DOI: 10.12890/2025_005467
Unmasking myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): CNS demyelination triggered by TNF-alpha Inhibition in a patient with ankylosing spondylitis
Authors
drsujathabaddam@gmail.com
Keywords
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), TNF-α inhibitors, central nervous system demyelination, autoimmune diseaseAbstract
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-alpha 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-alpha 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-alpha inhibitor exposure. Early recognition and treatment with immunotherapy can lead to significant clinical improvement.
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