Bell's Palsy — Presentation, Diagnosis, and Management

Bell’s palsy is idiopathic facial palsy — a rapid, unilateral, lower motor neuron paralysis of the facial nerve with no identifiable cause. It is the most common cause of acute unilateral facial paralysis, and it is a diagnosis of exclusion: the label is only applied once central lesions (stroke, tumour), infections (Lyme, Ramsay Hunt), autoimmune disease (Guillain–Barré, multiple sclerosis), and metabolic causes have been considered and ruled out. Because it is a peripheral (lower motor neuron) palsy, it weakens the whole half of the face — including the forehead — which is the first clue that separates it from a central cause (see localising a facial nerve palsy for the anatomical basis).

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Aetiology and pathophysiology

The leading proposed cause is reactivation of a latent herpes simplex virus type 1 (HSV-1) infection. The mechanism of injury is an inflammatory one — inflammation, oedema, and consequent compression of the nerve within its bony canal. The critical site is the labyrinthine segment of the facial nerve: its entrance, the meatal foramen, is the anatomically narrowest part of the fallopian (facial) canal, so a swollen nerve is squeezed hardest there. Causation is a leading theory rather than a settled fact — the HSV-1 attribution is the current best explanation, not proof.

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Clinical presentation

Onset is rapid, reaching its peak within 48–72 hours. The patient develops twitching, weakness, or complete paralysis of one side of the face. As a lower motor neuron lesion, the forehead is involved — on the House–Brackmann scale, higher grades (IV–VI) show no forehead movement, whereas a central (upper motor neuron) lesion tends to spare it.

Because the facial nerve carries more than motor fibres, the branches given off along its course produce associated features that also help localise the problem:

• Reduced lacrimation — a dry eye (greater petrosal nerve).
• Altered taste — the chorda tympani. (In diabetic patients, taste is often spared, suggesting the lesion sits distal to the chorda tympani.)
• Hyperacusis — sensitivity to loud sounds, from loss of the nerve to stapedius.
• Post-auricular pain / otalgia — often precedes or accompanies the weakness.

Bell’s palsy is more common in patients with diabetes.

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When it is not Bell’s palsy — red flags

Bell’s palsy is a diagnosis of exclusion, so the features that argue against it matter as much as those that fit. Each of the following should prompt MRI (with gadolinium) to look for another cause:

• No recovery by 4–6 months — mandates imaging to exclude neoplastic pathology.
• Bilateral facial paralysis — seen in fewer than 1% of Bell’s palsy; its presence warrants MRI.
• Recurrent paralysis — a red flag for a tumour or for Melkersson–Rosenthal syndrome.
• Additional cranial neuropathy — any other cranial nerve involvement points away from Bell’s palsy.

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Diagnosis and investigations

Bell’s palsy is a clinical diagnosis of exclusion; in the typical, new-onset case, routine laboratory tests and routine imaging are not required. Investigations are directed by the clinical picture:

• Serology — Lyme disease testing where there is a history of tick exposure; serum/CSF angiotensin-converting enzyme (ACE) if sarcoidosis is suspected.
• MRI with gadolinium — for the red-flag situations above (no recovery at 4–6 months, bilateral, recurrent, or additional cranial nerves).
• CT — when a neoplastic process is suspected, or for pre-operative planning of decompression.
• Electrodiagnostics — electroneuronography (ENoG) can be obtained from about 72 hours after onset and is the most accurate prognostic indicator within the first two weeks; electromyography (EMG) identifies voluntary motor units, with fibrillation potentials suggesting degeneration and polyphasic potentials suggesting reinnervation. These are reserved for patients with complete paralysis — they add little in incomplete palsy.

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Grading

Facial function is documented on the House–Brackmann scale, from Grade I (normal) to Grade VI (total paralysis). Grade is both the shared language for describing the palsy and, tracked over time, the measure of recovery.

