Acute idiopathic peripheral CN VII palsy with unilateral facial weakness involving the forehead.
Also known as: Bell palsy, Bell's palsy, idiopathic facial nerve palsy, facial nerve palsy, facial paralysis
Overview
Acute idiopathic peripheral palsy of the facial nerve (CN VII) producing unilateral lower motor neuron facial weakness, including the forehead. Considered a diagnosis of exclusion after secondary causes (Lyme, herpes zoster, otitis media, tumor, stroke) have been considered.
Epidemiology
Annual incidence ~15-30 per 100,000. Peak in 15-45 year-olds; equal in men and women. Risk increased in pregnancy (especially third trimester), diabetes, hypertension, obesity, and upper respiratory infection.
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Question 1NeurologyMedium
A 45-year-old male wakes with right-sided facial droop, inability to close his right eye, and loss of taste on the anterior two-thirds of the tongue. Forehead wrinkling on the right is absent. Limb strength and speech are normal. Which of the following is the most likely diagnosis?
AMiddle cerebral artery (MCA) stroke
BTrigeminal neuritis
CRamsay Hunt syndrome
DBell palsy
Reveal answer & full explanation
Correct answer: D — Bell palsy
AMiddle cerebral artery (MCA) stroke
BTrigeminal neuritis
CRamsay Hunt syndrome
DBell palsy✓
Why Bell palsy is correct
Idiopathic peripheral cranial nerve (CN) VII palsy affecting the entire half of the face, including the forehead, because both upper and lower facial motor fibers are involved at the peripheral level
Absence of forehead wrinkling confirms a peripheral lower motor neuron (LMN) lesion, distinguishing it from a central lesion
Loss of taste on the anterior two-thirds of the tongue (chorda tympani branch of CN VII) further localizes the lesion to peripheral CN VII
Sudden onset over hours, often noticed on waking, is characteristic
First-line treatment within 72 hours is prednisone, with valacyclovir added in severe cases
Eye protection (lubricant, taping) prevents corneal injury; most patients recover in 3-6 months
Why the others are wrong
Middle cerebral artery (MCA) stroke — a central upper motor neuron lesion spares the forehead due to bilateral cortical innervation; this patient's forehead involvement rules out a central cause (confused-with central VII palsy)
Trigeminal neuritis — CN V mediates facial sensation and mastication, not facial expression or taste; it would not cause motor droop or loss of taste (wrong-cranial-nerve trap)
Ramsay Hunt syndrome — also a peripheral CN VII palsy but from varicella-zoster reactivation in the geniculate ganglion, requiring a painful vesicular eruption in the ear canal or auricle, which is absent here (right-concept-wrong-setting)
Additional high-yield points
The forehead test is the key clinical maneuver: forehead spared = central (UMN); forehead involved = peripheral (LMN)
Chorda tympani involvement (altered taste) and hyperacusis (stapedius) help localize the lesion along the facial canal
Prognosis is worse with complete paralysis; consider Lyme disease, sarcoidosis, or tumor if bilateral, recurrent, or slowly progressive
Question 2NeurologyMedium
A 43-year-old man has acute unilateral facial weakness involving the forehead and mouth. He cannot close the affected eye. There is no limb weakness, aphasia, or visual field deficit. Which of the following is the most appropriate initial treatment?
AOral acyclovir as sole therapy
BSurgical facial nerve decompression
CIntravenous tissue plasminogen activator
DOral prednisone started within 72 hours
Reveal answer & full explanation
Correct answer: D — Oral prednisone started within 72 hours
AOral acyclovir as sole therapy
BSurgical facial nerve decompression
CIntravenous tissue plasminogen activator
DOral prednisone started within 72 hours✓
Why Oral prednisone started within 72 hours is correct
Forehead-involving acute peripheral facial palsy with incomplete eye closure is Bell palsy.
Corticosteroids begun within 72 hours of onset improve the odds of complete recovery.
Artificial tears and nighttime taping protect the cornea when eyelid closure is impaired.
Why the others are wrong
Oral acyclovir as sole therapy — Right-disease-wrong-step: antivirals are at most an adjunct to steroids and provide little benefit when used alone in typical Bell palsy.
Surgical facial nerve decompression — Premature closure: decompression is reserved for rare severe cases with >90% degeneration on electrophysiology, not initial treatment.
Intravenous tissue plasminogen activator — Buzzword-match to "facial droop": forehead sparing would point to central stroke, but full forehead involvement localizes to the peripheral nerve, so thrombolysis is wrong.
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Pregnancy (especially third trimester and early postpartum)
Diabetes mellitus
Hypertension
Obesity
Family history (small genetic component)
Immunosuppression
Pathophysiology
Inflammation and edema of the facial nerve within the bony facial canal of the temporal bone, leading to compression and demyelination/axonal injury. Reactivation of latent herpes simplex virus type 1 (HSV-1) within the geniculate ganglion is the most widely supported etiology; varicella-zoster reactivation produces a distinct syndrome (Ramsay Hunt). Edema in the narrow labyrinthine segment is the proposed mechanism for nerve compression.
