Autor(es): Sejvar James J,Leis A Arturo,Stokic Dobrivoje S,Van Gerpen Jay A,Marfin Anthony A,Webb Risa,Haddad Maryam B,Tierney Bruce C,Slavinski Sally A,Polk Jo Lynn,Dostrow Victor,Winkelmann Michael,Petersen Lyle R

Resumo: Acute weakness associated with West Nile virus (WNV) infection has previously been attributed to a peripheral demyelinating process (Guillain-Barré syndrome); however, the exact etiology of this acute flaccid paralysis has not been systematically assessed. To thoroughly describe the clinical, laboratory, and electrodiagnostic features of this paralysis syndrome, we evaluated acute flaccid paralysis that developed in seven patients in the setting of acute WNV infection, consecutively identified in four hospitals in St. Tammany Parish and New Orleans, Louisiana, and Jackson, Mississippi. All patients had acute onset of asymmetric weakness and areflexia but no sensory abnormalities. Clinical and electrodiagnostic data suggested the involvement of spinal anterior horn cells, resulting in a poliomyelitis-like syndrome. In areas in which transmission is occurring, WNV infection should be considered in patients with acute flaccid paralysis. Recognition that such weakness may be of spinal origin may prevent inappropriate treatment and diagnostic testing.

Imprenta: Emerging Infectious Diseases, v. 9, n. 7, p. 788-793, 2003

Identificador do objeto digital: 10.3201/eid0907.030129

Descritores: Guillain-Barre Syndrome - Cell ; Guillain-Barre Syndrome - Flaviviridae ; Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Viral infections ; Guillain-Barre Syndrome - Virus ; Guillain-Barre Syndrome - Transmission

Data de publicação: 2003

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