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Despite rapid dissemination of Borrelia burgdorferi throughout the body following initial inoculation, the clinical manifestations of this illness tend to involve specific organ systems preferentially. The nervous system, in particular, is frequently affected; involvement usually follows one of several distinct patterns. Most commonly, patients develop a lymphocytic meningitis, radiculoneuritis or cranial neuropathy, occurring singly or in combination. Patients with radicular involvement often have a myelopathic component as well. At the other extreme, rare patients will develop focal inflammation of the central nervous system, an encephalomyelitis, that appears to involve white matter more often than grey. More commonly, patients may develop cognitive and memory impairment-a mild encephalopathy. In some patients this may represent a subtle form of encephalomyelitis, while in others it is probably a “toxic-metabolic” effect of systemic infection.
Disease variability among patients probably is the result of multiple factors, including bacterial strain differences in virulence and organotropism, inoculum size, host immunity, and simultaneous co-infection with other tick-borne organisms. Accurate diagnosis remains somewhat problematic. The cerebrospinal fluid is almost always abnormal in the presence of active CNS infection. Intrathecal production of specific antibody can be demonstrated in over 90% of patients with meningitis or frank inflammatory encephalomyelitis; in patients with a milder encephalopathy this is less consistently observed. In most instances, diagnosis relies on a combination of demonstration of a specific immune response, and clinical judgment. In patients in whom the diagnosis is secure, appropriate antimicrobial therapy is highly effective in the vast majority of cases, although if there has been significant structural damage to the CNS, some residua may remain.