child and adolescent psychopathology - the...

Child and AdolescentPsychopathology

Child andAdolescent

Psychopathology

Second Edition

Edited by

Theodore P. BeauchaineStephen P. Hinshaw

John Wiley & Sons, Inc.

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Child and adolescent psychopathology / edited by Theodore P. Beauchaine,Stephen P. Hinshaw.— 2nd ed.

p. cm.Includes bibliographical references and index.ISBN 978-1-118-12094-1 (cloth)ISBN 978-1-118-43167-2 (e-bk)ISBN 978-1-118-41636-5 (e-bk)ISBN 978-1-118-41914-4 (e-bk)1. Child psychopathology. 2. Adolescent psychopathology. I. Beauchaine, Theodore P. II. Hinshaw,

Stephen P.RJ499.C48237 2012

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Printed in the United States of America

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Contents

Foreword vii

Preface xi

List of Contributors xv

Part I THE DEVELOPMENTAL PSYCHOPATHOLOGY APPROACHTO UNDERSTANDING MENTAL ILLNESS

1 Developmental Psychopathology as a Scientific Discipline 3Stephen P. Hinshaw

2 Developmental Psychopathology and the Diagnostic and StatisticalManual of Mental Disorders 29Theodore P. Beauchaine, Daniel N. Klein, Nora L. Erickson,and Alyssa L. Norris

3 Genetic and Environmental Influences on Behavior 111Theodore P. Beauchaine and Lisa M. Gatzke-Kopp

Part II VULNERABILITIES AND RISK FACTORS FORPSYCHOPATHOLOGY

4 Risk and Resilience in Child and Adolescent Psychopathology 143Bruce E. Compas and Charissa Andreotti

5 Child Maltreatment and Risk for Psychopathology 171Sara R. Jaffee and Andrea Kohn Maikovich-Fong

6 Impulsivity and Vulnerability to Psychopathology 197Emily Neuhaus and Theodore P. Beauchaine

7 Behavioral Inhibition as a Temperamental Vulnerability toPsychopathology 227Jerome Kagan

8 Beyond Allostatic Load 251Bruce J. Ellis, Marco Del Giudice, and Elizabeth A. Shirtcliff

9 Exposure to Teratogens as a Risk Factor for Psychopathology 285Nicole A. Crocker, Susanna L. Fryer, and Sarah N. Mattson

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vi Contents

10 Brain Injury as a Risk Factor for Psychopathology 317Katherine E. Shannon Bowen and Lisa M. Gatzke-Kopp

11 Emotion Dysregulation as a Risk Factor for Psychopathology 341Pamela M. Cole, Sarah E. Hall, and Nastassia J. Hajal

Part III EXTERNALIZING BEHAVIOR DISORDERS

12 Attention-Deficit/Hyperactivity Disorder 377Joel Nigg

13 Oppositional Defiant Disorder, Conduct Disorder, and JuvenileDelinquency 411Irwin D. Waldman and Benjamin B. Lahey

14 Development of Adult Antisocial Behavior 453Thomas J. Dishion and Kristina Hiatt Racer

15 Substance Use Disorders in Adolescence 489Sandra A. Brown, Kristin Tomlinson, and Jennifer Winward

Part IV INTERNALIZING BEHAVIOR DISORDERS

16 Anxiety Disorders 513Carl F. Weems and Wendy K. Silverman

17 Depressive Disorders 543Daniel N. Klein, Autumn J. Kujawa, Sarah R. Black,and Allison T. Pennock

18 The Development of Borderline Personality and Self-Inflicted Injury 577Sheila E. Crowell, Erin A. Kaufman, and Mark F. Lenzenweger

Part V OTHER DISORDERS

19 Bipolar Disorder 613Joseph C. Blader and Gabrielle A. Carlson

20 Autism Spectrum Disorders 649Susan Faja and Geraldine Dawson

21 Childhood Schizophrenia 685Robert F. Asarnow

22 Eating Disorders 715Eric Stice and Cara Bohon

Author Index 739

Subject Index 765

Foreword

THE FIELD OF DEVELOPMENTAL psychopathology first came into ascendance duringthe 1970s, predominantly by being highlighted as an important perspectiveby researchers conducting prospective longitudinal studies of children at riskfor developing schizophrenia. Epidemiological investigations of families exhibitingdiscord and disruption (but where there was no parental mental disorder), studiesof links between cumulative risk factors and developmental outcome, investigationsof children with handicapping conditions, and research on cognitive and socio-emotional development in children with autism were among those areas that wereinfluential in the field’s emergence. Conceptualizations of the nature of mentaldisorder, etiological models of risk and resilience, scientific questions that wereposed, and research designs and data analytic strategies were all reexamined,challenged, and cast in a new light by developmental psychopathologists.

The belief that the study of typical developmental processes informs understand-ing of pathological development and, conversely, that the study of pathologicaldevelopment informs the understanding of normative development, is one of thecentral tenets of developmental psychopathology—an interdisciplinary science thatstrives to reduce the schisms that so often separate scientific research from theapplication of knowledge to clinical populations. The field of developmental psy-chopathology owes its emergence and coalescence to a number of historicallybased endeavors in a variety of disciplines, including embryology, genetics, andthe neurosciences, as well as psychoanalysis, psychiatry, and psychology. As such,developmental psychopathology provides an example of the synergistic contribu-tions of previously disparate fields that result in the emergence of a new discipline.Somewhat surprisingly, given its historical roots, most of the research conductedon both the development of psychopathology and the processes contributing toresilience focused on relatively narrow domains of variables until the late 1990s andearly years of the present millennium.

Over the past several decades, there has been a veritable explosion in our knowl-edge of developmental neurobiology, that area of neuroscience that focuses on factorsregulating the development of neurons, neuronal circuitry, and complex neuronalorganization systems, including the brain. Additionally, technological advances inthe fields of neuroimaging and molecular genetics have contributed to progress inour understanding of normality, psychopathology, and resilience. Consequently,it has become increasingly acknowledged that the investigation of developmentalprocesses, both normal and abnormal, is an inherently interdisciplinary enterprise.

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It is now apparent from the nature of the questions addressed by developmentalpsychopathologists that progress toward a process-level understanding of mentaldisorders will require research designs and strategies that call for the assessment ofmultiple domains and multiple levels of variables, both within and outside the devel-oping person. Likewise, research on the developmental pathways to resilience, theachievement of positive adaptation in the face of significant adversity, must followthese interdisciplinary multiple-levels-of-analysis perspectives. To comprehend typ-ical development, psychopathology, and resilience fully, all levels of analysis mustbe examined and integrated. Multiple levels of analysis are necessary because noone level is sufficient to explain the complexity inherent in the study of developmentand psychopathology.

Developmental psychopathology is an exciting and complex field. A major goal ofgraduate and postdoctoral training in developmental psychopathology is to developthe next generation of scholars so that they can go on and launch their own researchcareers. An important early step in this process is student access to scholarly volumesthat demonstrate the depth and breadth of the field in a clear and accessible way.Thus, this edited volume is a long-awaited, much needed, unique and innovativecontribution to the field. It is organized around highlighting the principles and majortenets of developmental psychopathology into a work that does not shy away frompresenting students, scholars, and clinicians with our current knowledge regardingthe multilevel complexity of typical and atypical development.

The editors of this volume, Ted Beauchaine and Steve Hinshaw, are each leadingtheorists and researchers in developmental psychopathology. They both subscribeto multilevel research and also have engaged in impressive translational researchthrough developing and implementing preventive interventions for high-risk youththat were influenced by basic research findings.

Ted Beauchaine has made seminal contributions to the understanding of the bio-logical underpinnings of a number of mental and personality disorders in childrenand adolescents and has conducted exemplary research on the prevention of theseconditions. Beauchaine also has utilized numerous psychophysiological measuresin his research on attention deficit hyperactivity disorder, conduct problems, dis-inhibitory psychopathology, depression, and teen self-injury. Importantly, Ted alsopossesses superb quantitative skills that enable him to conduct data analyses acrossmultiple levels of analysis.

Steve Hinshaw has made classic contributions on the role of the family and peerrelationships to typical and atypical development. He also has completed impres-sive multilevel research on externalizing problems (i.e., conduct disorder, attentiondeficit disorder) and on behavior problems and psychopathology in girls. Further-more, Hinshaw has implemented combinations of psychosocial and pharmacologicintervention for children with externalizing expressions of dysfunction. Finally,Steve has been a major advocate and contributor to the importance of destigma-tizing mental illness. He has written two powerful volumes on this topic—one apersonal account of his father’s lifelong struggle with bipolar disorder (The Yearsof Silence Are Past: My Father’s Life with Bipolar Disorder, 2002), the other a scholarlyaccount of the history of the stigmatizing treatment of persons with mental illness

Foreword ix

that also reviews the extant research on stigma from various scientific perspectivesand provides recommendations for future research, intervention, and social policy(The Mark of Shame:Stigma of Mental Illness and an Agenda for Change, 2007).

