The relationships of deviant talk and role taking during peer interaction, association with deviant peers, and growth in overt and covert conduct problems during kindergarten and first grade were examined in a community sample of 267 boys and girls. At entry to kindergarten, high levels of overt and covert conduct problems predicted association with deviant peers, and deviant peer association predicted deviant talk and role taking during peer interaction during kindergarten. Association with deviant peers, and deviant talk and role taking predicted growth in overt and covert conduct problems on the playground, in the classroom, and at home during kindergarten and first grade. Peer processes associated with growth in conduct problems that escalate rapidly during late childhood and adolescence appear to occur in earlier childhood. These peer processes may play a central role in the evolution of conduct problems to include covert as well as overt forms.This research was supported by National Institute of Health Grant MH57342.

Although no prospective epidemiological studies have evaluated the relationship between family interactions and the development of borderline personality disorder (BPD), there is considerable evidence for the central role of family interactions in the development of BPD. This paper describes the role of family interactions or processes, especially those that might be regarded as invalidating or conflictual, negative or critical, and the absence of more validating, positive, supportive, empathic interactions, in the development of BPD. Perhaps more importantly, the proposed model considers how these parental and family behaviors transact with the child's own behaviors and emotional vulnerabilities, resulting in a developmental model of BPD that is neither blaming of the family member with BPD nor of her or his parents and caregivers, and has important and specific implications for both prevention and intervention.

Neuroimaging and behavioral studies have shown that children and adults with autism have impaired face recognition. Individuals with autism also exhibit atypical event-related brain potentials to faces, characterized by a failure to show a negative component (N170) latency advantage to face compared to nonface stimuli and a bilateral, rather than right lateralized, pattern of N170 distribution. In this report, performance by 143 parents of children with autism on standardized verbal, visual–spatial, and face recognition tasks was examined. It was found that parents of children with autism exhibited a significant decrement in face recognition ability relative to their verbal and visual spatial abilities. Event-related brain potentials to face and nonface stimuli were examined in 21 parents of children with autism and 21 control adults. Parents of children with autism showed an atypical event-related potential response to faces, which mirrored the pattern shown by children and adults with autism. These results raise the possibility that face processing might be a functional trait marker of genetic susceptibility to autism. Discussion focuses on hypotheses regarding the neurodevelopmental and genetic basis of altered face processing in autism. A general model of the normal emergence of social brain circuitry in the first year of life is proposed, followed by a discussion of how the trajectory of normal development of social brain circuitry, including cortical specialization for face processing, is altered in individuals with autism. The hypothesis that genetic-mediated dysfunction of the dopamine reward system, especially its functioning in social contexts, might account for altered face processing in individuals with autism and their relatives is discussed.The writing of this paper and the studies reported herein were funded by a grant from the National Institute of Child Health and Human Development (NICHD Grant U19HD34565), which is part of the NICHD Collaborative Program of Excellence in Autism, and a center grant from the National Institute of Mental Health (NIMH Grant U54MH066399), which is part of the NIH STAART Centers Program.

Inattention/hyperactivity and aggressive behavior problems were measured in 335 children from school entry throughout adolescence, at 3-year intervals. Children were participants in a high-risk prospective study of substance use disorders and comorbid problems. A parallel process latent growth model found aggressive behavior decreasing throughout childhood and adolescence, whereas inattentive/hyperactive behavior levels were constant. Growth mixture modeling, in which developmental trajectories are statistically classified, found two classes for inattention/hyperactivity and two for aggressive behavior, resulting in a total of four trajectory classes. Different influences of the family environment predicted development of the two types of behavior problems when the other behavior problem was held constant. Lower emotional support and lower intellectual stimulation by the parents in early childhood predicted membership in the high problem class of inattention/hyperactivity when the trajectory of aggression was held constant. Conversely, conflict and lack of cohesiveness in the family environment predicted membership in a worse developmental trajectory of aggressive behavior when the inattention/hyperactivity trajectories were held constant. The implications of these findings for the development of inattention/hyperactivity and for the development of risk for the emergence of substance use disorders are discussed.This work was supported by National Institute on Alcohol Abuse and Alcoholism grants (RO1 AA12217 to R.A.Z. and J.T.N. and R37 AA07065 to R.A.Z. and H.E.F.). We are indebted to Bengt Muthén for his advice on the statistical analyses for this study.

