Facial Palsy — Bell Palsy and Central vs Peripheral

Central (Upper Motor Neuron) Facial Palsy

• The corticobulbar tract innervates the facial motor nucleus, with the upper face (forehead and orbicularis oculi) receiving bilateral cortical innervation, while the lower face (orbicularis oris, buccalis) receives predominantly ipsilateral innervation
• Lesions rostral to the facial motor nucleus (stroke, mass, demyelination) spare the forehead and upper eyelid muscles on the affected side because of crossed supranuclear input to those muscles
• Results from disruption of pyramidal tracts in the internal capsule, cerebral cortex, or brainstem above the facial nucleus
• Contralateral hemispheric involvement produces ipsilateral facial weakness

Peripheral (Lower Motor Neuron) Facial Palsy

• Involves damage to the facial nerve nucleus in the pons or the facial nerve itself (CN VII) distal to the nucleus
• The facial nerve has an unusually long intracranial course, exiting the skull through the stylomastoid foramen after traversing the temporal bone (petrous portion)
• Peripheral lesions cause weakness of all facial muscles on the affected side, including forehead, eye, and mouth
• In Bell palsy, idiopathic inflammation and edema within the temporal bone canal lead to nerve compression, ischemia, and conduction block; proposed mechanisms include viral reactivation (HSV-1, VZV), autoimmunity, and microvascular ischemia
• Demyelination, axonal degeneration, or complete transection may occur depending on severity and duration of compression

Temporal Bone Anatomy and CN VII Vulnerability

• The facial nerve exits the brainstem at the cerebellopontine angle and enters the internal acoustic meatus
• Within the temporal bone, the nerve travels through a 30-mm bony canal with minimal space for swelling
• The genu (bend) of the facial nerve at the geniculate ganglion is the narrowest segment and most susceptible to ischemia
• Greater petrosal nerve (preganglionic parasympathetic) branches at the geniculate ganglion; chorda tympani (taste from anterior 2/3 tongue, parasympathetic to submandibular/sublingual glands) branches in the mastoid segment

Bell Palsy (Idiopathic Peripheral Facial Palsy)

• Most common cause; accounts for 60–75% of acute peripheral facial palsy cases
• Presumed HSV-1 reactivation within the geniculate ganglion is the leading hypothesis
• Risk factors: pregnancy (especially third trimester and immediate postpartum period), diabetes mellitus, hypertension, upper respiratory infection preceding onset, emotional stress, cold exposure
• Age peak: 15–60 years, rare in children <5 years and adults >75 years

Secondary Causes of Peripheral Facial Palsy (Must Always Be Excluded)

• Otitis media and mastoiditis — bacterial or viral infection extending into temporal bone
• Ramsay Hunt syndrome — VZV reactivation in the geniculate ganglion causing facial palsy with vesicles in the ear canal or hard palate; associated with severe otalgia and may include hearing loss, vertigo (CN VIII involvement)
• Lyme disease — Borrelia burgdorferi; often bilateral facial palsy (pathognomonic for Lyme); endemic regions (Northeast, Midwest USA); check for erythema migrans rash and systemic symptoms
• HIV/AIDS — increased incidence, may be bilateral
• Melkersson-Rosenthal syndrome — recurrent facial palsy with facial edema and lingua plicata (furrowed tongue); autosomal dominant with variable penetrance
• Möbius syndrome — congenital bilateral facial palsy with abducens nerve palsy; CNS hypoplasia
• Temporal bone fractures — may involve facial nerve within petrous bone; immediate vs. delayed paralysis has different prognoses
• Bell phenomenon — reflex upward eye deviation when attempting to close eyelids; intact with CN VII lesion but may be absent in severe cases or axonal injury
• Parotid malignancy or surgery — common iatrogenic cause; nerve compression or transaction
• Facial nerve tumors — schwannomas (acoustic neuroma), hemangiomas, cholesteatoma
• Hemifacial spasm — involuntary facial twitching (not true paralysis); hyperactivity of CN VII rather than palsy
• Melasma and other cosmetic conditions — differentiate from true weakness

Central Facial Palsy Causes

• Acute ischemic or hemorrhagic stroke — most common; contralateral hemispheric or brainstem involvement
• Space-occupying lesions — intracranial mass, tumor, abscess
• Demyelinating disease — multiple sclerosis
• Brainstem pathology — Foville syndrome, Millard-Gubler syndrome (ipsilateral CN VII palsy + contralateral hemiplegia from ventral pontine involvement)
• Myasthenia gravis — fatigue, not true palsy, but may present with facial weakness

