Developmental Psychopathology, Maladaptation and Psychopathology

By Dante Cicchetti

A comprehensive reference on external contributing factors in psychopathology

Developmental Psychopathology is a four-volume compendium of the most complete and current research on every aspect of the field. Volume Three: Risk, Disorder, and Adaptation explores the everyday effects and behaviors of those with behavioral, mental, or neurological disorders, and the disorder's real-world impact on their well-being. Now in its third edition, this comprehensive reference has been fully updated to better reflect the current state of the field, and detail the latest findings in causation, intervention, contextual factors, and the risks associated with atypical development. Contributions from expert researchers and clinicians explore the effects of abuse and traumatic stress, memory development, emotion regulation, impulsivity, and more, with chapters specifically targeted toward autism, schizophrenia, narcissism, antisocial behavior, bipolar disorder, and borderline personality disorder.

Advances in developmental psychopathology have burgeoned since the 2006 publication of the second edition, and keeping up on the latest findings in multiple avenues of investigation can be burdensome to the busy professional. This series solves the problem by collecting the information into one place, with a logical organization designed for easy reference.

• Learn how childhood experiences contribute to psychopathology
• Explore the relationship between atypical development and substance abuse
• Consider the impact or absence of other developmental traits
• Understand the full risk potential of any behavioral or mental disorder

The complexity of a field as diverse as developmental psychopathology deepens with each emerging theory, especially with consideration of the multiple external factors that have major effects on a person's mental and emotional development. Developmental Psychopathology Volume Three: Risk, Disorder, and Adaptation compiles the latest information into a cohesive, broad-reaching reference with the most recent findings.

• Language: English
• Publisher: Wiley
• Release date: Feb 10, 2016
• ISBN: 9781119125501

Book preview

Table of Contents

Title Page

Copyright

Dedication

Preface to Developmental Psychopathology, Third Edition

References

Contributors

Chapter 1: Developments in the Developmental Approach to Intellectual Disability

Developments in the Developmental Approach to Intellectual Disability

The Diagnosis of Intellectual Disability and Its (Lack of) Meaningfulness

The Origins of the Developmental Approach to the Study of Intellectual Disability

The Two-Group Approach and Beyond

Applying Developmental Principles to the Study of Persons With Intellectual Disability: Classic and Expanded Versions

The Importance of Mental Age

The Study of the Whole Person With Intellectual Disability

Neuroscience and the Developmental Approach: Benefits and Pitfalls in the Application of Cutting-Edge Technology

Conclusions

References

Chapter 2: Fragile X Syndrome as a Multilevel Model for Understanding Behaviorally Defined Disorders

Introduction

The Fragile X Genotype and Phenotype

Brain–Behavior Relations in Fragile X

Cognitive and Behavioral Patterns in Fragile X

Insights From Longitudinal Studies of Fragile X

The Challenges of Comorbidity

Relationships to the Principles of Developmental Psychopathology

Future Directions: The Importance of Longitudinal Comparisons Across Syndromes of Known Genetic Origin

Translational Implications

Concluding Thoughts

References

Chapter 3: Autism Spectrum Disorders

Historical Context

Core Characteristics

Diagnosis and Assessment of ASD

Related Symptoms and Comorbid Disorders

Early Identification

Epidemiology

Etiology

Brain Structure and Function

Interventions and Treatment

Future Directions

References

Chapter 4: Joint Attention and the Social Phenotype of Autism Spectrum Disorder: A Perspective From Developmental Psychopathology

Overview

A Historical Perspective on Autism Spectrum Disorder

Diagnostic Description of ASD

Joint Attention in Typical Development

The Neural Systems of Joint Attention

Dynamic Systems and the Joint Attention PDPM

Joint Attention and Defining the Social Deficits of ASD

Applying the Joint Attention PDPM to ASD

Summary

Future Directions

References

Chapter 5: Explicating the Developmental in Preschool Psychopathology

Preschool Psychopathology: What Have We Learned from a Traditional Categorical DSM-Based Approach?

Measurement Advances: Dimensional Operationalization of the Conceptualization and Theory

Cross-Cutting Developmental Domain-Based Approach to Preschool Psychopathology

Translational Application of Developmentally Sensitive Assessment

Conclusions and Future Directions

References

Chapter 6: The Development of Emotion Regulation: Implications for Child Adjustment

Setting the Stage

Definitional and Theoretical Considerations

Developmental and Contextual Issues

Empirical Approaches and Challenges

Contributions of Emotion Regulation to Developmental Outcomes

Integration, Implications, and Future Directions: Modeling Complex Pathways Between ER and Child Functioning

Translational Implications

Conclusions

References

Chapter 7: Interpersonal Theories of Developmental Psychopathology

Historical Perspectives on Interpersonal Relationships as Contexts of Development

Principles of Developmental Psychopathology Within an Interpersonal Context

General Interpersonal Theories of Developmental Psychopathology

Intersection Between Interpersonal Theories and Alternate Theories of Psychopathology

Disorder-Specific Integrative Interpersonal Theories of Psychopathology

Future Directions

References

Chapter 8: Cognitive Risks in Developmental Psychopathology

Introduction

Cognitive Processes

Cognitive Products

Discussion

References

Chapter 9: Traumatic Stress From a Multilevel Developmental Psychopathology Perspective

Traumatic Stress From Multiple Levels of Analysis: An Introduction

A Range of Psychopathologies Following Early Trauma: Trauma-Spectrum Disorders and the Multilevel Approach to the Assessment of the Trauma Response

Relevance of the Multiple Levels of Analysis Approach to Developmental Psychopathology

Psychological Trauma: The Long View

DSM-III Pluses and Minuses

Trauma and the Self

Risk Factors for the Development of Trauma-Related Psychopathology

The Interaction of Developmental Epoch and the Brain

Biological Responses to Trauma

The Neural Circuitry of PTSD

Effects of Trauma on the Body

Multiple Levels of Analysis

Translational Implications of the Multilevel Developmental Psychopathology Perspective

Future Directions

Conclusions

References

Chapter 10: Childhood Exposure to Interpersonal Trauma

Prevalence: Mediators and Moderators

Single Versus Cumulative Trauma

Manifestations and Child Outcomes

Environmental Interventions

Conclusion

References

Chapter 11: Child Maltreatment and Developmental Psychopathology: A Multilevel Perspective

Introduction

Definitional Considerations

Etiological Models of Child Maltreatment

Sequelae of Child Maltreatment

The Organizational Perspective on Development

Affect Differentiation and Emotion Regulation

Emotion Recognition

Formation of Attachment Relationships

Development of an Autonomous Self

Peer Relationships

Adaptation to School

Effects of Maltreatment on Memory

Personality Organization and Psychopathology

Gene–Environment Interaction

Maltreatment and Allostatic Load

Neuroendocrine Regulation and Reactivity

Adverse Physical Health Outcomes

Maltreatment Experiences and Neurobiological Development

Neuroimaging and Child Maltreatment

Child Maltreatment and Resilience

Race and Ethnicity

Methodological Issues in Maltreatment Research

Translational Research

Social Policy Perspectives

The Next Generation: New Frontiers in Child Maltreatment Research

References

Chapter 12: A Developmental Psychopathology Perspective on Foster Care Research

Introduction

A History of Foster Care and Foster Care Research

Early Adversity Increases the Likelihood of Atypical Emotional, Psychological, and Cognitive Development

Early Adversity Has the Potential to Alter Biological Development and to Increase Risk for Disease

The Timing and Duration of Adversity Is Associated With Differential Behavioral and Neurobiological Outcomes, With a General Trend of Longer Lasting Adversity Producing the Most Profound Effects

Neglect Is a Particular Cause for Concern Because of Its Pervasiveness and Its Propensity to Disrupt Healthy Development and Exert a Lasting Impact on Health and Well-Being

Transitions Among Primary Caregivers Are a Specific Class of Adverse Experience Worthy of Attention Because They Appear to Negatively Affect the Development of Key Cognitive and Behavioral Skills Needed for Social and Academic Success

