Bell's palsy: steroid within 72 hours, protect the eye, watch for stroke

What Bell’s palsy actually is

Bell’s palsy is an acute, idiopathic lower motor neuron palsy of the facial nerve (cranial nerve VII). It produces sudden weakness of the entire half of the face — including the forehead — on the affected side. The underlying mechanism is thought to be herpes simplex virus-1 reactivation in the geniculate ganglion, causing inflammatory oedema that compresses the facial nerve within its bony canal.

Onset is typically rapid: facial weakness develops over hours and is usually maximal within 72 hours. Many patients also notice post-auricular pain on the affected side in the hours before weakness appears. Associated features can include impaired taste on the anterior two-thirds of the tongue (chorda tympani involvement), hyperacusis (stapedius involvement), and reduced tearing (greater petrosal nerve involvement).

Bell’s palsy is common — it is the most frequent cause of acute facial nerve palsy in Australian general practice, with an annual incidence of approximately 20–30 per 100,000. eTG and RACGP guidelines both position this as a condition where the GP’s assessment and early prednisolone prescription determine the outcome.

The most urgent task in any acute facial weakness presentation is distinguishing Bell’s palsy from stroke. The second most urgent task, once Bell’s palsy is confirmed, is starting prednisolone within 72 hours of onset and initiating eye protection.

A. Core clinical — the AU general-practice framework

The single most important examination finding

The forehead. In Bell’s palsy, the entire ipsilateral face is weak — the patient cannot raise the eyebrow, wrinkle the forehead, close the eye fully, puff the cheek, or smile symmetrically. This is lower motor neuron (LMN) palsy: the entire facial nerve nucleus is affected because the nerve is damaged peripherally.

In a stroke or other upper motor neuron (UMN) lesion, the forehead is spared. Both cerebral hemispheres supply the frontalis muscle bilaterally; only one hemisphere supplies the lower face. So cortical or internal capsule pathology produces contralateral lower face weakness with preserved forehead movement. Forehead sparing in a patient with facial asymmetry = stroke until proven otherwise. Call 000.

Additional examination: inspect the external auditory canal and auricle carefully. Painful vesicles in the ear canal, concha, or posterior pharynx with facial palsy = Ramsay Hunt syndrome (varicella-zoster virus reactivation). This requires urgent ENT referral and mandatory antiviral plus corticosteroid treatment — it has a worse prognosis than idiopathic Bell’s palsy.

Bilateral facial palsy is almost never Bell’s palsy — it requires systemic workup for Lyme disease (in returned travellers from endemic regions), sarcoidosis (Heerfordt syndrome), Guillain-Barré syndrome (ascending weakness, areflexia, albumino-cytologic dissociation), lymphoma, or HIV.

The House-Brackmann grading scale

The AAO-HNS guideline uses House-Brackmann grading to quantify severity:

Grade	Description
I	Normal — full function
II	Mild — slight weakness, complete eye closure with effort, slight asymmetry at rest
III	Moderate — obvious weakness; full eye closure with effort; good to moderate movement
IV	Moderately severe — obvious weakness; incomplete eye closure; asymmetry at rest
V	Severe — barely perceptible movement; incomplete closure
VI	Total — no movement

Grade III and above warrants particular attention to eye care and consideration of adding an antiviral to prednisolone.

Investigations

Bell’s palsy is a clinical diagnosis. No routine investigations are needed for a typical presentation (acute onset, full hemiface involvement including forehead, no other neurological signs, no vesicles, no progressive course).

Bloods (selective): fasting glucose or HbA1c in all patients — diabetes is associated with increased Bell’s palsy risk and affects recovery. Lyme serology in returned travellers from endemic regions.

MRI brain and facial nerve: not routine for typical Bell’s palsy. Indicated if: no improvement at 3 months; progressive facial weakness (not acute onset); bilateral palsy; recurrent ipsilateral palsy; associated neurological signs; or suspected mass at the parotid, temporal bone, or cerebellopontine angle.

Audiogram: if there are hearing symptoms, suggesting Ramsay Hunt or acoustic neuroma.

Management

1. Prednisolone — first-line, start within 72 hours

Per eTG and RACGP: prednisolone 1 mg/kg (maximum 75 mg) orally daily for 5 days, then taper over 5 days (total 10 days). Equivalent regimens: prednisolone 60 mg daily for 5 days then reduce by 10 mg every 2 days; or prednisolone 50 mg daily for 10 days. The goal is to start within 72 hours of weakness onset. Check for contraindications: active peptic ulcer, uncontrolled diabetes, recent live vaccination. Add a PPI (omeprazole, pantoprazole) if gastrointestinal risk.