Cardinal Symptoms

• Acute onset of unilateral facial weakness (hours to overnight in Bell palsy; more gradual in neoplastic causes)
• Inability to smile, wrinkle forehead, or close eye on affected side
• Facial sagging and asymmetry
• Difficulty with eating or drinking (food accumulating in cheek)
• Speech changes (slurred) if severe
• Taste disturbance (anterior 2/3 tongue) when chorda tympani involved
• Hyperacusis (uncomfortable loudness) if stapedius branch affected

Physical Examination Findings — Peripheral Facial Palsy

• Complete hemiparesis of all facial muscles on affected side: forehead wrinkles absent, eyebrow droops, eye cannot close fully (incomplete eye closure → lagophthalmos), nasolabial fold flattened, mouth droops, inability to puff cheeks or whistle
• Bell phenomenon present: intact reflex upward deviation of eye when attempting closure (indicates nerve is intact; absent in severe axonal injury)
• Schirmer test abnormal if greater petrosal nerve involved (decreased tearing on affected side)
• Taste testing on anterior 2/3 tongue affected if chorda tympani involved
• Ear canal examination may reveal vesicles (Ramsay Hunt)
• Postauricular pain or tenderness may occur in Bell palsy
• Loss of nasal airway obstruction sensation (minor finding)

Physical Examination Findings — Central Facial Palsy

• Forehead and upper eyelid muscles spared — patient can raise eyebrow and wrinkle forehead on affected side despite lower facial weakness
• Asymmetric smile with contralateral mouth droop (affected side drops down)
• Other neurologic signs present: arm/leg weakness (stroke), cognitive changes, speech abnormalities, reflex abnormalities
• No lagophthalmos (eye closure intact)

Associated Findings by Syndrome

• Melkersson-Rosenthal: facial edema, lingua plicata, recurrent palsy
• Ramsay Hunt: severe otalgia, vesicles, hearing loss, vertigo
• Lyme disease: bilateral facial palsy (in ~25% of Lyme disease cases), erythema migrans rash, arthralgia, meningitis signs
• Möbius syndrome: inability to abduct eyes (CN VI), micrognathia, webbed fingers, autism spectrum features

Clinical Diagnosis of Bell Palsy (Excluding Other Causes)

• Diagnosis of exclusion — requires ruling out secondary causes
• House-Brackmann Grading Scale (I–VI) quantifies severity: Grade I = normal function; Grade II = minor weakness with effort; Grade III = obvious weakness at rest, mild synkinesis; Grade IV = obvious weakness at rest, moderate synkinesis; Grade V = barely perceptible movement; Grade VI = no movement
• Onset within 72 hours suggests Bell palsy; more gradual progression suggests neoplasm or other structural lesion
• Clinical presentation checklist for Bell palsy: acute unilateral peripheral facial palsy, no other neurologic deficits, no recent trauma, no recurrent episodes (unless Melkersson-Rosenthal)

Electrodiagnostic Testing (EMG/NCS)

• Electromyography (EMG) and nerve conduction studies (NCS) assess degree of nerve damage (neurapraxia vs. axonotmesis)
• Normal NCS with denervation on EMG (fibrillations, positive sharp waves) after 3 weeks indicates axonal injury; prognostic indicator
• Absent response on stimulation distal to lesion indicates conduction block or axonal degeneration
• Helpful when diagnosis unclear, severity assessment needed, or prognostication desired; perform at 2–3 weeks post-onset for optimal assessment
• Not routinely necessary in typical Bell palsy presentation with early corticosteroid initiation

Laboratory Testing

• CBC, comprehensive metabolic panel, ESR, CRP — nonspecific screening; elevated CRP may support inflammatory etiology
• Blood glucose and HbA1c — check for diabetes (risk factor and secondary cause)
• Lyme serology (ELISA ± Western blot) — if endemic region or risk factors present; obtain in all patients with bilateral facial palsy
• HIV testing — consider based on risk factors and clinical context; increased facial palsy incidence in AIDS
• Temporal bone imaging (CT/MRI) — NOT routinely recommended for isolated Bell palsy in typical presentation; order if:
• Atypical features present (gradual onset, recurrent, bilateral)
• Secondary cause suspected (trauma, infection, neoplasm)
• Failure to improve or deterioration despite treatment
• Ramsay Hunt syndrome suspected
• Evaluation of temporal bone fracture

