General practitioners in the United Kingdom will see about one patient with Bell's palsy every two years. Increasing evidence shows that the way the patient is managed has an important effect on outcome. Untreated Bell's palsy leaves some patients with major facial dysfunction and a reduced quality of life. Of patients with Bell's palsy registered by general practitioners between 1992 and 1996 a fifth were referred for specialist opinion, just over a third received oral steroids, and 0.6% received aciclovir.¹ Improving outcomes requires coordination between specialists and general practitioners so that patients are treated during the critical first 72 hours. We outline recent developments in Bell's palsy and current best evidence in its management.

Bell's palsy accounts for almost three quarters of all acute facial palsies, with the highest incidence in the 15 to 45 year old age group (table 1).² The annual incidence in the UK population is around 20 per 100 000, with one in 60 people being affected during their lifetime. Men and women are equally affected, although the incidence is higher in pregnant women (45 cases per 100 000).

The most alarming symptom of Bell's palsy is paresis; up to three quarters of affected patients think they have had a stroke or have an intracranial tumour. The palsy is often sudden in onset and evolves rapidly, with maximal facial weakness developing within two days. Associated symptoms may be hyperacusis, decreased production of tears, and altered taste (table 2).

Bell's palsy causes a peripheral lower motor neurone palsy, which manifests as the unilateral impairment of movement in the facial and platysma muscles, drooping of the brow and corner of the mouth, and impaired closure of the eye and mouth. Bell's phenomenon—upward diversion of the eye on attempted closure of the lid—is seen when eye closure is incomplete.

Herpes zoster virus has traditionally been associated with Ramsay Hunt syndrome, with typical cutaneous vesicles and cochleovestibular dysfunction. Vesiculation may not necessarily appear (zoster sine herpete) or may be delayed in up to half of patients. Dermatomal pain and dysaesthesia before vesiculation is termed preherpetic neuralgia and may be the only clinical indicator that herpes zoster virus is involved. Zoster sine herpete is thought to be the cause of almost a third of facial palsies previously diagnosed as idiopathic.⁹

Overall, Bell's palsy has a fair prognosis without treatment, with almost three quarters of patients recovering normal mimetical function and just over a tenth having minor sequelae. A sixth of patients are left with either moderate to severe weakness, contracture, hemifacial spasm, or synkinesis. Patients with a partial palsy fair better, with 94% making a full recovery. The outcome is worse when herpes zoster virus infection is involved in partial palsy. In patients who recover without treatment, major improvement occurs within three weeks in most. If recovery does not occur within this time, then it is unlikely to be seen until four to six months, when nerve regrowth and reinnervation have occurred. By six months it is clear who will have moderate to severe sequelae. Box 1 lists the poor prognostic indicators of Bell's palsy.

The main aims of treatment in the acute phase of Bell's palsy are to speed recovery and to prevent corneal complications. Treatment should begin immediately to inhibit viral replication and the effect on subsequent pathophysiological processes that affect the facial nerve. Psychological support is also essential, and for this reason patients may require regular follow up.

Patients with Bell's palsy should start treatment immediately and be referred to a specialist as soon as possible. In a few cases the diagnosis may be subsequently reassigned.² Patients should receive psychological support and eye care during follow up. Long term sequelae may be missed if patients are not monitored for a full year.