Traditional theories regarding the etiology of borderline personality disorder have focused on poor attachment figures and/or traumatic experience. The present review posits an additional pathogenic course for this disorder. Specifically, the proposed mechanism involves a basic disruption of the neural hardware that supports the formation and maintenance of unconscious emotional memory, hardware essential for the formation of early attachments. It is further theorized that this early disruption has ongoing effects on both behavioral and concomitant neural development. Within this model, adolescence is described as a period of intense change that serves as the tipping point for the onset of borderline personality disorder.

Empathic concern for others is an essential motive for challenges of self-regulation at all developmental stages. A child who never develops the capacity for empathic concern may become an ineffective parent, such that developmental psychopathology propagates across generations. We draw on evidence and theory by Panksepp and associates that indicates that infant–mother bonding is mediated by opiate mechanisms. We review the neural systems of pain perception and find these are closely aligned with those for attentional and cognitive self-regulation. Analysis of the limbic and neocortical representations for interpersonal reasoning suggests there are important contributions from visceral, affective, and somatic and cognitive levels. We draw on modern learning theory to propose a critical role for frustration training in development to allow the child to achieve the capacity for tolerating psychological pain that allows effective empathic concern in later relationships.

A longitudinal prospective design was used to test the generalizability of low levels of social preference and high levels of antisocial peer involvement as risk factors for delinquent behavior problems to African American (AA) and European American (EA) boys and girls (N = 384). Social preference scores were computed from peer reports in middle childhood (ages 6–9). Parents and adolescents reported antisocial peer involvement in early adolescence (ages 13–16) and adolescents reported on their own delinquent behavior in late adolescence (ages 17 and 18). Analyses tested for differences across four groups (AA boys, EA boys, AA girls, EA girls) in construct measurement, mean levels, and associations among variables. Few measurement differences were found. Mean-level differences were found for social preference and delinquent behavior. AA boys were least accepted by peers and reported the highest level of delinquent behavior. EA girls were most accepted by peers and reported the lowest level of delinquent behavior. Associations among peer experiences and delinquent behavior were equivalent across groups, with lower levels of social preference and higher levels of antisocial peer involvement associated with more delinquent behavior. Person-centered analyses showed the risk associated with low social preference and high antisocial peer involvement to be similar across groups, providing further evidence of the generalizability of the peer relationship experiences as risk factors for subsequent delinquent behavior problems.This research was supported by grants from the National Institute of Mental Health (MH 42498, MH 57095) and the National Institute of Child Health and Human Development (HD 30572 to G.S.P., K.A.D., and J.E.B.). We are grateful to the Child Development Project families for their participation. Special thanks to Jennifer Burczyk–Brown for her help in managing the analyses and to Michael M. Criss for his comments on an early version of the manuscript. This article has been approved for publication by the Director of the Louisiana Agricultural Experiment Station (manuscript 03-36-104).

