Objective. Offspring of parents with major depressive disorder (MDD) face three-fold higher risk for MDD than offspring without a family history. Although MDD is a major cause of morbidity and mortality, neural correlates of risk for MDD remain poorly understood. This study compares amygdala and nucleus accumbens activation in children and adolescents at high and low risk for MDD under varying attentional and emotional conditions. Methods. Thirty-nine juveniles, 17 offspring of parents with MDD (high-risk group) and 22 offspring of parents without histories of MDD, anxiety or psychotic disorders (low-risk group) completed a functional magnetic resonance imaging study. During imaging, subjects viewed faces that varied in intensity of emotional expressions across blocks of trials; while attention was unconstrained (passive viewing), and constrained (rate nose width on face; rate subjective fear while viewing face). Results. When attention was unconstrained, high-risk, relative to lowrisk, subjects showed greater amygdala and nucleus accumbens (NAcc)
This study investigates the relationship between childhood attention deficit hyperactivity disorder (ADHD) and later criminality. White boys (n = 207, ages 6-12) with ADHD, free of conduct disorder, were assessed at ages 18 and 25 by clinicians who were blind to childhood status. A non-ADHD group served as comparisons. Lifetime arrest records were obtained when subjects were 38 years old for subjects who resided in New York State throughout the follow-up interval (93 probands, 93 comparisons). Significantly more ADHD probands than comparisons had been arrested (47% vs. 24%), convicted (42% vs. 14%), and incarcerated (15% vs. 1%). Rates of felonies and aggressive offenses also were significantly higher among probands. Importantly, the development of an antisocial or substance use disorder in adolescence completely explained the increased risk for subsequent criminality. Results suggest that even in the absence of comorbid conduct disorder in childhood, ADHD increases the risk for developing antisocial and substance use disorders in adolescence, which, in turn, increases the risk for criminal behavior in adolescence and adulthood.
Objective-Animal studies report that age at stimulant exposure is positively related to later drug sensitivity. This study was designed to examine whether age at initiation of stimulant treatment in children with attention deficit hyperactivity disorder (ADHD) is related to subsequent development of substance use disorder (SUD).Method-Prospective longitudinal study of 176 methylphenidate-treated white boys (6-12 years) with ADHD but without conduct disorder, evaluated at mean ages 18 (94% retention) and 25 (85%), and 178 comparisons diagnosed by blinded clinicians. The Cox proportional hazards model included childhood predictor variables: age at initiation of methylphenidate treatment, total cumulative dose, treatment duration; IQ; severity of hyperactivity; socioeconomic status; also lifetime parent mental disorder. Separate models tested for four lifetime outcomes: Any SUD, Alcohol SUD, Non-Alcohol SUD, and Stimulant SUD. Other outcomes included antisocial personality disorder, mood and anxiety disorders.
Estimates of the proportion of children with ADHD who will experience symptoms of the childhood syndrome in adulthood are likely to vary considerably, as a function of multiple factors. Several recommendations are made for designing future follow-up investigations.
This study investigates whether low to moderate levels of childhood oppositional defiant disorder (ODD) and conduct disorder (CD) behaviors contribute to the development of clinically diagnosed CD in adolescence, in children with attention deficit hyperactivity disorder (ADHD). Participants were 207 White boys (ages 6-12) with ADHD free of conduct disorder diagnoses. Parent and teacher ratings were obtained. Participants were assessed at mean age 18 by clinicians blind to childhood status. A non-ADHD group (recruited in adolescence) was also studied. ODD behavior ratings did not predict CD in adolescence, whereas CD behavior ratings did. No single ODD or CD behavior predicted adolescent outcome. ADHD probands with very low ratings (Not at all, Just a little) by parents and teachers on all CD behaviors were still at significantly increased risk for CD in adolescence, compared to non-ADHD controls. The same relationships were found between childhood ODD and CD behaviors, and antisocial personality disorder in adulthood (mean age, 25). We conclude that childhood ADHD is a developmental precursor of later antisocial disorder, even in the absence of comorbid ODD or CD in childhood. However, low levels of CD-type problems are not innocuous, because they predict later CD among children with ADHD without comorbid CD.
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