01OverviewDefinition, clinical context and the essential points that orientate the chapter.
The facial nerve supplies muscles of facial expression and carries parasympathetic and sensory fibres through a long intracranial, temporal-bone and extracranial course. A lesion at or distal to the facial nucleus weakens the ipsilateral forehead, eyelid and lower face. A supranuclear hemispheric lesion often produces predominantly contralateral lower-face weakness because upper facial motor nuclei receive more bilateral input. Brainstem lesions can affect the facial nucleus or fascicle while also producing gaze, long-tract or cerebellar signs.
Bell palsy presents as rapid unilateral peripheral-pattern weakness without a better cause. Patients may report peri-auricular discomfort, altered taste, sound sensitivity or a subjective numb feeling, but objective trigeminal sensory loss is atypical. The diagnosis is weakened by gradual progression beyond several days, recurrent palsy on the same side, bilateral involvement, palpable mass, persistent severe pain, ear or skin vesicles, hearing loss, other cranial nerves, limb signs or constitutional disease.
Eye harm is preventable. Weak orbicularis oculi causes exposure, reduced blink and drying; altered tearing or corneal sensation increases risk. Ask about grittiness, photophobia, pain and visual blur and inspect closure and corneal clarity. Ophthalmology involvement is urgent for ocular symptoms, reduced corneal sensation, pre-existing eye disease, poor Bell phenomenon, severe exposure or uncertainty about protection.
Most people improve, but recovery varies with initial severity and axonal injury. Persistent weakness can cause synkinesis, crocodile tears, facial tightness and psychosocial distress. Follow-up should not simply wait for movement: reassess the original diagnosis, eye safety and onset of recovery, and refer persistent or progressive cases for facial-nerve, ENT, neurology or ophthalmic expertise.
Key points
- Bell palsy is an acute idiopathic unilateral lower motor neurone facial-nerve palsy diagnosed after excluding a recognisable alternative; symptoms usually evolve over hours and reach maximum within seventy-two hours.
- Observe eyebrow elevation, gentle and forced eye closure, nasolabial fold and smiling or showing teeth. True peripheral weakness affects upper and lower face on the same side, although effort and baseline asymmetry must be considered.
- Forehead sparing with lower facial weakness suggests a contralateral supranuclear lesion, but this is a localisation clue rather than a stand-alone stroke exclusion rule.
- Ask about exact onset, limb or speech symptoms, diplopia, vertigo, hearing change, dysphagia, severe headache, ear pain or vesicles, rash, tick exposure, trauma, surgery, parotid swelling, cancer and previous episodes.
- Examine all cranial nerves, limbs and coordination, and inspect the external ear, canal, tympanic region, oral cavity, parotid and skin. An isolated facial examination can miss brainstem or skull-base disease.
- Corneal protection begins immediately when closure is incomplete: frequent preservative-free lubricating drops by day, lubricating ointment and eyelid closure at night according to local eye-care advice.
- Oral corticosteroid started within seventy-two hours improves the chance of complete recovery in adults with Bell palsy when contraindications and individual risks are addressed.
- Do not use antiviral treatment alone for Bell palsy. Combined antiviral and steroid treatment is considered selectively through current local guidance, particularly in severe complete palsy or suspected herpetic disease.
- Ramsay Hunt syndrome may cause facial palsy with severe ear pain, vesicles in the canal, pinna or palate, hearing loss or vertigo; vesicles can appear after weakness and absence at first examination does not guarantee Bell palsy.
- Routine imaging or broad blood panels are unnecessary for a classic first isolated Bell palsy, but atypical tempo, recurrence, bilateral disease, other nerves, systemic features or failure to recover warrants specialist investigation.
- Document function and severity with a recognised scale where used locally, photograph only with consent on an approved clinical system and arrange follow-up of eye closure and neurological recovery.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Idiopathic inflammatory facial neuropathy
Bell palsy is an acute peripheral facial-nerve palsy without an identified alternative, thought to involve inflammatory swelling within the temporal bone facial canal.
Herpes-family infection
Varicella-zoster reactivation causes Ramsay Hunt syndrome, while herpes simplex may contribute to some idiopathic palsies; vesicles, severe ear pain, hearing loss or vertigo favour zoster.
Structural, infective and traumatic disease
Ear or mastoid infection, parotid or skull-base tumour, Lyme disease after relevant exposure, trauma and surgery can injure the nerve along its long course.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Facial-nerve inflammation
Immune or infectious injury causes oedema of the facial nerve, particularly where it traverses the narrow bony canal in the temporal bone.
- 2Conduction block or axonal loss
Compression and inflammation impair motor conduction; mild neurapraxia recovers rapidly, while axonal degeneration produces complete weakness, denervation and slower regrowth.
- 3Muscle and secretomotor dysfunction
Denervation weakens the ipsilateral forehead, eyelid and lower face and may disturb taste, lacrimation or sound tolerance depending on lesion level.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Rapid unilateral weakness of forehead, eye closure and mouth without other objective neurology, ear vesicles, parotid mass or progressive systemic illness supports Bell palsy after a focused exclusion assessment.
