There are one or two studies that have suggested that steroids may delay recovery if used in GBS/AIDP. There is no clear explanation of a mechanism by which steroids can do harm in AIDP in published literature as far as I have searched. Wondering why most if not all acute central nervous system demyelination states are aggressively treated with high dose steroids (eg., ADEM, Transverse myelitis, an MS flare, Optic neuritis, etc) while steroids may do harm in a peripheral demyelination process. Can anyone suggest reasons?
Hi Suraj
I do remember in a recent conference about the concept of good inflammation. If we believe that inflammatory reactions are sometimes beneficial (if not crucial) in some defence against some disorders, possibly including GBS, then it might make a little sense then. However at the level of translational medicine, I am not sure how we can prove or disprove this theory further.
Knowing my post is not connected to the initial question but:
Information added with regard to actuality (has been reported today in Austrian Newspaper for the first time):
MEYER SAUTEUR PM et al:
Research Article
Mycoplasma pneumoniae triggering the Guillain-Barré syndrome: A case-control study
Annals of Neurology, Volume 80, Issue 4 October 2016
Pages 566–580
First published: 26 August 2016
DOI: 10.1002/ana.24755
http://onlinelibrary.wiley.com/doi/10.1002/ana.24755/abstract
For (your) convenience only:
Abstract
Objective
Guillain-Barré syndrome (GBS) is an acute postinfectious immune-mediated polyneuropathy. Although preceding respiratory tract infections with Mycoplasma pneumoniae have been reported in some cases, the role of M. pneumoniae in the pathogenesis of GBS remains unclear. We here cultured, for the first time, M. pneumoniae from a GBS patient with antibodies against galactocerebroside (GalC), which cross-reacted with the isolate. This case prompted us to unravel the role of M. pneumoniae in GBS in a case-control study.
Methods
We included 189 adults and 24 children with GBS and compared them to control cohorts for analysis of serum antibodies against M. pneumoniae (n = 479) and GalC (n = 198).
Results
Anti–M. pneumoniae immunoglobulin (Ig) M antibodies were detected in GBS patients and healthy controls in 3% and 0% of adults (p = 0.16) and 21% and 7% of children (p = 0.03), respectively. Anti-GalC antibodies (IgM and/or IgG) were found in 4% of adults and 25% of children with GBS (p = 0.001). Anti-GalC-positive patients showed more-frequent preceding respiratory symptoms, cranial nerve involvement, and a better outcome. Anti-GalC antibodies correlated with anti–M. pneumoniae antibodies (p < 0.001) and cross-reacted with different M. pneumoniae strains. Anti-GalC IgM antibodies were not only found in GBS patients with M. pneumoniae infection, but also in patients without neurological disease (8% vs 9%; p = 0.87), whereas anti-GalC IgG was exclusively found in patients with GBS (9% vs 0%; p = 0.006).
Interpretation
M. pneumoniae infection is associated with GBS, more frequently in children than adults, and elicits anti-GalC antibodies, of which specifically anti-GalC IgG may contribute to the pathogenesis of GBS. Ann Neurol 2016;80:566–580
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