Nervous System & Special Senses

Bell palsy: diagnosis and management

Clinical Overview and When to Suspect Bell Palsy

— Annual incidence ~15–30 per 100,000; lifetime risk ~1 in 60

— Peak ages 15–45, but occurs across the lifespan

— Risk factors: pregnancy (especially third trimester and first postpartum week, ~3× risk), diabetes mellitus, obesity, hypertension, preeclampsia, upper respiratory infection in prior 2 weeks

— Otherwise healthy adult with sudden hemifacial weakness involving forehead AND lower face on the same side

— Inability to close the eye, drooling, food pocketing in the cheek, drooping of the corner of the mouth

— Often preceded by retroauricular pain, altered taste (dysgeusia), or hyperacusis

Board pearl: Step 3 stems will commonly place this patient in a primary-care or urgent-care setting; the highest-yield decisions are recognizing the LMN pattern, ruling out stroke clinically, starting prednisone within 72 hours, providing eye protection, and arranging short-interval follow-up. Avoid the trap of ordering routine MRI or Lyme serology in classic isolated unilateral disease.

Definition: Acute, idiopathic, unilateral lower motor neuron (LMN) facial nerve (CN VII) palsy that evolves over <72 hours and reaches maximum severity within ~1 week.

Epidemiology:

Pathophysiology: Inflammation, edema, and ischemic compression of CN VII within the bony facial canal (narrowest at the labyrinthine segment). Reactivation of HSV-1 in the geniculate ganglion is the leading mechanistic hypothesis; VZV reactivation produces Ramsay Hunt syndrome (a distinct entity).

When to suspect on a Step 3 stem:

Diagnostic framing: Bell palsy is a clinical diagnosis of exclusion in the ambulatory setting—no labs or imaging are required when the presentation is typical and isolated. The clinician's job is to (1) confirm LMN pattern, (2) screen for red flags suggesting alternative pathology, and (3) initiate timely steroid therapy within 72 hours of symptom onset.

Presentation Patterns and Key History

— Unilateral facial droop, inability to wrinkle forehead or close the eye fully (Bell phenomenon: eyeball rolls up on attempted closure—exposes sclera)

— Drooling, food trapping in the buccal sulcus, slurred labial speech

— Ipsilateral retroauricular or mastoid pain (50–60%) often preceding weakness by 1–2 days

— Dysgeusia (decreased taste anterior two-thirds of tongue—chorda tympani)

— Hyperacusis (stapedius muscle paralysis)

— Decreased tearing or, conversely, epiphora from poor lid closure

— Bilateral facial weakness → Lyme, sarcoidosis, GBS (Miller Fisher), HIV seroconversion

— Vesicles in ear canal or palate → Ramsay Hunt (VZV)—needs valacyclovir

— Tick exposure, erythema migrans, endemic area → Lyme neuroborreliosis

— Slowly progressive weakness over weeks, recurrent ipsilateral palsy, or facial twitching preceding weakness → parotid or CPA tumor

— Associated limb weakness, dysarthria, hemisensory loss, diplopia → stroke

— Hearing loss, vertigo, or otorrhea → otitis media, cholesteatoma, skull base lesion

— Trauma, recent dental/parotid surgery → mechanical injury

— Diabetes, pregnancy, immunocompromise

— Recent URI or vaccination

— Prior episodes (recurrent Bell palsy raises suspicion for Melkersson–Rosenthal syndrome: recurrent facial palsy, orofacial swelling, fissured tongue)

Key distinction: A patient who cannot wrinkle the forehead on the affected side has a peripheral (LMN) lesion; preserved forehead movement with lower-face weakness indicates a central (UMN) lesion—activate stroke workup immediately, not Bell palsy management.

Tempo: Onset over hours, maximal deficit by 72 hours; progression beyond 3 weeks argues strongly against Bell palsy and suggests tumor, chronic infection, or autoimmune cause.

Cardinal symptoms:

History red flags suggesting NOT Bell palsy:

Past medical and exposure history to elicit:

Physical Exam Findings and Neurologic Localization

— Loss of nasolabial fold, drooping mouth corner, widened palpebral fissure on the affected side

— Asymmetric blink, lagophthalmos (incomplete eye closure)

— Temporal — raise eyebrows / wrinkle forehead

— Zygomatic — close eyes tightly against resistance

— Buccal — smile, show teeth

— Mandibular — pucker lips, whistle

— Cervical — tense platysma

— Decreased taste anterior two-thirds of tongue

— Hyperacusis (stapedius)

— Decreased lacrimation (greater petrosal nerve—Schirmer test if performed)

— Full extraocular movements; no diplopia (rules out CN III, IV, VI involvement)

— Normal hearing and Weber/Rinne (rules out CN VIII, suggesting CPA lesion)

— No vesicles in external auditory canal, tympanic membrane, or palate (rules out Ramsay Hunt)

— Normal cerebellar testing, gait, and limb strength/sensation

— Otoscopy: normal TM, no cholesteatoma, no effusion

— Skin: no erythema migrans, no parotid mass on palpation

— Lymph nodes and parotid gland normal

Step 3 management: On the CCS, after confirming LMN pattern and a clean exam, document House–Brackmann grade, perform corneal exam with fluorescein if any irritation, and check that the patient can protect the eye—then move directly to steroid initiation and eye-care orders rather than imaging.

