Bell Palsy
Acute unilateral LMN facial nerve (CN VII) palsy of unknown cause (diagnosis of exclusion). Affects all muscles of facial expression on one side (forehead included — distinguishes from UMN lesion). Annual incidence ~20-30 per 100,000. Most recover spontaneously. Prednisolone within 72 hours improves outcomes.
Key Facts
Acute idiopathic LMN facial nerve palsy: diagnosis of exclusion; incidence ~20-30 per 100,000/year; peak age 15-45; equal sex; right = left LMN pattern: affects ALL muscles of facial expression on one side — including forehead (forehead sparing = UMN lesion); inability to close eye, loss of nasolabial fold, drooping mouth Distinguish from UMN facial weakness: UMN (stroke) spares forehead (bilateral UMN innervation of frontalis); LMN (Bell) affects entire ipsilateral face Likely cause: HSV-1 reactivation in geniculate ganglion → inflammation and oedema of CN VII within temporal bone (narrow fallopian canal) Treatment (NICE CKS): prednisolone 50mg OD × 10 days (or 60mg × 5 days then taper) started within 72 hours of onset; eye protection (artificial tears, tape at night) Prognosis: ~70% make full recovery without treatment; >90% with early prednisolone; ~15% have permanent residual weakness
Overview
Key Facts
Bell palsy is the commonest cause of acute facial nerve palsy. It is a diagnosis of exclusion — other causes must be considered. Early corticosteroids significantly improve outcome.
Epidemiology
Incidence ~20-30 per 100,000/year. Equal sex distribution. Peak age 15-45 years. More common in pregnancy (3rd trimester/early postpartum) and diabetes.
Aetiology
- Idiopathic by definition, but HSV-1 reactivation in the geniculate ganglion is the leading hypothesis
- Swelling of CN VII within the bony fallopian canal → nerve compression → demyelination ± axonal degeneration
- Risk factors: pregnancy, diabetes, family history, upper respiratory infection
Pathophysiology
Viral reactivation (HSV-1) in the geniculate ganglion → inflammation → oedema of the facial nerve within the rigid fallopian canal → nerve compression → ischaemia → demyelination (neuropraxia in mild cases) or axonal degeneration (in severe cases). Neuropraxia: good prognosis (recovery in weeks). Axonal degeneration: slower, incomplete recovery (months); risk of synkinesis (aberrant reinnervation).
Clinical Presentation
Typical Presentation
- Acute onset (hours to 1-2 days): unilateral facial weakness affecting ALL muscles of ipsilateral face
- Forehead involved: inability to raise eyebrow, wrinkle forehead (KEY distinguishing feature from UMN)
- Eye closure weakness: inability to close eye (lagophthalmos) → corneal exposure → risk of corneal ulceration
- Loss of nasolabial fold: drooping of ipsilateral mouth corner
- Mouth drooping: drooling, difficulty eating/drinking
- Postauricular/mastoid pain: may precede weakness by 1-2 days (~50%)
Associated Features
- Hyperacusis (stapedius muscle paralysis)
- Altered taste (anterior 2/3 of tongue — chorda tympani involvement)
- Reduced lacrimation (greater petrosal nerve involvement)
- Dry mouth (submandibular/sublingual gland — chorda tympani)
Red Flags (NOT Bell Palsy)
- Bilateral facial palsy → sarcoidosis, GBS, Lyme disease
- Gradual onset (>2 weeks) → tumour (parotid, CPA schwannoma)
- Associated vesicles in ear (Ramsay Hunt syndrome — VZV)
- Other cranial nerve involvement → brainstem lesion, skull base pathology
- Failure to improve by 3-4 months → reconsider diagnosis
Differential Diagnosis
| Diagnosis | Key Features | Investigation |
|---|---|---|
| Stroke (UMN facial weakness) | Forehead SPARED, associated limb weakness, speech disturbance | CT/MRI brain |
| Ramsay Hunt syndrome (VZV) | Vesicles in ear/palate, severe pain, worse prognosis than Bell | VZV PCR, clinical |
