scholarly journals Imaging predictors of outcome in acute spontaneous subarachnoid hemorrhage: a review of the literature

2018 ◽  
Vol 60 (2) ◽  
pp. 247-259 ◽  
Author(s):  
Isabel Fragata ◽  
Patrícia Canhão
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Early Brain Injury ◽  
High Morbidity ◽  
Predictors Of Outcome ◽  
Imaging Studies ◽  
Prediction Of Complications ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Very High

Spontaneous subarachnoid hemorrhage (SAH) accounts for about 5% of strokes, but has a very high morbidity and mortality. Many survivors are left with important cognitive impairment and are severely incapacitated. Prediction of complications such as vasospasm and delayed cerebral ischemia, and of clinical outcome after SAH, is challenging. Imaging studies are essential in the initial evaluation of SAH patients and are increasingly relevant in assessing for complications and prognosis. In this article, we reviewed the role of imaging studies in evaluating early brain injury and predicting complications as well as clinical and neuropsychological prognosis after acute SAH.

scholarly journals The Role of the Blood Neutrophil-to-Lymphocyte Ratio in Aneurysmal Subarachnoid Hemorrhage

2021 ◽  
Vol 12 ◽  
Author(s):  
Lingxin Cai ◽  
Hanhai Zeng ◽  
Xiaoxiao Tan ◽  
Xinyan Wu ◽  
Cong Qian ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Critical Role ◽  
Delayed Cerebral Ischemia ◽  
Early Brain Injury ◽  
Neutrophil To Lymphocyte Ratio ◽  
Lymphocyte Ratio ◽  
Novel Therapeutic Strategies ◽  
Improved Accuracy

Aneurysmal subarachnoid hemorrhage (aSAH) is an important type of stroke with the highest rates of mortality and disability. Recent evidence indicates that neuroinflammation plays a critical role in both early brain injury and delayed neural deterioration after aSAH, contributing to unfavorable outcomes. The neutrophil-to-lymphocyte ratio (NLR) is a peripheral biomarker that conveys information about the inflammatory burden in terms of both innate and adaptive immunity. This review summarizes relevant studies that associate the NLR with aSAH to evaluate whether the NLR can predict outcomes and serve as an effective biomarker for clinical management. We found that increased NLR is valuable in predicting the clinical outcome of aSAH patients and is related to the risk of complications such as delayed cerebral ischemia (DCI) or rebleeding. Combined with other indicators, the NLR provides improved accuracy for predicting prognosis to stratify patients into different risk categories. The underlying pathophysiology is highlighted to identify new potential targets for neuroprotection and to develop novel therapeutic strategies.

scholarly journals The Role of Oxidative Stress in Early Brain Injury after Subarachnoid Hemorrhage

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
M. Jelinek ◽  
M. Jurajda ◽  
K. Duris
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Molecular Mechanisms ◽  
Early Brain Injury ◽  
Pathophysiological Mechanisms ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Antioxidant Mechanisms

This review focuses on the problem of oxidative stress in early brain injury (EBI) after spontaneous subarachnoid hemorrhage (SAH). EBI involves complex pathophysiological mechanisms, including oxidative stress. In the first section, we describe the main sources of free radicals in EBI. There are several sources of excessive generation of free radicals from mitochondrial free radicals’ generation and endoplasmic reticulum stress, to hemoglobin and enzymatic free radicals’ generation. The second part focuses on the disruption of antioxidant mechanisms in EBI. The third section describes some newly found molecular mechanisms and pathway involved in oxidative stress after EBI. The last section is dedicated to the pathophysiological mechanisms through which free radicals mediate early brain injury.

New Mechanisms and Targets of Subarachnoid Hemorrhage: A Focus on Mitochondria

2021 ◽  
Vol 19 ◽  
Author(s):  
Zeyu Zhang ◽  
Anke Zhang ◽  
Yibo Liu ◽  
Xiaoming Hu ◽  
Yuanjian Fang ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Mitochondrial Dynamics ◽  
Delayed Cerebral Ischemia ◽  
Early Brain Injury ◽  
Adverse Outcomes ◽  
Heavy Burden ◽  
Poor Outcomes ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Membrane Organelle

