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NEUROLOGY 1990;40:1067
© 1990 American Academy of Neurology

The spectrum of neurologic disease associated with anti-GM1 antibodies

S. A. Sadiq, MD, F. P. Thomas, MD, K. Kilidireas, MD, S. Protopsaltis, MS, A. P. Hays, MD, K.-W. Lee, MD, S. N. Romas, N. Kumar, L. van den Berg, MD, M. Santoro, MD, D. J. Lange, MD, D. S. Younger, MD, R. E. Lovelace, MD, W. Trojaborg, MD, W. H. Sherman, MD, J. R. Miller, MD, J. Minuk, MD, M. A. Fehr, MD, R. I. Roelofs, MD, D. Hollander, MD, F. T. Nichols, III, MD, H. Mitsumoto, MD, J. J. Kelley, Jr., MD, T. R. Swift, MD, T. L. Munsat, MD and N. Latov, MD

Departments of Neurology (Drs. Sadiq, Thomas, Kilidireas, Lee, Santoro, Lange, Younger, Lovelace, Trojaborg, Miller, Latov, and van den Berg, and S. Protopsaltis, S.N. Romas, and N. Kumar), Pathology (Dr. Hays), and Medicine (Dr. Sherman), and the H. Houston Merritt Clinical Research Center for Muscular Dystrophy and Related Diseases of the Columbia Presbyterian Medical Center, College of Physicians and Surgeons, Columbia University, New York, NY; the Department of Neurology (Drs. Fehr and Roelofs), University of Minnesota Hospitals and Clinic, Minneapolis, MN; the Montreal Neurological Hospital (Dr. Minuk), Montreal, Canada; the Department of Neurology (Dr. Mitsumoto), the Cleveland Clinic, Cleveland, OH; the Department of Neurology (Drs. Nichols and Swift), the Medical College of Georgia, Augusta, GA; and the Department of Neurology (Drs. Hollander, Kelly, and Munsat), Tufts New England Medical Center, Boston, MA.

We compared anti-GM1 IgM antibody titers in patients with various neurologic diseases and in normal subjects. We found increased titers in patients with lower motor neuron disease, sensorimotor neuropathy, or motor neuropathy with or without multifocal conduction block. In patients with other diseases, titers are similar to those in normal individuals, suggesting that anti-GM1 antibody levels are not increased nonspecifically after neural injury or inflammatory diseases. Anti-GM1 antibodies in many of the patients occur as monoclonal gammopathies, predominantly of lambda light-chain type, but the antibodies are sometimes polyclonal with normal or increased serum IgM concentrations. Most of the anti-GM1 antibodies appear to react with the Gal(ß1-3)GalNAc epitope which is shared with asialo-GM1 and GD1b, but in some patients the antibodies are more specific for GM1 and associated with motor neuropathy. Patients with motor or sensorimotor peripheral neuropathy or lower motor neuron disease should be tested for anti-GM1 antibodies or anti-Gal(ß1-3)GalNAc antibodies, as therapeutic reduction in antibody concentrations was reported to result in clinical improvement in some patients.

Address correspondence and reprint requests to Dr. Saud A. Sadiq, Department of Neurology, Columbia University, Black Bldg. Rm 3-323, 630 W. 168th Street, New York, NY 10032.

Received October 6, 1989. Accepted for publication in final form December 21, 1989.

Supported by Center Grants from the Muscular Dystrophy Association and from the NIH (NINCDS NS11766) to the Department of Neurology, Columbia University. Drs. Thomas and Sadiq are the recipients of Postdoctoral Research Fellowships from the Muscular Dystrophy Association. Dr. Kilidireas is the recipient of a Fellowship from the State Scholarship Foundation of Greece.




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