Autism is a developmental disorder with variable severity, occurring at all levels of cognitive ability and having a number of slightly different clinical presentations. It is associated with neuropsychological deficits that occur in other conditions also, but its pattern may be specific to autism. Genetic and environmental early insults to brain development are etiological determinants of the disorder. Brain circuitries important for social, communicative, and integrational purposes have been suggested to be dysfunctional in autism. There could be at least two different pathways to autism, one connected with primary temporofrontal dysfunction (and late prenatal–early postnatal origins) and another linked to primary brain-stem dysfunction (and early prenatal origins). Further study of neurodevelopmental and neuropsychological processes in autism will help elucidate not only the pathological mechanisms involved in the specific syndromes but also the underpinnings of normal brain development.

One variant of substance-use disorder is characterized by behavioral disinhibition. In this report, we martial evidence for a model for the development of this variant. We hypothesize that genetic liability for this variant is reflected in a spectrum of risk indicators linked to the inability or unwillingness to inhibit behavioral impulses. Included in this spectrum are personality traits suggesting low constraint, and externalizing psychopathology, including conduct, oppositional defiant, and attention-deficit disorder in children and antisocial personality disorder and behavior in adults. We further hypothesize that these individual differences in behavioral disinhibition are manifestations of underlying central nervous system processes associated with various psychophysiological anomalies, some of which may index genetic risk for substance abuse. Support for the model is derived from the analysis of findings from the Minnesota Twin Family Study, an epidemiological investigation of approximately 2,700 adolescent twins and their parents.

In previous studies, infants of depressed mothers have been found to exhibit reduced left frontal brain electrical activity (EEG). The left frontal region has been hypothesized to mediate social approach behaviors and positive affective expression. These findings raise important questions about the cause and nature of atypical EEG patterns in infants of depressed mothers. The present study begins to address some of these questions by examining whether or not variations in patterns of frontal brain activity in infants of depressed and nondepressed mothers are related to variations in infant behavior as observed in naturalistic situations. If such relations exist, are they specific to certain behaviors hypothesized to be mediated by the frontal region (i.e., positive approach behaviors)? Frontal and parietal brain electrical activity was recorded from 14- to 15-month old infants of depressed versus nondepressed mothers during a baseline condition and during conditions designed to elicit interest and positive affect. Infant behavior was observed in naturalistic play conditions, with and without mother, on a separate day from EEG testing. Mothers provided information on infant temperament. Infants of depressed mothers showed less affection and touching of their mothers. For infants of depressed mothers only, reduced left frontal brain activity was found to be related to lower levels of affection toward mother, but not to infant temperament. Furthermore, increased generalized frontal activation was found to be related to higher levels of negative affect, hostility, and tantrums and aggression. Relations between infant brain activity and behavior were not found for parietal EEG activity. These results suggest that infant frontal electrical brain activity is related to variations in infant behavior, especially those involved in positive affiliative behavior and the expression and regulation of negative affect. The nature and cause of atypical patterns of brain activity and question of whether such atypical patterns of frontal brain activity predispose infants to affective disorders in later life are discussed.

Although it is well documented that intrapersonal and interpersonal risk factors are related to the frequency of marijuana use, much less is known about the initiation of marijuana use. This paper reports on a longitudinal study of the personality, family, peer, and ecological predictors of marijuana onset. Survival analysis was applied to a sample of nonusers of illegal drugs, followed from age 9 years to the 20s. The major findings indicate that (a) youngsters who are unconventional are at a higher risk for marijuana initiation; (b) youngsters who associate with peers who use marijuana or who smoke tobacco themselves are at increased risk for marijuana initiation; (c) youngsters who identify with their parents are less likely to begin marijuana use; and (d) the predictors related to marijuana onset emerged during preadolescence, early adolescence, middle adolescence, late adolescence, and the 20s. Results are discussed within the framework of a family interactional perspective of development. Implications for prevention are discussed.