Imaging Studies

• High-resolution CT temporal bone — assesses bony anatomy, fractures, cholesteatoma, otitis
• MRI brain and internal auditory canals (IAC) — evaluates for stroke, mass, demyelination, acoustic neuroma, geniculate ganglion inflammation (T2/STIR hyperintensity); superior for soft tissue evaluation and exclusion of central causes
• MRI with gadolinium — may show enhancement of facial nerve (geniculate ganglion, labyrinthine, tympanic, or mastoid segments) in Bell palsy and Ramsay Hunt; nonspecific but supports inflammatory diagnosis

Diagnostic Criteria for Bell Palsy (Clinical Diagnosis)

• Acute unilateral peripheral facial nerve palsy
• Rapid onset (hours to days)
• Involvement of all facial muscles on one side (upper + lower face)
• Absence of other neurologic signs
• Exclusion of secondary causes (no temporal bone pathology, no systemic disease)
• Hyperacusis, taste loss, or ear pain may be present but not required for diagnosis

Central vs. Peripheral Differentiation (Key Clinical Test)

• Forehead and upper eyelid sparing = Central (upper motor neuron)
• Forehead and upper eyelid involved = Peripheral (lower motor neuron)

Bell Palsy — First-Line Treatment

Corticosteroids

• Oral prednisone 1 mg/kg/day (max 80 mg) × 7 days, then taper over 7 days (total 14-day course) OR prednisolone 500 mg once daily × 5 days followed by 5-day taper (British approach); initiate within 72 hours of symptom onset for maximum benefit
• Evidence-based: Reduces time to complete recovery by ~7 days and increases rate of complete recovery at 3 months (approximately 75% vs. 60% without treatment)
• Mechanism: Reduces inflammation and edema within temporal bone canal, improving nerve perfusion
• Most effective in moderate-to-severe palsy (House-Brackmann III–VI); benefit in mild palsy less clear
• Contraindications: active infection (chickenpox, measles), recent live vaccine; use cautiously in diabetes (hyperglycemia risk)
• NNT = 7 to prevent one incomplete recovery

Antivirals (Controversial)

• Valacyclovir 1000 mg three times daily × 7 days or acyclovir 800 mg five times daily × 7–10 days
• Rationale: addresses presumed HSV-1 reactivation pathogenesis
• Evidence conflicting: Some trials show modest additional benefit when combined with corticosteroids; recent meta-analyses suggest limited independent benefit
• Generally NOT routinely recommended as monotherapy; may consider adjunctive use in severe cases (House-Brackmann V–VI) or Ramsay Hunt syndrome
• Ramsay Hunt syndrome: Definitely requires acyclovir or valacyclovir + corticosteroids (significantly better outcomes); start within 72 hours
• Renal function must be adequate; adjust dosing if creatinine clearance <50 mL/min

Eye Care (Critical — Prevent Corneal Complications)

• Artificial tears instilled frequently (hourly during day) to prevent drying
• Lubricating ointment at night (petrolatum, hypoallergenic formulations)
• Eye taping or protective eyeglasses during day to prevent corneal abrasion; protective eye patch or shield especially important at night
• Consider protective goggles for hazardous work environments
• Sleeping position: sleep on affected side to reduce eye exposure
• Humidified environment may help
• Eye tape should not cover nasal bridge to avoid obstruction of nasal airway during tape adherence
• Ophthalmology referral if corneal ulceration, scarring, or vision loss develops; may require lubricating drops with higher viscosity (carbomers), contact lens, or protective procedures

Monitoring for Improvement

• Clinical assessment at 3 weeks and 3 months post-onset
• Electrodiagnostic testing if prognosis unclear or no improvement by 3 weeks (indicates severe axonal injury)
• Most patients achieve complete recovery within 3–6 months even without treatment, but with corticosteroids, recovery is faster and more complete

Second-Line Therapies (Refractory Cases)

• Physical therapy and facial rehabilitation — particularly important if incomplete recovery or synkinesis develops
• Electromyography-guided therapy — can help retrain facial muscles and prevent aberrant reinnervation
• Botulinum toxin injection — for established synkinesis (unwanted facial movement synchronous with voluntary movement) or hemifacial spasm; typically 3–4 months post-onset if synkinesis evident
• Surgical decompression — rarely indicated; only in severe cases with acute complete denervation on EMG and failure to improve; complications include hearing loss and facial nerve injury; not standard of care given low evidence base
• Facial reanimation surgery — for chronic irreversible paralysis (nerve transfer, muscle transfer, reanimation procedures); requires specialized otologic/plastic surgical expertise

Non-Pharmacological Measures

• Reassurance and patient education — explain excellent prognosis, typical timeline (weeks to months for recovery)
• Counseling on risk of complications — particularly corneal abrasion/ulceration
• Avoid facial stimulation or massage in early stages (no strong evidence but traditional guidance)
• Electrical stimulation — not recommended; no evidence of benefit

Ocular — the complication that threatens organ loss

• Exposure keratopathy and corneal ulceration: orbicularis oculi paralysis plus loss of greater petrosal parasympathetic tearing leaves the cornea unprotected and dry; signaled by foreign-body sensation, injection, and a fluorescein-staining epithelial defect. A corneal ulcer, hypopyon, or acute vision loss is an ophthalmologic emergency — same-day slit-lamp evaluation. The AAO-HNS Bell palsy guideline makes eye protection a strong recommendation for exactly this reason.

