Nielsen V K
Muscle Nerve. 1985 Sep;8(7):545-55. doi: 10.1002/mus.880080702.
Pathologic and pathophysiologic findings in hemifacial spasm are reviewed in connection with recent theoretical and experimental studies of ectopic/ephaptic excitation. The intracranial segment of the normal facial nerve is ensheathed by an arachnoid membrane only and shows no fascicular organization. In hemifacial spasm, this segment shows signs of demyelination. Several electrical phenomena relating to ectopic excitation, ephaptic transmission between facial nerve fibers, and autoexcitation can be reproduced in clinical electrophysiologic studies of hemifacial spasm. These abnormalities gradually disappear after facial nerve decompression in the cerebellopontine recess. It is concluded that the normal facial nerve is vulnerable to minor compression, the primary pathophysiologic mechanism in hemifacial spasm is ectopic/ephaptic excitation due to compression and demyelination of the intracranial segment of the facial nerve, and the facial nerve in hemifacial spasm is a useful model for the study of ephaptic transmission, which has provided new information about the resolution of abnormal electrical events after decompression.
结合近期关于异位/突触旁兴奋的理论和实验研究，对面肌痉挛的病理和病理生理发现进行了综述。正常面神经的颅内段仅被蛛网膜包裹，且无束状结构。在面肌痉挛中，该段显示出脱髓鞘的迹象。在面肌痉挛的临床电生理研究中，可以重现与异位兴奋、面神经纤维间的突触旁传递和自发放电相关的几种电现象。在小脑脑桥角进行面神经减压后，这些异常逐渐消失。得出的结论是，正常面神经易受轻微压迫，面肌痉挛的主要病理生理机制是由于面神经颅内段受压和脱髓鞘导致的异位/突触旁兴奋，并且面肌痉挛中的面神经是研究突触旁传递的有用模型，这为减压后异常电活动的消退提供了新信息。