Recent research on the disorders of attention and activity has indicated inherited variants of genes controlling aspects of neurotransmission, abnormalities of structure and function in regions of frontal lobes and basal ganglia, failures to suppress inappropriate responses, and a cascade of failures in various kinds of cognitive performance and organization of behavior. This review integrates the neurodevelopmental findings with findings from developmental psychopathology. It outlines several developmental tracks by which constitutional factors interact with the psychological environment. In one set of tracks, altered brain states lead to cognitive alteration. An understimulating environment is evoked by (and may be genetically associated with) an inattentive and cognitively impulsive style during early childhood. In another track, impulsive and inattentive behavior shows direct continuity through childhood into late adolescence. In yet another track, impulsiveness evokes (and may be genetically associated with) critical expressed emotion from parents and inefficient coping strategies, which in turn contribute to the development of antisocial conduct. This formulation emphasizes the need for several types of research: the mapping of biological findings onto different components of disorder, the combination of genetically informative designs with direct measurement of relevant aspects of the environment, and the use of longitudinal studies to examine predictive and mediating factors separately for different aspects of outcome.

This paper reviews what is known about developmental dyslexia at three levels of analysis: cognitive, neurological, and genetic. It also considers the difficult problem of establishing causal links between these levels of analysis, and argues that solving the gene–behavior problem is paradoxically easier than solving the brain–behavior problem.

The current paper uses data from a longitudinal study of a high-risk sample to test the relation between adolescent alcohol and drug use and later young adult autonomy, positive activity involvement, and perceived competence. Participants (children of alcoholics and demographically matched controls) were assessed in three annual interviews in adolescence (mean age: 12.7 years at Time 1) and then again 5–7 years later, in young adulthood (median age: 20 years). Path analyses and latent growth curve models tested the effects of adolescent substance use on both self-reported and collateral-reported outcomes, controlling for correlated risk factors (parental alcoholism, adolescent psychopathology, and parental support), preexisting levels of the outcome, and concurrent young adult substance use. Results showed that adolescent drug use had a significant, unique negative effect on later autonomy and perceived competence. Alcohol use effects were more complex. Adolescent heavy drinking was associated with less positive adult outcomes, but more so in collateral reports than in self-reported outcomes. Moreover, young adult heavy drinking was either uncorrelated with or positively correlated with higher levels of perceived competence, suggesting different developmental significance of alcohol use in adolescence than in young adulthood.

In 1987, we began a longitudinal study of the offspring of alcoholic parents and have been following this group of young adults from their freshman year in college throughout their transition into later young adulthood. The goal of this review is to highlight some of the findings we consider most important and relevant to the development of pathological alcohol involvement in young adulthood. Courses of pathological alcohol involvement in young adulthood are outlined. Predictors of both the development and course of pathological alcohol use in young adulthood are also addressed, including family history of alcoholism, personality, alcohol use motivations, and role transitions. While certainly a problem in its own right, pathological alcohol involvement can also affect the attainment of important life tasks and success in various life roles. Consequently, we also examine the effects of pathological alcohol involvement on later role transitions and role attainment. Finally, prevention, policy, and treatment issues surrounding this stage of life are discussed.

This paper explores the parenting of drug-dependent women and the contributions of comorbid psychopathology to their parenting. A sample of 32 children whose mothers were dependent on opioid drugs during pregnancy and 37 children whose mothers were not drug users were followed from birth to middle childhood. Multivariate regression analyses were conducted contrasting whether maternal substance abuse or psychopathology was more closely linked to parenting behaviors and continuity in parenting over time. Maternal drug dependence was related to whether mothers were able to remain primary caregivers for their children over time, even after controlling for psychopathology. Maternal drug use was related to unresponsive and negative parenting behavior during mother–infant interaction, but this relation was largely accounted for by the effects of comorbid maternal psychopathology on parenting, particularly symptoms of antisocial and related personality disorders. For those children whose mothers continued to care for them into middle childhood, perceptions of their mothers as rejecting were related to maternal antisocial personality and maternal depression. Substance-abuse treatment for women should be integrated with interventions addressing their mental health and parenting needs.