Elizabeth C. Finger,
Abigail A. Marsh,
Derek G. Mitchell,
Marguerite E. Reid,
Courtney Sims,
Salima Budhani,
David S. Kosson,
Gang Chen,
Kenneth E. Towbin,
Ellen Leibenluft,
Daniel S. Pine &
James R. Blair
Abstract
Context — Children and adults with psychopathic traits and conduct or oppositional defiant disorder demonstrate poor decision making and are impaired in reversal learning. However, the neural basis of this impairment has not previously been investigated. Furthermore, despite high comorbidity of psychopathic traits and attention deficit/hyperactivity disorder, to our knowledge,
no research has attempted to distinguish neural correlates of childhood psychopathic traits and
attention-deficit/hyperactivity disorder.
Objective—To determine the neural regions that underlie the reversal learning impairments in children with psychopathic traits plus conduct or oppositional defiant disorder.
Design — Case-control study.
Setting — Government clinical research institute.
Participants — Forty-two adolescents aged 10 to 17 years: 14 with psychopathic traits and oppositional defiant disorder or conduct disorder, 14 with attention-deficit/hyperactivity disorder only, and 14 healthy controls.
Main Outcome Measure — Blood oxygenation level–dependent signal as measured via functional magnetic resonance imaging during a probabilistic reversal task.
Results — Children with psychopathic traits showed abnormal responses within the ventromedial prefrontal cortex (Brodmann area 10) during punished reversal errors compared with children wit hattention deficit/hyperactivity disorder and healthy children (P < .05 corrected for multiple comparisons).
Conclusions — To our knowledge, this study provides the first evidence of abnormal
ventromedial prefrontal cortex responsiveness in children with psychopathic traits and
demonstrates this dysfunction was not attributable to comorbid attention-deficit/hyperactivity
disorder. These findings suggest that reversal learning impairments in patients with developmental
psychopathic traits relate to abnormal processing of reinforcement information.