Abstract / Summary
Abstract We describe a 57-year-old male patient who developed an autoimmune neurological syndrome sequentially following resection of a type B2 thymoma. One year after surgery, the patient presented with acetylcholine receptor (AChR) antibody-positive myasthenia gravis (MG), which responded well to intravenous immunoglobulin and glucocorticoids. Approximately six months later, he developed acute transverse myelitis. Spinal MRI revealed longitudinally extensive transverse myelitis (LETM) spanning T5–T10. Serological testing by live cell-based assay demonstrated positive MOG-IgG (titer 1:10) with negative aquaporin-4 antibodies. Concurrent screening showed positive antinuclear antibodies (1:320) and anti–SS-A/Ro52 antibodies. Following high-dose methylprednisolone pulse therapy followed by maintenance immunosuppression, the patient achieved marked neurological improvement, with near-complete resolution of spinal lesions at the 12-week follow-up. This temporal sequence—B2 thymoma → MG → MOGAD-associated myelitis—supports the hypothesis that the thymoma may have acted as an autoimmune amplifier, driving epitope spreading and sequential loss of immune tolerance to peripheral (neuromuscular junction) and central (spinal cord myelin) self-antigens. We discuss the immunopathological links among thymoma, MG, and MOG-IgG-associated disease, highlighting the importance of comprehensive autoantibody screening when new central nervous system symptoms emerge in patients with known paraneoplastic syndromes. This case expands the recognized spectrum of thymoma-associated paraneoplastic neurological disorders and underscores the need for thorough autoantibody profiling and vigilant neurological monitoring in patients with advanced thymoma.