Attention-deficit/hyperactivity disorder (ADHD) is a behavioral syndrome that arises in early childhood, often co-occurs with conduct disorder and leads, developmentally, to antisocial behavior and substance abuse. Models from cognitive and affective neuroscience have been invoked in an effort to understand the development of ADHD, leading to a broad array of interrelated theories and hypothesized mechanisms. In this paper, we highlight core mechanisms that may cut across several theories and constructs, and thus provide some leverage for further study and conceptualization from a neuroscience perspective. We emphasize the joint operations of frontostriatal and frontocerebellar neural loops in detecting and predicting what and when important events in the environment will occur and their interaction with frontoamygdala loops in assigning emotional significance to these events. We note that weaknesses in the development of these basic operations could lead to decrement in the development of cognitive and affective control and other mental operations mediated by prefrontal cortex during development. In turn, such decrement could lead to many of the phenotypic cognitive and neuropsychological features seen in children with ADHD.This work was supported by National Institute of Mental Health Grants R01-MH59105 and R01-MH63146 to J.T.N. and NIMH R01 MH63255 and NIDA R21 DA15882 to B.J.C.

From their early roots in embryology, parallels are drawn between the major psychological and biological foci of organismic theories. Neural plasticity and concepts of causality in developmental systems are discussed. Because the nature of the developmental process necessitates addressing the nonlinear dynamics of complex systems, it is theorized that causal explanations in neural development, just as is the case with psychological processes, should emphasize the individual's active strivings for self-organization as the major determinant of ontogenesis. Whether or not they cohere to form an integrated self, it is hypothesized that the homeostatic, self-regulatory structures of the mind are the major stabilities in the chaotic dynamics of psychological and neural development.

The utility and flexibility of recent advances in statistical methods for the quantitative analysis of developmental data—in particular, the methods of individual growth modeling and survival analysis—are unquestioned by methodologists, but have yet to have a major impact on empirical research within the field of developmental psychopathology and elsewhere. In this paper, we show how these new methods provide developmental psychpathologists with powerful ways of answering their research questions about systematic changes over time in individual behavior and about the occurrence and timing of life events. In the first section, we present a descriptive overview of each method by illustrating the types of research questions that each method can address, introducing the statistical models, and commenting on methods of model fitting, estimation, and interpretation. In the following three sections, we offer six concrete recommendations for developmental psychopathologists hoping to use these methods. First, we recommend that when designing studies, investigators should increase the number of waves of data they collect and consider the use of accelerated longitudinal designs. Second, we recommend that when selecting measurement strategies, investigators should strive to collect equatable data prospectively on all time-varying measures and should never standardize their measures before analysis. Third, we recommend that when specifying statistical models, researchers should consider a variety of alternative specifications for the time predictor and should test for interactions among predictors, particularly interactions between substantive predictors and time. Our goal throughout is to show that these methods are essential tools for answering questions about life-span developmental processes in both normal and atypical populations and that their proper use will help developmental psychopathologists and others illuminate how important contextual variables contribute to various pathways of development.

The onset of adolescence, and more specifically the advent of pubertal maturation, represents a key developmental window for understanding the emergence of psychopathology in youth. The papers in this special section examine normative differences in the neurobiology of stress and emotional functioning over the peripubertal period. The work in this special section helps to fill in gaps in our understanding of key mechanisms that may contribute to increased vulnerabilities in behavioral and psychiatric morbidity during this developmental period.

The current study was initiated to increase understanding of developmental cascades in childhood in a sample of at-risk boys (N = 291; 52% White). Mothers, teachers, and boys reported on boys' externalizing problems, internalizing difficulties, and academic competence. Consistent with hypotheses regarding school-related transitions, high levels of externalizing problems were associated with both low levels of academic competence and high levels of internalizing problems during the early school-age period, and with elevations in internalizing problems during the transition to adolescence. Low levels of academic competence were associated with high levels of internalizing problems in middle childhood, and with high levels of externalizing problems during the transition from elementary school to middle school. Shared risk factors played a minimal role in these developmental cascades. Results suggest that there are cascading effects of externalizing problems and academic competence in childhood and early adolescence, and that some cascading effects are more likely to occur during periods of school-related transitions. Implications of developmental cascade effects for research and intervention are discussed.

