Polyneuropathies associated with IgM monoclonal gammopathies
J. J. Kelly, L. S. Adelman, E. Berkman and I. Bhan
Department of Neurology, Tufts Medical School, Boston.
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.
