Within days to weeks, B. burgdorferi spreads hematogenously. The organism also probably enters the CNS at this time (B. burgdorferi DNA, outer surface protein antigens, and the organism itself have been recovered from CSF as early as 18 days after inoculation). One to two months postinfection, B. burgdorferi localizes and becomes sequestered in certain tissues, including the CNS.

The CNS is involved in up to 20% of untreated North American patients (50% in European populations). Meningitis (typically lymphocytic) is the most common neuropathologic abnormality in early disseminated Lyme disease. Systemic symptoms can be present, but EM, fever, and lymphadenopathy are usually gone by the time neurologic complications develop. In fact, neurologic deficits, including seizure, can occur without antecedent EM and can be the initial disease manifestation. Neurologic abnormalities that have been reported to be associated with early CNS Lyme disease include:

• acute aseptic meningitis
• acute purulent meningitis
• chronic lymphocytic meningitis
• recurrent meningitis
• acute meningoencephalitis
• acute focal encephalitis
• encephalomyelitis
• leukoencephalitis
• acute cerebellar ataxia
• acute parkinsonian syndrome
• acute transverse myelitis
• subacute myelitis
• cognitive deficits
• affective disturbance
• seizures

Adapted from: Goldstein MA and Harden CL. Infectious states. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;83-133.
With permission from Elsevier (www.elsevier.com).
Reviewed and revised March 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.