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

DiagnosisKey FeaturesInvestigation
Stroke (UMN facial weakness)Forehead SPARED, associated limb weakness, speech disturbanceCT/MRI brain
Ramsay Hunt syndrome (VZV)Vesicles in ear/palate, severe pain, worse prognosis than BellVZV PCR, clinical
Lyme diseaseTick exposure, erythema migrans, bilateral palsy possibleLyme serology
Parotid tumourGradual onset, parotid mass, selective branch involvementUSS/MRI parotid
Cholesteatoma/otitis mediaEar discharge, hearing loss, chronic ear diseaseOtoscopy, CT temporal bone
Sarcoidosis (Heerfordt syndrome)Bilateral palsy, parotid swelling, uveitis, feverACE, 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

GradeDescriptionRecovery
INormal
IISlight weakness, complete eye closureGood
IIIObvious weakness, complete eye closureGood
IVObvious weakness, incomplete eye closureModerate
VBarely perceptible movementPoor
VITotal paralysisPoor

UMN vs LMN Facial Weakness

FeatureUMN (Stroke)LMN (Bell Palsy)
ForeheadSPARED (bilateral UMN supply)AFFECTED
PatternLower face onlyEntire ipsilateral face
Eye closurePreservedImpaired
Associated featuresLimb weakness, speechHyperacusis, taste change
OnsetSudden (stroke)Acute (hours)