THE PATHOGENESIS of Bell's palsy is generally assumed to be compression of the nerve or its blood supply in the rigid fallopian canal due to edema1-3 resulting in an entrapment syndrome with paralysis not unlike that of the median nerve in the carpal tunnel.4 The etiology is unknown, but most authors accept ischemia as the primary mechanism.1,2,4 The main evidence for this view is the observation that on slitting the nerve sheath, ie, the perineurium and epineurium, of the facial nerve during the decompression operation for Bell's palsy the nerve bulges outward.5,6 Proponents of this theory maintain that the deleterious pressure is exerted in the descending portion of the fallopian canal, and that the facial nerve should, therefore, be decompressed in this part of its course.7 Approximately 20% of patients with Bell's palsy do not recover spontaneously, and it is claimed that early relief of
SADE J, LEVY E, CHACO J. Surgery and Pathology of Bell's Palsy. Arch Otolaryngol. 1965;82(6):594–602. doi:10.1001/archotol.1965.00760010596007
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