In order to have this volume adhere to the tenets of developmental psychopathol-ogy, Beauchaine and Hinshaw instructed the contributors to take a multiple-levels-of-analysis approach to their assigned chapter topic. All of the authors in thisvolume are world-class scholars in their area of expertise. Importantly, each contrib-utor communicates clearly, thus enabling graduate students and professionals froma variety of disciplines to develop a firm grasp of psychopathology and resilience intheir multi-system entirety.

Major high-risk conditions and mental disorders are given excellent coverage, asare processes contributing to the development of resilient functioning in individ-uals experiencing significant adverse experiences. The breadth and depth of eachchapter’s content provides the reader with a deep appreciation of the complex natureof normality, psychopathology, and resilience. The topics and issues addressed inthese chapters are immensely important – not only for the developmental sciences,but also for a number of other scientific fields.

I have been teaching graduate courses in developmental psychopathology forover 30 years. I have often searched for appropriate textbooks on psychopathologyto assign to students that were undergirded by the principles of developmentalpsychopathology. Although there were a number of good textbooks available, fewwere truly developmental in their organization and content. One of the books thatwas guided by the tenets of developmental psychopathology was a multi-volume setthat Donald Cohen and I co-edited on Developmental Psychopathology. These extensivevolumes were not practical to assign to graduate students for a semester-long course.Thus, I have never assigned a required textbook for my courses on developmentalpsychopathology. My course syllabus was composed solely of journal articles andbook chapters that the students were required to read.

Now that I have read this excellent volume edited by Ted Beauchaine and SteveHinshaw, I believe that I have finally found the answer to my 30-plus-year search fora developmental psychopathology textbook. The volume is full of rich and excitingideas that will help students develop a passion for the field of developmentalpsychopathology. I fully anticipate that my colleagues across the country will feelsimilarly and that the Beauchaine and Hinshaw text will play an important role inthe training of future generations of developmental psychopathologists.

Dante Cicchetti, Ph.D.McKnight Presidential Chair

William Harris Professorand Professor of Child Psychology and Psychiatry

Institute of Child DevelopmentUniversity of Minnesota

Preface

SOCIETAL COSTS OF mental illness—in terms of both morbidity and mortality—arestaggering. In 2002, the most recent year for which data are available, 154million people worldwide suffered from depression, 106 million suffered analcohol or drug use disorder, 25 million suffered from schizophrenia, and nearly1 million died by suicide (World Health Organization, 2012). In low- and middle-income countries, mental disorders account for 25% and 34%, respectively, of totalyears lived with disability, yet the large majority of those affected receive no formof treatment (WHO World Mental Health Survey Consortium, 2004). Althoughtreatment rates are slightly higher in wealthy countries, mental disorders continueto carry significant stigma. As a result, many avoid seeking help, and a lack oftreatment parity remains for mental disorders vs. other health-related conditions(Hinshaw, 2007).

When we wrote the preface to the first edition of this book, we noted howimportant it is to elucidate the causes of mental illness. After all, the better weunderstand etiology across all relevant levels of analysis, including genetic, neural,familial, and cultural (to name a few), the better position we are in to formulateeffective prevention and intervention programs (Beauchaine, Neuhaus, Brenner,& Gatzke-Kopp, 2008). Thus, even though this is not a text about treatment, wehope readers will keep in mind while digesting each chapter how important it isto identify the causes of mental illness in our efforts to reduce human suffering. Inthis regard, we live in an exciting and promising time. The Human Genome Project,completed only 10 years ago, sequenced 3 billion chemical base pairs that comprisehuman DNA. Following from this and major advances in psychiatric genetics,our understanding of molecular genetic vulnerabilities to mental illness continuesto improve, even though new paradigms are constantly emerging. Similarly, theapplication of modern neuroimaging techniques—particularly fMRI—has advancedour understanding of neural vulnerabilities to psychopathology. Especially excitingis recent research demonstrating how neural functioning mediates links betweengenetic vulnerability and high risk personality traits that predispose individuals topsychopathology (e.g., Buckholtz et al., 2008).

Traditionally, most of what we learned about mental illness was obtained throughobservation and classification of symptoms (see Chapter 2). Although useful in theearly stages of identifying different forms of mental illness, symptom classificationoften tells us little if anything about underlying causal processes—be they biolog-ical or environmental—that lead to a particular disorder. Accordingly, in editing

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this book we sought authors with expertise in the developmental psychopathologyperspective, which emerged only about 30 years ago (see Chapter 1). This perspec-tive follows from the observation that human behavioral traits—including thosethat predispose to psychopathology—almost always arise from complex transactionsbetween biological vulnerabilities and exposure to environmental risks across devel-opment. For example, heritable disorders such as depression, schizophrenia, andsubstance dependence are affected strongly by environmental experiences, and theeffects of environmentally-transmitted risks such as child maltreatment are moder-ated by genes and other biological predispositions. Furthermore, through epigeneticmechanisms, the expression of several genes implicated in behavior regulation canbe altered by experience including exposure to stress and trauma—findings thatdefy anachronistic distinctions between nature and nurture.

This shift in the scientific landscape—from a relatively static view of psychopathol-ogy based on specific clusters of behavior to a dynamic view of disorders emergingfrom complex transactions between vulnerabilities and risks across time—servedas the impetus for the first edition of this book. It continues to drive the currentsecond edition, which includes considerable new material. Before the first editionwas published, most graduate-level psychopathology texts were organized aroundsymptom-based approaches to classifying mental illness, with limited considerationof the genetic and neural underpinnings of behavior, or of unfolding of interactionsbetween biological vulnerabilities and environmental risk across time. However, inthe five years since the first edition was published, appreciation for the complexityof such transactions in the development of psychopathology has increased, andmany new and exciting findings have emerged. The timing was therefore right fora second edition.

Some readers will likely note that a few disorders often covered in psy-chopathology texts are not included in this book. For example, we do not addressdevelopmental disabilities or mental retardation. In omitting these disorders, weare not implying that they are unimportant. Rather, the ever expanding literatureaddressing developmental disabilities makes it difficult to cover the topic adequatelyin a text that already includes 22 chapters. Thus, we were left with a difficult choice,and we decided not to limit coverage of the conditions contained herein. We referinterested readers to other sources (e.g., Jacobson, Mulick, & Rojahn, 2007) forexcellent coverage of developmental disabilities and mental retardation.

We now invite you to join us in the quest for a deepened understanding ofmental disorders and conditions that originate in childhood and adolescence. Wehope that our emphases on genetic and other biological vulnerabilities, and howthese interact with environmental risk factors and contexts, will challenge yourpreconceived notions as to what is ‘‘biological’’ and what is ‘‘environmental’’ inrelation to normal and atypical development and psychopathology. We hope aswell that our coverage will prompt a new generation of investigators, clinicians, andpolicymakers to pursue the daunting but essential goal of explaining, treating, andpreventing the devastation that so often accompanies psychopathology.

Theodore P. BeauchaineStephen P. Hinshaw

Preface xiii

REFERENCES

Jacobson, J. W., Mulick, J. A., & Rojahn, J. (Eds.) (2007). Handbook of intellectual anddevelopmental disabilities. New York: Springer.

Beauchaine, T. P., Neuhaus, E., Brenner, S. L., & Gatzke-Kopp, L. (2008). Ten goodreasons to consider biological processes in prevention and intervention research.Development and Psychopathology, 20, 745–774.

Buckholtz, J. W., Callicott, J. H., Kolachana, B. K., Hariri, A. R., Goldberg, T.E., Genderson, M., . . . Meyer-Lindenberg, A. (2008). Genetic variation in MAOAmodulates ventromedial prefrontal circuitry mediating individual differences inhuman personality. Molecular Psychiatry, 13, 313–324.

Hinshaw, S. P. (2007). The mark of shame: Stigma of mental illness and an agenda forchange. New York: Oxford University Press.

WHO World Mental Health Survey Consortium (2004). Prevalence, severity, andunmet need for treatment of mental disorders in the World Health OrganizationWorld Mental Health Surveys. Journal of the American Medical Association, 291,2581–2590.

