Autoimmune Cerebellar Ataxia Following TNF ‐α Inhibitor Therapy for Rheumatoid Arthritis: A Case Report

Background Tumor necrosis factor‐α (TNF‐α) inhibitors are widely used to treat autoimmune diseases, but accumulating evidence has linked TNF‐α inhibitor therapy to inflammatory central nervous system (CNS) disorders. While an association with demyelinating disease has been established, the relationship between TNF‐α inhibitors and autoimmune cerebellar ataxia (ACA) or autoimmune encephalitis remains poorly defined. Case Presentation We report a 55‐year‐old woman with rheumatoid arthritis who developed progressive gait ataxia and dysarthria 1 month after starting golimumab, a TNF‐α inhibitor. Cerebrospinal fluid analysis showed an elevated IgG index (1.44) with normal cell count, cytokine levels, and negative oligoclonal bands. Brain magnetic resonance imaging (MRI) revealed mild cerebellar atrophy, and single‐photon emission computed tomography demonstrated cerebellar hypoperfusion. A tissue‐based immunofluorescence assay using rat brain sections showed the patient's Cerebrospinal fluid (CSF) IgG binding to the neuropil of the cerebellar molecular layer, suggesting cell‐surface anti‐neuronal antibodies. Intravenous methylprednisolone pulse therapy and discontinuation of golimumab led to clinical improvement, partial normalization of cerebellar perfusion, and a decrease in IgG index. Conclusion This case suggests that TNF‐α inhibitor therapy may trigger ACA through the production of anti‐neuronal antibodies. Clinicians should consider drug‐induced autoimmunity when new‐onset cerebellar ataxia develops during TNF‐α inhibitor treatment and promptly initiate immunologic evaluation and treatment.