The main aims of this study were to investigate if children with high-functioning autism (HFA) and children with Tourette syndrome (TS) can be differentiated in their executive functioning (EF) profile compared to normal controls (NCs) and compared to each other and to investigate whether children with HFA or children with TS and a comorbid group of children with both disorders are distinct conditions in terms of EF. Four groups of children participated in this study: HFA, TS, comorbid HFA + TS, and a NC group. All children were in the age range of 6 to 13 years. The groups were compared on five major domains of EF: inhibition, visual working memory, planning, cognitive flexibility, and verbal fluency. Children with HFA scored lower than NC children on all the EFs measured. Children with TS and NC children showed the same EF profile. The HFA group scored lower than the TS group for inhibition of a prepotent response and cognitive flexibility. Children with HFA performed poorer than children with comorbid HFA + TS on all functions, with the exception of inhibiting an ongoing response, interference control, and verbal fluency. Children with TS and children with comorbid HFA + TS could not be differentiated from one another in terms of EF. This study indicates that EF deficits are highly characteristic of children with HFA in comparison to children with TS and NC. The results suggest that for the comparison between HFA and TS groups, it is important to take into account comorbidity. A reevaluation of the EF hypothesis in children with TS is suggested.We thank the children and parents without whose participation this research would not have been possible.

Borderline personality disorder is a particularly devastating, yet understudied form of psychopathology. One of the most significant gaps in existing knowledge is the lack of systematic, prospective empirical attention to the developmental precursors of borderline personality. The present investigation was an exploratory attempt to address this limitation through (a) development of a psychometrically sound self-report instrument that assesses borderline personality features in childhood, the Borderline Personality Features Scale for Children (BPFS-C); (b) examination of the stability of BPF in childhood; (c) evaluation of gender differences in BPF in childhood; and (d) evaluation of the specificity of the BPFS-C for assessing borderline personality features. These goals were achieved through the prospective study of a normative sample of 400 (54% female) fourth though sixth graders who were assessed during the Fall of Year 1, Spring of Year 1, and Fall of Year 2. The use of linear mixed modeling techniques provided evidence for the construct validity of the BPFS-C. Further, borderline personality features as assessed with the BPFS-C were found to be moderately stable over the course of the study, with girls reporting higher levels of BPF than boys. Results also demonstrated that children's scores on the BPFS-C were uniquely related to indicators of borderline personality pathology above and beyond their scores on the Children's Depression Inventory. The implications of these results for the study of the development and etiology of borderline pathology are discussed.This research was supported by a grant to the first author from the National Institute of Mental Health (MH063684). We acknowledge Leslie Morey and Carol Rockhill for their extensive assistance with the development of the BPFS-C. We also thank the staff of the School Buddies Project and the teachers and children who participated in this study for their significant contributions.

The present study attempted to determine the direction and etiology of the robust relationship between childhood externalizing (EXT) symptoms and parent–child conflict using a genetically informative longitudinal model and data from the ongoing Minnesota Twin Family Study. Participants consisted of 1,506 same-sex twins assessed at ages 11 and 14, and their parents. The relationship between EXT and parent–child conflict from ages 11 to 14 was examined within a biometrical cross-lagged design. The results revealed three primary findings: first, the stability of conflict and externalizing over time is largely, although not solely, a result of genetic factors. Second, there appears to be a bidirectional relationship between conflict and EXT over time, such that both conflict and EXT at 11 independently predict the other 3 years later. Finally, the results are consistent with the notion that parent–child conflict partially results from parental responses to their child's heritable externalizing behavior, while simultaneously contributing to child externalizing via environmental mechanisms. These results suggest a “downward spiral” of interplay between parent–child conflict and EXT, and offer confirmation of a (partially) environmentally mediated effect of parenting on child behavior.This research was funded in part by USPHS grants (DA05147, DA13240, AA09367, AA00175, MH 65137), a National Institutes of Mental Health training grant (MH17069 to S.A.B.), and a Doctoral Dissertation Fellowship (S.A.B.). We also thank Hennepin County Medical Center in Minneapolis for the research time that enabled the primary author to conduct this study.

