Because many serious adolescent offenders reduce their antisocial behavior after court involvement, understanding the patterns and mechanisms of the process of desistance from criminal activity is essential for developing effective interventions and legal policy. This study examined patterns of self-reported antisocial behavior over a 3-year period after court involvement in a sample of 1,119 serious male adolescent offenders. Using growth mixture models, and incorporating time at risk for offending in the community, we identified five trajectory groups, including a “persister” group (8.7% of the sample) and a “desister” group (14.6% of the sample). Case characteristics (age, ethnicity, antisocial history, deviant peers, a criminal father, substance use, psychosocial maturity) differentiated the five trajectory groups well, but did not effectively differentiate the persisting from desisting group. We show that even the most serious adolescent offenders report relatively low levels of antisocial activity after court involvement, but that distinguishing effectively between high-frequency offenders who desist and those who persist requires further consideration of potentially important dynamic factors related to this process.

The Relational Psychotherapy Mothers' Group (RPMG), a developmentally informed, supportive psychotherapy designed to serve heroin-addicted mothers with children up to 16 years of age, aims at addressing psychosocial vulnerabilities, and facilitating optimal parenting, among at-risk mothers. We present preliminary evidence on the efficacy of RPMG as an “add on” treatment in comparison with standard methadone counseling alone. At the end of the 24-week treatment period, mothers receiving RPMG plus standard methadone counseling demonstrated lower levels of risk for child maltreatment, greater involvement with their children, and more positive psychosocial adjustment than women who received methadone counseling alone. Children of RPMG participants also reflected fewer problems in multiple areas. At 6 months posttreatment, RPMG recipients continued to be at a relative advantage, although the magnitude of group differences was often attenuated. Notably, urinalyses indicated that RPMG mothers showed greater improvements in levels of opioid use over time than comparison mothers.

The last 25 years have seen significant advances in our conceptualization of alcohol use and alcohol use disorders within a developmental framework, along with advances in our empirical understanding that have been potentiated by advances in quantitative methods. These include advances in understanding the heterogeneity of trajectories of alcohol outcomes; new insights about early childhood antecedents, and adolescence and emerging adulthood as important developmental periods for alcohol outcomes; a more nuanced understanding of the influences of developmental transitions, and their timing and contexts; a greater appreciation for the importance of considering multiple levels of analysis (including an increasing number of genetically informative studies); a continuing focus on studying multiple pathways underlying alcohol outcomes; and an increasing focus on studying the effects of alcohol exposure on future development. The current paper reviews these advances and suggests directions for future study.

Within the last decade, many investigators have focused on the physical, neurodevelopmental, and neuropsychological effects of prenatal cocaine exposure on infants and young children. Although inconclusive on many crucial issues, published studies reveal the beginnings of a profile of possible cocaine-related effects on neuropsychological functions subserving arousal and attention regulation. That profile is informed by preclinical studies in which important factors such as duration and type of exposure as well as environmental conditions may be more adequately controlled. In the developing brain, there are a number of candidate mechanisms that account for how prenatal cocaine exposure may interfere with neural ontogeny. This review focuses on the monoamine system, one of the primary sites of action of cocaine in the adult. In the developing organism, monoamines play critical trophic roles through all phases of central nervous system (CNS) ontogeny—cell proliferation, neural migration, growth, maturation, and synaptogenesis. Because of their trophic role in CNS ontogeny, cocaine effects on developing nervous system may be mediated in part through effects on monoamine system ontogeny. In turn, these effects may be expressed behaviorally in disrupted patterns of arousal and attention regulation given that these domains are connected intimately to monoaminergic systems.

Although much has been written about the utility of applying Sameroff and Chandler's transactional perspective to the study of child psychopathology, relatively few researchers have used such an approach to trace the emergence of child problem behavior from infancy to adolescence. Using a sample of 289 male toddlers from predominantly low-income families, the current study examined associations between various forms of early child disruptive behavior, subsequent trajectories of maternal depressive symptoms over the course of 8 years, and adolescent problem behavior. Results indicated that early child noncompliance was the most robust predictor of more chronic and elevated trajectories of maternal depression, which in turn discriminated teacher and youth reports of adolescent antisocial behavior but not internalizing symptoms. The findings were consistent with transactional perspectives of developmental psychopathology that have emphasized the dynamic interplay between child and parent characteristics.

