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Electrophysiology of the facial nerve in hemifacial spasm: Ectopic/ephaptic excitation
Author(s) -
Nielsen Viggo Kamp
Publication year - 1985
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880080702
Subject(s) - hemifacial spasm , facial nerve , cerebellopontine angle , medicine , facial muscles , microvascular decompression , pathophysiology , neuroscience , anatomy , surgery , psychology , magnetic resonance imaging , radiology , pathology , trigeminal neuralgia
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 (1) the normal facial nerve is vulnerable to minor compression, (2) 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 (3) 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.

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