REVIEW article
Front. Neurol.
Sec. Neurocritical and Neurohospitalist Care
Volume 16 - 2025 | doi: 10.3389/fneur.2025.1587091
Pathophysiological mechanisms underlying early brain injury and delayed cerebral ischemia in the aftermath of aneurysmal subarachnoid haemorrhage: a comprehensive analysis
Provisionally accepted
Hendrik Stragier1,2*
Hans Vandersmissen2Sofie Ordies2Steven Thiessen2,3Dieter Mesotten2,3Dieter Peuskens4
Hugo Ten Cate5,6- 1School for Cardiovascular Diseases, Faculty of Health, Medicine and Life Sciences, Maastricht University, Maastricht, Netherlands, Netherlands
- 2Department of Anaesthesiology, Intensive Care Medicine, Emergency Medicine and Pain Therapy, Ziekenhuis Oost-Limburg, Genk, Belgium
- 3Faculty of Medicine and Life Sciences, UHasselt, Diepenbeek, Belgium
- 4Department of Neurosurgery, Ziekenhuis Oost-Limburg, Genk, Belgium
- 5Thrombosis Expertise Center, Maastricht University Medical Centre, Maastricht, Netherlands
- 6Center for Thrombosis and Hemostasis, University Medical Centre, Johannes Gutenberg University Mainz, Mainz, Rhineland-Palatinate, Germany
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Early brain injury (EBI) and delayed cerebral ischemia (DCI) are pivotal contributors to morbidity and mortality following aneurysmal subarachnoid haemorrhage (aSAH). Despite advances that have reduced mortality and incidence, aSAH remains a significant public health concern due to its early onset, leading to prolonged periods of diminished quality of life for affected individuals. EBI mechanisms, including endothelial dysfunction, blood-brain barrier disruption, cerebral edema, neuro-inflammation, cortical spreading depolarizations, and oxidative damage, trigger cell death and apoptosis, setting the stage for DCI development in later clinical phases. DCI arises not only from large-vessel vasospasm, but also from other complex pathophysiological processes, including thrombo-inflammation, neuro-inflammation, microcirculatory dysfunction, and glycocalyx disruption. Recognizing and understanding these mechanisms is essential, as early interventions could potentially reduce long-term disability in this population. This comprehensive review offers an in-depth analysis of these pathophysiological mechanisms. As our understanding of these processes continues to evolve, further research is crucial to improving outcomes and reducing the long-term impact of aSAH.
Keywords: Aneurysmal subarachnoid hemorrhage (aSAH), Delayed cerebral ischemia (DCI), Early brain injury (EBI), Thrombo-inflammation, Neuro-inflammation
Received: 03 Mar 2025; Accepted: 12 May 2025.
Copyright: © 2025 Stragier, Vandersmissen, Ordies, Thiessen, Mesotten, Peuskens and Ten Cate. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Hendrik Stragier, School for Cardiovascular Diseases, Faculty of Health, Medicine and Life Sciences, Maastricht University, Maastricht, 6229 ER, Netherlands, Netherlands
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