Abstract
Varicella zoster virus (VZV), a ubiquitous human herpesvirus, causes chicken pox on primary infection and then establishes lifelong latency in all cranial nerve, dorsal root, and autonomic ganglia. When VZV-specific cell-mediated immunity declines, such as in elderly and immunocompromised individuals, virus reactivates in one or more ganglia and typically travels peripherally to cause herpes zoster in the corresponding dermatomes. Herpes zoster can be complicated by stroke and has been described clinically as VZV vasculopathy, granulomatous angiitis, post varicella arteriopathy, and herpes zoster ophthalmicus (HZO) with delayed contralateral hemiparesis. The likely mechanism for stroke caused by VZV is direct viral infection of cerebral arteries. This assertion is supported by animal studies identifying afferent fibers from trigeminal and dorsal root ganglia to both intracranial and extracranial blood vessels, providing an anatomic pathway for spread of the virus,1,2 and observations of viral particles, antigens, and DNA in affected arterial vessels in VZV vasculopathy cases.3,4 Several studies have examined varicella and the risk of stroke in children,5,6 but large studies in the adult population regarding the frequency and risk of …
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