Bell's Palsy – ClinicalJunior.com

Clinical Reminder: Bell's palsy is a diagnosis of exclusion. Always rule out stroke, Ramsay Hunt syndrome, parotid malignancy, cholesteatoma, and other treatable causes before applying this label. Always consult a senior if you are uncertain.

What Is Bell's Palsy?

Bell's palsy is an idiopathic, acute-onset lower motor neuron (LMN) palsy of the facial nerve (cranial nerve VII). It is the most common cause of acute unilateral facial weakness, accounting for approximately 60–75% of all cases of acute facial palsy. The aetiology is believed to be reactivation of herpes simplex virus type 1 (HSV-1) within the geniculate ganglion, causing oedema, ischaemia, and compression of the nerve within the narrow fallopian canal. Many patients report a preceding viral illness, stress, or fatigue.

The diagnosis is one of exclusion — it is only appropriate once other causes of facial nerve palsy have been considered and excluded on clinical grounds (or by investigation where necessary).

UMN vs LMN Facial Palsy — A Critical Distinction

This is the first and most important question to answer at the bedside, as it determines whether the patient may be having a stroke.

Upper motor neuron (UMN) facial palsy — caused by a lesion above the facial nerve nucleus (e.g., cortical stroke, intracerebral tumour). The forehead is spared because the forehead muscles receive bilateral cortical innervation. The upper face appears relatively normal while the lower face (nasolabial fold, corner of mouth) is weak. The patient can wrinkle their forehead and raise their eyebrows despite lower facial weakness. This pattern should prompt immediate stroke assessment and referral to the medical team.
Lower motor neuron (LMN) facial palsy — caused by a lesion at or below the facial nerve nucleus, including the nerve itself (e.g., Bell's palsy, Ramsay Hunt, parotid tumour, cholesteatoma). The entire ipsilateral face is affected, including the forehead. The patient cannot wrinkle the forehead on the affected side, cannot close the eye, and has weakness of the lower face. This is the pattern seen in Bell's palsy.

Memory aid: In an UMN lesion the "upper" face is spared. In an LMN lesion the whole face is affected, including the forehead.

Presentation of Bell's Palsy

Bell's palsy typically presents with:

Rapid onset — the palsy usually develops over hours and is maximal within 48–72 hours. Onset over more than a week or a gradually progressive palsy should prompt investigation for an alternative cause (e.g., parotid tumour or cholesteatoma).
Complete LMN facial weakness — all branches of the facial nerve are affected to varying degrees: inability to close the eye (orbicularis oculi), weakness of the mouth and cheek (buccinator, orbicularis oris), flattening of the nasolabial fold, and inability to wrinkle the forehead (frontalis).
Reduced tear flow (epiphora or paradoxically reduced lacrimation) — the greater petrosal nerve, the first branch of the facial nerve after the geniculate ganglion, carries parasympathetic fibres to the lacrimal gland. Reduced lacrimation is one of the earliest features.
Hyperacusis — oversensitivity to loud sounds, due to loss of the stapedius reflex. The stapedius muscle, innervated by the facial nerve, normally dampens the vibration of the stapes in response to loud noise. When the nerve is injured, the reflex is lost and sounds appear unnaturally loud.
Loss of taste / metallic taste — the chorda tympani branch of the facial nerve (the last branch before the nerve exits the stylomastoid foramen) carries taste sensation from the anterior two-thirds of the tongue. Patients often report a metallic taste on the affected side rather than complete taste loss.
Post-auricular pain — often precedes the weakness by 1–2 days. The pain follows the course of the sensory branch of the facial nerve (nervus intermedius).
Preceding viral illness or stress — many patients report a recent upper respiratory tract infection or a period of physical or emotional stress.

Epidemiology and Risk Factors

Bell's palsy can occur at any age but is slightly more common in older adults. The following groups have an increased risk:

Diabetics — diabetes mellitus is associated with microvascular ischaemia and impairs nerve recovery
Pregnant women — particularly in the third trimester and those with pre-eclampsia; the incidence is approximately three times higher than in the non-pregnant population
The immunocompromised
Those with a family history of Bell's palsy (suggesting a genetic predisposition to narrow facial canals)

Examination

House-Brackmann Grading System

The House-Brackmann (HB) scale is the internationally accepted system for grading facial nerve function. It should be documented at presentation and at each follow-up visit to track recovery. Severity at presentation is the single strongest predictor of long-term outcome.

