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The causative agent of
Lyme disease, Borrelia burgdorferi, is a highly neurotropic organism that not only can produce symptomatic neurologic
disease but also can exist dormant within the central nervous system (CNS) for long periods. Two distinct types of neuroborreliosis occur at different stages of
Lyme disease. Second-stage
Lyme meningitis resembles aseptic meningitis and is often associated with facial palsies, peripheral nerve involvement, and/or radiculopathies.
Lyme meningitis may be the first evidence of
Lyme disease, occurring without a history of erythema chronicum migrans or flu-like illness. Third-stage parenchymal involvement causes a multitude of nonspecific CNS manifestations that can be confused with conditions such as multiple sclerosis, brain tumor, and psychiatric derangements. Manifestations of CNS parenchymal involvement in
Lyme disease are generally associated, however, with a history of erythema chronicum migrans, meningitis, or carditis. Both second- and third-stage
Lyme neuroborrelioses are commonly misdiagnosed because they are relatively uncommon and because they mimic many better-known disorders.