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Background <p>Myelin oligodendrocyte glycoprotein-associated disease (MOG-AD) is a central nervous system (CNS) demyelinating disorder linked to anti-MOG antibodies, whereas anti-myelin associated glycoprotein (MAG) antibodies are associated with peripheral nervous system (PNS) demyelination. Their coexistence in a single patient has not been previously reported.</p> Case presentation <p>We describe a 38-year-old male who developed rapidly progressive paraparesis, visual impairment, and sensory deficits. MRI revealed multifocal CNS demyelinating lesions, while nerve conduction studies later confirmed a demyelinating polyneuropathy. Serum testing showed concurrent anti-MOG and high-titer anti-MAG antibodies. Despite treatment with corticosteroids, IVIg, and plasma exchange, the patient exhibited a severe, relapsing course with persistent disability.</p> Conclusion <p>This is the first documented case of anti-MOG and anti-MAG antibody coexistence, causing simultaneous CNS and PNS demyelination and suggesting a shared autoimmune mechanism. Anti-MAG antibodies may indicate a more aggressive course, warranting routine testing and intensive therapy. Further research is needed to clarify their pathogenic interplay and refine treatment strategies.</p>

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Coexistence of anti-MOG and anti-MAG antibodies in combined central and peripheral nervous system demyelination: a case of dual myelinopathy

  • 期刊论文

  • 发表日期：

    2025年5月26日

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  • Rihab Ben Dhia,
  • Yasmine Saad,
  • Mariem Mhiri,
  • Narjes Gouta,
  • Mahbouba Frih-Ayed

摘要

Background

Myelin oligodendrocyte glycoprotein-associated disease (MOG-AD) is a central nervous system (CNS) demyelinating disorder linked to anti-MOG antibodies, whereas anti-myelin associated glycoprotein (MAG) antibodies are associated with peripheral nervous system (PNS) demyelination. Their coexistence in a single patient has not been previously reported.

Case presentation

We describe a 38-year-old male who developed rapidly progressive paraparesis, visual impairment, and sensory deficits. MRI revealed multifocal CNS demyelinating lesions, while nerve conduction studies later confirmed a demyelinating polyneuropathy. Serum testing showed concurrent anti-MOG and high-titer anti-MAG antibodies. Despite treatment with corticosteroids, IVIg, and plasma exchange, the patient exhibited a severe, relapsing course with persistent disability.

Conclusion

This is the first documented case of anti-MOG and anti-MAG antibody coexistence, causing simultaneous CNS and PNS demyelination and suggesting a shared autoimmune mechanism. Anti-MAG antibodies may indicate a more aggressive course, warranting routine testing and intensive therapy. Further research is needed to clarify their pathogenic interplay and refine treatment strategies.