Clinical presentation
Symptoms
Acute onset over hours; maximal weakness within 72 hours
Unilateral facial weakness/paralysis affecting BOTH upper and lower face (cannot raise eyebrow, close eye, smile symmetrically)
Inability to close affected eye → dry eye, corneal exposure
Drooling and food pocketing on the affected side
Hyperacusis (loss of stapedius dampening)
Decreased taste on anterior 2/3 of tongue (chorda tympani)
Decreased lacrimation, retroauricular pain (often precedes weakness by 1-2 days)
HIV seroconversion — Facial palsy can be presenting feature; consider in at-risk patients
Trauma (temporal bone fracture) — History of head injury, CT temporal bone
Diagnostic workup
Diagnostic criteria
Clinical diagnosis of acute peripheral LMN facial weakness in the absence of identifiable cause. Onset over <72 hours, no other cranial nerve involvement, no signs of central or otologic pathology.
Labs
Usually none required — clinical diagnosis
Consider: Lyme serology in endemic areas; HIV testing if risk factors; A1c if undiagnosed diabetes suspected
If bilateral, recurrent, or atypical: more extensive evaluation (Lyme, HIV, sarcoid, autoimmune)
Imaging
Not routinely indicated for typical presentation
MRI brain with contrast if: atypical features (slow onset >72 h, gradual progression beyond 3 weeks, no recovery by 3-4 months, other cranial nerves involved, recurrence, bilateral, mass found) → exclude tumor (schwannoma, parotid), stroke, demyelinating disease
CT temporal bone if trauma or otologic findings
Electroneurography (ENoG) and EMG at 3-14 days for prognostication in severe (House-Brackmann V-VI) cases — >90% degeneration on ENoG predicts poor recovery and may indicate surgical decompression candidacy
Diagnostic algorithm
Feature
Bell Palsy (LMN, CN VII)
Cortical Stroke (UMN, face)
Forehead
Weak (cannot wrinkle)
Spared (can wrinkle)
Eye closure
Impaired; lagophthalmos
Preserved
Smile
Drooping ipsilateral corner
Drooping contralateral corner
Other CN/limb signs
Absent (isolated)
Present (hemiparesis, dysarthria, neglect)
Onset
Hours, peaks <72 h
Sudden, seconds to minutes
Hyperacusis / taste loss / retroauricular pain
Often present
Absent
Treatment
Prednisone (± antiviral), eye care
Stroke protocol (tPA, thrombectomy, ASA)
Peripheral (Bell) vs. central (stroke) facial weakness.
Treatment
First-line
Corticosteroids — high-dose oral prednisone 60 mg/day x 5 days, then taper over 5 days (or prednisolone equivalent), started within 72 hours of symptom onset for best benefit (improves complete recovery rate; SCANDINAVIAN BELL trial, Sullivan trial)
Eye protection (essential to prevent exposure keratopathy): artificial tears every 1-2 hours, lubricating ointment at bedtime, tape eyelid shut at night, consider moisture chamber/eye patch
Antiviral therapy (acyclovir 400 mg 5x/day or valacyclovir 1 g TID for 7 days) — limited additive benefit alone but reasonable when added to steroids in severe cases (House-Brackmann IV-VI); routinely used for Ramsay Hunt syndrome
Reassurance — most patients begin to recover within 3 weeks; ~70-85% recover completely without intervention
Second-line / adjunct
Ophthalmology referral if exposure keratopathy, persistent epiphora, or corneal abrasion
Physical therapy / facial neuromuscular retraining for persistent weakness or synkinesis
Surgical decompression — controversial; consider only in severe cases within 14 days when ENoG shows >90% degeneration
Botulinum toxin for synkinesis or hemifacial spasm in late phase
Tarsorrhaphy or upper-lid weight (gold or platinum) for chronic lagophthalmos
If recurrent or bilateral, evaluate for systemic disease (Lyme, sarcoid, GBS, HIV, autoimmune)
Complications
Exposure keratopathy and corneal ulceration (most important early complication)
Forehead-sparing facial weakness = stroke until proven otherwise; forehead-involved = peripheral (LMN) cause such as Bell palsy.
Begin steroids within 72 hours of symptom onset for maximum benefit; later initiation may still help.
Eye protection is the most important and most often forgotten step — corneal injury can be sight-threatening.
Bilateral facial palsy is rarely Bell palsy — think Lyme disease, GBS (Miller Fisher), sarcoid, HIV.
Ramsay Hunt syndrome (zoster oticus): more pain, vesicles, hearing/vestibular involvement, and worse prognosis than Bell palsy — give acyclovir/valacyclovir AND steroids.
Pregnancy-associated Bell palsy is more common in the third trimester and immediate postpartum; steroids are generally considered safe in pregnancy.
Failure to improve at all by 3-4 months should prompt MRI to evaluate for tumor (vestibular schwannoma, parotid).
References
AAN 2012 — Evidence-based Guideline Update: Steroids and Antivirals for Bell Palsy (Gronseth & Paduga, Neurology 2012)
AAO-HNS 2013 — Clinical Practice Guideline: Bell's Palsy (Baugh et al., Otolaryngol Head Neck Surg 2013)
Sullivan Trial — Early Treatment with Prednisolone or Acyclovir in Bell's Palsy (Sullivan et al., NEJM 2007)
Engstrom Trial — Prednisolone and Valaciclovir in Bell's Palsy (Engstrom et al., Lancet Neurol 2008)
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