: Autism Spectrum Disorder

Figure 22.1 Experience-based risk processes in autism.

List of Tables

Chapter 8: The Adaptive Calibration Model of Stress Responsivity: Concepts, Findings, and Implications for Developmental Psychopathology

Table 8.1 Comparison of Adaptive Calibration Model (ACM) and Allostatic Load Model (ALM)

Chapter 13: Attention-Deficit/Hyperactivity Disorder

Table 13.1 Summary of Brain Imaging Findings in ADHD

Table 13.2 Summary of Neuropsychological Findings in ADHD

Child and Adolescent Psychopathology

Third Edition

Edited by

Theodore P. Beauchaine

Stephen P. Hinshaw

Copyright © 2017 by John Wiley & Sons, Inc. All rights reserved.

Published by John Wiley & Sons, Inc., Hoboken, New Jersey.

Published simultaneously in Canada.

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Library of Congress Cataloging-in-Publication Data

Names: Beauchaine, Theodore P., editor. | Hinshaw, Stephen P., editor.

Title: Child and adolescent psychopathology / edited By Theodore P. Beauchaine, Stephen P. Hinshaw.

Description: Third edition. | Hoboken, N.J. : John Wiley & Sons Inc., [2017] | Includes bibliographical references and index.

Identifiers: LCCN 2016026246 | ISBN 9781119169956 (cloth) | ISBN 9781119169963 (epdf) | ISBN 9781119169970 (epub)

Subjects: LCSH: Child psychopathology. | Adolescent psychopathology.

Classification: LCC RJ499 .C48237 2016 | DDC 618.92/89—dc23 LC record available at https://lccn.loc.gov/2016026246

THIRD EDITION

Foreword

The remarkable third edition of Child and Adolescent Psychopathology represents an academic tour de force presenting the science of development associated with progressions to mental disorder. These processes are typically multiple and interacting. Indeed, their importance is clear, as neurodevelopmental models of psychopathology are dominant today. Sadly, both stigmatization—primarily from profound misunderstanding of mental disorders—and low economic status remain barriers to research and treatment (Martinez & Hinshaw, 2016; Merikangas et al., 2011).

The chapters show remarkable breadth, including the challenge of integrating genetics, brain imaging, brain trauma, and prenatal and physiological as well as environmental variables in a clinically meaningful way. Clinicians have already benefitted from studies detailing patterns of continuity and discontinuity. Indeed, such investigations can help to prevent premature prediction and labeling that in itself may be harmful. These models, as well as the transactional nature of many dysfunctional behaviors, preclude simplistic causal pathways.

Brain imaging has yet to contribute to clinical diagnosis and care, even though longitudinal and large-sample cross-sectional studies are starting to indicate subpopulation developmental brain phenotypes that have integrative potential for developmental psychopathology (Giedd et al., 2015; Gur, 2016). For example, it is possible that different developmental trajectories in attention-deficit/hyperactivity disorder reflect alternate clinical forms, as delayed cortical developmental may well relate to greater improvement in adolescence (Shaw et al., 2013).

In our sister science of developmental neurobiology, true “clinical breakthroughs” have emerged, such as the use of rapamycin for tuberous sclerosis (Franz et al., 2006), and magnesium infusion for prevention of cerebral palsy (Rouse et al., 2008). These are large-effect-size interventions of interest to child psychiatrists because of associated psychopathologies in these conditions. Both were serendipitous discoveries, which by definition cannot be planned. At the same time, it remains troubling how much risk remains embedded in political arenas of community infrastructure (e.g., support for schools, housing, and law enforcement). We must transcend psychobiology to incorporate multiple levels of analysis, as amply shown in the following chapters.

The Research Domain Criteria (RDoC; Cuthbert, 2014), highlighted in a number of chapters, do not represent a truly new approach. Dimensional as well as categorical measures have been hallmarks of NIH-funded psychiatric research for decades (Weinberger, Glick, & Klein, 2015), and neurobiologically founded, multiple-levels-of analysis research has contributed to key advances in our understanding of etiology since at least the mid-20th century (Beauchaine & Thayer, 2015). Evidence is mounting for age- and category-related interactions with dimensional brain MRI measures (e.g., Wiggins et al., 2016). In all, the RDoC provides a useful and surprisingly interactive set of measures.

Finally, I found inspiration in the several authors who reviewed the predictive and possible treatment implications of regulatory physiological measures for developmental psychopathology. Ultimately, these models will be judged on when and how these regulatory processes can be changed, given the complexity of initial measurements and the potential for highly individualized treatment plans. One might read this entire volume as a basis for future personalized therapies, paralleling the present movement in medicine. In all, the chapters herald considerable promise for the future.

Judith L. Rapoport, MDChief, Child Psychiatry BranchNational Institute of Mental Health10 Center Drive Building 10, Room 3 N202Bethesda, MD 20892-1600

REFERENCES

Beauchaine, T. P., & Thayer, J. F. (2015). Heart rate variability as a transdiagnostic biomarker of psychopathology.

