This paper examines the conceptual and empirical connections between competence and psychopathology, two historically rich traditions for the study of adaptation in development, and what might be gained from their integration. Historical roots of these two traditions are reviewed, then overlaps in their definition are considered, with a focus on the ways in which judgments about competence enter into the nosology of mental disorders. DSM-IV is analyzed from the perspective of competence, and the debate about “harmful dysfunction” in defining mental disorder is discussed in relation to competence. Different models explaining the empirical associations of competence and psychopathology are delineated, and illustrative empirical evidence is provided. Potential explanations include confounded concepts and methods, symptoms undermining the effectiveness of adaptation in the environment, failures in age-salient developmental tasks leading to emotional and behavioral problems, transactional influences, shared vulnerability or risk factors producing both kinds of difficulties, and more complex models. The potential benefits of integrating competence and psychopathology as two major approaches to adaptation are discussed in regard to theory, classification of mental disorder, research, and intervention.

The prospective relation of maternal emotion philosophy to children's emotion understanding and regulation and positive and negative adjustment was investigated. Sixty-nine African American youth (50% male; M age = 11.29 years) and their maternal caregivers living in high violence areas of a midsized city participated in this interview study. Caregivers' meta-emotion philosophy predicted child emotion understanding and emotion regulation, which also were associated with Time 2 grades, internalizing behaviors, externalizing behaviors, and social skills after controlling for Time 1 adjustment. Emotional understanding mediated the relationship between caregivers' emotional socialization and boys' internalizing behaviors and between caregivers' emotional socialization and girls' social skills. In addition, emotion regulation mediated the relationships between emotional socialization and all four outcomes for boys. Implications for future work on emotion socialization and clinical intervention, particularly related to emotion regulation, are discussed.

Autistic symptoms begin in the first years of life, and recent magnetic resonance imaging studies have discovered brain growth abnormalities that precede and overlap with the onset of these symptoms. Recent postmortem studies of the autistic brain provide evidence of cellular abnormalities and processes that may underlie the recently discovered early brain overgrowth and arrest of growth that marks the first years of life in autism. Alternative origins and time tables for these cellular defects and processes are discussed. These cellular and growth abnormalities are most pronounced in frontal, cerebellar, and temporal structures that normally mediate the development of those same higher order social, emotional, speech, language, speech, attention, and cognitive functions that characterize autism. Cellular and growth pathologies are milder and perhaps nonexistent in other structures (e.g., occipital cortex), which are known to mediate functions that are often either mildly affected or entirely unaffected in autistic patients. It is argued that in autism, higher order functions largely fail to develop normally in the first place because frontal, cerebellar, and temporal cellular and growth pathologies occur prior to and during the critical period when these higher order neural systems first begin to form their circuitry. It is hypothesized that microstructural maldevelopment results in local and short distance overconnectivity in frontal cortex that is largely ineffective and in a failure of long-distance cortical–cortical coupling, and thus a reduction in frontal–posterior reciprocal connectivity. This altered circuitry impairs the essential role of frontal cortex in integrating information from diverse functional systems (emotional, sensory, autonomic, memory, etc.) and providing context-based and goal-directed feedback to lower level systems.The authors were supported by funds from the National Institute of Mental Health (2-ROI-MH36840) and National Institute of Neurological Disorders and Stroke (2-ROI-NS19855) awarded to Eric Courchesne.

The question of whether to view psychopathology as categorical or dimensional continues to provoke debate. We review the many facets of this argument. These include the pragmatics of measurement; the needs of clinical practice; our ability to distinguish categories from dimensions empirically; methods of analysis appropriate to each and how they relate; and the potential theoretical biases associated with each approach. We conclude that much of the debate is misconceived in that we do not observe pathology directly; rather, we observe its properties. The same pathology can have some properties that are most easily understood using a dimensional conceptualization while at the same time having other properties that are best understood categorically. We suggest replacing Meehl's analogy involving qualitatively distinct species with an alternative analogy with the “duality” of light, a phenomenon with both wave- and particle-like properties.

