Neural Circuitry Engaged During Unsuccessful Motor Inhibition in Pediatric Bipolar Disorder

双相情感障碍 心理学 冲动性 扣带回前部 前额叶皮质 功能磁共振成像 神经科学 注意缺陷多动障碍 易怒 精神科 听力学 医学 认知
作者
Ellen Leibenluft,Brendan A. Rich,Deborah Vinton,Eric E. Nelson,Stephen J. Fromm,Lisa H. Berghorst,Paramjit T. Joshi,Adelaide S. Robb,Russell Schachar,Daniel P. Dickstein,Erin B. McClure,Daniel S. Pine
出处
期刊:American Journal of Psychiatry [American Psychiatric Association]
卷期号:164 (1): 52-60 被引量:109
标识
DOI:10.1176/ajp.2007.164.1.52
摘要

Objective: Deficits in motor inhibition may contribute to impulsivity and irritability in children with bipolar disorder. Studies of the neural circuitry engaged during failed motor inhibition in pediatric bipolar disorder may increase our understanding of the pathophysiology of the illness. The authors tested the hypothesis that children with bipolar disorder and comparison subjects would differ in ventral prefrontal cortex, striatal, and anterior cingulate activation during unsuccessful motor inhibition. They also compared activation in medicated versus unmedicated children with bipolar disorder and in children with bipolar disorder and attention deficit hyperactivity disorder (ADHD) versus those with bipolar disorder without ADHD. Method: The authors conducted an event-related functional magnetic resonance imaging study comparing neural activation in children with bipolar disorder and healthy comparison subjects while they performed a motor inhibition task. The study group included 26 children with bipolar disorder (13 unmedicated and 15 with ADHD) and 17 comparison subjects matched by age, gender, and IQ. Results: On failed inhibitory trials, comparison subjects showed greater bilateral striatal and right ventral prefrontal cortex activation than did patients. These deficits were present in unmedicated patients, but the role of ADHD in mediating them was unclear. Conclusions: In relation to comparison subjects, children with bipolar disorder may have deficits in their ability to engage striatal structures and the right ventral prefrontal cortex during unsuccessful inhibition. Further research should ascertain the contribution of ADHD to these deficits and the role that such deficits may play in the emotional and behavioral dysregulation characteristic of bipolar disorder.

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