There is controversy over the existence and nature of blind children's limitations in symbolic play. In this study we tested 13 5- to 9-year-old congenitally blind children for the ability to symbolize when an adult provided scaffolding for their play. The blind children were selected on the basis that they did not have the syndrome of autism, and they comprised two groups matched for age (MA) and verbal ability on the Wechsler Intelligence Scale for Children who contrasted in their ability to engage in social relations. We also tested a group of sighted children who were MA matched with the more socially able blind children. On the basis of an hypothesis about the social–developmental sources of symbolic play deficits in congenitally blind children, we predicted differences between the socially able and socially impaired groups of blind children in the following respects: the attribution of symbolic meanings to play materials, the ascription of individual roles to play figures, and the anchorage of play in the scenario as presented by the adult. The results accorded with these predictions. Whereas the more socially able blind children showed symbolic play that was very similar to that of sighted children, the MA- and IQ-matched socially impaired blind children were limited in the three aspects of their play. On the other hand, even the socially impaired children showed instances of symbolizing. The findings suggest a way to reconcile conflicting reports of symbolic play deficits in young blind children, and may be relevant for explaining the association between autism and congenital blindness.This study was supported by a PhD studentship from the Mary Kitzinger Trust to Martin Bishop. The Hayward Foundation also contributed financial support. We thank the pupils and staff of the following schools, who were so generous in making the study possible: Dorton House School, Sevenoaks; West of England School, Exeter; Joseph Clarke School, London; Linden Lodge School, Wimbledon; Temple Bank School, Bradford; St. Vincent's School for the Blind, Liverpool; RNIB Sunshine House School, Northwood; and Priestley Smith School, Birmingham.

The circumplex model of affect proposes that all affective states arise from cognitive interpretations of core neural sensations that are the product of two independent neurophysiological systems. This model stands in contrast to theories of basic emotions, which posit that a discrete and independent neural system subserves every emotion. We propose that basic emotion theories no longer explain adequately the vast number of empirical observations from studies in affective neuroscience, and we suggest that a conceptual shift is needed in the empirical approaches taken to the study of emotion and affective psychopathologies. The circumplex model of affect is more consistent with many recent findings from behavioral, cognitive neuroscience, neuroimaging, and developmental studies of affect. Moreover, the model offers new theoretical and empirical approaches to studying the development of affective disorders as well as the genetic and cognitive underpinnings of affective processing within the central nervous system.This work was supported in part by NIMH Grants MH01232, MH59139, MH36197, MHK02-74677, and MH068318; a grant from the National Alliance for Research in Schizophrenia and Affective Disorders (NARSAD); NSF Grant BSC-0421702; and funding from the Thomas D. Klingenstein and Nancy D. Perlman Family Fund and the Suzanne Crosby Murphy Endowment at Columbia University.

Potential precursors to borderline personality disorder (BPD) were investigated in a sample of 185 maltreated and 175 nonmaltreated school-aged children attending a summer camp research program. Self-report, peer-report, and counselor-report measures were utilized to assess developmental constructs conceptualized to constitute vulnerability for later emerging BPD. These areas, including personality features, representational models of self, parent, and peers, interpersonal relationship difficulties with peers and adults, and suicidal/self-harm behavior, were used to develop a BPD precursors composite. Additionally, the efficiency of three attention networks was assessed with a computerized task. Maltreated children had higher mean scores on the BPD precursors composite, and children classified as having high levels of these precursors were more prevalent in the maltreatment group. No maltreatment group differences were found for the efficiency of the three attention networks; however, children with high levels of BPD precursors evinced less efficient processing of the conflict attention network, comparable to findings observed among adult patients with BPD. Child maltreatment and efficiency of the conflict attention network independently predicted scores on the BPD precursors composite. Experiential and biological contributions to risk for BPD and recommendations for prevention and intervention are discussed.This research was supported by funding from the National Institute on Drug Abuse (DA11741) and the Spunk Fund, Inc.

