Volume 9, Number 7—July 2003
Research
Acute Flaccid Paralysis and West Nile Virus Infection
James J. Sejvar*
, 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*
, 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*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.
