Pathophysiological Study of Facial Nerve Paralysis Induced by Herpes Simplex Virus Type 1 Infection.

Bell's palsy is the most common cause of peripheral facial nerve paralysis. Although herpes simplex virus type 1 (HSV-1) infection has been strongly suggested as a cause of Bell's palsy, the pathomechanism of the facial nerve paralysis is unclear. Previously, we had succeeded in producing an animal model of acute, transient and homolateral facial paralysis by inoculating HSV-1 into the auricle, simulating Bell's palsy. To clarify the mechanism of this facial nerve paralysis, electrophysiological testing of the trigemino-facial reflex (blink reflex) and electroneuronography (ENoG) were carried out, and a histopathological study of the facial nerve was subsequently performed. The blink reflex and ENoG were examined twice ; during facial paralysis on day 10 and after recovery on day 17. The R1 latency of the blink reflex was prolonged or disappeared on the paralyzed side during facial paralysis, but recovered in all animals with the corresponding recovery of facial nerve paralysis. ENoG values were inconsistent during facial nerve paralysis and did not normalize even after complete recovery of the facial nerve paralysis. The histopathological studies demonstrated that mixed nerve damage, demyelination and axonotomesis, were present, although demyelination was dominant. Collectively, the electrophysiological and histopathological findings suggested that the pathomechanism of facial nerve paralysis caused by HSV-1 infection is mainly due to demyelination of the nerve, which was represented as a conduction block in electrophysiological testing. The present study suggested that the facial nerve damage underlying Bell's palsy involves mixed nerve damage including demyelination and axonotomesis, and the prognosis of facial nerve paralysis is dependent on the balance of these two kinds of nerve damage.