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The aetiology of flaccid paralysis in West Nile virus infection
  1. A A Leis1,
  2. J A Van Gerpen2,
  3. J J Sejvar3
  1. 1Methodist Rehabilitation Center, Jackson, MS, USA
  2. 2Ochsner Clinic, New Orleans, LA, USA
  3. 3Centers for Disease Control and Prevention, Atlanta, GA, USA
  1. Correspondence to:
 J J Sejvar;
 zea3cdc.gov

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We read with interest the recent article by Park et al,1 describing a syndrome of acute anterior radiculitis associated with West Nile virus (WNV) infection. Although admittedly there is still much to learn about the clinical spectrum of disease associated with WNV, we were troubled by several of the assertions raised by the article, and the conclusions drawn.

Recent evidence has suggested that the majority of patients developing acute asymmetrical weakness in the setting of WNV infection suffer from damage to spinal anterior horn cells, resulting in a poliomyelitis-like syndrome.2–5 This has been supported by electrodiagnostic data2–5 and by pathology demonstrating the destruction of anterior spinal grey matter.6–9 Park et al assert that “the mechanism of weakness associated with WNV infection continues to be unclear”, and they subsequently “propose an alternate explanation for the associated weakness”. This alternative explanation of “acute anterior radiculitis” is based on MRI findings that showed intradural lumbosacral nerve root enhancement in a patient with unilateral leg weakness.

However, the authors do not describe MRI findings in the anterior spinal cord, and the MRI images provided are at the L1–L2 and L2–L3 levels, which lie caudal to the cord segments giving rise to lumbar …

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