Inspection:

Motor testing of CN VII branches (all five must be weak on affected side in Bell palsy):

House–Brackmann grading (I–VI): Document baseline severity—Grade I normal, VI total paralysis. Grades III–IV predict slower but generally good recovery; V–VI predicts higher risk of incomplete recovery and synkinesis.

Adjunct CN VII findings:

Required negative exam to support Bell palsy:

Vital signs: Generally normal; fever or systemic illness should prompt search for alternative etiology.

Diagnostic Workup — Initial Labs and Imaging

— Lyme serology (ELISA → Western blot) if patient lives in or recently traveled to an endemic area (Northeast/Upper Midwest US), has erythema migrans, arthralgias, tick exposure, summer onset, or bilateral facial palsy

— HIV testing if risk factors, bilateral palsy, lymphadenopathy, or other systemic features

— HbA1c / fasting glucose if undiagnosed diabetes is suspected—diabetes worsens prognosis and is a comorbidity to address

— ACE level, chest x-ray if sarcoidosis is suspected (bilateral palsy, uveitis, parotid enlargement = Heerfordt syndrome)

— CBC, ESR/CRP only if systemic inflammatory or infectious process suspected

— RPR if syphilis risk

— Pregnancy test in reproductive-age women before steroid dosing decisions (though prednisone is acceptable in pregnancy)

— Atypical course: no improvement at 3 weeks, progression beyond 3 weeks, or worsening after initial plateau

— Recurrent ipsilateral palsy

— Associated cranial neuropathies, hearing loss, vertigo, or focal neuro signs

— Suspected trauma, mass, or otologic pathology

— MRI brain with gadolinium, dedicated internal auditory canal/temporal bone protocol — best test; may show enhancement of the facial nerve (nonspecific in Bell palsy but useful to rule out schwannoma, hemangioma, parotid tumor, CPA mass)

— CT temporal bone for trauma, cholesteatoma, or bony erosion

— Noncontrast head CT acutely if stroke cannot be excluded clinically (rare in true LMN presentations)

Board pearl: A stem describing bilateral simultaneous facial palsy is almost never Bell palsy—work up Lyme, sarcoidosis, GBS, HIV, and leukemia/lymphoma. Order Lyme serology, HIV, CXR, and consider LP.

Core principle: Classic isolated unilateral Bell palsy requires no labs or imaging. Diagnosis is clinical. Step 3 will reward you for not ordering reflexive testing.

Selective testing — order only when red flags are present:

Imaging — not routine. Reserve for:

Imaging modalities when indicated:

Diagnostic Workup — Advanced and Confirmatory Studies

— Electroneurography (ENoG): Compares compound muscle action potential (CMAP) amplitude on affected vs unaffected side. >90% degeneration within 3 weeks is a marker of poor prognosis and the historical threshold for considering surgical decompression.

— Needle EMG: Useful after 2–3 weeks; presence of voluntary motor units predicts good recovery; fibrillations alone indicate denervation.

— Bilateral facial palsy with suspicion of GBS/Miller Fisher (albuminocytologic dissociation) or neuroborreliosis (lymphocytic pleocytosis, intrathecal Lyme antibody production)

— Suspected meningeal carcinomatosis, sarcoidosis, or CNS infection

— Neurology: atypical course, recurrent palsy, suspected central lesion

— Otolaryngology/Neurotology: complete paralysis being considered for decompression, otologic findings, suspected temporal bone pathology

— Ophthalmology: corneal abrasion, exposure keratopathy, or inability to protect the eye

Key distinction: ENoG and EMG are prognostic tools, not used to make the diagnosis of Bell palsy. Step 3 stems that ask "what test confirms the diagnosis?" in a classic case—the answer is no test; diagnose clinically.

Electrodiagnostic testing — prognostic, not diagnostic. Reserve for patients with complete or near-complete paralysis (House–Brackmann V–VI) at 3–14 days from onset who may be candidates for surgical decompression or who need prognostic counseling.

Lumbar puncture: Consider when:

MRI findings supportive but not diagnostic of Bell palsy: Smooth enhancement of the geniculate ganglion, labyrinthine, tympanic, and mastoid segments of CN VII without a discrete mass. A mass lesion, asymmetric enhancement, or progressive enlargement should redirect workup toward schwannoma, perineural spread of cutaneous malignancy, or parotid tumor.

Audiometry: Indicated when hearing loss, tinnitus, or vertigo accompanies the facial palsy to evaluate CN VIII involvement (suggests CPA pathology).

Schirmer test and stapedial reflex testing: Historically used to localize the lesion along CN VII; rarely changes management today.

Specialty referral triggers for advanced workup:

Risk Stratification and First-Line Management Logic

— HB II–IV (incomplete paralysis): Most recover fully (>90%) with or without treatment; steroids still offered to improve speed and completeness of recovery.

— HB V–VI (severe/complete paralysis): ~60–70% complete recovery; benefit greatest from prompt combination steroid + antiviral therapy and consideration of electrodiagnostic prognostication.

