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

One variant of substance-use disorder is characterized by behavioral disinhibition. In thisreport, we martial evidence for a model for the development of this variant. We hypothesize thatgenetic liability for this variant is reflected in a spectrum of risk indicators linked to the inabilityor unwillingness to inhibit behavioral impulses. Included in this spectrum are personality traitssuggesting low constraint, and externalizing psychopathology, including conduct, oppositionaldefiant, and attention-deficit disorder in children and antisocial personality disorder and behaviorin adults. We further hypothesize that these individual differences in behavioral disinhibition aremanifestations of underlying central nervous system processes associated with variouspsychophysiological 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 FamilyStudy, an epidemiological investigation of approximately 2,700 adolescent twins and theirparents.

In previous studies, infants of depressed mothers have been found to exhibit reduced leftfrontal brain electrical activity (EEG). The left frontal region has been hypothesized to mediatesocial approach behaviors and positive affective expression. These findings raise importantquestions 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 notvariations in patterns of frontal brain activity in infants of depressed and nondepressed mothersare related to variations in infant behavior as observed in naturalistic situations. If such relationsexist, 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 recordedfrom 14- to 15-month old infants of depressed versus nondepressed mothers during a baselinecondition and during conditions designed to elicit interest and positive affect. Infant behaviorwas observed in naturalistic play conditions, with and without mother, on a separate day fromEEG testing. Mothers provided information on infant temperament. Infants of depressed mothersshowed 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 towardmother, but not to infant temperament. Furthermore, increased generalized frontal activation wasfound 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 infantbehavior, especially those involved in positive affiliative behavior and the expression andregulation of negative affect. The nature and cause of atypical patterns of brain activity andquestion of whether such atypical patterns of frontal brain activity predispose infants to affectivedisorders in later life are discussed.

Although it is well documented that intrapersonal and interpersonal risk factors are related tothe frequency of marijuana use, much less is known about the initiation of marijuana use. Thispaper reports on a longitudinal study of the personality, family, peer, and ecological predictors ofmarijuana onset. Survival analysis was applied to a sample of nonusers of illegal drugs, followedfrom age 9 years to the 20s. The major findings indicate that (a) youngsters who areunconventional are at a higher risk for marijuana initiation; (b) youngsters who associate withpeers who use marijuana or who smoke tobacco themselves are at increased risk for marijuanainitiation; (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, earlyadolescence, middle adolescence, late adolescence, and the 20s. Results are discussed within theframework of a family interactional perspective of development. Implications for prevention arediscussed.

Recent research on the disorders of attention and activity has indicated inherited variants ofgenes controlling aspects of neurotransmission, abnormalities of structure and function in regionsof frontal lobes and basal ganglia, failures to suppress inappropriate responses, and a cascade offailures in various kinds of cognitive performance and organization of behavior. This reviewintegrates the neurodevelopmental findings with findings from developmental psychopathology.It outlines several developmental tracks by which constitutional factors interact with thepsychological 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) aninattentive and cognitively impulsive style during early childhood. In another track, impulsiveand inattentive behavior shows direct continuity through childhood into late adolescence. In yetanother track, impulsiveness evokes (and may be genetically associated with) critical expressedemotion from parents and inefficient coping strategies, which in turn contribute to thedevelopment of antisocial conduct. This formulation emphasizes the need for several types ofresearch: the mapping of biological findings onto different components of disorder, thecombination of genetically informative designs with direct measurement of relevant aspects ofthe environment, and the use of longitudinal studies to examine predictive and mediating factorsseparately for different aspects of outcome.

The current paper uses data from a longitudinal study of a high-risk sample to test therelation between adolescent alcohol and drug use and later young adult autonomy, positiveactivity involvement, and perceived competence. Participants (children of alcoholics anddemographically 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 ofadolescent substance use on both self-reported and collateral-reported outcomes, controlling forcorrelated risk factors (parental alcoholism, adolescent psychopathology, and parental support),preexisting levels of the outcome, and concurrent young adult substance use. Results showed thatadolescent drug use had a significant, unique negative effect on later autonomy and perceivedcompetence. Alcohol use effects were more complex. Adolescent heavy drinking was associatedwith less positive adult outcomes, but more so in collateral reports than in self-reportedoutcomes. Moreover, young adult heavy drinking was either uncorrelated with or positivelycorrelated with higher levels of perceived competence, suggesting different developmentalsignificance of alcohol use in adolescence than in young adulthood.

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 causallinks between these levels of analysis, and argues that solving the gene–behavior problemis paradoxically easier than solving the brain–behavior problem.

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

This paper explores the parenting of drug-dependent women and the contributions ofcomorbid psychopathology to their parenting. A sample of 32 children whose mothers weredependent on opioid drugs during pregnancy and 37 children whose mothers were not drug userswere followed from birth to middle childhood. Multivariate regression analyses were conductedcontrasting whether maternal substance abuse or psychopathology was more closely linked toparenting behaviors and continuity in parenting over time. Maternal drug dependence was relatedto whether mothers were able to remain primary caregivers for their children over time, evenafter controlling for psychopathology. Maternal drug use was related to unresponsive andnegative parenting behavior during mother–infant interaction, but this relation was largelyaccounted for by the effects of comorbid maternal psychopathology on parenting, particularlysymptoms of antisocial and related personality disorders. For those children whose motherscontinued to care for them into middle childhood, perceptions of their mothers as rejecting wererelated to maternal antisocial personality and maternal depression. Substance-abuse treatment forwomen should be integrated with interventions addressing their mental health and parentingneeds.