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Published on: November 9, 2017
Guillain-barré syndrome
1Department of Neurology, Chiba University School of Medicine, Chiba, Japan. kuwabara-s@faculty.chiba-u.jp
Current Neurology and Neuroscience Reports
|January 16, 2007
Summary
Guillain-Barré syndrome (GBS) subtypes like AMAN involve antibodies targeting gangliosides on motor nerves. This molecular mimicry, often triggered by Campylobacter jejuni, leads to nerve damage and conduction block.
Area of Science:
- Neurology
- Immunology
- Microbiology
Background:
- Guillain-Barré syndrome (GBS) comprises acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN).
- Pathophysiology of AMAN is increasingly understood, contrasting with unidentified targets in AIDP.
Purpose of the Study:
- To review recent publications on Guillain-Barré syndrome pathophysiology, focusing on AMAN.
- To elucidate the molecular mechanisms underlying AMAN.
Main Methods:
- Review of recent scientific literature.
- Analysis of molecular mimicry mechanisms between bacterial lipo-oligosaccharides and human gangliosides.
- Examination of electrodiagnostic findings and therapeutic outcomes.
Main Results:
- Molecular mimicry involving bacterial lipo-oligosaccharides and gangliosides (GM1, GM1b, GD1a, GalNAc-GD1a) is a key cause of AMAN.
- Antibody deposition at nerve nodes/paranodes leads to reversible conduction block and axonal degeneration.
- Campylobacter jejuni genetic polymorphisms influence ganglioside expression and AMAN pathogenesis.
- Plasmapheresis and immunoglobulin therapy accelerate recovery in GBS; corticosteroids are ineffective.
Conclusions:
- Understanding AMAN pathophysiology involves ganglioside-targeting antibodies and bacterial mimicry.
- Therapeutic strategies for GBS should focus on immunotherapy like plasmapheresis and immunoglobulin.
- Further research is needed to identify AIDP targets.
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