Leibenluft Ellen, Rich Brendan A, Vinton Deborah T, Nelson Eric E, Fromm Stephen J, Berghorst Lisa H, Joshi Paramjit, Robb Adelaide, Schachar Russell J, Dickstein Daniel P, McClure Erin B, Pine Daniel S
Emotion and Development Branch, mood and Anxiety Disorders Program, NIMH, NIH, Health and Human Services, Bldg. 15K, MSC-2670, Bethesda, MD 20892-2670, USA.
Am J Psychiatry. 2007 Jan;164(1):52-60. doi: 10.1176/ajp.2007.164.1.A52.
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.
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.
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.
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.
运动抑制功能缺陷可能导致双相情感障碍患儿出现冲动和易怒症状。对小儿双相情感障碍患者运动抑制失败时所涉及的神经回路进行研究,可能会增进我们对该疾病病理生理学的理解。作者检验了以下假设:在运动抑制未成功时,双相情感障碍患儿与对照受试者在腹侧前额叶皮质、纹状体和前扣带回的激活情况会有所不同。他们还比较了双相情感障碍患儿中服药与未服药者的激活情况,以及双相情感障碍合并注意力缺陷多动障碍(ADHD)的患儿与无ADHD的双相情感障碍患儿的激活情况。
作者进行了一项事件相关功能磁共振成像研究,比较双相情感障碍患儿与健康对照受试者在执行运动抑制任务时的神经激活情况。研究组包括26名双相情感障碍患儿(13名未服药,15名合并ADHD)和17名在年龄、性别和智商方面匹配的对照受试者。
在抑制失败的试验中,对照受试者双侧纹状体和右侧腹侧前额叶皮质的激活程度高于患者。这些缺陷在未服药患者中也存在,但ADHD在其中的介导作用尚不清楚。
与对照受试者相比,双相情感障碍患儿在抑制未成功时,调动纹状体结构和右侧腹侧前额叶皮质的能力可能存在缺陷。进一步的研究应确定ADHD对这些缺陷的影响,以及这些缺陷在双相情感障碍特征性的情绪和行为失调中可能发挥的作用。