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面肌痉挛的电生理研究:面部肌肉的F波

Electrophysiological investigation of hemifacial spasm: F-waves of the facial muscles.

作者信息

Ishikawa M, Ohira T, Namiki J, Gotoh K, Takase M, Toya S

机构信息

Department of Neurosurgery, School of Medicine, Keio University, Tokyo, Japan.

出版信息

Acta Neurochir (Wien). 1996;138(1):24-32. doi: 10.1007/BF01411719.

Abstract

In patients with hemifacial spasm (HFS), the spasm is due to cross-compression of the facial nerve by a blood vessel. There are currently two hypotheses for the mechanism of HFS: 1) the spasm is caused by ephaptic transmission and an increase in excitability at the site of compression; and 2) the spasm is caused by hyperexcitability in the facial nerve nucleus. In peripheral nerves, F-waves, which result from the backfiring of antidromically activated anterior horn cells, have been proposed as indices of proximal motoneuron conduction and anterior horn cell excitability. Enhancement of the F-waves indicates increased anterior horn cell excitability. We have therefore measured F-waves in the facial muscle of HFS patients in order to investigate the excitability of the facial nerve nucleus. The authors obtained facial nerve evoked responses from 20 HFS patients before microvascular decompression (MVD), 10 HFS patients after MVD and 10 healthy controls. The F-waves, obtained with surface electrodes from the mentalis muscle, were the second response after the M-wave. On the patient's spasm side, the F-wave duration, F/M amplitude ratio and frequency of F-wave appearance significantly increased compared with those of the normal side or healthy controls; minimum latency and chronodispersion did not significantly differ between these groups. In patients whose spasm disappeared completely following MVD, the abnormal muscle response (lateral spread), which is a characteristic sign of HFS, and the enhancement of the F-wave eventually also disappeared. Because of the correlation between HFS and F-waves, the authors' study supports the hypothesis that the cause of HFS is hyperexcitability of the facial motonucleus.

摘要

在半面痉挛(HFS)患者中,痉挛是由血管对面神经的交叉压迫所致。目前关于HFS的发病机制有两种假说:1)痉挛是由突触外传递以及压迫部位兴奋性增加引起的;2)痉挛是由面神经核的兴奋性过高引起的。在周围神经中,F波是由逆行激活的前角细胞的回返放电产生的,已被提议作为近端运动神经元传导和前角细胞兴奋性的指标。F波增强表明前角细胞兴奋性增加。因此,我们测量了HFS患者面部肌肉的F波,以研究面神经核的兴奋性。作者获取了20例微血管减压(MVD)术前的HFS患者、10例MVD术后的HFS患者以及10例健康对照者的面神经诱发反应。用表面电极从颏肌记录到的F波是继M波之后的第二个反应。在患者的痉挛侧,与正常侧或健康对照相比,F波持续时间、F/M波幅比值和F波出现频率显著增加;这些组之间的最小潜伏期和时间离散度无显著差异。在MVD后痉挛完全消失的患者中,作为HFS特征性体征的异常肌肉反应(侧向扩散)以及F波增强最终也消失了。由于HFS与F波之间存在相关性,作者的研究支持HFS病因是面神经运动核兴奋性过高这一假说。

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