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Neurology›Condition·Updated Jun 27, 2026·v1

Bell Palsy

Bell palsy is an acute, idiopathic, unilateral lower motor neuron facial nerve palsy. It is a clinical diagnosis of exclusion with excellent prognosis when treated early with prednisolone. Eye protection and recognition of red flags (stroke mimic, Ramsay Hunt syndrome, Lyme disease) are critical. Surgery is rarely indicated. Synkinesis and other sequelae are managed with botulinum toxin.

High Evidence38 references·948 words·4 min read·v1
Bell palsyfacial nerve palsyidiopathic facial paralysisHouse-Brackmannprednisolonestroke mimicRamsay Hunt syndromesynkinesisneurology

Quick Reference

RxDrug of choicePrednisolone 1 mg/kg/day (max 60 mg) PO × 7-10 days; start within 72 hours of onset.
AltAlternativesMethylprednisolone 1 g IV × 3 days (for severe cases or intolerant to oral); no advantage over oral prednisolone. Prednisone (bioequivalent).
⊘AvoidAntiviral monotherapy (acyclovir/valacyclovir without steroids), no benefit and delays effective treatment. Surgical decompression after 3 weeks or for incomplete paralysis, no benefit and risks complications.
DxTest of choiceClinical diagnosis. Electroneuronography (ENoG), CMAP ≤10% of unaffected side within 14 days predicts poor recovery and may guide consideration for decompression.
ScKey scoreHouse-Brackmann grading scale (I-VI), assesses severity and guides prognosis.
→When to referOphthalmology for corneal complications; otolaryngology/skull-base surgery if complete paralysis with >90% denervation within 14 days (possible decompression); neurology for atypical presentations, poor recovery, or synkinesis management.
Bell palsy is a clinical diagnosis of exclusion. Start prednisolone 1 mg/kg/day within 72 hours of onset, protect the eye, and do not routinely image or prescribe antivirals for mild cases. Recovery is excellent with early steroids (NNT = 7). Refer for surgical decompression only in complete paralysis with >90% denervation within 2 weeks.
Bell palsy is an acute, unilateral, peripheral facial nerve palsy of unknown etiology, causing rapid-onset weakness of facial expression. It is the most common cause of acute facial paralysis, with an annual incidence of 20-30 per 100,000 [5]. Early recognition and corticosteroid therapy improve outcomes.

Overview and Recommendations

Background

  • •Bell palsy is an acute, idiopathic, unilateral lower motor neuron facial nerve palsy, accounting for approximately 75% of all acute peripheral facial paralyses and affecting 20-30 per 100,000 persons annually worldwide. It carries significant functional and psychosocial morbidity during the acute phase, but complete spontaneous recovery occurs in about 70% of untreated patients within 3-6 months.
  • •The condition is named after Sir Charles Bell, the Scottish anatomist who first described the facial nerve's role in facial expression. It is also called idiopathic facial nerve palsy, a term that underscores its unknown cause; the non-possessive form 'Bell palsy' is preferred in contemporary medical literature.
  • •The pathogenetic paradigm centers on an inflammatory demyelinating neuritis, likely triggered by herpes simplex virus type 1 reactivation within the geniculate ganglion, leading to edema and secondary ischemic compression of the facial nerve within the rigid fallopian canal. The labyrinthine segment (0.68 mm diameter) is the narrowest and most vulnerable site.
  • •Despite being self-limiting, Bell palsy is a clinical emergency: early treatment with prednisolone 1 mg/kg/day (max 60 mg) for 10 days improves the rate of complete recovery at 3 months from 70% to 85% (number needed to treat [NNT] = 7), and delayed therapy beyond 72 hours is associated with significantly worse outcomes.
  • •Severity is graded using the House-Brackmann scale (I-VI). Grade I is normal, grade VI is total paralysis. This grading guides prognosis and treatment decisions, including the threshold for considering electroneuronography (ENoG) and surgical decompression in complete paralysis with >90% denervation within 14 days.
  • •Bell palsy can mimic stroke (the most common stroke mimic), and up to 30% of patients develop residual synkinesis or hemifacial spasm due to aberrant nerve regeneration. Long-term sequelae, though often mild, can cause persistent functional impairment and cosmetic concern requiring botulinum toxin therapy.

