J Am Acad Child Adolesc Psychiatry
December 2018
Objective: Although the neural underpinnings of antisocial behavior have been studied extensively, research on pharmacologic interventions targeting specific neural mechanisms remains sparse. Hypoactivity of the amygdala and ventromedial prefrontal cortex (vmPFC) has been reported in antisocial adolescents, which could account for deficits in fear learning (amygdala) and impairments in decision making (vmPFC), respectively. Limited clinical research suggests positive effects of methylphenidate, a dopamine agonist, on antisocial behavior in adolescents.
View Article and Find Full Text PDFAltered structural connectivity has been reported in antisocial juveniles, but findings have been inconsistent. Given the phenotypical heterogeneity among individuals showing antisocial behavior, specification of the association between structural connectivity and the dimensions of psychopathic traits (i.e.
View Article and Find Full Text PDFChildren diagnosed with a Disruptive Behavior Disorder (DBD, i.e. Oppositional Defiant Disorder or Conduct Disorder), especially those with psychopathic traits, are at risk of developing persistent and severe antisocial behavior.
View Article and Find Full Text PDFTraditionally, neurobiological research on psychopathy has focused on categorical differences in adults. However, there is evidence that psychopathy is best described by a set of relatively independent personality dimensions, that is, callous-unemotional, grandiose-manipulative, and impulsive-irresponsible traits, which can be reliably detected in juveniles, allowing investigation of the neural mechanisms leading to psychopathy. Furthermore, complex psychiatric disorders like psychopathy are increasingly being conceptualized as disorders of brain networks.
View Article and Find Full Text PDFBackground: Children with early-onset disruptive behavior disorder (DBD), especially those with callous-unemotional traits, are at risk of developing persistent and severe adult antisocial behavior. One possible underlying mechanism for persistence is deficient reward and loss sensitivity, i.e.
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