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通过磁脑刺激研究单侧脑损伤后运动皮层的抑制作用。

Inhibitory actions of motor cortex following unilateral brain lesions as studied by magnetic brain stimulation.

作者信息

von Giesen H J, Roick H, Benecke R

机构信息

Department of Neurology, Heinrich-Heine-University, Düsseldorf, Germany.

出版信息

Exp Brain Res. 1994;99(1):84-96. doi: 10.1007/BF00241414.

DOI:10.1007/BF00241414
PMID:7925799
Abstract

Noninvasive transcranial magnetic stimulation (TMS) of the motor cortex not only induces short-latency, motor-evoked potentials (MEP) in contralateral muscles, but also inhibitory phenomena. One type of inhibitory action appears directly after the MEP in contralateral muscles and can be visualized by blockade of tonic, voluntary electromyographic (EMG) activity (postexcitatory inhibition, PI). Evidence for a cortical origin of PI, especially in its later part, was derived from double cortical stimulation in previous studies and is further supported by examination of PI in patients with focal hemispheric unilateral brain lesions in the present study. Thirty patients with different sites of vascular or tumour lesions were studied by TMS. In 6 patients with circumscribed lesions of the primary sensorimotor cortex a significant shortening of PI to contralateral muscles was observed. In 7 patients with focal lesions of the thalamus or internal capsule, in 6 patients with lesions of the premotor cortex and in 5 patients with lesions restricted to the parietal or temporal lobe, a significant prolongation of PI to the contralateral muscles was detected. Six patients with transient ischemic attacks showed either prolongation or shortening of PI. We conclude that PI is predominantly generated in the primary motor cortex, correspondingly its damage causes shortening of PI. In contrast, damage to brain areas that project to the primary motor cortex is followed by prolongation of PI. This remote effect on the primary motor cortex may result from disinhibition of cortical interneurones.

摘要

对运动皮层进行无创性经颅磁刺激(TMS)不仅会在对侧肌肉中诱发短潜伏期的运动诱发电位(MEP),还会产生抑制现象。一种抑制作用在对侧肌肉的MEP之后直接出现,并且可以通过阻断强直性、随意肌电图(EMG)活动来显现(兴奋性后抑制,PI)。PI起源于皮层的证据,尤其是在其后期阶段,来自先前研究中的双皮层刺激,并且在本研究中对患有局灶性半球单侧脑损伤的患者进行PI检查时得到了进一步支持。通过TMS对30例患有不同部位血管或肿瘤病变的患者进行了研究。在6例原发性感觉运动皮层有局限性病变的患者中,观察到对侧肌肉的PI明显缩短。在7例丘脑或内囊局灶性病变的患者、6例运动前皮层病变的患者以及5例局限于顶叶或颞叶病变的患者中,检测到对侧肌肉的PI明显延长。6例短暂性脑缺血发作患者的PI显示延长或缩短。我们得出结论,PI主要在初级运动皮层产生,相应地其损伤会导致PI缩短。相反,投射到初级运动皮层的脑区受损后,PI会延长。对初级运动皮层的这种远程效应可能是由于皮层中间神经元的去抑制作用所致。

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