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Volume 9, Number 7—July 2003

Research

Acute Flaccid Paralysis and West Nile Virus Infection

James J. Sejvar*Comments to Author , A. Arturo Leis†, Dobrivoje S. Stokic†, Jay A. Van Gerpen‡, Anthony A. Marfin*, Risa Webb§, Maryam B. Haddad*, Bruce C. Tierney*, Sally A. Slavinski§, Jo Lynn Polk†, Victor Dostrow†, Michael Winkelmann†, and Lyle R. Petersen*
Author affiliations: *Centers for Disease Control and Prevention, Atlanta, Georgia, USA; †Methodist Rehabilitation Center, Jackson, Mississippi, USA; ‡Ochsner Clinic, New Orleans, Louisiana, USA; §Mississippi State Department of Health, Jackson, Mississippi, USA

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Table 4

Clinical characteristics of patients with West Nile virus–associated acute flaccid paralysis compared with patients with typical Guillain-Barré syndrome (25–27)a

Characteristic West Nile virus–associated flaccid paralysis Guillain-Barré syndrome
Timing of onset
Acute phase of infection
1–8 weeks after acute infection
Fever and leukocytosis
Present
Absent
Weakness distribution
Asymmetric; occasional monoplegia
Generally symmetric; proximal and distal muscles
Sensory symptoms
Absence of numbness, paresthesias, or sensory loss; occasional myalgias
Painful distal paresthesias and sensory loss
Bowel/bladder involvement
Often present
Rare
Concurrent encephalopathy
Often present
Absent
CSF profile
Pleocytosis and elevated protein
No pleocytosis; elevated protein (albuminocytologic dissociation)
Electrodiagnostic features Anterior horn cell/motor axon: reduced/absent CMAPs, preserved SNAPs; asymmetric denervation Demyelination: marked slowing of conduction velocity; conduction block, temporal dispersion; reduced SNAPs

aCSF, cerebrospinal fluid; CMAPs, compound muscle action potentials; SNAPSs, sensory nerve action potentials.

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