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Updated: Jun 2, 2026

Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients
Published on: April 14, 2014
Varicella zoster virus ischemic optic neuropathy and subclinical temporal artery involvement
Richard Salazar1, Andrew N Russman, Maria A Nagel
1Department of Neurology, Henry Ford Hospital, Detroit, Michigan, USA.
Objective:
To demonstrate varicella zoster virus (VZV) infection in an asymptomatic extracranial (temporal) artery in a patient with ischemic optic neuropathy produced by VZV vasculopathy in whom the pathological changes were mistakenly identified as giant cell arteritis.
Design:
Case report.
Setting:
Teaching hospital, pathology and virology laboratory.
Patient:
An 80-year-old man with left ophthalmic distribution zoster who developed left ischemic optic neuropathy.
Intervention:
An ipsilateral temporal artery biopsy revealed inflammation that was mistakenly identified as giant cell arteritis. The patient was initially treated with steroids but his condition did not improve. When the diagnosis of VZV vasculopathy was confirmed virologically and the patient was treated with intravenous acyclovir, his vision improved.
Results:
Pathological and virological studies provided proof of VZV vasculopathy in the asymptomatic temporal artery. Varicella zoster virus antigen was abundant in arterial adventitia and scattered throughout the media. With intravenous antiviral therapy, the patient's vision improved.
Conclusion:
Although in previously studied patients who died of chronic VZV vasculopathy after 10 to 12 months, VZV antigen was present exclusively in the intima, collective analyses of chronic cases and the asymptomatic VZV-infected temporal artery suggest that virus enters arteries through the adventitia and spreads transmurally to the intima.
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