Bell's palsy, or idiopathic facial nerve palsy, is a relatively common disorder. Its annual incidence in the USA is 20-25 per 100,000, 9 with higher rates in individuals with diabetes or hypertension. 4 A diagnosis of Bell's palsy is one of exclusion, and several potentially treatable disorders are included in the differential diagnosis, including middle ear or mastoid infection, temporal bone fracture, tumors in the parotid gland or cerebellopontine angle, multiple sclerosis, and Guillain-Barre Β΄syndrome. Several bacterial infectious diseases cause facial nerve weakness, including Lyme disease, syphilis, diphtheria, and leprosy. In addition, viral infectious diseases can cause facial nerve weakness, notably herpes zoster (reactivation of varicella zoster virus, the cause of the Ramsay-Hunt syndrome) and poliomyelitis. The causeeffect relationship between these infections and facial weakness is well accepted. 10 A causal relationship between reactivation of herpes simplex virus type 1 (HSV-1) infection in the geniculate ganglion, leading to direct injury to the facial nerve and subsequent palsy, has been debated for many years. Recent studies provide convincing support for this hypothesis.
Many studies have examined serologic responses to HSV in patients with Bell's palsy. Morgan reviewed the results of serologic studies conducted between 1972 and 1988. 10 Of 2043 patients, a significant increase in HSV antibody titer was seen in only 3.7%. However, several of the reviewed studies showed increased prevalence of immunoglobulin G (IgG) antibody or higher titers of IgG antibody to HSV in patients with Bell's palsy, consistent with reactivation of previously acquired infection. This finding should be interpreted in light of the fact that about 50% of the general population is HSV-1 seropositive. 5 Latent HSV-1 has been detected by polymerase chain reaction (PCR) or by histology in 70-90% of unselected geniculate ganglia collected at au-