The Combined Effects of Prenatal Stress (Especially Prenatal Substance Exposure) and Early Adversity on Neurobehavioral Development Are Additive and Produce Worse Outcomes Than Prenatal Stress or Early Adversity Alone

Resilience (i.e., Typical Development in the Face of Adversity) Is Evident in All Samples of Foster Children (Although What Contributes to It Is Not Well Understood)

Family-Based Care (Including Foster Care) Is, as a General Rule, Better Than Institutional Care

Family-Based Interventions That Can Mitigate the Effects of Early Adversity

Conclusions, Translational Implications, and Directions for Future Research

References

Chapter 13: Memory Development, Emotion Regulation, and Trauma-Related Psychopathology

Conceptual Framework

Overview of Memory Development

Emotion Regulation and Memory

Effects of Child Maltreatment

Theories of Trauma and Memory

Empirical Studies of Memory in Traumatized Children and Memory for Stressful Events in Typical Development

References

Chapter 14: Attention and Impulsivity

Introduction

Attention-Deficit/Hyperactivity Disorder: Background

Etiologies

Attention and Impulse Control in Development: Dual-Process Perspective

Attention: Conceptual Framework and Key ADHD-Related Effects

Impulse Control: Conceptual Framework and Key ADHD Effects

Future Directions and Conclusions

References

Chapter 15: The Development and Ecology of Antisocial Behavior: Linking Etiology, Prevention, and Treatment

A Brief History

Building Models of Antisocial Behavior

Coercion and Contagion Dynamics

Early Childhood: Coercion in Families

Middle Childhood: Coercion and Contagion

Adolescent Problem Behavior

Summary and Future Directions

References

Chapter 16: Narcissism

Introduction

History of Narcissism

Narcissism and Its Manifestations

Assessment of Narcissism in Children and Adolescents

Theories of Narcissism

Development and Etiology of Narcissism

Clinical Perspectives on Narcissism

Controversies

Conclusion and Future Research

References

Chapter 17: A Multilevel Perspective on the Development of Borderline Personality Disorder

Introduction

What Is Borderline Personality Disorder?

Key Ideas in the Mentalization-Based Approach to BPD

Attachment, Mentalizing, and BPD

Secondary Attachment Strategies, Mentalizing, and the Neurobiology of BPD

Adolescence and the Emergence of BPD

Implications for Intervention

Conclusions

References

Chapter 18: Alcohol Use and the Alcohol Use Disorders Over the Life Course: A Cross-Level Developmental Review

Introduction

Epidemiology

The Developmental Progression of Use and Disorder: A Multilevel Matrix

Variations in Risk and Course of Disorder: Alcohol-Nonspecific Risk, Behavioral Disinhibition, and a Hierarchical Model of General and Specific Risk for Alcoholism

Variations in Risk and Course of the Disorder: Emergence and Course of Alcohol-Specific Risk

The Genetics of Alcohol Use, Problems, and AUD

Intermediate-Level Etiology in Brain

Future Work and Concluding Comments

References

Chapter 19: Substance Use and Substance Use Disorders

Chapter Overview

Clinical Substance Use Disorders

Epidemiological Trends in Adolescent Substance Use

Relations With Demographic Factors

Use of Multiple Substances: Patterns Over Time

Age-Related Trajectories of Substance Use: Typical Age-Related Patterns

Individual Variability in Substance Use Trajectories: The Significance of Age of Onset and Time to Disorder

Etiological Pathways: General and Substance-Specific Biopsychosocial Mechanisms of Risk and Age and Stage Differences in Risk Pathways

The Externalizing Pathway

The Internalizing Pathway

The Negative Affect–Drug Use Relation

An Internalizing Developmental Pathway

Specificity in the Affect–Drug Association

Implications of the Externalizing and Internalizing Pathways for Treatment and Prevention

Genetic Influences on Substance Use Effects

Models of the Development of Chronic Effects and Dependence

The Yin and the Yang of Dependence: Dual-Process Approaches to Understanding Addiction

Behavioral Assessment of Impulsive Processes: Implicit Cognition

Treatment Implications of the Drug Effects Pathways

Macro Influences

Conclusions

References

Chapter 20: Bipolar Disorder from a Developmental Psychopathology Perspective: Focusing on Phenomenology, Etiology, and Neurobiology

Bipolar Disorder: Conceptualized Within a Developmental Psychopathology Framework

Classification and Phenomenology: Historical Context and Recent Advances

Etiology of Bipolar Disorder

Neuroimaging Findings in Pediatric Bipolar Disorder and High-Risk Populations

Translational Implications

Summary and Conclusion

References

Chapter 21: Childhood Schizophrenia

Introduction

Diagnosis

Cognition

Social Cognition

Risk Factors

Imaging Overview

Normal Brain Development

Schizophrenia

Genetics

Treatment

Future Directions

References

Chapter 22: Multilevel Approaches to Schizophrenia and Other Psychotic Disorders: The Biobehavioral Interface

The Symptoms and Modal Course

The Origins of Vulnerability to Schizophrenia and Other Psychoses

Epidemiology and Postnatal Environmental Exposures

Developmental Stages in the Emergence of Psychosis

Neurobiological Mechanisms

Treatment and Preventive Intervention

Future Research Directions

References

Chapter 23: Toward a Unifying Perspective on Personality Pathology Across the Life Span

Considering Personality Pathology in a Developmental Psychopathology Framework

Defining Normal Personality

Defining PD Across the Life Span

Critical Developmental Periods for PD

Conclusions and Future Directions

References

Chapter 24: Toward a Developmental Psychopathology of Personality Disturbance: A Neurobehavioral Dimensional Model Incorporating Genetic, Environmental, and Epigenetic Factors

Background and Context for a Developmental Model of Personality Disturbance

Prior Attempts to Understand Personality Disorder: Lexical Traits, Hybrid Constructs, and Axis I Disorders Extended

Neurobehavioral Systems Underlying Higher Order Personality Traits and Their Modification by Experience

Concluding Remarks and Future Directions

References

Author Index

Subject Index

End User License Agreement

List of Illustrations

Chapter 4: Joint Attention and the Social Phenotype of Autism Spectrum Disorder: A Perspective From Developmental Psychopathology

Figure 4.1 Illustrations of different types of infant social attention coordination behaviors: (a) responding to joint attention (RJA): following another person's gaze and pointing gesture; (b) initiating joint attention (IJA): using a conventional gesture (such as pointing) to share attention regarding a room poster; (c1,2,3) IJA: using an alternation of eye contact to share attention with respect to a toy; (d) initiating behavior requests: pointing to elicit aid in obtaining an out of reach object; (e) responding to behavior requests: following an adult's open-palm give-it-to-me gesture.

Figure 4.2 Illustration depicting the referential mapping problem encountered by infants in incidental social word learning situations.

Figure 4.3 Illustration of the range and stability of individual differences in IJA alternating eye contact in 95 infants between 9 and 18 months of age (left panel), and the meaningful nature of individual differences in IJA alternating eye contact for a combined measure of receptive and expressive vocabulary development at 24 months.

Figure 4.4 Illustration of the default network (circles with black background and white dots), frontoparietal network (circles in grayscale), and the dorsal attention network (circles with white background and black dots) in the top panel, and connectivity within and across networks in the bottom panel.

Figure 4.5 Illustration depicting the lateral (top) and medial (bottom) illustrations of Brodmann's cytoarchitectonic areas of the cerebral cortex associated with initiating joint attention and the anterior attention system, as well as RJA and the posterior attention systems. The former include areas 8 (frontal eye fields), 9 (prefrontal association cortex), 24 (anterior cingulate), 11, and 47 (orbital prefrontal association cortex). The latter include areas 7 (precuneus, posterior parietal association area), 22, 41, and 42 (superior temporal cortex), and 39 and 40 (parietal, temporal, occipital association cortex).

