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Related Experiment Video

Updated: Jul 16, 2026

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

Published on: May 8, 2016

[VZV-related myelitis: a pathophysiological hypothesis].

O Outteryck¹, V Deramecourt, S Bombois

¹Clinique Neurologique, Hôpital Roger Salengro, CHRU de Lille, 59037 Lille Cedex.

Revue Neurologique

|February 17, 2007

Summary

Varicella zoster virus (VZV) infection can cause myelitis, a rare spinal cord inflammation. Early diagnosis and combined treatment with acyclovir and corticosteroids improve outcomes for VZV-related myelitis.

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Last Updated: Jul 16, 2026

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

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Published on: May 8, 2016

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4

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Isolating Central Nervous System Tissues and Associated Meninges for the Downstream Analysis of Immune cells

Isolating Central Nervous System Tissues and Associated Meninges for the Downstream Analysis of Immune cells

Published on: May 19, 2020

Area of Science:

Neurology
Infectious Diseases
Immunology

Background:

Complications of Varicella Zoster Virus (VZV) infection in the central nervous system are diverse.
VZV-related myelitis, a rare complication of herpes zoster, presents diagnostic and therapeutic challenges.

Observation:

A 55-year-old man with intercostal herpes zoster developed subacute medullar syndrome.
MRI revealed extensive cervico-thoracic spinal cord hyperintensity on T2-weighted images.
Cerebrospinal fluid analysis showed pleocytosis, elevated protein, negative VZV PCR, and positive anti-VZV IgG, supporting VZV myelitis.

Findings:

The case presented three potential pathophysiological mechanisms: infectious, immune post-infectious, and vascular.
The patient experienced a partially favorable outcome after a short course of corticosteroids and prolonged acyclovir infusion.
This case highlights the potential vascular tropism of VZV, suggesting a more severe prognosis.

Implications:

Early diagnosis of VZV-related myelitis is crucial for timely intervention.
Combination therapy with acyclovir and corticosteroids appears beneficial for managing VZV myelitis.
Understanding VZV's vascular tropism may guide future treatment strategies and prognostic assessments.