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Richard B. Tenser, MD
Department of Medicine (Neurology) and Microbiology The Pennsylvania State College of Medicine Hershey, PA 17033

Arch Neurol. 1985;42(7):626.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—Feinberg et al¹ presented an interesting case of neurologic illness following Epstein-Barr virus (EBV) infection, but I believe that their suppositions of direct EBV infection of the nervous system were overstated. Elevated antibody levels to EBV in cerebrospinal fluid (CSF) three weeks after the onset of illness were taken to indicate nervous system infection. The CSF antibody levels, which were half of the serum levels, were not believed by the authors to be the result of the relatively slight amount of blood-brain barrier disruption that was present, indicated by the total CSF protein level of 71 mg/dL. However, this protein value was almost twice the admission value of 38 mg/dL. The evidence of ongoing blood-brain barrier disruption and the lack of increase of the CSF IgG level argue more strongly toward a peripheral rather than a central origin of antibody synthesis.

The authors speculated that EBV . . . [Full Text PDF of this Article]

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