Ramsay Hunt syndrome (herpes zoster oticus)
Overview and clinical importance
Ramsay Hunt syndrome is reactivation of varicella‑zoster virus (VZV) involving the geniculate ganglion, producing a peripheral (lower motor neuron) facial palsy together with a vesicular rash affecting the ear, external auditory canal, pinna or ipsilateral oral mucosa.
It is an important emergency department (ED) diagnosis because it is typically more painful, more often associated with hearing and vestibular dysfunction, and has a worse prognosis than idiopathic (Bell’s) palsy.
Prompt recognition, early antiviral therapy and appropriate referral (ENT/audiology/neurology) affect outcome and have public‑health implications for varicella exposure (see NICE NG127, NG98; GOV.UK Green Book/PEP guidance).
Pathophysiology
Reactivation of latent VZV in the geniculate ganglion causes inflammation and neuritis of the facial nerve. Viral spread can involve adjacent cochlear and vestibular structures producing tinnitus, sensorineural hearing loss and vertigo.
Vesicles arise from viral replication in the sensory distribution; in some cases (zoster sine herpete) facial palsy occurs without initial visible vesicles - vesicles may appear later or not at all.
Typical presentation
- Acute peripheral (LMN) facial weakness affecting the whole hemiface, including the forehead.
- Severe ipsilateral ear pain often precedes or accompanies the paralysis.
- Vesicular rash on the pinna, conchal bowl, external auditory canal or ipsilateral oral mucosa.
- Auditory and vestibular symptoms such as tinnitus, hearing loss (often sensorineural), and vertigo with...