The influence of perceived teacher support on trajectories of depression and self-esteem in middle school was examined using multigroup latent growth cross-domain models. A longitudinal sample of 2,585 students was followed from the sixth through the eighth grades. Students' perceptions of teacher support and general self-esteem declined and depressive symptoms increased over the course of middle school. We further found that, for both boys and girls, changes in perceptions of teachers' support reliably predicted changes in both self-esteem and depression. In particular, those students perceiving increasing teacher support showed corresponding decreases in depressive symptoms and increases in self-esteem. Gender differences were found for the initial levels of both perceptions of teacher support and general self-esteem. A competing model was also tested, which gave additional support for pathways of influence from perceptions of teacher support to depression and self-esteem, rather than the reverse. This study underscores the role of teacher support in facilitating students' adjustment to middle school and highlights the importance of using idiographic methodologies in the study of developmental processes. Implications and future directions are discussed.

Using cross-domain latent growth modeling, we examined trajectories of externalizing and internalizing problems in disadvantaged boys followed from ages 2 to 6 years (N = 303). On average, externalizing problems gradually decreased and internalizing problems gradually increased. However, we found significant variability in individual-level trajectories. Higher levels of externalizing problems were associated with higher levels of internalizing problems; rates of change were also positively correlated across domains. In addition, high levels of externalizing problems predicted rapid increases in internalizing problems. In follow-up analyses involving child and parenting factors, the combination of high negative emotionality, low fearfulness, and high negative maternal control preceded high, nondecreasing externalizing trajectories. The combination of high negative emotionality, high fearfulness, and high negative maternal control preceded high, increasing internalizing trajectories. Taken together, the results indicate both general and specific processes in the development of early externalizing and internalizing problems.This research was supported by National Institute of Mental Health (NIMH) Grants MH50907 and MH01666 to the second author and NIMH National Research Service Award 1F31MH12226 to the first author. We thank Emily Winslow and Elizabeth Owens for developing the Early Parenting Coding System and the Negative Emotionality Coding System, respectively. We also thank the study participants for teaching us about child development.

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

Studies with nonhuman primates and rodents, as well as with human children, have suggested that early separations from caregivers are often associated with changes in the functioning of the hypothalamus–pituitary–adrenal (HPA) axis. On the basis of these findings, we designed a relational intervention that was intended to normalize HPA functioning among children in foster care. This paper presents findings from a randomized clinical trial that assessed the effectiveness of a relational intervention (Attachment and Biobehavioral Catch-up [ABC]) with regard to HPA functioning. The ABC intervention was intended to enhance children's ability to regulate physiology and behavior. The control intervention (Developmental Education for Families) was intended to enhance children's cognitive skills. A comparison group of children who had never been in foster care was also included. Children's cortisol production was assessed upon arrival at the lab, and 15 and 30 min following the Strange Situation. Random effects analyses of variance were performed to assess differences in initial values and change between children in the two intervention groups. Children in the ABC intervention and comparison group children showed lower initial values of cortisol than children in the treatment control group, considering arrival at lab as initial values (p < .05). Groups did not differ significantly in change over time. These results suggest that the ABC intervention is effective in helping children regulate biology in ways more characteristic of children who have not experienced early adversity.

This paper presents information pertaining to attachment processes as risk factors in the development of disruptive behavior in young children. In recognition of the fact that attachment is not the only or necessarily most important risk factor in the prediction of behavior problems, attachment is considered in the context of other domains of variables, including child biologic factors, family ecology, and parental management and socialization practices. Within the attachment domain, we describe three complementary processes that may lead to disruptive behavior: the information-processing aspects of affective-cognitive structures, the function of observable attachment patterns, and the motivational consequences of attachment security. The indirect effects of maternal representations of attachment on child disruptive behavior are also considered. Examples of protypical risk factor combinations involving attachment and other domains are provided. The implications of the attachment perspective for research and clinical work with young disruptive children are discussed.

