Neurology 2003;61:55-59
© 2003 American Academy of Neurology
West Nile virus infection
A new acute paralytic illness
L. E. Jeha, MD,
C. A. Sila, MD,
R. J. Lederman, MD PhD,
R. A. Prayson, MD PhD,
C. M. Isada, MD and
S. M. Gordon, MD
From the Departments of Neurology (Drs. Jeha, Sila, and Lederman), Pathology (Dr. Prayson), and Infectious Disease (Drs. Isada and Gordon), The Cleveland Clinic Foundation, OH.
Address correspondence and reprint requests to Dr. L. E. Jeha, Department of Neurology, The Cleveland Clinic Foundation, 9500 Euclid Ave., S-91, Cleveland, OH 44195; e-mail: jehal{at}ccf.org
Objective: To determine the clinical, laboratory, electrodiagnostic, radiologic, and pathologic characteristics that define the spectrum of CNS disease caused by West Nile virus (WNV) infection.
Methods: The records of all patients hospitalized at the Cleveland Clinic from August 2002 to September 2002 with WNV infection were reviewed.
Results: Of 23 cases, the median age was 74 years old, and 74% were men. Symptoms included fever (100%), altered mental status (74%), gastrointestinal complaints (43%), back pain (35%), and rash (26%). In half, meningitis or encephalitis overlapped with flaccid weakness that progressed over 3 to 8 days, with a tendency to be proximal and asymmetric. Laboratory abnormalities included hyponatremia (30%) and initial CSF neutrophilic pleocytosis. Electrodiagnostic studies in two patients showed reduced motor amplitudes with normal conduction velocities and active denervation. In two other patients, reduced sensory amplitudes were also seen. MRI changes included cauda equina enhancement and parenchymal spinal cord signal abnormalities and parenchymal or leptomeningeal signal changes in the brain. Autopsy in three cases showed chronic perivascular inflammation in the brain and inflammatory changes with anterior horn cell loss in the spinal cord.
Conclusion: An overlapping spectrum of meningitis, encephalitis, and myeloradiculitis occurs in CNS WNV infection. Fever, rash, abdominal and back pain, preceding a proximal, asymmetric flaccid weakness, with CSF pleocytosis help distinguish the motor syndrome from Guillain–Barré syndrome. Pathologic changes in the CNS resembled poliomyelitis.
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