The onset of Bell’s palsy is acute; about one-half of cases attain maximum paralysis in 48 h and practically all within 3 or 4 days. Pain behind the ear may precede the paralysis by a day or two and in a few patients is intense and persistent. Although a report by the patient of fullness or numbness in the face is common, in a small number there is hypesthesia in 1 or more branches of the trigeminal nerve. The explanation of this finding is not clear. Impairment of taste is present in most patients but it rarely persists beyond the second week of paralysis. This indicates that the lesion has extended proximal to the point at which the chorda tympani joins the facial nerve. Hyperacusis or distortion of sound is then experienced in the ipsilateral ear and, as mentioned, indicates paralysis of the stapedius muscle.
The facial nerve in Bell’s palsy often displays abnormal signal on gadolinium-enhanced MRI although this may be difficult to appreciate in axial sections if the change is in the vertical part of the facial canal. There is a mild increase of lymphocytes and mononuclear cells in the CSF in a few instances. Cases with more pronounced contrast enhancement of the facial nerve apparently have a worse prognosis (Kress). The enhancement presumably reflects inflammation and swelling along the course of the facial nerve.
Fully 70 percent of patients recover completely within a month or two and 85 percent achieve near-normal facial function, as reviewed by Gilden. Recovery of taste precedes recovery of motor function; if taste returns in the first week, it is a good prognostic sign. But early recovery of some motor function in the first 5 to 7 days is the most favorable sign. EMG may be of value in distinguishing temporary conduction defects from a pathologic interruption of nerve fibers; if there is evidence of denervation after 10 days, one may expect a long delay in the onset of recovery, measured in terms of months. Recovery then proceeds by axonal regeneration, a process that may take 2 years or longer and is often incomplete.
Bell’s palsy recurs in approximately 8 percent of cases in several series (van Amstel and Devriese; Pitts et al), presumably as a result of reactivation of the latent herpes virus. The palsy reemerges during an infection or pregnancy, or for no apparent reason. The interval between episodes is unpredictable but averages about 10 years. Recurrent forms of facial paralysis also occur with Lyme disease and sarcoidosis, and in a familial variety as mentioned below.
Treatment Protection of the eye during sleep is generally employed in the management of Bell’s palsy. There is no evidence that surgical decompression of the facial nerve is effective, and it may be harmful. The administration of prednisone (40 to 60 mg/d, or an equivalent glucocorticoid) during the first week to 10 days after onset was shown to be beneficial in randomized placebo controlled trials by Sullivan and colleagues and by Engstrom and colleagues. Glucocorticoids are thought to decrease the possibility of permanent paralysis from swelling of the nerve in the tight facial canal.
The finding of viral genome surrounding the seventh nerve suggested that antiviral agents might be useful in the management of Bell’s palsy. Most evidence from large randomized trials, however, particularly the one conducted by Sullivan and colleagues, fails to support the use of these drugs alone or in combination with steroids. On the other hand, a study by Hato and colleagues suggested an additive benefit of treatment with valacyclovir and prednisolone compared to treatment with prednisolone alone, particularly in the group of patients presenting with complete facial palsy. An earlier trial by De Diego and colleagues did not affirm this.
In appropriate circumstances, testing should be undertaken for infectious causes that would require alternative therapy (e.g., Lyme, HIV, and perhaps mycoplasma) but this is not routinely required. The treatment of facial palsy caused by VZV (Ramsay Hunt syndrome) with antiviral drugs is discussed later.