Abstract

In patients with hemifacial spasm, it has been said that the spasm is due to cross compression of the facial nerve by a blood vessel and that microvascular decompression (MVD) of the facial nerve is an effective treatment. The F waves, which result from backfiring of antidromically activated motor neurons of the facial motor nucleus, are indices of the excitability of the facial motor nucleus and are enhanced in patients with hemifacial spasm. Measuring blink reflexes and abnormal muscle responses (lateral spread), a characteristic sign of hemifacial spasm, has been used to investigate the mechanism of hemifacial spasm pathophysiologically. Thus the authors measured F waves of the facial muscle, blink reflexes, and abnormal muscle responses before and after MVD in patients suffering from hemifacial spasm to investigate the excitability of the facial motor nucleus and the course of the cure of hemifacial spasm after MVD. The authors obtained facial nerve-evoked electromyograms in 20 patients with hemifacial spasm before and after the MVD procedure. On the spasm side, the F waves and blink reflexes were enhanced preoperatively compared to those on the normal side and abnormal muscle responses were recorded in all patients. In 12 patients whose hemifacial spasm had not disappeared completely for 5.1 +/- 1.7 (mean +/- standard error) months following the MVD procedure, F waves were still enhanced significantly and abnormal muscle responses were still recordable, albeit at lower amplitude. Within 1 month after the hemifacial spasm had disappeared completely. F waves were still significantly enhanced in 17 patients and abnormal muscle responses were recorded in seven of 15 patients. Subsequently, the enhanced F waves and abnormal muscle responses disappeared completely. The authors' study supports the hypothesis that the cause of hemifacial spasm is hyperexcitability of the facial motor nucleus and suggests that additional surgery should not be performed for at least 2 years after MVD, because that period is necessary for the disappearance of the hyperexcitability of the facial motor nucleus.

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