This article examines what it means to have a self. My focus is on the essential components of self-experience, the kind of psychological architecture required to construct a self, rather than on the configurations or qualities of individual “selves.” I adopt a developmental perspective and indicate how early childhood autism may afford unique insights into the role of perceptual-affective and interpersonal experience in determining the normal child's developing awareness of self.

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.

This article presents an overview of work conducted at the Institute of Psychiatry over the past 30 years on childhood depression. The work began with the basic question of definition and measurement. Epidemiological studies showed that depressive symptoms were quite common in children and were a good, if nonspecific, indicator of psychological disturbance. Further work in both epidemiological and clinical samples provided some evidence for the validity of a depressive syndrome. However, this work also showed that these depressive syndromes represented a heterogeneous group of phenomena. The validity of major depressive disorder in children was therefore tested further in longitudinal and family-genetic studies. These studies supported the validity of the concept but confirmed that there was heterogeneity in respect to both developmental stage at the time of onset and comorbidity with conduct disorder. We concluded that there are probably several different kinds of depressive syndromes in children. Some are strongly linked with depressive disorders in adulthood, but others are probably better conceptualized as part of another psychopathological problem altogether.

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.

We hypothesized that hyperactivity defines the first stage and that antisocial problems define a second stage in a progression that leads eventually to early-onset delinquency. As expected, a structural equation model (SEM) showed that a latent construct for hyperactivity was significantly related to a latent construct for antisocial problems. We hypothesized that this path reflected a shared mechanism, disrupted parental discipline. A second SEM showed that the relation between hyperactivity and antisocial behavior really reflected a shared disruption in parental discipline. A third SEM showed that having antisocial parents was uniquely correlated with antisocial children but not with hyperactivity. A fourth SEM showed that early-onset delinquency was predicted by a latent construct for antisocial child; but when this was partialed out, the contribution for hyperactivity was nonsignificant.

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.

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.

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.

Longitudinal effects of child maltreatment on cortisol regulation in infants from age 1 to 3 years were investigated in the context of a randomized preventive intervention trial. Thirteen-month-old infants from maltreating families (N = 91) and their mothers were randomly assigned to one of three intervention conditions: child–parent psychotherapy, psychoeducational parenting intervention, and a control group involving standard community services (CS). A fourth group of infants from nonmaltreating families (N = 52) and their mothers comprised a nonmaltreated comparison (NC) group. The two active interventions were combined into one maltreated intervention (MI) group for statistical analyses. Saliva samples were obtained from children at 10:00 a.m. before beginning a laboratory observation session with their mothers when the children were 13 months of age (preintervention), 19 months (midintervention), 26 months (postintervention), and 38 months (1-year postintervention follow-up). At the initial assessment, no significant differences among groups in morning cortisol were observed. Latent growth curve analyses examined trajectories of cortisol regulation over time. Beginning at midintervention, divergence was found among the groups. Whereas the MI group remained indistinguishable from the NC group across time, the CS group progressively evinced lower levels of morning cortisol, statistically differing from the MI and NC groups. Results highlight the value of psychosocial interventions for early child maltreatment in normalizing biological regulatory processes.

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.

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.

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.

This article offers a multilevel perspective on resilience to depression, with a focus on interactions among social and neurobehavioral systems involved in emotional reactivity and regulation. We discuss models of cross-contextual mediation and moderation by which the social context influences or modifies the effects of resilience processes at the biological level, or the biological context influences or modifies the effects of resilience processes at the social level. We highlight the socialization of emotion regulation as a candidate process contributing to resilience against depression at the social context level. We discuss several factors and their interactions across levels—including genetic factors, stress reactivity, positive affect, neural systems of reward, and sleep—as candidate processes contributing to resilience against depression at the neurobehavioral level. We then present some preliminary supportive findings from two studies of children and adolescents at high risk for depression. Study 1 shows that elevated neighborhood level adversity has the potential to constrain or limit the benefits of protective factors at other levels. Study 2 indicates that ease and quickness in falling asleep and a greater amount of time in deep Stage 4 sleep may be protective against the development of depressive disorders for children. The paper concludes with a discussion of clinical implications of this approach.

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.

Emotional distress experienced by mothers increases young children's risk of externalizing problems through suboptimal parenting and child self-regulation. An integrative structural equation model tested hypotheses that mothers’ parenting (i.e., low levels of inductive discipline and maternal warmth) would mediate adverse effects of early maternal distress on child effortful control, which in turn would mediate effects of maternal parenting on child externalizing behavior. This longitudinal study spanning ages 3, 6, and 10 included 241 children, mothers, and a subset of teachers. The hypothesized model was partially supported. Elevated maternal distress was associated with less inductive discipline and maternal warmth, which in turn were associated with less effortful control at age 3 but not at age 6. Inductive discipline and maternal warmth mediated adverse effects of maternal distress on children's effortful control. Less effortful control at ages 3 and 6 predicted smaller relative decreases in externalizing behavior at 6 and 10, respectively. Effortful control mediated effects of inductive discipline, but not maternal warmth, on externalizing behavior. Findings suggest elevated maternal distress increases children's risk of externalizing problems by compromising early parenting and child self-regulation.

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.

Learning to respond to others' distress with well-regulated empathy is an important developmental task linked to positive health outcomes and moral achievements. However, this important interpersonal skill set may also confer risk for depression and anxiety when present at extreme levels and in combination with certain individual characteristics or within particular contexts. The purpose of this review is to describe an empirically grounded theoretical rationale for the hypothesis that empathic tendencies can be “risky strengths.” We propose a model in which typical development of affective and cognitive empathy can be influenced by complex interplay among intraindividual and interindividual moderators that increase risk for empathic personal distress and excessive interpersonal guilt. These intermediate states in turn precipitate internalizing problems that map onto empirically derived fear/arousal and anhedonia/misery subfactors of internalizing disorders. The intraindividual moderators include a genetically influenced propensity toward physiological hyperarousal, which is proposed to interact with genetic propensity to empathic sensitivity to contribute to neurobiological processes that underlie personal distress responses to others' pain or unhappiness. This empathic personal distress then increases risk for internalizing problems, particularly fear/arousal symptoms. In a similar fashion, interactions between genetic propensities toward negative thinking processes and empathic sensitivity are hypothesized to contribute to excess interpersonal guilt in response to others' distress. This interpersonal guilt then increases the risk for internalizing problems, especially anhedonia/misery symptoms. Interindividual moderators, such as maladaptive parenting or chronic exposure to parents' negative affect, further interact with these genetic liabilities to amplify risk for personal distress and interpersonal guilt as well as for consequent internalizing problems. Age-related increases in the heritability of depression, anxiety, and empathy-related constructs are consistent with developmental shifts toward greater influence of intraindividual moderators throughout childhood and adolescence, with interindividual moderators exerting their greatest influence during early childhood. Efforts to modulate neurobiological and behavioral expressions of genetic dysregulation liabilities and to promote adaptive empathic skills must thus begin early in development.

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.