Jay A Van Gerpen

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Publications (2)36.19 Total impact

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    Article: Neurologic manifestations and outcome of West Nile virus infection.
    James J Sejvar, Maryam B Haddad, Bruce C Tierney, Grant L Campbell, Anthony A Marfin, Jay A Van Gerpen, Aaron Fleischauer, A Arturo Leis, Dobrivoje S Stokic, Lyle R Petersen
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    ABSTRACT: The neurologic manifestations, laboratory findings, and outcome of patients with West Nile virus (WNV) infection have not been prospectively characterized. To describe prospectively the clinical and laboratory features and long-term outcome of patients with neurologic manifestations of WNV infection. From August 1 to September 2, 2002, a community-based, prospective case series was conducted in St Tammany Parish, La. Standardized clinical data were collected on patients with suspected WNV infection. Confirmed WNV-seropositive patients were reassessed at 8 months. Clinical, neurologic, and laboratory features at initial presentation, and long-term neurologic outcome. Sixteen (37%) of 39 suspected cases had antibodies against WNV; 5 had meningitis, 8 had encephalitis, and 3 had poliomyelitis-like acute flaccid paralysis. Movement disorders, including tremor (15 [94%]), myoclonus (5 [31%]), and parkinsonism (11 [69%]), were common among WNV-seropositive patients. One patient died. At 8-month follow-up, fatigue, headache, and myalgias were persistent symptoms; gait and movement disorders persisted in 6 patients. Patients with WNV meningitis or encephalitis had favorable outcomes, although patients with acute flaccid paralysis did not recover limb strength. Movement disorders, including tremor, myoclonus, and parkinsonism, may be present during acute illness with WNV infection. Some patients with WNV infection and meningitis or encephalitis ultimately may have good long-term outcome, although an irreversible poliomyelitis-like syndrome may result.
    JAMA The Journal of the American Medical Association 08/2003; 290(4):511-5. · 30.03 Impact Factor
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    Article: 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, Lyle R Petersen
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    ABSTRACT: Acute weakness associated with West Nile virus (WNV) infection has previously been attributed to a peripheral demyelinating process (Guillain-Barré syndrome); however, the exact etiology of this acute flaccid paralysis has not been systematically assessed. To thoroughly describe the clinical, laboratory, and electrodiagnostic features of this paralysis syndrome, we evaluated acute flaccid paralysis that developed in seven patients in the setting of acute WNV infection, consecutively identified in four hospitals in St. Tammany Parish and New Orleans, Louisiana, and Jackson, Mississippi. All patients had acute onset of asymmetric weakness and areflexia but no sensory abnormalities. Clinical and electrodiagnostic data suggested the involvement of spinal anterior horn cells, resulting in a poliomyelitis-like syndrome. In areas in which transmission is occurring, WNV infection should be considered in patients with acute flaccid paralysis. Recognition that such weakness may be of spinal origin may prevent inappropriate treatment and diagnostic testing.
    Emerging infectious diseases 08/2003; 9(7):788-93. · 6.17 Impact Factor
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