International Journal of Psychophysiology

, 98, 338–350.

Cuthbert, B. N. (2014). The RDoC framework: Facilitating transition from ICD/DSM to dimensional approaches that integrate neuroscience and psychopathology.

World Psychiatry

, 13, 28–35.

Franz, D. N., Leonard, J., Tudor, C., Chuck, G., Care, M., Sethuraman, G.,…Crone, K. R. (2006). Rapamycin causes regression of astrocytomas in tuberous sclerosis complex.

Annals of Neurology

, 59, 490–498.

Giedd, J. N., Raznahan, A., Alexander-Bloch, A., Schmitt, E., Gogtay, N., & Rapoport, J. L. (2015). Child psychiatry branch of the National Institute of Mental Health longitudinal structural magnetic resonance imaging study of human brain development.

Neuropsychopharmacology

, 40, 43–49.

Gur, R. C. (2016). Prospective community studies linking cognitive deficits to subclinical symptoms and a step toward precision medicine.

JAMA Psychiatry

, 73, 109–110.

Martinez, A., & Hinshaw, S. P. (2016). Mental health stigma: Theory, developmental issues, and research priorities. In D. Cicchetti (Ed.),

Developmental psychopathology: Vol. 4. Risk, resilience, and intervention

(3rd ed., pp. 997–1039). Hoboken, NJ: Wiley.

Merikangas, K. R., He, J. P., Burstein, M., Swendsen, J., Avenevoli, S., Case, B.,…Olfson, M. (2011). Service utilization for lifetime mental disorders in U.S. adolescents: Results of the National Comorbidity Survey-Adolescent Supplement (NCS-A).

Journal of the American Academy of Child and Adolescent Psychiatry

, 50, 32–45.

Rouse, D. J., Hirtz, D. G., Thom, E., Varner, M. W., Spong, C. Y., Mercer, B. M.,…Roberts, J. M. (2008). A randomized, controlled trial of magnesium sulfate for the prevention of cerebral palsy.

New England Journal of Medicine

, 359, 895–905.

Shaw, P., Malek, M., Watson, B., Greenstein, D., de Rossi, P., & Sharp, W. (2013). Trajectories of cerebral cortical development in childhood and adolescence and adult attention-deficit/hyperactivity disorder.

Biological Psychiatry

, 74, 599–606.

Weinberger, D. R., Glick, I. D., & Klein, D. F. (2015). Whither Research Domain Criteria (RDoC)?: The good, the bad, and the ugly.

JAMA Psychiatry

, 72, 1161–1162.

Wiggins, J. L., Brotman, M. A., Adleman, N. E., Kim, P., Oakes, A. H., Reynolds, R. C.,…Leibenluft, E. (2016). Neural correlates of irritability in disruptive mood dysregulation and bipolar disorders.

American Journal of Psychiatry

. Epub ahead of print.

Preface

As we noted in the preface of the second edition of Child and Adolescent Psychopathology (Beauchaine & Hinshaw, 2013), global costs of mental illness—in terms of morbidity, mortality, and other forms of human suffering—are staggering. In many developed countries including the United States, over one third of individuals suffer from a major psychiatric disorder at some point in their lives (Kessler et al., 2009). In low- and middle-income countries, mental disorders account for 25% and 34%, respectively, of total years lived with disability, yet most of those affected receive no treatment (WHO World Mental Health Survey Consortium, 2004). Although treatment rates are slightly higher in wealthy countries, mental disorders continue to carry significant stigma. As a result, many avoid seeking help, and a lack of treatment parity remains for mental disorders vs. other health-related conditions (Hinshaw, 2007; Martinez & Hinshaw, 2016).

When the two of us met nearly 18 years ago, knowledge of the causes of mental illnesses was quite limited compared to today. Although behavioral genetics studies had shown that most psychiatric disorders are at least moderately heritable, little was known about molecular genetic, neural, or hormonal mechanisms of heritability. Moreover, neither epigenetic alterations in gene expression, nor rare structural variants, had been identified as possible mechanisms through which environment might confer vulnerability to psychopathology. Many prevailing models of mental illness still pitted nature and nurture against each other as competing causes of psychopathology. Transactional models, in which biological vulnerabilities are presumed to interact with environmental risk factors to eventuate in mental illness, were few in number and limited in specification of neurobiological mechanisms, as advanced neuroimaging was in still in its infancy.