When children experience emotions, do they view their primary caregiver as reacting in a different manner depending on the children's different emotions? Parental socialization of negative emotions and child psychopathology were examined among 161 inner city youth ages 11–14 years. These early adolescents were more likely to perceive their parents as responding in a different manner to different emotions than responding in the same way to different emotions. In addition, we asked if emotion-specific socialization strategies tell us more about child psychopathology than global socialization strategies do. Exploratory analyses suggest that a mixture of both emotion-specific and global socialization strategies may best predict child psychopathology. It remains important to clarify the emotional context of socialization strategies.This research was supported by an NIMH Predoctoral Fellowship, National Research Service Award (F31 MH12322), and an NIMH Postdoctoral Fellowship, Institutional Training Grant (T32 MH19890-07). We thank the principal, parents, and students of Junior High School 275 and the Police Athletic League Brownsville Beacon Community Center for their support and participation in this project. Patrick Shrout gave invaluable feedback in the development of this paper. Colleen R. O'Neal is now at the NYU Child Study Center, NYU School of Medicine.

Interest in the effects of early adversity on children's development reflects contemporary emphases on early experience in the behavioral sciences and plasticity in the neurosciences. Over the past decade, powerful new tools and approaches for understanding the neural circuitry involved in emotion have become increasingly available. Yet, research in developmental psychopathology has not reaped the full benefits of affective neuroscience approaches and methods. Integration of affective neuroscience approaches can excavate developmental mechanisms, thereby advancing knowledge about the etiology, prevention, and treatment of mental health problems in children. Here, we consider two general principles that can guide understanding of plasticity in the neural circuitry of emotion systems and the development of psychopathology.The author was generously supported by the National Institutes of Mental Health (MH 61285, MH 68858) and by the University of Wisconsin. Elizabeth Shirtcliff, Alison Wismer Fries, Jessica Shackman, and Julia Kim–Cohen provided thoughtful comments on an early draft of this paper. The author also thanks Dante Cicchetti and Michael Posner for their critical reviews of the manuscript and Erin Henigan for help with preparation of this manuscript.

Research linking basal cortisol levels with internalizing and externalizing behavior problems in youths has yielded inconsistent results. We hypothesize that the high moment to moment variation in adrenocortical activity requires an analytical strategy that separates variance in cortisol levels attributable to “stable traitlike” versus “state or situationally specific” sources. Early morning saliva samples were obtained from 724 youths (M age = 13.5 years; range = 6–16 years in Year 1) on 2 successive days 1 year apart. Latent state–trait modeling revealed that 70% of the variance in cortisol levels could be attributed to statelike sources, and 28% to traitlike sources. For boys only, higher levels of externalizing problem behaviors were consistently associated with lower cortisol attributable to traitlike sources across 3 years of behavioral assessment. The inverse association between individual differences in cortisol and externalizing problem behavior has previously only been reported in studies of at-risk or clinical groups. The present findings suggest the relationship is a stable phenomenon that spans both normative and atypical child development. Studies are needed to reveal the biosocial mechanisms involved in the establishment and maintenance of this phenomenon, and to decipher whether individual differences in this hormone–behavior link confers risk or resilience.This research was supported in part by the Behavioral Endocrinology Laboratory, and the Population Research Institute (PRI) at Pennsylvania State University, as well as the W. T. Grant Foundation (Grant 9617796). PRI has core support from the National Institute of Child Health and Development (Grant 1-HD28263). Collection of data on family process and child psychosocial functioning was supported by two grants from the National Institute of Child Health and Human Development (HD 32336 and HD 29409) to Ann Crouter and Susan McHale.