Figure 4.6 An illustration of the parallel distributed information processing system model of joint attention and social cognition. In this model, different types of lines depict the multiple paths of joint attention development. The posterior attention system path associated with RJA development is illustrated with a dotted line and the anterior attention system path associated with IJA development is illustrated with a dashed line . The central solid line in the Figure depicts the developments of other processes during infancy that influence joint attention development, such as representational ability, speed of processing, motivation, and executive attention control, as well as each other, during infancy. The diagonal arrows connect all paths throughout early development. This reflects the dynamic and coactive nature of joint attention development, whereby the maturation of attention, cognitive, and affective systems interact in reciprocal cause and effect relations with experience, including the experiences children create for themselves through their own actions. Finally, the development of integrated self and other attention processing is considered to be a social attention executive function of the anterior system that emerges in the 4- to 9-month period. This is represented by the box. The capacity to integrate and share overt aspects of attention provides a foundation for the ability to share covert aspects of attention, such as representations, and social cognition.

Figure 4.7 An illustration of the decrease in response latency to left and right RJA trials on the Early Social-Communication Scales (Mundy, Hogan, & Doehring, 1996) between 9 and 18 months of age. Also illustrated is the decrease in response latency across a sequence of RJA trials exhibited by infants at 9 months of age.

Figure 4.8 An illustration of the continuous information processing model of social attention, joint attention, and social-cognition. Here development is modeled as a spiral, in which the initial acquisition of the capacity for integrated processing of information about self- and other- attention (joint attention) remains an active but deeper layer of cognitive activity throughout life that supports symbolic thought, language, and cultural social exchange.

Figure 4.9 In the first year, the development of joint attention involves the learning-to phase. This period comprises the integration of executive, motivational, and imitative processes to support the routine, rapid, and efficient (error-free) execution of behavioral patterns, which enable infants' coordination of overt processing of aspects of visual self-attention, with processing of the social attention of other people. In the latter part of the first year and the second year, infants can better monitor their own experiences and integrate them with information about social partners during joint attention events. This provides a critical multimodal source of information to the infants about the convergence and divergence of self- and other-experience and behavior during sharing information in social interactions. Theoretically, this provides the stage for the learning-from phase of joint attention development. In this stage, infants can control their attention to self-organize and optimize information processing in social learning opportunities. The integration of anterior and posterior self–other attention processing (Figure 4.5) provides a neural network that enriches encoding in social learning. The internalization of the overt joint processing of attention to the covert joint processing of attention to representations is part of an executive system that facilitates symbolic development and the social cognition. Both symbolic thought and social cognition may be characterized by a transition from learning to socially coordinate overt attention to the capacity to socially coordinate covert mental representations of the attention of self and others.

Figure 4.10 Illustration of the moderating effect of mental age on diagnostic group differences on RJA versus IJA.

Figure 4.11 Illustration of the IJA and RJA conditions in the Kim & Mundy (2012) joint attention and memory paradigm. In the IJA condition (panel A), the participant first views the avatar, then chooses to shift attention to a stimulus window to the left or right of the avatar. Eye-tracking data then flows to a WorldViz© software program to trigger gaze following in the Avatar and onset of the study picture. The final illustration in panel A indicates that, after a study trial ended, the participant returned to midline, but the Avatar remained fixated on the target area to insure that the participant recognized that the avatar had followed his or her gaze. In the RJA condition, the participant fixated the Avatar and followed the direction of gaze of the avatar to choose a picture to study. Eye tracking control of stimulus onset ensured the picture did not appear until the participant followed the Avatar's gaze. This equated the study time that was available on each trial across IJA and RJA conditions. The Avatar again returned to midline gaze after the participant returned to midline.

Chapter 5: Explicating the Developmental in Preschool Psychopathology

Figure 5.1 Relation of temper loss to externalizing disorders (left). Relation of temper loss to internalizing disorders (right).

Figure 5.2 Normal–abnormal spectrum of MAP-DB noncompliance.

Chapter 7: Interpersonal Theories of Developmental Psychopathology

Figure 7.1 Models of person–environment (PxE) interactions. Childhood adversity and youth depression: The role of gender and pubertal status. Development and Psychopathology, 19, 497–521.

Figure 7.2 Theoretical model of the interpersonal context of adolescent depression.

Figure 7.3 A developmental model of the attachment-moderated interaction of risk factors in the development of anxiety disorders.

Figure 7.4 A biopsychosocial model of the development of conduct disorder.

Chapter 9: Traumatic Stress From a Multilevel Developmental Psychopathology Perspective

Figure 9.1 Model of how traumatic stress affects the brain. Stress is associated with acute increases in cortisol and norepinephrine. With chronic stress there is dysregulation of these systems with increased amygdala function and decreased hippocampal and medial prefrontal function. Outputs through the hypothalamus and medial prefrontal cortex increase peripheral sympathetic and cortisol function, increasing the risk of heart disease.

Figure 9.2 Hippocampal volume in PTSD on a coronal MRI. The hippocampus is visibly smaller in the PTSD patient compared with a normal control.

Figure 9.3 Replicated findings in PTSD. The most replicated findings related to symptom provocation are decreased medial prefrontal function. Other findings include decreased hippocampal and dorsolateral prefrontal function and increased amygdala function.

Figure 9.4 Amygdala function in PTSD. With classical fear conditioning (pairing of an unconditioned stimulus [shock] with conditioned stimulus [seeing a blue square on a screen] there was increased amygdala activation in PTSD relative to controls, suggesting increased sensitivity of the amygdala in the learning of fear.

Figure 9.5 Effects of combat related slides and sounds on brain function. Outlined area shows decreased blood flow with combat slides in sounds in combat veterans with PTSD. This area normally inhibits the amygdala (involved in fear responses).

Chapter 14: Attention and Impulsivity

Figure 14.1 Correlations among child disorders.

Figure 14.2 Molecular genetic meta-model.

Figure 14.3 Vulnerability versus susceptibility models of G×E effect.

Figure 14.4 Brain attention networks. Panel a: Attention networks. The dorsal attention network = interparietal sulcus (IPS), frontal eye fields (FEF); it is associated with strategic direction of attention. The vental attention network includes temporal-parietal junction (TPJ), inferior frontal gyrus (IFG). It is associated with bottom-up capture of attention. Panel b: Executive control networks involved in higher order attentional allocation and control on task. Frontoparietal network includes dorsolateral PFC (dlpfc), IPS, medial cingulate (mCC); cingulo-opercular network includes dorsal anterior cingulate (dACC), anterior pole (aPFC), fronto-operculum (Al/fO), and thalamus as well as regions of striatum not shown. These canonical networks are inferred from functional connectivity as well as task based functional MRI data. For detailed discussion see Petersen & Posner (2012).

Figure 14.5 Altered brain activation during attention tasks in ADHD. ADHD associated on attention tasks with decreased activation in the right dorsolateral prefrontal cortex (DLPFC), left putamen and globus pallidus, right posterior thalamus (pulvinar) and caudate tail extending into the posterior insula, in the right inferior parietal lobe, and in the precuneus and superior temporal lobe. Increased activation in the left cuneus and in the right cerebellum.

Figure 14.6 Figure 6: White matter microstructure and ADHD. Meta-analysis results for fractional anisotropy effects ADHD versus non-ADHD (all effects z > 3, p < .05 corrected). Top row: Coronal view. Bottom row: Axial few. L = Left, R = Right.

Figure 14.7 Ex-Gaussian decomposition of reaction time components. Reaction time distributions are usually positively skewed (third display on right), rendering a standard statistical analysis suspect. One solution is decomposing the distribution components. Left panel: μ reflects the mean of the normal (Gaussian) portion of the distribution, and σ captures the standard deviation of the normal portion of the distribution. Middle panel: τ reflects both the mean and standard deviation of the exponential portion of the distribution. Right panel: combining these describes the skewed distribution.