Neurologic sequelae of aberrant reinnervation

• Synkinesis: regenerating axons misroute into the wrong muscle groups, so voluntary smiling produces eye closure (oral-ocular synkinesis) or blinking pulls up the corner of the mouth. Appears months after onset and is the usual reason for botulinum toxin referral.
• Crocodile tears (gustatory lacrimation): salivary fibers of the chorda tympani/greater petrosal system regrow toward the lacrimal gland, so eating provokes tearing — the classic Bogorad syndrome.
• Facial contracture and hemifacial spasm: chronic denervation-reinnervation yields a tightened nasolabial fold that can be mistaken for weakness on the opposite side.
• Incomplete recovery: most likely after complete (House-Brackmann V–VI) palsy with EMG evidence of axonal degeneration.

Missed alternative diagnoses — the true emergencies

• Acute stroke presenting as forehead-sparing weakness: activate stroke protocols per AHA/ASA, do not treat as Bell palsy.
• Guillain-Barré/Miller Fisher with bilateral palsy: monitor vital capacity for neuromuscular respiratory failure.
• Necrotizing (malignant) otitis externa, coalescent mastoiditis, or cholesteatoma eroding the fallopian canal — requires urgent imaging and ENT involvement.

Treatment-related

• Corticosteroids: hyperglycemia and hyperosmolar crisis in diabetics, insomnia, mood change/psychosis, and dissemination of untreated infection; unmasked VZV if Ramsay Hunt is missed and steroids are given alone.
• Acyclovir/valacyclovir: crystal nephropathy and neurotoxicity (confusion, myoclonus) in renal impairment or underhydration.
• Surgical decompression: sensorineural hearing loss, CSF leak, worsened palsy — a major reason it is not standard care.
• Botulinum toxin: diffusion causing ptosis or worsened lagophthalmos.

• The forehead is the whole question: forehead and eye closure involved = peripheral (LMN, CN VII nucleus or nerve); forehead spared = central (UMN), because the upper facial nucleus receives bilateral corticobulbar input. Examiners test this before anything else.
• Single best next step in forehead-sparing palsy: emergent noncontrast head CT and stroke pathway activation per AHA/ASA — not prednisone, not MRI of the temporal bone. Look in the stem for arm weakness, dysarthria, or gaze deviation.
• Single best next step in typical Bell palsy: oral corticosteroids (prednisone) started within 72 hours, plus aggressive eye protection with artificial tears by day and lubricating ointment with taping/shield at night (AAO-HNS). Routine labs and imaging are not indicated in a typical unilateral presentation.
• Vesicles in the ear canal, concha, or hard palate with severe otalgia = Ramsay Hunt syndrome (VZV, geniculate ganglion). This is the one scenario where an antiviral plus a corticosteroid is clearly indicated together, and outcomes are worse than Bell palsy.
• Bilateral facial palsy is never Bell palsy until proven otherwise: think Lyme neuroborreliosis (serologic testing per IDSA/AAN/ACR 2020 Lyme guideline), Guillain-Barré, sarcoidosis (Heerfordt syndrome: uveitis, parotitis, fever), and HIV seroconversion.
• Localize by the associated deficit: hyperacusis implies a lesion proximal to the nerve to stapedius; loss of taste on the anterior two-thirds of the tongue and reduced salivation implies involvement at or above the chorda tympani; dry eye implies involvement at the geniculate ganglion.
• Common distractor — antiviral monotherapy: antivirals alone do not improve Bell palsy outcomes (AAN); the corticosteroid is the agent that matters.
• Common distractor — "MRI everyone": reserve imaging for gradual onset over weeks, recurrent or bilateral palsy, other cranial neuropathies, or failure to improve, which suggest neoplasm (parotid malignancy, schwannoma).
• Association tested most: pregnancy (third trimester/peripartum) and diabetes mellitus raise Bell palsy risk; diabetics need glucose monitoring once steroids start.