Background: 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., deficient incentive processing. However, little is known about the relation between deficient incentive processing and persistence of antisocial behavior into adulthood or its relation with callous-unemotional and other psychopathic traits. In this study, we investigate the relationship between the neural correlates of incentive processing and both DBD persistence and psychopathic traits.
Methods: In a sample of 128 adolescents (mean age 17.7) with a history of criminal offending before age 12, functional magnetic resonance imaging was performed during a monetary incentive delay task designed to assess neural responses during incentive processing. Neural activation during incentive processing was then associated with DBD persistence and psychopathic traits, measured with the Youth Psychopathic Traits Inventory.
Results: Compared with both healthy control subjects and youths who had desisted from DBD, persistent DBD subjects showed lower neural responses in the ventral striatum during reward outcomes and higher neural responses in the amygdala during loss outcomes. Callous-unemotional traits were related to lower neural responses in the amygdala during reward outcomes, while other psychopathic traits were not related to incentive processing.
Conclusions: In the current study, aberrant incentive processing is related to persistence of childhood antisocial behavior into late adolescence and to callous-unemotional traits. This mechanism may underlie treatment resistance in a subgroup of antisocial youth and provide a target for intervention.
Keywords: Antisocial behavior; Callous-unemotional; Persistence; Psychopathy; Reward; fMRI.
Copyright © 2015 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.