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Cerebellar dysfunction caused by autoimmune processes is the hallmark of immune-mediated cerebellar ataxia (IMCA), a rare neurological condition that is most frequently idiopathic or paraneoplastic. It is scarce and still poorly understood to be associated with rheumatoid arthritis (RA). We describe the case of a 58-year-old man with long-standing seropositive RA who had growing gait instability and imbalance for a week without focal neurological abnormalities or a flare-up of the systemic illness. Gait ataxia, poor tandem walking, and mild limb dysmetria were found during a neurological evaluation. A thorough examination revealed minor cerebellar cortical alterations, suggesting inflammatory involvement, despite the initial brain magnetic resonance imaging being classified as normal. Vascular, viral, metabolic, demyelinating, and drug-related causes were ruled out after a thorough investigation. Neuronal autoantibody testing and cerebrospinal fluid analysis were not possible due to patient refusal and resource limitations. Therefore, clinical presentation, elimination of other etiologies, imaging results, and a positive response to immunotherapy were used to establish the diagnosis of IMCA secondary to RA. After receiving high-dose intravenous corticosteroid therapy, the patient demonstrated significant clinical improvement and continued to recover at follow-up. Even in the absence of active systemic disease, this example underscores the importance of considering immune-mediated cerebellar ataxia when patients with systemic autoimmune disorders present with acute cerebellar symptoms.
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Ahmad et al. (2026) studied this question.
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