Evaluation

  • •Suspect Bell palsy in any patient presenting with acute (<72 hours), unilateral facial weakness involving both the upper and lower face (forehead is affected), with ipsilateral effacement of the nasolabial fold, widened palpebral fissure, and drooping of the mouth corner.
  • •Ask about onset timing (sudden vs. gradual), associated symptoms: ear pain, hyperacusis, taste disturbance (dysgeusia or ageusia on the anterior two-thirds of the tongue), decreased tearing, and subjective facial numbness (often due to trigeminal nerve overlap rather than true CN V involvement).
  • •Also ask for red-flag symptoms: vesicular rash in the ear canal or auricle (suggests Ramsay Hunt syndrome), headache, fever, stiff neck, recent tick bite or erythema migrans (Lyme disease), bilateral or recurrent facial palsy, or concomitant limb weakness/diplopia (suggests central cause or Guillain-Barré syndrome).
  • •Examine the face at rest and during voluntary movement: ask the patient to raise eyebrows, close eyes tightly, puff cheeks, and show teeth. Document the House-Brackmann grade (I-VI). Confirm that the forehead is involved, this distinguishes lower motor neuron (Bell palsy) from upper motor neuron (stroke) weakness, which spares the forehead.
  • •Inspect the ear canal and tympanic membrane carefully for vesicular lesions (Ramsay Hunt syndrome) and palpate the parotid gland for masses. Perform a full neurological exam including assessment of extraocular movements, hearing, taste on the anterior tongue (if feasible), and testing of CN V, VIII, IX, X, XI, XII for other neuropathies.
  • •The diagnosis of Bell palsy is clinical and a diagnosis of exclusion. No routine imaging or laboratory tests are needed if the history and exam are classic and no atypical features are present.
  • •Order noncontrast head CT or MRI brain with diffusion-weighted imaging if there is any suspicion of central (upper motor neuron) weakness, especially forehead sparing, associated limb weakness, speech disturbance, or acute headache with vomiting, to rule out ischemic stroke or intracranial hemorrhage. Bell palsy is the most common stroke mimic in both adults and children.
  • •Order contrast-enhanced MRI of the internal auditory canal and facial nerve with gadolinium if atypical features are present: gradual progression >3 weeks, age <18 years (to exclude congenital anomalies or tumors), recurrent ipsilateral palsy, bilateral palsy, vesicular rash, fever, parotid mass, or failure to improve after 3 months. In acute Bell palsy, MRI reveals enhancement of the geniculate, labyrinthine, or tympanic segments in up to 90% of patients, but this finding is not specific.
  • •Consider serologic testing (Lyme ELISA/Western blot, VZV serology, HIV, ANA, ACE, syphilis) based on exposure history and clinical suspicion. In endemic areas or if there is a history of tick exposure with erythema migrans, test for Lyme disease, as facial palsy may be the presenting feature of early disseminated Lyme in children and adults.
  • •Perform electroneuronography (ENoG) and needle electromyography (EMG) in patients with complete paralysis (House-Brackmann grade VI) within 14 days of onset to quantify denervation. A compound muscle action potential (CMAP) amplitude ≤10% of the unaffected side (i.e., ≥90% denervation) predicts poor recovery and defines a narrow window in which surgical decompression is sometimes considered. The presence of voluntary motor unit potentials on needle EMG within the first 10 days is a favorable sign.
  • •Also consider Ramsay Hunt syndrome (varicella-zoster virus reactivation) if vesicles are present in the ear canal, auricle, or oral mucosa, or if there is severe otalgia, hearing loss, or vertigo. VZV PCR of vesicular fluid or serum VZV IgM can confirm the diagnosis; treatment requires acyclovir 800 mg 5 times daily for 7-10 days plus corticosteroids.
  • •In children, the differential includes acute otitis media (may cause facial palsy from middle ear infection or cholesteatoma), Lyme disease (especially in endemic regions), and stroke. Children with Bell palsy typically recover well, but MRI with contrast is advised if there is no improvement within 3 weeks or if recurrent or bilateral.

