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Axonal excitability properties in hemifacial spasm
Author(s) -
Krishnan Arun V.,
Hayes Michael,
Kiernan Matthew C.
Publication year - 2007
Publication title -
movement disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.352
H-Index - 198
eISSN - 1531-8257
pISSN - 0885-3185
DOI - 10.1002/mds.21512
Subject(s) - facial nerve , hemifacial spasm , stimulation , depolarization , neuroscience , medicine , facial muscles , psychology , anatomy
Hemifacial spasm (HFS) is characterized by involuntary, irregular contractions of muscles innervated by the facial nerve. Whether the facial nerve has a relative predisposition for ectopic activity has not been clarified. Nerve excitability techniques, which provide information about membrane potential and axonal ion channel function, were initially measured in 12 control subjects looking for biophysical differences that may predispose the facial nerve to generate ectopic activity. In a second series of studies, facial nerve excitability was assessed in nine HFS patients. In both series, stimulus–response behavior, threshold electrotonus, a current threshold relationship, and the recovery of excitability following supramaximal stimulation were recorded following stimulation of the facial nerve. When compared to normative data from nerves in the upper and lower limbs, there was a relative “fanning‐in” of threshold electrotonus, reduced superexcitability, and increased subexcitability in facial nerve studies from control subjects ( P < 0.05), consistent with relative axonal depolarization. These findings may underlie the propensity for the facial nerve to develop ectopic impulse activity in motor axons. In the HFS patient study, there were no significant differences in distal facial nerve excitability properties from the affected side in HFS patients when compared either to the unaffected side or to normative facial nerve data. It is concluded that the impulse generator underlying HFS must consequently be sited more proximally and does not cause a generalized disturbance of motor axon excitability. © 2007 Movement Disorder Society

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