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.

This review summarizes the last decade of work by the ENIGMA (Enhancing NeuroImaging Genetics through Meta Analysis) Consortium, a global alliance of over 1400 scientists across 43 countries, studying the human brain in health and disease. Building on large-scale genetic studies that discovered the first robustly replicated genetic loci associated with brain metrics, ENIGMA has diversified into over 50 working groups (WGs), pooling worldwide data and expertise to answer fundamental questions in neuroscience, psychiatry, neurology, and genetics. Most ENIGMA WGs focus on specific psychiatric and neurological conditions, other WGs study normal variation due to sex and gender differences, or development and aging; still other WGs develop methodological pipelines and tools to facilitate harmonized analyses of "big data" (i.e., genetic and epigenetic data, multimodal MRI, and electroencephalography data). These international efforts have yielded the largest neuroimaging studies to date in schizophrenia, bipolar disorder, major depressive disorder, post-traumatic stress disorder, substance use disorders, obsessive-compulsive disorder, attentiondeficit/hyperactivity disorder, autism spectrum disorders, epilepsy, and 22q11.2 deletion syndrome. More recent ENIGMA WGs have formed to study anxiety disorders, suicidal thoughts and behavior, sleep and insomnia, eating disorders, irritability, brain injury, antisocial personality and conduct disorder, and dissociative identity disorder. Here, we summarize the first decade of ENIGMA's activities and ongoing projects, and describe the successes and challenges encountered along the way. We highlight the advantages of collaborative large-scale coordinated data analyses for testing reproducibility and robustness of findings, offering the opportunity to identify brain systems involved in clinical syndromes across diverse samples and associated genetic, environmental, demographic, cognitive, and psychosocial factors.

Background:We examined whether conduct disorder (CD) is associated with deficits in facial expression recognition and, if so, whether these deficits are specific to the early-onset form of CD, which emerges in childhood. The findings could potentially inform the developmental taxonomic theory of antisocial behaviour, which suggests that early-onset and adolescence-limited forms of CD are subject to different aetiological processes.Method:Male adolescents with either early-onset CD (n =42) or adolescence-onset CD (n =39), and controls with no history of serious antisocial behaviour and no current psychiatric disorder (n =40) completed tests of facial expression and facial identity recognition. Dependent measures were: (a) correct recognition of facial expressions of anger, disgust, fear, happiness, sadness, and surprise, and (b) the number of correct matches of unfamiliar faces.Results:Relative to controls, recognition of anger, disgust, and happiness in facial expressions was disproportionately impaired in participants with early-onset CD, whereas recognition of fear was impaired in participants with adolescence-onset CD. Participants with CD who were high in psychopathic traits showed impaired fear, sadness, and surprise recognition relative to those low in psychopathic traits. There were no group differences in facial identity recognition.Conclusions:Both CD subtypes were associated with impairments in facial recognition, although these were more marked in the early-onset subgroup. Variation in psychopathic traits appeared to exert an additional influence on the recognition of fear, sadness and surprise. Implications of these data for the developmental taxonomic theory of antisocial behaviour are discussed.

The results demonstrate that gray matter volume reductions in brain regions involved in processing socioemotional stimuli are associated with conduct disorder, regardless of age of onset. Brain structural abnormalities may contribute to the emergence of adolescent-onset as well as early-onset conduct disorder.

Conduct disorder (CD) is a common and highly impairing psychiatric disorder that usually emerges in childhood or adolescence and is characterized by severe antisocial and aggressive behaviour. It frequently co-occurs with attention-deficit/hyperactivity disorder (ADHD) and often leads to antisocial personality disorder in adulthood. CD affects ~3% of schoolaged children and is twice as prevalent in males than in females. This disorder can be subtyped according to age at onset (childhood-onset versus adolescent-onset) and the presence or absence of callous-unemotional traits (deficits in empathy and guilt). The aetiology of CD is complex, with contributions of both genetic and environmental risk factors and different forms of interplay among the two (gene-environment interaction and correlation). In addition, CD is associated with neurocognitive impairments; smaller grey matter volume in limbic regions such as the amygdala, insula and orbitofrontal cortex, and functional abnormalities in overlapping brain circuits responsible for emotion processing, emotion regulation and reinforcement-based decision-making have been reported. Lower hypothalamic-pituitary-adrenal axis and autonomic reactivity to stress has also been reported. Management of CD primarily involves parent-based or family-based psychosocial interventions, although stimulants and atypical antipsychotics are sometimes used, especially in individuals with comorbid ADHD.