: Spontaneous subarachnoid hemorrhage (SAH) accounts for 5-10% of all strokes, and is a subtype of hemorrhagic stroke that places a heavy burden on health care. Despite great progress in surgical clipping and endovascular treatment for ruptured aneurysms, cerebral vasospasm (CVS) and delayed cerebral ischemia (DCI) threaten the long-term outcomes of patients with SAH. Moreover, there are limited drugs available to reduce the risk of DCI and adverse outcomes in SAH patients. New insight suggests that early brain injury (EBI), which occurs within 72 h after the onset of SAH, may lay the foundation for further DCI development and poor outcomes. The mechanisms of EBI mainly include excitotoxicity, oxidative stress, neuroinflammation, blood-brain barrier (BBB) destruction, and cellular death. Mitochondria are a double-membrane organelle, and they play an important role in energy production, cell growth, differentiation, apoptosis, and survival. Mitochondrial dysfunction, which can lead to mitochondrial membrane potential (ΔΨm) collapse, overproduction of reactive oxygen species (ROS), release of apoptogenic proteins, disorders of mitochondrial dynamics, and activation of mitochondria-related inflammation, is considered a novel mechanism of EBI related to DCI as well as post-SAH outcomes. In addition, mitophagy is activated after SAH. In this review, we discuss the latest perspectives on the role of mitochondria in EBI and DCI after SAH. We emphasize the potential of mitochondria as therapeutic targets, and summarize the promising therapeutic strategies targeting mitochondria for SAH.

scholarly journals The Role of the Glycocalyx in the Pathophysiology of Subarachnoid Hemorrhage-Induced Delayed Cerebral Ischemia

2021 ◽  
Vol 9 ◽  
Author(s):  
Hanna Schenck ◽  
Eliisa Netti ◽  
Onno Teernstra ◽  
Inger De Ridder ◽  
Jim Dings ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Brain Damage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Neurovascular Unit ◽  
Delayed Cerebral Ischemia ◽  
Treatment Strategies ◽  
Early Brain Injury

The glycocalyx is an important constituent of blood vessels located between the bloodstream and the endothelium. It plays a pivotal role in intercellular interactions in neuroinflammation, reduction of vascular oxidative stress, and provides a barrier regulating vascular permeability. In the brain, the glycocalyx is closely related to functions of the blood-brain barrier and neurovascular unit, both responsible for adequate neurovascular responses to potential threats to cerebral homeostasis. An aneurysmal subarachnoid hemorrhage (aSAH) occurs following rupture of an intracranial aneurysm and leads to immediate brain damage (early brain injury). In some cases, this can result in secondary brain damage, also known as delayed cerebral ischemia (DCI). DCI is a life-threatening condition that affects up to 30% of all aSAH patients. As such, it is associated with substantial societal and healthcare-related costs. Causes of DCI are multifactorial and thought to involve neuroinflammation, oxidative stress, neuroinflammation, thrombosis, and neurovascular uncoupling. To date, prediction of DCI is limited, and preventive and effective treatment strategies of DCI are scarce. There is increasing evidence that the glycocalyx is disrupted following an aSAH, and that glycocalyx disruption could precipitate or aggravate DCI. This review explores the potential role of the glycocalyx in the pathophysiological mechanisms contributing to DCI following aSAH. Understanding the role of the glycocalyx in DCI could advance the development of improved methods to predict DCI or identify patients at risk for DCI. This knowledge may also alter the methods and timing of preventive and treatment strategies of DCI. To this end, we review the potential and limitations of methods currently used to evaluate the glycocalyx, and strategies to restore or prevent glycocalyx shedding.

scholarly journals Role of Endothelin-1 in Human Aneurysmal Subarachnoid Hemorrhage: Associations with Vasospasm and Delayed Cerebral Ischemia

2011 ◽  
Vol 15 (1) ◽  
pp. 19-27 ◽  
Author(s):  
Bhavani P. Thampatty ◽  
Paula R. Sherwood ◽  
Matthew J. Gallek ◽  
Elizabeth A. Crago ◽  
Dianxu Ren ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Endothelin 1

scholarly journals White Matter Injury in Early Brain Injury after Subarachnoid Hemorrhage