Given limitations in technology, most of what we learned about mental illness has traditionally been obtained through observation and classification of symptoms (see Chapter 2 [Beauchaine & Klein]). Although useful in early stages of identifying different forms of mental illness, symptom classification often tells us little if anything about underlying causal processes—be they biological or environmental—that lead to particular disorders. In editing this book, we therefore sought authors with expertise in the developmental psychopathology perspective, which emerged only about 35 years ago (see Chapter 1 [Hinshaw]). This perspective follows from the observation that human behavioral traits—including those that predispose to psychopathology—almost always arise from complex transactions between biological vulnerabilities and exposure to environmental risks across development. For example, heritable conditions such as attention-deficit/hyperactivity disorder, depression, schizophrenia, and substance dependence are shaped strongly by environmental influences, and effects of environmentally transmitted risks such as child maltreatment are moderated by genes and other biological predispositions (see e.g., Beauchaine & McNulty, 2013). Furthermore, through epigenetic mechanisms, the expression of several genes that are implicated in behavior regulation can be altered by experience, including exposure to stress and trauma—findings that defy anachronistic distinctions derived from reductionistic models. Thus, we asked all authors to identify both biological and environmental contributors to psychopathology and to discuss how these interact and transact across development to amplify risk.

This dynamic view of mental disorders served as the impetus for both the first and second editions of this book, and continues as a driving force behind the current third edition, which includes substantially updated material. Before the first edition was published, most graduate-level psychopathology texts were organized around the symptom-based approach to classifying mental illness, with limited consideration of the genetic and neural underpinnings of behavior or the interplay between biological vulnerabilities and environmental risk factors across development. However, in the nine years since the first edition was published, appreciation for the complexity of such transactions in the development of psychopathology has increased, and many new and exciting findings have emerged (see e.g., Beauchaine & Goodman, 2015).

Elucidating causes of mental illness is an international public health concern. The better we understand etiology across all relevant levels of analysis, including genetic, neural, familial, and cultural (to name a few), the better position we are in to devise more effective prevention and intervention programs (Beauchaine, Neuhaus, Brenner, & Gatzke-Kopp, 2008). Thus, even though this text does not address treatment, we hope readers will keep in mind while digesting each chapter how important it is to identify causes of mental illness in our efforts to reduce human suffering. This motivation played a central role in the National Institute of Mental Health (2015) establishing the Research Domain Criteria (RDoC) project. RDoC is a collaboration between NIMH and researchers around the world to develop a neuroscience-informed system of characterizing psychopathology that identifies genetic, neural, hormonal, and social determinants of major behavioral systems that contribute to human function, and at the extremes, mental illness (see Chapter 2 [Beauchaine & Klein]).

Readers will likely note that some disorders that are often addressed in psychopathology texts are not included in this book. For example, we do not cover developmental disorders or intellectual disability. In omitting these disorders, we are not implying that they are unimportant. Rather, the vast literature on developmental disabilities makes it difficult to cover the topic adequately in a text that already includes 24 chapters. Thus, we were left with a difficult choice, and we decided not to limit coverage of the conditions contained herein. We refer interested readers to other sources (e.g., Burack, Hodapp, Iarocci, & Zigler, 2011) for excellent coverage of this domain.

We now invite you to join us in the quest for a deeper understanding of the development of mental disorders, which almost always originate in childhood and adolescence. We hope that our emphases on genetic and other biological vulnerabilities, and how these interact with environmental risk factors and contexts will challenge any preconceived notions you may have about what is “biological” and what is “environmental” in relation to normal and atypical development. We hope as well that our coverage will prompt the next generation of investigators, clinicians, and policymakers to pursue the daunting but essential goal of explaining, treating, and preventing the devastation that so often accompanies psychopathology.

Theodore P. BeauchaineStephen P. Hinshaw

REFERENCES

Beauchaine, T. P., & Goodman, S. H. (Eds.). (2015). Ontogenic process models of psychopathology [Special Section].

Journal of Abnormal Psychology

,

124

, 771–877.

Beauchaine, T. P., & Hinshaw, S. P. (2013). Preface. In T. P. Beauchaine & S. P. Hinshaw (Eds.),

Child and adolescent psychopathology

(2nd ed., pp. xi–xiii). Hoboken, NJ: Wiley.

Beauchaine, T. P., & McNulty, T. (2013). Comorbidities and continuities as ontogenic processes: Toward a developmental spectrum model of externalizing behavior.

Development and Psychopathology

,

25

, 1505–1528.

Beauchaine, T. P., Neuhaus, E., Brenner, S. L., & Gatzke-Kopp, L. (2008). Ten good reasons to consider biological processes in prevention and intervention research.

Development and Psychopathology

,

20

, 745–774.

Burack, J. A., Hodapp, R. M., Iarocci, G., & Zigler, E. (Eds.). (2011).

The Oxford handbook of intellectual disability and development

. New York, NY: Oxford University Press.

Hinshaw, S. P. (2007).

The mark of shame: Stigma of mental illness and an agenda for change

. New York, NY: Oxford University Press.

Kessler, R. C., Aguilar-Gaxiola, S., Alonso, J., Chatterji, S., Lee, S., Ormel, J.,…Wang, P. S. (2009). The global burden of mental disorders: An update from the WHO World Mental Health (WMH) Surveys.

Epidemiologia e Psichiatria Sociale

,

18

, 23–33.

Martinez, A., & Hinshaw, S. P. (2016). Mental health stigma: Theory, developmental issues, and research priorities. In D. Cicchetti (Ed.),

Developmental psychopathology. Vol. 4: Risk, resilience, and intervention

(3rd ed., pp. 997–1039). Hoboken, NJ: Wiley.

