Neurological Complications of VZV Reactivation #MMPMID24792344
Nagel MA; Gilden D
Curr Opin Neurol 2014[Jun]; 27 (3): 356-60 PMID24792344show ga
Purpose of the review: Varicella zoster virus (VZV) reactivation results in zoster, which may be complicated by postherpetic neuralgia, myelitis, meningoencephalitis and VZV vasculopathy. This review highlights the clinical features, laboratory abnormalities, imaging changes and optimal treatment of each of those conditions. Because all of these neurological disorders produced by VZV reactivation can occur in the absence of rash, the virological tests proving that VZV caused disease are discussed. Recent findings: After primary infection, VZV becomes latent in ganglionic neurons along the entire neuraxis. With a decline in VZV-specific cell-mediated immunity, VZV reactivates from ganglia and travels anterograde to the skin to cause zoster, which is often complicated by postherpetic neuralgia. VZV can also travel retrograde to produce meningoencephaltis, myelitis and stroke. When these complications occur without rash, VZV-induced disease can be diagnosed by detection of VZV DNA or anti-VZV antibody in CSF and treated with intravenous acyclovir. Summary: Awareness of the expanding spectrum of neurological complications caused by VZV reactivation with and without rash will improve diagnosis and treatment.
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Curr+Opin+Neurol 2014 ; 27 (3): 356-60
