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Category: Neurology | ENT

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Bell’s palsy overview

Published: April 03, 2010. Updated: April 03, 2010


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Bell’s palsy, also known as facial palsy, is an inflammatory swelling of the facial nerve (the nerve supplying the muscles of the face) in the facial canal of the middle ear, leading in severe cases to an acute compression neuropathy which results in a temporary loss of function (temporary weakness in the facial muscles).

The cause is unkown (idiopathic); however, recent evidence suggests that herpes simplex virus type 1 invasion may trigger the process (an association with herpes simplex virus type 1 DNA in endoneurial fluid and posterior auricular muscle has been documented).

The incidence rate of this disorder is about 23 per 100,000 annually, or about 1 in 60 or 70 persons in a lifetime.

Clinical suspicion

The patient may have been exposed to a mild draft or a common infection. Usually begins with mild pain behind the ear, followed within several hours by paralysis of the muscles supplied by the facial nerve. 


Lower motor neuron lesion of facial nerve (whole face on one side shows weakness of the facial muscles) accompanied by unilateral loss of taste (chorda tympani).


One very important aspect in the treatment of Bell’s palsy is to prevent corneal ulceration. This can be accomplished by the use of paper tape to depress the upper eyelid during sleep and prevent corneal drying. Massage of the weakened muscles may also be useful.

A course of glucocorticoids, given as prednisone 60 to 80 mg daily during the first 5 days and then tapered over the next 5 days, appears to shorten the recovery period and modestly improve the functional outcome. In one double-blind study, patients treated within 3 days of onset with both prednisone and acyclovir (400 mg five times daily for 10 days) had a better outcome than patients treated with prednisone alone.

N.B. note that in facial palsy laughter is preserved because it is supplied by extrapyramidal fibers (as it is an emotion) just as crying is present in dysarthric patients.


Recovery usually begins within 2 months, and within 9 months to 1 year. 80% of patients report virtually normal function.

Electromyography may be of some prognostic value; evidence of denervation after 10 days indicates that there has been axonal degeneration and that there will be a long delay (3 months, as a rule) before regeneration occurs and that it may be incomplete. The presence of incomplete paralysis in the first week is the most favorable prognostic sign.

Previous: Acute autoimmune brachial plexopathy Next: Carpal tunnel syndrome

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