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Write a short note on Bell's palsy.

General Medicine · Final Professional

Definition

Bell's palsy is an acute, idiopathic, unilateral lower motor neurone facial nerve palsy, and is the commonest cause of acute facial paralysis, accounting for around 70% of cases. It is a diagnosis of exclusion, made when no other cause is identified.

Aetiology

The prevailing view is reactivation of latent herpes simplex virus type 1 in the geniculate ganglion, producing inflammation and oedema of the nerve within the narrow facial canal, causing compression and ischaemic demyelination. Risk is increased in pregnancy (especially the third trimester), diabetes mellitus, hypertension, obesity and immunosuppression.

Anatomy That Explains the Signs

The facial nerve supplies the muscles of facial expression, carries taste from the anterior two-thirds of the tongue (chorda tympani), supplies the stapedius, and carries parasympathetic fibres to the lacrimal and salivary glands. The level of the lesion determines the additional features — a lesion proximal to the chorda tympani causes loss of taste; proximal to the nerve to stapedius causes hyperacusis; and involvement of the greater petrosal nerve causes reduced tearing.

Clinical Features

Abrupt onset, typically progressing over hours and maximal within 72 hours.
Unilateral facial weakness involving the WHOLE side of the face, including the forehead — the patient cannot wrinkle the forehead or close the eye on the affected side.
Bell's phenomenon — the eyeball rolls upwards on attempted eye closure, exposing the sclera.
Loss of the nasolabial fold, drooping of the angle of the mouth, drooling, difficulty with speech articulation, and food collecting in the cheek.
Hyperacusis (loss of stapedius damping), loss of taste over the anterior two-thirds of the tongue, and reduced lacrimation, depending on the level of the lesion.
Pain behind the ear for a day or two before or with the onset — common and often the first symptom.
Incomplete eye closure with exposure keratitis — the main risk to the patient's long-term wellbeing.

DANGER / REMEMBER

The single most important clinical decision is whether the forehead is spared. In an upper motor neurone (supranuclear) lesion — a stroke — the forehead is SPARED, because the upper facial muscles receive bilateral cortical innervation; the patient can wrinkle the forehead and close the eye, and emotional facial movement may be preserved. Lower motor neurone lesions involve the whole hemiface. A patient with facial weakness sparing the forehead has had a stroke until proved otherwise and must be managed as such, not treated as Bell's palsy.

DIFFERENTIAL DIAGNOSIS — features that make it NOT Bell's palsy

Bilateral facial palsy — GBS, sarcoidosis, Lyme disease, HIV, leukaemia, leprosy.
Vesicles in the external auditory canal or pinna with severe pain — Ramsay Hunt syndrome (herpes zoster oticus), which has a worse prognosis and requires antivirals.
Gradual onset or progression beyond 3 weeks, or no recovery by 4 months — suspect a tumour (parotid malignancy, cerebellopontine angle tumour, cholesteatoma).
Other cranial nerve involvement or limb signs — brainstem lesion.
Parotid mass — parotid malignancy infiltrating the nerve.
Recurrent palsy — consider tumour, sarcoidosis, or Melkersson–Rosenthal syndrome (recurrent facial palsy, facial oedema, fissured tongue).
Trauma, otitis media, diabetes and hypertension as contributory factors.

Investigations

Typical Bell's palsy requires no investigation. Investigate when atypical features are present:

Blood glucose and HbA1c, blood pressure — commonly associated and worth checking in all.
Serology for Lyme disease (in endemic areas), HIV, and VZV.
MRI brain with contrast — for atypical presentation, progression, no recovery, other cranial nerve involvement or suspected mass.
Nerve conduction studies and electroneuronography after 1–2 weeks in severe cases, to assess the degree of degeneration and prognosis.
Slit lamp examination if there is any corneal concern.

Management

1. Corticosteroids — the key treatment

Oral prednisolone, started within 72 hours of onset, significantly improves the rate and completeness of recovery. This is the intervention with the strongest evidence, and the window matters — the earlier the better.

2. Antivirals

Aciclovir or valaciclovir added to steroids may confer modest additional benefit in severe or complete palsy, and are definitely indicated in Ramsay Hunt syndrome. They are not recommended as monotherapy.

3. EYE CARE — the most important practical measure

Corneal exposure is the one complication that can cause permanent harm.

Artificial tears frequently during the day and lubricating ointment at night.
Tape or patch the eye closed at night; protective glasses outdoors.
Urgent ophthalmology referral for any redness, pain or visual disturbance.

4. Supportive

Facial exercises and massage; reassurance about the very good prognosis; analgesia for the retroauricular pain; and psychological support, since facial disfigurement is distressing.

5. For incomplete recovery — physiotherapy, botulinum toxin for synkinesis and contracture, and surgical procedures (tarsorrhaphy, gold weight implant, facial reanimation) in selected patients.

Prognosis

Excellent — 70–85% recover completely, most beginning to improve within 3 weeks and completing recovery by 3–4 months. Recovery is less complete with complete palsy at onset, older age, diabetes, hypertension, severe pain, and Ramsay Hunt syndrome. Complications of incomplete recovery include synkinesis (involuntary co-movement, such as eye closure on smiling), crocodile tears (gustatory lacrimation from aberrant regeneration), contracture and hemifacial spasm.

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