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Abstract & Commentary
Source: Flaherty ML, et al. Clinical and electrophysiologic patterns of flaccid paralysis due to West Nile virus. Mayo Clin Proc. 2003;78:1245-1248.
West Nile virus may present as meningitis, encephalitis, meningoencephalomyelitis, and Guillain Barré syndrome. Poliomyelitis, as 2 well-documented cases demonstrate, must also be added to the list. In the first case, a 34-year-old man developed rapidly progressive, asymmetric, flaccid arm and bifacial muscle weakness 6 days following the onset of a febrile illness characterized by headache, tinnitus, photophobia, and upper respiratory tract symptoms. Reflexes were diminished in the weak muscles and sensation was normal. Cerebrospinal fluid (CSF) examination initially revealed elevated protein with a neutrophilic lymphocytosis that converted to lymphocytic pleocytosis 3 days later. CSF West Nile IgM titer was positive. Cervical spine and brain MRI with gadolinium enhancement were normal. Nerve conduction studies and needle EMG were consistent with anterior horn cell involvement. He partially improved over 9 months. In the second case, a 48-year-old man became acutely febrile and delirious with positive CSF West Nile IgM. Several days following recovery, he developed leg weakness and mild paresthesiae. Electrodiagnostic studies 3 months following presentation were consistent with anterior horn cell involvement. Improvement occurred within 3 weeks but plateaued. West Nile virus may result in clinical poliomyelitis, and physicians should be alert to this possibility, particularly in the summertime.
West Nile virus, a single stranded RNA virus, belongs to the genus Flavivirus that includes St. Louis encephalitis virus and dengue.1 It can be transmitted through blood transfusion, organ transplantation, or breast-feeding but is most commonly transmitted through the bite of an infected Culex species mosquito. Only 1 in 150 infected persons develop neurologic sequelae. Diagnosis requires presence of IgM West Nile virus antibody in the CSF, West Nile RNA in CSF, four-fold elevation of IgG between acute and convalescent sera, or isolation of West Nile virus from brain or spinal cord. Falsely positive results may arise from cross reactivity with other flaviviruses, and titer positivity must be confirmed by the plaque-reduction neutralization assay in cell culture. CSF findings are typically those of an aseptic meningitis, and treatment remains supportive. An ongoing NIH trial of intravenous immunoglobulin (IVIG) rich in West Nile virus antibodies (obtained from Israel following a Y2K epidemic) will determine whether it will be of benefit. Meanwhile, recovery is slow and often incomplete. — Michael Rubin, MD, Professor of Clinical Neurology, New York Presbyterian Hospital-Cornell Campus, Assistant Editor, Neurology Alert.
1. Roos KL. Mayo Clin Proc. 2003;78:1205-1206.