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NEUROLOGY 2005;65:1114-1116
© 2005 American Academy of Neurology
Brief Communications

Autoantibodies in postinfectious acute cerebellar ataxia

Ayumi Uchibori, MD, Manabu Sakuta, MD, Susumu Kusunoki, MD and Atsuro Chiba, MD

From the Department of Neurology (Drs. Uchibori, Sakuta, and Chiba), School of Medicine, Kyorin University, Tokyo; and the Department of Neurology (Dr. Kusunoki), School of Medicine, Kinki University, Osaka, Japan.

Address correspondence and reprint requests to Dr. Atsuro Chiba, Department of Neurology, School of Medicine, Kyorin University, 6-20-2 Shinkawa, Mitaka, Tokyo 181-8611, Japan; e-mail: achiba-tky{at}umin.ac.jp

The authors found serum immunoglobulin M (IgM) autoantibody in a patient with typical acute cerebellar ataxia (ACA) and identified the antigen molecule as triosephosphate isomerase (TPI). TPI antigenicity to the patient’s antibody was the highest in the cerebellar tissue. Eight of 23 patients with ACA had increased IgM anti-TPI antibody titers vs those of healthy controls. Preceding Epstein–Barr virus infection was confirmed serologically in all 8 patients. Anti-TPI antibody decreased with clinical improvement.

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 11 issue to find the title link for this article.

Supported by a Grant-in-Aid for Scientific Research (16590844) from the Ministry of Education, Culture, Sports, Science and Technology of Japan.

Disclosure: The authors report no conflicts of interest.

Received December 22, 2004. Accepted in final form June 14, 2005.


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October 11 Highlights
Neurology 2005 65: 976-977. [Full Text] [PDF]





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