Children with persistent antisocial and aggressive behavior are diagnosed as having disruptive behavior disorder. The authors review evidence that antisocial children, and especially those who persist with this behavior as they grow older, have a range of neurobiological characteristics. It is argued that serotonergic functioning and stress-regulating mechanisms are important in explaining individual differences in antisocial behavior. Moreover, low fear of punishment and physiological underactivity may predispose antisocial individuals to seek out stimulation or take risks and may help to explain poor conditioning and socialization. The authors propose a theoretical model highlighting the interplay between neurobiological deficits and cognitive and emotional functioning as mediators of the link between early adversity and antisocial behavior problems in childhood. Implications for intervention programs are discussed.

Patterns of lower autonomic nervous system~ANS! and hypothalamic-pituitary-adrenal~HPA! axis activity have been found in children with oppositional defiant disorder~ODD!. The aim of the present study was to investigate whether children with attention-deficit0hyperactivity disorder~ADHD! differ from ODD children with~OD0AD! or without comorbid ADHD in ANS and HPA axis activity under baseline and stressful conditions. The effects of stress on cortisol, heart rate~HR!, and skin conductance level~SCL! were studied in 95 children~26 normal control @NC# children and 69 child psychiatric patients referred for externalizing behavior problems @15 ODD, 31 OD0AD, and 23 ADHD#!. No baseline differences were found in cortisol between the four groups. However, the ODD and OD0AD groups showed a significantly weaker cortisol response to stress compared to the ADHD and NC groups; the ADHD group had a similar cortisol response as the NC group. Within the ODD group this pattern of low cortisol responsivity was most clearly present in the more severely affected inpatients. With respect to HR, the ODD group had a significantly lower HR during baseline and stressful conditions. The higher HR levels in the OD0AD and ADHD groups were likely to be caused by methylphenidate. The externalizing groups had significantly lower SCL levels, and no differences were found between these groups. It was concluded that differences in cortisol responsivity during stress exposure are important in distinguishing within a group of children with externalizing behavior between those with ODD and ADHD.

Objective: Many previous studies have surveyed associations between Tourette syndrome (TS) and co-morbid psychiatric disorders, but they usually did not include oppositional defiant disorder (ODD), conduct disorder (CD), separation anxiety disorder (SAD), and post-traumatic stress disorder (PTSD). Method: The subjects were children and adolescents with TS who visited a child and adolescent psychiatric clinic, and who were interviewed using DSM-IV diagnostic criteria. Characteristics of their tics were examined by the Yale-Global Tic Severity Scale (Y-GTSS). Behavioral problems were surveyed by the Child Behavior Checklist (CBCL) filled in by the parents. Results: About 87.9% of the subjects were boys. The mean age of the subjects was 11.8 years.The most common psychiatric disorders were attention deficit hyperactivity disorder (ADHD), ODD, nail biting, and obsessive compulsive disorder (OCD). Only one subject was affected by TS without co-morbidities. Among TS patients with co-morbidities, those with disruptive behavioral disorders (DBD) have significantly higher mean scores than patients without DBD on the Externalizing scale, Social problems, Attention problems, Delinquent and Aggression scales. Co-morbidity of anxiety disorders was not related to the CBCL scores. Conclusion: Many of our results were similar to those reported in studies conducted in other parts of the world. TS is more common in boys and nearly all of them had at least one co-morbid disorder. The most common co-morbidity was ADHD. Behavioral problems in TS are related to the co-morbidity with the DBD, and possibly not to the anxiety disorders.

The findings do not support the hypothesis that ODD and ODD/ADHD children have a deficit in executive inhibitory control; rather, they emphasise that they have problems in regulating their behaviour under motivational inhibitory conditions.