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.

Recent advances in the discipline of developmental psychopathology highlight the contributions of developmental thought to the study of persons with autism. This article briefly outlines primary developmental innovations in theory, methodology, and the interpretation of findings. Specifically, we discuss two sets of issues that arise from the general notion of developmental level. One set is relevant to the choice of persons that comprise the comparison group and the other to the various implications of the subjects' levels of functioning. In sum, we contend that researchers need to frame their empirical work within the context of developmental theory and methodology and interpret their findings accordingly. This will lead to scientifically compelling work and an increasingly heuristic approach to the study of persons with autism.

Previous work based on observations of home videotapes indicates that differences can be detected between infants with autism spectrum disorder and infants with typical development at 1 year of age. The present study addresses the question of whether autism can be distinguished from mental retardation by 1 year of age. Home videotapes of first birthday parties from 20 infants later diagnosed with autism spectrum disorder, 14 infants later diagnosed with mental retardation (without autism), and 20 typically developing infants were coded by blind raters with respect to the frequencies of specific social and communicative behaviors and repetitive motor actions. Results indicated that 1-year-olds with autism spectrum disorder can be distinguished from 1-year-olds with typical development and those with mental retardation. The infants with autism spectrum disorder looked at others and oriented to their names less frequently than infants with mental retardation. The infants with autism spectrum disorder and those with mental retardation used gestures and looked to objects held by others less frequently and engaged in repetitive motor actions more frequently than typically developing infants. These results indicate that autism can be distinguished from mental retardation and typical development by 1 year of age.

This study examined the association between fathers' alcoholism and other risk factors such as parental depression, family conflict, infant temperament, and parent–infant attachment. The quality of parent–infant interactions was hypothesized to be a proximal mediator of the associations among alcoholism and other risk factors and attachment. The participants were 223 families (104 nonalcoholic families and 119 alcoholic families) with 12-month-old infants recruited through birth records. Infants in families with two parents with alcohol problem had significantly higher rates of insecure attachment with both parents. Structural Equations Modeling indicated that the fathers' alcohol problem was associated with lower paternal sensitivity (higher negative affect, lower positive engagement, and lower sensitive responding) during father–infant play interactions, and this in turn was associated with higher risk for infant attachment insecurity with fathers. The association between the fathers' alcohol problem and infant attachment security with the mother was mediated by maternal depression, and maternal alcohol problems and family conflict were associated with maternal sensitivity during play interactions. These results indicate that the fathers' alcoholism is associated with higher family risk including the quality of the parent–infant relationship; infant attachment develops in a family context; and this context has a significant association with attachment security.

The development of joint attention skills is a major milestone of infancy. Recent research suggests that the development of these skills may be affected by disorganized (D) attachment. This hypothesis was examined in a longitudinal study of attachment and joint attention skill development in a sample of infants at risk for developmental–behavioral morbidity. The results revealed that toddlers with D classifications initiated joint attention with an experimenter significantly less often than did secure, or even other insecure, toddlers. However, no group differences in the capacity to respond to the joint attention bids of others were observed in this study. These data suggest that a disturbance in the tendency to initiate episodes of joint attention with others may be indicative of early social–cognitive and social–emotional disturbance among infants affected by disorganized attachment status. Theory and research is reviewed to suggest that an early impairment in joint attention facility may make a significant contribution to risk for negative cognitive and emotional outcomes among these infants.

In light of evidence that the effects of attachment security on subsequent development may be contingent on the social context in which the child continues to develop, we examined the effect of attachment security at age 15 months, cumulative contextual risk from 1 to 36 months, and the interaction of attachment and cumulative risk to predict socioemotional and cognitive linguistic functioning at age 3 years, using data from the National Institute of Child Health and Human Development Study of Early Child Care. Results indicated that early attachment predicts both socioemotional development and language skills, but not cognitive functioning as indexed by a measure of school readiness, and that the effect of attachment on socioemotional development and expressive language varied as a function of social-contextual risk. Insecure–avoidant infants proved most vulnerable to contextual risk, not children classified as secure or insecure more generally, although in one instance security did prove protective with respect to the adverse effects of cumulative contextual risk. Findings are discussed in terms of risk and resilience and in light of the probabilistic nature of the relation between early attachment and later development.