Grade	Description	Clinical Features
I	Normal	Normal facial function in all areas
II	Slight dysfunction	Slight weakness only on close inspection; normal symmetry at rest; eye closes completely with minimal effort
III	Moderate dysfunction	Obvious weakness but not disfiguring; normal symmetry at rest; eye closes with maximal effort but requires effort to do so
IV	Moderately severe dysfunction	Disfiguring weakness; inability to close the eye fully even with effort; mouth asymmetrical even on maximal effort
V	Severe dysfunction	Barely perceptible movement; asymmetry at rest; eye cannot close
VI	Total paralysis	No movement whatsoever

Ear and Head Examination

At a minimum, the following should be examined in every patient with facial palsy:

The ear — look carefully at the conchal bowl, external auditory canal, and tympanic membrane. The presence of vesicles in the conchal bowl, pinna, or ear canal indicates Ramsay Hunt syndrome (herpes zoster oticus — reactivation of the varicella-zoster virus in the geniculate ganglion). Ramsay Hunt causes a more severe, less favourable palsy and requires antiviral treatment (valaciclovir or aciclovir) in addition to steroids. Cholesteatoma or middle ear disease affecting the nerve are other findings that could be seen.
The parotid gland — palpate for any mass along the course of the extratemporal facial nerve. A parotid tumour can present as a partial or complete facial palsy. Parotid malignancy tends to cause a gradually progressive palsy rather than the rapid onset seen in Bell's palsy.
Regional lymph nodes — lymphadenopathy may suggest malignancy, lymphoma, or sarcoidosis

Other Differentials to Consider

Stroke — UMN pattern (forehead spared); associated neurological signs
Ramsay Hunt syndrome — LMN palsy with ipsilateral ear vesicles, severe otalgia, sensorineural hearing loss, and vertigo; poorer prognosis than Bell's palsy
Lyme disease — consider if history of tick bite or residence in endemic area; may cause bilateral facial palsy
Sarcoidosis — may cause facial palsy, often with other systemic features (bilateral hilar lymphadenopathy, uveitis, parotid swelling — Heerfordt syndrome)
Cholesteatoma / otitis media — ear examination abnormality
Parotid tumour — parotid mass palpable; gradual onset
Acoustic neuroma (vestibular schwannoma) — rarely causes acute facial palsy; more commonly causes gradual sensorineural hearing loss and tinnitus
Guillain-Barré syndrome — may cause bilateral facial palsy with ascending weakness

Management

Steroids (First-Line)

Corticosteroids are the mainstay of treatment for Bell's palsy and have strong evidence behind them. The landmark Sullivan et al. (2007) trial — published in the Lancet — demonstrated that prednisolone given within 72 hours of symptom onset significantly improved the rate of complete recovery (83% vs 63% in the placebo group). The standard regimen is:

Prednisolone 50 mg orally once daily for 10 days (some centres use 1 mg/kg/day up to 60 mg)
Must be started within 72 hours of onset for maximum benefit; the evidence for starting after 72 hours is less clear, but most authorities treat if within one week of onset

Standard precautions apply: prescribe a proton pump inhibitor (PPI) for gastric protection and counsel about side-effects. Steroids are relatively contraindicated in uncontrolled diabetes, active peptic ulcer disease, and active untreated infection.

Antivirals — What the Evidence Shows

The role of antiviral agents in Bell's palsy has been contentious. Two large, high-quality randomised controlled trials clarified the picture:

Sullivan et al. (Lancet, 2007) — showed that aciclovir plus prednisolone was no better than prednisolone alone. Aciclovir alone was inferior to prednisolone alone. Conclusion: do not give aciclovir instead of or in addition to prednisolone for Bell's palsy.
Engström et al. (Lancet, 2008) — confirmed that valaciclovir added to prednisolone conferred no additional benefit over prednisolone alone in Bell's palsy.

Therefore, for a straightforward clinical picture of Bell's palsy, steroids alone are the evidence-based treatment. Antivirals should not be routinely added. However, if Ramsay Hunt syndrome is suspected or confirmed (vesicles present), valaciclovir should be given alongside prednisolone — Ramsay Hunt has a different, more severe natural history and antiviral therapy does have a role there.

