Maria A Nagel1, Don Gilden. 1. aDepartment of Neurology bDepartment of Microbiology, University of Colorado School of Medicine, Aurora, Colorado, USA.
Abstract
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.
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.
Authors: J M Menerath; M Gerard; H Laurichesse; P Goldschmidt; H Peigue-Lafeuille; F Rozenberg; J Beytout Journal: J Fr Ophtalmol Date: 1995 Impact factor: 0.818
Authors: Ralph P Insinga; Robbin F Itzler; James M Pellissier; Patricia Saddier; Alexander A Nikas Journal: J Gen Intern Med Date: 2005-08 Impact factor: 5.128
Authors: D H Gilden; B R Beinlich; E M Rubinstien; E Stommel; R Swenson; D Rubinstein; R Mahalingam Journal: Neurology Date: 1994-10 Impact factor: 9.910
Authors: Leonard H Calabrese; Fenglong Xie; Huifeng Yun; Kevin L Winthrop; John W Baddley; Cassandra Calabrese; Jeffrey R Curtis Journal: Arthritis Rheumatol Date: 2017-02 Impact factor: 10.995
Authors: Jaqueline R Silva; Alexandre H Lopes; Jhimmy Talbot; Nerry T Cecilio; Mateus F Rossato; Rangel L Silva; Guilherme R Souza; Cassia R Silva; Guilherme Lucas; Benedito A Fonseca; Eurico Arruda; Jose C Alves-Filho; Fernando Q Cunha; Thiago M Cunha Journal: J Neurosci Date: 2017-06-02 Impact factor: 6.167