— Pregnancy, diabetes, hypertension, immunocompromise—still treat with steroids in most cases; monitor glucose and BP closely

— Age >60, severe paralysis, hyperacusis, and dysgeusia at onset all predict slower recovery

— Confirm LMN pattern and rule out red flags

— Start prednisone within 72 hours

— Add valacyclovir if severe (HB V–VI) or if Ramsay Hunt is being considered

— Aggressive eye protection (artificial tears, lubricating ointment at night, taping/patching, sunglasses)

— Patient education on expected course and red-flag return precautions

— Follow-up at 1–2 weeks, then at 1 month and 3 months until resolution

— MRI, CT, Lyme serology, EMG/ENoG, or specialist referral in classic isolated cases

— Acyclovir/valacyclovir monotherapy (inferior to steroids; only adjunct)

— Physical therapy or electrical stimulation in acute phase (evidence weak; facial retraining therapy is appropriate later for synkinesis)

Step 3 management: The CCS-style answer for an otherwise healthy adult presenting at day 2 with isolated unilateral LMN facial weakness is: prednisone 60 mg PO daily × 7 days, artificial tears and overnight ocular lubrication, return precautions, follow-up in 1–2 weeks. Add valacyclovir for severe cases.

Time is the dominant variable: Steroid efficacy is greatest when started within 72 hours of symptom onset; benefit diminishes thereafter but is still reasonable up to 7 days.

Stratify by severity (House–Brackmann grade):

Stratify by patient-specific factors:

Core management bundle (ambulatory, first visit):

Do NOT routinely order:

Pharmacotherapy — First-Line Drug Regimen

— Prednisone 60–80 mg PO daily × 7 days, then either stop or taper over 5 days (common regimen: 60 mg × 5 days then taper by 10 mg/day)

— Alternative: prednisolone 25 mg PO BID × 10 days

— Start within 72 hours of symptom onset for maximal benefit; reasonable up to 7 days

— NNT ~10 for complete recovery at 9 months

— Mechanism: reduces inflammatory edema of CN VII within the facial canal

— Valacyclovir 1000 mg PO TID × 7 days OR acyclovir 400 mg 5× daily × 10 days

— Indicated in addition to steroids for severe/complete paralysis (HB V–VI), and standard of care if Ramsay Hunt suspected (vesicles → use higher antiviral doses)

— Antiviral monotherapy is inferior to steroids and should not be used alone in suspected Bell palsy

— Combination therapy may offer modest additional benefit in severe disease

— Preservative-free artificial tears every 1–2 hours while awake

— Lubricating ophthalmic ointment (e.g., Lacri-Lube, mineral oil/petrolatum) at bedtime

— Tape eyelid closed at night or use moisture chamber/eye patch to prevent exposure keratopathy

— Sunglasses outdoors to reduce wind/UV exposure

— Avoid empiric antibiotics unless Lyme or otitis is documented

— Caution with steroids in poorly controlled diabetes (monitor and adjust hypoglycemics), active peptic ulcer disease, severe psychiatric disease, or systemic infection

Board pearl: A common Step 3 distractor is valacyclovir monotherapy—it is the wrong answer. Prednisone alone > valacyclovir alone, and combination is reserved for severe cases. Always start steroids unless contraindicated.

Corticosteroids (cornerstone, AAN Level A evidence):

Antivirals (adjunctive, AAN Level C):

Ocular pharmacotherapy (essential—prevents the most common complication):

Analgesia: Acetaminophen or NSAIDs for retroauricular pain.

Drugs to avoid or use cautiously:

Counseling on steroid side effects: Insomnia, mood lability, hyperglycemia, GI upset, fluid retention, increased appetite—typically self-limited with the short course.

Procedures and Expanded Adjunctive Management

— Highly selective indication: severe/complete paralysis (HB V–VI) AND ENoG showing >90% degeneration within 14 days AND no voluntary EMG motor units

— Procedure: middle cranial fossa approach to decompress the labyrinthine segment of CN VII

— Performed by neurotology/skull base surgery; must be done within ~2 weeks of onset to confer benefit

— Evidence is limited; not routinely recommended; reserved for centers with expertise

— Neuromuscular retraining/mime therapy improves outcomes and reduces synkinesis in patients with incomplete recovery at 3 months

— Referral indication: persistent HB III or worse at 3 months, or development of synkinesis

— Electrical stimulation in the acute phase is NOT recommended—may worsen synkinesis

— Indicated for synkinesis, hemifacial spasm post-Bell palsy, and hyperlacrimation ("crocodile tears")

— Injected into overactive muscles (e.g., orbicularis oculi, platysma) every 3–4 months

— Refer to facial nerve clinic, otolaryngology, or oculoplastics

— Gold or platinum eyelid weights for persistent lagophthalmos

— Tarsorrhaphy for severe exposure keratopathy

— Static slings, dynamic muscle transfers, cross-facial nerve grafts, free gracilis transfer for persistent paralysis with cosmetic and functional deficit

CCS pearl: Do not advance the simulated clock weeks without scheduling a follow-up visit at 1–2 weeks to reassess for improvement, confirm eye protection adherence, and screen for steroid side effects. If no improvement by 3 weeks, order MRI and refer to neurology/ENT.

