Varicella-zoster virus is part of the Herpesviridae family. The primary infection is usually self-limited. The virus remains dormant in the neurosensory ganglia and can be reactivated, resulting in the cutaneous presentation affecting V1 distribution of trigeminal nerve, labelled as Herpes Zoster Ophthalmicus (HZO).

PATIENT PRESENTATION: A 68 years-old immunocompetent female presented to the clinic with two-week history of severe headaches in the temporal region bilaterally without accompanying visual changes. Initially giant cell arteritis was suspected given elevated ESR (70) and was started on prednisone along with temporal artery biopsy. Within a week she developed chemosis, a new erythematous rash with pustules on the right side of forehead and right upper eyelid swelling in the V1 dermatome. HZO was suspected based on the pattern of rash, and oral valacyclovir and prednisone were initiated. Two weeks later, she noted drooping of the right eyelid and diplopia, examination revealed right oculomotor nerve palsy with complete ptosis and limited ductions. Workup with brain MRI showed enhancement of right third, fourth, sixth and ophthalmic branch of the trigeminal nerve, seventh cranial nerve nucleus enhancement in the right lower pons, indicating multiple cranial nerve palsies in the setting of zoster ophthalmicus. Intravenous acyclovir was initiated for a total course of 3 weeks. Symptomatic management was offered with gabapentin and amitriptyline for post-herpetic neuralgia. The patient significantly recovered post treatment with mild remanence of ptosis and mild anisocoria.

The prevalence of HZO is estimated to be 0.05% in immunocompetent patients. Most commonly HZO can affect periorbital skin, eyelid, cornea.  Diplopia from cranial nerve palsy occurs in less than 30% HZO, whereas optic neuropathy is seen in less than 1% HZO.  Pathology suggests this is related to perineural vasculitis and treatment with long term systemic antiviral medication is indicated in the setting of neurological involvement.