The current study examined the interactive effects of infant activity level and fear on growth trajectories of behavior problems in early childhood (age 4 to 8 years) using maternal ratings. The sample was drawn from the National Longitudinal Survey of Youth (NLSY) and included children who were between 1 and 11 months in 1986. Findings suggested that boys characterized by high activity level and low levels of fear in infancy escalated in both externalizing and internalizing symptoms. Also, boys characterized by high fear and low activity level increased in internalizing symptoms and these effects seemed to be specific to depression rather than anxiety. Temperament did not predict escalation in externalizing symptomatology for girls, but low levels of fear predicted increases in internalizing symptoms. There was also evidence for a decline in depression specific symptoms for girls characterized by high fear and low activity in infancy. These findings suggest the importance of examining interactive models of temperament risk and considering gender specific pathways to behavior problems.

In a chapter on the historical roots of the discipline of developmental psychopathology, Cicchetti (1990) predicted that this then-emerging field would, among other integrative functions, help to bridge the gap between basic and applied research and between theoretical and clinical efforts for children, adolescents, and adults (see also Cicchetti & Toth, 1991, 1992, 1998). Despite this hopeful assertion, in the dozen years since its appearance, there has not been a complete closing of the gap (which, at worst, can resemble a chasm).

Frith has argued that people with autism show “weak central coherence,” an unusual bias toward piecemeal rather than configurational processing and a reduction in the normal tendency to process information in context. However, the precise cognitive and neurological mechanisms underlying weak central coherence are still unknown. We propose the hypothesis that the features of autism associated with weak central coherence result from a reduction in the integration of specialized local neural networks in the brain caused by a deficit in temporal binding. The visuoperceptual anomalies associated with weak central coherence may be attributed to a reduction in synchronization of high-frequency gamma activity between local networks processing local features. The failure to utilize context in language processing in autism can be explained in similar terms. Temporal binding deficits could also contribute to executive dysfunction in autism and to some of the deficits in socialization and communication.

In a recent article, Cowan, Harter, and Kandel (2000) concluded that much of the success and excitement engendered by modern neuroscience can be attributed to the incorporation of several previously independent disciplines into one intellectual framework. During the 1950s and 1960s, neuroanatomy, neurochemistry, neuropharmacology, and neurophysiology, disciplines that had largely functioned in a separate and distinct fashion, gradually merged into a unified field of neuroscience. The penultimate step in the coalescence of neuroscience occurred in the early 1980s, when neuroscience integrated with molecular biology and molecular genetics. The confluence of these fields enabled scientists to understand the genetic basis of neurological diseases for the first time without requiring foreknowledge of the underlying biochemical abnormalities. The final phase of the merger of neuroscience into a single discipline took place in the mid-1980s, when cognitive psychology joined with neuroscience, leading to the formation of cognitive neuroscience.

Recent advances in the discipline of developmental psychopathology highlight the contributions of developmental thought to the study of persons with autism. This article briefly outlines primary developmental innovations in theory, methodology, and the interpretation of findings. Specifically, we discuss two sets of issues that arise from the general notion of developmental level. One set is relevant to the choice of persons that comprise the comparison group and the other to the various implications of the subjects' levels of functioning. In sum, we contend that researchers need to frame their empirical work within the context of developmental theory and methodology and interpret their findings accordingly. This will lead to scientifically compelling work and an increasingly heuristic approach to the study of persons with autism.

An understanding of developmental phenomena demands a relational or coactive concept of causality, as opposed to a conceptualization that assumes that singular causes can act in isolation. In this article we present a developmental psychobiological systems view of relational (bidirectional, coactional) causality, in which it is proposed that developmental outcomes are a consequence of at least two specific components of coaction from the same or different levels of a developmental system. The levels are genetic, neural, behavioral, and environmental; the latter level includes the cultural, social, and physical aspects of an organism's environment. We show the applicability of this view to the understanding of the development of normal and abnormal behavioral and psychological phenotypes through illustrations from the existing animal and human literature. Finally, we discuss future possibilities and potential stumbling blocks in the implementation of a more fully realized bidirectional, coactional perspective in developmental psychopathological research.

