Ramsay-Hunt Syndrome

Ramsay-Hunt syndrome is caused by VZV reactivation in the geniculate ganglion. After primary varicella infection, VZV achieves latency in the satellite cells surrounding sensory ganglion neurons. Reactivation involves transition from the latent circular episome to lytic replication, with viral progeny traveling anterograde via axonal transport to cutaneous sensory terminals (producing vesicles) and simultaneously causing inflammatory destruction of ganglion neurons and the facial nerve trunk. The facial nerve traverses the narrow bony fallopian canal, where inflammatory edema causes compressive ischemia. The degree of nerve injury ranges from neuropraxia (demyelination with intact axons, good prognosis) through axonotmesis (axonal disruption with preserved endoneurium, variable recovery) to neurotmesis (complete transection, poor recovery). Electroneurography (ENoG) within 2 weeks of onset predicts prognosis: >90% degeneration suggests poor spontaneous recovery and possible need for surgical decompression. The clinician must differentiate Ramsay-Hunt from Bell's palsy (no vesicles), central facial palsy (stroke), parotid tumors, otitis media complications, Lyme disease, sarcoidosis, and Guillain-Barré syndrome. The clinician also manages complex pharmacotherapy, assesses for complications, and determines need for specialist referral.