Iwao Yamakami1, Nobuo Oka, Yoshinori Higuchi. 1. Neurosurgery, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuoku, Chiba 260-8670, Japan. yamakami@faculty.chiba-u.jp
Abstract
OBJECTIVE: There are two hypotheses for the pathogenesis of hemifacial spasm (HFS): abnormal cross-transmission between the facial nerve fibers at a site of vascular compression, and hyperactivity of the facial nucleus. To further elucidate the mechanism of HFS, we established an animal model. We applied chronic electrical stimulation (CES) to the facial nucleus in rats, and clarified functional and morphological changes in the nucleus. METHOD: Under anesthesia, a novel intracranial electrode was stereotactically implanted in the facial nucleus of six rats. CES of the facial nucleus via the implanted electrode was applied for 5 min daily for three weeks (CES animals). Facial electromyograms (EMGs) were recorded at rest and during electrical stimulation to study the excitability of the facial nucleus at 1, 2, and 4 weeks after initiating CES. As control animals, six rats were implanted with intracranial electrodes, but did not undergo CES. Electrophysiological studies of the control animals were performed using the same protocol as in the CES animals. RESULT: Spontaneous abnormal movement of the facial muscle mimicking HFS did not occur. Four weeks after starting CES, one of the six CES animals developed an abnormal EMG response with a latency of 10 ms. No control animals developed such a response. CONCLUSIONS: CES of the facial nucleus can produce an abnormal EMG response very similar to the abnormal muscle response (AMR) characteristic of HFS patients. Kindling-like hyperactivity of the facial nucleus induced by CES is the cause of the AMR, suggesting a pathogenesis of HFS.
OBJECTIVE: There are two hypotheses for the pathogenesis of hemifacial spasm (HFS): abnormal cross-transmission between the facial nerve fibers at a site of vascular compression, and hyperactivity of the facial nucleus. To further elucidate the mechanism of HFS, we established an animal model. We applied chronic electrical stimulation (CES) to the facial nucleus in rats, and clarified functional and morphological changes in the nucleus. METHOD: Under anesthesia, a novel intracranial electrode was stereotactically implanted in the facial nucleus of six rats. CES of the facial nucleus via the implanted electrode was applied for 5 min daily for three weeks (CES animals). Facial electromyograms (EMGs) were recorded at rest and during electrical stimulation to study the excitability of the facial nucleus at 1, 2, and 4 weeks after initiating CES. As control animals, six rats were implanted with intracranial electrodes, but did not undergo CES. Electrophysiological studies of the control animals were performed using the same protocol as in the CES animals. RESULT: Spontaneous abnormal movement of the facial muscle mimicking HFS did not occur. Four weeks after starting CES, one of the six CES animals developed an abnormal EMG response with a latency of 10 ms. No control animals developed such a response. CONCLUSIONS:CES of the facial nucleus can produce an abnormal EMG response very similar to the abnormal muscle response (AMR) characteristic of HFSpatients. Kindling-like hyperactivity of the facial nucleus induced by CES is the cause of the AMR, suggesting a pathogenesis of HFS.