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Lyme disease is a multisystem infectious
disease with frequent nervous system involvement. It affects peripheral nerves, the meningeal lining 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 stages, as has been done with syphilis–the other well-known spirochetosis that 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, although radiculoneuropathy and cranial neuropathies may also occur later. Less fulminant forms of peripheral nerve or CNS involvement may present 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 studies have relied on indirect methods. Demonstration of intrathecal production of anti-Borrelia burgdorferi antibodies provides the strongest evidence, but correction for the amount of peripheral blood immunoreactivity to B. burgdorferi that crosses the blood-brain barrier is essential. Newer technologies have been applied in an effort to improve detection of B. burgdorferi itself–polymerase chain reaction may provide a sensitive tool for organism detection to complement immunologic techniques. The optimal treatment regimen for
Lyme disease has not been defined, but a course of ceftriaxone (2 g/day) or cefotaxime (6 g/day) for 3-4 weeks is commonly prescribed. Intravenous penicillin and oral doxycycline (200 mg/day) for 2 weeks have been used successfully to treat
Lyme meningitis, but these results require confirmation.

Am J Med. 1995 Apr 24;98(4A):52S-56S; discussion 56S-59S. Review

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