Spinal Cord Involvement in Uncomplicated Herpes Zoster

Abstract

We prospectively evaluated herpes zoster patients during the acute phase of the disease for central nervous system involvement. Of 24 patients with spinal zoster, 13 (54%) had spinal cord abnormality, which was asymptomatic in 12 of the 13. Age but not lack of acyclovir treatment was associated with such involvement. In all but 2, neurological involvement resolved within 6 months. Although the mechanism responsible for the neurological abnormalities is unknown, findings may support the hypothesis that zoster is associated with spread of viral infection into the spinal cord and therefore support the possibility that zoster is due to active viral replication in the ganglion.The three neurotropic herpes viruses, herpes simplex virus type 1 (HSV-1), HSV-2, and varicella-zoster virus (VZV), reside latently in peripheral sensory ganglia (PSG) and reactivate to produce recurrent mucocutaneous disease (for reviews, see references 2, 4, and 7). However, although they belong to the same family of viruses and colonize the same tissue, there are major clinical differences between the reactivation of HSV-1 and -2 and that of VZV. Unlike cold or genital sores, herpes zoster is usually a single episode affecting the entire dermatome and is associated with severe sensory symptomatology and sometimes with short or even long-lasting sensory abnormalities. Moreover, while HSV-1 and -2 reactivations are usually not associated with meningitis, herpes zoster is accompanied by cerebrospinal fluid pleocytosis in at least a third of patients (3). The site of latency for HSV-1 in PSG is ganglion cells. However, some data suggest that in addition to neurons, nonneuronal cells also harbor the latent VZV genome (1, 6). Based on these differences, several groups proposed that nonneuronal cells might give rise to reactivated VZV, leading to active viral replication, propagation of infectious viral particles throughout the ganglion, and spread of the infection via nerve axons to the entire respective dermatome and the meninges. (5). On the other hand, HSV-1 reactivation is associated with either restricted or no viral replication in the ganglion and spread of viral particles to the cutaneous distribution of a single neuron.If indeed the cause of herpes zoster is infectious viral particles that spread from the ganglion into the periphery, one might expect a similar spread orthodromically from the ganglion into the spinal cord in cases of spinal herpes zoster and into the brain stem in cranial herpes zoster. We therefore examined central nervous system (CNS) involvement in patients with uncomplicated herpes zoster.Between the years 1997 and 1999, we enrolled all patients who presented to the neurological and/or dermatological departments and outpatient clinics in our institute, within the first week of herpes zoster. Patients underwent a thorough neurological examination and were followed up for at least 6 months after the herpes zoster episode by the same neurologist at time intervals of 1 to 2 months. In all patients, diagnosis of zoster infec...

Acyclovir responsive brain stem disease after the Ramsay Hunt syndrome

“…The first possibility is that VZV migrated transaxonally or transynaptically into the brain stem parenchyma without arterial involvement. The notion that VZV migrates transaxonally to the CNS after reactivation from ganglia is supported by earlier imaging studies that demonstrated segmental spinal cord or focal brainstem abnormalities after zoster [6,7]. Transaxonal spread of virus into the CNS is also supported by the fact that our patient developed progressive neurological deficit, not transient ischemic attacks, until treatment with intravenous acyclovir was instituted.…”

“…The MRI finding of bilateral contrast enhancement in the brainstem and cerebellum corroborated evidence of CNS involvement. Previous reports have revealed MRI abnormalities on T2-weighted images of the brainstem or spinal cord in patients with acute zoster [6,7]. In these studies, only a subset of the patients with MRI abnormalities had symptoms or signs that suggested CNS dysfunction.…”

Shingles with secondary asymptomatic CNS involvement!

“…There was strong evidence of VZV in the CSF in 14 of 46 patients (35%), either in the form of a positive PCR or as anti-VZV antibodies. A prospective study by Steiner et al 6 to evaluate CNS involvement in the acute phase of HZ infection showed clinical evidence of spinal cord involvement (long tract signs, sensory level, pyramidal limb weakness and/or sphincter involvement) in 12 of 24 patients without any clinical symptoms. This study suggested that the mechanisms responsible for CNS involvement could be immune-mediated or infectious.…”

Zona zoster enfeksiyonu sırasında gelişen aseptik menenjit

“…CNS complications related to ZZ infection include myelitis, aseptic meningitis, encephalitis and ventriculitis (2,4,5). Myelitis and aseptic meningitis are thought to be caused by dissemination of the virus directly into the CNS from the related nerve.…”