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John J. Kelly, MD; Lester S. Adelman, MD; Eugene Berkman, MD; Ina Bhan, MD

Arch Neurol. 1988;45(12):1355-1359.

Abstract
• We studied ten patients with IgM monoclonal gammopathies. Five had M proteins that reacted with myelin-associated glycoprotein (MAG) and five had no recognizable antinerve activity. The neuropathy in the MAG-reactive patients was homogeneous by clinical and laboratory analysis, while the neuropathy in the MAG-nonreactive patients varied considerably. Both groups responded well to immunosuppressive therapy, which lowered the concentration of the serum M protein. The homogeneity of the MAG-reactive patients and their response to sustained lowering of the M protein levels support the concept that the IgM M protein directly damages nerve fibers and is the proximate cause of the polyneuropathy.

Author Affiliations
From the Departments of Neurology (Dr Kelly), Pathology (Drs Adelman and Bhan), and Internal Medicine (Dr Berkman), Tufts Medical School and New England Medical Center, Boston.

Footnotes
Accepted for publication June 20, 1988.

Reprints not available.

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