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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SpringerOpen
2025-05-01
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| Series: | Annals of Intensive Care |
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| 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. |
| format | Article |
| id | doaj-art-33f5396c853246d281a141fe5fa92167 |
| institution | DOAJ |
| issn | 2110-5820 |
| language | English |
| publishDate | 2025-05-01 |
| publisher | SpringerOpen |
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| series | Annals of Intensive Care |
| 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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