Unmasking Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): CNS Demyelination Triggered by TNF-α Inhibition in a Patient with Ankylosing Spondylitis.

Background: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a rare but emerging central nervous system demyelinating disorder that can mimic other neurological conditions. The use of TNF-α inhibitors in patients with autoimmune diseases has been linked to central nervous system demyelinating events, but the relationship remains poorly understood. Case description: We present a 64-year-old male with a history of ankylosing spondylitis previously treated with a TNF-α inhibitor who developed progressive dizziness, ataxia, visual disturbances and cognitive changes. Despite extensive workup, including imaging and cerebrospinal fluid analysis, initial evaluations were inconclusive. MRI was non-diagnostic, and cerebrospinal fluid lacked oligoclonal bands. Ultimately, a serum MOG antibody titre of 1:1,000 confirmed the diagnosis of MOGAD. The patient improved with intravenous corticosteroids and was discharged on a tapering dose of oral prednisone. This case highlights an MRI-negative presentation of MOGAD with strong serologic findings. Conclusion: This case emphasises the diagnostic challenge of MOGAD in patients with autoimmune backgrounds and neurologic symptoms without clear imaging findings. Clinicians should consider MOGAD in the differential diagnosis when evaluating such patients, particularly those with prior TNF-α inhibitor exposure. Early recognition and treatment with immunotherapy can lead to significant clinical improvement. LEARNING POINTS: Clinicians should maintain a high index of suspicion for MOGAD in patients with atypical neurological symptoms, even when MRI findings are negative.TNF-α inhibitors may act as potential immunologic triggers for central nervous system demyelination, especially in patients with autoimmune conditions.Strong MOG antibody positivity can guide diagnosis in diagnostically ambiguous presentations and warrants the timely initiation of immunotherapy.