World Health Organization (2012). Mental health. Retrieved April 17, 2012, www.who.int/en/

http://www.who.int/en/

List of Contributors

Charissa AndreottiVanderbilt University, TN

Robert F. AsarnowUCLA School of Medicine

Theodore P. BeauchaineWashington State University

Sarah R. BlackUniversity at Stony Brook, NY

Joseph C. BladerStony Brook University School ofMedicine, NY

Cara BohonUniversity of California, Los Angeles

Katherine Shannon BowenUniversity of Wisconsin

Sandra A. BrownVeterans Affairs San Diego HealthcareSystem, CA

Gabrielle A. CarlsonStony Brook University School ofMedicine, NY

Pamela M. ColePennsylvania State University

Bruce E. CompasVanderbilt University, TN

Nicole A. CrockerSDSU/UCSD Joint Doctoral Programin Clinical Psychology, CA

Sheila E. CrowellUniversity of Utah

Geraldine DawsonAutism Speaks, NY

Marco Del GiudiceCenter for Cognitive Science,Department of Psychology, Universityof Turin, Italy

Thomas J. DishionArizona State University

Bruce J. EllisJohn and Doris Norton School ofFamily and Consumer Sciences, AZ

Nora L. EricksonWashington State University

Susan FajaUniversity of Washington

Susanna L. FryerUniversity of California, San Francisco

Lisa M. Gatzke-KoppPennsylvania State University

Nastassia J. HajalPennsylvania State University

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xvi List of Contributors

Sarah E. HallWheaton College, IL

Stephen P. HinshawUniversity of California, Berkeley

Sara R. JaffeeInstitute of Psychiatry, London

Jerome KaganHarvard University

Erin A. KaufmanUniversity of Utah

Daniel N. KleinUniversity at Stony Brook, NY

Autumn J. KujawaUniversity at Stony Brook, NY

Benjamin B. LaheyUniversity of Chicago

Mark F. LenzenwegerState University of New York atBinghamton

Andrea Kohn Maikovich-FongColorado Blood Cancer Institute atPresbyterian/St. Luke’s Hospital

Sarah N. MattsonSan Diego State University, CA

Emily NeuhausUniversity of Colorado School ofMedicine

Joel NiggOregon Health and Science University

Alyssa L. NorrisWashington State University

Allison T. PennockUniversity at Stony Brook, NY

Kristina Hiatt RacerUniversity of Oregon

Elizabeth A. ShirtcliffUniversity of New Orleans, LA

Wendy K. SilvermanFlorida International University

Eric SticeOregon Research Institute

Kristin TomlinsonUniversity of California, San Diego

Irwin D. WaldmanEmory University, GA

Carl F. WeemsUniversity of New Orleans, LA

Jennifer WinwardUniversity of California, San Diego

P A R T I

THE DEVELOPMENTALPSYCHOPATHOLOGY

APPROACH TOUNDERSTANDINGMENTAL ILLNESS

C H A P T E R 1

Developmental Psychopathologyas a Scientific Discipline

Rationale, Principles, and Advances

STEPHEN P. HINSHAW

FROM ITS ‘‘LAUNCH’’ BETWEEN three and four decades ago (see Achenbach, 1974;Cicchetti, 1984; Sroufe & Rutter, 1984), developmental psychopathology (DP)has become a force to be reckoned with. DP is at once a perspective on theorigins of mental disorders that begin during childhood and adolescence, a multidis-ciplinary conceptual approach linking normative development to psychopathology,and a scientific discipline closely tied to clinical child/adolescent psychology andpsychiatry but transcending the usual diagnosis-based emphasis of these fields(Cicchetti & Cohen, 2006; Cicchetti & Toth, 2009). Through its focus on the dynamicinterplay of biology and context, genes and environments, and ‘‘inner’’ versus‘‘outer’’ influences on the development of healthy and atypical functioning, it hascome to dominate current thinking and research on psychopathology. Some of itscore ideas are not new, having emerged in the context of embryology, systems the-ory, philosophy, and genetics long ago (see Cicchetti, 2006; Gottlieb & Willoughby,2006, for elaboration). Yet the syntheses represented in this volume, reflecting DP’scontinuing growth, are truly cutting edge, given the relatively recent emergence ofDP and given the knowledge explosion in recent years related to psychobiologicalinfluences as they transact with contextual forces. Today, scientists from diversedisciplines contribute to ever-expanding knowledge of this enterprise while clini-cians benefit from and utilize its core principles. The underlying perspectives are nolonger revolutionary; instead, they have come to comprise the dominant paradigm.

In this, our second edition of a graduate-level compendium on core aspectsof this vast topic, we continue our tradition of providing current, conceptuallybased, clinically relevant, and developmentally informed information on causalmechanisms underlying child and adolescent psychopathology. Leading scientistsacross the entire field have contributed state-of-the-art summations of their particular

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4 The Developmental Psychopathology Approach to Understanding

areas of expertise; we owe them a great debt for their efforts toward translating thecomplex findings into each chapter synthesis. Indeed, every entry in this edition isbrand new, which is entirely necessary given how much the science has advancedacross the several years since the first edition (Beauchaine & Hinshaw, 2008).

WHY DEVELOPMENTAL PSYCHOPATHOLOGY?

To contextualize and put into perspective why this entire area is so important, onemust first consider the high levels of suffering involved in child and adolescentpsychopathology, including the severe pain and restricted life opportunities expe-rienced by not only affected children and adolescents but also by families, schools,and in some cases communities and society at large. Emotional and behavioralproblems in youth are not only distressingly prevalent but also hugely impairing,leading to serious problems in such crucial domains as academic achievement,interpersonal competencies, and independent living skills. Distress is often intense;individuals may engage in behavior patterns that are highly destructive to their owndevelopment as well as the well-being of others.

For example, depression is associated with high degrees of hopelessness anddespair, anxiety disorders with severe restrictions on exploration, bipolar disorderwith disruption and chaos as well as high risk for suicidality, attention-deficithyperactivity disorder with major deficits in academic and social arenas as well asrisk for accidental injury, conduct problems with both violence and victimization,eating disorders with threats to physical well-being and healthy self-image, autismand other pervasive developmental disorders with severe isolation and major skilldeficits, and substance use/abuse with squandered opportunities and major healthrisks. Child maltreatment is linked, in too many instances, to tragic developmentalconsequences, and the origins of personality disturbance are linked to major risk forself-harm and interpersonal disasters. Although lifelong pain and impairment arenot inevitable, as we know from investigations of resilience (e.g., Luthar & Brown,2007; Sapienza & Masten, 2011), mental disorders are quite likely to ‘‘up the ante’’for devastation.

Second, the costs of mental disturbance are huge in other ways. Health careexpenditures rise dramatically, educational and occupational milestones are likelyto be hugely delayed or lost altogether, and deficits in later employability are oftenstaggering, with major economic consequences (e.g., Murray & Lopez, 1996; Robbet al., 2011). Thus, beyond personal and family suffering, disabling skill deficits andharsh economic realities frequently accrue from mental disorder.

Third, not only do behavioral, emotional, and developmental disturbances inchildhood and adolescence typically persist into adulthood, but what are oftenconsidered to be ‘‘adult’’ mental disorders often have precursors in the early yearsof development (Kessler et al., 2005). All too often, symptoms and impairments startearly and remain problematic for years to come.

Given this set of deeply human, enormously costly, and persistent needs, whynot rely on traditional clinical efforts in psychology and psychiatry, with their long,venerable histories? As detailed in earlier treatises, these efforts have too often

Developmental Psychopathology as a Scientific Discipline 5

yielded overly broad and static categories of mental disorders, with insufficientattention paid to biological vulnerabilities, contextual influences, multilevel chainsof causation, dynamic and transactional influences, and divergent life-course path-ways within a given diagnostic category (e.g., Cicchetti, 1990). The reciprocallydeterministic nature of development, both typical and atypical, is not well capturedin such diagnostic systems. As a function of the huge expansion of knowledge in ahost of related fields and subfields, the complex yet compelling perspectives offeredby DP have taken hold with increasing pace. Without them, traditional models seemsterile and impoverished.

Yet despite the utter scientific and clinical urgency surrounding this topic, impor-tant barriers stand in the way of increased scientific understanding and access toevidence-based treatment. Perhaps the primary reason is that mental disturbanceat any age is still highly stigmatized (e.g., Hinshaw, 2007; Hinshaw & Stier, 2008).Intensive stigma and shame prevent help seeking and serve to render mental healtha lower priority than physical health, despite the inextricable linkages between thetwo. Intriguingly, although we appear to be a far more open and accepting cultureregarding mental health than half a century ago—and although public knowledge ofmental illness has grown considerably since the 1950s—the U.S. public is more likelyto link mental illness with dangerousness, and it wishes for greater social distancefrom those with mental disorders, than in the past (see Phelan, Link, Stueve, &Pescosolido, 2000). The reasons are complex but may relate to (a) increased numbersof seriously impaired individuals on the streets, without needed community servicesand resources; (b) enhanced public awareness that ‘‘dangerousness’’ is one of thefew reasons that can still lead to involuntarily commitment; and (c) the tenuousnessof the evidence that biogenetic ascriptions to mental illness (i.e., that it is a ‘‘braindisease’’ or a ‘‘disease like any other’’) can eliminate stigmatization (see Hinshaw,2007; Jorm & Griffiths, 2008; Martinez, Piff, Mendoza-Denton, & Hinshaw, 2011;Pescosolido et al., 2010). DP perspectives promote complex as opposed to simplisticor reductionistic conceptions of mental disorder, leading to both enhanced scientificprogress and, it is hoped, a more realistic view on the part of the general public,emphasizing multidetermined pathways but not personal weakness or blame.