This study examined the relation of negative emotionality in infancy to child social and cognitive developmental outcomes among low birth weight (LBW) preterm infants participating in the Infant Health and Development Program (IHDP), a comprehensive compensatory education intervention beginning in infancy and lasting through age 3 years. In this analysis, intervention effects at age 36 months on maternal report of child behavior as assessed by the Child Behavior Checklist externalizing and internalizing scales and on intelligence as measured by the Stanford–Binet scale were largest among children characterized by higher levels of negative emotionality in infancy. Findings indicate that for LBW preterm infants characterized by negative emotionality at age 12 months the intervention was associated with a twofold decrease in the occurrence of clinically meaningful levels of behavior problems at age 3 years and a fourfold decrease in the occurrence of a high-risk profile in which both internalizing and externalizing scores are in the clinically meaningful range. The intervention was also associated with a fivefold decrease in the occurrence of IQ ≤ 75 at age 3 years among children with higher levels of negative emotionality and heavier LBW (2001–2500 g). However, specific aspects of temperamental difficulty such as fearfulness and anger were related to internalizing and externalizing, respectively, in both the intervention and control groups. Findings are consistent with research linking negative emotionality in infancy with social and cognitive developmental outcomes in early childhood among normal birth weight infants. Results suggest the need for further attention to child temperament in early intervention research.

Research suggests that disruptions in early caretaking can have long-term effects on the hypothalamic–pituitary–adrenal (HPA) axis, which mediates the stress response. Children of depressed mothers are at increased risk for developing internalizing problems in part because of disruptions in their caretaking environment. The present study investigated whether children of depressed mothers exhibit elevated salivary cortisol levels. Salivary cortisol samples were collected from 45 7- to 8-year-old children of mothers with a history of depression and 29 children of nondepressed mothers. Samples were collected soon after arrival to the laboratory and after a mild laboratory stressor and at home after wakeup and before bedtime. Children who had elevated levels of internalizing symptoms and whose mothers had a history of depression showed elevated laboratory baseline cortisol levels. Children who were reported to have clinically significant internalizing symptoms were also more likely to show an elevated stress response to a mild laboratory stressor. When the longitudinal history of maternal depression was examined, maternal depression during the child's first 2 years of life was the best predictor of elevations in baseline cortisol at age 7 years. This study provides evidence that internalizing symptoms exist in conjunction with a more reactive hormonal stress system in children of depressed mothers. The results also provide preliminary evidence that exposure to maternal depression in the first 2 years of life may be related to children's cortisol levels later in life.

Smoking during pregnancy is associated with adverse consequences for children. Most recently, it has been established as a risk factor for developmental psychopathology, specifically Conduct Disorder (CD). Although this association has been shown to be robust, developmental pathways from exposure to CD have not been established. We examined how prenatal exposure to cigarettes interacts with child and family factors to increase risk of CD symptoms in a longitudinal study of 10-year-old urban, African-American youth (N = 77). The effects of prenatal exposure at school age were moderated by child sex. Boys whose mothers smoked during pregnancy were significantly more likely to develop CD symptoms, but exposure did not increase risk in girls. A similar trend was found during infancy: prenatal smoking was associated with low sociability/negative emotionality only for boys. The effects of smoking during pregnancy were also moderated by the quality of the early caregiving environment. Exposed boys whose mothers were unresponsive during infancy were at increased risk of CD symptoms, but exposed boys with early responsive mothers were not. Prospective studies, with developmentally based measures of behavior across time, are critical for further elucidating pathways from prenatal exposure to cigarettes to the development of clinical disorder. The identification of a potentially modifiable, prenatal risk factor for early onset developmental psychopathology has important implications for prevention.

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.

The present study uses a population-based sample of 6,806 adult twins from same-sex and opposite-sex twin pairs to examine sex differences in the underlying genetic and environmental architecture of the development of antisocial behavior (AB). Retrospective reports of AB during three different developmental periods were obtained: prior to age 15 years (childhood), age 15–17 years (adolescent), and age 18 years and older (adult). Structural equation modeling analyses revealed that there was no evidence for sex-specific genetic or sex-specific shared family environmental influences on the development of AB; that is, the types of genetic and environmental influence were similar for males and females. For both sexes, a model that allowed for genetic influences on adolescent and adult AB that were not shared with childhood AB fit better than a model with a single genetic factor. In contrast, shared environmental influences on adolescent and adult AB overlapped entirely with shared environmental influences on childhood AB. Genetic factors played a larger role in variation in childhood AB among females, whereas shared environmental factors played a larger role among males. However, heritability of AB increased from childhood to adolescence and adulthood for both sexes, and the magnitude of genetic and environmental influences on adolescent and adult AB was approximately equal across sex. We speculate that sex differences in timing of puberty may account for the earlier presence of genetic effects among females.