Surgical decompression of the facial nerve:

Facial rehabilitation therapy (subacute/chronic phase):

Botulinum toxin (chronic management):

Surgical management of chronic sequelae (>9–12 months):

Acupuncture, physical therapy modalities, vitamin B12, hyperbaric oxygen: Insufficient evidence; not standard.

Special Populations — Elderly and Renal/Hepatic Impairment

— Worse prognosis: higher rates of incomplete recovery, synkinesis, and persistent weakness

— Higher comorbidity burden (diabetes, hypertension, vascular risk factors)—lower threshold for stroke workup given overlapping presentations; if any doubt about central vs peripheral, obtain neuroimaging

— Steroid dose unchanged but monitor BP, glucose, and mental status closely; consider PPI if PUD risk

— Higher rate of comorbid herpes zoster oticus (Ramsay Hunt)—examine ear canal carefully

— Falls risk if vertigo or visual disturbance from eye patching—counsel

— 4–5× higher incidence of Bell palsy

— Worse prognosis with delayed and incomplete recovery

— Prednisone will raise blood glucose—instruct patient on home glucose monitoring 2–4× daily during steroid course; adjust insulin or oral agents; coordinate with primary diabetes management

— Consider shorter taper or lower dose only if hyperglycemia becomes uncontrolled

— Prednisone does not require renal dose adjustment

— Valacyclovir requires dose adjustment for CrCl <50 mL/min (e.g., CrCl 30–49: 1 g q12h; CrCl 10–29: 1 g q24h; <10: 500 mg q24h)—failure to adjust risks acute kidney injury and neurotoxicity (confusion, hallucinations, tremor)

— Ensure adequate hydration during antiviral therapy

— Prednisone metabolism reduced; usually no dose change but monitor for cushingoid effects

— Valacyclovir generally safe; acyclovir metabolites mostly renally cleared

— Higher index of suspicion for VZV, CMV, lymphoma, opportunistic infection

— Steroids must be balanced against infection risk—involve specialists

— Consider broader workup including MRI and LP earlier

Step 3 management: In a 72-year-old diabetic with HbA1c 8.5%, still start prednisone 60 mg × 7 days, but add home glucose monitoring QID, sliding-scale or temporary basal insulin uptitration, and dose-adjust valacyclovir if CKD is present. Do not withhold steroids based on diabetes alone.

Elderly (>60 years):

Diabetes mellitus:

Renal impairment:

Hepatic impairment:

Immunocompromised patients (HIV, transplant, chemotherapy):

Special Populations — Pregnancy and Pediatrics

— Incidence ~3× higher, especially third trimester and first postpartum week

— Associated with preeclampsia and gestational hypertension—check BP, urine protein, and screen for preeclampsia features (headache, RUQ pain, visual changes, hyperreflexia) in any pregnant patient presenting with Bell palsy

— Prednisone is generally safe in pregnancy (Category C; small risk of cleft palate with first-trimester exposure is debated and modest); use at standard doses if benefit outweighs risk, especially in second/third trimester

— Valacyclovir is Category B and considered safe in pregnancy; reserve for severe disease per usual criteria

— Coordinate care with obstetrics; document shared decision-making

— Prognosis in pregnancy-associated Bell palsy may be slightly worse than in nonpregnant patients, especially with complete paralysis

— Children generally have excellent prognosis (>90% complete recovery), often without treatment

— Lyme disease is a major cause of facial palsy in children in endemic areas—always test (Lyme ELISA → Western blot) in endemic geography, bilateral palsy, summer presentation, or tick exposure; treat confirmed Lyme with doxycycline (age ≥8) or amoxicillin/cefuroxime (younger) × 14–21 days

— Steroid use in children with idiopathic Bell palsy is less clearly beneficial than in adults; reasonable in severe cases, typically prednisone/prednisolone 1 mg/kg/day (max 60 mg) × 5–7 days

— Eye care principles identical

— Rule out otitis media and cholesteatoma with thorough otoscopy

Board pearl: A child in Connecticut presenting in July with unilateral facial droop and a recent "rash that looked like a target"—the diagnosis is Lyme neuroborreliosis, not Bell palsy. Send Lyme serology and start doxycycline (age ≥8) or amoxicillin (younger); steroids are not the answer here.

Pregnancy:

Pediatrics:

Recurrent or bilateral palsy in any age: Workup for Lyme, sarcoidosis (Heerfordt), GBS, HIV, leukemia/lymphoma, and Melkersson–Rosenthal syndrome.

Postpartum care: Standard treatment; lactation compatible with prednisone and valacyclovir.

Complications and Adverse Outcomes

— Caused by lagophthalmos plus reduced lacrimation and impaired blink

— Symptoms: foreign body sensation, redness, pain, photophobia, blurred vision

— Prevention: aggressive lubrication, nighttime taping, ointment, sunglasses

— Management: ophthalmology referral for any persistent eye complaint; fluorescein staining to detect abrasion; topical antibiotics for infectious ulcer

— ~70% of all patients achieve complete recovery; 30% have residual weakness or sequelae

— Worse prognostic factors: complete paralysis at onset, age >60, diabetes, hypertension, severe pain, hyperacusis, delayed treatment, >90% degeneration on ENoG

— Most recovery occurs by 3–6 months; minimal further improvement after 9–12 months

— Aberrant reinnervation causing involuntary co-contraction (e.g., eye closes with smiling, mouth twitches when blinking)

— Develops months after the acute episode

— Treated with neuromuscular retraining and botulinum toxin

— Steroid-induced hyperglycemia, insomnia, mood lability, hypertension, gastritis

— Valacyclovir-associated AKI or neurotoxicity (esp. if not renally dosed)

Key distinction: New-onset eye pain or redness in a Bell palsy patient is a corneal emergency until proven otherwise—immediate fluorescein exam and ophthalmology referral; do not assume it is benign irritation.

