NEUROBORRELIOSIS

Lyme disease is a multisystem infectious disease with frequent nervous system involvement. It affects peripheral nerves, the meningeal linin g of the central nervous system (CNS), and the CNS parenchyma, but the underlying pathophysiology remains unclear. Considerable data suggest that dividing Lyme neuroborreliosis into early and late disease stage s, as has been done with syphilis-the other well-known spirochetosis t hat affects the nervous system-lacks pathophysiologic validity. Early CNS seeding has been demonstrated, however, and lymphocytic meningitis and facial paralysis tend to occur relatively early in infection, alt hough radiculoneuropathy and cranial neuropathies may also occur later . Less fulminant forms of peripheral nerve or CNS involvement may pres ent later in the disease course. Encephalomyelitis may occur early or late but is rare; encephalopathy is far more common and tends to occur in patients with evidence of systemic (but not necessarily CNS) Lyme disease. Diagnosis of CNS infection has been difficult, and most studi es have relied on indirect methods. Demonstration of intrathecal produ ction of anti-Borrelia burgdorferi antibodies provides the strongest e vidence, but correction for the amount of peripheral blood immunoreact ivity to B. burgdorferi that crosses the blood-brain barrier is essent ial. Newer technologies have been applied in an effort to improve dete ction of B. burgdorferi itself-polymerase chain reaction may provide a sensitive tool for organism detection to complement immunologic techn iques. The optimal treatment regimen for Lyme disease has not been def ined, but a course of ceftriaxone (2 g/day) or cefotaxime (6 g/day) fo r 3-4 weeks is commonly prescribed. Intravenous penicillin and oral do xycycline (200 mg/day) for 2 weeks have been used successfully to trea t Lyme meningitis, but these results require confirmation.