Clinical: The Basics - Understanding and care of Bell's palsy

Diagnosis of Bell's palsy is usually made on presentation, as Dr Honor Merriman explains.

Bell's palsy is named after Sir Charles Bell, a Scottish surgeon who studied the facial nerve and its innervation of the facial muscles 200 years ago.

The facial nerve provides the motor supply to the muscles of the face.

When the nerve is damaged, the most obvious presentation is weakness of the muscles of facial expression leading to failure to close the eye on the affected side and an asymmetrical smile - the corner of the mouth droops on the affected side.

The symptoms and signs appear over hours or days, and damage to the nerve (lower motor neurone disease or LMN) needs to be distinguished from damage to the brain (upper motor neurone disease or UMN).

UMN lesions are commonly caused by cerebrovascular disease and multiple sclerosis, or by less common disorders such as syphilis and HIV.


The facial nerve supplies not only the muscles of facial expression but is also the nerve supply to the lacrimal gland, salivary glands, taste receptors on the tongue and the stapedius muscle in the middle ear.

So the immediate clinical picture will be of facial asymmetry, eyebrow droop, loss of forehead and nasolabial folds, drooping of the corner of the mouth, inability to close the eye, inability to keep the lips tightly together and there is difficulty keeping food in the mouth.

Rarely, cases are bilateral and these are non-idiopathic. There are several possible causes including sarcoidosis and Guillain-Barre's syndrome.

Other features include pain near the mastoid process (50 per cent), excess tear formation (33 per cent), hyperacusis (effect on stapedius), and lacrimation is mildly affected in some patients. Taste is not clinically significantly changed in most patients.

Sensory loss is present on the face or tongue in a few cases - on the side of the paralysis - which is possibly related to involvement of the greater superficial petrosal nerve.

Most commonly no cause is found. However, it is important to be aware that in a few cases there may be a cause that should be investigated.

Prevalence and diagnosis

There is a lifetime prevalence of 6.4-20 per 1,000 and the incidence increases with age. The overall incidence is 0.5 per 1,000 per year, at age 20 this is 0.1 per 1,000 per year and at age 80 the incidence is 0.6 per 1,000 per year. It is equally common in men and women.

Recurrence occurs in 7 per cent. The right side is affected in 63 per cent of cases. There is an increased incidence with diabetes and in pregnant women.

The prognosis is better if there is incomplete paralysis, early improvement - in a few weeks - slow progression, occurrence is at a younger age (<60 years), and if salivary flow and taste are normal.

The prognosis is worse if there are no signs of recovery in three weeks, when associated with Ramsay Hunt's syndrome, or there is an association with hypertension, diabetes or pregnancy.

The diagnosis is usually made on clinical features but serology may be helpful if Lyme disease or herpes zoster are suspected. Paired samples of sera - over four weeks - are needed, so may not help in initial management.

If there is concern that the palsy may be due to a tumour, neurological disease or middle ear disease, specialist referral is needed.

Treatment in primary care

Mild cases where paralysis is minor and no underlying cause is suspected need no medication, although the cornea on the affected side should be protected by a pad at night and artificial tears.

Medication may be helpful, although recent Cochrane reviews have questioned how effective either steroids and/or antivirals can be.

A recent article in the BMJ suggests that patients should be started on both antivirals and oral steroids to counteract the effects of occult herpes virus infection and to reduce swelling and inflammation around the nerve. This regimen is not accepted as best practice by all.

However there is agreement on some aspects of medication. There is more benefit if treatment is started within three days of onset. There is no benefit from treatment starting more than 10 days after onset.

Corticosteroids should be commenced within one week of onset. Adults should be given prednisolone 1mg/kg/day to a maximum of 80mg/day, in divided doses, for seven days. After the initial dosage taper off over 7-10 days.

Aciclovir should be used within three days of onset at a dosage of 800mg five times a day for five days in adults. Aciclovir is more effective in Ramsay Hunt's syndrome.An alternative antiviral is valaciclovir.

- Dr Merriman is a GP in Oxford.

More common causes of LMN seventh nerve damage
- Herpes virus type 1
- Herpes zoster
- Ramsay Hunt's syndrome, typical lesions can be seen on the ear, palate
and tongue on the affected side
- Lyme disease
- Otitis media or cholesteatoma

Uncommon causes
- Posterior fossa tumours
- Guillain-Barre's syndrome
- Sarcoidosis
- Parotid gland tumours


Lower motor neurone disease

- Patient cannot wrinkle forehead.

- Nerve damage in posterior fossa, bony canal, middle ear or outside skull.

Upper motor neurone disease

- Can move muscles of forehead because of alternative nerve pathways in the brainstem.

- CVA may cause loss of voluntary facial movement but involuntary movements (e.g. smiling) may be preserved.


- The most useful patient leaflets may be found at

- BUPA also publish a simple patient guide:

- The Bell's Palsy Association also offers support, particularly for patients who have a slow recovery:

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