Asymmetric flaccid paralysis: A neuromuscular presentation of West Nile virus infection

• Published in: Annals of neurology 2003-06, Vol.53 (6), p.703-710
• Main Authors: Li, Jun, Loeb, Jeffrey A., Shy, Michael E., Shah, Aashit K., Tselis, Alex C., Kupski, William J., Lewis, Richard A.
• Format: Article
• Language: English
• Subjects: Acute Disease; Adult; Biological and medical sciences; Biopsy; Electromyography - instrumentation; Enzyme-Linked Immunosorbent Assay; Female; Human viral diseases; Humans; Immunoglobulin M - blood; Infectious diseases; Lumbosacral Region; Magnetic Resonance Imaging; Male; Medical sciences; Middle Aged; Motor Neurons - pathology; Motor Neurons - virology; Muscle Fibers, Skeletal - pathology; Muscle Fibers, Skeletal - virology; Muscle, Skeletal - pathology; Muscle, Skeletal - virology; Neural Conduction - physiology; Paraplegia - diagnosis; Paraplegia - immunology; Paraplegia - virology; Spinal Cord - pathology; Spinal Cord - virology; Spinal Nerve Roots - pathology; Spinal Nerve Roots - virology; Viral diseases; Viral diseases of the nervous system; West Nile Fever - cerebrospinal fluid; West Nile Fever - complications; West Nile Fever - diagnosis; West Nile virus - isolation & purification
• ISSN: 0364-5134; 1531-8249
• DOI: 10.1002/ana.10575

The neuromuscular aspects of West Nile virus (WNV) infection have not been characterized in detail. We have studied a group of six patients with proven WNV infection. All cases presented with acute, severe, asymmetric, or monolimb weakness, with minimal or no sensory disturbance after a mild flu‐like prodrome. Four cases also had facial weakness. Three of our cases had no encephalitic signs or symptoms despite cerebrospinal fluid pleocytosis. Electrophysiological studies showed severe denervation in paralyzed limb muscles, suggesting either motor neuron or multiple ventral nerve root damage. This localization is supported further by the finding of abnormal signal intensity confined to the anterior horns on a lumbar spine magnetic resonance imaging. Muscle biopsies from three patients showed scattered necrotic fibers, implicating mild direct or indirect muscle damage from the WNV infection. In summary, we describe a group of patients with acute segmental flaccid paralysis with minimal or no encephalitic or sensory signs. We have localized the abnormality to either the spinal motor neurons or their ventral nerve roots. It will be important for physicians to consider WNV infection in patients with acute asymmetric paralysis with or without encephalitic symptoms. Ann Neurol 2003;53:703–710