Predominantly lower facial weakness with relatively preserved forehead movement, especially with contralateral limb deficit, aphasia, neglect, gaze or field abnormality, supports an acute cerebral lesion and demands stroke assessment.
Peripheral facial palsy with prominent otalgia, vesicles in or around the ear or palate, hearing loss or vestibular symptoms suggests varicella-zoster reactivation. Early lesions may be subtle or delayed.
An ipsilateral peripheral-pattern facial weakness accompanied by abduction or gaze disturbance, contralateral limb signs, ataxia or altered facial sensation localises to the pons rather than an isolated extracranial nerve.
Slow progression, recurrent same-side weakness, facial pain, multiple branch involvement, a parotid mass, other cranial neuropathies or cancer history suggests neoplastic, infiltrative or compressive disease.
Bilateral palsy is not typical Bell palsy and raises inflammatory neuropathy, sarcoidosis, infection, brainstem disease, malignancy and systemic causes; assess limb reflexes, respiratory and bulbar function urgently.
Incomplete blink or closure with redness, foreign-body sensation, photophobia, pain, epithelial haze or reduced vision indicates corneal surface injury and requires urgent eye-service advice.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Complete neurological and cranial-nerve examinationFirst step - Why
- Confirm the distribution of facial weakness and identify supranuclear, brainstem, multifocal or systemic neurological disease.
- Interpretation and limitations
- Record each facial region and eye closure plus speech, gaze, hearing, palate, tongue, limbs and coordination. Forehead movement is helpful but cannot safely overrule accompanying stroke features.
- 02
Ear, oral, skin and parotid examination - Why
- Find zoster lesions, otitis or cholesteatoma, trauma, tumour and local inflammatory causes along the facial-nerve course.
- Interpretation and limitations
- Inspect canal, pinna and palate with adequate light and palpate the parotid and neck. Re-examine if severe otalgia persists because vesicles may follow initial weakness.
- 03
Ocular-surface and closure assessment - Why
- Determine exposure risk and whether same-day ophthalmic treatment is needed.
- Interpretation and limitations
- Observe spontaneous and forced closure and ask about pain, photophobia and blur. Fluorescein assessment and corneal sensation require appropriate competence; symptoms or epithelial damage mandate eye review.
- 04
Glucose or HbA1c and targeted blood tests - Why
- Investigate diabetes or specific infectious, inflammatory and systemic causes only when history or atypical features support them.
- Interpretation and limitations
- Routine broad serology in a classic first palsy has low yield. Bilateral disease, tick exposure, systemic inflammation, pregnancy or recurrent neuropathies justifies a tailored plan with specialist advice.
- 05
MRI brain, internal auditory canal or facial-nerve pathway - Why
- Evaluate progressive, recurrent, multifocal or non-recovering palsy and suspected brainstem, skull-base or parotid disease.
- Interpretation and limitations
- Imaging is selected by lesion level and urgency. Non-specific facial-nerve enhancement may occur in Bell palsy and should not distract from a concerning clinical course.
- 06
Electroneurography or facial electromyography - Why
- Characterise severe axonal injury, prognosis and reinnervation in selected complete or persistent palsies.
- Interpretation and limitations
- Timing strongly affects yield and routine early testing is unnecessary. Facial-nerve specialists decide when results will change decompression, rehabilitation or reanimation planning.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Supranuclear stroke
Predominant contralateral lower-face weakness with limb, language, gaze or sensory signs supports a cerebral lesion, although forehead sparing is not an infallible rule.
Ramsay Hunt syndrome
Severe ear pain, vesicles in the canal, pinna or palate, hearing change or vertigo favours zoster; lesions may appear after facial weakness begins.
Ear, parotid or skull-base lesion
Gradual progression, recurrence on the same side, a palpable mass, hearing loss or multiple cranial neuropathies should prompt targeted imaging and specialist assessment.
Lyme or systemic neuropathy
Bilateral palsy, relevant tick exposure, meningitic symptoms or other neuropathies broadens assessment beyond a first isolated idiopathic facial palsy.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Acute isolated peripheral patternTreat Bell palsy early and protect visionFirst stepAlternativeUnilateral upper and lower facial weakness reaching maximum within seventy-two hours, with no alternative features after examination.+
- 1Confirm onset and exclusion features, examine all cranial nerves and limbs, inspect ear, palate and parotid, and assess corneal closure and symptoms before applying the Bell palsy label.
- 2Start an appropriate oral corticosteroid within seventy-two hours when safe, institute preservative-free lubrication and night closure measures, and follow local advice on selective antiviral addition.
- 3Give written eye and neurological safety-netting and arrange follow-up of closure and recovery; refer if progression continues, no improvement begins in the expected interval or function remains incomplete.
02Stroke or brainstem concernDo not let forehead movement delay imagingSudden facial weakness accompanies limb, language, visual, gaze, coordination or conscious-level abnormality, or onset is uncertain.+
- 1Perform ABCDE, glucose and a concise stroke examination, establish last known well, deficit severity, anticoagulation and pre-event function and activate the local stroke service immediately.
