An Animal Model of Ischemic Facial Palsy.

Abstract

Although the pathogenesis of idiopathic facial palsy remains to be clarified, ischemia is thought to be one of the most probable factors. The intratemporal portion of the facial nerve receives its blood supply from three major sources: the internal auditory artery, the petrosal branch of the middle meningeal artery and the stylomastoid artery. The petrosal branch of the middle meningeal artery, the so-called petrosal artery, provides the main arterial supply to the geniculate ganglion, where the vascularity is much richer than elsewhere in the course of the facial nerve. We confirmed in a previous experiment that interruption of the petrosal artery resulted in a marked decrease in the facial nerve blood flow at the geniculate ganglion. This ischemic change could cause functional disorders in the facial nerve. In the present study the petrosal artery of the guinea pigs was transected, and the motor function and electrophysiological and histologic changes of the facial nerve was investigated. 1) Interruption of the petrosal artery produced facial palsy within 3 days in 52.6% of the guinea pigs. 2) Antidromically evoked facial nerve responses and histological findings suggested that facial palsy was caused by nerve conduction block due to edema of the nerve distal to the geniculate ganglion.