Bell Palsy

Bell palsy is an acute, unilateral, lower motor neuron paralysis of the facial nerve (cranial nerve VII), most often attributed to reactivation of latent herpes simplex virus type 1 within the geniculate ganglion, producing inflammation and edema of the nerve as it passes through the narrow bony facial canal.^[1] Because the nerve is compressed within that fixed bony channel, this swelling is what actually threatens the nerve fibres — the same mechanism that makes early anti-inflammatory treatment time-sensitive. Bell palsy is a diagnosis of exclusion: it must never be presumed until other causes of facial weakness — most urgently stroke, but also Ramsay Hunt syndrome and Lyme disease — have been considered and excluded (see Assessment & Diagnosis).^[2] Most patients recover completely without any specific intervention, but corticosteroid therapy has been shown to reduce the rate of incomplete recovery,^[3] and that benefit is meaningfully greater, and more complete, when treatment is started early — within 72 hours, and ideally within 48 hours, of symptom onset — which makes the timing of this single decision one of the highest-yield counselling points a pharmacist will encounter in this condition.^[4]

Typical presentation

Acute onset (hours to 1-3 days) of unilateral facial weakness or paralysis affecting both the upper and lower face — this is the single most important examination finding in the whole condition, because it is what separates a peripheral facial nerve palsy from a central (stroke) cause. Ask the patient to raise their eyebrows and wrinkle their forehead: preserved forehead movement on the weak side points to a central lesion instead, since the forehead has bilateral cortical innervation and is spared in stroke but not in Bell palsy.

Commonly accompanying features include post-auricular or ear pain (which may precede the facial weakness by a day or two), hyperacusis (increased sensitivity to sound from stapedius muscle weakness), and altered taste over the anterior two-thirds of the tongue (chorda tympani involvement). Decreased tearing, or paradoxically excessive tearing or drooling from poor eyelid and mouth closure, drooping of the mouth corner, and difficulty with speech articulation are also common.

Time course

Weakness typically progresses over hours to a few days and then plateaus. Continued progression beyond 3 weeks, or a very slowly progressive course from the outset, is atypical for Bell palsy and should prompt reconsideration of the diagnosis (see Red Flags & Refer).

• Pregnancy, particularly the third trimester and the first few postpartum weeks.^[5]
• Hypertension.
• Diabetes mellitus.
• Recent immunization (e.g., COVID-19 vaccination) has been associated with a modestly increased risk in some studies — vaccine benefits still clearly outweigh this risk, and vaccination should not be withheld or delayed because of it.
• A preceding upper respiratory illness, consistent with the proposed viral-reactivation mechanism.
• A personal history of a prior episode — recurrence on the same or the opposite side occurs in a minority of patients and should prompt reconsideration of the diagnosis and specialist referral rather than automatic retreatment (see Red Flags & Refer).

Differential diagnosis of unilateral (and bilateral) facial weakness

Confirm the presentation truly fits idiopathic Bell palsy before treating for it — the table below covers every entity that can present as facial weakness and needs to be actively considered, not just stroke.

Rarely, diabetic ischemic cranial neuropathy, HIV infection, and tuberculosis can also cause facial palsy and should be considered when the history supports them.

History

• Exact time since symptom onset — the single most time-critical piece of information, since it determines whether the corticosteroid window is still open.
• Ear pain, hearing changes, vertigo, and any rash in or around the ear.
• Tick exposure, travel to or residence in a Lyme-endemic area, and any erythema migrans-type rash.
• Immunocompromising conditions or medications.
• Pregnancy status.
• Prior episodes of facial palsy.

Examination

• Forehead movement — the key test distinguishing a peripheral palsy from a central (stroke) cause.
• A full cranial nerve examination and a brief limb/gait assessment to look for any other focal neurological deficit.
• Otoscopic examination for vesicles, discharge, or mastoid tenderness.
• Palpation of the parotid gland for a mass.
• Assessment of eyelid closure — critical for determining eye-protection intensity (see Non-Pharmacologic Treatment).

Grading severity

Objective grading is not required before starting treatment, but it is useful for documenting baseline severity, informing the corticosteroid-plus-antiviral decision, and tracking recovery. The House-Brackmann grading system is the most widely used scale internationally; it is a descriptive, categorical 6-grade classification assigned by clinical judgment, not a point-sum score, so no calculator applies to it.^[6]

The Sunnybrook Facial Grading System is a more detailed, continuously-scored alternative used mainly by specialists following patients with an inadequate recovery; it is more sensitive to partial change over time than House-Brackmann but requires more training to administer and is not needed for routine assessment.^[7]

Investigations

Investigations are seldom needed once a complete history and examination have excluded the other causes of facial weakness above — Bell palsy remains a clinical diagnosis, and waiting on results should never delay starting corticosteroid therapy within the effective window.

