Evidence map›Paper›PMID 40418511›Full record

ArticleActa neurologica Belgica2025

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

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

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Article in Acta neurologica Belgica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

5 authors.

Rihab Ben DhiaDepartment of Neurology, Fattouma Bourguiba University Hospital, Monastir, Tunisia.
Yasmine SaadDepartment of Neurology, Fattouma Bourguiba University Hospital, Monastir, Tunisia. yasmin.saad@hotmail.fr.
Mariem MhiriDepartment of Neurology, Fattouma Bourguiba University Hospital, Monastir, Tunisia.
Narjes GoutaDepartment of Neurology, Fattouma Bourguiba University Hospital, Monastir, Tunisia.
Mahbouba Frih-AyedDepartment of Neurology, Fattouma Bourguiba University Hospital, Monastir, Tunisia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyelin 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.

conclusionThis 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.

Indexed as

AutoantibodiesDemyelinating Autoimmune Diseases, CNSDemyelinating DiseasesMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinPeripheral Nervous System DiseasesAdultHumansMaleAutoantibodiesMAG protein, humanMOG protein, humanMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinAnti-myelin-associated glycoprotein (MAG) antibodyAnti-myelin oligodendrocyte glycoprotein (MOG) antibodyAutoimmune demyelinationCombined central and peripheral demyelinationMOG-associated disease

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