Exposure keratopathy and corneal ulceration (most common preventable complication):

Incomplete recovery:

Synkinesis:

Hemifacial spasm: Tonic and clonic contractions of facial muscles; treat with botulinum toxin

Crocodile tears (gustatory lacrimation): Aberrant reinnervation of lacrimal gland by salivary fibers—lacrimation during eating; managed with botulinum toxin to the lacrimal gland

Contracture and facial asymmetry at rest

Psychosocial impact: Depression, anxiety, social withdrawal due to facial disfigurement—screen and counsel; refer to mental health resources as needed

Recurrent ipsilateral Bell palsy: ~7% lifetime recurrence—heightens suspicion for tumor; consider MRI on second episode

Iatrogenic complications:

When to Escalate Care

— Forehead is spared (UMN pattern) → suspect stroke

— Sudden onset with any limb weakness, dysarthria, hemisensory loss, ataxia, diplopia, or vertigo

— Altered mental status, severe headache, neck stiffness

— Acute trauma with facial palsy

— Atypical course: progression beyond 3 weeks, no improvement at 3–4 months, or worsening after initial stabilization

— Recurrent ipsilateral palsy

— Bilateral simultaneous facial palsy (consider admission for GBS workup with LP, spirometry, NIF)

— Associated cranial neuropathies or systemic neurologic findings

— Otologic findings (vesicles, otorrhea, cholesteatoma, mass)

— Complete paralysis (HB V–VI) considering electrodiagnostic testing and possible decompression

— Hearing loss or vertigo accompanying facial palsy

— Suspected parotid or temporal bone tumor

— Corneal abrasion, ulcer, or persistent exposure keratopathy

— Severe lagophthalmos requiring tarsorrhaphy or eyelid weight

— Persistent vision changes

— Suspected Lyme neuroborreliosis with CNS involvement

— HIV-associated facial palsy

— Complex zoster oticus

— Inability to protect the eye and lack of caregiver support

— Suspected GBS, meningitis, or stroke

— Severe comorbid decompensation (e.g., DKA precipitated by steroid initiation)

— Need for IV antiviral therapy (severe Ramsay Hunt with CNS involvement)

CCS pearl: On the CCS, if the stem describes a patient with forehead sparing or any focal limb finding, immediately switch to a stroke workup: noncontrast head CT, NIHSS, glucose, then MRI/MRA—do not order prednisone for this patient.

Refer to Emergency Department or activate stroke protocol if:

Refer to Neurology if:

Refer to Otolaryngology/Neurotology if:

Refer to Ophthalmology if:

Refer to Infectious Disease if:

Inpatient admission criteria (uncommon for isolated Bell palsy):

Key Differentials — Same-Category (Peripheral CN VII Lesions)

— VZV reactivation in geniculate ganglion

— Vesicles in ear canal, tympanic membrane, or palate + facial palsy + otalgia

— Often accompanied by hearing loss, tinnitus, vertigo (CN VIII involvement)

— Worse prognosis than Bell palsy; treat aggressively with prednisone + valacyclovir 1 g TID × 7–10 days, started ASAP

— Endemic exposure, EM rash, summer presentation, bilateral palsy in 30% of cases

— Serology + LP if CNS symptoms; treat with doxycycline 100 mg BID × 14–21 days (or IV ceftriaxone if meningitis)

— Steroids are controversial in Lyme-associated palsy; some evidence of worse outcome—prioritize antibiotics

Key distinction: Vesicles in the ear = Ramsay Hunt, not Bell palsy—the antiviral is now mandatory (not optional), and prognosis is materially worse. Always inspect the external auditory canal.

Ramsay Hunt syndrome (herpes zoster oticus):

Lyme neuroborreliosis:

Acute otitis media or cholesteatoma: Facial palsy with otologic findings; treat infection, urgent ENT referral

Parotid tumor (benign or malignant): Gradual onset weakness, palpable mass, often with progressive course over weeks; warrants MRI and parotid evaluation

Facial nerve schwannoma or hemangioma: Slowly progressive or recurrent ipsilateral palsy; MRI diagnostic

Traumatic facial nerve injury: Temporal bone fracture; CT temporal bone; ENT urgent

Iatrogenic injury: Parotidectomy, mastoidectomy, dental nerve block injury

Skull base tumor (e.g., nasopharyngeal carcinoma, perineural spread of cutaneous SCC): Multiple cranial neuropathies, prior head/neck cancer, persistent regional pain

Sarcoidosis (Heerfordt syndrome): Uveitis, parotid enlargement, fever, facial palsy (often bilateral); CXR shows hilar adenopathy; treat sarcoidosis

Melkersson–Rosenthal syndrome: Recurrent facial palsy + orofacial edema + fissured tongue; rare granulomatous condition