Normal adolescent development is often accompanied by transient emotional and behavioral problems. For most individuals with postpubertal-onset adjustment problems, there is a resolution by early adulthood and relative stability through the adult life span. But for a minority, adjustment problems escalate during adolescence and portend the development of serious mental illness in adulthood. In this article, we explore adolescent behavioral changes and neurodevelopmental processes that might contribute to stress sensitivity and vulnerability for the emergence of the mental disorders. Of particular interest is the role that hormonal changes might play in the expression of genetic vulnerabilities for psychopathology. Drawing on recent findings from clinical research and behavioral neuroscience, we describe the ways in which postpubertal hormones might alter brain function and, thereby, behavior. It is concluded that there are both activational and organization effects of hormones on the adolescent brain, and these contribute to developmental discontinuities in behavioral adjustment. Implications for adult psychopathology and preventive intervention are discussed.

We tested the hypothesis that attachment security at 12 months can be predicted from infant response to the mother's still-face interaction during the first half-year. Subjects were 66 primiparous mother-infant pairs drawn from the working- and middle-socioeconomic strata (SES). Half of the mothers had experienced a postpartum depression. Infants were observed longitudinally in the still-face paradigm at 2, 4, and 6 months and in the Strange Situation at 12 months. Positive expressions in response to the still-face at 6 months predicted secure attachment at 12 months. Absence of positive expressions predicted avoidant attachment. In infants of postpartum depressed mothers, hours of nonmaternal care positively correlated with secure attachment. Variables associated with infant proneness to distress and sociability were unrelated to attachment security. These results suggest that attachment formation is underway by 6 months of age and that indicators of 12-month attachment security can be detected as early as 6 months. Similar mechanisms of affect regulation and coping may underlie infant response in the still-face and Strange Situation procedures.

Analyzing gene–brain–behavior linkages in childhood neurodevelopmental disorders, a research approach called “behavioral neurogenetics,” has provided new insights into understanding how both genetic and environmental factors contribute to complex variations in typical and atypical human development. Research into etiologically more homogeneous disorders, such as fragile X syndrome, in particular, allows the use of more precise metrics of genetic risk so that we can more fully understand the complex pathophysiology of childhood onset neurodevelopmental disorders. In this paper, we review our laboratory's behavioral neurogenetics research by examining gene–brain–behavior relationships in fragile X syndrome, a single-gene disorder that has become a well-characterized model for studying neurodevelopmental dysfunction in childhood. Specifically, we examine genetic influences, trajectories of cognition and behavior, variation in brain structure and function, and biological and environmental factors that influence developmental and cognitive outcomes of children with fragile X. The converging approaches across these multilevel scientific domains indicate that fragile X, which arises from disruption of a single gene leading to the loss of a specific protein, is associated with a cascade of aberrations in neurodevelopment, resulting in a central nervous system that is suboptimal with respect to structure and function. In turn, structural and functional brain alterations lead to early disruption in emotion, cognition, and behavior in the child with fragile X. The combination of molecular genetics, neuroimaging, and behavioral research have advanced our understanding of the linkages between genetic variables, neurobiological measures, IQ, and behavior. Our research and that of others demonstrates that neurobehavior and neurocognition, genetics, and neuroanatomy are all different views of the same intriguing biological puzzle, a puzzle that today is rapidly emerging into a more complete picture of the intricate linkages among gene, brain, and behavior in developing children. Understanding the complex multilevel scientific perspective involved in fragile X will also contribute to our understanding of normal development by highlighting developmental events throughout the life span, thereby helping us to delineate the boundaries of pathology.

Previous research has documented differences in the pattern of EEG activation between 3-month-old infants of depressed mothers and infants of nondepressed mothers. In the present study, EEG was recorded in even younger 1-month-old infants of depressed and nondepressed mothers. The infants of depressed mothers exhibited greater relative right frontal EEG asymmetry (due to reduced left frontal activation), and this pattern at 1 month was significantly related to 3-month EEG asymmetry. Right frontal EEG asymmetry was also related to more frequent negative facial expressions (sad and pre-cry faces) during the Brazelton exam. Finally, the infants of depressed mothers showed more indeterminate sleep, were less active, and cried less than infants of nondepressed mothers.

