Cerebellar ataxia as a possible organ-specific autoimmune disease

HADJIVASSILIOU, M., BOSCOLO, S., TONGIORGI, E., GRÜNEWALD, R. A., SHARRACK, B., SANDERS, D. S., WOODROOFE, N. and DAVIES-JONES, G. A. B. (2008). Cerebellar ataxia as a possible organ-specific autoimmune disease. Movement disorders, 23 (10), 1370-1377.

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Link to published version:: https://doi.org/10.1002/mds.22129


The purpose of this study was to investigate the possibility that autoimmunity is responsible for some cases of sporadic idiopathic ataxia. We prospectively investigated 400 patients with progressive ataxia and identified a group of patients with idiopathic sporadic ataxia. A comparison of the prevalence of autoimmune diseases, the autoimmunity linked HLA DQ2, and serum anticerebellar antibodies was made between patients with idiopathic sporadic and those with genetically characterized ataxia. Ninety-one of 400 (23%) patients with progressive ataxia had idiopathic sporadic ataxia. The prevalence of autoimmune diseases in this group was 47% as compared with 6% in the group of patients with genetic ataxias (P < 0.0001). The HLA DQ2 was found in 71% of patients with sporadic ataxia, in 34% in patients with genetic ataxia, and in 36% of healthy local population (P = 0.0005 by Chi squared test). Anticerebellar antibodies were detected in 12 out of 20 patients with idiopathic sporadic as opposed to one of 20 patients with genetic ataxia. The significantly higher prevalence of autoimmune diseases, HLA DQ2 and anti-cerebellar antibodies in patients with idiopathic sporadic ataxia compared to genetic ataxia supports the notion that autoimmunity may account for some cases of idiopathic sporadic cerebellar ataxia.

Item Type: Article
Research Institute, Centre or Group - Does NOT include content added after October 2018: Biomedical Research Centre
Identification Number: https://doi.org/10.1002/mds.22129
Page Range: 1370-1377
Depositing User: Users 4 not found.
Date Deposited: 04 Jun 2010 12:56
Last Modified: 18 Mar 2021 21:15
URI: https://shura.shu.ac.uk/id/eprint/2117

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