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Guillain–Barré Syndrome

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Myelin

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 1190))

Abstract

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.

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Correspondence to Kenichi Kaida .

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© 2019 Springer Nature Singapore Pte Ltd.

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Kaida, K. (2019). Guillain–Barré Syndrome. In: Sango, K., Yamauchi, J., Ogata, T., Susuki, K. (eds) Myelin. Advances in Experimental Medicine and Biology, vol 1190. Springer, Singapore. https://doi.org/10.1007/978-981-32-9636-7_20

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