FACIAL NERVE PARALYSIS INDUCED BY HERPES SIMPLEX VIRUS INFECTION IN MICE

Abstract

The etiology of Bell's palsy remains unknown but clinical serological investigations have suggested herpes simplex virus (HSV) induced facial neuritis to be a potential cause. In order to verify the viral etiology of Bell's palsy it must be proved by animal experimentation. The author first succeeded in producing a transient facial paralysis of mice, with a herpes simplex viral neuritis simulating human Bell's palsy. Type 1 HSV (strain KOS, 4.5 X 10⁶ pfu/ml) was inoculated into the posterior aspect of the auricle. Fifty-nine out of 104 mice (56.7%) developed facial paralysis, on the experimental side, 6 to 9 days after the inoculation. The facial paralysis continued for 3 to 7 days and resolved spontaneously. In 36. 8% of the animals with facial palsy, HSV antigens were identified mainly in the geniculate ganglion cells, satellite cells, Schwann cells and nerve fibers of the involved side using immunohistochemical methods. No HSV antigen was demonstrated in the facial nerve of the contralateral side in animals with facial paralysis, bilateral facial nerves in animals without facial palsy or in control animals. Histopathologically, the involved nerve showed findings of viral neuritis such as round cell infiltration and vacuolar degeneration of nerve fibers. Inflammatory changes were noted in and around the geniculate ganglion but were more pronounced in nerve fibers proximal to the ganglion. These findings persisted for as long as a month after normal facial function had been restored. Round cell infiltration and vacuolar degeneration have been reported in histopathological studies of Bell's palsy. The results presented here indicate that HSV caused facial paralysis and provide substantial support for the viral hypothesis of the etiology of Bell's palsy.