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VZV vasculopathy and postherpetic neuralgia

Progress and perspective on antiviral therapy

From the Departments of Neurology (Drs. Gilden, Cohrs, and Mahalingam) and Microbiology (Dr. Gilden), University of Colorado Health Sciences Center, Denver.

Address correspondence and reprint requests to Dr. Donald H. Gilden, Department of Neurology, Mail Stop B182, University of Colorado Health Sciences Center, 4200 East 9th Avenue, Denver, CO 80262; e-mail: don.gilden{at}uchsc.edu

Two serious complications of varicella-zoster virus (VZV) reactivation are vasculopathy and postherpetic neuralgia (PHN). Clinical-virologic analyses have proven that VZV vasculopathy is caused by chronic active virus infection in cerebral arteries. Conclusive evidence that PHN is caused by persistent or productive VZV infection is less compelling because human ganglia are not accessible during life for pathologic and virologic examination. However, the notion that PHN may reflect a smoldering VZV ganglionitis is supported by 1) the detection of VZV DNA and proteins in peripheral blood mononuclear cells of many patients with PHN; 2) studies of multiple patients with zoster sine herpete, which indicate a productive VZV ganglionitis; and 3) a favorable response of some patients with zoster sine herpete and PHN to antiviral treatment. Few studies have used antiviral therapy to manage PHN with conflicting results. Larger, double-blind studies, which give IV antiviral drug, are needed.

Received May 26, 2004. Accepted in final form August 18, 2004.

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