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NEUROLOGY 1992;42:278
© 1992 American Academy of Neurology

Demyelinating disease after neurologically complicated primary Epstein-Barr virus infection

P. F. Bray, MD, K. W. Culp, BS, D. E. McFarlin, MD, H. S. Panitch, MD, R. D. Torkelson, MD and J. P. Schlight, BS

From the Departments of Neurology and Pediatrics (Dr. Bray, and K.W. Culp and J.P. Schlight), University of Utah, Salt Lake City, UT; the Section on Neuroimmunology (Dr. McFarlin), National Institute of Neurologic Disease and Stroke, NIH, Bethesda, MD; the Department of Neurology (Dr. Panitch), University of Maryland, Baltimore, MD; and the Division of Pediatric Neurology (Dr. Torkelson), University of Nebraska, Omaha, NE.

This report describes five patients who, following a neurologically complicated primary Epstein-Barr virus infection, developed progressive or relapsing neurologic deficits. The sequelae in four patients followed 4 to 12 years led to the diagnosis of multiple sclerosis (MS). The fifth patient presented with acute disseminated sclerosis and exhibits diffuse neurologic deficits that have persisted for 2 years. We suggest that the diagnosis of an unexplained acute neurologic or psychiatric syndrome should raise the question of a primary EBV etiology. A precisely timed serologic and hematologic study of the blood is imperative to capture the essential evidence. The data presented represent a clinical association between a neurologically complicated primary EBV infection and both chronic and acute demyelinating disease. The evidence does not justify a conclusion that EBV virus causes MS.

Address correspondence and reprint requests to Dr. Patrick F. Bray, 50 No. Medical Drive, University Hospital, Salt Lake City, UT 84132.

Supported in part by the Clipped Wings (flying personnel, United Airlines), Richard Uriarte, and the Utah Association of Life Underwriters.

Received May 13, 1991. Accepted for publication in final form July 29, 1991.




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