Examined associations between effortful control temperament and externalizing problems in 220 3-year-old boys and girls, controlling for co-occurring cognitive and social risk factors. We also considered possible additive and/or interactive contributions of child dispositional anger and psychosocial adversity, and whether relations between effortful control and early externalizing problems were moderated by child gender. Individual differences in children's effortful control abilities, assessed using behavioral and parent rating measures, were negatively associated with child externalizing problems reported by mothers, fathers, and preschool teachers. These associations were not overshadowed by other cognitive or social risk factors, or by other relevant child temperament traits such as proneness to irritability. Further analyses revealed that associations between externalizing problem behavior and effortful control were specific to components of child problem behavior indexing impulsive-inattentive symptoms. Thus, children's effortful control skills were important correlates of children's early disruptive behavior, a finding that may provide insight into the developmental origins of chronic behavioral maladjustment.This research was supported by a grant from the National Institute of Mental Health (RO1MH57489) to Sheryl Olson and Arnold Sameroff. We are very grateful to the children, parents, teachers, and preschool administrators who participated, and to the many individuals who gave us invaluable help with data collection and coding, especially Gail Benninghoff, Meribeth Gandy Pezda, Lisa Alvarez, Sara Miceli, and Felicia Kleinberg. We also thank the administrators of the University of Michigan Children's Center for their generous assistance, Grazyna Kochanska for allowing us to use her behavioral battery of effortful control tasks, Kathy Murray for helping us with numerous details concerning the behavioral battery, and Mary Rothbart, Jack Bates, Patricia Kerig, and Thomas Power for allowing us to use their parent self-report measures.

Inconsistencies exist in literature examining hypothalamic–pituitary–adrenal (HPA) axis activity in children and adults who have experienced childhood abuse. Hence, the extent and manner to which childhood abuse may disrupt HPA axis development is largely unknown. To address these inconsistencies, the developmental course of nonstress cortisol in a long-term longitudinal study was assessed at six time points from childhood through adolescence and into young adulthood to determine whether childhood abuse results in disrupted cortisol activity. Nonstress, morning cortisol was measured in 84 females with confirmed familial sexual abuse and 89 nonabused, comparison females. Although dynamically controlling for co-occurring depression and anxiety, hierarchical linear modeling (HLM) showed that relative to comparison females, the linear trend for abused females was significantly less steep when cortisol was examined across development from age 6 to age 30, t (1, 180) = −2.55, p < .01, indicating attenuation in cortisol activity starting in adolescence with significantly lower levels of cortisol by early adulthood, F (1, 162) = 4.78, p < .01. As a more direct test of the attenuation hypothesis, supplemental HLM analyses of data arrayed by time since the disclosure of abuse indicated that cortisol activity was initially significantly higher, t (1, 425) = 2.18, p < .05, and slopes were significantly less steep t (1, 205) = −2.66, p < .01, for abused females. These findings demonstrate how the experience of childhood abuse might disrupt the neurobiology of stress, providing some support for the attenuation hypothesis that victims of abuse may experience cortisol hyposecretion subsequent to a period of heightened secretion.

This study investigated the correlates of childhood depressive symptoms in an African American sample. We included processes that are likely to operate for all children, regardless of race or ethnicity, as well as events and circumstances that are largely unique to children of color. These various constructs were assessed at both the individual and community level. The analyses consisted of hierarchical linear modeling with a sample of 810 African American families living in Iowa and Georgia. Three individual-level variables were associated with childhood depressive symptoms: uninvolved parenting, racial discrimination, and criminal victimization. At the community level, prevalence of both discrimination and criminal victimization were positively related and community ethnic identification was negatively related to depressive symptoms. Further, there was evidence that community ethnic identification and neighborhood poverty serve to moderate the relationship between criminal victimization and depressive symptoms. Overall, the findings underscore the importance of considering factors unique to the everyday lives of the cultural group that is the focus of study, while demonstrating the dangers of a “one model fits all” approach to studying children of color.