• Electromyography and facial nerve conduction studies can help with prognosis, but only once performed 8-10 days after onset — ordering them earlier does not give useful information.
• CT imaging is appropriate when trauma is a plausible cause.
• MRI may be indicated when atypical features are present — fever, immunocompromised state, or other focal neurological symptoms or signs.
• Lyme serology when the history supports possible exposure — endemic area, tick bite, erythema migrans, joint symptoms.
• No routine laboratory testing is otherwise useful.

• Maximize the probability of complete recovery of facial nerve function by limiting further denervation — achieved primarily through prompt, appropriately-dosed corticosteroid therapy.
• Protect the cornea from exposure keratopathy for as long as eyelid closure remains incomplete.
• Control pain and inflammation during the acute phase.
• Correctly exclude stroke and the other mimics in the differential before committing to a Bell palsy diagnosis and treatment plan.
• Identify the specific patients — severe or complete paralysis, immunocompromised, suspected Ramsay Hunt syndrome — who may gain additional benefit from adding an antiviral to the corticosteroid.

Eye protection — essential in every patient with incomplete eyelid closure

Because incomplete or absent voluntary eyelid closure prevents the normal blink reflex from keeping the cornea moist and protected, any patient who cannot fully close the affected eye is at real risk of exposure keratopathy and corneal abrasion — start protection on the day of diagnosis, not after eye symptoms appear.

• Lubricate the eye with preservative-free artificial tears or lubricating drops frequently during the day — at least every 1-2 hours while awake if the eye feels dry or irritated, more often if needed.
• Apply a thicker lubricating, petrolatum-based ophthalmic ointment at bedtime, then gently tape the eyelid closed overnight — this is the single most effective way to prevent overnight corneal drying, since blinking stops entirely during sleep.
• Wear wraparound glasses or goggles during the day to reduce airflow and debris reaching an incompletely-protected eye.
• Review taping technique directly with the patient or caregiver — the tape should close the lid without pressing on the globe, and a skin-friendly tape should be used to avoid periocular skin irritation with nightly use.
• Continue eye protection until eyelid closure has visibly recovered, not just until the facial weakness subjectively feels better — reassess this specifically at every follow-up.

Facial exercises and physical therapy

Facial muscle exercises, ideally taught and supervised by a physiotherapist, may help recovery when started in the early stages of Bell palsy; overall evidence quality for this intervention is low, but it is a reasonable, low-risk adjunct to offer alongside corticosteroid therapy, not a substitute for it.^[11]

Acupuncture

No high-quality trial evidence establishes a clear benefit for acupuncture in Bell palsy. If a patient wants to pursue it, position it as an adjunct that has not been proven to change outcomes, never as a substitute for timely corticosteroid therapy.

General counselling

• Most patients recover completely — reassure the patient early, while being honest that recovery may take weeks to months.
• Reinforce that starting corticosteroid treatment as early as possible is the single action within the patient's control most likely to improve the chance of complete recovery.
• Counsel specifically on chewing carefully and protecting the mouth from biting the inside of the cheek on the weak side, since sensation and muscle control are both reduced.

Pregnancy

Breastfeeding

Prednisone is considered compatible with breastfeeding — transfer into breast milk is low, and no harm has been reported in exposed infants. Valacyclovir and acyclovir are the preferred antivirals in breastfeeding, given minimal transfer into breast milk and a reassuring reported safety record; data for famciclovir in breastfeeding are limited, so prefer valacyclovir or acyclovir when an antiviral is genuinely needed.

Pediatrics

Current randomized-trial evidence does not demonstrate a benefit from corticosteroid therapy in children with Bell palsy — a large placebo-controlled trial found no improvement in complete recovery with prednisolone compared with placebo.^[12] The risk of incomplete recovery from Bell palsy in children is low regardless of treatment, since the great majority recover fully without any specific therapy. Routine corticosteroid use in children is therefore not currently recommended outside specialist direction; supportive care — eye protection, analgesia as needed, and reassurance — remains the mainstay. There is no evidence available for antiviral use in children with Bell palsy, and it should not be used outside specialist direction.

Renal and hepatic impairment

A short, 10-day corticosteroid course as used for Bell palsy does not require renal dose adjustment. Use caution and closer blood-glucose monitoring in patients with diabetes and in those with hepatic impairment affecting corticosteroid metabolism. The antiviral agents are renally cleared, so acyclovir, valacyclovir, and famciclovir all require dose reduction in significant renal impairment — see each drug's individual Drug Database entry for the specific adjustment.

Other populations requiring caution with corticosteroid therapy

• Systemic fungal infection is a contraindication to corticosteroid therapy — do not start prednisone in this setting.
• Peptic ulcer disease — use corticosteroids with caution, and avoid adding an NSAID on top of the corticosteroid course when possible.
• Poorly controlled diabetes — corticosteroids will worsen glycemic control for the duration of the course; counsel on more frequent blood-glucose monitoring during treatment.
• Immunocompromised patients — this group is specifically one where adding an antiviral to the corticosteroid is favoured (see Choose Initial Treatment).

