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Herpes zoster myelitis.

O Devinsky1, E S Cho, C K Petito

  • 1Department of Neurology, New York Hospital-Cornell University Medical Center, NY 10003.

Brain : a Journal of Neurology
|June 1, 1991
PubMed
Summary
This summary is machine-generated.

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Herpes zoster myelitis in immunosuppressed patients involves direct varicella-zoster virus infection of the spinal cord. Early antiviral therapy may help prevent or reduce myelopathy progression.

Area of Science:

  • Neurology
  • Virology
  • Immunology

Background:

  • Herpes zoster myelitis is a serious complication of varicella-zoster virus (VZV) reactivation.
  • Immunosuppression increases the risk and severity of VZV infections, including myelitis.

Purpose of the Study:

  • To investigate the clinical and pathological features of herpes zoster myelitis in immunosuppressed patients.
  • To explore the role of direct VZV infection and vasculitis in the pathogenesis of myelitis.
  • To provide a rationale for antiviral therapy in managing herpes zoster myelitis.

Main Methods:

  • Retrospective analysis of clinical and pathological findings in 13 patients with herpes zoster myelitis.
  • Immunohistochemical staining for VZV antigens.
  • Histopathological examination for viral inclusions, demyelination, vasculitis, and necrosis.

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Main Results:

  • Median interval from rash onset to myelitis was 12 days; median interval to maximal deficit was 10.5 days.
  • Neurological symptoms were predominantly motor, ipsilateral to the rash, with sensory deficits.
  • Pathological findings included direct VZV infection of neuroectodermal cells (oligodendrocytes), focal demyelination, and VZV vasculitis with leptomeningitis and necrosis in some cases.

Conclusions:

  • Direct VZV infection of the spinal cord is a key mechanism in herpes zoster myelitis.
  • The documented viral pathogenesis supports the use of antiviral agents to manage or prevent myelopathy progression.