Bells Palsy

Bell's palsy is characterized by a sudden onset of facial paresis or paralysis. Bell's palsy is the most common cause of facial paralysis worldwide, with an incidence of up to 30 cases per 100,000 individuals (33). It may be associated with facial numbness, otalgia, hyperacusis, decreased tearing, or taste changes. Other neurologic symptoms should be absent because Bell' s palsy remains a diagnosis of exclusion.

In some patients, the inflammation along the nerve can be detected by an enhancing signal using magnetic resonance imaging with gadolinium contrast agent.

Herpes simplex virus has been implicated using polymerase chain reaction (PCR) techniques as the likely causative agent in Bell's palsy (33). The mechanism of injury appears to be viral insult with direct injury to ganglion cells as well as Schwann cells, resulting in secondary edema and inflammatory demyelination (34). Fisch, using intraoperative-evoked electromyography (EMG), determined that the pathologic constriction of the facial nerve is at the meatal foramen of the intralabyrinthine segment in 94% of patients (1).

Prognosis is good, with 85% of patients achieving complete recovery. A study of over 1000 patients followed for at least 15 years demonstrated that all patients had some recovery within six months: 71% achieved normal function, 13% had slight dysfunction, 12% had mild dysfunction, and 4% had severe dysfunction (35). Treatment is controversial, but recent studies advocate corticosteroid and antiviral therapy over corticosteroid therapy alone. A

double blind prospective trial of prednisone versus prednisone and acyclovir in Bell's palsy patients demonstrated that acyclovir 500 mg 5 times a day for 10 days with prednisone did produce a statistically significant improvement in outcome. This included improved return of volitional muscle motion and prevention of nerve degeneration on ENoG over prednisone therapy alone (36). Prednisone dosing is a 1 mg/kg/day (divided) taper over 7 to 10 days, and acyclovir dosing is 1000mg/day (5 times/day) for seven days. Surgical therapy remains an extremely controversial topic, with strong advocates both for and against its use. All agree that for patients with incomplete paralysis, the prognosis is excellent and surgical therapy should not be considered. ENoG has been shown to predict which patients are most likely to have a poor prognosis. It is in those patients where some would advocate surgical decompression of the nerve. Gantz et al. have advocated that for patients with more than 90% degeneration of ENoG after two weeks along, with no voluntary motor unit EMG potentials, the overall outcome is poor enough (58% chance of a poor outcome of House-Brackmann grade III or IV) to warrant surgical decompression using a middle fossa approach. Using this protocol, the outcome improved to a 91% chance of achieving a House-Brackmann grade I or II in the same patient population. Decompression medial to the geniculate ganglion appears to be most critical, with many studies demonstrating that decompression of the vertical segment alone has dubious efficacy. Late decompression beyond two weeks was also of no clinical benefit (37).

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