As part of a larger investigation of very low income families, this study examined the characteristics that differentiated resilient from nonresilient school-age youths, with a focus on self-regulation (e.g., executive function, emotion regulation) skills. Resilience was operationally defined in a robust and comprehensive manner using well-established instruments that measured children's emotional well-being and mental health. Controlling for other explanatory variables, including differences in the experience of negative life events and chronic strains, resilient youths were notably different from nonresilient youths in terms of having greater self-regulatory skills and self-esteem, as well as in receiving more active parental monitoring. Study findings are discussed with regard to the theoretical framework of self-regulation and their implications for preventive intervention.

Although an extensive literature has accumulated documenting the maladaptive outcomes associated with childhood victimization, a limited body of knowledge addresses resilience. This paper sought to operationalize the construct of resilience across a number of domains of functioning and time periods and to determine the extent to which abused and neglected children grown up demonstrate resilience. Substantiated cases of child abuse and neglect from 1967 to 1971 were matched on gender, age, race, and approximate family social class with nonabused and nonneglected children and followed prospectively into young adulthood. Between 1989 and 1995, 1,196 participants (676 abused and neglected and 520 controls) were administered a 2-hr in-person interview, including a psychiatric assessment. Resilience requires meeting the criteria for success across six of eight domains of functioning: employment, homelessness, education, social activity, psychiatric disorder, substance abuse, and two domains assessing criminal behavior (official arrest and self-reports of violence). Results indicate that 22% of abused and neglected individuals meet the criteria for resilience. More females met the criteria for resilience and females were successful across a greater number of domains than males. We speculate on the meaning of these findings and discuss implications for the child maltreatment field. Limitations of the study are also acknowledged.

Achieving progress in understanding the cause, nature, and treatment of autism requires an integration of concepts, approaches, and empirical findings from genetic, cognitive neuroscience, animal, and clinical studies. The need for such integration has been a fundamental tenet of the discipline of developmental psychopathology from its inception. It is likely that the discovery of autism susceptibility genes will depend on the development of dimensional measures of broader phenotype autism traits. It is argued that knowledge of the cognitive neuroscience of social and language behavior will provide a useful framework for defining such measures. In this article, the current state of knowledge of the cognitive neuroscience of social and language impairments in autism is reviewed. Following from this, six candidate broader phenotype autism traits are proposed: (a) face processing, including structural encoding of facial features and face movements, such as eye gaze; (b) social affiliation or sensitivity to social reward, pertaining to the social motivational impairments found in autism; (c) motor imitation ability, particularly imitation of body actions; (d) memory, specifically those aspects of memory mediated by the medial temporal lobe–prefrontal circuits; (e) executive function, especially planning and flexibility; and (f) Language ability, particularly those aspects of language that overlap with specific language impairment, namely, phonological processing.

The developmental interplay between nature and nurture is discussed, with particular reference to implications for research in developmental psychopathology. The general principles include individual differences in reactivity to the environment, two-way interplay between intraindividual biology and environmental influences, and the need to consider broader social contextual features. Individuals actively process their experiences; they also act on their environment to shape and select their experiences, and individual characteristics change over time. Key findings on genetic effects include their ubiquitous influence, the multifactorial origin of most psychopathology, the involvement of several genes in most mental disorders, some genetic effects operate through dimensional risk features rather than directly on disorder, some genetic effects are dependent on gene–environment correlations and interactions, and genetic effects increase with age. Key findings on environmental effects include their ubiquitous influence, the genetic mediation of some supposed environmental effects, the importance of passive gene–environment correlations, the paucity of evidence regarding environmental effects on lifetime liability to psychopathology, the lack of understanding of environmental effects on the organism, and the importance of nonshared environmental effects. Research strategies to investigate environmental risk mediation include the range of genetically sensitive designs, migration studies, secular trend investigations, studies of nonfamilial environments, and examination of intraindividual change in relation to measured environmental alterations. Proximal processes involved in person–environment interplay are discussed in relation to person–environment interactions and evocative and active person–environment correlations.