Figure 14.8 Diffusion decomposition of reaction time components. Drift rate (v) = rate at which information accumulates as reflected by the average slope of the line. It is determined by speed of information processing and noise (represented by the hypothetical jagged deviations from the average slope). Larger values of v indicate faster processing. Boundary separation (a) = conservativeness of the response criterion with wider separations indicating more conservative responding. Nondecision time (Ter) includes all nondecision processes, such as stimulus encoding and motor preparation.

Figure 14.9 Temporal discounting hypothetical curve in addiction. This Figure shows the predicted values of two reinforcers as a function of the delay until their receipt as predicted by the exponential model (left panel, A) and hyperbolic model (right pane, B). The height of the vertical lines represents the magnitude of subjective value on the future reward.

Figure 14.10 Temporal discounting curve in children with ADHD and typically developing control children.

Figure 14.11 Brain model of response inhibition. Response inhibition has been mapped through a series of animal and human studies. The network now considered to be involved includes the subthalamic nucleus (STN), caudate, premotor cortex (PMC), presupplemental motor area, and inferior frontal cortex (IFC) and their interconnecting white matter tracts.

Figure 14.12 Race model of response inhibition. Two processes compete in this model. The go process launches when the go signal is perceived; the stop process launches when the stop signal is perceived. Depending on the timing of the stop signal and the speed of the two processes, the response will be executed or interrupted. SSRT = Go RT minus stop signal delay. The relative speed of the component processes is illustrative only and not to scale.

Figure 14.13 Altered brain activation during inhibition tasks in ADHD. Meta-analytic results. IFC = inferior prefrontal cortex; SMA = supplementary motor area (SMA), ACC = anterior cingulate cortex (ACC) Color picture available online

Figure 14.14 ADHD physiology and CU subgroup. Three groups are depicted: typically developing children (typical, n = 128), ADHD (n = 54), and ADHD with callous-unemotional features (ADHD-CU; n = 21). The x axis depicts four emotion conditions: (1) negative and (2) positive emotion (NE, PE); (3) emotional induction (Y); and (4) suppression (Su). Panel A: Preejection period on the y axis; higher value = lower sympathetic arousal. Panel B: Respiratory sinus arrhythmia (*100) difference from baseline (at 0) on y axis; higher value = greater regulatory engagement.

Figure 14.15 ADHD neuropsychological subtypes suggested by empirical clustering. Derived from graph theory analysis. Control group scaled to 0, all measures are in standard deviation units scaled on control group mean; high scores=poor performance.

Figure 14.16 ADHD temperament types suggested by empirical clustering. Three temperament based subtypes of ADHD based on a graph theory analysis of maternal ratings. N = 310 ADHD, 180 typically developing. Control children scores are scaled to 0 on all scales; the y axis is standard deviation units scaled to the control group.

Chapter 15: The Development and Ecology of Antisocial Behavior: Linking Etiology, Prevention, and Treatment

Figure 15.1 A developmental cascade model: parenting contributions and amplifying mechanisms.

Figure 15.2 A state space grid summarizing parent–child interaction in early childhood.

Figure 15.3 Early development of oppositional and aggressive behavior.

Figure 15.4 A cross-lagged model for observed parent–child dyadic positive engagement and coercive interactions.

Figure 15.5 A multilevel analysis of intervention effects on family microsocial dynamics in early childhood.

Figure 15.6 Peers and the emergence of covert antisocial behavior in middle childhood.

Figure 15.7 Life history perspective on peer influence in adolescence.

Figure 15.8 Self-organized peer groups and adolescent problem behavior.

Figure 15.9 Self-organized peer groups and progressions to adolescent ADU dependence.

Figure 15.10 Adolescent friendship influence on the ADU progression.

Figure 15.11 Dyadic coregulation as a moderator for friendship influence progressions in substance use.

Figure 15.12 Adolescent friendship influence on violence progression.

Figure 15.13 Unique contributions of trauma to adolescent violence.

Figure 15.14 From family to peers: microsocial coercion in the development of violence.

Figure 15.15 Normative and antisocial development and young adult rehabilitation.

Chapter 17: A Multilevel Perspective on the Development of Borderline Personality Disorder

Figure 17.1 Mentalizing profile of the prototypical BPD patient.

Figure 17.2 A biobehavioral switch model of the relationship between stress and controlled versus automatic mentalization.

Chapter 18: Alcohol Use and the Alcohol Use Disorders Over the Life Course: A Cross-Level Developmental Review

Figure 18.1 Harm caused by drugs.

Figure 18.2 Past 30-day alcohol use (any, binge, or heavy) according to age.

Figure 18.3 Probability of alcoholism (risk) over the life course: the envelope of risk expression as a function of genes, intermediate traits, environment, and life stage.

Figure 18.4 The multigenerational linkage of life-course trajectories in individual/developmental time, life-stage time, family time, and historical time: an example.

Figure 18.5 Cross-level/multidomain mechanistic structure of risk for alcohol use and AUD.

Figure 18.6 Multilevel mechanistic structure in developmental perspective.

Figure 18.7 Model of behavioral disinhibition and early-onset substance use disorders. Note: the Figure depicts the interplay among heritable individual differences characteristics and environmental influences on the development of three substance use disorders and antisocial personality disorder. Ellipses are latent variables that represent generalized risk factors. The variables in the boxes are conceptualized to represent specific and observable manifestations of these generalized risk factors. Specific genetic and environmental effects represented by the box at the far right work to differentiate the adult disorder from one another. Dots between the boxes are meant to indicate that other risk factors in addition to those depicted in the Figure contribute to the development of substance use disorders.

Figure 18.8 Externalizing symptoms in different risk/adversity groups.

Figure 18.9 Internalizing symptoms in different risk/adversity groups.

Figure 18.10 Growth curve trajectories of binge drinking from adolescence through emerging adulthood. Note: solid lines represent estimated growth trajectories for the three groups from the mixture modeling. Dashed lines represent observed means of binge drinking at each age for each group. Observed frequencies of binge drinking (past year) ranged from 0 (none) to 5 (1–2 times a week). Nonbinger group, N = 176, 39.5% of the sample. Early–heavy group, N = 93, 20.9% of the sample. Late–moderate group, N = 134, 30.0% of the sample. Infrequent group, N = 43, 9.6% of the sample.

Figure 18.11 Course of the comorbid alcoholisms and the primary alcoholisms.

Figure 18.12 Cross-level mechanistic structure of undercontrol and related intermediate phenotypes.

Chapter 21: Childhood Schizophrenia

Figure 21.1 Lateral and superior surface cortical brain regions.

Figure 21.2 Right lateral and top views of the dynamic sequence of gray matter maturation over the cortical surface. The side bar shows a color representation in units of gray matter volume. Fifty-two scans from 13 subjects each scanned 4 times at approximately 2-year intervals.

Figure 21.3 Average rates of gray matter loss in normal adolescents and in schizophrenia. (A) Three-dimensional maps of brain changes, derived from high-resolution magnetic resonance images (MRI scans) acquired repeatedly from the same subjects, reveal profound, progressive gray matter loss in schizophrenia (Right). Average rates of gray matter loss from 13 to 18 years of age are displayed on average cortical models for the group. Severe loss is observed (red and pink; up to 5% annually) in parietal, motor, and temporal cortices, whereas inferior frontal cortices remain stable (blue; 0–1% loss). Dynamic loss is also observed in the parietal cortices of normal adolescents, but at a much slower rate. (B) Average gray matter loss rates were computed for all 24 subjects in superior frontal gyri (SFG), lateral temporal cortices (LTC), and superior parietal lobules (SPL) in both brain hemispheres. Error bars indicate the standard error of the sample means, by region, in controls and patients. Individual loss rates (in percent per year) are plotted ( 1 , patients; 1 , controls), showing significant group separation, despite some outliers.

