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Anticerebellar antibodies in neurologically normal patients with ovarian neoplasms

From the Department of Neurology, University of Virginia Health Sciences Center, Charlottesville, VA; and the Neurology Service, Veterans Administration Medical Center, and Department of Neurology, University of Utah Medical Center, Salt Lake City, UT.

Several groups of investigators have confirmed the occurrence of antibodies to Purkinje and other cerebellar neuronal populations in the serum and spinal fluid of patients with paraneoplastic cerebellar degeneration. Although this antibody response suggests that paraneoplastic cerebellar degeneration may have an autoimmune basis, it is not known what role anticerebellar antibodies play in the pathogenesis of this disorder or whether the presence of antibodies invariably results in cerebellar injury. We identified 3 patients with ovarian malignancies in whom high titers of circulating anticerebellar antibodies were present without clinical evidence of cerebellar disease. We followed these patients clinically and serologically until their deaths from their neoplasms. All 3 patients remained neurologically normal. In 2 of the patients, anticerebellar antibodies persisted at high titer. CSF obtained from 1 of these patients postmortem did not contain detectable levels of anticerebellar antibody, but histopathologic examination of her cerebellum revealed patchy loss of Purkinje cells. In the 3rd patient, antibody titers fell with removal of the primary tumor and chemotherapy but did not rise with tumor recurrence. Indirect immunonuorescence did not reveal anticerebellar antibodies in the serum or CSF of other patients with neoplasms, patients with other cerebellar disease, or normal controls. The present study demonstrates that patients with ovarian malignancies may occasionally develop antibodies that react with cerebellar neuronal antigens and can maintain this antibody response for protracted periods of time without clinically evident cerebellar injury. Tumor recurrence may not be accompanied by rise in titers of anticerebellar antibodies.

Address correspondence and reprint requests to Dr. Brashear, Department of Neurology—Box 394, University of Virginia Health Sciences Center, Charlottesville, VA 22908.

Supported in part by Research Advisory Group and Merit Review Awards from the Veterans Administration.

Received April 4, 1989. Accepted for publication in final form June 5, 1989.

This article has been cited by other articles:

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