The mechanism of hemifacial spasm: a new understanding of the offending artery
Authors:
- Ning-Ning DouNDNing-Ning Dou
- Jun ZhongJZJun Zhong
- Qiu-Meng ZhouQZQiu-Meng Zhou
- Jin ZhuJZJin Zhu
- Yong-Nan WangYWYong-Nan Wang
- Lei XiaLXLei Xia
- Xiao-Sheng YangXYXiao-Sheng Yang
- Ting-Ting YingTYTing-Ting Ying
- Xue-Sheng ZhengXZXue-Sheng Zheng
- Shi-Ting LiSLShi-Ting Li
- 8 July 2014
- journal article
- review article
- Published by Taylor & Francis in Neurological Research
- Vol. 37 (2) , 184-188
Abstract
Although neurovascular confliction was believed to be the cause of hemifacial spasm (HFS), the mechanism of the disorder remains unclear to date. Current theories, merely focusing on the facial nerve, have failed to explain the clinical phenomenon of immediate relief following a successful microvascular decompression surgery (MVD). With the experience of thousands of microvascular decompression surgeries and preliminary investigations, we have learned that the offending artery may play a more important role than the effect of merely mechanical compression in the pathogenesis of the disease. We believe that the attrition of neurovascular interface is the essence of the etiology, and the substance of the disease is emersion of ectopic action potentials from the demyelinated facial nerve fibers, which were triggered by the sympathetic endings from the offending artery wall. In this paper, we put forward evidence to support this hypothesis, both logically and theoretically.Keywords
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