RESEARCH ed with other flaviviruses (21–23), as well as anterior myelitis associated with WNV infection (24). The assertion that WNV infection involves anterior horn cells and causes a polio-type syndrome has a patho- logic basis. The neuropathology of experimental WNV infection in monkeys was most pronounced in the cerebel- lum, medulla, and the cervical and lumbar regions of the spinal cord (25). Anterior horn cells showed degeneration and neuronal cell death; conversely, no changes were seen in the oligodendroglia or peripheral nerves. Similarly, WNV-infected horses displayed multifocal polioen- cephalomyelitis, with involvement of the ventral and later- al horns of the thoracic and lumbar spinal cord (26,27). WNV antigen was mainly localized within the gray matter of the spinal cord, with no lesions apparent in peripheral nerves or ganglia. In WNV-infected birds, lesions and viral antigen were most prominent in the cerebellum and the gray matter of the spinal cord (28). Previous case studies have attributed WNV-associated acute flaccid paralysis to Guillain-Barré syndrome, motor axonopathy, or severe axonal polyneuropathy (4–6). The clinical signs and symptoms and electrodiagnostic findings reported in those cases, and those described here, are most consistent with a polio-like condition, and would be atypi- cal for Guillain-Barré syndrome or other peripheral nerve disorders. Although acute poliomyelitis and polio-like con- ditions may occasionally simulate Guillain-Barré syn- drome (29), our cases had several clinical, laboratory, and electrodiagnostic features that differed from typical Guillain-Barré syndrome (30–32; Table 4). In Guillain-Barré syndrome, electrodiagnostic findings generally suggest peripheral nerve demyelination or, less commonly, a combined demyelinating and axonal process (30,31). The cases reported here displayed reduced or absent CMAPs with preserved SNAPs, no evidence of demyelination, a neurogenic pattern of recruitment, and widespread denervation; combined with the clinical pic- ture of an asymmetric paralysis, these findings are typical for a polio-like condition and uncommon for Guillain- Barré syndrome. A pure axonal variant of Guillain-Barré syndrome has been described (33) and may be confused with poliomyelitis and polio-like conditions; however, such cases are generally characterized by distally promi- nent weakness and show subclinical sensory nerve involvement on electrodiagnostic testing. Thus, in the con- text of WNV infection, electrodiagnostic studies previous- ly interpreted as motor axonal polyneuropathy or motor axonopathy without sensory nerve involvement (4–6) are more suggestive of anterior horn cell loss than of Guillain- Barré syndrome. Three of the seven patients had acute flaccid paralysis without other findings, suggestive of severe central nerv- ous system involvement caused by WNV infection. Physicians should suspect WNV infection in patients from areas where WNV is being transmitted and who have acute, painless, asymmetric weakness, even if unaccompa- nied by fever or apparent meningoencephalitis. Diagnostic studies should include testing for WNV-specific IgM anti- body in CSF or acute- and convalescent-phase serum sam- ples. In patients from such areas who have acute flaccid paralysis, CSF analysis, thorough electrodiagnostic stud- ies, and spinal imaging should be considered before initi- ating diagnostic evaluations or therapies directed at Guillain-Barré syndrome, stroke, inflammatory myopathies, or other peripheral inflammatory processes. These therapies are ineffective for polio-like syndromes and can produce serious sequelae (34–37). Continued surveillance and investigation of WNV- infected patients are needed to fully define the scope of clinical illness and determine the incidence of acute flaccid paralysis. In addition to assessing clinical outcome, the identification of risk factors and the pathologic confirma- tion of anterior horn cell involvement in patients with WNV-associated acute flaccid paralysis remain important public health goals. 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 Painful distal paresthesias and sensory loss sensory loss; occasional myalgias 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 Demyelination: marked slowing of conduction velocity; CMAPs, preserved SNAPs; asymmetric denervation conduction block, temporal dispersion; reduced SNAPs aCSF, cerebrospinal fluid; CMAPs, compound muscle action potentials; SNAPSs, sensory nerve action potentials. 792 Emerging Infectious Diseases • Vol. 9, No. 7, July 2003