Lyme disease, first recognized in 1975, typically begins in summer with erythema chronicum migrans (ECM) followed some months later by neurological symptoms (meningoencephalitis, cranial neuropathy), associated with carditis and arthritis. Bannwarth’s syndrome is characterized by an ECM followed by radicular pain and radicular sensory and motor disturbances, accompanied by aseptic meningitis. In both cases the cerebrospinal fluid typically shows marked lymphocytic pleocytosis accompanied by an oligoclonal reaction. Despite differences in the clinical symptoms, a borrelia isolated from ticks has been implicated as the etiologic agent of both diseases, and specific antibody titers usually reach a peak between the third and sixth week after onset of the
disease. Investigations in 5 patients who developed neurologic symptoms after tick-borne borrelia infection revealed specific antibodies (IgM, IgG) against Borrelia burgdorferi in all sera, and all the patients recovered, one of them without treatment and the others under penicillin or tetracyclines. None developed major complications (carditis, arthritis).