- 2Proceed to urgent brain and vascular imaging selected by the stroke pathway, including posterior-circulation assessment when a peripheral-pattern palsy has crossed or ocular signs.
- 3Follow specialist reperfusion, antithrombotic, swallow and observation decisions and reconsider additional peripheral pathology only after time-critical cerebral care is protected.
03Atypical or persistent palsySearch along the entire nerveGradual onset, recurrent same-side or bilateral palsy, severe pain, vesicles, hearing loss, mass, other nerves, systemic disease or incomplete recovery.+
- 1Remap cranial and limb signs and examine ear, oral cavity, skin, parotid and neck; review trauma, surgery, malignancy, immune disease, infection, pregnancy and medication context.
- 2Refer to ENT, neurology, ophthalmology or a facial-nerve service according to level and eye risk, arranging targeted MRI, audiology, blood tests or neurophysiology rather than routine indiscriminate panels.
- 3Continue corneal protection and offer facial rehabilitation and psychosocial support while monitoring for synkinesis, contracture, exposure and a newly emerging diagnosis.
Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
Prednisolone for adult Bell palsy
Start within seventy-two hours: use either prednisolone 50 mg once daily for ten days, or 60 mg once daily for five days followed by a 10 mg daily reduction, according to local guidance.Review diabetes, infection, peptic-ulcer risk, severe hypertension, psychiatric history, pregnancy and interacting medicines; do not let steroid treatment substitute for stroke exclusion or ocular protection.
Preservative-free ocular lubricants
Use lubricating drops frequently while awake and a lubricating ointment at night, with dosing intensified to symptoms and ophthalmic advice while eyelid closure remains incomplete.Ointment blurs vision and taping or closure must not abrade the cornea; pain, photophobia, redness or reduced vision needs urgent examination rather than simply more lubricant.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Exposure keratopathy
Incomplete blink and eyelid closure dry the cornea, causing abrasion, ulceration, infection and potentially permanent visual loss unless protection is reliable.
Persistent weakness and contracture
Severe axonal injury may leave facial asymmetry, oral incompetence and tightness, affecting speech, eating, eye closure and social confidence.
Aberrant reinnervation
Regrowing fibres may connect to unintended muscles or glands, producing synkinesis, hemifacial spasm, crocodile tears and discomfort during facial movement.
Psychosocial distress
Visible asymmetry and impaired expression can affect identity, communication, mood and participation even when clinicians judge motor recovery as functionally adequate.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Recheck ability to close the eye gently and forcibly, blink quality, ocular symptoms and corneal appearance until exposure risk has resolved.
- Record facial movement by region and a recognised severity scale where used locally, noting the date recovery first becomes evident.
- Monitor glucose and steroid adverse effects in patients at risk, with medicine-specific sick-day and infection advice appropriate to the short course.
- Review for new vesicles, hearing loss, vertigo, other cranial neuropathies or limb signs that would overturn the original Bell palsy diagnosis.
- Refer persistent weakness for synkinesis, contracture, facial therapy and diagnostic reassessment rather than repeating unsupervised steroid courses.
- Safety-net severe headache, limb or speech symptoms, ocular pain, photophobia, visual loss, dysphagia and breathing difficulty with explicit emergency routes.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Subjective numbness is common
Patients may describe the weak side as numb because facial movement and sensory feedback feel altered. Reproducible trigeminal sensory loss is not a usual Bell palsy feature and widens localisation.
Vesicles can appear late
Zoster-related facial palsy may precede a visible eruption. Prominent otalgia, hearing or vestibular symptoms justify careful repeat ear and palate inspection and urgent specialist advice.
Eye closure deserves priority
Motor recovery takes time, whereas corneal epithelial injury can occur quickly. Lubrication, safe night closure and prompt ophthalmic escalation are active treatment rather than comfort extras.
Forehead sparing is imperfect
Some central lesions produce more extensive facial weakness and examination effort varies. Sudden onset and accompanying cortical, limb or gaze signs carry more weight than one eyebrow movement.
Synkinesis reflects miswiring
During axonal recovery, eye closure may accompany smiling or mouth movement may accompany blinking. Specialist facial therapy and selected treatments differ from management of persistent flaccid weakness.
Recurrence changes probability
A second episode can still be idiopathic, but recurrent same-side, bilateral or progressively incomplete recovery raises tumour, inflammation, infection and hereditary or metabolic causes.
11Common pitfallsFrequent interpretation and management errors.
- 01
Diagnosing Bell palsy from facial asymmetry without examining limbs, language, gaze and coordination.
- 02
Using preserved forehead movement as a reason to dismiss other acute stroke features.
- 03
Prescribing steroids while omitting corneal protection and explicit eye-symptom safety-netting.
- 04
Using antiviral monotherapy for an otherwise typical Bell palsy.
- 05
Failing to inspect the ear canal and palate when pain suggests zoster.
- 06
Repeating empirical treatment for gradual or recurrent same-side palsy instead of imaging the nerve pathway.
- 07
Assuming absent improvement is cosmetic only and missing eye injury or an alternative diagnosis.