Abstract
Although the pathogenisis of idiopathic facial palsy still remains to be clarified, ischemia is thought to be one of the most possible factors. We confirmed in our previous study that the interruption of the petrosal artery, which provides the main arterial supply to the geniculate ganglion, resulted in a marked decrease in the facial nerve blood flow around the geniculate ganglion, and this thus later caused ischemic facial palsy. In the present study we investigated the natural course of facial palsy induced by an interruption of the petrosal artery. The results were as follows: 1) In 68 of 80 animals (85%) facial palsy developed (severe: 21, moderate: 22, slight: 25 animals), 2) In animals with severe palsy, a complete recovery of the facial palsy took about two months and pathological synkinesis was often accompanied in the recovery stage, 3) Animals with moderate or slight palsy improved within one month and the duration of palsy depended on the severity, 4) Regarding the behavioral course of facial movement, ischemic facial palsy caused by an interruption of the petrosal artery seemed to be analogous to idiopathic facial palsy in humans. Thus, this animal model might provides useful informations for evaluating the pathogenesis of idiopathic facial palsy.
