Case 5 On August 11, 2002, severe nausea, vomiting, headache, and diarrhea in the absence of fever developed in a 50-year-old male Mississippi resident with a history of alcohol abuse; the next day, progressive right arm weak- ness developed. He was hospitalized on August 14. Neurologic examination on admission showed flaccid paralysis of the right arm and mild weakness of the right leg, with normal sensation in all limbs (Table 2). Laboratory values are shown in Table 3; a lumbar puncture was not performed. Acute stroke was diagnosed, and the patient was treated with heparin. Mental status changes, dysarthria, and dysphagia subsequently developed but resolved. Upon transfer to a rehabilitation center on day 12, the patient had paralysis and areflexia limited to the right arm, with normal sensation and diffuse tremor in all limbs. Brain MRI results were normal; cervical spine MRI displayed mild multilevel foraminal stenosis on the left. Electrodiagnostic studies showed markedly reduced motor responses in the right arm with normal sensory responses, consistent with a severe asymmetric process affecting anterior horn cells. Case 6 On August 16, 2002, a 46-year-old male Louisiana res- ident with a history of coronary artery disease was hospi- talized with fever, headache, fatigue, and leg weakness of 3 days’ duration. He reported no nuchal rigidity or mental status changes, although family members described him as intermittently confused. Neurologic examination showed a plegic and areflexic right leg and mild left leg weakness; sensation was intact throughout. A bilateral tremor of the upper extremities and jaw was noted (Table 2). Laboratory abnormalities included a CSF pleocytosis (Table 3). He was diagnosed with Guillain-Barré syndrome and started on IVIG. Brain CT and MRI results were normal. Results of an enhanced MRI of the spine suggested meningitis involving the conus medullaris and cauda equina. Electrodiagnostic studies performed on day 4 demonstrat- ed early denervation and absent activation in muscles of the right leg and reduced activation of muscles in the right arm. CMAPs and SNAPs in the right arm and leg were normal. These findings were consistent with a severe, asymmetric process affecting anterior horn cells or motor axons. He was transferred to a rehabilitation facility on day 6 with no improvement of weakness. Case 7 On September 1, 2002, a previously healthy, 39-year- old male Louisiana resident had onset of fever, headache, and nuchal rigidity followed the next day by dysphagia and bilateral arm and leg weakness that was worse on the left. He was hospitalized on September 6 for acute respiratory RESEARCH failure and intubated. Neurologic examination showed normal cognition, asymmetric flaccid paralysis of the left arm and leg with absent reflexes, hyporeflexic weakness of the right arm and leg, and weakness of bulbar muscles (Table 2). A partial supranuclear gaze palsy, cogwheel rigidity, and bilateral Babinski signs were also evident. Admission laboratory findings showed peripheral leukocy- tosis and CSF pleocytosis (Table 3). Brain MRI showed increased T2 signal in the periaqueductal gray matter, sub- stantia nigra, and trigeminal motor nuclei. Electrodiagnostic studies performed on day 15 showed dif- fuse denervation in all myotomes, reduced CMAPs (worse on the left), and preserved SNAPs. On day 25, he was transferred to a long-term care facility with no improve- ment of limb weakness. Discussion The clinical and electrodiagnostic findings in these patients with WNV infection suggest involvement of spinal cord gray matter, specifically anterior horn cells, and a resulting acute poliomyelitis-like syndrome. All patients exhibited features typical for polio, including acute flaccid paralysis without paresthesias or sensory loss, marked asymmetric weakness, diminished or absent deep tendon reflexes in the affected limbs, and weakness that developed during an acute infectious process. Other typical features of poliomyelitis included CSF pleocytosis in five of six patients with CSF examination, acute respi- ratory distress in four, and acute changes in bowel or blad- der function in two. In addition, electrodiagnostic findings showed asymmetric muscle denervation, reduced CMAPs, and preserved SNAPs. No patients had evidence of demyelinating polyneuropathy or myopathy. The absence of new sensory abnormalities localizes the disease process to the anterior horn cells or motor axons. Although muscle denervation and reduced CMAP amplitudes do not distin- guish loss of anterior horn cells from loss of motor axons (15), these patients’ clinical features can be explained only by anterior horn cell disease, since no known infectious processes limited to motor axons produce widespread, asymmetric paralysis without sensory involvement. While MRI signal abnormalities in the anterior spinal cord have been noted in patients with poliomyelitis (16,17), these findings are inconsistent (18,19), and the absence of such changes in our four patients in which imaging was per- formed does not preclude a diagnosis of a poliomyelitis- like syndrome. Since immunization has eradicated wild-type poliovirus from the developed world, most cases of para- lytic polio-like conditions in the United States have been linked to other RNA viruses, including echoviruses, enteroviruses, and coxsackieviruses (20). Case reports have documented a poliomyelitis-type syndrome associat- Emerging Infectious Diseases • Vol. 9, No. 7, July 2003 791