National Institute of Mental Health. (2015).

NIMH strategic plan for research

. Retrieved from

http://www.nimh.nih.gov/about/strategic-planning-reports/index.shtml

WHO World Mental Health Survey Consortium. (2004). Prevalence, severity, and unmet need for treatment of mental disorders in the World Health Organization World Mental Health Surveys.

Journal of the American Medical Association

,

291

, 2581–2590.

List of Contributors

Peter Arnett

Pennsylvania State University

Robert F. Asarnow

UCLA School of Medicine

Theodore P. Beauchaine

The Ohio State University

Alexandra H. Bettis

Vanderbilt University

Joseph C. Blader

University of Texas Health Science Center at San Antonio

Deepika Bose

University of California, Los Angeles

Sandra A. Brown

University of California, San Diego

Gabrielle A. Carlson

State University of New York at Stony Brook

Pamela M. Cole

Pennsylvania State University

Bruce E. Compas

Vanderbilt University

Sheila E. Crowell

University of Utah

Nicole A. Crocker

San Francisco VA Medical Center

Geraldine Dawson

Duke University School of Medicine

Marco Del Giudice

University of New Mexico

Lauren R. Doyle

San Diego State University

Bruce J. Ellis

University of Utah

Susan Faja

Harvard Medical School

Megan Finsaas

State University of New York at Stony Brook

Jennifer K. Forsyth

UCLA Department of Psychology

Susanna L. Fryer

University of California San Francisco

Lisa Gatzke-Kopp

Pennsylvania State University

Brandon L. Goldstein

State University of New York at Stony Brook

Meredith Gruhn

Vanderbilt University

Sarah E. Hall

Wheaton College

Nastassia J. Hajal

University of California, Los Angeles

Stephen P. Hinshaw

University of California, Berkeley

Sara R. Jaffee

University of Pennsylvania

Wesley G. Jennings

University of South Florida

Jerome Kagan

Harvard University

Erin A. Kaufman

University of Utah

Daniel N. Klein

State University of New York at Stony Brook

Benjamin B. Lahey

University of Chicago

Mark F. Lenzenweger

State University of New York at Binghamton and Weill Cornell Medical College

Deanna Linville

University of Oregon

Sarah N. Mattson

San Diego State University

Victoria C. Merritt

Pennsylvania State University

Jessica E. Meyer

Pennsylvania State University

Emily Neuhaus

Seattle Children's Research Institute

Joel Nigg

Oregon Health and Science University

Nicholas M. Perez

University of South Florida

John Piacentini

University of California, Los Angeles

Bruce D. Perry

Child Trauma Academy

Houston, TX

Emily Ricketts

University of California, Los Angeles

Donna J. Roybal

University of Texas Health Science Center at San Antonio

Colin L. Sauder

University of Texas Health Science Center at San Antonio

Katherine E. Shannon Bowen

University of Washington

Elizabeth A. Shirtcliff

Iowa State University

Wendy K. Silverman

Yale University School of Medicine

Eric Stice

Oregon Research Institute

Kristin L. Tomlinson

University of California, San Diego

Ian R. Gizer

University of Missouri

Irwin D. Waldman

Emory University

Carl F. Weems

Iowa State University

Jennifer Winward

University of California, San Diego

PART I

THE DEVELOPMENTAL PSYCHOPATHOLOGY APPROACH TO UNDERSTANDING MENTAL ILLNESS

Chapter 1

Developmental Psychopathology as a Scientific Discipline: A 21st-Century Perspective

Stephen P. Hinshaw

Information continues to accumulate, at an increasingly rapid pace, about the complex processes and mechanisms underlying the genesis and maintenance of child and adolescent forms of mental disorder. Our major goal for this, the third edition of Child and Adolescent Psychopathology—in chapters written by international experts on the topics of interest—is to present current information, particularly surrounding core vulnerabilities and risk factors for major dimensions and categories of behavioral and emotional problems of youth. As in our prior editions (Beauchaine & Hinshaw, 2008, 2013), we emphasize psychobiological vulnerabilities in the active context of environmental forces that shape development. Framed somewhat differently, an important objective for each chapter is to delineate potential ontogenic processes in progressions to mental disorder, signifying mechanisms underlying individual development, with the realization that multiple vulnerabilities and risk factors interact and transact in case-specific yet ultimately predictable ways (Beauchaine & Hinshaw, 2016; Beauchaine & McNulty, 2013; Hinshaw, 2015). Parallel to the first two editions, we do not prioritize assessment or treatment-related information in this book, given that such coverage would necessitate a second or even third volume (e.g., Mash & Barkley, 2006, 2007).

