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Neurological complications of varicella zoster virus reactivation
#MMPMID24792344
Nagel MA
; Gilden D
Curr Opin Neurol
2014[Jun]; 27
(3
): 356-60
PMID24792344
show ga
PURPOSE OF 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
meningoencephalitis, 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 cerebrospinal fluid 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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