In all, despite the major advances in basic science and clinical applications inrecent years, which we highlight in the following pages, the field’s knowledge ofdeveloping brains and minds in multiple, interacting contexts is still rudimentary.How could it be otherwise, given the sheer complexity of our topic matter? Still,for those who enjoy a challenge—and those who are excited by questions that willtake many years and many great minds to answer, with the potential for a payoffof bettering the human condition—we sincerely hope that our chapters serve asa call to join the major scientific and clinical efforts needed in the decades ahead.Indeed, if the field is to continue to make headway toward understanding, treating,and preventing the serious clinical conditions that emerge during childhood andadolescence, the best minds of the current generation are required.

We admit that the multilayered nature of the topic at hand, paired with thehuge numbers of risk factors (biological, experiential, and contextual) that promotedisturbed functioning and the many protective factors that might mitigate such


risk, can serve to delay needed translational efforts from DP-related insights toevidence-based treatment strategies (Cicchetti & Toth, 2009). Although this book is,by design, not a volume on intervention, our ultimate hope is that the intentionalapplication of advances in basic science to clinical practice and prevention will occurat an ever-increasing pace.

OVERVIEW OF APPROACH

In the chapters that follow, our core objective is to bring to life DP’s core tenetsand principles into a useful guide for students, clinicians, and scholars, in orderto facilitate deepened understanding of the major forms of child and adolescentbehavioral and emotional disturbance. To meet this aim, we have asked leadersin the field to present up-to-date material that is simultaneously developmentallybased, clinically relevant, and directly inclusive of the types of psychobiologicalformulations that are gaining ascendancy in the entire mental health enterprise. Inother words, we aim to supplement the kinds of developmental, process-orientedconstructs typically linked to DP with appreciation of core findings in behavioraland molecular genetics, neural pathways, and brain plasticity that have risen toprominence in recent years.

Thus, in our instructions to the volume’s contributors, we asked explicitly forcoverage of historical context, epidemiologic factors, diagnostic issues, sex differ-ences, cultural variables, developmental processes, and important psychobiologicalmechanisms that can illuminate the forms of pathology under discussion in theirparticular chapter. At the same time, we emphasized that neurobiological pro-cesses must not be represented in reductionistic fashion. Indeed, those contextualfactors—familial, cultural, school-related—viewed as the predominant causal mech-anisms throughout much of the last century are now known to interact and transactwith biological vulnerabilities and risk variables to produce both maladaptation andhealthy adaptation across development. Thus, we urged our authors to considervulnerability and risk across multiple levels of analysis, emphasizing transactionacross a range of individual and contextual factors in the genesis of (or desistancefrom) psychopathology. Indeed, modern views of behavioral and molecular geneticshave placed into sharp relief the unique and interactive roles that environmentaland cultural forces exert on development (e.g., Cicchetti & Curtis, 2006; Dodge &Rutter, 2011; Rutter, Moffitt, & Caspi, 2006).

Given page limitations and our desire for focused rather than exhaustive cov-erage, each chapter is relatively brief, with the goal of providing cogent, recent,and incisive commentary on conceptual issues, clinically relevant material, neuro-scientific advances, and interactive models. We strongly hope that readers use thesecontributions as a springboard for further exploration of conceptual frameworks,empirical research on etiology and mechanisms, and bases for prevention andtreatment.

As noted earlier, despite the considerable advances that have been made, the roadahead is long. One can only wonder at what scholars a century from now will makeof our preliminary attempts to model the hugely complex developmental pathways,


processes, and trajectories linked to psychopathology. After all, the human genomewas decoded only a decade ago, and high-resolution brain scanning is still arelatively young field of endeavor. Still, throughout the following pages, I highlightkey advances that have been made in recent years regarding DP processes, methods,and models, signifying that the enterprise has already yielded unprecedentedinsights and discoveries.

DP CONCEPTS AND PRINCIPLES

What characterizes a truly developmental view of psychopathology, as opposed tothe kinds of descriptive, symptom-focused presentations that still dominate mostclassification systems and that still permeate many ideas in the field? As discussed inkey readings (e.g., Cicchetti & Cohen, 2006; Cicchetti & Toth, 2009; Mash & Dozois,2003; Rutter & Sroufe, 2000; Sameroff, Lewis, & Miller, 2000), several core points arecommonly viewed as central to the DP perspective. These include the necessity of(a) interweaving studies of normal development and pathological functioning into atrue synthesis; (b) examining developmental continuities and discontinuities of traits,behavior patterns, emotional responses, and disorders; (c) evaluating evidence acrossmultiple levels of analysis (from genes to cultures, including the intermediate levelsof individuals, families, schools, and neighborhoods); (d) incorporating distinctperspectives, including clinical and developmental psychology, child and adolescentpsychiatry, genetics, neurology, public health, philosophy of science, and manyothers, into a truly multidisciplinary effort; (e) exploring both risk and protectivefactors and their interplay, so that competence, strength, and resilience as well aspathology and impairment can be understood; (f) involving reciprocal, transactionalmodels of influence in the field’s causal models, through which linear patternsof association and causation are replaced by probabilistic, dynamic, nonlinear,and complex conceptual models; and (g) capturing the importance of social andcultural context both in understanding the function and meaning of behavioraland emotional patterns and in interacting with biological predisposition to yielddisordered functioning.

Three related principles bear emphasis. The first is that multiple pathwaysto pathology exist. Indeed, disparate routes may lead to a common conditionor outcome, exemplifying the construct of equifinality. For example, aggressivebehavior (or, diagnostically speaking, ‘‘conduct disorder’’) can result from physicalabuse (Chapter 5), from a heritable tendency toward disinhibition (Chapter 3),from injury to the frontal lobes (Chapter 10), from coercive parenting interchangeswith the developing child (Chapter 14), from prenatal and perinatal risk factorsacting in concert with early experiences of insecure attachment or parental rejection(Chapter 9), or from different combinations of these vulnerabilities and risk factors(e.g., Jaffee, Strait, & Odgers, 2012; Raine, Brennan, & Mednick, 1997; Tremblay, 2010).In other words, separate—and in many cases interacting—causal influences can yieldsimilar clinical endstates. In addition, the concept of multifinality applies when agiven risk factor or initial state yields disparate outcomes across development. Forinstance, abuse may or may not lead to severe malaptation, depending on a host of


intervening factors; extremes of inhibited temperament may produce shyness andsocial withdrawal, but other, healthier outcomes are also possible, depending on thepresence or absence of additional risk or protective factors (see Cicchetti & Rogosch,1996). Both equifinality and multifinality imply that linear models of associationand simplistic categorical conceptions of disorder are incapable of facilitating fullunderstanding of child and adolescent psychopathology. Indeed, such simplisticmodels may actually be misleading.

Second, DP models place emphasis on person-centered research designs, in whichthe typical practice of examining global effects of one or more risk/protectivevariables across an entire sample or population is supplemented by considera-tion of unique subgroups—whether defined by genotypes, personality variables,socialization practices, neighborhoods, or other key factors—and their particulardevelopmental journeys across the life span (Bergman, von Eye, & Magnusson,2006). Framed from a slightly different perspective, developmental continuities anddiscontinuities may well differ across homogeneous subgroups of participants. Evenin variable-centered research, key moderator variables and mediator processes mustalways be considered (e.g., Fairchild & MacKinnon, 2009; Hinshaw, 2002; Howe,Reiss, & Yuh, 2002; Kraemer, Stice, Kazdin, Offord, & Kupfer, 2001) to ensure that(a) results are applicable to subsets of participants grouped on the basis of the mod-erator variable of interest (e.g., male versus female participants, those from differentethnic groups, those with different patterns of comorbidity) and (b) underlyingmechanisms of change are considered explicitly.

Third, given the rapid growth in recent years of genetic and genomic modelsand brain imaging methods, DP researchers in the 21st century must pay increasingattention to the role of the brain—and to neuroscientific principles in general—toaccount for the wide range of extant pathologies and their devastating effects(Cicchetti & Curtis, 2006). Clearly, we have come a long way from the mid-20thcentury, when biological and temperamental factors were virtually ignored inaccounts of child development and psychopathology.