Although the book's title focuses on children and adolescents, I note immediately that psychopathology, in many (if not most) cases, unfolds across the entire lifespan. Most so-called adult manifestations of mental disorder have origins, if not outright symptom presentations, prior to age 18. Moreover, even the earliest-appearing forms of behavioral and emotional disturbance typically portend escalating symptoms and impairments that can persist for decades (e.g., Kessler, Berglund, Demler, Jin, & Walters, 2005). Because resilience is also a possibility (Luthar, 2006), lifespan approaches to the topics of interest in this book are increasingly mandated for thorough understanding, carrying profound clinical as well as scientific implications. The child is the father of the man—and the mother of the woman—given that adults emerge from a cascading set of processes set in motion years before.

Before delving further, I immediately acknowledge the major debt that Ted Beauchaine and I owe to all of our contributors, as each is a major force in the scientific literature. We asked them to integrate state-of-the-art knowledge into the chapters that follow. Indeed, given the fast-escalating sophistication of mechanistic accounts of the development of psychopathology—which are now integrating genetic vulnerability and brain architecture in the presence of contextual forces across development, providing unprecedented levels of synthesis (Hinshaw, 2015)—no current compendium can afford to rest on the laurels of previous editions. The field's work is emerging at ever-more-detailed levels of analysis, with the promise of accounts that should, in the future, better inform evidence-based practice in the context of validated knowledge structures that can be applied to the clinical phenomena under consideration. In this initial chapter, I delineate the clinical and policy-related importance of the subject matter at hand, explicate core principles of developmental psychopathology (DP), and provide a general overview of the sequence of the chapters and their contents. In so doing I aim to set the stage for the cutting-edge advances and wisdom provided in the remainder of the volume.

RELEVANCE AND IMPORTANCE

The subject matter under consideration in this volume is at once clinically compelling and conceptually fascinating. Mental disorders yield substantial impairment, pain, and suffering for individuals, families, communities, and even cultures. The levels of personal and family tragedy involved are often devastating (Hinshaw, 2008a). At the same time, multifactorial vulnerabilities and risk factors—along with the complex, transactional developmental progressions that produce symptoms and impairments—challenge investigators from disciplines as diverse as neuroscience, genomics, public health, psychology, psychiatry, and public policy to emerge with new insights and syntheses. Overall, the clinical need is urgent and the scientific motivation compelling.

I begin with the concept of impairment. As elaborated in nearly every working guide to psychopathology (e.g., American Psychiatric Association, 2013; Wakefield, 1992), a designation of mental illness mandates, beyond behavior patterns or symptoms, that the individual in question display impairment or “harm” before a diagnosis is made. Clinically, then, attention must be paid to the often-excruciating pain and suffering attending to conditions as diverse as autism-spectrum disorders, various sequelae of maltreatment, severe attention deficits and impulsivity, interpersonal aggression, significant anxiety and mood disorders, thought disorders (including schizophrenia), eating-related conditions, self-destructive behavior patterns and personality configurations, and substance use disorders. Each is linked to setback and suffering, societal reverberations, and significant costs, the latter measurable in terms of huge expenditures borne by society, not related just to treatment per se but to the long-range outcomes of interpersonal, educational, and vocational failure that often attend to mental disorders (for an example of the huge costs linked to attention-deficit/hyperactivity disorder [ADHD], see Hinshaw & Scheffler, 2014).

Of course, impairment and harm—whether personal or experienced by others—are not sufficient for designating individuals as suffering from a mental disorder. In the view of Wakefield (1992), both harm (which involves a value-laden component) and dysfunction (a scientific construct) are required before mental illness should be diagnosed. Per Wakefield, dysfunction is “the failure of a mental mechanism to perform a natural function for which it was designed by evolution” (p. 373). Although mental health fields lack the objective markers and pathognomonic signs1 as those found in medicine and neurology (see Chapter 2 [Beauchaine & Klein]), our aim for the accumulated work in the present volume is to propel knowledge of dysfunctional mechanisms related to child and adolescent psychopathology. At the same time, findings from each chapter remind us that the origins of mental health conditions are reciprocal, dynamic, multilevel, and fully linked with processes linked to environmental context.

Not every aspect of psychopathology is necessarily impairing. At the level of evolution, it cannot be the case that mental disorder is inevitably or inexorably linked to personal failure or reduced fecundity; otherwise, how would conditions such as severe thought and mood disorders have perpetuated across human history (for evolutionary psychological explanations of mental disorder, see Neese, 2005)? Partial genetic loadings or vulnerabilities in biological relatives may well carry adaptive advantage; at least some aspects of symptoms could yield inspiration or thriving. Still, clinical and population-level facts regarding impairment linked to mental illness are stark. Emotional and behavioral problems among children and adolescents are distressingly prevalent and often lead to serious impairments in such crucial life domains as academic achievement, interpersonal competencies, and independent living skills (for thorough accounts, see Mash & Barkley, 2014). These conditions incur intensive pain for individuals, families, and communities at large, delimiting life opportunities and triggering major burdens for caregivers, school districts, and health care systems. In short, far too many young lives are compromised by mental illness.