Key Differentials — Other-Category (Central and Systemic Mimics)

— Forehead spared due to bilateral cortical innervation of the upper face

— Often with limb weakness, dysarthria, sensory loss, gaze deviation

— Pontine stroke may rarely produce isolated LMN-pattern palsy with crossed signs (Millard–Gubler: ipsilateral CN VI + VII palsy with contralateral hemiparesis)—still requires emergent imaging

— Work up with NIHSS, noncontrast CT, MRI/MRA, glucose, ECG

— Bilateral facial weakness, ascending limb weakness, areflexia, ophthalmoplegia, ataxia

— Recent GI (Campylobacter) or respiratory infection

— LP: albuminocytologic dissociation; monitor respiratory function (NIF, FVC)

— Treat with IVIG or plasmapheresis; admit

Board pearl: "Forehead-sparing weakness" = stroke until proven otherwise, regardless of how convincing other features sound. This is the single most testable distinction on Step 3 facial-palsy stems.

Ischemic or hemorrhagic stroke (UMN facial palsy):

Guillain–Barré syndrome (especially Miller Fisher variant):

Multiple sclerosis: Recurrent or relapsing neurologic deficits in young adult; MRI brain shows demyelinating lesions; CN VII palsy can be a presenting feature

Myasthenia gravis: Fatigable weakness, ptosis, diplopia, bulbar symptoms; not typically isolated unilateral facial palsy

Brain tumor or CPA mass (vestibular schwannoma, meningioma): Slowly progressive palsy, often with hearing loss and tinnitus; MRI internal auditory canal

HIV seroconversion or AIDS-related opportunistic infection: Bilateral palsy at seroconversion; CMV, toxoplasmosis, lymphoma in advanced disease

Diabetic mononeuropathy: Isolated cranial nerve palsy in poorly controlled diabetes; usually CN III (pupil-sparing) but can affect CN VII; resolves over weeks

Vasculitis (GPA, polyarteritis nodosa, GCA): Multiple cranial neuropathies, systemic symptoms, elevated ESR

Leukemic or lymphomatous infiltration of cranial nerves: Bilateral palsy with B symptoms or known hematologic malignancy

Botulism: Descending paralysis, cranial nerves first; canned food, infants and honey

Preeclampsia: Pregnant patient with hypertension, proteinuria, and new facial palsy—evaluate for preeclampsia

Secondary Prevention and Long-Term Plan

— Tight diabetes control: HbA1c target individualized, generally <7%

— Blood pressure control: <130/80 per ACC/AHA in most adults; especially important if Bell palsy occurred during pregnancy (future cardiovascular risk marker)

— Weight management, smoking cessation, lipid management as indicated

— Prednisone course (typically 7 days ± taper)—instructions to complete the course

— Valacyclovir if prescribed—renal dose-adjusted; ensure hydration

— Artificial tears and ophthalmic ointment—continue until full eyelid closure returns

— Acetaminophen or NSAIDs for residual pain

— Most patients begin to improve within 3 weeks

— Maximum recovery typically by 3–6 months; minimal further improvement after 9–12 months

— 70–85% complete recovery overall; higher with prompt treatment

— ~7% lifetime recurrence (ipsilateral or contralateral)

— A second episode warrants MRI brain with IAC protocol to exclude tumor and consideration of Melkersson–Rosenthal syndrome

— Synkinesis, hemifacial spasm, crocodile tears → botulinum toxin and facial rehabilitation

— Persistent lagophthalmos → eyelid weights, tarsorrhaphy

— Psychosocial support: depression screening, support groups

— Shingles vaccine (Shingrix) at age ≥50 reduces zoster reactivation, including Ramsay Hunt—encourage age-appropriate vaccination

— No contraindication to routine vaccines after Bell palsy

Step 3 management: At the 1-month follow-up visit, address diabetes control, BP, eye protection adherence, mental health, and arrange physical/facial therapy if House–Brackmann grade has not improved to II or better—this is the secondary-prevention bundle the exam wants you to think about.

There is no proven primary prevention for idiopathic Bell palsy, but identifying and treating modifiable risk factors reduces recurrence and improves overall neurovascular health:

Discharge/post-visit medication summary:

Counseling on natural history:

Recurrence:

Long-term sequelae management:

Vaccination considerations:

Pregnancy planning: Counsel on increased risk during future pregnancies, particularly with history of preeclampsia.

Follow-Up, Monitoring, and Rehabilitation

— 1–2 weeks after presentation: reassess House–Brackmann grade, eye protection adherence, steroid tolerance and glucose, screen for complications

— 1 month: most patients show improvement; if HB unchanged or worse, order MRI and refer to neurology/ENT

— 3 months: if persistent HB III or worse, refer to facial nerve clinic or physical therapy for neuromuscular retraining

— 6 and 9 months: assess for synkinesis and residual deficits; refer for botulinum toxin or surgical options if indicated

— Blood glucose (especially diabetics on prednisone)

— Blood pressure

— Mood and sleep (steroid side effects)

— Renal function if on valacyclovir and risk factors present

— Eye comfort and vision (ask explicitly; examine with fluorescein if any complaint)