As noted in the introductory chapter to the first edition (Hinshaw, 2008), a basicmathematical calculation may help to elucidate the underlying complexities here:Adults have approximately 100 billion neurons in their brains; children are born witheven higher numbers, perhaps double that figure. Indeed a major developmental‘‘task’’ over the earliest years of postnatal development is the pruning and migrationof such neurons into a working, functional brain. But what is the rate of neuraldevelopment during the 40 weeks of human gestation? To figure this out, one mustdivide 200 billion (a fair estimate of the number of neurons with which an infant isborn) by the number of seconds in 40 weeks. The result—of dividing the numeratorof 2 times 10 to the 11th power (the number of neurons) by the denominator of2.4192 times 10 to the 7th power (the number of seconds)—is the astonishing figurethat, on average, the embryo and fetus are producing approximately 8,000 newneurons every second throughout the entire course of prenatal development. Thisaverage is not constant, of course, given that the neural tube and brain do not evenform for some weeks. Thus, in some crucial periods, this figure is even higher (seeGiedd, Shaw, Wallace, Gogtay, & Lenroot, 2006, for additional information on the


precise timing of neural development across pregnancy and childhood). Rates ofconnectivity in the developing brain yield numbers that are exponentially higher.As the cortex matures, revealing characteristic patterns of thickening and thinning,and as cortical neurons form rich and lasting connections with other brain regions,the number of synaptic connections goes into the trillions and beyond.

Given such staggering statistics, a key question involves the joint influenceof genes, hormones, nutrition, life experiences, and contextual influences on theplasticity of the brain’s development across childhood and adolescence. Withoutconsideration of transactional processes, multilevel models, computational frame-works, gene-environment interplay, and a host of technological and conceptualadvances related to the overall field of developmental neuroscience, we will not beable to solve the problem of gaining deep understanding of relevant mechanisms(see also Blakemore, Burnett, & Dahl, 2010; Romer & Walker, 2007; and Steinberg,2010, for considerations of adolescent brain and behavioral development).

Key concepts and principles related to DP have been stated and restated across alarge number of articles, chapters, and books. Indeed, detailed discussion of any oneof them could easily fill a volume unto itself. The challenge for the current chapter isto encapsulate these tenets, in the service of foreshadowing and illuminating contenton specific risk factors and specific disorders that fill the rest of the book. Becauseexplanations of these concepts too often remain at a rather global and abstract level,leaving unresolved precisely what they suggest for the investigation and treatmentof behavioral and emotional disorders, I try, in the following section, to bring thesepercepts to life.

Normal and Atypical Development Are Mutually Informative

As opposed to the study of discrete, mutually exclusive categories of ‘‘disorder,’’DP models emphasize that phenomena defined as abnormal represent aberrationsin normal developmental pathways and processes. Hence, without a full under-standing of typical development, the study of pathology will remain incompleteand decontextualized. Taking just one example, illuminating the nature of attention-deficit/hyperactivity disorder (ADHD) requires thorough understanding of thenormative development of attention, impulse control, and self-regulation (Nigg,2006; Nigg, Hinshaw, & Huang-Pollack, 2006; Chapter 12). Similarly, investigationsof autism must be fully integrated with the development of interpersonal awarenessand empathy, which typically takes place over the first several years of life. With-out such developmental templates, understanding autism may become an emptyexercise of counting symptoms (for a developmental approach, see Dawson & Toth,2006; Chapter 20). Additional instances exist across all forms of disordered emotionand behavior. Currently, few doubt the wisdom of understanding developmentalsequences and processes associated with healthy outcomes as extremely relevant tothe elucidation and explication of pathology.

Yet the process is conceptualized as a two-way street, with the corresponding viewthat investigations of pathological conditions—sometimes referred to as adaptationalfailures in DP terms (see Sroufe, 1997)—can and should provide a unique perspective


on normal developmental mechanisms. In other words, the study of disrupteddevelopmental progressions illuminates our understanding of what is normative.

Overall, this core tenet of DP—of the mutual interplay between the study ofnormality and pathology, along with the perspective that progress in each domain isdependent on progress in the other—is now widely held. Neurology abounds withrelevant examples. For example, there is a long tradition utilizing the study of dis-rupted neural systems to enhance understanding of healthy brain functioning andvice versa. ‘‘Split-brain’’ patients (those who have had their cerebral hemispheresseparated to provide relief from specific neurological disorders) provide unprece-dented insights into normative brain processes, such that separable functions andeven ‘‘personalities’’ subserved by the right versus left hemispheres become evidentas a function of the pathology and resultant surgery. In parallel, famous case studiessuch as HM, in which key brain structures/regions have been surgically removed(in his case the hippocampus), greatly facilitate knowledge about human memorysystems (see Gazzaniga, Ivry, & Mangun, 2009). Cicchetti and Curtis (2006) providelucid detail on neuroscience-related approaches. For a specific example, the study ofphenylketonuria (PKU) has implications for elaborating the normative developmentof executive functions (Diamond, Prevor, Callender, & Druin, 1997).

How might this perspective inform our understanding of psychological or psy-chiatric disorders that are the core subject matter of DP? In other words, beyondneurological conditions and formulations per se, can investigations of pathologyinform normal development? Once again, it is now commonly accepted that themore we know about basic emotion, cognition, attention, memory, social awareness,self-regulation, and the like, the more investigations of psychopathology can benefit.Almost no form of mental disorder constitutes a clearly demarcated, qualitativelydistinct category or taxon, meaning that processes applying to individuals near thecenter of the bell curve are likely to apply to those further out on the continuumas well. Nearly all forms of mental pathology appear consistent with a quantita-tive, dimensional perspective (Beauchaine, 2003), emphasizing the need for flow ofinformation from normal developmental pathways to pathological functioning.

But what about the other direction? Specifically, what has been learned aboutnormal developmental processes from studies of child and adolescent psychopathol-ogy? At first glance, the situation doesn’t seem to be as heuristic as that in neurology;it may be that we have not gained the kinds of dramatic insights about typical psy-chological development from studies of child and adolescent psychopathology thathave been realized in ‘‘harder’’ scientific endeavors. In other words, the complex-ity of mental disorders may limit parallels to more simply caused neurologicalconditions. In short, there are few behavioral and emotional equivalents to thesurgical procedures of creating lesions in certain brain tracts or single-gene forms ofpathology such as PKU.

Yet consider the work on autism by Baron-Cohen (2000). Relevant findings suggestthat the lack of social connectedness experienced by individuals with autism mayrelate to a failure in attainment of a basic ‘‘theory of mind,’’ which deals with thedeveloping realization that other humans have mental states that differ from one’sown. Most normal 4-year-olds can master theory-of-mind tests, suggesting that basic


social understanding is predicated on a domain-specific cognitive module that, onceoperative, occurs almost automatically. On the other hand, a high percentage ofyouth with autistic disorder, even those with high levels of intellectual functioning,do not ‘‘pass’’ such psychological tests, suggesting that they have not come to thecore realization that fellow humans have different minds and different psychologicalperspectives from their own.

I note that a number of individuals with high-functioning autism can eventu-ally learn to pass the kinds of experimental tests used to test for theory of mind.Through effortful processing, they come to deduce that other children and adultshave a different understanding of events in the world than they do. Yet this effortfulskill does not mean that their social interactions become smooth, effortless, and‘‘automatic.’’ Indeed, the laborious kinds of calculations and inferences made bypeople with high-functioning autism to understand interpersonal dynamics are notusually accompanied by perfectly functional social interactions (Grandin, 2006). Akey implication is that ‘‘normal’’ social-cognitive and social functioning is highlyautomatic and qualitatively distinct from the ability to deduce social situationsanalytically more typical in autism—which is time consuming and not perceivedas skillful by peers. Thus, disruptions in social cognition and social performancein persons with autism may help to clarify the automatic and highly developednature of the social cognitions and processes that underlie skilled interpersonalperformance in normal development. Parenthetically, I note that current viewsof theory of mind posit that at least some aspects of understanding false beliefsappear far earlier in life, even toddlerhood and infancy, further challenging devel-opmental models of both normative and atypical development (see, for example,Sodian, 2011).

Another example pertains to work on the reward sensitivity of individuals withADHD (e.g., Sagvolden, Johansen, Aase, & Russell, 2005). Here, considerable evi-dence reveals that in people with this condition, large performance decrementsoccur when rewards are suddenly stopped, presumably related to a dopaminergi-cally mediated problem with responding during extinction. More recent research(Volkow et al., 2009) reveals, in fact, that never-medicated adults with ADHD havemarkedly deficient numbers of dopamine receptors and transporters in reward andmotivational brain pathways than do non-ADHD comparison subjects. This find-ing has served to revive ‘‘motivational’’ theories regarding the origins of ADHD,revealing a biologically driven undersensitivity to reward. Not only is extrinsicreward necessary to enhance task performance of affected individuals, but rewardcessation would be expected to lead to larger-than-normal drop-off of task perfor-mance. In all, these insights foster understanding of basic developmental processesand mechanisms underlying dysregulated attention and impulse control, suchthat ADHD-related reward processes may well elucidate normative patterns ofmotivation, persistence, and effort.