Moreover, child and adolescent conditions and mental-health-related issues are growing in impact. As just one harrowing example, recent data from the World Health Organization reveal that, worldwide, the number-one cause of death for girls aged 15–19 years is now suicide (World Health Organization, 2014). Rates of self-injury have escalated rapidly over the past decades, and conditions like autism and ADHD are undergoing huge increases in diagnosed prevalence (e.g., Visser et al., 2014). The age of onset of serious mood disorders appears to be dropping, signaling the importance of contextual “push” in unearthing vulnerability (Hinshaw, 2009). In both the developing and developed world, serious mental disorder in youth portends major life consequences and even tragedy (see, for example, Sawyer et al., 2002).

Moving beyond childhood and adolescence per se, each year the Global Burden of Disease findings convey that a number of mental health conditions (along with neurological and substance use disorders) are among the world's most impairing illnesses (Whiteford, Ferrari, Degenhardt, Feigin, & Vos, 2015). Indeed, the variable called “years lived with disability” is dominated by individuals with mental disorders in our current era, on par with and often surpassing so-called physical diseases. By the time of adulthood, economic costs related to mental illness escalate with respect to employment-related impairments, yielding huge public-entitlement expenditures and lack of productivity. In short, from a number of important lenses, mental disorders are tragically impairing, robbing individuals of opportunities to thrive and be productive, often in the prime of their lives. If readers sense a call to action in these words, they have read my intentions precisely.

Crucially, mental health and physical health are inexplicably intertwined. It is now well known that serious mental disorder is associated with reductions in life expectancy averaging from 10 to 25 years (e.g., Chang et al., 2011). The reasons here are plentiful: high-risk lifestyles, lack of access to medical care, suicide, homicide, co-occurring chronic (e.g., cardiovascular disease; diabetes), and infectious (e.g., HIV) illnesses, and related unhealthy practices such as smoking and substance abuse. Even nonpsychotic disorders (e.g., ADHD; many forms of depression) are linked to long-term health risks (e.g., Barkley, Murphy, & Fischer, 2008). Recent findings reveal links between a range of mental disorders and a startling list of chronic physical illnesses (Scott et al., 2016).

Given this set of enormously costly, persistent, and deeply human consequences and needs, why not rely on traditional clinical efforts in psychology and psychiatry for solutions, given their long, venerable histories? As detailed in earlier accounts, however, these efforts have led to static views of psychopathology, with priority given to categorical diagnoses that inevitably lump together individuals with substantially different etiologic pathways into the same “condition” (e.g., Cicchetti, 1984, 1990). Moreover, the reciprocally deterministic nature of development, both typical and atypical, is not well captured by such static diagnostic systems (or nosologies, see Chapter 2 [Beauchaine & Klein]). Because of the huge expansion of knowledge in a host of related fields and subfields, the complex yet compelling perspectives offered by DP have taken hold with increasing rapidity, providing a call to investigators from a host of seemingly disparate disciplines regarding the promise of uncovering relevant mechanisms. Absent the multifaceted nature of DP models and paradigms, traditional perspectives are too often sterile and impoverished, carrying huge potential for treatments and prevention efforts to be directed at the wrong targets.

Despite scientific and clinical urgency surrounding this entire topic, barriers stand in the way of increased scientific understanding and access to evidence-based treatment. Perhaps the primary issue is that mental disturbance, at any age, remains highly stigmatized (e.g., Hinshaw, 2007; Hinshaw & Stier, 2008; Martinez & Hinshaw, 2016). Intensive stigma and shame—related to the unpredictability of the behavior patterns in question, the threat they convey to perceivers' well-being, and their media-propelled linkages to violence and incompetence—too often preclude help seeking, prevent empathic responses, and serve to render mental health a lower priority than physical health, despite inextricable linkages between the two. Depressingly, although public knowledge of mental illness has grown considerably since the 1950s, the U.S. public is far more likely to link mental illness with dangerousness than in the past (see Phelan, Link, Stueve, & Pescosolido, 2000). Moreover, rates of stigma and social distance related to mental illness have not changed appreciably in recent decades (Pescosolido et al., 2010). Reasons are complex but may relate to (a) increased numbers of seriously impaired individuals on the streets, without needed community services and resources; (b) enhanced public awareness that “dangerousness” is one of the few mandates for involuntary commitment to hospitals—along with frequent media attention linking mental illness to mass shootings, oftentimes inaccurately; and (c) the tenuousness of evidence that biogenetic ascriptions to mental illness (i.e., that it is a “brain disease” or a “disease like any other”) can eliminate stigmatization (see Haslam & Kvaale, 2015; Martinez, Piff, Mendoza-Denton, & Hinshaw, 2011; Pescosolido et al., 2010). Indeed, although biological perspectives are a necessary antidote to the “blaming the family” and “castigating the individual” perspectives that dominated psychology and psychiatry for much of the 20th century, their reductionistic promotion is neither accurate nor aiding the cause of stigma reduction, in part because they appear to promote pessimism and dehumanization. Instead, DP perspectives offer complex as opposed to simplistic or reductionistic conceptions of mental disorder, potentially leading to appreciation of the multidetermined biological and contextual factors related to psychopathology instead of personal or family weakness or blame, or notions of genetic flaw (e.g., Haslam & Kvaale, 2015; Martinez & Hinshaw, 2016).

