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Node of Ranvier disruption in Guillain–Barré syndrome
Author(s) -
Susuki Keiichiro
Publication year - 2016
Publication title -
clinical and experimental neuroimmunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.297
H-Index - 15
ISSN - 1759-1961
DOI - 10.1111/cen3.12338
Subject(s) - guillain barre syndrome , axolemma , node of ranvier , autoantibody , medicine , chronic inflammatory demyelinating polyneuropathy , neuroscience , pathophysiology , nodal , sodium channel , overlap syndrome , immunology , pathology , antibody , myelin , biology , chemistry , anatomy , disease , central nervous system , organic chemistry , sodium
Guillain–Barré syndrome is an autoimmune polyneuropathy characterized by acute and progressive limb weakness. Recent evidence shows that disruption of the nodes of Ranvier is the key pathophysiology in axonal forms of Guillain–Barré syndrome. Rapid and efficient propagation of action potentials along myelinated nerve fibers depends on the high density of voltage‐gated Na + channels on the nodal axolemma. Complement‐mediated autoimmune attacks against gangliosides cause dysfunction and structural damage at and near nodes, resulting in nerve conduction failure. Furthermore, the proteins highly enriched at and near the nodes can be a direct target of autoimmune reactions, and these autoantibodies might exacerbate immune‐mediated demyelinating neuropathies. The present review focuses on disruption of the nodes of Ranvier during Guillain–Barré syndrome and related disorders.