The Role Of Offending Artery Wall And Transmembrane Proteins In Generation Of Hemifacial Spasm

Objectives: Despite vascular compression of the facial nerve has been confirmed asthe cause of hemifacial spasm (HFS), the mechanism is still unknown. We’ve foundthat the autonomic nervous system in the offending artery may play a role in themechanism of HFS. To further study the pathogenesis, we performed a series ofexperiments in SD rats.Methods: Moller’s HFS model in SD rats was adopted in this study and theabnormal muscle response (AMR) wave was electrophysiologically monitored. Theanimals were grouped according to the results of AMR monitoring. Afterelectromyography, both the facial nerve and offending artery were cut off in all therats for scanning electron microscope and transmission electron microscope,respectively. Then the immunohistochemistry was used to detect the expression ofNav1.1, Nav1.3, Nav1.6, Nav1.7and Nav1.8in the facial nerve of different groups.Results: After completion of HFS model,11/18rats were recorded AMR.Electron microscopy found lesions of both the epineuria and the adventitia in all therats from AMR-positive group, while in3/7rats from AMR-negative group (P<0.05).Immunohistochemical experiments showed up-regulation of Nav1.8in13/14rats fromAMR positive group, while in0from AMR-negative group (P<0.05). Conclusion: An interface lesion of both the facial nerve root and the offendingartery was necessary for development of HFS. Up-regulation of Nav1.8was foundin the damaged facial nerve, which could be the base of facial nerve hyperexcitability.