2. Antivirals — selective use

Per Cochrane reviews, antivirals used alone provide no clear benefit for Bell’s palsy. The AAO-HNS guideline makes a weak recommendation to add valaciclovir 1 g three times daily for 7 days (or aciclovir 400 mg five times daily for 7 days) to prednisolone in moderate-to-severe palsy (House-Brackmann grade IV–VI), where a small additional benefit has been suggested by some meta-analyses. For mild-to-moderate palsy, prednisolone alone is appropriate per current AU practice.

Ramsay Hunt syndrome: antiviral + corticosteroid is mandatory. Same-day ENT referral.

3. Eye care — essential from day 1

Incomplete eye closure in Bell’s palsy is a direct corneal injury risk. Initiating eye protection at the first consultation prevents sight-threatening exposure keratitis:

• Preservative-free artificial tears (Refresh Plus, Systane Ultra single-use vials) every 1–2 hours during waking hours
• Lubricating gel or ointment at night (Lacri-Lube, GenTeal Gel overnight)
• Eye closure assistance: micropore tape across the closed lid, or a moisture chamber, or a sleep mask — overnight every night until eye closure is fully restored
• Sunglasses outdoors to reduce drying and particulate exposure
• Urgent ophthalmology review if any corneal redness, pain, photophobia, or change in vision

B. Evidence: why prednisolone works and when antivirals add value

The Sullivan 2007 NEJM trial

The landmark evidence base for prednisolone comes from Sullivan FM et al. NEJM 2007 — a Scottish double-blind 2×2 factorial RCT of 551 patients with Bell’s palsy randomised to prednisolone, aciclovir, both, or neither within 72 hours of onset. At 3 months, complete recovery occurred in 83% of prednisolone recipients versus 63.6% of those not on prednisolone (number needed to treat approximately 7). There was no significant benefit from aciclovir alone. The combination was not superior to prednisolone alone in this trial.

The Cochrane systematic review of corticosteroids for Bell’s palsy includes seven high-quality RCTs and robustly supports prednisolone as first-line, consistent with the AAO-HNS guideline. The evidence is strong enough to qualify as standard of care.

Antivirals: nuanced not negligible

The Cochrane review of antivirals for Bell’s palsy found no significant benefit from antivirals alone compared with placebo or prednisolone. However, meta-analyses of combination therapy — antiviral plus prednisolone versus prednisolone alone — show a modest reduction in incomplete recovery at 6 months, particularly in more severe presentations. The effect size is small. The AAO-HNS makes this a weak recommendation limited to moderate-to-severe palsy.

For Ramsay Hunt syndrome (VZV, not HSV), the antiviral benefit is substantially larger: antiviral plus steroid significantly outperforms steroid alone, and early ENT management reduces the risk of permanent deafness and balance impairment.

Facial physiotherapy and neuromuscular retraining

Emerging evidence supports physiotherapy-led facial retraining and neuromuscular retraining — particularly for moderate-to-severe palsy and for patients developing synkinesis during recovery. The technique involves biofeedback, mirror exercises, and targeted muscle activation patterns. Access in Australia is through physiotherapists with facial palsy expertise (some hospital outpatient departments; private referral under the GP Chronic Condition Management Plan).

C. Long-term complications: synkinesis and persistent palsy

Synkinesis

Synkinesis — involuntary co-movements during recovery — is the most common long-term complication of Bell’s palsy. It occurs when regenerating facial nerve axons reconnect to muscles other than their original targets: the eye closes when smiling; the mouth pulls when the eye closes. It typically appears 3–6 months after onset as the nerve regenerates.

Synkinesis management: specialist facial physiotherapy with neuromuscular retraining is first-line. Targeted botulinum toxin (Botox) injections into the overactive muscles are highly effective and are the standard specialist approach for significant synkinesis.

Incomplete recovery and refractory cases

If there is no measurable facial movement recovery at 3 months, refer to neurology. Nerve conduction studies (electromyography, electroneuronography) quantify the degree of denervation and provide prognostic information. MRI of the brain and facial nerve excludes structural pathology that may have been misdiagnosed as idiopathic Bell’s palsy. Surgical facial reanimation (dynamic reinnervation procedures, static slings, gold weight implants) is a rare but valid option for permanent severe palsy — specialist plastic/ENT surgery.

Recurrent Bell’s palsy

Recurrent Bell’s palsy — ipsilateral or contralateral — occurs in approximately 5–10% of patients. Recurrent ipsilateral Bell’s palsy warrants investigation for structural causes: parotid tumour, perineural malignant spread, cholesteatoma. Refer to neurology and ENT.

D. Australian operations

PBS medications

AMH and eTG confirm:

• Prednisolone 1 mg/kg daily (maximum 75 mg) × 5 days, taper × 5 days — PBS general benefit; inexpensive
• Valaciclovir 1 g three times daily × 7 days — PBS general benefit (HSV reactivation indication)
• Aciclovir 400 mg five times daily × 7 days — PBS general benefit alternative
• PPI (omeprazole, pantoprazole) — PBS general benefit; prescribe with steroid in at-risk patients

Eye care products (preservative-free tears, lubricating ointment, eye patch) are OTC and not PBS-subsidised.

