The clinical disorders of B. burgdorferi infection continue to be elucidated. The neurologic disorders, especially those that produce progressive paralytic syndromes, have been reasonably well described. They frequently occur in conjunction with syndromes affecting other body systems. The appropriate use of antibiotics is usually effective in eradicating the infection. However, some individuals may have residual deficits as a result of the infectious process, even after the bacterial infection is eradicated. These are treated by appropriate supportive and symptomatic therapies, not by endless, useless courses of antibiotics. Finally, although early discussions of the pathophysiology and the clinical syndromes associated with B. burgdorferi infection compared the neurologic syndromes of with those of T. pallidum, raising the specter of another Great Imitator, this frame of reference has lost its usefulness. Modern laboratory techniques have allowed much better definition of the syndromes associated with this disorder. Whereas I once subscribed to the slogan, "Remember the Great Imitator," I now recommend that neurologists "Imitate Great Thinkers and Forget the Great Imitator."