Figure 21.4 Clusters showing significant alterations in the gyrification index in adolescents with schizophrenia. Top panel: Clusters displayed on inflated average image (fsaverage). Bottom panel: Clusters displayed on the pial surface of the fsaverage image. Left hemisphere is shown on the left, right hemisphere is on the right.

Figure 21.5 White Matter Tracts. SLF II and III = Superior longitudinal fascicle, ILF = Inferior longitudinal fascicle, MdLF = Middle longitudinal fascicle, UF = Uncinate fascicle, EC = External capsule. EMc = Extreme capsule.

Figure 21.6 Subject MRI scan identifying the sub-regions of the corpus callosum.

Figure 21.7 Connectivity-based segmentation of the thalamus in a single subject. (a) Division of the cerebral cortex according to anatomical landmarks (see Methods). (b) An axial section based on a histological atlas of the human thalamus with nuclei outlined by black lines. Nuclei have been color-coded according to the cortical zone to which we predict they would show the strongest connections, on the basis of data from nonhuman primates. (c,d) Classifying thalamic voxels based on the zone with the highest probability of connection resulted in clusters of commonly-connected voxels. The clusters correspond to histologically defined locations of major nuclei as in b. The medial, anterior purple area in c and d is thought to include the mediodorsal nucleus and nuclei within the anterior complex, which are connected to prefrontal cortex and the temporal lobe. The more posterior purple area is thought to include parts of the lateral and inferior pulvinar which connect to the temporal lobe. The yellow area is thought to include the anterior pulvinar and the lateral posterior nucleus which project mainly to posterior parietal and extrastriate areas. The blue area is thought to include the ventral posterior lateral nucleus, which projects to somatosensory cortices. The orange area is thought to include the ventral lateral and ventral anterior nuclei, which project to motor and premotor cortices.

Figure 21.8 Cortico-cerebellar-thalamic-cortical circuit.

Figure 21.9 Cortical activity during semantic and syntactic task in Healthy Control (HC) and Childhood Onset Schizophrenia Groups (COS). a. Several clusters of significant activity in frontotemporal language regions were observed in HC children for both the semantic (top) and syntactic (bottom) conditions as compared with resting baseline. Activation maps are displayed at a threshold of t > 3.85, p < 0.001 for magnitude, p < .05, corrected for spatial extent. b. Children with COS also showed significant task-related activity during the semantic (top) and syntactic (bottom) conditions as compared with resting baseline, albeit to a lesser degree than observed in the HC group. Activation maps are displayed at a threshold of t >3.85, p < 0.001 for magnitude, p < .05, corrected for spatial extent.

Chapter 22: Multilevel Approaches to Schizophrenia and Other Psychotic Disorders: The Biobehavioral Interface

Figure 22.1 Risk factors and developmental stages psychosis.

Chapter 24: Toward a Developmental Psychopathology of Personality Disturbance: A Neurobehavioral Dimensional Model Incorporating Genetic, Environmental, and Epigenetic Factors

Figure 24.1 A multidimensional model of personality disturbance.

Figure 24.2 A minimum threshold for elicitation of anxiety and negative emotions is illustrated as a trade-off function between eliciting stimulus magnitude (left vertical axis) and postsynaptic receptor activation of a neurobiological variable underlying the personality trait of neuroticism (horizontal axis). Range of effective (eliciting) stimuli is illustrated on the right vertical axis as a function of level of receptor activation. Two hypothetical individuals with low and high trait postsynaptic receptor activation (demarcated on the horizontal axis as A and B, respectively) are shown to have narrow (A) and broad (B) ranges of effective stimuli, respectively. Threshold effects due to a modulator of neuroticism neurobiology are illustrated as well.

Figure 24.3 Illustration of the components of the gene (SLC6A4) that codes for the serotonin transporter (5-HTT). Polymorphism of the promotor region yields two common alleles (S and L) that differ in length of nucleotide number.

Figure 24.4 Anterior cingulate–amygdala circuitry that provides negative feedback to modulate activity of the amygdala.

Figure 24.5 Components of the central and peripheral corticotrophin releasing-hormone (CRH) systems. Abbreviations: Ce (central amygdala nucleus), BNST (bed nucleus of the stria terminalis), LH (lateral hypothalamus), PGi (paragiganticocellularis), PVN (paraventricular nucleus of the hypothalamus), ACTH (corticotropic hormone from the anterior pituitary).

Figure 24.6 Rats raised by mothers that display low licking-and-grooming behavior exhibit more anxiety-related behavior than rats raised by high licking-and-grooming mothers. Cross-fostering studies show that the offspring of low licking-and-grooming mothers raised by high licking-and-grooming mothers are less prone to anxiety-related behavior as adults. This indicates that the effect is mediated by postnatal maternal environment. However, offspring of high licking-and-grooming mothers raised by low licking-and-grooming mothers do not have an increased tendency to develop anxiety-related behavior in adulthood, indicating that specific factors inherited by the high licking-and-grooming offspring protect them from the effects of being mothered by low licking-and-grooming females.

Figure 24.7 General scheme of chromatin remodeling. a) Picture of a nucleosome showing a DNA strand wrapped around a histone octamer composed of two copies each of the histones. b) Chromatin can be conceptualized as existing in two primary structural states: as active or open (top left) in which histone acetylation (a) is associated with opening the nucleosome to allow binding of the basal transcriptional complex and other activators of transcription; or as condensed or closed where all gene activity is permanently silenced (bottom left). In reality, chromatin exists in a continuum of several functional states (active; permissive (top right); repressed (bottom right; and inactive).

Figure 24.8 Five effects of high LG maternal care in the hippocampus on gene expression.

Figure 24.9 A summary of the effects of maternal experience and genetic polymorphisms on gene expression of glucocorticoid receptors during an early postnatal period.

Figure 24.10 Six effects of early aversive experience on glucocorticoid and DA systems in the VTA and NAS.

Figure 24.11 The interaction of an emotional trait with the higher order trait of constraint, forming a diagonal of behavioral stability extending from labile to rigid.

Figure 24.12 Rats differing in dopamine (DA) functioning show a different course of acquisition of self-administration of amphetamine over days.

Figure 24.13 Effects of increasing levels of childhood maltreatment on antisocial behavior as a function of a genetic polymorphism in MAOA.

Figure 24.14 Effects of increasing levels of childhood maltreatment on depression as a function of a genetic polymorphism in 5-HTT (s- vs l-alleles).

Figure 24.15 Nature of the interaction between environmental and neurobiological variables in the development of personality disturbance.

List of Tables

Chapter 1: Developments in the Developmental Approach to Intellectual Disability

Table 1.1 Summary of Studies Using Neuroscience Tools Among Individuals With Developmental Disabilities

Chapter 3: Autism Spectrum Disorders

Table 3.1 DSM-5 Diagnostic Criteria for Autism Spectrum Disorder

Table 3.2 Red flags indicating need for further evaluation for ASD

Table 3.3 Brain Regions and Structures Implicated in in ASD and Their Purported Function

Chapter 4: Joint Attention and the Social Phenotype of Autism Spectrum Disorder: A Perspective From Developmental Psychopathology

Table 4.1 Behavioral Intervention Studies With Effects on Joint Attention in Children With ASD

Chapter 5: Explicating the Developmental in Preschool Psychopathology

Table 5.1 Illustrative Behaviors Across Normal–Abnormal Dimensional Spectrum

Table 5.2 Illustrating the Normal–Abnormal Spectrum: Cross-Cutting Developmental Domains and Variation in Behavior in Preschool Psychopathology

Chapter 8: Cognitive Risks in Developmental Psychopathology

Table 8.1 Examples of Commonly Used EF Tasks

Table 8.2 Summary of Recent EF Meta-Analyses

Table 8.3 Summary of Recent Attention Meta-Analyses

Table 8.5 Examples of Commonly Used Memory Measures

Table 8.4 Examples of Commonly Used Attention Measures

Table 8.6 Summary of Memory Meta-Analyses

Table 8.7 Commonly Used Cognitive Product Measures

Table 8.8 Summary of Findings

Chapter 13: Memory Development, Emotion Regulation, and Trauma-Related Psychopathology

