Varicella zoster virus (VZV) infection of cerebral arteries produces a vasculopathy, manifesting most often as ischemic stroke and less often as hemorrhagic stroke. Vasculopathy can occur after either primary infection with VZV (ie, varicella; chickenpox) or after viral reactivation (ie, herpes zoster; shingles) .
This topic will review the pathogenesis, epidemiology, risk factors for, clinical features, diagnosis, and treatment of VZV vasculopathy. The major clinical manifestations and complications of chickenpox and herpes zoster are discussed separately. (See "Epidemiology of varicella-zoster virus infection: Chickenpox" and "Treatment of varicella-zoster virus infection: Chickenpox" and "Vaccination for the prevention of varicella-zoster virus infection: Chickenpox" and "Clinical manifestations of varicella-zoster virus infection: Herpes zoster" and "Prevention of varicella-zoster virus infection: Herpes zoster".)
VZV vasculopathy has previously been called granulomatous angiitis, VZV vasculitis, or post-varicella arteriopathy; a subset of patients has specific ocular and motor findings known as herpes zoster ophthalmicus with delayed contralateral hemiparesis.
Early reports described ischemic large vessel strokes, although it is now appreciated that both large and small arteries are commonly involved. An expanded spectrum of stroke caused by VZV infection has been increasingly recognized including aneurysm, subarachnoid and intracerebral hemorrhage, arterial ectasia, and possibly dissection [2-4].
VZV is a ubiquitous human DNA virus of the herpesvirus family. Primary infection occurs via respiratory aerosols or contact with vesicles from an infected individual and results in the characteristic, disseminated rash of varicella (ie, chickenpox).