We present a multilevel approach to developing potential explanations of cognitive impairments and psychopathologies common to individuals with chromosome 22q11.2 deletion syndrome. Results presented support our hypothesis of posterior parietal dysfunction as a central determinant of characteristic visuospatial and numerical cognitive impairments. Converging data suggest that brain development anomalies, primarily tissue reductions in the posterior brain and changes to the corpus callosum, may affect parietal connectivity. Further findings indicate that dysfunction in “frontal” attention systems may explain some executive cognition impairments observed in affected children, and that there may be links between these domains of cognitive function and some of the serious psychiatric conditions, such as attention-deficit/hyperactivity disorder, autism, and schizophrenia, that have elevated incidence rates in the syndrome. Linking the neural structure and the cognitive processing levels in this way enabled us to develop an elaborate structure/function mapping hypothesis for the impairments that are observed. We show also, that in the case of the catechol-O-methyltransferase gene, a fairly direct relationship between gene expression, cognitive function, and psychopathology exists in the affected population. Beyond that, we introduce the idea that variation in other genes may further explain the phenotypic variation in cognitive function and possibly the anomalies in brain development.We thank the children and families that participated in our studies and the staff of the 22q and You Center at the Children's Hospital of Philadelphia. This work was supported by grants from the NIH (R01HD42974 and R01HD46159) and the Philadelphia Foundation to T.J.S., Grant PO1DC02027 to B.S.E., and Grant M01-RR00240 to the Children's Hospital of Philadelphia.

A longitudinal model that linked involved–supportive parenting and siblings' ability-camouflaging self-presentations to peers with the development of externalizing and internalizing symptoms was tested with 152 pairs of first- and second-born African American siblings (mean ages 12.7 years and 10.2 years at the first wave of data collection). Three waves of data were collected at 1-year intervals. Teachers assessed siblings' externalizing symptoms, internalizing symptoms, and academic competence; siblings reported their own self-presentations and desire for peer acceptance; and mothers and siblings provided multiinformant assessments of involved–supportive parenting. Involved–supportive parenting at Wave 1 was linked with peer-directed self-presentations at Wave 2. Wave 2 self-presentations were linked indirectly with changes from Wave 1 to Wave 3 in externalizing and internalizing symptoms through their association with academic competence.This study was supported by a grant (2 R01 HD30588) from the National Institute of Child Health and Human Development.

Borderline personality disorder (BPD) is characterized by a broad pattern of impulsivity and suicidality. BPD usually begins in adolescence; the full clinical picture of the disorder is associated with developmental increases in impulsivity. However, BPD also has childhood precursors. The developmental pathways are similar to those found in other impulsive spectrum disorders, but children who later develop BPD probably have both externalizing and internalizing symptoms. Research in this area has made use of retrospective data from adults, prospective data from community studies, follow-up studies from children at risk, as well as research on “borderline pathology of childhood” (a condition with symptoms similar to adult BPD). Existing evidence suggests that both temperamental and environmental risk factors play a role in the development of the behavioral patterns associated with the disorder. These pathways also help account for the life course and outcome of BPD in adulthood.This paper benefited from suggestions made by Jenny Macfie.

Within-family covariation between interparental hostility and adolescent behavior across three interactions over a 2-year period was explored in a sample that included 37 typical adolescents and 35 adolescents recently hospitalized for psychiatric difficulties. More interparental hostility across the three interactions was associated with more adolescent hostility and more positive engagement (at a trend level) regardless of psychiatric background. Parent-to-child hostility in each interaction mediated the link for adolescent hostility but not for positive adolescent engagement. Emotion regulation capacities and age were linked to variability in adolescents' behavior in the presence of interparental conflict. In interactions with more interparental hostility, adolescents with greater capacity to tolerate negative affect were more likely to show increased positive engagement, and adolescents who were better able to modulate their emotional expression were less likely to show increased hostility. Covariation between interparental and adolescent hostility across the three family interactions decreased as the adolescent aged. These findings are consistent with the theory that exposure to interparental hostility is emotionally disequilibrating, and that adolescent responses may reflect differences in emotion regulation and other developmentally based capacities. Gender and variations across families in overall levels of hostile parenting were also linked with adolescent behavior in the presence of interparental hostility.This research was supported, in part, by a grant from the National Institute of Mental Health (RO1 MH 4493). The authors thank J. Heidi Gralinski–Bakker and Rebecca Billings for their valuable assistance with this research.