Research on the Pathogenesis of Hemifacial Spasm through Electrophysiological Studies

Abstract

The cause of hemifacial spasm (HFS) is commonly linked to vascular compression of the facial nerve at the root exit zone. Microvascular decompression has become the most effective treatment for HFS. However, despite numerous electrophysiological studies investigating factors such as ephaptic transmission, ectopic excitation between individual nerve fibers, and hyperexcitability of the facial motor nucleus, there is still debate about the exact pathogenesis of HFS. For over 40 years, researchers have been conducting electrophysiological studies in clinical settings to better understand the pathogenesis of HFS. These studies have employed techniques including the lateral spread response, blink reflex test, facial F-waves, and transcranial electrical stimulation. Although a peripheral nerve mechanism was historically considered most likely to be responsible for this condition, recent studies are increasingly pointing to a central mechanism as the primary culprit behind HFS. This article seeks to shed light on the pathogenesis of HFS by reviewing the key findings from electrophysiological studies carried out over the years.