Eye Care — This Is Critical

Protection of the cornea is paramount, particularly in patients with HB Grade IV or above who cannot close the eye. An exposed, insensate cornea rapidly dries out and can develop exposure keratitis, corneal ulceration, and even perforation — resulting in permanent visual loss. Implement the following:

Lubricating eye drops (artificial tears) — e.g., hypromellose 0.3% drops, used frequently during waking hours (every 1–2 hours in severe cases)
Lubricating eye ointment — applied at night (e.g., lacrilube or simple eye ointment); provides longer-lasting lubrication than drops but causes temporary blurred vision
Tape the eye closed at night — using micropore or surgical tape applied horizontally across the closed lid; this is the most reliable method to prevent nocturnal corneal exposure
Eye shield or moisture chamber glasses — during the day for additional protection, particularly in windy environments
Ophthalmology referral — if there is any concern about corneal involvement (redness, pain, visual change), arrange an urgent ophthalmology review. In severe or prolonged palsy, early ophthalmology involvement is advisable.

Follow-Up

Patients should be followed up in the ENT outpatient clinic at 4–6 weeks to assess recovery (using House-Brackmann grading) and address any ongoing eye concerns. Patients who show no signs of recovery by 3 months, who have an atypical presentation, or in whom an alternative diagnosis is suspected should have an MRI of the internal auditory meati and facial nerve to exclude an alternative structural cause.

Prognosis

The prognosis for Bell's palsy is generally good:

Approximately 85% of untreated patients have some recovery within 3 weeks
Approximately 80–85% achieve full recovery by 3 months without any treatment
Steroid treatment with prednisolone improves complete recovery rates from approximately 63% to 83%
Patients with an incomplete palsy (HB II–III) at presentation have a better and faster recovery than those with complete paralysis (HB V–VI)
Younger patients recover more quickly and more completely than older patients
More severe initial symptoms (post-auricular pain, metallic taste) and risk factors (diabetes, pregnancy) are associated with a slower and less complete recovery
A small proportion develop sequelae including synkinesis (involuntary co-movement of facial muscles during voluntary movement, caused by aberrant nerve regeneration) or hemifacial spasm

Frequently Asked Questions

How do you distinguish Bell's palsy from a stroke at the bedside?

The key is forehead involvement. In a stroke (UMN lesion), the forehead is spared because the frontalis muscle receives bilateral cortical innervation — the patient can still raise their eyebrows and wrinkle their forehead, despite weakness of the lower face. In Bell's palsy (LMN lesion), the entire face is affected on the ipsilateral side, including the forehead — the patient cannot raise their eyebrow or close their eye. Always also look for other neurological signs (limb weakness, dysarthria, ataxia) that would indicate a central cause. If in any doubt, treat as a possible stroke and obtain urgent neurological assessment and CT head.

What is Ramsay Hunt syndrome and how does it differ from Bell's palsy?

Ramsay Hunt syndrome (herpes zoster oticus) is caused by reactivation of the varicella-zoster virus (VZV) in the geniculate ganglion of the facial nerve. It differs from Bell's palsy in several important ways: (1) There is a characteristic painful vesicular rash in the ear — look in the conchal bowl, ear canal, and on the pinna. (2) Patients often have more severe otalgia. (3) Sensorineural hearing loss and vertigo may be present (VZV affects the cochlear and vestibular branches of the VIII nerve). (4) The palsy tends to be more severe and the prognosis is worse — only about 50–60% of patients fully recover versus 80–85% with Bell's palsy. (5) Unlike Bell's palsy, Ramsay Hunt requires antiviral treatment (valaciclovir 1 g three times daily for 7 days) in addition to steroids.

What is the House-Brackmann grading system and why does it matter?

The House-Brackmann (HB) scale grades facial nerve function from I (normal) to VI (complete paralysis). It is important because: (1) It provides a standardised, reproducible assessment that allows comparison between clinicians and at different time points. (2) It guides management — patients with HB IV–VI are at significant risk of corneal exposure and require aggressive eye protection. (3) Severity at presentation is the strongest single predictor of outcome. (4) Failure to progress through grades at follow-up suggests a poorer prognosis and should prompt investigation for an underlying cause. Always document the grade at presentation and at each subsequent review.

Should I prescribe antivirals alongside steroids for Bell's palsy?

