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KMID : 1201420110040000042
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Journal of Neurocritical Care
2011 Volume.4 No. 0 p.42 ~ p.46
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Diagnosis and Immunotherapy of Guillain-Barre Syndrome
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Kwon Ki-Han
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Abstract
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There are several subtypes in Guillain-Barre syndrome (GBS), including acute inflammatory demyelinating polyradiculoneuropahty (AIDP), acute motor axonal neuropathy (AMAN), acute motor and sensory axonal neuropathy (AMSAN), and Miller-Fisher syndrome (MFS). Recently Guillain-Barre syndrome has been regarded complement-mediated autoimmune disorder. Many of patients with AMAN is caused by antibodies to lipo-oligosaacharides (LOS) of Campylobacter jejuni (c. jejuni) cell wall. The antibodies to LOS of C. jejuni bind to GM1, GM1b, GD1a, or GalNAc-GD1a exposed in the axolemma at the node of Ranvier and activate complement with formation of membrane attack complexes (MAC). Activation of complement and MAC formation cause only disruption of clusters of sodium channels on axolemma at the rode of Ranvier, which explains of acute motor conduction block neuropathy (AMCBN) or “arrested” AMAN. In severe case they even can cause Wallerian degeneration of axon. In AIDP, autoantibodies bound to unknown molecules of the outer surface of Schwann cell also activate complement and form MAC, which result in segmental dymelination. The clinical and electrophysiological diagnosis, and pathogenesis of GBS will be presented. In the last part of this article, intravenous immunoglobuli (IVIg) and plasma exchange (PE), which are effective in GBS and new emerging treatment, including nafamostat mesilate and eculizumab will be presented.
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KEYWORD
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Tuberculous meningitis, Spontaneous regression
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