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From the Departments of Neurology (Drs. de Silva, Mark, Balish, Sandbrink, and Houff), Veterans Affairs Medical Center and Georgetown University, Washington, DC; the Department of Neurology (Drs. Gilden and Mahalingam) and the Department of Microbiology (Dr. Gilden), University of Colorado Health Sciences Center, Denver, CO; the Department of Neurology (Dr. de Silva) Uniformed Services University of the Health Sciences, Bethesda, MD.
Supported in part by Public Health Service Grants from the National Institutes of Health (AG 06127 and NS 32623).
Received December 1, 1995. Accepted in final form February 9, 1996.
Address correspondence and reprint requests to Dr. Shari de Silva, Department of Neurology (Mailstop 127), Veterans Affairs Medical Center, 50 Irving Street NW, Washington, DC 20422.
This report describes two patients with acquired immunodeficiency syndrome (AIDS) and herpes zoster myelopathy.Patient one had a T-8 myelitis that preceded the onset of T-8-distribution zoster and was followed by cervical myelopathy. Antibody to varicella zoster virus (VZV) was present in the CSF. He never received steroids or other immunosuppressive drugs, and his condition improved dramatically after treatment with intravenous acyclovir. The second patient had a rapidly progressive myelitis with paralysis of both legs. Detection of VZV DNA and antibody to VZV in his CSF led to successful treatment with famciclovir despite discontinuation of dexamethasone and earlier treatment failure with acyclovir. These cases support the idea that VZV myelopathy in the immunosuppressed host is caused by virus invasion. CSF analysis for antiviral antibody and for VZV DNA by polymerase chain reaction are helpful in establishing the diagnosis. Aggressive antiviral therapy is advised.
NEUROLOGY 1996;47: 929-931
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