THE PATTERNS OF VARICELLA-ZOSTER VIRUS ENCEPHALITIS

Varicella tester virus (VZV) encephalitis has become increasingly prev alent in the era of acquired immunodeficiency syndrome (AIDS), and a w idening spectrum of pathological lesions has defined the disease in th ese and ether severely immunosuppressed patients. VZV produces three d istinct morphological patterns of brain damage. VZV can cause bland or hemorrhagic infarctions secondary to a large or medium vessel vasculo pathy. Deep white matter, ovoid mixed necrotic, and demyelinative lesi ons occur as a consequence of small vessel vasculopathy, with demyelin ation dependent on the degree of additional oligodendrocyte infection, Distinctive Cowdry A intranuclear viral inclusions are rare in either large or small blood vessels or near infarctions, but are commonly fo und in glial cells at the edge of the smaller ovoid, demyelinative les ions, Ependymal and periventricular necrosis occurs as a result of vas culopathy of subependymal vessels and secondary infection of ependymal and other glial cells in the periventricular region. To clarify these patterns of VZV encephalitis and shed light on their pathogenesis, th e authors have examined all cases of VZV encephalitis seen at our inst itution since 1984. Additionally, the authors review the extensive lit erature in an attempt to classify the patterns of VZV encephalitis int o (1) large/medium vessel vasculopathy with bland or hemorrhagic infar ctions, (2) small vessel vasculopathy with mixed ischemic/demyelinativ e lesions, and (3) ventriculitis/periventriculitis. Although one of th ese three patterns often predominates clinically and radiographically, careful histological examination at autopsy shows mixed features in m any cases. Copyright (C) 1996 by W.B. Saunders Company