| Lyme disease | Tick exposure, erythema migrans, bilateral palsy possible | Lyme serology |
| Parotid tumour | Gradual onset, parotid mass, selective branch involvement | USS/MRI parotid |
| Cholesteatoma/otitis media | Ear discharge, hearing loss, chronic ear disease | Otoscopy, CT temporal bone |
| Sarcoidosis (Heerfordt syndrome) | Bilateral palsy, parotid swelling, uveitis, fever | ACE, CXR, biopsy |
Diagnosis / Investigation
Clinical Diagnosis
- Bell palsy is a clinical diagnosis of exclusion
- No routine investigations required for typical presentation in a young, otherwise healthy patient
When to Investigate
- Atypical features: bilateral, gradual onset, recurrent, other CN involvement, vesicles
- Lyme serology: if risk factors (tick exposure, endemic area)
- MRI brain/temporal bone: if progressive, no improvement by 3 months, suspected tumour
- Blood glucose/HbA1c: screen for diabetes (associated)
- Pregnancy test: if appropriate
- VZV serology: if vesicles present (Ramsay Hunt)
Grading
- House-Brackmann scale: grades I (normal) to VI (total paralysis); guides prognosis and treatment assessment
Management
Pharmacological (NICE CKS)
- Prednisolone 50mg OD × 10 days (or 25mg BD × 10 days; or 60mg × 5 days then taper over 5 days): started within 72 hours of onset; NNT ~10 for complete recovery
- Antivirals: aciclovir 400mg 5×/day or valaciclovir 1g TDS × 7 days — NO proven benefit for Bell palsy when added to steroids (but use for Ramsay Hunt syndrome); NICE does not recommend routine antiviral for Bell palsy
Eye Protection (Essential)
- Artificial tears (hypromellose drops): during the day for corneal dryness
- Eye ointment (Lacri-Lube): at night
- Tape eyelid closed at night (micropore tape)
- Moisture chamber (cling film over eye): if severe lagophthalmos
- Urgent ophthalmology referral if corneal symptoms (pain, redness, visual change)
Physiotherapy
- Facial exercises (gentle) once some recovery begins
- Avoid aggressive electrical stimulation (may worsen synkinesis)
Surgical (Rare)
- Tarsorrhaphy: if persistent lagophthalmos and corneal risk
- Facial nerve decompression: controversial; not standard practice
- Facial reanimation surgery: for severe permanent paralysis (nerve grafts, muscle transfers)
Referral Criteria
- ENT/neurology: atypical features, no improvement by 3 months, complete paralysis at onset (HB grade VI)
- Ophthalmology: corneal complications
- Plastic surgery: if permanent severe paralysis requiring reanimation
Prognosis
~70% make full recovery without treatment. With prednisolone within 72 hours: >90% recover completely. Incomplete paralysis: ~95% full recovery. Complete paralysis: ~60-70% full recovery. Recovery usually begins within 3 weeks; most recovery by 3 months. ~15% have permanent residual weakness. ~5% develop synkinesis (involuntary movement of one facial region during voluntary movement of another — e.g., eye closure when smiling). Ramsay Hunt syndrome: worse prognosis than Bell palsy (~50% full recovery).
Other Relevant Information
House-Brackmann Facial Nerve Grading
| Grade | Description | Recovery |
|---|---|---|
| I | Normal | — |
| II | Slight weakness, complete eye closure | Good |
| III | Obvious weakness, complete eye closure | Good |
| IV | Obvious weakness, incomplete eye closure | Moderate |
| V | Barely perceptible movement | Poor |
| VI | Total paralysis | Poor |
UMN vs LMN Facial Weakness
| Feature | UMN (Stroke) | LMN (Bell Palsy) |
|---|---|---|
| Forehead | SPARED (bilateral UMN supply) | AFFECTED |
| Pattern | Lower face only | Entire ipsilateral face |
| Eye closure | Preserved | Impaired |
| Associated features | Limb weakness, speech | Hyperacusis, taste change |
| Onset | Sudden (stroke) | Acute (hours) |