Chaudhry V, Cornblath DR, Corse A, Freimer M, Simmons-O'Brien E, Vogelsang
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.
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
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
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
PMID: 12499476 [PubMed - in process]