Altered cortical excitability in obsessive-compulsive disorder
Altered cortical excitability in obsessive-compulsive disorder
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DOI：
10.1212/wnl.54.1.142
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发表时间：
2000-01-11
期刊：
影响因子：
9.9
通讯作者：
Wassermann, EM
中科院分区：
文献类型：
--
作者：
Greenberg, BD;Ziemann, U;Wassermann, EM
目的：探讨强迫症（OCD）的皮层抑制和兴奋机制。背景资料：经颅磁刺激（TMS）研究发现，在图雷特综合征、局灶性肌张力障碍和其他被认为涉及皮质下结构（包括基底神经节）功能障碍的疾病中，主要运动区的神经元抑制减少，皮质沉默期减少。基底神经节和相关区域的功能障碍也与强迫症有关，强迫症与抽动障碍在临床和家族方面有显着的重叠。研究方法：我们应用TMS技术先前用于抽动秽语综合征的一组16名强迫症患者（7名未用药）和II年龄匹配的健康志愿者广泛筛查精神病理学。运动皮层兴奋性的措施包括休息和主动运动阈值，皮质沉默期的持续时间，和皮质内抑制和促进使用成对脉冲TMS技术与阈下条件刺激。结果如下：与最近在抽动秽语综合征和局灶性肌张力障碍中的发现类似，本研究报告了相对于志愿者在2至5毫秒的刺激间隔处皮质内抑制（ICI）显著降低。我们还发现强迫症患者的活动和静息运动诱发电位阈值降低，这是皮质兴奋性增加的另一个迹象。两项异常均未显示与药物相关。ICI和运动阈值的降低在有共病关系的强迫症患者中最大，但在无关系的患者中仍然显著。结论：这些数据表明，异常的皮质兴奋性强迫症。这些研究结果是一致的假设，抽动秽语综合征和强迫症（OCD）是类似的疾病重叠功能障碍的皮质基底神经回路。抽动相关强迫症患者可能比无抽动的强迫症患者有更多的运动皮层兴奋性异常。
Objective: To assess cortical inhibitory and excitatory mechanisms in obsessive-compulsive disorder (OCD). Background: Transcranial magnetic stimulation (TMS) studies have found decreased neuronal inhibition and a reduced cortical silent period in the primary motor area in Tourette's syndrome, focal dystonia, and other disorders believed to involve dysfunction of subcortical structures, including the basal ganglia. Dysfunction of the basal ganglia and linked regions also has been implicated in OCD, which has significant clinical and familial overlap with tic disorders. Methods: We applied the TMS techniques previously used in Tourette's syndrome to a group of 16 OCD patients (seven unmedicated) and II age-matched healthy volunteers extensively screened for psychopathology. Measures of motor cortex excitability included resting and active motor threshold, cortical silent period duration, and intracortical inhibition and facilitation using a paired-pulse TMS technique with a subthreshold conditioning stimulus. Results: Similar to recent findings in Tourette's syndrome and focal dystonia, this study reports significantly decreased intracortical inhibition (ICI) relative to the volunteers at interstimulus intervals from 2 to 5 msec. We also found decreased active and resting motor evoked potential threshold in the OCD patients, another indication of increased cortical excitability. Neither abnormality appeared medication related. The decreases in ICI and motor threshold were greatest in OCD patients with comorbid ties, but remained significant in patients without ties. Conclusions: The data suggest abnormal cortical excitability in obsessive-compulsive disorder. These findings are congruent with the hypothesis that Tourette's syndrome and obsessive compulsive disorder (OCD) are analogous disorders with overlapping dysfunction in corticobasal circuits. Patients with tic-related OCD may have more abnormal motor cortex excitability than OCD patients without tics.