We describe recent progress in our program of research that aims to use functional magnetic resonance imaging (fMRI) to identify and delineate the brain systems involved in social perception and to chart the development of those systems and their roles as mechanisms supporting the development of social cognition in children, adolescents, and adults with and without autism. This research program was initiated with the intention of further specifying the role of the posterior superior temporal sulcus (STS) region in the network of neuroanatomical structures comprising the social brain. Initially, this work focused on evaluating STS function when typically developing adults were engaged in the visual analysis of other people's actions and intentions. We concluded that that the STS region plays an important role in social perception via its involvement in representing and predicting the actions and social intentions of other people from an analysis of biological–motion cues. These studies of typically developing people provided a set of core findings and a methodological approach that informed a set of fMRI studies of social perception dysfunction in autism. The work has established that dysfunction in the STS region, as well as reduced connectivity between this region and other social brain structures including the fusiform gyrus and amygdala, play a role in the pathophysiology of social perception deficits in autism. Most recently, this research program has incorporated a developmental perspective in beginning to chart the development of the STS region in children with and without autism.

Emotion dysregulation is defined as patterns of emotional experience or expression that interfere with goal-directed activity. This paper considers this functionalist definition from a developmental perspective with the goal of elaborating this approach with respect to its central questions. What are the goals that are impeded by emotionally dysregulated responding, and what alternative goals might motivate emotion dysregulation? What are the developmental processes by which these goals take shape, and what are the influences of the family context, and especially of central relationships in the family, in their emergence? How does this functionalist account address the complex interaction of experience and developing biological processes that also influence emotion regulation and dysregulation? Drawing on research literature concerning children at risk for affective psychopathology and considering relevant examples of the interaction of biology and context, this discussion offers a portrayal of emotion dysregulation as a biologically dynamic, experience-based aspect of adaptation to environments and relationships that, in conditions of risk for the emergence of developmental psychopathology, motivates patterns of emotional responding that serve immediate coping often at the cost of long-term maladaptation. Implications for emotions theory and the study of developmental psychopathology are also considered.

A three-wave longitudinal study conducted with preadolescent boys and girls (N = 231 at Time 1 [T1]) was used to assess the hypotheses that aspects of social withdrawal would be predictors of a “snowball” cascade of depressed affect, and that friendship experiences would moderate these effects. Consistent with these hypotheses, multilevel modeling showed that measures of avoidance and exclusion at T1 were associated with concurrent levels of depressed affect and were antecedent to escalating trajectories of depressed affect over time. These accelerating growth curves fit a snowball cascade model. The analyses also showed the protective effects of friendship. Specifically, the snowball effect was limited to avoidant and excluded children who were friendless. Depressed affect did not increase among avoidant and excluded children who were friended.

Relations between attachment and child emotional and behavioral regulation were studied longitudinally in a sample of 223 children from urban, low-income families. Attachment in the Strange Situation at 12 and 18 months was scored using the infant classification system and at 24 months was scored using a preschool classification system. Only modest stability was found in attachment whether within or across classification systems, with the percentage of insecure attachments consistently increasing over time. Results indicated both concurrent and predictive associations with indices of child regulation based on observer ratings or maternal report. However, only the 24-month classification predicted maternal report of externalizing and internalizing behavior problems at age 3.5 years, with additional variance accounted for by selected measures of child emotional and behavior regulation from the same assessment. Attachment security (B) and atypical attachment classifications (D, A/C, and AD) appear to provide the most consistently useful information about child functioning. Results are discussed in terms of continuity and change from the perspective of developmental psychopathology.

Early antisocial behavior has its origins in childhood behavior problems, particularly those characterized by aggressive and destructive behavior. Deficits in self-regulation across multiple domains of functioning, from the physiological to the cognitive, are associated with early behavior problems, and may place children at greater risk for the development of later antisocial behavior. Data are presented from a longitudinal study of early self-regulation and behavior problems, the RIGHT Track Research Project, demonstrating that children at greatest risk for early and persistent problem behavior display patterns of physiological and emotional regulation deficits early in life. Parenting behavior and functioning have also been examined as predictors of trajectories of early problem behavior, and some data support the interaction of parenting and self-regulation as significant predictors of patterns of problematic behavior and ongoing problems with the regulation of affect. Peer relationships also affect and are affected by early self-regulation skills, and both may play a role in academic performance and subsequent school success. These data provide evidence that the social contexts of early family and peer relationships are important moderators of the more proximal mechanism of self-regulation, and both types of processes, social and biobehavioral, are likely implicated in early antisocial tendencies. Implications of these findings on self-regulation and early behavior problems are discussed in terms of future research and treatment approaches.