For straightforward Bell's palsy, the evidence — from two large RCTs (Sullivan et al., Lancet 2007; Engström et al., Lancet 2008) — clearly shows that adding aciclovir or valaciclovir to prednisolone provides no additional benefit over prednisolone alone. Steroids alone are the evidence-based treatment. Do not add antivirals routinely. However, if there are any vesicles present in the ear (suggesting Ramsay Hunt syndrome), valaciclovir should be prescribed alongside steroids, as this is a different condition with a different natural history and the antiviral treatment does have a role.

Why is eye care so important in Bell's palsy and what does it involve?

In patients with grade IV or above, the inability to close the eye (lagophthalmos) leaves the cornea exposed. The cornea depends on the blinking reflex to stay moist and clear — without it, it rapidly dries out (exposure keratitis), which can progress to corneal ulceration and potentially permanent visual loss. Daytime eye care involves frequent lubricating drops (e.g., hypromellose). At night, the eye must be actively closed with tape (micropore across the lid) and lubricating ointment applied. Eye shields provide additional protection. If there is any suspicion of corneal involvement — redness, pain, photophobia, or reduced visual acuity — urgent ophthalmology assessment is required.

ST3 interview: How would you manage a patient presenting with acute facial weakness?

I would approach this systematically. First, I would determine whether this is an UMN or LMN pattern: if the forehead is spared, I would immediately treat this as a possible stroke and involve the medical or neurology team urgently. If it is an LMN pattern, I would take a detailed history of onset (sudden versus gradual — gradual onset raises suspicion of a parotid tumour), associated symptoms (vesicles in the ear suggests Ramsay Hunt; hearing loss and tinnitus may point to cholesteatoma or acoustic neuroma). I would examine the ear carefully for vesicles and cholesteatoma, palpate the parotid gland, and perform a full cranial nerve examination. If the clinical picture is consistent with Bell's palsy, I would grade the palsy using House-Brackmann, prescribe prednisolone 50 mg daily for 10 days if within 72 hours of onset, provide comprehensive eye care instructions, and arrange ENT follow-up at 4–6 weeks. I would not routinely prescribe antivirals for Bell's palsy given the RCT evidence.

What is the prognosis for Bell's palsy and when should an MRI be arranged?

The overall prognosis is good — 80–85% of patients fully recover, and prednisolone treatment improves this further to approximately 83%. However, MRI of the facial nerve and internal auditory meati should be arranged if: the palsy fails to show any recovery by 3 months (suggesting an alternative structural cause such as a facial nerve schwannoma or parotid malignancy), the onset was gradual rather than acute, or if there are other atypical features such as recurrence on the same side, associated mass, or other cranial nerve involvement. Routine MRI is not required for straightforward Bell's palsy presenting acutely.

Can Bell's palsy occur in pregnancy and is prednisolone safe to prescribe?

Yes — pregnant women, particularly in the third trimester and those with pre-eclampsia, have approximately three times the risk of Bell's palsy compared with the general population. Prednisolone is generally considered safe in pregnancy and is used for other conditions (e.g., asthma) without evidence of teratogenicity at standard doses. The decision to treat should involve discussion with the obstetric team. The risks of untreated severe facial palsy (corneal exposure, incomplete recovery) generally outweigh the small risks of a short course of prednisolone. Antivirals should be avoided in pregnancy if possible unless Ramsay Hunt is confirmed.

References

Sullivan FM, Swan IR, Donnan PT, et al. Early treatment with prednisolone or acyclovir in Bell's palsy. N Engl J Med. 2007;357(16):1598–1607.
Engström M, Berg T, Stjernquist-Desatnik A, et al. Prednisolone and valaciclovir in Bell's palsy: a randomised, double-blind, placebo-controlled, multicentre trial. Lancet Neurol. 2008;7(11):993–1000.
Hato N, Yamada H, Kohno H, et al. Valacyclovir and prednisolone treatment for Bell's palsy: a multicenter, randomized, placebo-controlled study. Otol Neurotol. 2007;28(3):408–413.
National Institute for Health and Care Excellence. Bell's palsy. NICE CKS. London: NICE; 2023 (updated).
Watkinson JC, Clarke RW, eds. Scott-Brown's Otorhinolaryngology, Head and Neck Surgery. 8th ed. Boca Raton: CRC Press; 2018.
Gilden DH. Clinical practice: Bell's palsy. N Engl J Med. 2004;351(13):1323–1331.
House JW, Brackmann DE. Facial nerve grading system. Otolaryngol Head Neck Surg. 1985;93(2):146–147.