— Neuromuscular facial retraining (mime therapy) with a trained therapist is the evidence-supported rehab modality—introduced when voluntary motion returns (usually after 3 months if recovery is incomplete)

— Avoid aggressive electrical stimulation and forced gross facial exercises in the acute phase—may worsen synkinesis

— Teach gentle range-of-motion and symmetrical facial movements with a mirror

— Reassure about natural history and high overall recovery rate

— Explain that Bell palsy is not stroke and not contagious

— Address cosmetic concerns and offer mental health resources

— Provide written instructions for eye care and red flags (eye pain, vision change, new neurologic symptoms, no improvement at 3 weeks)

CCS pearl: Schedule a return visit at 1–2 weeks explicitly—the exam rewards proactive follow-up. At that visit, recheck HB grade, ask about eye symptoms (fluorescein exam if any), check glucose and BP, and adjust the plan rather than passively advancing time.

Follow-up cadence (ambulatory):

Monitoring parameters during treatment:

Rehabilitation:

Counseling points:

Driving and work: Generally safe to continue if vision is protected and no other neurologic deficits; counsel on sun and wind protection with eyewear.

Ethical, Legal, and Patient Safety Considerations

— Discuss benefits (NNT ~10 for complete recovery) and risks (hyperglycemia, insomnia, mood changes, infection risk, rare avascular necrosis)

— Document shared decision-making, especially in patients with diabetes, pregnancy, peptic ulcer disease, psychiatric history, or active infection

— In pregnancy, document discussion of fetal risk and maternal benefit; consult OB

— Missing a stroke masquerading as Bell palsy is one of the highest-liability errors in ambulatory medicine—always test forehead movement and perform a complete neuro exam; document findings

— Conversely, unnecessary CT/MRI exposes patients to cost, radiation, and incidental findings—Choosing Wisely supports clinical diagnosis without routine imaging

— Missing Lyme disease in endemic regions or Ramsay Hunt delays appropriate antiviral/antibiotic treatment and worsens outcomes—always inspect the ear and ask about ticks/rash

— Failure to protect the cornea can lead to permanent vision loss

— Verify patient and caregiver understanding; provide written instructions

— Document counseling

— If diagnosed in ED or urgent care, ensure primary care follow-up within 1–2 weeks with explicit handoff; closed-loop communication of the prednisone course and eye care plan

— Provide patient with a discharge summary including expected course and red flags

— Lyme disease, when diagnosed, is reportable in most US states

— Suspected child abuse if pediatric facial findings are inconsistent with history—mandatory reporting

— Counsel on impaired vision from eye patching and potential safety considerations for occupations requiring binocular vision or facial expression (e.g., commercial driving, performance professions)

— Facial disfigurement carries significant stigma; provide empathetic counseling and address mental health

— Use medical interpreters as needed to ensure understanding of eye-care instructions—this is a major safety issue when language barriers exist

Board pearl: A Step 3 vignette ending with an ED-discharged Bell palsy patient who returns at week 4 with a corneal ulcer is almost always testing transition-of-care failure: no PCP follow-up scheduled, no written eye-care instructions, no documented counseling. The fix is closed-loop discharge planning.

Informed consent for steroid therapy:

Diagnostic error and patient safety:

Eye protection — patient safety priority:

Transitions of care:

Mandatory reporting and public health:

Driver and occupational safety:

Cultural and psychosocial considerations:

High-Yield Associations and Rapid-Fire Clinical Facts

Key distinction: Anterior two-thirds of tongue taste = chorda tympani (CN VII); posterior one-third = CN IX. Bell palsy affects taste in the anterior two-thirds ipsilaterally.

Bell phenomenon: Upward rolling of the eyeball on attempted eye closure—exposes white sclera; classic LMN CN VII finding

Forehead sparing = UMN lesion = think stroke, not Bell palsy

Pregnancy 3rd trimester / postpartum: 3× risk; check for preeclampsia

Diabetes: 4–5× risk; worse prognosis

Lyme disease: Most common cause of pediatric facial palsy in endemic US regions; bilateral palsy in 30%

Ramsay Hunt: Vesicles in ear/palate + facial palsy ± hearing loss/vertigo; treat with prednisone + valacyclovir

Heerfordt syndrome (uveoparotid fever): Sarcoidosis with uveitis + parotid enlargement + fever + facial palsy

Melkersson–Rosenthal syndrome: Recurrent facial palsy + orofacial swelling + fissured tongue

Millard–Gubler syndrome: Pontine stroke causing ipsilateral CN VI + VII palsy with contralateral hemiparesis

Treatment window: Prednisone within 72 hours; latest reasonable benefit by 7 days

Prednisone dose: 60 mg PO daily × 7 days (or 25 mg BID × 10 days of prednisolone)

Valacyclovir dose: 1 g PO TID × 7 days (adjunct in severe disease)

House–Brackmann grading: I (normal) to VI (total paralysis); HB V–VI predicts incomplete recovery

ENoG >90% degeneration at 2 weeks: Poor prognosis; consider surgical decompression

Recovery timeline: Most by 3 months; complete by 6–9 months in 70–85%

Recurrence rate: ~7% lifetime

Synkinesis: Aberrant reinnervation; treat with botulinum toxin and neuromuscular retraining

