Developmental Psychopathology, Volume 3, Maladaptation and Psychopathology E-Book
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- Herausgeber: John Wiley & Sons
- Kategorie: Geisteswissenschaft
- Sprache: Englisch
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.
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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
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Guide
Cover
Table of Contents
Begin Reading
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 (, patients; , 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
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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).
