Abstract

About three-quarters of the lesions of the facial nerve fall into the category termed Bell's palsy. The pathological process involved is unknown. It is generally presumed to be swelling and hyperemia of the nerve sheath, with compression of the axons in the narrow facial canal. Park and Watkins 1 made a comprehensive survey of 500 cases of Bell's palsy observed over a period of 18 years. They listed the causes as idiopathic, 87.2%; trauma, 6%; infection, 6%; and tumor, 0.8%. Forty-two of the patients with idiopathic cases gave a history of exposure to drafts or colds. Several specific theories as to the etiology of Bell's palsy have been advanced. Among these are a specific infectious neuritis, subclinical mastoid infection involving the fallopian canal region, congenital stenosis of the fallopian canal associated with some precipitating factor, and refrigeration. Kettel 2 advanced the theory that the facial nerve impairment is a disease

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