Ishikawa M, Ohira T, Namiki J, Ishihara M, Takase M, Toya S
Department of Neurosurgery, Keio University, Tokyo, Japan.
Neurol Res. 1996 Feb;18(1):2-8. doi: 10.1080/01616412.1996.11740368.
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 how the cross compression can cause HFS: 1. the spasm is caused by ephaptic transmission and hyperexcitability at the site of compression; and 2. the spasm is caused by hyperexcitability in the facial motonucleus. In peripheral nerves, F-waves, which result from the backfiring of antidromically activated anterior horn cells, have been proposed as indices of anterior horn cell excitability. Enhancement of the F-waves in facial muscles also indicates increased excitability of the facial motonucleus. On the other hand, abnormal muscle response (AMR), which can be elicited by stimulating one branch of the facial nerve and recording electromyographically from muscles innervated by other branches of the facial nerve, is specific for patients with HFS. We have therefore measured the AMRs and the F-waves in the facial muscle of HFS patients under anesthesia in order to investigate the excitability of the facial motonucleus. We obtained facial nerve evoked electromyograms from 14 HFS patients during microvascular decompression (MVD) operation. The F-waves, obtained with surface electrodes from the mentalis muscle, were defined as the second response after the M-wave. The F-waves in facial muscles cannot usually be elicited during surgical anesthesia using inhalation anesthetics. However, the F-waves were elicited on the spasm side in 10 out of 14 patients with HFS and the F-waves disappeared after MVD under anesthesia, as the early responses (R1) of the blink reflex were elicited on the spasm side before MVD under anesthesia. The F-waves elicited during anesthesia were suppressed significantly, compared with those before MVD. These results suggest that excitability in facial motonucleus increased on the spasm side.
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。目前有两种关于交叉压迫如何导致HFS的假说:1. 痉挛是由压迫部位的ephaptic传递和兴奋性过高引起的;2. 痉挛是由面神经运动核的兴奋性过高引起的。在周围神经中,由逆向激活的前角细胞的反向放电产生的F波,已被提议作为前角细胞兴奋性的指标。面部肌肉中F波的增强也表明面神经运动核的兴奋性增加。另一方面,异常肌肉反应(AMR)可通过刺激面神经的一个分支并从面神经其他分支支配的肌肉进行肌电图记录来引出,它是HFS患者所特有的。因此,我们在麻醉下测量了HFS患者面部肌肉的AMR和F波,以研究面神经运动核的兴奋性。我们在微血管减压(MVD)手术期间从14例HFS患者获得了面神经诱发肌电图。用表面电极从颏肌获得的F波被定义为M波后的第二个反应。在使用吸入麻醉剂的手术麻醉期间,通常无法引出面部肌肉的F波。然而,14例HFS患者中有10例在痉挛侧引出了F波,并且在麻醉下MVD后F波消失,因为在麻醉下MVD前痉挛侧眨眼反射的早期反应(R1)被引出。与MVD前相比,麻醉期间引出的F波明显受到抑制。这些结果表明痉挛侧面神经运动核的兴奋性增加。