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Review
. 2025 May 21;15(1):67.
doi: 10.1186/s13613-025-01464-w.

Critical insights for intensivists on Guillain-Barré syndrome

Nicolas Weiss  1   2   3 , Clémence Marois  4   5 , Loic Le Guennec  4   6 , Benjamin Rohaut  4   7 , Sophie Demeret  4   5
Affiliations
Review

Critical insights for intensivists on Guillain-Barré syndrome

Nicolas Weiss et al. Ann Intensive Care. .

Abstract

Guillain-Barré Syndrome (GBS) is a leading cause of acute flaccid tetraplegia worldwide, with an incidence of 1-2 cases per 100,000 people per year. Characterized by an immune-mediated polyneuropathy, GBS often follows infections or immunological triggers, including vaccinations. The syndrome is classified into three main subtypes based on electrophysiological findings: acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN). The pathophysiology of GBS involves molecular mimicry between microbial antigens and nerve structures, particularly affecting gangliosides and myelin proteins. Diagnosis primarily relies on clinical history, with lumbar puncture and electroneuromyogram used to confirm and differentiate subtypes. Treatment includes intravenous immunoglobulins or therapeutic plasma exchange associated with symptomatic treatment, especially mechanical ventilation if needed. Prognosis is generally favorable with a low mortality rate (< 5%) overall, but neurological sequelae can occur. Current research continues to explore novel therapeutic approaches, including complement-targeted therapies. Despite advancements, progress in specific treatments has been limited, and ongoing evaluation of potential biomarkers such as neurofilament light chains may enhance prognosis prediction and management strategies.

Keywords: Acute polyradiculoneuritis; Bickerstaff encephalitis; Guillain-Barré syndrome; Miller-Fisher.

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Conflict of interest statement

Declarations. Ethics approval and consent to participate: Not applicable, review article. Consent for publication: Not applicable, review article. All authors consent to the submission of the current version of the manuscript. Competing interests: Nicolas Weiss perceived consultant fees from Owkin and Alexion. Clémence Marois perceived consultant fees from UCB.

Figures

Fig. 1
Fig. 1
Pathophysiology of Guillain-Barré syndrome A, schematic view of the peripheral nerve showing the axon, the myelin sheath and the saltatory conduction from one node of Ranvier to another in normal condition; B, schematic view of the node of Ranvier showing voltage-gated sodium channel and gangliosides; C, immune system recognizes gangliosides expressed on the surface of Campylobacter jejuni and induces the production of gangliosides antibodies that are able to fix gangliosides expressed on the node of Ranvier; this correspond to what is coined as molecular mimicry. Antibodies fixation will lead to complement activation and then after macrophage recruitment
Fig. 2
Fig. 2
Different forms of Guillain-Barré syndrome Black areas represent localization of the neurological symptoms. The blurred representation stands for ataxia. The bed represents altered consciousness
Fig. 3
Fig. 3
Initial management of Guillain-Barré syndrome Abbreviations: CSF, cerebrospinal fluid; FVC, forced vital capacity; MRC, medical research council motor score; SBC, single breath count
Fig. 4
Fig. 4
Proposed mechanical ventilation weaning algorithm Abbreviations: HR, heart rate; P/F, PaO2/FiO2 ratio; PEEP, Positive end expiratory pressure; PSV, Pressure support ventilation; RR, respiratory rate; SBP, systolic blood pressure; SBT, spontaneous breathing trial; ZEEP, zero end expiratory pressure
See this image and copyright information in PMC

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