Abstract SNACC-47

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Investigating the pathophysiology of hemifacial spasm using desflurane

Chowdhury T, Wilkinson M, Kaufmann A
University of Manitoba, Winnipeg, Manitoba, Canada

Hemifacial spasm (HFS) is characterized by progressive unilateral facial muscle contractions. A signature feature of HFS is the lateral spread response (LSR). The LSR results when electrical stimulation of one branch of the facial nerve produces contractions of facial muscles innervated by a different branch. The “spreading” of this response is thought to be a reflection of the progressive nature of HFS. There is debate as to the pathophysiological mechanism of the LSR. One hypothesis is that chronic vascular contact of the facial nerve causes ephaptic transmission of nerve impulses resulting in the “spreading” phenomena. An alternative hypothesis is that the facial motor neurons in the brainstem acquire a hyperexcitable state leading to the LSR.
LSR can be measured during MVD surgery using standard stimulation and electromyography techniques. In a prospective study we sought to investigate the mechanism of the LSR by using a total intravenous anesthesia (TIVA) or anesthesia using desflurane. If the LSR is entirely peripheral in nature (i.e. ephaptically transmitted) then the addition of desflurane to the anesthesia should have no effect on the LSR. If the LSR is due to central hyperactivity then desflurane should inhibit the LSR by virtue of the central locus of action of desflurane.
22 HFS patients undergoing MVD sugery participated in this study with informed and signed consent. The LSR was recorded from 3 facial muscles. LSR was produced in the o. oculi following stimulation of the mandibular branch of the facial nerve and LSR from the o. oris and mentalis was generated following stimulation of the zygomatic branch. All data were obtained prior to MVD and dural opening. Onset latency and peak to peak amplitude of the LSR were determined under TIVA and TIVA plus 1 MAC desflurane. Under each anesthetic condition EEG was recorded simultaneously and analyzed using density spectral analysis (DSA). Statistical analysis utilized the Wilcoxon Signed Rank test (before/after treatment design) and the Fisher Exact test for rates and proportions with significance at the 5% level.
The amplitudes of the LSR under TIVA and desflurane are shown in figure 1. Desflurane significantly decreased the LSR amplitude in all 3 facial muscles (p < 0.01). When data from all 3 facial muscles were pooled desflurane inhibited the LSR amplitude 44%. No effects were observed on the latency of the LSR. EEG fit into 2 categories: burst suppression or alpha/delta activity. There were no statistical differences in EEG state between the 2 test conditions.
The effects of dseflurane on the LSR suggest that a central mechanism is involved in the genesis of this signature HFS response.

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