The maturation of corticolimbic systems that neurobiologically mediate essential affective and social regulatory functions is experience dependent. During the first and second years of life, the infant's affective experiences, especially those embedded in the relationship with the primary caregiver, elicit patterns of psychobiological alterations that influence the activity of subcortically produced trophic bioamines, peptides, and steroids that regulate the critical period growth and organization of the developing neocortex. Interactive attachment experiences of psychobiological attunemcnt, stressful misattunement, and stress-regulating repair and reattunement that maximize positive and minimize negative affect are imprinted into the orbitofrontal cortex — the hierarchical apex of the limbic system that is expanded in the early developing right hemisphere. During the critical period of maturation of this system, prolonged episodes of intense and unregulated interactive stress are manifest in disorganizing experiences of heightened negative affect and altered levels of stress hormones, and this chaotic biochemical alteration of the internal environment triggers an extensive apoptotic panellation of corticolimbic circuitries. In this manner less than optimal affect-regulating experiences with the primary caregiver are imprinted into the circuits of this frontolimbic system that is instrumental to attachment functions, thereby producing orbitofrontal organizations that neurobiologically express different patterns of insecure attachments. Such pathomorphogenetic outcomes result in structurally defective systems that, under stress, inefficiently regulate subcortical mechanisms that mediate the physiological processes that underlie emotion. The functional impairments of the cortical-subcortical circuitries of this prefrontal system are implicated in an enduring vulnerability to and the pathophysiology of various later forming psychiatric disorders.

The current study examines outcomes at Grade 8 for boys who, at Grade 6, displayed elevated, though not necessarily clinical, levels of conduct problems and depressive symptoms. An at-risk community sample of 203 early adolescent boys in the Oregon Youth Study, a multimethod/multiagent study, was divided into the following groups at Grade 6: (a) co-occurring conduct problems and depressed mood, (b) conduct problems only, (c) depressed mood only, and (d) neither problem. The four groups were compared at Grade 8 on family management and boy's adjustment, using multivariate analyses of variance. The groups were compared also on relationships with parents, delinquency, and suicidal ideation. As hypothesized, conduct problems showed higher stability than depressive symptoms from Grade 6 to Grade 8. The conduct-problem-only boys and boys with co-occurring conduct problems and depressive symptoms continued to show considerable adjustment deficits at Grade 8, whereas boys with only depressive symptoms showed some improvement. The co-occurring group showed elevated levels of suicidal ideation. As hypothesized, conduct problems at Grade 6 were predictive of increases in depressed mood by Grade 8, but depressed mood was not predictive of an increase in the conduct problems measure. Results are consistent with a failure model whereby lack of skill and noxious behavior lead to pervasive failures and vulnerability to depressed mood.

Childhood abuse is an important public health problem; however, little is known about the effects of abuse on the brain and neurobiological development. This article reviews the behavioral and biological consequences of childhood abuse and places them in a developmental context. Animal studies show that both positive and negative events early in life can influence neurobiological development in unique ways. Early stressors such as maternal separation result in lasting effects on stress-responsive neurobiological systems, including the hypothalamic–pituitary–adrenal (HPA) axis and noradrenergic systems. These studies also implicate a brain area involved in learning and memory, the hippocampus, in the long-term consequences of early stress. Clinical studies of patients with a history of abuse also implicate dysfunction in the HPA axis and the noradrenergic and hippocampal systems; however, there are multiple questions related to chronicity of stress, developmental epoch at the time of the stressor, presence of stress-related psychiatric disorders including posttraumatic stress disorder and depression, and psychological factors mediating the response to trauma that need to be addressed in this field of research. Understanding the effects of abuse on the development of the brain and neurobiology will nevertheless have important treatment and policy implications.