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 Volume 61, Number 7, October 14, 2003
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NEUROLOGY 2003;61:891-896
© 2003 American Academy of Neurology

Autoantibodies to NMDA receptor in patients with chronic forms of epilepsia partialis continua

Y. Takahashi, PhD, H. Mori, PhD, M. Mishina, PhD, M. Watanabe, PhD, T. Fujiwara, PhD, J. Shimomura, PhD, H. Aiba, MD, T. Miyajima, PhD, Y. Saito, MD, A. Nezu, PhD, H. Nishida, PhD, K. Imai, MD, N. Sakaguchi and N. Kondo, PhD

From the Department of Pediatrics (Drs. Takahashi and Kondo, N. Sakaguchi), Gifu University School of Medicine, and Department of Neurology (Dr. Nishida), Gifu Prefectural Gifu Hospital; Department of Molecular Neurobiology and Pharmacology (Drs. Mori and Mishina), Graduate School of Medicine, University of Tokyo, and Department of Pediatrics (Dr. Saito), Tokyo Women’s Medical University; Department of Anatomy (Dr. Watanabe), Hokkaido University School of Medicine; National Epilepsy Center (Drs. Takahashi, Shimomura, and Fujiwara), Shizuoka MIND; Department of Neurology (Dr. Aiba), Shizuoka Children’s Hospital; Department of Pediatrics (Dr. Miyajima), Shiga Medical Center for Children; Department of Pediatrics (Dr. Nezu), Urafune Hospital, Yokohama City University School of Medicine; and Department of Pediatrics (Dr. Imai), Faculty of Medicine, Osaka University, Japan.

Address correspondence and reprint requests to Dr. Y. Takahashi, National Epilepsy Center, Shizuoka MIND, 886 Urushiyama, Shizuoka 420-8688, Japan; e-mail: takahashi-ped{at}umin.ac.jp

Background: Antibody-mediated and cytotoxic T cell-mediated pathogenicity have been implicated as the autoimmune pathophysiologic mechanisms in Rasmussen’s encephalitis.

Methods: The authors investigated autoantibodies against the NMDA glutamate receptor (GluR) {epsilon}2 subunit and their epitopes in serum and CSF samples from 15 patients with chronic epilepsia partialis continua (EPC), 17 with West syndrome, 10 with Lennox–Gastaut syndrome, and 11 control subjects.

Results: In 15 patients with chronic EPC, we detected NMDA-type GluR {epsilon}2 autoantibodies in histologically proven Rasmussen’s encephalitis (3/3 patients), clinical Rasmussen’s encephalitis (6/7 patients), acute encephalitis/encephalopathy (2/3 patients), and nonprogressive EPC (2/2 patients). Serum IgM autoantibodies were found in the early phase of EPC and became negative later in four patients. The autoantibodies were not detected in West syndrome, Lennox–Gastaut syndrome, or controls. Among 10 patients with histologically proven or clinical Rasmussen’s encephalitis, epitope analyses showed that the autoantibodies were predominantly against C-terminal epitopes and rarely against N-terminal epitope, with inconsistency in profile during the courses of disease. Epitope recognition spectrum of autoantibodies was broader in CSF than in serum, and the serum or CSF profile showed an increase in number of epitopes as disease progressed in some patients.

Conclusions: The presence of autoantibodies against NMDA GluR {epsilon}2 suggests autoimmune pathologic mechanisms but is not a hallmark of Rasmussen’s encephalitis. Patients with Rasmussen’s encephalitis may have autoantibodies against several neural molecules, and these autoantibodies may be produced in the CNS after cytotoxic T cell-mediated neuronal damage.

Received April 6, 2003. Accepted in final form June 16, 2003.

The authors have not received any financial support or equity positions from manufacturers of drugs or products cited in this manuscript.

Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the October 14 issue to find the title link for this article.

See also page 875




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