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From the Departments of Neurology (Drs. Chaudhry, Cornblath, and Corse), Dermatology (Dr. Simmons-O’Brien), and Oncology (Dr. Vogelsang), Johns Hopkins University School of Medicine, Baltimore, MD; and Department of Neurology (Dr. Freimer), Ohio State University School of Medicine, Columbus.
Address correspondence and reprint requests to Dr. V. Chaudhry, 601 N. Caroline Street, Suite 5072 A, Baltimore, MD 21287; e-mail: vchaudh{at}jhmi.edu
Background: Thalidomide is effective for the treatment of some refractory dermatologic and oncologic diseases. Toxic neuropathy limits its use, as embryopathy can be avoided by contraceptive measures.
Objective: To describe the clinical, electrophysiologic, and pathologic features of thalidomide-induced peripheral neuropathy.
Methods: Clinical and electrophysiologic examinations were performed in seven patients with thalidomide-induced peripheral neuropathy. Thalidomide was used for graft-vs-host disease, pyoderma gangrenosum, and discoid lupus with dosages ranging from 100 to 1,200 mg/day for 5 to 16 months (cumulative dosages of 24 to 384 g).
Results: All seven patients had clinical and electrophysiologic evidence of a sensory more than motor, axonal, length-dependent polyneuropathy that presented as painful paresthesias or numbness. Sural nerve biopsies, done in three patients, showed evidence of Wallerian degeneration and loss of myelinated fibers. The symptoms, signs, and electrophysiologic data correlated with total cumulative dose of thalidomide.
Conclusions: Thalidomide induces a dose-dependent sensorimotor length-dependent axonal neuropathy; it should be judiciously used with close neurologic monitoring.
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