Management

  • •Initiate oral prednisolone as soon as possible, ideally within 72 hours of symptom onset. Adults: 1 mg/kg/day (maximum 60-80 mg/day) for 7-10 days. No taper is needed for short courses. This is the single most effective intervention: NNT = 7 for complete recovery at 3 months. Treatment beyond 7 days offers no additional benefit.
  • •For severe Bell palsy (House-Brackmann grade IV-VI), consider adding oral valacyclovir 1 g three times daily for 7 days (or acyclovir 800 mg five times daily) to prednisolone. The combination provides a modest additional benefit (OR 1.48; NNT = 12) compared with steroids alone, though it is not standard for mild cases. For Ramsay Hunt syndrome, combination therapy is mandatory.
  • •Do not prescribe antiviral monotherapy without corticosteroids for Bell palsy, it is no better than placebo and delays effective treatment. Antivirals are reserved for severe cases or when varicella-zoster virus is suspected (Ramsay Hunt syndrome).
  • •Do not routinely order MRI or CT for classic Bell palsy. Imaging is reserved for atypical presentations (see Evaluation) and for patients who fail to improve after 3 months, where it reveals an alternative cause in <2% of cases. Overuse of imaging delays treatment and incurs unnecessary cost.
  • •Protect the eye in patients with lagophthalmos (incomplete eye closure). Prescribe preservative-free artificial tears every 1-2 hours while awake, a lubricating ophthalmic ointment at bedtime, and tape the eye closed at night or use a moisture chamber. If corneal exposure persists, refer to ophthalmology for temporary tarsorrhaphy or botulinum toxin-induced protective ptosis.
  • •Monitor for corneal abrasion and exposure keratopathy. Assess visual acuity and perform fluorescein staining if eye pain, photophobia, or decreased vision occur. Urgent ophthalmology referral for any corneal ulceration or persistent epithelial defect.
  • •Counsel patients about recovery expectations: spontaneous improvement typically begins within 3 weeks in 85% of patients; most achieve near-complete recovery by 3-6 months. Prognosis is more guarded if complete paralysis persists beyond 3 weeks without improvement. Residual weakness or synkinesis occurs in up to 30%.
  • •For post-Bell palsy synkinesis (e.g., eye closure causing mouth twitching or mouth movement causing eyelid closure), first-line therapy is botulinum toxin A (Botox) injections: 1.25-5 units per injection site into the involved orbicularis oculi or other hyperactive muscles. Effects last 3-4 months and can be repeated. Refer to a neurologist or facial nerve specialist for this.
  • •For hemifacial spasm or neuropathic otalgia after Bell palsy, consider gabapentin 300-900 mg daily (titrated as tolerated) or pregabalin 75-150 mg twice daily. If symptoms are severe or persistent, refer to a neurologist for further evaluation (e.g., MRI to exclude vascular compression). Botulinum toxin remains the most effective treatment for hemifacial spasm.
  • •Surgical facial nerve decompression is rarely indicated and remains controversial. It may be offered only to patients with: (1) complete paralysis (House-Brackmann grade VI), (2) ENoG showing >90% denervation (CMAP ≤10% of unaffected side) within 14 days of onset, and (3) no spontaneous recovery by day 14. The procedure must be performed within 2-3 weeks of onset to have any potential benefit; beyond that, it does not improve outcomes. Refer to a skull-base surgeon who performs this procedure.
  • •Do not perform surgical decompression after 3 weeks from onset, for incomplete paralysis, or for patients with partial recovery, it offers no benefit and risks hearing loss and other complications.
  • •Avoid non-dihydropyridine calcium channel blockers (verapamil, diltiazem), tricyclic antidepressants, and SSRIs where possible in patients with comorbid cardiovascular disease because of potential interaction with corticosteroids (hyperglycemia, hypertension). For pain, acetaminophen or ibuprofen are safe; avoid opioids unless severe otalgia.
  • •In children, prednisolone 1-2 mg/kg/day (max 60 mg) for 7-10 days is equally effective and safe. A pediatric series showed 98% recovery at 6 months with prednisolone vs. 93% with placebo (absolute difference 5%, NNT = 20, not statistically significant). However, guidelines still recommend steroid treatment given the favorable safety profile and trend toward benefit. Eye protection is equally important.
  • •Hospital admission is rarely needed for Bell palsy. Indications include: inability to eat or drink due to severe facial weakness (risk of aspiration), suspected life-threatening alternative diagnosis (e.g., bacterial meningitis, brainstem stroke), need for urgent surgical evaluation (e.g., temporal bone fracture), or need for IV hydration or IV steroids if oral not tolerated.
  • •Discharge criteria: no corneal ulceration, patient/caregiver able to provide eye care, ability to take oral medications and maintain oral intake, safe swallow, no signs of alternative acute neurological disease (e.g., stroke). Arrange outpatient follow-up with primary care or neurology in 2-4 weeks to monitor recovery and manage sequelae.
  • •Refer to otolaryngology or facial nerve clinic if: no recovery by 3 months, worsening symptoms beyond 2 weeks, recurrent ipsilateral or bilateral palsy, suspected secondary cause (parotid mass, cholesteatoma), or consideration for surgical decompression. Refer to ophthalmology for any corneal complication.
  • •Advise against common alternative therapies: acupuncture, facial exercises, electrical stimulation, none have proven benefit and may promote synkinesis. Physical therapy for facial retraining (neuromuscular retraining) may be considered after 3 months if synkinesis or persistent weakness, but evidence is limited. Chiropractic manipulation of the cervical spine is contraindicated (risk of vertebral artery dissection causing stroke).