MBS items

Standard GP consultation items (23, 36, 44) cover the initial assessment and follow-up visits. The GP Chronic Condition Management Plan (items 965 and 967) funds physiotherapy referral for prolonged recovery or synkinesis rehabilitation. The Better Access Mental Health Treatment Plan (item 2715) can fund psychology input if the psychosocial impact of facial palsy is significant. The ATSI Health Assessment (item 715) for eligible patients.

MRI brain and facial nerve is Medicare-rebatable for atypical features or no improvement at 3 months, with specialist referral. Audiometry (items 82300–82332) for hearing concerns.

Driving

The Austroads Assessing Fitness to Drive 2022 guideline does not specifically exclude Bell’s palsy patients from driving, but if lid closure is severely impaired and visual field is compromised, document a driving review discussion. Advise patients to avoid driving when the affected eye requires patching that restricts their visual field.

Consumer resources

HealthDirect — Bell’s palsy and Better Health Channel provide clear, evidence-aligned patient information in plain English.

E. Special populations

Pregnancy and postpartum: Bell’s palsy incidence is approximately 3 times higher in the third trimester and early postpartum period. Prednisolone is appropriate during pregnancy — the benefit for the mother substantially outweighs the theoretical fetal risk at doses used for Bell’s palsy. Involve the obstetric team, particularly in the third trimester. Eye care is the same as for non-pregnant patients.

Diabetes: patients with diabetes have a higher incidence of Bell’s palsy and often have slower, less complete recovery. Monitor blood glucose carefully during prednisolone treatment — steroid-induced hyperglycaemia is common in diabetes and may require temporary insulin adjustment. This does not negate the indication for prednisolone; it requires active glucose management.

Children and adolescents: the evidence for prednisolone in children is less robust than for adults — paediatric RCT data are limited. The AAO-HNS guideline makes the paediatric prednisolone recommendation weaker (optional rather than recommended). In older children and adolescents with moderate-to-severe palsy, many clinicians extrapolate the adult evidence with paediatric dose adjustment, under specialist guidance. Refer to a paediatrician or paediatric neurologist for children under 12.

Older adults: both higher incidence and poorer prognosis. Prednisolone carries greater risks of blood pressure elevation, hyperglycaemia, and delirium in the elderly. Start at the weight-appropriate dose, monitor closely, and co-prescribe PPI and glucose monitoring as standard in this group.

When to escalate

Refer or seek urgent input in any of the following scenarios:

Same-day emergency review (call 000 or send to ED): facial weakness with forehead sparing (upper motor neuron pattern — stroke until proven otherwise); acute facial weakness with limb weakness, dysarthria, dysphagia, diplopia, or severe sudden headache; haemodynamic instability or reduced consciousness.

Urgent ENT referral (same day or next day): suspected Ramsay Hunt syndrome — vesicles in or around the ear with facial palsy; hearing loss accompanying facial palsy; significant otological signs on examination.

Urgent ophthalmology review: corneal involvement (red eye, pain, photophobia, reduced vision), persistent incomplete closure beyond 2 weeks despite maximum eye care.

Neurology outpatient: no recovery at 3 months; progressive facial weakness; recurrent ipsilateral palsy; bilateral facial palsy; associated systemic features suggesting Lyme, sarcoidosis, or Guillain-Barré syndrome.

What this article is and is not

This is general health information drawn from current Australian clinical guidelines — Therapeutic Guidelines, RACGP, Australian Medicines Handbook — and the major published trial evidence including Sullivan 2007 and Cochrane systematic reviews. It is not personal medical advice and does not create a doctor–patient relationship. Treatment decisions — including steroid dosing, antiviral use, and specialist referral — are made with your own GP and treating clinicians.

For patient-facing information: HealthDirect — Bell’s palsy, Better Health Channel.

For acute emergency: if you or someone near you develops sudden facial weakness, call 000 and do not wait to see whether it is Bell’s palsy or stroke.

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Sources cited

1. Therapeutic Guidelines (eTG) — Neurology: Bell’s palsy
2. RACGP — Bell’s palsy clinical resources
3. Australian Medicines Handbook
4. NPS MedicineWise
5. Sullivan FM et al. — Bell’s Palsy Trial, NEJM 2007
6. Cochrane review — Corticosteroids for Bell’s palsy
7. Cochrane review — Antivirals for Bell’s palsy
8. AAO-HNS Clinical Practice Guideline: Bell’s Palsy (2013)
9. HealthDirect — Bell’s palsy
10. Better Health Channel — Bell’s palsy
11. Austroads — Assessing Fitness to Drive 2022