A third instance, noted briefly, pertains to the horrific ‘‘experiments of nature’’that occur when infants and toddlers are subjected to brutal institutionalization andlack of human contact during the earliest years of development (for review, seeO’Connor, 2006). The development of specific symptom patterns (e.g., inattention


and overactivity, as opposed to aggression; see Kreppner, O’Connor, Rutter, &the English and Romanian Adoptees Study Team, 2001), and the extent of socialand cognitive ‘‘catch-up’’ following removal from the institutions, are extremelyinformative about normal-range development of secure relationships and cognitiveperformance. Such work has even incorporated experimental methods to understandwhether in-home foster placements can mitigate the effects of early deprivation interms of cognitive growth (Nelson et al., 2007). Indeed, for the previously institu-tionalized girls in this randomized trial, foster care placement led to improvementsin girls’ internalizing behavior patterns, mediated by the gaining of attachmentsecurity via the change from institutional care to family placements (McLaughlin,Zeanah, Fox, & Nelson, 2012). Thus, even in a harshly abandoned and deprived sam-ple, attachment processes are implicated in reductions of anxiety and depression.Mediators of competence in more normative samples are still open to exploration.

Developmental Continuities and Discontinuities

With this principle, it is commonly asserted that DP models must emphasize bothcontinuous and discontinuous processes at work in the development of pathology.What precisely does this mean? Taking the example of externalizing and antisocialbehavior, it is well known that antisocial behaviors show strong stability acrosstime—meaning that correlations are substantial between early measures of aggres-sive and antisocial tendencies and those made at later times. In other words, therank order remains relatively preserved, such that the most aggressive individuals atearly points in development remain high in such behavior patterns across develop-ment. But does this mean that the precise forms of externalizing antisocial behaviorremain constant? Clearly not, given that those children with extremes of tempertantrums and defiance during the toddler and preschool years are not especiallylikely to exhibit high rates of tantrums during adolescence. Rather, they have ahigh likelihood of displaying physical aggression in grade school, covert antisocialbehaviors in preadolescence, and various forms of delinquency by their teen years(e.g., sexual assault, property crime, violence), followed by adult manifestations ofantisocial behavior after adolescence (e.g., Moffitt, 1993, 2006). In short, continu-ities exist, but these are heterotypic in nature, as the actual form of the underlyingantisocial trait changes form with development.

Another important consideration is that patterns of continuity may differ consid-erably across separable subgroups that display different developmental patterns ortrajectories. Not all highly aggressive or antisocial children remain so, as some areprone to desist with the transition to adolescence. Others, however—the so-calledearly starter or life-course-persistent subgroup—maintain high rates through at leastearly adulthood (although, as just noted, the specific forms of the antisocial actionsmay well change with development). In addition, a large subset does not displaymajor externalizing problems in childhood but instead shows a sharp increase withadolescence (for a review, see Moffitt, 2006). Understanding such continuities anddiscontinuities via homogeneous subgroups is likely to yield greater understandingthan basic plots of overall curves of ‘‘growth’’ across the population. Sophisticated


statistical strategies (e.g., growth mixture modeling; group-based trajectory model-ing) are increasingly used to facilitate the search for separable trajectories or classesdefined on patterns of change of the relevant dependent variable, leading to majorinsights about predictors, moderators, and mediators and emphasizing the majorheterogeneity in multiple aspects of psychopathological functioning (see Muthén &Muthén, 2000; Nagin & Odgers, 2010a, 2010b).

Multiple Levels of Analysis

The greatest potential for progress (and complexity) in the DP field is made wheninvestigators travel back and forth between ‘‘micro’’ and ‘‘macro’’ levels, includingintermediate steps or pathways, to understand mechanisms underlying the develop-ment of adjustment and maladjustment. The essential task for the next generationsof DP investigators is to link events at the level of the gene (e.g., genetic polymor-phisms; transcription and translation; epigenetic influences) to neurotransmissionand neuroanatomical development, and subsequently into individual differencesin temperament, social cognition, and emotional response patterns (for detaileddiscussion, see Cicchetti, 2008). At the same time, such bottom-up conceptions mustbe supplemented by top-down understanding of the ways in which family interac-tion patterns, peer relations, school factors, and neighborhood/community variablesinfluence the developing, plastic brain, even at the level of gene expression, invokingthe concept of epigenetic influences. Overall, progress in understanding pathologicalbehavior will require multidisciplinary efforts in which investigators ranging fromgeneticists and biochemists, clinicians focusing on individual pathology, experts onfamily and neighborhood processes, investigators of clinical service systems, andpublic health officials must work collaboratively and in increasingly diversifiedways. The phenomena under consideration are too complex, too dynamic, and toomultifaceted to be understood by focusing exclusively on psychobiological pro-cesses, family factors, peer processes, or cultural factors in isolation. Performing thenecessary kinds of investigations often mandates large scale, complex, and inter-disciplinary/multidisciplinary work, necessitating collaborations across traditionalacademic boundaries. Although such collaboration is not simple, these kinds ofefforts are undoubtedly where the payoffs will lie (for a key example, see Caspi,Hariri, Holmes, Uher, & Moffitt, 2010).

Risk and Protective Factors

The key focus of a discipline such as DP—with the term psychopathology embedded inits title—is to discover the nature of behavioral and emotional problems, syndromes,and disorders. Many different definitional schemes have been invoked to define andexplain psychopathological functioning, with none able to provide a complete pic-ture (see Hinshaw, 2007, Chapter 1). Indeed, it is clear that biological vulnerabilities,psychological handicaps, environmental potentiators, and cultural-level norms allplay a major role in defining and understanding behavioral manifestations that areconsidered abnormal and/or pathological in a particular social context. Risk factors


(and constitutional vulnerabilities) are those antecedent variables that predict suchdysfunction, and the ultimate goal is to discover those variables that are bothmalleable and potentially causal of the disorder in question (Kraemer et al., 1997).

Yet disordered behavior is not uniform, and risk factors are not inevitablepredictors. Being female is a protective factor against most forms of psychopathologyin the first decade of life but serves as a risk factor for internalizing conditions duringadolescence (e.g., Hinshaw, 2009). As noted earlier, maltreatment is sometimes butnot always a risk factor for later pathology. Furthermore, for most individuals withdiagnosable forms of mental disorder, symptoms and impairments tend to wax andwane over time. It is often difficult to know when dysfunction precisely begins; itis also quite normative for periods of serious problems to be followed by healthieradjustment. In fact, the myth that mental disturbance is uniformly debilitating,handicapping, and permanent is a key reason for the continuing stigmatization ofmental illness (Hinshaw, 2006, 2007).

Resilience is the term often used to define unexpectedly good outcomes, orcompetence, despite the presence of adversity or risk (Luthar, 2006; Sapienza &Masten, 2011). Indeed, the concept of multifinality, noted earlier, directly impliesthat, depending on a host of biological, environmental, and contextual factors,variegated outcomes will emanate from common risk factors, with the distinctpossibility of positive adaptation in some cases.

DP is therefore centrally involved in the search for what have been calledprotective factors—those variables and processes that mitigate risk and promotemore successful outcomes than would be expected. Yet controversy surrounds theconstruct of resilience, the nature of protective factors, and the nature of competentfunctioning (see Luthar & Brown, 2007; Masten, Burt, & Coatsworth, 2006). In fact,some have claimed that there is no need to invoke a set of special processes thatare involved, given that a certain percentage of any sample exposed to a risk factorwill show better-than-expected outcomes and that protective factors are all toooften simply the opposite poles of what we typically think of as risk variables orvulnerabilities (e.g., higher rather than lower IQ; easier rather than more difficulttemperament; warm and structured rather than cold and lax parenting). Even so,it is crucial to examine processes that may be involved in promoting competenceand strength rather than disability and despair, given that such processes may beharnessed for prevention efforts and may provide key conceptual leads toward theunderstanding of both pathology and competence.

Indeed, recent advances in the study of resilience show that some aspects ofresilient functioning have psychobiological and even genetic underpinnings andthat a systemic, transactional, and even epigenetic model is needed to under-stand the multipronged nature of resilience-enhancing processes (see review inSapienza & Masten, 2011). Furthermore, Luthar and Brown (2007) remind us thatrelationships are central to any conception of resilience, despite current work in psy-chobiological undercurrents. In short, gaining understanding of why some childrenborn into poverty fare well in adolescence and adulthood, why some individualswith alleles that tend to confer risk for pathological outcomes do not evidence


psychopathology, why some youth with difficult temperamental features developinto highly competent adults, and why some people who lack secure attachmentsor enriching environments during their early years nonetheless show academic andsocial competence, is essential for knowledge of both health and maladjustment. Itis not just a luxury but a necessity to investigate positive developmental outcomes.Competence can shed light on the pathways that deflect away from pathology and, inso doing, may provide otherwise hidden insights into the necessary developmentalcomponents of adjustment versus maladjustment.