Previous studies have revealed a “theory of mind” impairment in children with autism. The aim of this study was to assess whether it is possible to intervene by teaching children with autism to understand the mental states of emotion, belief, or pretence. Results showed that it is possible to teach children with autism to pass tasks that assess emotion and belief understanding. Introducing unfamiliar materials in structurally similar tasks did not adversely influence teaching effects, either immediately after teaching, or 2 months later. However, teaching effects did not generalize to tasks in domains where children received no teaching. In addition, no significant progress in spontaneous pretend play resulted from teaching. These results indicate that children may be passing tasks using rules rather than any genuine understanding of the concepts involved.

One reason for looking at a person's eyes may be to diagnose their goal, because a person's eye direction reliably specifies what they are likely to act upon next. We report an experiment that investigates whether or not young normal infants use eye contact for this function. We placed them in situations in which the adult's action toward them was either ambiguous or unambiguous in its goal. Results showed that the majority of normal infants and young children with mental handicap made instant eye contact immediately following the ambiguous action but rarely after the unambiguous action. Young children with autism, in contrast, made eye contact equally (little) in both conditions. These results are discussed in relation to the function of eye contact, to our understanding of infant cognition, and to the theory of mind hypothesis of autism.

Salivary cortisol concentrations (10:30–11:30 a.m.) and social behavior (observations and teacher reports) were examined in 33 maltreated (26 boys) and 16 comparison (8 boys) children. The maltreated children were studied for 31 days while they attended a therapeutic preschool for abused and neglected children. Children in the comparison sample were studied while attending a preschool serving economically disadvantaged families. Each child's cortisol values over days were used to compute measures of basal activity (median cortisol) and reactivity (ratio of quartile ranges). Median cortisol was not significantly correlated with social behavior measures. Cortisol reactivity was positively correlated with social competence and negatively correlated with shy/internalizing behavior. Maltreated children exhibited less cortisol reactivity then did comparison children. Maltreated children also scored lower in social competence and higher in shy/internalizing and acting out/externalizing behaviors. In additional analyses, maltreated children failed to show elevations in cortisol on days of high versus low social conflict in the classroom. Social competence was also found to correlate positively with cortisol levels on high-conflict days. In all, the results suggest a reduction in cortisol reactivity in maltreated children related to the impairment in social competence frequently noted among these children.

Studies in animals showing hippocampal atrophy and associated memory deficits in stress and aging have implications for stress and aging in humans. Clinical studies in traumatized human populations with posttraumatic stress disorder (PTSD) have replicated studies in animals, showing reduction in volume of the hippocampus measured with magnetic resonance imaging and associated memory deficits. Trauma at different stages of development (early childhood abuse versus trauma in later life due to combat) may influence the nature of memory deficits and hippocampal atrophy. Studies in aging human subjects are consistent with animal studies, although future research is needed in this area. The similarities between biological findings related to cortisol and the hippocampus in stress and aging in both animal and human studies raises the question of whether PTSD can be seen as a form of accelerated aging. Evidence that stress affects the hippocampus and the capacity for learning has broad implications for public health policy, underlying the need for additional resources in this important area and a reexamination of our understanding of factors influencing academic achievement.

Protective and risk factors were examined in three samples, each of about 500 boys. Cross-sectional analyses examined a large number of independent variables for their potential protective and risk effects on different levels of seriousness of boys' delinquency. The results showed that protective and risk effects often co-occurred in the same variables, that few variables had risk effects only, and none had protective effects oniy. Protective effects were as likely to promote nondelinquency as to suppress serious delinquency, whereas risk effects were as likely to suppress nondelinquency as to promote serious delinquency. Certain variables were mostly associated with distinctions between nondelinquency and minor delinquency, other variables were related to the distinction between minor delinquency and serious delinquency, and a third group of variables was associated with both distinctions. Developmental analyses indicated that the magnitude of protective and risk effects increased with age. Implications of the findings for research and clinical practice are discussed.