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Management

Management is guideline-led (the AAO-HNS Clinical Practice Guideline) and centres on three things:

• Oral corticosteroids — the one intervention with clear benefit. Recommended within 72 hours of onset for patients aged 16 and over — high-dose prednisone (around 1 mg/kg) for roughly 10 days. In the landmark randomised trial, early prednisolone raised the proportion recovering facial function from about 64% to 83% at 3 months.
• Antivirals — not on their own. Antiviral monotherapy is not recommended; the trial evidence shows no benefit from acyclovir given alone, and only a possible small additional benefit when combined with steroids. Antivirals are used in immunocompromised patients.
• Eye protection — imperative. With impaired eye closure the cornea is at risk of exposure keratitis: ocular lubricants, daytime coverage, and taping/patching of the eye at night.

Surgical decompression of the nerve is controversial and carries no formal guideline recommendation for or against. Where it is considered, it is for the small subset with the worst electrophysiology — >90% degeneration on ENoG and no motor units on EMG within two weeks — and, in the trial data, must be performed within two weeks of the onset of total paralysis to be effective.

Detailed treatment decisions are for the treating clinician; this page summarises published guidance and is not a substitute for it.

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Prognosis

The outlook is generally good, and steroids improve it:

• With early prednisolone, about 83% recover facial function by 3 months and 94% by 9 months (versus roughly 64% and 82% without).
• The degree of degeneration on ENoG is the key prognostic marker: patients with less than 90% degeneration are expected to recover partially or fully, while those exceeding 90% within two weeks have a higher risk of a poor outcome. In one multicentre trial, severe cases (>90% degeneration) treated with steroids alone had about a 42% chance of a good result (House–Brackmann I–II), rising to 91% in those who underwent decompression within two weeks.
• Synkinesis — involuntary movement accompanying voluntary movement — is the characteristic long-term complication; it can be managed with botulinum toxin.

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Differential diagnosis

Because Bell’s palsy is defined by exclusion, the alternatives must be actively considered:

Condition	The distinguishing feature
Ramsay Hunt syndrome	Severe otalgia + vesicular rash on the ipsilateral ear/face (present in up to 80%)
Stroke	Other ipsilateral cranial nerve palsies; central pattern
Tumour (CPA mass, facial neuroma)	Facial paralysis as the sole symptom is rare; usually other structures involved
Lyme disease	Erythema chronicum migrans rash and a flu-like illness; tick exposure
Sarcoidosis	Non-caseating granulomas in multiple organs (commonly the lungs)
Multiple sclerosis	CSF oligoclonal bands; serial MRI
Melkersson–Rosenthal syndrome	Triad of recurrent facial palsy, lip swelling, and a furrowed tongue
Guillain–Barré syndrome	Weakness begins distally and ascends

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Frequently Asked Questions

Why is Bell’s palsy called a diagnosis of exclusion? Because there is no confirmatory test — the label is only applied after other causes of facial weakness (stroke, tumour, Ramsay Hunt, Lyme, sarcoidosis, and others) have been considered and excluded on history, examination, and, where indicated, investigation. Not everyone with a facial palsy has Bell’s palsy.

How do you tell Bell’s palsy from a stroke? Bell’s palsy is a lower motor neuron lesion, so it weakens the whole half of the face, forehead included. A stroke is an upper motor neuron lesion and tends to spare the forehead, and it is usually accompanied by other neurological signs. Any additional cranial nerve involvement argues against Bell’s palsy and warrants imaging.

Do steroids actually help, and when should they be given? Yes — corticosteroids are the one treatment with clear evidence of benefit. They should be started within 72 hours of onset in patients aged 16 and over. In the landmark randomised trial, early prednisolone raised the 3-month recovery rate from about 64% to 83%.

Should antivirals be prescribed? Not by themselves. Antiviral monotherapy is not recommended and shows no benefit in the trial evidence; there may be a small additional benefit when combined with steroids, and antivirals are used in immunocompromised patients — but steroids are the mainstay.

What is the chance of full recovery? Good, especially with early steroids — roughly 83% recover by 3 months and 94% by 9 months. The strongest predictor of a poor outcome is more than 90% degeneration on electroneuronography (ENoG) within the first two weeks.

Why does the eye need protecting? If the eye cannot close fully, the cornea is exposed and at risk of drying and keratitis. Lubricating drops or ointment, daytime coverage, and taping the eye closed at night protect it while function recovers.