Primary infection with Varicella zoster virus (VZV) causes varicella (chickenpox). Following primary infection, this ubiquitous human neurotropic virus establishes latency in cranial nerve ganglia, dorsal root ganglia and autonomic ganglia, sites from which it can reactivate, most often occurring as cell-mediated immunity wanes with advancing age and immunosuppression. Reactivation results in zoster (shingles), a painful dermatomal rash occasionally followed by postherpetic neuralgia. Centripetal spread at the time of reactivation may result in other neurological complications including meningoencephalitis, myelopathy and VZV vasculopathy. Diagnosis of these neurological conditions is aided by polymerase chain reaction (PCR) to detect VZV DNA in CSF and serological studies of antibody in the CSF to VZV in CSF.
Relation is Part of
NANOS Annual Meeting 2018: Varicella Zoster Virus (VZV) in Neuro-Ophthalmology
Joseph Berger, MD
Spencer S. Eccles Health Sciences Library, University of Utah
2018 North American Neuro-Ophthalmology Society Annual Meeting