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Clinical and electrophysiologic findings in chronic neuropathy of Lyme disease.

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We evaluated 25 patients with
Lyme disease and chronic peripheral neuropathy. All had immunologic evidence of exposure to Borrelia burgdorferi and no other identifiable cause of neuropathy. Neuropathic symptoms began a median of 8 months (range, 0 to 165) after erythema migrans and had been present for a median of 12 months (range, 2 to 168) prior to evaluation. Twelve patients (48%) had generally symmetric distal, nonpainful paresthesia, and another 12 (48%) had generally asymmetric radicular pain. One patient (4%) had asymptomatic neuropathy. The most common physical finding was multimodal sensory loss, which was observed in 13 patients (52%); weakness and hyporeflexia were less common. Motor or sensory nerve conduction was slightly slow in 16 patients (64%). The paresthesia group more often had abnormalities on physical examination and on nerve conduction testing than did the radicular group. In 75% to 80% of patients from both groups, however, needle examination showed denervation in paraspinal and limb muscles. Among 20 patients who underwent lumbar puncture, only one had a slight spinal fluid pleocytosis. Six months after treatment with intravenous ceftriaxone, 19 patients (76%) were clinically improved. We conclude that
Lyme disease can be associated with a reversible, mild chronic axonal sensorimotor polyradiculoneuropathy or polyradiculopathy.

Neurology. 1992 Feb;42(2):303-11.

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