Table 13.1 Hypothesized Developmental Psychopathology Model of the Effects of Childhood Adversity on Memory

Chapter 14: Attention and Impulsivity

Table 14.1 Type 1 and Type 2 Regulation and Commonly Used Terminology

Table 14.2 Arousal-Related Concepts

Chapter 15: The Development and Ecology of Antisocial Behavior: Linking Etiology, Prevention, and Treatment

Table 15.1 Peer Clustering on ADU as a Mediator for Progressing to Late-Adolescence Dependence

Chapter 17: A Multilevel Perspective on the Development of Borderline Personality Disorder

Table 17.1 Mentalizing Strengths and Impairments in BPD Across the Four Vectors

Chapter 18: Alcohol Use and the Alcohol Use Disorders Over the Life Course: A Cross-Level Developmental Review

Table 18.1 Lifetime and 12-Month Prevalence of DSM-IV Substance Use Disorders

Table 18.2 Parallelisms Between Longitudinal Subtype Typology and Prospective Trajectory Class Studies Traversing Early Childhood to Late Middle Adulthood

Chapter 19: Substance Use and Substance Use Disorders

Table 19.1 Neurobiological Substrates for the Acute Reinforcing Effects of Drugs of Abuse

Chapter 21: Childhood Schizophrenia

Table 21.1 Positive and Negative Psychotic Symptoms

Table 21.2 Questions on Delusions for Children

Table 21.3 Definition and Examples of Thought Disorder

Table 21.4 Developmental Approach to Differential Diagnosis of Childhood and Adolescent Onset Schizophrenia

Table 21.5 Childhood Triad of Putative Antecedents of Adult Onset Schizophrenia

Table 21.6 Risk Factors for Schizophrenia (Sz)

Table 21.7 Symptoms, Cognition, and Frontal Lobe Regional Structural Abnormalities

Table 21.8 Thalamo-cortical connectivity and functions

Chapter 22: Multilevel Approaches to Schizophrenia and Other Psychotic Disorders: The Biobehavioral Interface

Table 22.1 Diagnostic Criteria for Schizophrenia and Other Psychotic Disorders (DSM-V, 2013)

Table 22.2 Catatonia Associated with Another Mental Disorder (DSM-V, 2013)

DEVELOPMENTAL PSYCHOPATHOLOGY

THIRD EDITION

Volume Three: Maladaptation and Psychopathology

Editor

DANTE CICCHETTI

Title Page

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Library of Congress Cataloging-in-Publication Data:

Developmental psychopathology / editor, Dante Cicchetti. – Third edition.

pages cm

Includes index.

ISBN 978-1-118-12087-3 (volume 1 : cloth : alk. paper) – ISBN 978-1-118-12091-0 (volume 2 : alk. paper) – ISBN 978-1-118-12092-7 (volume 3 : alk. paper) – ISBN 978-1-118-12093-4 (volume 4 : alk. paper) 1. Mental illness–Etiology. 2. Developmental psychology. 3. Mental illness–Risk factors. 4. Adjustment (Psychology) I. Cicchetti, Dante.

RC454.4.D483 2016

616.89–dc23

These volumes are dedicated to Marianne Gerschel in recognition of her great vision and staunch support of the field of developmental psychopathology.

Preface to Developmental Psychopathology, Third Edition

A decade has passed since the second edition of Developmental Psychopathology was published. The two prior editions (Cicchetti & Cohen, 1995, 2006) have been very influential in the growth of the field of developmental psychopathology. The volumes have been highly cited in the literature and have served as an important resource for developmental scientists and prevention and intervention researchers alike. In the present third edition, we have expanded from the three volumes contained in the second edition to four volumes. The increased number of volumes in this current edition reflects the continued knowledge gains that have occurred in the field over the past decade.

A not insignificant contributor to this growth can be found in the very principles of the discipline (Cicchetti, 1984, 1990, 1993; Cicchetti & Sroufe, 2000; Cicchetti & Toth, 1991, 2009; Rutter & Sroufe, 2000; Sroufe & Rutter, 1984). Theorists, researchers, and prevention scientists in the field of developmental psychopathology adhere to a life span framework to elucidate the numerous processes and mechanisms that can contribute to the development of mental disorders in high-risk individuals as well as those operative in individuals who already have manifested psychological disturbances or who have averted such disorders despite their high-risk status (Cicchetti, 1993; Masten, 2014; Rutter, 1986, 1987, 2012). Not only is knowledge of normal genetic, neurobiological, physiological, hormonal, psychological, and social processes very helpful for understanding, preventing, and treating psychopathology, but also deviations from and distortions of normal development that are seen in pathological processes indicate in innovative ways how normal development may be better investigated and understood. Similarly, information obtained from investigations of experiments of nature, high-risk conditions, and psychopathology can augment the comprehension of normal development (Cicchetti, 1984, 1990, 1993; Rutter, 1986; Rutter & Garmezy, 1983; Sroufe, 1990; Weiss, 1969).

Another factor that has expedited growth within the field of developmental psychopathology has been its ability to incorporate knowledge from diverse disciplines and to encourage interdisciplinary and translational research (Cicchetti & Gunnar, 2009; Cicchetti & Toth, 2006). In keeping with its integrative focus, contributions to developmental psychopathology have come from many disciplines of the biological and social sciences. A wide array of content areas, scientific disciplines, and methodologies has been germane. Risk and protective factors and processes have been identified and validated at multiple levels of analysis and in multiple domains.

The increased emphasis on a multilevel, dynamic systems approach to psychopathology and resilience, the increased attention paid to gene–environment interplay in the development of psychopathology and resilience, and the application of a multiple levels of analysis developmental perspective to mental illnesses that have traditionally been examined nondevelopmentally (e.g., bipolar disorder, schizophrenia, and the personality disorders) not only have contributed to a deeper understanding of the dysfunctions but also have educated the public about the causes and consequences of mental disorder (see Cicchetti & Cannon, 1999; Cicchetti & Crick, 2009a, 2009b; Miklowitz & Cicchetti, 2006, 2010; Tackett & Sharp, 2014).

Advances in genomics, GxE interactions, and epigenetics; growth in our understanding of neurobiology, neural plasticity, and resilience; and progress in the development of methodological and technological tools, including brain imaging, neural circuitry, hormone assays, immunology, social and environmental influences on brain development, and statistical analysis of developmental change, pave the way for interdisciplinary and for multiple levels of analysis research programs that will significantly increase the knowledge base of the development and course of maladaptation, psychopathology, and resilience. Moreover, randomized control prevention and intervention trials are being conducted based on theoretical models and efforts to elucidate the mechanisms and processes contributing to developmental change at both the biological and psychological levels (Belsky & van IJzendoorn, 2015; Cicchetti & Gunnar, 2008).

Despite the significant advances that have occurred in the field of developmental psychopathology, much important work lies ahead. Undoubtedly these future developments will build on the venerable contributions of the past; however, as work in the field becomes increasingly interdisciplinary, multilevel, and technologically sophisticated, it is essential that even more emphasis be directed toward the process of development (Harter, 2006; Sroufe, 2007, 2013). It is not only genes and environments but also the cumulative developmental history of the individual that influences how future development will unfold (Sroufe, 2007, 2013).

Developmental psychopathologists have incorporated concepts and methods derived from other disciplinary endeavors that are too often isolated from each other, thereby generating advances in knowledge that might have been missed in the absence of cross-disciplinary dialogue. The continuation and elaboration of the mutually enriching interchanges that have occurred within and across disciplines interested in normal and abnormal development not only will enhance the science of developmental psychopathology but also will increase the benefits to be derived for individuals with high-risk conditions or mental disorders, families, and society as a whole.

Dante Cicchetti, Ph.D.

Minneapolis, MN

January 2015

References

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Cicchetti, D. (1984). The emergence of developmental psychopathology. Child Development, 55(1), 1–7.

