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Handb Clin Neurol. 2013;115:383-402. doi: 10.1016/B978-0-444-52902-2.00021-7.

The Guillain-Barré syndrome.

Author information

1
Department of Neurology, Toneyama National Hospital, Toneyama, Toyonaka, Japan. Electronic address: hfujim@toneyama.hosp.go.jp.

Abstract

The latest estimation for the frequency of Guillain-Barré syndrome (GBS) is 1.1 to 1.8 per 100000 persons per year. Guillain-Barré syndrome is today divided into two major subtypes: acute inflammatory demyelinating polyneuropathy (AIDP) and the axonal subtypes, acute motor axonal neuropathy (AMAN) and acute motor and sensory axonal neuropathy (AMSAN). The axonal forms of GBS are caused by certain autoimmune mechanisms, due to a molecular mimicry between antecedent bacterial infection (particularly Campylobacter jejuni) and human peripheral nerve gangliosides. Improvements in patient management in intensive care units has permitted a dramatic drop in mortality rates. Immunotherapy, including plasma exchange (PE) or intravenous immunoglobulin (IVIg), seems to shorten the time to recovery, but their effect remains limited. Further clinical investigations are needed to assess the effect of PE or IVIg on the GBS patients with mild affection, no response, or relapse.

KEYWORDS:

Campylobacter jejuni; Guillain–Barré syndrome; acute inflammatory demyelinating polyneuropathy; acute motor axonal neuropathy; ganglioside; intravenous immunoglobulin; molecular mimicry; plasma exchange

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