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Antineuronal antibodies in acute cerebellar ataxia following Epstein-Barr virus infection

Department of Neurology, Kitasato University East Hospital (Drs. Ito, Sayama, Irie, Saito, and Kowa) and Research Division of East Hospital (N. Kanazawa), School of Medicine, Kitasato University, Sagamihara, Kanagawa; and the Psychiatric Research Institute of Tokyo (Drs. Haga and Ikeda), Tokyo, Japan.

A 29-year-old man developed acute cerebellar ataxia following Epstein-Barr virus infection. Serum IgG and IgM antibodies reacted with both nuclear and cytoplasmic elements of neurons. Western blot revealed IgG binding to the 34- and 29-kd bands and IgM binding to the 44-, 37-, and 29-kd bands. The IgM reactivity gradually reduced. There was no identifiable neoplasm and the ataxia gradually improved. These findings suggest a role for autoimmune mechanisms in the pathogenesis of acute cerebellar ataxia.

Address correspondence and reprint requests to Dr. Hiroaki Ito, Department of Neurology, Kitasato University East Hospital, 2-1-1 Asamizodai, Sagamihara, Kanagawa, 228, Japan.

Supported in part by a grant from the Neuroimmunological Disorder Research Committee, Ministry of Health and Welfare, Japan.

Received October 19, 1993. Accepted in final form January 26, 1994.

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