2018 ◽  
Vol 28 (1) ◽  
pp. 26-35 ◽  
Author(s):  
Jinwei Pang ◽  
Jianhua Peng ◽  
Ping Yang ◽  
Li Kuai ◽  
Ligang Chen ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
White Matter ◽  
Early Brain Injury ◽  
Therapeutic Strategies ◽  
White Matter Injury ◽  
High Morbidity ◽  
Normal Brain ◽  
Neurological Outcomes ◽  
Multiple Substrates

Subarachnoid hemorrhage (SAH) is a major cause of high morbidity, disability, and mortality in the field of neurovascular disease. Most previous SAH studies have focused on improving cerebral blood flow, reducing cerebral vasospasm, reducing neuronal calcium overload, and other treatments. While these studies showed exciting findings in basic science, therapeutic strategies based on the findings have not significantly improved neurological outcomes in patients with SAH. Currently, the only drug proven to effectively reduce the neurological defects of SAH patients is nimodipine. Current advances in imaging technologies in the field of stroke have confirmed that white matter injury (WMI) plays an important role in the prognosis of types of stroke, and suggests that WMI protection is essential for functional recovery and poststroke rehabilitation. However, WMI injury in relation to SAH has remained obscure until recently. An increasing number of studies suggest that the current limitations for SAH treatment are probably linked to overlooked WMI in previous studies that focused only on neurons and gray matter. In this review, we discuss the biology and functions of white matter in the normal brain, and discuss the potential pathophysiology and mechanisms of early brain injury after SAH. Our review demonstrates that WMI encompasses multiple substrates, and, therefore, more than one pharmacological approach is necessary to preserve WMI and prevent neurobehavioral impairment after SAH. Strategies targeting both neuronal injury and WMI may potentially provide a novel future for SAH knowledge and treatment.

Abstract 192: The Relationship of Platelet-leukocyte Aggregates and Early Brain Injury After Subarachnoid Hemorrhage

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Jennifer A Frontera ◽  
Vladimir Katyshev ◽  
Thomas M McIntyre ◽  
Fatima A Sehba ◽  
Jonathan M Weimer ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Delayed Cerebral Ischemia ◽  
Early Brain Injury ◽  
Aneurysm Rupture ◽  
Acute Brain Injury ◽  
Unruptured Aneurysms ◽  
Major Predictor ◽  
A Prospective Study ◽  
And Control

Introduction: Acute brain injury incurred after aneurysm rupture in subarachnoid hemorrhage (SAH) is a major predictor of poor functional outcome. We hypothesize that platelet-leukocyte aggregates (PLA) form early after SAH and contribute to acute brain injury. Methods: A prospective study of antiplatelet-naive SAH patients and controls (patients with unruptured aneurysms undergoing repair) was conducted from 3/2014-3/2016. Platelet-monocyte, platelet-lymphocyte and platelet-neutrophil aggregates in whole blood were measured with and without exposure to a platelet agonist (Thrombin receptor activating peptide [TRAP]) using flow cytometry. PLA within 24h and averaged over 72h from ictus (prior to the onset of delayed cerebral ischemia/vasospasm) were compared between patients with mild (admission Hunt-Hess [HH] 1-3) versus severe early brain injury (EBI; HH 4-5). Results: We enrolled 60 SAH patients and 13 controls. PLA were significantly lower in those with severe EBI compared to those with mild EBI (Platelet-monocyte-aggregates 36% versus 53%, P=0.011; Platelet-neutrophil-aggregates 15.2 versus 23.1%, P=0.002) within 24h of ictus and prior to aneurysm repair and remained significantly lower over 72h (both P<0.05). Platelet-monocyte, platelet-neutrophil and platelet-lymphocyte aggregates were also significantly lower in those with severe EBI compared to controls (all P<0.05). The ability of platelets to be stimulated/activated by TRAP to form PLA was also lower in severe EBI patients compared to mild EBI and control patients over 72h (platelet-neutrophil-aggregates 79.7, 88.2 and 92.7%, respectively, P=0.003; platelet-lymphocyte aggregates 9.2, 11.0 and 14.6%, respectively, P=0.022), consistent with prior platelet activation/degranulation. Conclusions: PLA are lower, and respond less to stimulation in patients with severe EBI after SAH compared to those with mild EBI and controls. These data suggest that in severe EBI: PLA may form earlier and are cleared, are adherent to endothelium and not shed in the blood, or have migrated into the parenchyma. These hypotheses bear further study.

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