VZV vasculopathy and postherpetic neuralgia: Progress and perspective on antiviral therapy

Department of Neurology, Mail Stop B182, University of Colorado Health Sciences Center, 4200 East 9th Avenue, Denver, CO 8026, USA.
Neurology (Impact Factor: 8.29). 02/2005; 64(1):21-5. DOI: 10.1212/01.WNL.0000148484.19070.4D
Source: PubMed


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.

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    • "More debate persists about the preferred antiviral treatment (valaciclovir or famciclovir versus acyclovir) and the use of steroids (Gilden et al. 2007). Treatment of encephalopathy and cerebral vasculitis requires intravenous acyclovir treatment, as oral treatment may be insufficient (Gilden et al. 2005). Concurrent steroid treatment may have a beneficial role in immunocompetent patients with severe VZV encephalitis (Steiner et al. 2005). "
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