Previous studies have repeatedly shown verbal intelligence deficits in adolescent antisocial individuals, but it is not known whether these deficits are in place prior to kindergarten or, alternatively, whether they are acquired throughout childhood. This study assesses whether cognitive deficits occur as early as age 3 years and whether they are specific to persistently antisocial individuals. Verbal and spatial abilities were assessed at ages 3 and 11 years in 330 male and female children, while antisocial behavior was assessed at ages 8 and 17 years. Persistently antisocial individuals (N = 47) had spatial deficits in the absence of verbal deficits at age 3 years compared to comparisons (N = 133), and also spatial and verbal deficits at age 11 years. Age 3 spatial deficits were independent of social adversity, early hyperactivity, poor test motivation, poor test comprehension, and social discomfort during testing, and they were found in females as well as males. Findings suggest that early spatial deficits contribute to persistent antisocial behavior whereas verbal deficits are developmentally acquired. An early-starter model is proposed whereby early spatial impairments interfere with early bonding and attachment, reflect disrupted right hemisphere affect regulation and expression, and predispose to later persistent antisocial behavior.

This paper addresses the issue of whether prevention research methods, particularly those involving randomized prevention trials, can be used to test theories concerning the etiology of psychopathology. Based on recent empirical and theoretical work in developmental psychopathology, three aspects of etiologic theory are discussed: risk and protective mechanisms, the integration of environmental and genetic factors, and patterns of developmental progression in psychopathology across the life span. It is suggested that integration of prevention trial methods with methods from passive correlational designs, behavioral genetics, and longitudinal studies allows for unique opportunities to test hypotheses about etiology. Empirical literature on the development and prevention of internalizing disorders, particularly depression, is presented to support this argument. Limitations of prevention trials for testing theory are also reviewed.

Previous work based on observations of home videotapes indicates that differences can be detected between infants with autism spectrum disorder and infants with typical development at 1 year of age. The present study addresses the question of whether autism can be distinguished from mental retardation by 1 year of age. Home videotapes of first birthday parties from 20 infants later diagnosed with autism spectrum disorder, 14 infants later diagnosed with mental retardation (without autism), and 20 typically developing infants were coded by blind raters with respect to the frequencies of specific social and communicative behaviors and repetitive motor actions. Results indicated that 1-year-olds with autism spectrum disorder can be distinguished from 1-year-olds with typical development and those with mental retardation. The infants with autism spectrum disorder looked at others and oriented to their names less frequently than infants with mental retardation. The infants with autism spectrum disorder and those with mental retardation used gestures and looked to objects held by others less frequently and engaged in repetitive motor actions more frequently than typically developing infants. These results indicate that autism can be distinguished from mental retardation and typical development by 1 year of age.

A significant discrepancy between intelligence and daily adaptive functioning, or adaptive disability (AD), has been previously found to be a associated with significant psychological morbidity in preschool children with disruptive behavior (DB). The utility of AD as a predictor of later developmental risks was examined in a 3-year longitudinal study of normal ( N= 43) and DB preschool children. The DB children were grouped into those with AD (DB+AD; N = 28) and those without AD (DB-only; N = 98). All children were followed with annual evaluations to the end of second grade. Both DB groups demonstrated substantial and pervasive psychological and educational morbidity at 3-year follow-up. In comparison to DB-only children, DB+AD children had more symptoms of attention-deficit hyperactivity disorder (ADHD) and conduct disorder (CD), more severe and pervasive behavior problems at home, more parent-rated externalizing and internalizing, and lower academic competence and more behavioral problems at school. Parents of DB+AD children also reported greater parenting stress than did parents in the other groups. A significant contribution of AD to adverse outcomes in the DB group remained on some measures even after controlling for initial severity of DB. AD also contributed significantly to CD symptoms at follow-up after controlling for initial DB severity and initial CD symptoms. The results corroborate and extend earlier findings of the utility of AD as a risk indicator above severity of DB alone. They also imply that AD in the context of normal intellectual development may arise from both the deficient self-regulation associated with ADHD and from disrupted parenting, with exposure to kindergarten moderating these adverse effects.