Arrange follow-up contact within 1-2 weeks of starting treatment to confirm the expected trajectory — most patients begin to show some improvement within the first few weeks, with continued recovery over the following months. Reassess eyelid closure specifically at this visit, since eye-protection intensity should track the actual degree of closure, not the patient's overall sense of improvement. Confirm the full corticosteroid course, and antiviral course if prescribed, was completed as directed. If electromyography or facial nerve conduction studies were ordered for prognosis, remember these are only informative once performed 8-10 days after onset — earlier results should not be used to guide decisions. Watch specifically for delayed complications over the following months: synkinesis (unwanted, linked movements — for example, the eye closing involuntarily during a smile), gustatory lacrimation (tearing while eating, sometimes called crocodile tears), and other signs of aberrant nerve regeneration. Ask about eye symptoms at every contact for as long as eyelid closure remains incomplete, and refer urgently to ophthalmology for any new eye redness, pain, photophobia, or visual change.

1. Re-confirm the diagnosis before assuming treatment has failed — re-examine specifically for forehead sparing, other neurological deficits, a vesicular rash that may have appeared after the initial visit, or systemic features pointing to Lyme disease or another alternative diagnosis (see Assessment & Diagnosis).
2. Confirm the corticosteroid, and antiviral if prescribed, was started within the effective window and the full course was actually completed at the correct dose.
3. If eyelid closure is still incomplete, escalate eye-protection intensity (more frequent drops, confirm nightly ointment and taping are actually being done) and refer to ophthalmology if there are any signs of corneal irritation or damage.
4. If there is no meaningful improvement, or the condition is worsening, by about 3 months from onset, refer to otolaryngology or neurology — electromyography/nerve conduction studies (if not already done) and formal facial grading can help with prognosis and further management planning.
5. Persistent, unwanted synkinetic movements or excessive tearing appearing months after the acute illness are managed with referral for consideration of botulinum toxin injection by a specialist experienced with facial palsy.^[13]
6. Surgical facial nerve decompression is not a routine treatment-failure step — current evidence is of low quality and insufficient to determine whether it helps or harms, so it remains a specialist-directed option considered only in select, carefully evaluated cases.^[14]

• Delaying corticosteroid initiation to wait for a specialist referral, imaging, or lab results — treat empirically once red flags have been reasonably excluded, since delay past the 48-72 hour window meaningfully reduces the achievable benefit.
• Starting an antiviral without a corticosteroid — antiviral monotherapy has no proven benefit in Bell palsy.
• Reflexively adding an antiviral to every case — reserve it for severe/complete paralysis, immunocompromised patients, or suspected Ramsay Hunt syndrome.
• Missing forehead sparing or another focal neurological deficit that indicates a central (stroke) cause requiring urgent stroke workup instead of Bell palsy treatment.
• Failing to counsel on eye protection — especially nightly ointment and taping — a major, often-overlooked source of preventable harm (exposure keratopathy) in a condition that is otherwise usually self-limited.
• Assuming pediatric Bell palsy should be treated the same way as adult Bell palsy — current trial evidence does not support routine corticosteroid use in children.
• Restarting or continuing corticosteroids for a presentation now more than 7 days old on the assumption that some treatment is better than none — the evidence does not support benefit in that window, and the adverse-effect burden is not free.
• Missing Lyme disease as the actual cause in a patient with a relevant exposure history or endemic-area residence — this needs its own specific antimicrobial treatment, not standard Bell palsy management.
• Treating a recurrence exactly like a first episode without reconsidering the diagnosis and involving a specialist.

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

Antiviral agents are always used together with a corticosteroid in Bell palsy, never alone.

Corticosteroids

The cornerstone of Bell palsy treatment — start as early as possible, ideally within 48 hours and no later than 72 hours of symptom onset.

Antivirals (adjunct only — never monotherapy)

Reserve for severe or complete paralysis, immunocompromised patients, or suspected Ramsay Hunt syndrome; always co-prescribed with, never instead of, the corticosteroid course.

Analgesics

For pain and edema, usually only needed for the first 1-2 days.

Eye protection

Essential adjunct in any patient with incomplete eyelid closure — start on the day of diagnosis, not after eye symptoms appear.

Other therapies (specialist-directed, later stage)

Not initiated in primary or pharmacy care — included so pharmacists recognize them and can counsel appropriately when a patient is referred for them.

Evidence note: Drug selection, dosing, adverse effects, and comments reflect the AAN 2012 evidence-based guideline update, the AAO-HNSF 2013 clinical practice guideline, and the 2014 Canadian (CMAJ) clinical practice guideline.^[4][15][2]