Bell Palsy vs Ramsay Hunt Syndrome
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Direct answer
Painful facial palsy with vesicles on the ear is Ramsay Hunt syndrome — reactivation of varicella zoster virus in the geniculate ganglion — and it behaves far more aggressively than Bell palsy, the painless idiopathic paralysis attributed to herpes simplex virus reactivation and inflammation within the facial canal. Ramsay Hunt adds severe otalgia, herpetic vesicles on the concha, external canal or postauricular skin, frequently sensorineural hearing loss, tinnitus and vertigo from VIII nerve involvement, and carries a distinctly worse outlook for facial recovery. Both are treated with corticosteroids, but the antiviral (aciclovir or valaciclovir) is not optional in zoster: it must run alongside the steroid, ideally within 72 hours of rash or palsy onset.
What you must remember
- Bell palsy: acute, unilateral, lower motor neurone facial paralysis over 24–72 hours, no vesicles, no significant otalgia, no hearing loss; about 85 per cent recover fully, and steroids within 72 hours improve those odds.
- Ramsay Hunt (herpes zoster oticus): VZV reactivation in the geniculate ganglion; the full triad is facial palsy, ear vesicles and vestibulocochlear symptoms, but all three need not coexist.
- Pain precedes the rash and palsy may precede vesicles by days — severe otalgia with facial weakness should be treated as zoster even before vesicles appear, since vesicles can also be limited to the pharynx or absent (zoster sine herpete).
- Hearing loss in Ramsay Hunt is sensorineural (cochlear involvement), may be permanent, and hearing prognosis correlates with the severity of the palsy.
- CSF in Ramsay Hunt shows lymphocytic pleocytosis, reflecting true neuritis; imaging is reserved for atypical, progressive or non-resolving cases.
- Treatment of Ramsay Hunt: aciclovir 10 mg/kg three times daily intravenously (or oral valaciclovir at zoster doses) plus prednisolone, started together within 72 hours; analgesia is often opioid-level for the neuralgic pain.
- Only about two-thirds of Ramsay Hunt patients achieve good facial recovery even with treatment, against the overwhelmingly good natural history of Bell palsy — the single most exam-tested difference.
- Post-herpetic neuralgia, residual synkinesis and hearing loss are the long-term worries after zoster oticus.
A clinical comparison, case against case
Put two patients side by side in casualty. The first is a 30-year-old woman with a two-day droopy left face, mild retro-auricular discomfort, taste disturbance and hyperacusis; ear examination is normal, hearing is normal, and no vesicles exist anywhere. Her picture fits Bell palsy: prescribe prednisolone (about 1 mg/kg for a week, tapering), explain the 85 per cent spontaneous-recovery odds, protect the eye, and review at one and four weeks. Adding an antiviral here is common practice but the evidence adds little to steroids alone.
The second is a 68-year-old man with three days of agonising right ear pain, then facial droop, then clusters of tense vesicles filling the concha and canal, with muffled hearing and a spinning sensation. Examine him fully: the tympanic membrane may be intact under the vesicles; test hearing (a sensorineural drop on the right), look for nystagmus, and check the mouth — vesicles may extend to the anterior tongue and palate via chorda tympani distribution. This is Ramsay Hunt syndrome. Admit or treat aggressively: intravenous aciclovir plus steroid, strong analgesia, eye care, and vestibular sedatives for the vertigo. Warn him honestly — his facial recovery chances are roughly a coin-flip to two-thirds, far below the Bell palsy patient beside him, and his hearing may not return.
The physiological reason for the difference is worth one line in a viva: zoster produces actual neuronal destruction with inflammatory infiltration of the ganglion (hence pleocytosis and axonal loss on electrodiagnostics), whereas Bell palsy is chiefly conduction block from oedema in a tight bony canal — conduction block recovers, destroyed axons regenerate imperfectly, if at all.
How the exam frames it
The discriminator the MCQ wants is the presence of otalgia plus vesicles — answer Ramsay Hunt and its causative agent, VZV in the geniculate ganglion. Reversals are tested too: a "Bell palsy" that keeps worsening after three weeks, develops vesicles late, or leaves a dry eye with absent lacrimation should push you to image the temporal bone and CP angle. A favourite multi-part question gives vesicles plus hearing loss plus vertigo and asks the antiviral of choice and the prognosis. Expect one assertion-type item: "Ramsay Hunt is caused by herpes simplex virus" — false; HSV is implicated in Bell palsy, VZV in Ramsay Hunt. Lastly, remember the immunocompromised: disseminated zoster with multiple cranial neuropathies demands ophthalmology review, HIV and malignancy screening.
Frequently asked questions
What distinguishes Ramsay Hunt syndrome from Bell palsy clinically?
Severe otalgia with herpetic vesicles on the pinna or canal, frequent VIII nerve features (sensorineural hearing loss, tinnitus, vertigo), older age and much poorer facial recovery in Ramsay Hunt; Bell palsy is painless, vesicle-free and largely self-limiting.
Which virus and which ganglion cause Ramsay Hunt syndrome?
Varicella zoster virus reactivating in the geniculate ganglion of the facial nerve.
Can Ramsay Hunt be diagnosed before vesicles appear?
Yes — zoster sine herpete exists, and severe otalgia preceding facial palsy with rising VZV titres justifies empirical antiviral treatment; waiting for the rash delays therapy.
What is the treatment protocol for Ramsay Hunt syndrome?
Aciclovir (or oral valaciclovir at zoster doses) combined with corticosteroid, both within 72 hours of onset when possible, plus aggressive analgesia and eye protection.
Why does Ramsay Hunt recover less well than Bell palsy?
Zoster neuritis destroys ganglion neurones and axons, whereas Bell palsy is mainly oedematous conduction block; axonal loss regenerates incompletely, leaving weakness and synkinesis.