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From the Department of Neurology, Institute for Brain Research (Drs. Chiba, Kusunoki, and Kanazawa), and the Department of Pathology (Drs. Obata and Machinami), School of Medicine, University of Tokyo, Tokyo, Japan.
To determine the significance of serum anti-GQ1b IgG antibody, we studied the disease spectrum associated with this antibody and GQ1b epitope in the human nervous system. We examined sera from 19 patients with typical Miller Fisher syndrome (MFS), five patients with acute postinfectious ophthalmoplegia without ataxia (atypical MFS), six patients with Guillain-Barré syndrome (GBS) with ophthalmoplegia (GBS-OP[+]), and 23 patients with GBS without ophthalmoplegia (GBS-OP[-]). We also examined sera from 84 patients with other neurologic or non-neurologic disorders and from 16 normal control subjects. Eighteen of the 19 patients with typical MFS, all the patients with atypical MFS, and five of the six patients with GBS-OP(+) had increased anti-GQ1b IgG activity in ELISA, but none of the patients in the other groups, including GBS-OP(-), had it. All the patients' sera that had anti-GQ1b IgG antibody showed anti-GT1a IgG activity. Results of absorption studies suggested that the same antibody reacted with GQ1b and GTla. An anti-GQ1b mouse monoclonal antibody immunostained the paranodal regions of the extramedullary portion of the human oculomotor, trochlear, and abducens nerves. Biochemical analysis showed that the human oculomotor nerve contained a larger amount of GQ1b than did the ventral and dorsal roots of the spinal cord. We conclude that serum IgG antibody against GQ1b is very closely associated with acute postinfectious ophthalmoplegia in MFS and GBS.
Address correspondence and reprint requests to Dr. S. Kusunoki, Department of Neurology, Institute for Brain Research, School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113, Japan.
Supported in part by a Grant-in-Aid for Scientific Research (04670485, 04250202) from the Ministry of Education, Science, and Culture of Japan and a grant from the Ministry of Health and Welfare of Japan.
Received October 13,1992. Accepted for publication in final form February 16,1993.
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