Ugawa Y, Genba-Shimizu K, Rothwell J C, Iwata M, Kanazawa I
Department of Neurology, School of Medicine, University of Tokyo, Japan.
Ann Neurol. 1994 Jul;36(1):90-6. doi: 10.1002/ana.410360117.
We studied the effect of electrical stimulation over the cerebellum on electromyographic responses evoked by magnetic stimulation over the cerebral motor cortex in 41 normal volunteers and 32 patients with ataxia due to various disorders. In all the normal subjects, stimulation over the cerebellum significantly reduced the size of electromyographic response in the first dorsal interosseous muscle evoked by magnetic cortical stimulation, when the cerebellar stimulus preceded the cortical stimulus by 5, 6, and 7 msec. This suppression was absent or reduced in ataxic patients who had atrophy of the cerebellar hemispheres as demonstrated by magnetic resonance imaging and in patients with dysfunction of the cerebellothalamocortical pathway who had lesions in the superior cerebellar peduncle or in the motor thalamus. In contrast, suppression was normal in ataxic patients who had pontine lesions that affected the pontocerebellar afferent pathway to the cerebellum. Results were also normal in patients without cerebellar ataxia, such as those with Parkinson's disease, sensory ataxia, and cerebrovascular disease without ataxia. We conclude that electrical stimulation activates cerebellar structures that suppress motor cortical excitability through a cerebellothalamocortical pathway and that the afferent systems to the cerebellum make no or little contribution to the effect. The technique described here would be useful for distinguishing ataxia due to lesions of cerebellar afferent pathway from other types of cerebellar ataxia.
我们研究了在41名正常志愿者和32名因各种疾病导致共济失调的患者中，对小脑进行电刺激对大脑运动皮层磁刺激诱发的肌电图反应的影响。在所有正常受试者中，当小脑刺激比皮层刺激提前5、6和7毫秒时，对小脑的刺激显著降低了磁皮层刺激诱发的第一背侧骨间肌的肌电图反应大小。在磁共振成像显示小脑半球萎缩的共济失调患者以及小脑丘脑皮质通路功能障碍、上小脑脚或运动丘脑有病变的患者中，这种抑制作用不存在或减弱。相比之下，患有桥脑病变影响小脑桥脑传入通路的共济失调患者的抑制作用正常。在没有小脑共济失调的患者中，如帕金森病、感觉性共济失调和无共济失调的脑血管疾病患者，结果也正常。我们得出结论，电刺激激活了通过小脑丘脑皮质通路抑制运动皮层兴奋性的小脑结构，并且小脑的传入系统对这种效应没有或几乎没有贡献。这里描述的技术将有助于区分由小脑传入通路病变引起的共济失调与其他类型的小脑共济失调。
