Please use this identifier to cite or link to this item: https://doi.org/10.1212/WNL.0b013e3181ff94c2
DC FieldValue
dc.titleMultifocal motor neuropathy: Association of anti-GM1 IgM antibodies with clinical features
dc.contributor.authorCats, E.A.
dc.contributor.authorJacobs, B.C.
dc.contributor.authorYuki, N.
dc.contributor.authorTio-Gillen, A.P.
dc.contributor.authorPiepers, S.
dc.contributor.authorFranssen, H.
dc.contributor.authorVan Asseldonk, J.-T.
dc.contributor.authorVan Den Berg, L.H.
dc.contributor.authorVan Der Pol, W.-L.
dc.date.accessioned2016-09-06T08:19:16Z
dc.date.available2016-09-06T08:19:16Z
dc.date.issued2010-11-30
dc.identifier.citationCats, E.A., Jacobs, B.C., Yuki, N., Tio-Gillen, A.P., Piepers, S., Franssen, H., Van Asseldonk, J.-T., Van Den Berg, L.H., Van Der Pol, W.-L. (2010-11-30). Multifocal motor neuropathy: Association of anti-GM1 IgM antibodies with clinical features. Neurology 75 (22) : 1961-1967. ScholarBank@NUS Repository. https://doi.org/10.1212/WNL.0b013e3181ff94c2
dc.identifier.issn00283878
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/126739
dc.description.abstractObjective: To determine the prevalence and specificity of antibodies against single gangliosides and ganglioside complexes in serum from 88 patients with multifocal motor neuropathy (MMN) and to study the association with clinical features. Methods: ELISA was used to detect immunoglobulin (Ig)M, IgG, and IgA antibodies against GM1, GM2, GD1a, GD1b, GM1b, GT1a, GT1b, GQ1b, GalNAc-GD1a, and the glycolipid SGPG; absorption studies were performed to study cross-reactivity. Presence of antibodies against ganglioside complexes consisting of any of combinations of GM1, GM2, GD1a, GD1b, GT1b, and GQ1b was also tested. Results: Anti-GM1 IgM, IgG, and IgA antibodies were detected in serum from 43%, 1%, and 5% of patients with MMN. Anti-GM2 IgM antibodies were detected in 6% and anti-GD1b IgM antibodies in 9% of patients. Patients with MMN with anti-GM1 IgM antibodies had more severe weakness (p < 0.01), more disability (p < 0.01), and more axon loss (p = 0.05) than patients without anti-GM1 IgM antibodies. Anti-GM1 IgM antibody titers correlated with Medical Research Council scores (correlation coefficient = 0.43; p < 0.0001). Anti-GD1b IgM antibody activity was associated with reduced vibration sense (p < 0.01). Absorption studies showed that anti-GD1b and anti-GM2 IgM antibodies cross-reacted with GM1. Antibodies against ganglioside complexes were not detected. Complexes containing GD1a, GD1b, GT1b, or GQ1b with GM1 lowered antibody activity against GM1. Conclusion: Anti-ganglioside IgM antibodies in MMN display limited specificity and are associated with severity and clinical characteristics. Results of this study suggest that anti-GM1 IgM antibodies may play a role in MMN pathogenesis. Copyright © 2010 by AAN Enterprises, Inc.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1212/WNL.0b013e3181ff94c2
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentMICROBIOLOGY
dc.description.doi10.1212/WNL.0b013e3181ff94c2
dc.description.sourcetitleNeurology
dc.description.volume75
dc.description.issue22
dc.description.page1961-1967
dc.description.codenNEURA
dc.identifier.isiut000284685800008
Appears in Collections:Staff Publications

Show simple item record
Files in This Item:
There are no files associated with this item.

SCOPUSTM   
Citations

80
checked on May 24, 2019

WEB OF SCIENCETM
Citations

65
checked on May 24, 2019

Page view(s)

27
checked on May 24, 2019

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.