Critical insights for intensivists on Guillain-Barré syndrome

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 syndro...

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Main Authors: Nicolas Weiss, Clémence Marois, Loic Le Guennec, Benjamin Rohaut, Sophie Demeret
Format: Article
Language:English
Published: SpringerOpen 2025-05-01
Series:Annals of Intensive Care
Subjects:
Online Access:https://doi.org/10.1186/s13613-025-01464-w
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author Nicolas Weiss
Clémence Marois
Loic Le Guennec
Benjamin Rohaut
Sophie Demeret
author_facet Nicolas Weiss
Clémence Marois
Loic Le Guennec
Benjamin Rohaut
Sophie Demeret
author_sort Nicolas Weiss
collection DOAJ
description 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.
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spelling doaj-art-33f5396c853246d281a141fe5fa921672025-08-20T03:08:44ZengSpringerOpenAnnals of Intensive Care2110-58202025-05-0115111810.1186/s13613-025-01464-wCritical insights for intensivists on Guillain-Barré syndromeNicolas Weiss0Clémence Marois1Loic Le Guennec2Benjamin Rohaut3Sophie Demeret4Département de neurologie, Service de Médecine Intensive Réanimation à orientation neurologique, Sorbonne Université, AP-HP.Sorbonne Université, Hôpital de la Pitié-SalpêtrièreDépartement de neurologie, Service de Médecine Intensive Réanimation à orientation neurologique, Sorbonne Université, AP-HP.Sorbonne Université, Hôpital de la Pitié-SalpêtrièreDépartement de neurologie, Service de Médecine Intensive Réanimation à orientation neurologique, Sorbonne Université, AP-HP.Sorbonne Université, Hôpital de la Pitié-SalpêtrièreDépartement de neurologie, Service de Médecine Intensive Réanimation à orientation neurologique, Sorbonne Université, AP-HP.Sorbonne Université, Hôpital de la Pitié-SalpêtrièreDépartement de neurologie, Service de Médecine Intensive Réanimation à orientation neurologique, Sorbonne Université, AP-HP.Sorbonne Université, Hôpital de la Pitié-SalpêtrièreAbstract 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.https://doi.org/10.1186/s13613-025-01464-wGuillain-Barré syndromeMiller-FisherAcute polyradiculoneuritisBickerstaff encephalitis
spellingShingle Nicolas Weiss
Clémence Marois
Loic Le Guennec
Benjamin Rohaut
Sophie Demeret
Critical insights for intensivists on Guillain-Barré syndrome
Annals of Intensive Care
Guillain-Barré syndrome
Miller-Fisher
Acute polyradiculoneuritis
Bickerstaff encephalitis
title Critical insights for intensivists on Guillain-Barré syndrome
title_full Critical insights for intensivists on Guillain-Barré syndrome
title_fullStr Critical insights for intensivists on Guillain-Barré syndrome
title_full_unstemmed Critical insights for intensivists on Guillain-Barré syndrome
title_short Critical insights for intensivists on Guillain-Barré syndrome
title_sort critical insights for intensivists on guillain barre syndrome
topic Guillain-Barré syndrome
Miller-Fisher
Acute polyradiculoneuritis
Bickerstaff encephalitis
url https://doi.org/10.1186/s13613-025-01464-w
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