Board Review — High Yield

  • •Forehead-sparing vs. forehead-involved, Bell palsy affects the entire ipsilateral face including the forehead (lower motor neuron); stroke spares the forehead (upper motor neuron).
  • •House-Brackmann grade I-VI, Standard severity scale. Grade VI = total paralysis; grade I = normal function.
  • •NNT = 7, Prednisolone 1 mg/kg/day × 7-10 days for complete recovery at 3 months (from ~70% to ~85%).
  • •Labyrinthine segment, The narrowest region of the fallopian canal (0.68 mm) where entrapment edema occurs; most common site of nerve enhancement on MRI.
  • •ENoG cutoff, CMAP ≤10% of unaffected side within 14 days = >90% denervation; predicts poor recovery and defines the window for possible surgical decompression.
  • •Ramsay Hunt syndrome, Vesicular rash in ear canal/auricle; requires acyclovir 800 mg 5×/d + prednisolone. Worse prognosis than Bell palsy if untreated.
  • •Post-Bell palsy synkinesis, Ocular-oral or oral-ocular; first-line treatment: botulinum toxin A (1.25-5 U per injection site) into involved orbicularis oculi.
  • •MRI enhancement pattern, Geniculate ganglion (80%), labyrinthine (60%), tympanic (50%), intracanalicular (40%); not specific, also seen in Ramsay Hunt syndrome and schwannoma.
  • •Bilateral facial palsy, Rare (<1%); think Guillain-Barré, sarcoidosis, Lyme, HIV, meningitis. Not Bell palsy.
  • •Vaccine association, mRNA SARS-CoV-2 vaccines: reported increased risk (IRR 2.50), absolute risk 0.5-1/10,000; overall low and should not deter vaccination.

Deep Dive — Evidence Details

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