Myelin pp 323-331 | Cite as

Guillain–Barré Syndrome

  • Kenichi KaidaEmail author
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 1190)


Guillain–Barré syndrome (GBS) is an acute immune-mediated polyradiculoneuropathy, and pathophysiologically classified into acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), and acute motor and sensory axonal neuropathy (AMSAN). The main pathophysiological mechanism is complement-mediated nerve injury caused by antibody–antigen interaction in the peripheral nerves. Antiglycolipid antibodies are most pathogenic factors in the development of GBS, but not found in 40% of patients with GBS. One of the principal target regions in GBS is the node of Ranvier where functional molecules including glycolipids are assembled. Nodal dysfunction induced by the immune response in nodal axolemma, termed “nodopathy,” can electrophysiologically show reversible conduction failure, axonal degeneration, or segmental demyelination. To detect new target molecules in antiglycolipid antibody-negative GBS and to elucidate the pathophysiology in the subacute and the subsequent phases of the disorder are the next problems.


Guillain–Barré syndrome Glycolipid Antibody Complement Neuropathy Nodopathy 


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© Springer Nature Singapore Pte Ltd. 2019

Authors and Affiliations

  1. 1.Division of Neurology, Department of Internal MedicineNational Defense Medical CollegeSaitamaJapan

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