In all, despite major advances in both basic science and clinical applications in recent years, as highlighted in the following chapters, the field's knowledge of developing brains and minds in multiple, interacting contexts is still rudimentary. It is hard to imagine otherwise, given the sheer complexity of the subject matter under consideration. As noted in introductory chapters to the earlier editions of this volume (Hinshaw, [2008b, 2013]), the trajectory of human prenatal neural development is nothing short of staggering, with literally thousands of new neurons proliferating during each second of development after the first few weeks following conception, as well as massive pruning and synaptogenesis in the first several years of life. Still, for those who enjoy a challenge and are excited by questions that will take both many decades and many great minds and scientific teams to answer—with the potential payoff of bettering the human condition—the hope is that this volume will serve as a call to join the major scientific and clinical efforts so urgently needed. Indeed, if the field is to continue to make headway toward understanding, treating, and preventing the serious clinical conditions that emerge during childhood and adolescence, the best minds of the current and forthcoming generations of scholars and clinicians need to join the effort.

At this point, I provide a review of core axioms and principles of DP. These points reflect the multidisciplinarity and transactional nature of the field, signifying that static models and unidimensional conceptions are simply not able to explain the fascinating and troubling development of maladaptive behavior patterns comprising the domain of psychopathology.

PRINCIPLES OF DP

Many of the conceptual bases for integrating developmental principles and models into the study of child and adolescent psychopathology have been present for several centuries, spanning diverse fields and disciplines (e.g., Cicchetti, 1990). Yet it is only in the past 40 years that DP has taken formal shape as a perspective on behavioral and emotional disturbance throughout the lifespan, and as a major conceptual guidepost for the study of both normal and atypical development. During this period, DP has exerted a major force on clinical child psychology, child psychiatry, developmental psychology, developmental neuroscience, and a number of other disciplines in both behavioral and neurological sciences. Not only have new courses been formed at major universities, but journals have been created and new paradigms of conceptualizing mental disorder have gained traction (Insel et al., 2010; see Chapter 2 [Beauchaine & Klein]). It is remarkable how pervasive the DP perspective has become, galvanizing a host of clinical and scientific efforts and in the process becoming mainstream.

DP simultaneously comprises a theoretical model regarding the origins of mental disorders, a multidisciplinary approach linking principles of normative development to the genesis and maintenance of psychopathology, and a scientific discipline closely tied to clinical child and adolescent psychology and psychiatry but transcending the usual diagnosis-based emphases of these fields (Cicchetti, 2016; Lewis & Randolph, 2014). Through its focus on the dynamic interplay of biology and context, genes and environments, and transactional processes linking multilevel influences to the development of healthy and atypical functioning, DP has come to dominate current conceptual models of psychopathology. Many of its core ideas emerge from disciplines such as philosophy, systems theory, and embryology (see Gottlieb & Willoughby, 2006, for elaboration). The syntheses represented in this volume, reflecting DP's continuing growth into the first two decades of the 21st century, are cutting-edge, given the major knowledge explosion in recent years, related largely to greater understanding of psychobiological influences as they transact with contextual forces.

What characterizes a truly developmental view of psychopathology, versus descriptive, symptom-focused presentations dominating most classification systems? DP's originators contended with this core question (e.g., Achenbach, 1974; Cicchetti, 1990; Rutter & Sroufe, 1984; Sroufe & Rutter, 2000), and current syntheses still grapple with the fundamental issues involved (Cicchetti, 2016; Lewis & Rudolph, 2014). From my perspective the key issues constitute multidisciplinarity; acknowledgment of dynamic, multilevel processes; and appreciation of systems-level change in producing developmental transitions (whether the systems are biological or social). Despite the many gains that have been made, it is important to realize at the same time how far we must still travel to comprehend the development and maintenance of psychopathology via the tools and models of DP. The trail ahead is long and steep.

I list several core points that are commonly viewed as central to the DP perspective. These include the necessity of (a) interweaving studies of normal development and pathological functioning into a true synthesis; (b) examining developmental continuities and discontinuities of traits, behavior patterns, emotional responses, and disorders; (c) exploring both risk and protective factors and their interplay, so that competence, strength, and resilience as well as pathology and impairment can be understood; (d) involving reciprocal, transactional models of influence in the field's causal models through which linear patterns of association and causation are replaced by probabilistic, dynamic, nonlinear, and complex conceptual models; and (e) capturing the importance of both psychobiological vulnerabilities and social/cultural context in understanding the function of behavioral and emotional patterns.