Accumulating evidence suggests that social contexts in early life have important and complex effects on childhood psychopathology. Spurred by the lack of an explicit operational definition that could guide the study of such effects, we define a social context operationally as “a set of interpersonal conditions, relevant to a particular behavior or disorder and external to, but shaped and interpreted by, the individual child.” Building on this definition, we offer a series of recommendations for future research, based on five theoretically derived propositions: (a) Contexts are nested and multidimensional; (b) contexts broaden, differentiate, and deepen with age, becoming more specific in their effects; (c) contexts and children are mutually determining; (d) a context's meaning to the child determines its effects on the child and arises from the context's ability to provide for fundamental needs; and (e) contexts should be selected for assessment in light of specific questions or outcomes. As reflected in an increasingly rich legacy of literature on child development and psychopathology, social contexts appear to influence emerging mental disorders through dynamic, bidirectional interactions with individual children. Future research will benefit from examining not only statistical interactions between child- and context-specific factors, but also the actual transactions between children and contexts and the transduction of contextual influences into pathways of biological mediation. Because adverse contexts exert powerful effects on the mental health of children, it is important for the field to generate new, more theoretically grounded research addressing the contextual determinants of psychological well-being and disorder.

This study attempted to replicate previous findings that indicated that preschool-aged children with significant externalizing problems are more likely to have insecure attachment relations than nonproblem peers (Speltz, Greenberg, & DeKlyen, 1990). Fifty children (ages 3–6) and their mothers participated; 25 referred to a child psychiatry clinic for one of the DSM-IIIR Disruptive Behavior Disorders, and 25 matched comparisons without externalizing behavior problems. Attachment was measured at the time of referral using two separation and reunion sequences in a clinic context. We found that 80% of the clinic-referred children were classified as insecure, whereas only 28% of the comparisons were so classified (p <.001). Further, a high percentage of clinic insecure children showed a controlling pattern of attachment. Thus, the present study, with improved methodological rigor, provided an almost exact replication to previous results. The discussion focuses on what contribution attachment research can provide to a developmental psychopathology perspective on early externalizing disorders.

This study identified profiles of 13 risk factors across child, family, school, and neighborhood domains in a diverse sample of children in kindergarten from four US locations (n = 750; 45% minority). It then examined the relation of those early risk profiles to externalizing problems, school failure, and low academic achievement in Grade 5. A person-centered approach, latent class analysis, revealed four unique risk profiles, which varied considerably across urban African American, urban White, and rural White children. Profiles characterized by several risks that cut across multiple domains conferred the highest risk for negative outcomes. Compared to a variable-centered approach, such as a cumulative risk index, these findings provide a more nuanced understanding of the early precursors to negative outcomes. For example, results suggested that urban children in single-parent homes that have few other risk factors (i.e., show at least average parenting warmth and consistency and report relatively low stress and high social support) are at quite low risk for externalizing problems, but at relatively high risk for poor grades and low academic achievement. These findings provide important information for refining and targeting preventive interventions to groups of children who share particular constellations of risk factors.

This article uses a developmental pathway model to consider the role of attachment processes in adolescents' reports of depressive symptoms. Teen attachments were assessed with both interview and observational methods. Assessments of teens' strategies in the Adult Attachment Interview (AAI) indicated that insecure and preoccupied strategies were associated with increased reports of depressive symptoms. Observations of mother-teen problem-solving revealed that depressed teens engaged in interactions characterized by high levels of maternal dominance and dysfunctional anger. Maternal reports of teens' negative life events contributed additional variance to a regression model for depressive symptoms. Gender differences further specified pathways to depressive symptoms. Females reported more depressive symptoms, while depressed males engaged in problem-solving interactions characterized by high levels of dysfunctional anger. Competency-based treatments of depressive symptoms designed to improve parent-teen communication and meta-monitoring skills are discussed.

The complex interplay between bullying/victimization and defending was examined using a longitudinal social network approach (stochastic actor-based models). The (co)evolution of these relations within three elementary schools (Grades 2–5 at Time 1, ages 8–11, N = 354 children) was investigated across three time points within a year. Most bullies and defenders were in the same grade as the victims, although a substantial number of bullies and defenders were in other grades (most often one grade higher). Defenders were usually of the same gender as the victims, whereas most bullies were boys, with boys bullying both boys and girls. In line with goal-framing theory, multiplex network analyses provided evidence for the social support hypothesis (victims with the same bullies defended each other over time) as well as the retaliation hypothesis (defenders run the risk of becoming victimized by the bullies of the victims they defend). In addition, the analysis revealed that bullies with the same victims defended each other over time and that defenders of bullies initiated harassment of those bullies' victims. This study can be seen as a starting point in unraveling the relationship dynamics among bullying, victimization, and defending networks in schools.