Crocodile tears: Lacrimation while eating from aberrant reinnervation

Eye care: Artificial tears, ointment at night, tape eye closed, sunglasses

Choosing Wisely: Don't routinely obtain neuroimaging in classic isolated unilateral LMN facial palsy

Antiviral monotherapy is the wrong answer in most Step 3 stems—steroids first

Shingrix vaccine at age ≥50 reduces Ramsay Hunt risk via VZV protection

Pediatric Bell palsy: Excellent prognosis; consider lower threshold to skip steroids in mild cases

Bilateral simultaneous palsy: Almost never idiopathic Bell palsy—work up Lyme, GBS, sarcoid, HIV, leukemia

Pregnancy + Bell palsy: Still treat with prednisone after OB discussion

Board Question Stem Patterns

Step 3 management: When in doubt between answer choices, pick prednisone within 72 hours + eye protection + close follow-up for classic Bell palsy; pick stroke workup if forehead is spared; pick antibiotics if Lyme features are present.

Stem 1 — Classic Bell palsy: 32-year-old healthy woman with 1-day history of left facial droop, inability to close left eye, drooling, and retroauricular pain. Exam: complete left-sided LMN facial weakness; otherwise normal. Best next step? → Prednisone 60 mg daily × 7 days + artificial tears and overnight lubrication + 1–2 week follow-up. Do not order MRI, Lyme serology, or valacyclovir monotherapy.

Stem 2 — Stroke mimic: 68-year-old hypertensive man with sudden left facial droop, forehead spared, slurred speech, and right arm weakness. → Activate stroke protocol, noncontrast head CT, NIHSS, glucose, MRI/MRA. Not Bell palsy.

Stem 3 — Ramsay Hunt: 55-year-old with facial palsy, severe ear pain, vertigo, vesicles on the auricle and ear canal. → Prednisone + valacyclovir 1 g TID × 7–10 days, ENT referral, audiometry.

Stem 4 — Lyme: 10-year-old in Connecticut in July with new facial droop and a "ring-shaped rash" on the thigh. → Lyme ELISA, doxycycline (age ≥8) or amoxicillin × 14–21 days, eye protection. Steroids not first-line.

Stem 5 — Pregnancy: 28-year-old at 36 weeks with facial palsy and BP 152/98 with proteinuria. → Evaluate for preeclampsia; OB consult; if isolated Bell palsy, prednisone is acceptable.

Stem 6 — Diabetic: 60-year-old with HbA1c 9.2% and new facial palsy. → Start prednisone, home glucose monitoring QID, adjust diabetic regimen, expect somewhat worse prognosis.

Stem 7 — Bilateral palsy: 24-year-old with bilateral facial weakness and ascending limb weakness after recent diarrheal illness. → GBS; admit, LP, monitor respiratory status, IVIG.

Stem 8 — Recurrent ipsilateral palsy: Third episode of left facial palsy in 5 years. → MRI brain with internal auditory canal protocol to evaluate for schwannoma; consider Melkersson–Rosenthal.

Stem 9 — Slow progression: Facial weakness progressing over 6 weeks with palpable parotid mass. → MRI and ENT/oncology referral; not Bell palsy.

Stem 10 — Eye complication: Bell palsy patient returns at 2 weeks with eye pain and redness. → Fluorescein exam; corneal abrasion or exposure keratopathy; ophthalmology referral; reinforce nighttime taping and ointment.

Stem 11 — Late presentation: Patient presents day 10 with new Bell palsy. → Steroid benefit reduced but still consider; emphasize eye care and follow-up.

One-Line Recap

Bell palsy is an acute, idiopathic, lower-motor-neuron unilateral facial nerve palsy diagnosed clinically and best treated with prednisone within 72 hours plus aggressive eye protection, with antivirals reserved for severe cases or Ramsay Hunt, while always ruling out stroke, Lyme disease, and other mimics.

Board pearl: The Step 3 winning answer for the classic stem is almost always "prednisone now, lubricate the eye, see me in two weeks" — and the highest-yield trap to avoid is reflexive neuroimaging, antiviral monotherapy, or missing a forehead-sparing stroke.

Diagnosis is clinical — no routine imaging or labs in classic isolated unilateral LMN palsy; reserve MRI, Lyme, HIV, and CXR for atypical, bilateral, recurrent, or red-flag presentations.

First-line therapy — prednisone 60 mg PO daily × 7 days started within 72 hours of symptom onset; add valacyclovir 1 g TID × 7 days for severe paralysis (HB V–VI) or suspected Ramsay Hunt; antiviral monotherapy is wrong.

Eye protection is non-negotiable — preservative-free artificial tears during the day, lubricating ointment and taped eye closure at night, sunglasses outdoors; corneal ulceration is the most common preventable serious complication.

Forehead sparing means stroke, not Bell palsy — the single most tested distinction; bilateral palsy means Lyme, GBS, sarcoidosis, or HIV; slowly progressive palsy means tumor.

Follow-up at 1–2 weeks, 1 month, 3 months — reassess House–Brackmann grade, screen for steroid side effects (especially glucose in diabetics), check eye protection adherence, and refer to facial rehabilitation or ENT/neurology if no improvement by 3 weeks or persistent HB III+ at 3 months.