Most of the major psychiatric disorders have been analyzed at each of several different levels. For example, at the broadest level, epidemiological studies have served to establish the incidence of disorders like schizophrenia and major depression in a number of different populations. Family and twin studies have been important in determining the heritability of certain mental illnesses, and chromosomal and linkage analyses have identified a number of discrete loci that appear to be implicated in disease susceptibility or, even directly, in the pathogenesis of some disorders. In a few cases, specific genes have been found to be mutated or polymorphic and proteins they encode are currently being analyzed. This article reviews how these different levels contribute to our understanding of a number of psychiatric disorders, including drug addiction, which has been the focus of much of our own work.

The design of effective interventions for antisocial adolescents has been greatly influenced by research-based developmental theories. However, randomized clinical trials (RCTs) demonstrating effectiveness of these treatments have contributed minimally to alterations and refinements of these theories. In this article, nine guidelines for research that may enhance the contributions of RCTs to developmental theory are proposed: (1) use mediational analyses to test and refine theories of change; (2) use moderator analyses to test differential pathways to change; (3) assess change processes separately for different types of antisocial behavior; (4) use constructive and dismantling designs to isolate effects of intervention components on targeted mediators and outcomes; (5) assess the time-sensitive nature of change mechanisms with theoretically relevant spacing of multiple assessments and long-term follow-ups; (6) expand the nomological net of developmental theories by assessing intervention effects on nontargeted constructs; (7) use RCTs to disentangle direction of effects questions in developmental theories; (8) conduct secondary analyses of RCTs to assess extra-treatment influences on antisocial behavior; and (9) assess the generalizability of mediator and moderator effects. Use of these guidelines may promote a recursive and iterative relationship between RCTs and theory building. Improved developmental theories may yield more effective interventions, and theory-testing interventions may engender more comprehensive and better informed theories.

This paper tries to make three points. First, current constructs in personality and psychopathology are based on the restrictive evidence contained in self-reports. As a result, heterogeneous categories of individuals are assigned to the same category. Second, it is suggested that when different sources of evidence are included, theoretically distinct groups will be detected within the prior heterogeneous category. Third, the authors argue that physiological information has the potential to parse individuals with similar phenotypes on self-report data into distinct groups that reveal the temperamental origins of their phenotype.

This study examined the effects of being victimized by peers on children's behavioral, social, emotional, and academic functioning. We assessed an ethnically diverse sample of 2,064 first, second, and fourth graders and followed them over 2 years, locating 1,469 of the participants at the follow-up. Correlation and partial correlation analyses revealed that prior victimization predicted externalizing, internalizing, and social problems 2 years later for the sample as a whole. However, not all victimized children experienced the same types of outcomes; instead, there was heterogeneity in children's responses to victimization. Using cluster analysis, we identified eight outcome patterns that represented different patterns of functioning. These were labeled as externalizing, internalizing, symptomatic, popular, disliked, absent, low achieving, and high achieving. Discriminant function analyses revealed that the symptomatic, externalizing, and disliked patterns were systematically related to victimization. Moreover, significant gender and age differences in the severity of effects were obtained. The discussion highlights the complexity of victimization effects.

This article reviews major issues of a developmental psychopathology understanding of youth violence and related insights gained from violence prevention efforts to date. Based in a perspective that emphasizes three areas of knowledge, epidemiology, risk factors and models, and developmental trajectories, findings are reviewed that help clarify theoretical propositions about the developmental patterns, influences, and pathways related to youth violence. Extant research is able to support several major contentions of basic developmental psychopathology theories of youth violence. Support is most robust for risk factors central to prevailing models of the development of youth violence. In addition to noting current knowledge contributions, the review suggests areas of needed additional analytic progress and theoretical extension to refine knowledge and expand understanding of the development of violence risk and its prevention.

