Introduction: Complications of VZV infection in the central nervous system are multiple. VZV-related myelitis is an uncommon complication of herpes zoster.
Observation: We report the case of a 55-year old man with intercostal herpes zoster who presented a subacute medullar syndrome. MRI demonstrated an extended cervico-thoracic medullar hyperintensity on the T2-weighted images. Cerebrospinal fluid (CSF) analysis showed 100 leukocytes/mm3, 0.94 g/L protein, negative VZV PCR, elevated rate of anti-VZV IgG and no oligoclonal bands. Clinical, biological and radiological presentations were compatible with the diagnosis of VZV-related myelitis with three potential pathophysiological mechanisms: infectious, immune post-infectious, vascular. The course was partially favorable after a 3-day regimen of corticosteroid and 3 weeks of acyclovir infusions.
Discussion: Parainfectious myelitis is often the consequence of a viral infection with a post-infectious pathogenesis. Most often, the clinical outcome is good. In this case report, we highlight the VZV vascular tropism and its more severe outcome.
Conclusion: VZV-related myelitis should be diagnosed early. The combination of aciclovir and corticoids infusions seems to be beneficial.
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http://dx.doi.org/10.1016/s0035-3787(07)90359-8 | DOI Listing |
Rev Med Virol
July 2024
Department of Medical Laboratory Sciences, College of Applied Medical Sciences, Prince Sattam bin Abdulaziz University, Al-Kharj, Saudi Arabia.
The Varicella-zoster virus (VZV), classified as a neurotropic member of the Herpesviridae family, exhibits a characteristic pathogenicity, predominantly inducing varicella, commonly known as chickenpox, during the initial infectious phase, and triggering the reactivation of herpes zoster, more commonly recognized as shingles, following its emergence from a latent state. The pathogenesis of VZV-associated neuroinflammation involves a complex interplay between viral replication within sensory ganglia and immune-mediated responses that contribute to tissue damage and dysfunction. Upon primary infection, VZV gains access to sensory ganglia, establishing latent infection within neurons.
View Article and Find Full Text PDFNeurol Sci
September 2008
Department of Clinical Neurology, C. Mondino IRCCS Foundation, Pavia, Italy.
Objective: To describe clinical, MRI and cerebrospinal fluid (CSF) features of a varicella zoster virus (VZV) related meningo-encephalo-myelitis (MEM) without rash in an immunocompetent female.
Patient: An 85 year old immunocompetent woman with mild hyperthermia and acute, severe MEM.
Intervention: Serum antibodies and CSF PCR were searched for several viruses.
Rev Neurol (Paris)
January 2007
Clinique Neurologique, Hôpital Roger Salengro, CHRU de Lille, 59037 Lille Cedex.
Introduction: Complications of VZV infection in the central nervous system are multiple. VZV-related myelitis is an uncommon complication of herpes zoster.
Observation: We report the case of a 55-year old man with intercostal herpes zoster who presented a subacute medullar syndrome.
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