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Lauren B. Krupp, MD; Patricia K. Coyle, MD
Department of Neurology Health Science Center T12-020 State University of New York, Stony Brook Stony Brook, NY 11794-8121

John J. Halperin, MD
Department of Neurology North Shore University Hospital 300 Community Dr Manhasset, NY 10013

Arch Neurol. 1992;49(10):1011.

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

In Reply.

—We appreciate Cameron's comments and the opportunity to discuss the management of patients with Lyme disease who have been previously treated with oral antibiotics. Although objective cognitive deficits were present in 60% of our sample,¹ we do not suspect that for most of the patients this was due to continued brain infection. Only one patient had intrathecal antibody synthesis. No patient showed pleocytosis or protein level elevation in the cerebrospinal fluid. Therefore, we suspect that indirect consequences of infection may be a better explanation for the continued symptoms. In contrast to our group of patients where continued spirochetal infection was unlikely, Logigian and colleagues² noted that 75% (18/24) of their patients with encephalopathy had abnormal findings in the cerebrospinal fluid, including intrathecal Borrelia burgdorferi—antibody synthesis, pleocytosis, or protein level elevation, findings which suggest that continued brain infection was present.

The subsequent management of the patients . . . [Full Text PDF of this Article]

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