Cicchetti, D. (1990). A historical perspective on the discipline of developmental psychopathology. In J. Rolf, A. Masten, D. Cicchetti, K. Nuechterlein, & S. Weintraub (Eds.), Risk and protective factors in the development of psychopathology (pp. 2–28). New York, NY: Cambridge University Press.

Cicchetti, D. (1993). Developmental psychopathology: Reactions, reflections, projections. Developmental Review, 13, 471–502.

Cicchetti, D., & Cannon, T. (1999). Neurodevelopmental processes in the ontogenesis and epigenesis of psychopathology. Development and Psychopathology, 11, 375–393.

Cicchetti, D., & Cohen, D. (Eds.). (1995). Developmental psychopathology (Vols. 1–2). New York, NY: Wiley.

Cicchetti, D., & Cohen, D. (Eds.). (2006). Developmental psychopathology (2nd ed., Vols. 1–3). New York, NY: Wiley.

Cicchetti, D., & Crick, N. R. (Eds.) (2009a). Precursors of and diverse pathways to personality disorder in children and adolescents. [Special Issue, Part 1]. Development and Psychopathology, 21(3), 683–1030.

Cicchetti, D., & Crick, N. R. (Eds.). (2009b). Precursors of and diverse pathways to personality disorder in children and adolescents. [Special Issue, Part 2]. Development and Psychopathology, 21(4), 1031–1381.

Cicchetti, D., & Gunnar, M. R. (2008). Integrating biological processes into the design and evaluation of preventive interventions. Development and Psychopathology, 20, 737–743.

Cicchetti, D., & Gunnar, M. R. (Eds.). (2009). Meeting the challenge of translational research in child psychology: Minnesota symposia on child psychology (Vol. 35). New York, NY: Wiley.

Cicchetti, D., & Sroufe, L. A. (2000). The past as prologue to the future: The times they've been a changin'. Development and Psychopathology, 12, 255–264.

Cicchetti, D., & Toth, S. L. (1991). The making of a developmental psychopathologist. In J. Cantor, C. Spiker, & L. Lipsitt (Eds.), Child behavior and development: Training for diversity (pp. 34–72). Norwood, NJ: Ablex.

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Cicchetti, D., & Toth, S. L. (2009). The past achievements and future promises of developmental psychopathology: The coming of age of a discipline. Journal of Child Psychology and Psychiatry, 50, 16–25.

Harter, S. (2006). Self-processes and developmental psychopathology. In D. Cicchetti & D. Cohen (Eds.), Developmental psychopathology (2nd ed., 370–418). New York, NY: Wiley.

Masten, A. S. (2014). Ordinary magic: Resilience in development. New York, NY: Guilford Publications, Inc.

Miklowitz, D. J., & Cicchetti, D. (2006). Toward a life span developmental psychopathology perspective on bipolar disorder. Development and Psychopathology, 18, 935–938.

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Contributors

Steve Balsis, PhD

Texas A&M University

College Station, Texas

Raphael Bernier, PhD

University of Washington

Seattle, Washington

Joy L. Brasfield, MA

Emory University

Atlanta, Georgia

J. Douglas Bremner, MD

Emory University

Atlanta, Georgia

Katrina C. Bridgman Goines, MA

Emory University

Atlanta, Georgia

Eddie Brummelman, MA

Utrecht University

Utrecht, Netherlands

Sara J. Bufferd, PhD

California State University San Marcos

San Marcos, California

Jacob A. Burack, PhD

McGill University

Montreal, Canada

and

Hôpital Rivière-des-Prairies

Montreal, Canada

Susan D. Calkins, PhD

University of North Carolina

Greensboro, North Carolina

Rochelle Caplan, MD

University of California

Los Angeles, California

Laurie Chassin, PhD

Arizona State University

Tempe, Arizona

Ann T. Chu, PhD

A Better Way, Inc.

