Presynaptic Neuromuscular Transmission Defect in Anti-GQ1b IgG Antibody-Related DisordersYL Lo1*, A Seah1, LL Lim1, TH Leoh2, YF Dan2, S Fook-Chong3 and P Ratnagopal1
- Corresponding Author:
- Dr. A/Prof Lo
Department of Neurology
National Neuroscience Institute
Singapore General Hospital, Outram Road
Singapore 169608, Singapore
Tel: 65 63265003
Fax: 65 62203321
E-mail: [email protected] sgh.com.sg
Received date: November 25, 2010; Accepted date: April 06, 2011; Published date: April 08, 2011
Citation: Shah D, Nandakumar S, Jaishankar GB, Chilakala S, Wang K, et al. (2011) Pre-Term Exposure Patterns in Neonatal Intensive Care Unit Alters Immunological Outcome in Neonates. J Aller Ther 2:106. doi:10.4172/2155-9562.1000111
Copyright: ©2011 Lo YL, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, hich permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: In vitro studies of Miller Fisher syndrome (MFS) have demonstrated anti-GQ1b IgG antibodymediated presynaptic damage at the neuromuscular junction. Previous studies have provided electrophysiological evidence of presynaptic neuromuscular transmission defect in MFS in anti-GQ1b positive patients, which persisted up to 3 months from initial presentation. Methods and results: In this study, we show that incremental responses were significantly greater in antibodypositive MFS and Bickerstaff's brainstem encephalitis, compared with antibody-negative Guillain-Barre and MFS variants. These responses return to normality by 6 months, in tandem with clinical recovery. Conclusions: The findings have pertinent implications on developing management strategies of these conditions.