This study examined the association between fathers' alcoholism and other risk factors such as parental depression, family conflict, infant temperament, and parent–infant attachment. The quality of parent–infant interactions was hypothesized to be a proximal mediator of the associations among alcoholism and other risk factors and attachment. The participants were 223 families (104 nonalcoholic families and 119 alcoholic families) with 12-month-old infants recruited through birth records. Infants in families with two parents with alcohol problem had significantly higher rates of insecure attachment with both parents. Structural Equations Modeling indicated that the fathers' alcohol problem was associated with lower paternal sensitivity (higher negative affect, lower positive engagement, and lower sensitive responding) during father–infant play interactions, and this in turn was associated with higher risk for infant attachment insecurity with fathers. The association between the fathers' alcohol problem and infant attachment security with the mother was mediated by maternal depression, and maternal alcohol problems and family conflict were associated with maternal sensitivity during play interactions. These results indicate that the fathers' alcoholism is associated with higher family risk including the quality of the parent–infant relationship; infant attachment develops in a family context; and this context has a significant association with attachment security.

Self-regulatory processes are believed to be critical to early personality and behavioral adjustment. Such processes can be observed on multiple levels, including the physiological, attentional, emotional, cognitive, and interpersonal domains of functioning. Data from several longitudinal studies suggest links between early temperamental tendencies such as behavioral inhibition and frustration tolerance, and regulatory developments at the levels of physiological, attentional, and emotional regulation. Deficits in these particular levels of self-regulation may underlie childhood social withdrawal and aggression. Significant gaps remain in our knowledge of the pathways to disordered behavior and the role that self-regulation plays in such pathways. Suggestions are made for the ways in which future longitudinal studies might address these gaps.

The goal of this study was to examine sexual harassment in early adolescence. Available data indicate that peer to peer sexual harassment is prevalent in high school and is associated with psychosocial problems for both victims and perpetrators. For the present study, we adopted a developmental contextual model to examine the possibility that this behavior develops during the late elementary and middle school years and is linked to the biological and social changes that occur at this time. Youths from Grades 6–8 (N = 1,213) enrolled in seven elementary and middle schools in a large south-central Canadian city were asked to report on their sexual harassment behaviors with same- and cross-gender peers; their pubertal development, and the gender composition of their peer network. The results revealed that cross-gender harassment was distinct from same-gender harassment, increased in frequency from Grade 6 to Grade 8, and was linked to pubertal maturation and participation in mixed-gender peer groups. The implications of a developmental contextual model for understanding the emergence of this problematic behavior in adolescence are discussed.

This paper addresses the role of family-based studies of preventive and therapeutic interventions in our understanding of normal development and psychopathology. The emphasis is on interventions designed to improve parent–child and/or marital relationships as a way of facilitating development and reducing psychopathology in children and adolescents. Intervention designs provide the gold standard for testing causal hypotheses. We begin by discussing the complexity of validating these hypotheses and the implications of the shift from a traditional emphasis on theories of etiology to developmental psychopathology's newer paradigm describing risks → pathways → outcomes. We summarize correlational studies that document the fact that difficult and ineffective parent–child and marital relationships function as risk factors for children's cognitive, social, and emotional problems in childhood and adolescence. We then review prevention studies and therapy evaluation studies that establish some specific parenting and marital variables as causal risk factors with respect to these outcomes. Our discussion focuses on what intervention studies have revealed so far and suggests an agenda for further research.

The development of joint attention skills is a major milestone of infancy. Recent research suggests that the development of these skills may be affected by disorganized (D) attachment. This hypothesis was examined in a longitudinal study of attachment and joint attention skill development in a sample of infants at risk for developmental–behavioral morbidity. The results revealed that toddlers with D classifications initiated joint attention with an experimenter significantly less often than did secure, or even other insecure, toddlers. However, no group differences in the capacity to respond to the joint attention bids of others were observed in this study. These data suggest that a disturbance in the tendency to initiate episodes of joint attention with others may be indicative of early social–cognitive and social–emotional disturbance among infants affected by disorganized attachment status. Theory and research is reviewed to suggest that an early impairment in joint attention facility may make a significant contribution to risk for negative cognitive and emotional outcomes among these infants.