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Department of Neurology, Tufts-New England Medical Center, Boston, MA.
We evaluated the clinical characteristics and electromyographic features of 39 patients with monoclonal gammopathy of undetermined significance (MGUS) and neuropathy. Twenty-three patients had a monoclonal IgM protein, 13 had an IgG, and three had an IgA. In 15 patients of the IgM group, the M protein reacted with myelin-associated glycoprotein (MAG). Comparing IgM-MGUS and IgG-MGUS neuropathies, we found the following differences: (1) There was a statistically significant higher frequency of sensory loss in the IgM group. (2) Nine attributes of nerve conduction abnormality were statistically worse in the IgM group, with slowing of conduction velocities and prolonged distal latencies. (3) The frequency of monoclonal IgM was overrepresented in the MGUS neuropathy group. In general, the clinical and electrophysiologic features of the IgM-MGUS MAG-reactive group were not significantly different than the MAG-nonreactive group. Our cases are similar to those previously reported and suggest that monoclonal IgM-MGUS should be separated conceptually from monoclonal IgG neuropathies.
Presented in part at the 44th annual meeting of the American Academy of Neurology, San Diego, CA, May 1992.
Address correspondence and reprint requests to Dr. Guillermo A. Suarez, Mayo Clinic, Peripheral Nerve Center, 200 First Street SW, Rochester, MN 55905.
Supported in part by a grant from the Muscular Dystrophy Association.
Received August 28,1992. Accepted for publication in final form November 12, 1992.
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