We studied the F wave of the facial muscles on both the normal side and the spastic side in 14 patients with hemifacial spasm. The purpose of this study was to determine if the mechanism of hemifacials spasm originates in ephaptic transmission in the facial nerve at the site of vascular compression or in a hyperexcited facial motor nucleus. Larger amplitude, longer duration and shorter latency F waves in the peripheral nerves than in normals indicate anterior horn cell hyperexcitability. We found abnormal potentials exhibiting synkinesis (lateral spread), a typical electrophysiological finding in hemifacial spasm, in the facial nerve evoked electromyograms of the 14 patients, none of whom had experienced facial palsy or facial nerve block. Electrical stimulation was delivered transcutaneously to the most distal portion of the marginal mandibular branch of the facial nerve. Using surface electrodes the F waves were obtained over the mentalis muscle as the second response after the M wave. While the F waves were normal on the patients' normal side, on the spastic side, their duration was longer (mean duration about 1.9 times that of the normal side), their onset latency was slightly shorter, and their F/M amplitude latency was greater than on the normal side. After microvascular decompression, the facial spasm and abnormal F-wave findings resolved. Onset latency was not increased, and on the spastic side some patients displayed facial spasm clinically and electrophysiologically for one year after MVD. In other words, there was hardly any focal demyelination of the facial nerve, so it is possible that ephaptic transmission and ectopic excitation are the mechanism of HFS. In conclusion, the abnormal F-wave findings on the spastic side indicate hyperexcitability of the facial nucleus. This supports the facial motor nucleus kindling theory as the pathophysiological mechanism of HFS.
|ジャーナル||Brain and Nerve|
|出版ステータス||Published - 1994 5 18|
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