One of the most dramatic findings from quantitative genetic research is that environmental influences shared by siblings in a family do not make the siblings similar in terms of psychopathology. Sibling resemblance for psychopathology appears to be genetic rather than environmental in origin; environmental influences that affect the development of psychopathology must be nonshared and make children in the same family different rather than similar. This study sets out to identify environmental factors that differ for young siblings and to assess associations between such nonshared factors and differences in the older siblings' outcome in two domains: internalizing and externalizing behavior problems. Maternal interview and observations of differential maternal and sibling behavior were compared within 67 sibling dyads (younger and older siblings aged 4 and 7 years, respectively, on average), and differential experiences were related to the adjustment of the older sibling, as assessed by mother and teacher. Differential maternal behavior appeared to be particularly important as a predictor of adjustment problems. Older siblings showed internalizing problems in families in which mothers were less affectionate to the older than to the younger sibling. Greater maternal control toward the older than the younger sibling predicted both internalizing and externalizing problems. Differential maternal behavior explained 34% of the variance of internalizing behavior and 27% of the variance of externalizing behavior problems, independent of variance explained by family structure variables. Although the sample was unselected for psychopathology and was too small to permit analyses of the diagnosable extremes of internalizing and externalizing dimensions, these results are encouraging in relation to the goal of identifying systematic sources of nonshared environment that affect the development of psychopathology.

Utilizing attachment theory as a basis for conceptualizing close relationships among adolescents, this study investigated two important relationship risk factors (child maltreatment, and adolescent self-perceived insecure attachment style) as predictors of “offender” and “victim” experiences in youth relationships. In addition to considering the influence of these risk factors, we further considered their interaction in predicting conflict in close relationships. Of interest was the extent to which attachment styles may function as a moderator of the relationship between childhood abuse and current abuse in teen close relationships. High school students (N = 321) in grades 9 and 10 completed questionnaires tapping their histories of maltreatment, currently viewed styles of attachment, and conflict in close relationships over the past 6 months. Maltreatment alone emerged as the most consistent predictor, accounting for 13–18% of the variance in male's physically, sexually, and verbally abusive behaviors; in contrast, it was not highly predictive of female's abusive behaviors. Maltreatment was predictive of victimization experiences for both males and females. Attachment style did not substantially add to the prediction of relationship conflict beyond maltreatment; however, avoidant attachment style emerged repeatedly as a significant predictor of female abusiveness and victimization. Attachment self-ratings were found to function as a moderator of child maltreatment in predicting primarily male coercive behavior towards a relationship partner as well as predicting male's experience of coercion from a partner. Thus, the presence of childhood maltreatment and adolescent self-perceived insecure attachment style applies predominantly to male youth. The implication of these gender differences for understanding relationship violence is discussed.

The pursuit of rewarding experiences motivates everyday human behavior, and can prove beneficial when pleasurable, positive consequences result (e.g., satisfying hunger, earning a paycheck). However, reward seeking may also be maladaptive and lead to risky decisions with potentially negative long-term consequences (e.g., unprotected sex, drug use). Such risky decision making is often observed during adolescence, a time in which important structural and functional refinements occur in the brain's reward circuitry. Although much of the brain develops before adolescence, critical centers for goal-directed behavior, such as frontal corticobasal ganglia networks, continue to mature. These ongoing changes may underlie the increases in risk-taking behavior often observed during adolescence. Further, typical development of these circuits is vital to our ability to make well-informed decisions; atypical development of the human reward circuitry can have severe implications, as is the case in certain clinical and developmental conditions (e.g., attention-deficit/hyperactivity disorder). This review focuses on current research probing the neural correlates of reward-related processing across human development supporting the current research hypothesis that immature or atypical corticostriatal circuitry may underlie maladaptive behaviors observed in adolescence.

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.