San Francisco, California

Dante Cicchetti, PhD

Institute of Child Development

University of Minnesota

Minneapolis, Minnesota

Craig R. Colder, PhD

University at Buffalo

State University of New York

Buffalo, New York

Bryna Cooper, BA

University of Oregon

Eugene, Oregon

Luke Cooper

Texas A&M University

College Station, Texas

Ingrid M. Cordon, PhD

University of California, Davis

Davis, California

Kim Cornish, PhD

Monash University

Victoria, Australia

Kathryn R. Cullen, MD

University of Minnesota

Minneapolis, Minnesota

Geraldine Dawson, PhD

Duke University

Durham, North Carolina

Brianna Delker, MS

University of Oregon

Eugene, Oregon

Richard A. Depue, PhD

Cornell University

Ithaca, New York

Thomas J. Dishion, PhD

Arizona State University

Tempe, Arizona

Brianna Doherty, BS, MSc

University of Oxford

Oxford, England

Margaret W. Dyson, PhD

University of California, San Diego

La Jolla, California

Philip A. Fisher, PhD

University of Oregon

Eugene, Oregon

Peter Fonagy, OBE, PhD, FMedSci, FBA

University College London

London, United Kingdom

Deborah Goldfarb, JD

University of California, Davis

Davis, California

Gail S. Goodman, PhD

University of California, Davis

Davis, California

Sandra M. Goulding, MPH, MA

Emory University

Atlanta, Georgia

Cathryn Gordon Green, BA

McGill University

Montreal, Canada

Lauren D. Gulley, MA

University of Denver

Denver, Colorado

Benjamin L. Hankin, PhD

University of Denver

Denver, Colorado

Iseli G. Hernandez, BA

Northwestern University

Chicago, Illinois

Kathrin Herzhoff, MA

Northwestern University

Chicago, Illinois

Houston, Texas

Mary M. Heitzeg, PhD

University of Michigan

Ann Arbor, Michigan

Brian M. Hicks, PhD

University of Michigan

Ann Arbor, Michigan

Andrea Hussong, PhD

University of North Carolina

Chapel Hill, North Carolina

Grace Iarocci, PhD

Simon Fraser University

Burnaby, Canada

Annette Karmiloff-Smith, CBE, FBA, FMedSci, MAE, CPscyhol

Birkbeck University of London

London, United Kingdom

Kevin P. Kennedy, BA

University of California

Berkeley, California

Bonnie Klimes-Dougan, PhD

University of Minnesota

Minneapolis, Minnesota

Oriane Landry, PhD

LaTrobe University

Bendigo, Australia

Jennifer E. Lansford, PhD

Duke University

Durham, North Carolina

Mark F. Lenzenweger, PhD

State University of New York

Binghamton, New York

and

Weill Cornell Medical College

New York, New York

Leslie D. Leve, PhD

University of Oregon

Eugene, Oregon

Alicia F. Lieberman, PhD

University of California, San Francisco

San Francisco, California

Patrick Luyten, PhD

University of Leuven

Leuven, Belgium

and

University College London

London, United Kingdom

Allison Macdonald, MA

Emory University

Atlanta, Georgia

Helen Milojevich, MA

University of California, Irvine

Irvine, California

Peter Mundy, PhD

University of California, Davis MIND Institute &

School of Education

Sacramento, California

Rachel K. Narr, MA

University of Virginia

Charlottesville, Virginia

Joel T. Nigg, PhD

Oregon Health & Science University

Portland, Oregon

Derek M. Novacek, MA

Emory University

Atlanta, Georgia

Tasha Oswald, PhD

University of California, Davis MIND Institute

Sacramento, California

Gerald R. Patterson, PhD

Oregon Social Learning Center

Eugene, Oregon

Nicole B. Perry, PhD

University of North Carolina

Greensboro, North Carolina

Jodi A. Quas, PhD

University of California, Irvine

Irvine, California

Philip C. Rodkin, PhD

University of Illinois, Urbana-Champaign

Urbana, Illinois

Leslie E. Roos, MS

University of Oregon

Eugene, Oregon

Karen D. Rudolph, PhD

University of Illinois, Urbana-Champaign

Champaign, Illinois

Natalie Russo, PhD

Syracuse University

Syracuse, New York

Arthur T. Ryan, MA

Emory University

Atlanta, Georgia

Gaia Scerif, BSc, PhD

University of Oxford

Oxford, England

Kenneth J. Sher, PhD

University of Missouri

Columbia, Missouri

Hannah R. Snyder, PhD

University of Denver

Denver, Colorado

Jennifer L. Tackett, PhD

Northwestern University

Chicago, Illinois

Sander Thomaes, PhD

University of Southampton

Southampton, England

and

Utrecht University

Utrecht, Netherlands

Sheree L. Toth, PhD

University of Rochester

Rochester, New York

Hanan D. Trotman, PhD

Emory University

Atlanta, Georgia

Amy Vaughan Van Hecke, PhD

Marquette University

Milwaukee, Wisconsin

Lauren S. Wakschlag, PhD

Northwestern University

Chicago, Illinois

Elaine F. Walker, PhD

Emory University

Atlanta, Georgia

Robert A. Zucker, PhD

University of Michigan

Ann Arbor, Michigan

Chapter 1

Developments in the Developmental Approach to Intellectual Disability

Jacob A. Burack, Natalie Russo, Cathryn Gordon Green, Oriane Landry, and Grace Iarocci

Make for yourself a teacher, acquire for yourself a friend, and judge everyone in a positive light… Ethics of the Fathers (Pirkei Avot, 1, 6). We dedicate this chapter in honor of Ed Zigler for all his contributions to the science and welfare of so many children, including those with intellectual disability. He is the most inspiring teacher, loyal friend, and positive influence to all who know him. As with so much of his work, his articulation of the developmental approach to intellectual disability helped humanize our understanding of a population that for too long had been underserved and kept at the fringes of society. We are especially grateful to Dante Cicchetti for inviting us to contribute this chapter, on a topic about which we are so passionate and about which he was a visionary. His leadership both in the world of science and in making the world a better place for children is an example to us all. We thank Jillian Stewart, Johanna Querengesser, Ashley Reynolds, Icoquih Badillo-Amberg, David McNeil, Eric Keskin, and Martina Tiberi as well as other members of the McGill Youth Study Team for their help in preparing the manuscript.

DEVELOPMENTS IN THE DEVELOPMENTAL APPROACH TO INTELLECTUAL DISABILITY

THE DIAGNOSIS OF INTELLECTUAL DISABILITY AND ITS (LACK OF) MEANINGFULNESS

Diagnostic Criteria and Assessment

THE ORIGINS OF THE DEVELOPMENTAL APPROACH TO THE STUDY OF INTELLECTUAL DISABILITY

THE TWO-GROUP APPROACH AND BEYOND

Zigler's Emphasis on Familial Intellectual Disability

Differentiating Among Organic Etiologies: Extending Beyond the Two-Group Approach in the Quest for Increased Precision

APPLYING DEVELOPMENTAL PRINCIPLES TO THE STUDY OF PERSONS WITH INTELLECTUAL DISABILITY: CLASSIC AND EXPANDED VERSIONS

Zigler and the Classic Developmental Approach

Cicchetti's Expansion of the Developmental Approach to Persons With Organic Etiologies: A Focus on Persons With Down Syndrome

THE IMPORTANCE OF MENTAL AGE

Considering Developmental Level

THE STUDY OF THE WHOLE PERSON WITH INTELLECTUAL DISABILITY

Social Competence

Language Development

The Impact of a Child With Intellectual Disability on the Family

NEUROSCIENCE AND THE DEVELOPMENTAL APPROACH: BENEFITS AND PITFALLS IN THE APPLICATION OF CUTTING-EDGE TECHNOLOGY

A Primer on What fMRI and ERP Measure

Neuroscience and the Developmental Approach: A Messy Meeting of Disciplines

CONCLUSIONS

From Genes to Brain to Behavior in Intellectual Disability: Future Directions in Research

Summary

REFERENCES

Developments in the Developmental Approach to Intellectual Disability

The developmental study of intellectual disability is a long-established forerunner of developmental psychopathology with origins that predate the formal emergence of the latter discipline by decades, and yet is still in its early, and sometimes apparently regressive, stages of developmental emergence relative to other areas of work. It was largely shaped by scholars, such as Heinz Werner, Edward Zigler, and Dante Cicchetti, who were also seminal to the emergence of the scholarly discipline of developmental psychopathology, and yet it is often conceptualized as a separate unrelated entity. These complex relationships provide a lens through which we can understand the advances, and setbacks, in the study of intellectual disability, and its place in the domain of developmental psychopathology (and thereby in this volume). Within this framework, we highlight the thinking and research that led to and continue to maintain the developmental approach to intellectual disability and consider them with regard to developments in the study and understanding of intellectual disability since Hodapp and Burack's (2006) chapter in the last edition of this handbook (Cicchetti & Cohen, 2006).

As intellectual disability is essentially defined by the development of cognitive abilities and, to a considerably lesser extent, social skills that are so delayed and ultimately impaired that it only involves a small percentage of persons, it is a paradigmatic example of the construct of development at the extreme that is so essential to the field of developmental psychopathology (Burack, 1997; Cicchetti & Pogge-Hesse, 1982). In this way, intellectual disability also exemplifies Urie Bronfenbrenner's notion of an experiment of nature, which could never be replicated in an experimental setting but in this case is informative for understanding the course of typical cognitive and social development. Thus, consistent with Cicchetti's (1984) dictum that you can learn more about typical functioning by studying its pathology and more about its pathology by studying its typical state (p. 4), intellectual disability is a window into addressing issues and questions about cognitive and social development that cannot be fully answered when only considering typically developing persons (Burack, 1997; Cicchetti & Pogge-Hese, 1982; Hodapp, Burack, & Zigler, 1990). In providing the example of extreme delay, or impairment, intellectual disability would appear to allow us the opportunity to examine the integrity of the developmental system from the unique perspective of especially slowed or delayed development (Cicchetti & Beegly, 1990; Hodapp & Burack, 1990; Hodapp & Zigler, 1990). As is often the case in nature, this slow motion analysis of cognitive and social development allows for a particularly intense level of scrutiny that cannot be attained with events occurring at their typical speed.

The converse of Cicchetti's dictum is also particularly relevant to the study of intellectual disability as the theories and methodologies that have governed the study of development among typically developing persons have, during the past half century, transformed the way that persons with intellectual disability and their families are studied, understood, educated, and supported (for related collections, see Burack, Hodapp, Iarocci, & Zigler, 2012; Burack, Hodapp, & Zigler, 1998; Cicchetti & Beeghly, 1990; Hodapp, Burack, & Zigler, 1990). These advances are the focus of this chapter as we highlight the ongoing and evolving conceptual, methodological, and interpretive contributions of the so-called developmental approach to the study of persons with intellectual disability and the ways that they have led to a more precise and sophisticated science (Burack, Dawkins, Stewart, Flores, Iarocci, & Russo, 2012; Burack, Russo, Flores, Iarocci, & Zigler, 2012; Cicchetti & Ganiban, 1990; Hodapp, Burack, & Zigler; 1990).

The Diagnosis of Intellectual Disability and Its (Lack of) Meaningfulness

Although the diagnosis has far-reaching implications for the development and outcomes of the affected persons, intellectual disability cannot be considered at all tangible. Virtually unique among the phenomena addressed in this volume, the designation of intellectual disability is essentially based on a behavioral classification culled from scores on single measures used to operationalize each of two constructs—in this case, primarily the construct of intelligence but often also that of social adaptation. Typically, people who score in approximately the lowest 3% of the population, or two or more standard deviations below the mean, on standardized tests of intelligence and behavioral adaptation are considered to be intellectually disabled. However, the utility of this designation is compromised in two essential ways. One, the cutoff score is entirely arbitrary. Two, the low IQ, or behavioral, scores can be attained