Adolescence is associated with an increase in the rate of certain psychiatric symptoms, and it is typically the developmental period when prodromal features of the major psychiatric disorders emerge. This is especially true of schizophrenia, with the majority of patients showing a marked postpubertal rise in schizotypal signs that predates the onset of clinical symptoms in early adulthood. Cross-sectional studies of youth have revealed a positive correlation between age and saliva cortisol level, suggesting a normative maturational increase in activity of the hypothalamic–pituitary–adrenal (HPA) axis. It has been hypothesized that this increase may trigger the expression of symptoms in vulnerable individuals. The present longitudinal study measured cortisol secretion and its relation with symptom development in samples of youth with schizotypal personality disorder (SPD), other personality disorders, or no Axis II disorder. The findings indicate moderate stability in cortisol levels across a 2-year period, with a longitudinal increase in cortisol levels over time. Cortisol levels at the first and second assessments were correlated with the severity of SPD symptoms at follow-up. The results are consistent with the notion that the HPA axis undergoes a postpubertal maturational process that moderates the expression of psychiatric symptoms.

Although the majority of research attention to the hypothalamic–pituitary–adrenal (HPA) axis in stress-related disorders and as a marker of allostatic load has focused on overactivation of this stress system, theory and data clearly indicate that underactivation is also an important type of dysregulation. In the current study we focused on low cortisol, exploring a constellation of risk factors including stress exposure, maternal depression, and attenuated basal and stress reactive cortisol in two samples of children. The first sample was comprised of 110 preschoolers living in high-stress environments. Cortisol was assessed across the day at home and at child care as well as across two stress paradigms. These data were used to classify whether children's HPA axis activity was attenuated. Serious family financial strain, maternal depression, and attenuated cortisol all made unique contributions in models predicting current clinical levels of internalizing symptoms as rated by mothers and teachers. The second sample was 166 third, sixth, and ninth graders studied five times across a 1-year period. Maternal and child depression were determined through structured clinical interviews, and stress exposure was assessed via checklist and interview techniques with the child and parent. Cortisol was assessed multiple times across a lab visit at Time 1, and these data were combined into a single continuous measure. Cortisol concentrations across the lab visit interacted with stress exposure across the year such that children with lower average cortisol at Time 1 and increased stress across the 12 months showed elevated levels of internalizing symptoms. Based on these and related data we propose that prior to puberty low cortisol may be an important marker of allostatic load, particularly for risk of depression and anxiety.

Proposed changes in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V) include replacing current personality disorder (PD) categories on Axis II with a taxonomy of dimensional maladaptive personality traits. Most of the work on dimensional models of personality pathology, and on personality disorders per se, has been conducted on young and middle-aged adult populations. Numerous questions remain regarding the applicability and limitations of applying various PD models to early and later life. In the present paper, we provide an overview of such dimensional models and review current proposals for conceptualizing PDs in DSM-V. Next, we extensively review existing evidence on the development, measurement, and manifestation of personality pathology in early and later life focusing on those issues deemed most relevant for informing DSM-V. Finally, we present overall conclusions regarding the need to incorporate developmental issues in conceptualizing PDs in DSM-V and highlight the advantages of a dimensional model in unifying PD perspectives across the life span.

It has been reported that borderline personality related characteristics can be observed in children, and that these characteristics are associated with increased risk for the development of borderline personality disorder. It is not clear whether borderline personality related characteristics in children share etiological features with adult borderline personality disorder. We investigated the etiology of borderline personality related characteristics in a longitudinal cohort study of 1,116 pairs of same-sex twins followed from birth through age 12 years. Borderline personality related characteristics measured at age 12 years were highly heritable, were more common in children who had exhibited poor cognitive function, impulsivity, and more behavioral and emotional problems at age 5 years, and co-occurred with symptoms of conduct disorder, depression, anxiety, and psychosis. Exposure to harsh treatment in the family environment through age 10 years predicted borderline personality related characteristics at age 12 years. This association showed evidence of environmental mediation and was stronger among children with a family history of psychiatric illness, consistent with diathesis–stress models of borderline etiology. Results indicate that borderline personality related characteristics in children share etiological features with borderline personality disorder in adults and suggest that inherited and environmental risk factors make independent and interactive contributions to borderline etiology.