Reciprocal, Transactional Models

Linear models of causation, in which static psychological variables are assumedto respond in invariant ways to the influence of risk or protective factors, arenot adequate to the task of explaining psychopathology and its development(see Richters, 1997, who highlights that quite different explanatory systems areneeded to deal with open systems such as individual people). Pathways fromchildhood to adolescent and adult functioning are marked by reciprocal patternsor chains, in which children influence parents, teachers, and peers, who shape thefurther individual development of the child. Such mutually interactive processescan themselves escalate over time, leading to what are termed transactional models.Furthermore, some developmental processes appear to operate via cascading, esca-lating chains (Masten et al., 2006; Masten & Cicchetti, 2010), whereas others may,as just noted, be dampened or altered by mediating, protective factors. Given thestrong potential for nonlinear change in all of the above processes, dynamic systemsmodels are needed to help explicate core developmental phenomena (see Granic &Hollenstein, 2006).

To be specific, it is now well known that a great many cognitive and personalityoutcomes are at least moderately heritable, meaning that genetic factors explain asizable proportion of individual differences in the trait, attribute, or disorder in ques-tion. But via gene-environment correlations, environments (genetically associatedwith the trait in question) may amplify the expression of the trait, and individualsmay seek or evoke environmental responses that further promote the trait’s unfold-ing. Furthermore, as noted explicitly in Chapter 3, early-maturing brain regionsthat give rise to expression of key emotional and behavioral characteristics mayinfluence the developmental maturation of other, later-maturing regions; environ-mental events and factors may actually aid in the ‘‘turning on’’ of genes that furtherreinforce similar neural and behavioral actions, through epigenetic processes. Inaddition, certain genotypes may become expressed only in the context of certainenvironmental factors, signifying the operation of gene-environment interactions(Rutter et al., 2006). Finally, as just noted, processes of development may operatein highly nonlinear ways, requiring a new set of tools and conceptual models forunderstanding change processes (Granic & Hollenstein, 2006). Sensitive data ana-lytic strategies and innovative research designs are crucial tools for fostering greaterunderstanding of such nonlinear phenomena.


The Importance of Context

A key tenet of DP, directly related to the above points, is that family, school-related,neighborhood, and wider cultural contexts are central for the unfolding of aberrantas well as adaptive behavior. This point cannot be overemphasized: What mayhave been adaptive behaviors at one point in human evolutionary history may bemaladaptive in current times, given the major environmental and cultural changesthat render certain genetically mediated traits far less advantageous than previously.As just two examples, consider [1] the storage of fat in times of uncertain mealsand sudden need for survival-related activity, and [2] the presence of undue anxietyin relation to certain feared stimuli when conditions have markedly changed withrespect to indoor, sedentary lifestyles. There are few absolutes in terms of eitherbehavior patterns that are inherently maladaptive or risk factors that inevitablyyield dysfunction. Cultural settings and context are all-important for shaping andeven defining healthy versus unhealthy adaptation.

Similarly, key environmental factors (such as parenting styles) are not alwaysuniformly positive or uniformly negative in terms of their developmental effects.Deater-Deckard and Dodge (1997) have shown, for example, that harsh, author-itarian parenting predicts antisocial behavior in white, middle-class children butnot necessarily in African-American families. (On the other hand, parenting thatcrosses the line into abuse is uniformly harmful.) Many forms of mental disorder arepresent at roughly equivalent rates across multiple cultures, revealing key evidencefor universality; but the effects of risk or protective factors may differ markedlydepending on their developmental timing, the family and social context in whichthey are experienced by the developing child, and the niche or space that exists ina given culture for their expression and resolution (see, for example, Serafica &Vargas, 2006). In short, the DP perspective tells us clearly that setting and contextare all-important (Cicchetti, 2006).

This discussion throws into sharp relief the surge of interest, in recent years,regarding the specific effects environments play, once biological vulnerabilities aretaken into account. Rutter, Pickles, Murray, and Eaves (2001) provide a masterfulaccount of how to understand specific, causal environmental forces and factors; Jaffeeet al. (2012) provide an extremely useful guide to how nonexperimental designsand recent statistical advances can help facilitate just such understanding. As notedby Caspi et al. (2010), the leap in knowledge between environmental correlatesand environmental ‘‘pathogens’’ (i.e., environmental factors that are causal) is alarge one.

Along these lines, the process known as gene-environment interaction, discussedin more detail in Chapter 3 (and in the comprehensive volume of Dodge & Rutter,2011), remains a hot topic. After groundbreaking research a decade ago on this topic(e.g., Caspi et al., 2003) revealing that genotypes may yield pathological outcomesonly in certain environmental contexts, meta-analyses have challenged the size andstrength of such findings (e.g., Risch et al., 2009). However, in an incisive rejoinder,Caspi et al. (2010) examine animal as well as human models of gene productsand genetically mediated vulnerabilities, laying the groundwork for much-neededpsychobiological pathways through which such moderated effects may occur. They


also make the key point that many large-sample investigations—which receivethe most ‘‘weight’’ in meta-analytic efforts—tend to utilize inferior assessments ofenvironmental influences, such as those that are self-reported and retrospective.More precise environmental measures, in smaller studies, are thus discounted.Finally, Caspi et al. (2010) highlight that the serotonin transporter gene, implicatedin a host of gene-environment interaction findings, exerts its effects not by conferringrisk for any particular form of psychopathology but by enhancing sensitivity to keyaspects of the environment—revealing the core DP principle that ‘‘nature’’ and‘‘nurture’’ cannot fundamentally be separated.

Importantly, current models are moving away from the idea that certain geneticconfigurations are inevitably ‘‘risk’’ factors for psychopathology. Some, in fact, mayyield better-than-expected outcomes in optimal contexts. In other words, they mayserve as plasticity factors as opposed to risk factors per se, yielding differentialsusceptibility to both positive and negative environmental settings (e.g., Belsky &Pluess, 2009).

Equifinality and Multifinality

As suggested earlier, there is overwhelming evidence that multiple pathways existto both health and illness. It is a myth to think that all individuals displayingsymptoms of a given mental disorder ‘‘got there’’ through similar mechanismsand processes. We know, for instance, that the broad syndrome of depressionmay emanate from heritable risks in some cases, from severe life losses andstressors in others, from the interaction of the two in a great many more, andfrom other early or contemporaneous risk factors in still others. ADHD, for example,is substantially heritable but the constituent symptomatology may also emergefrom low birthweight, severe early deprivation, effects of teratogens like nicotineor tobacco in utero, or even from what were formerly thought to be low levels ofenvironmental lead (Barkley, 2006; Nigg, 2006). In short, equifinality—the presence ofmultiple pathways leading to apparently similar outcome states—clearly operateswith regard to the major entities of mental disturbance that we now recognize(Cicchetti & Rogosch, 1996).

In parallel, although inhibited temperament in infancy and toddlerhood is clearlypredictive of risk for subsequent social anxiety, there is far from a 1:1 correspon-dence. Other risk and protective factors, including the presence of childrearingenvironments that gently but firmly ‘‘push’’ the child out of inhibited, withdrawnbehavior patterns, may deflect any inevitable association between early inhibitionand later internalizing conditions (see Kagan, 1997, and Chapter 7). Similarly, childmaltreatment does not lead to a uniform set of outcomes but may instead yielda range of subsequent behavioral and emotional patterns even when the type orseverity of abuse is held constant (Cicchetti & Valentino, 2006). Hence, throughprocesses of multifinality, complex causal chains of influence render the operationof early risk factors as probabilistic rather than deterministic. In cases of pathology,the chain tends to intensify and widen, in a process termed developmental cascades(Masten & Cicchetti, 2010).


Thus, the DP model emphasizes malleability, flexibility, and plasticity in devel-opment, although the presence of multiple risk factors is clearly linked to loweredchances of recovery. Core issues in this regard involve, first, the attempt to disentan-gle the many potential developmental influences that may tip the individual towardhealth and competence versus disorder and failure; and second, the necessity ofincorporating what is termed probabilistic epigenesis (Gottlieb & Willoughby, 2006)into causal models. This term means that genes do not provide a one-way causalinfluence on neural structures and behavior, because of highly interactive, reciprocal,and bidirectional influences with epigenetic factors (e.g., other brain structures andproducts, behavioral patterns, and environmental influences). Here we see that sev-eral DP principles—for example, nonlinear causal patterns, reciprocal/transactionalmodels, and the importance of context—are closely linked. In an elegant musicalmetaphor, Boyce (2006) presents the notion of ‘‘symphonic causation’’ to illustratethe confluence of biological and contextual influences on development.

