Abstract

Varicella zoster virus (VZV) reactivation results in zoster, which may be complicated by postherpetic neuralgia. Other, less frequent complications are cranial nerve palsies, zoster paresis, meningoencephalitis, myelitis, and varicella zoster vasculopathy. All these neurological disorders produced by VZV reactivation can occur in the absence of rash. They are caused mainly by the direct spread of the virus. The risk of neurological complications is increased in immunocompromised patients, who are also likely to have more severe forms of central nervous system complications. To confirm VZV as the cause of the condition, detection of anti-VZV IgG antibody in cerebrospinal fluid with intrathecal synthesis and detection of VZV DNA in cerebrospinal fluid are used. For those diseases in which viral replication likely plays an important role in pathogenesis (e.g., meningitis, encephalitis, and myelitis and VZV vasculopathy), therapy with intravenous acyclovir is recommended. Outcome of the central nervous system complications varies from full recovery to death, being worse in immunocompromised. Most patients with segmental zoster paresis or cranial nerve involvement show good or complete recovery.

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