Three related principles bear emphasis:

Multiple pathways to pathology exist. Indeed, disparate routes may lead to behaviorally indistinguishable conditions or outcomes, exemplifying the construct of

equifinality

. For example, aggressive behavior can result from physical abuse, from a heritable tendency toward disinhibition, from injury to the frontal lobes, from coercive parenting interchanges with the developing child, from prenatal and perinatal risk factors acting in concert with early experiences of insecure attachment or parental rejection, or—as is probably most often the case—from different combinations of these vulnerabilities and risk factors. A key problem with static nosologies is their assumption that everyone receiving a similar psychiatric diagnosis has the “same” underlying patterns and processes of psychopathology. Similarly,

multifinality

pertains when a given vulnerability, risk factor, or initial state fans out into disparate outcomes across different individuals (Cicchetti & Rogosch, 1996). Maltreatment may or may not lead to severe maladaptation, depending on a host of intervening factors. As another example, extremes of inhibited temperament may induce intense shyness and social withdrawal; but other, healthier outcomes are also possible, depending on the presence or absence of additional risk or protective factors.

DP models often place emphasis on person-centered research designs, in which the typical practice of examining global effects of one or more risk/protective variables across an entire sample or population is supplemented by consideration of unique subgroups—whether defined by genotypes, personality variables, socialization practices, neighborhoods, or other key factors—and their unique developmental journeys across the lifespan (see Bergman, von Eye, & Magnusson, 2006). From a slightly different perspective, developmental continuities and discontinuities may well differ across homogeneous subgroups of participants. Even in variable-centered research, key moderator variables and mediator processes must always be considered (e.g., Hinshaw, 2002; Kraemer, Stice, Kazdin, Offord, & Kupfer, 2001), to ensure that (a) results are applicable to subsets of participants grouped on moderator variable of interest (males versus females, those from different ethnic groups, or those with different patterns of comorbidity) and (b) underlying mechanisms of change, gleaned from mediator variables, are taken into account.

Given the rapid growth in recent years of genomic models as well as brain imaging methods, DP researchers in the 21st century must pay increasing attention to the role of the brain, and neuroscientific principles in general, toward accounting for the wide range of extant pathologies and their devastating effects. The field has come a long way from the middle of the 20th century, when biological and temperamental factors were virtually ignored in accounts of child development and psychopathology. Again, however, progress will be stalled if the psychosocial reductionism of prior generations is replaced by biological and genetic reductionism in the current era. A key antidote is for students and investigators to embrace a multiple-levels-of-analysis approach, integrating across genes and gene products, neural systems, and temperamental traits and core behavioral patterns, in contexts of families, schools, and neighborhoods, including the general culture (Cicchetti, 2008; Insel et al., 2010). Isolated, single-factor or single-level models and paradigms are inadequate to the task.

In other words, the greatest potential for progress in the DP field is made when investigators travel back and forth between “micro” and “macro” levels—including intermediate steps or pathways—to understand mechanisms that underlie development of adjustment and maladjustment. The essential task is to link events at the level of genes (e.g., genetic polymorphisms; transcription and translation), neurotransmitters, and neuroanatomical development, into individual differences in temperament, social cognition, and emotional response patterns. At the same time, such bottom-up conceptions must be supplemented by top-down understanding of ways in which family interaction patterns, peer relations, school factors, and neighborhood/community variables influence the developing, plastic brain, even at the level of gene expression (see Chapter 3 [Beauchaine, Gatzke-Kopp, & Gizer]). Overall, progress toward understanding pathological behavior will require multidisciplinary efforts in which investigators ranging from geneticists and biochemists, scientists focusing on basic psychological processes and individual psychopathology, experts on family and neighborhood processes, examiners of clinical service systems, and public health officials as well as policy experts must work collaboratively and in increasingly diversified ways. The phenomena under consideration are too complex, too dynamic, and too multifaceted to be understood by an exclusive focus on psychobiological processes, family factors, peer processes, or cultural factors in isolation. Performing the necessary kinds of investigations often mandates large-scale, complex, and interdisciplinary work, necessitating collaborations across traditional disciplinary boundaries.

Note that key concepts and principles of DP have been stated and restated across a large number of articles, chapters, and books. Indeed, detailed discussion could easily fill a volume unto itself. The challenge for the current chapter is to encapsulate several core tenets, in the service of foreshadowing and illuminating content on specific processes and specific mental dimensions and disorders.

NORMAL AND ATYPICAL DEVELOPMENT ARE MUTUALLY INFORMATIVE

As opposed to the study of discrete, mutually exclusive categories of disorder, DP models emphasize that nearly all relevant phenomena represent aberrations in continua of normal developmental pathways and processes—and, accordingly, that without understanding typical development, the study of pathology will remain incomplete and decontextualized. As just one example, related to a research area within my own expertise, illuminating the nature of ADHD requires thorough understanding of normative development of attention, impulse control, and self-regulation (e.g., Barkley, 2015; Hinshaw & Scheffler, 2014; Nigg, Hinshaw, & Huang-Pollack, 2006; Sonuga-Barke, Bitsakou, & Thompson, 2010; see also Chapter 13