{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T04:50:44Z","timestamp":1791348644520,"version":"4.3.1"},"reference-count":211,"publisher":"Oxford University Press (OUP)","license":[{"start":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T00:00:00Z","timestamp":1785283200000},"content-version":"am","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Multifocal motor neuropathy (MMN) is an immune-mediated, pure motor neuropathy characterized by slowly progressive, asymmetric limb weakness. It predominantly affects men in mid-adulthood and often presents with distal upper limb weakness, such as wrist or finger drop. Although the disease course is typically chronic, slowly and sometimes stepwise progressive, timely recognition is critical, as early immunotherapy can prevent irreversible axonal loss and long-term disability.<\/jats:p>\n                  <jats:p>This review aims to provide a comprehensive and clinically integrated overview of MMN, spanning pathogenesis, clinical presentation, diagnostic challenges and current and emerging therapeutic strategies. Emphasis is placed on translating mechanistic insights into practical diagnostic and treatment frameworks, and on identifying priorities for future research.<\/jats:p>\n                  <jats:p>Pathophysiologically, MMN is best understood as an antibody-mediated nodo-paranodopathy. IgM antibodies directed against GM1 gangliosides bind to GM1-enriched domains at the nodes of Ranvier, activate the classical complement cascade and disrupt sodium channel clustering and axo-glial integrity. The resulting conduction block constitutes the electrophysiological hallmark of the disease and may initially be reversible. Persistent immune-mediated injury, however, can lead to secondary axonal degeneration and fixed disability. While GM1 IgM antibodies are detected in a substantial proportion of patients, seronegativity does not exclude MMN, potentially reflecting mechanistic heterogeneity and\/or assay limitations.<\/jats:p>\n                  <jats:p>Diagnosis relies on the combination of a characteristic clinical phenotype and electrophysiological evidence of motor conduction block with preserved sensory conduction. However, conduction block can be difficult to demonstrate because of proximal lesions, temporal dispersion or superimposed axonal loss, contributing to diagnostic uncertainty. High-resolution nerve ultrasound and magnetic resonance neurography offer valuable complementary information by revealing focal nerve enlargement or plexus abnormalities, though neither technique is independently diagnostic.<\/jats:p>\n                  <jats:p>Intravenous immunoglobulin remains the established standard of care and the only approved therapy, producing rapid but often transient improvement that necessitates individualized maintenance regimens. Subcutaneous immunoglobulin provides an effective long-term alternative for many patients. Conventional immunosuppressants have shown limited efficacy, whereas emerging complement inhibitors targeting upstream components of the classical pathway represent a promising, mechanism-based strategy currently under clinical evaluation.<\/jats:p>\n                  <jats:p>Despite advances, significant gaps remain. Reliable biomarkers to predict treatment response, monitor disease activity and detect early axonal injury are lacking. Future progress will require integrated translational models, harmonized outcome measures and well-designed clinical trials to move towards more durable and personalized therapeutic approaches in MMN.<\/jats:p>","DOI":"10.1093\/brain\/awag260","type":"journal-article","created":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T11:16:22Z","timestamp":1785237382000},"source":"Crossref","is-referenced-by-count":0,"title":["Revisiting multifocal motor neuropathy: mechanisms, diagnosis and future directions"],"prefix":"10.1093","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4258-0579","authenticated-orcid":false,"given":"Nicolas","family":"Dubuisson","sequence":"first","affiliation":[{"name":"Nuffield Department of Clinical Neurosciences, University of Oxford , Oxford OX3 9DU ,","place":["UK"]},{"name":"Neuromuscular Reference Centre UCL Saint-Luc, University of Louvain , Brussels 1200 ,","place":["Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yusuf A","family":"Rajabally","sequence":"additional","affiliation":[{"name":"Inflammatory Neuropathy Service, Department of Neurology, University Hospitals Birmingham , Birmingham B15 2TH ,","place":["UK"]},{"name":"Aston Medical School, Aston University , Birmingham B4 7ET ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Clive","family":"Philips","sequence":"additional","affiliation":[{"name":"Making the Most of Now , Richmond 7081 ,","place":["New Zealand"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Harbo","sequence":"additional","affiliation":[{"name":"Department of Neurology, Aarhus University Hospital , 8200 Aarhus ,","place":["Denmark"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simon","family":"Rinaldi","sequence":"additional","affiliation":[{"name":"Nuffield Department of Clinical Neurosciences, University of Oxford , Oxford OX3 9DU ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2026,7,29]]},"reference":[{"key":"2026100700163614400_awag260-B1","first-page":"416","article-title":"Motor neuropathy with proximal multifocal persistent conduction block, fasciculations and myokymia. 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