Psychobiological Principles and Discoveries

The genomic era is upon us, and advances in brain imaging research and clinicaltechniques have made the developing brain far more accessible to scientific viewthan ever before (e.g., Giedd et al., 2006; Rende & Waldman, 2006). Although it ismistaken, as noted earlier, to give primacy to any given level of analysis in a DPperspective—brain, contextual, or other (Cicchetti & Toth, 2009)—we have askedcontributors to pay particular attention to psychobiological factors and processes intheir coverage.

Part of the reason is historical: Family systemic and environmental views dom-inated the field for much of the 20th century, and recent work on a range ofpsychobiological processes is not always featured in reviews and texts (Boyce,2006). Another issue pertains to explanatory power: We now know that withoutunderstanding the potential effects of genes, physiological processes, and bio-logical risk factors on psychopathology, we have little hope of understandingthe most severe forms of disorder. Because the brain is remarkably plastic andbecause context influences biological unfolding, we have—as noted throughoutthis chapter—asked authors to emphasize contextualization of the psychobiologicalperspectives they present. In fact, reductionistic accounts of the primacy of singlegenes, the inevitable predictability of later functioning from early temperament,or the ‘‘placement’’ of psychopathology completely inside brightly colored brainimages on journal or chapter pages are as short-sighted as the exclusively environ-mental accounts of psychopathology that dominated a half-century ago, such asthe blaming of autism on emotional refrigeration by parents or schizophrenia byschizophregenic mothers.

Summary

Clearly, the development of psychopathological functioning is multidetermined,complex, interactive, transactional, and in many if not most instances nonlinear. It isnearly impossible to imagine otherwise, given the staggering complexity of the brain


and the myriad influences, ranging from the microsocial to the macrosocial, thatimpinge on the developing infant, toddler, and child. For those who like problemsand solutions wrapped in neat packages, the study of DP will undoubtedly be afrustrating endeavor, perhaps even unfathomable. On the other hand, for thosewho are intrigued by the diverse clinical presentations of various pathologicalconditions in childhood and adolescence; who are fascinated with how muchremains to be learned about antecedent conditions and maintaining factors; who arepossessed by an intense ‘‘need to know’’ about the underlying mechanisms of theconditions discussed in this volume; and who realize the need to consider healthyoutcomes and competence as well as maladaptation, the DP perspective is a vitalframework for the rapidly growing scientific enterprise linking normal and atypicaldevelopment. Longitudinal, multilevel investigations are often required to gain thetypes of knowledge needed to understand psychopathology and competence froma developmental perspective, with the potential of high yield for developmentalscience and for informing prevention and intervention efforts. The study of DP is everexpanding, engaging scientists from large numbers of disciplines and perspectives.Progress is emerging quickly, but the territory to explore is vast and the roadahead is long.

A GUIDE TO THE BOOK’S CONTENTS

Immediately following this chapter, Theodore P. Beauchaine, Daniel N. Klein, NoraL. Erickson, and Alyssa L. Norris (Chapter 2) provide a history of attempts to classifythe vast domain of child and adolescent psychopathology, culminating in the newesteditions of the Diagnostic and Statistical Manual of Mental Disorders and the Interna-tional Classification of Diseases. This historical perspective throws into sharp relief thetensions between categorical versus continuous conceptions of psychopathologicalbehavior and the still-vast territories to be investigated in order to reconcile basicscience and current classifications. In Chapter 3, Theodore P. Beauchaine and LisaM. Gatzke-Kopp provide rich detail on gene-environment interplay and on psy-chobiological forces more generally, given their strong implications in the genesisof child and adolescent psychopathology. This material is essential background formany of the disorder-specific chapters that follow later in the volume.

In the next section (Part II), Bruce E. Compas and Charissa Andreotti (Chapter 4)lead off by writing about cultural and contextual factors linked to the develop-mental of psychopathology. As discussed in the present chapter, such influencesdeserve equal billing with psychobiological factors and forces in current DP concep-tualizations. In Chapter 5, Sara R. Jaffee and Andrea Kohn Maikovich-Fong covermaltreatment, which is known to be a clearly ‘‘environmental’’ contributor to psy-chopathology but one that (a) correlates and interacts with biological vulnerabilitiesand (b) may well produce biological as well as psychological consequences. Then, inChapter 6, Emily Neuhaus and Theodore P. Beauchaine discuss the role of impulsiv-ity as a risk factor for diverse forms of externalizing psychopathology. Providing richhistorical coverage, they debunk earlier myths about the neural underpinnings ofimpulsivity and bring to life a host of core DP constructs. Chapter 7, by Jerome Kagan,is a witty and engaging account of behavioral inhibition and its consequences for


a range of internalizing behavior patterns. This work also highlights many core DPprinciples, serving as a needed antidote to reductionism, either environmental or bio-logical. In Chapter 8 Bruce J. Ellis, Marco Del Giudice, and Elizabeth A. Shirtcliff detailhow exquisitely adaptive the human stress response system is, and the implicationsof this adaptability for both vulnerability to and protection from psychopathology.In Chapter 9, Nicole A. Crocker, Susanna L. Fryer, and Sarah N. Mattson discussteratogens—substances either (a) transmitted from a pregnant mother to her embryoor fetus, or (b) encountered in the postnatal environment—that promote dysfunctionin the developing organism. This work emphasizes the probabilistic rather than thedeterministic nature of this pernicious risk factor. In Chapter 10, Katherine ShannonBowen and Lisa M. Gatzke-Kopp cover various forms of brain injury, with emphasison risk for dysfunction and potential recovery. This chapter deals with the specific‘‘pathogens’’ of physical trauma and hypoxia, the construct of neural plasticity,and the potential for genetic factors to interact with trauma in the development ofmaladaptation. In Chapter 11, Pamela M. Cole, Sarah E. Hall, and Nastassia J. Hajalwrite a theoretically rich account of emotion dysregulation and its implicationsfor psychopathological outcomes. In their view, emotions are inherently activatingand organizing, but if attempts at their regulation are insufficient, if emotions aredisplayed in context-inappropriate fashion, or if emotions change either too quicklyor too slowly, implications for dysfunction become apparent.

Part III covers disruptive or externalizing conditions. In Chapter 12, Joel Niggprovides rich coverage on the core processes of inattention, impulsivity, andhyperactivity that characterize ADHD, with an integration of psychological andpsychobiological processes—and of both genetic and often-neglected environmen-tal risk factors for this condition. Explicitly embracing the core tenets of DP, thischapter emphasizes the great need for integrated theoretical models in future workon this prevalent and distressing disorder. Chapter 13, by Irwin D. Waldman andBenjamin B. Lahey, presents a comprehensive, multilevel, integrative view of thedevelopment of aggressive and antisocial behavior, with specific reference to thediagnostic categories of oppositional defiant disorder and conduct disorder. A keyissue for this domain of inquiry is the sheer number of pertinent risk factors,spanning intra-individual, familial, and wider contextual variables; Waldman andLahey’s integrative account is a welcome antidote to the often-chaotic feel of litera-ture in this area. Thomas J. Dishion and Kristina Hiatt Racer, in Chapter 14, discussprinciples and concepts underlying the development of antisocial personality, takinga life-span perspective as they do so, and featuring interplay among the myriad riskfactors (individual, parental, peer-related, neighborhood level) that together yieldadult antisocial outcomes and in some cases psychopathy. Chapter 15, by Sandra A.Brown, Kristin Tomlinson, and Jennifer Winward, discusses developmental trajec-tories of alcohol and substance problems, an area ripe for all of the DP principlesdiscussed in this chapter, with major public health implications given the scope andconsequences of early drug use and abuse.

Next, Part IV features internalizing conditions. Chapter 16, by Carl F. Weemsand Wendy K. Silverman, covers the range of anxiety disorders, providing an inte-grative perspective on their origins and maintenance. Building from dimensional


conceptions of anxiety and fear, they emphasize genetic and psychophysiologicalfactors, social learning and cognitive processes, social and interpersonal variables,and interactions across these levels. Daniel N. Klein, Autumn J. Kujawa, Sarah R.Black, and Allison T. Pennock comprehensively review, in Chapter 17, known riskfactors for and developmental issues related to child and adolescent depression.Covering the wide-ranging precursors to depressive outcomes (e.g., maladaptivecognitive patterns, stress reactivity, genetic vulnerability, disrupted parent–childrelationships, to name some of the more salient), they provide an integrative devel-opmental model. In Chapter 18, Sheila E. Crowell, Erin A. Kaufman, and Mark F.Lenzenweger provide essential commentary on borderline personality, self-injuriousbehavior, and their developmental antecedents. They emphasize genetic and neu-ral risk factors, the clear role of parenting disruptions, and interactions amongthem, concluding that borderline personality and intentional self-injury constituteextremes of impulse control problems, particularly in relation to severe stressors.Note that the placement of this chapter in Part IV is somewhat arbitrary, giventhe admixture of dysphoric, i

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