Predictors of Delayed Cerebral Ischemia in Patients with Aneurysmal Subarachnoid Hemorrhage with Asymptomatic Angiographic Vasospasm on Admission

Aldakkan, Abdulrahman; Mansouri, Alireza; Jaja, Blessing N.R.; Alotaibi, Naif M.; Macdonald, R. Loch; Noble, Adam; Molyneux, Andrew; Quinn, Audrey; Schatlo, Bawarjan; Lo, Benjamin; Johnston, Clay; Hänggi, Daniel; Hasan, David; Wong, George Kwok-Chu; Lantigua, Hector; Fukuda, Hitoshi; Torner, James C.; Singh, Jeffrey M.; Spears, Julian; Schaller, Karl; Stienen, Martin N.; Vergouwen, Mervyn D.I.; Cusimano, Michael D.; Todd, Michael M.; Tseng, Ming-Yuan; Roux, Peter Le; Yamagata, Sen; Mayer, Stephan A.; Schenk, Thomas; Schweizer, Tom A.

doi:10.1016/j.wneu.2016.09.096

Cited by 19 publications

(20 citation statements)

References 22 publications

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“…These data had modified the management protocols of aSAH in our institute to allow for intervention when EEG and TCD changes reach levels detecting DCI to avoid the possibility of irreversible neuronal damage. These results are in accordance with the work of Aldakkan and colleagues [15] and with that of Mortimer and colleagues [16] who specified that severe angiographic vasospasm is associated with increased risk of DCI and poorer functional outcome following aSAH.…”

Section: Discussionsupporting

confidence: 92%

“…At the same time, patients who progressed to DCI had earlier EEG and/or TCD onset of vasospasm manifestations than those passed a regressive course. This result is in accordance with Aldakkan and colleagues [15] as well as Phan and colleagues [17] who stated that earlier ultrasonographic signs of vasospasm are associated with higher incidence of clinically evident DCI, and they recommend early intervention and aggressive therapy in this sector of patients.…”

Section: Discussionsupporting

confidence: 91%

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Vasospasm following aneurysmal subarachnoid hemorrhage: prediction, detection, and intervention

Nassar

Ghali

Bahnasy

et al. 2019

Egypt J Neurol Psychiatry Neurosurg

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BackgroundVasospasm of the cerebral blood vessels is a common complication of aneurysmal subarachnoid hemorrhage (aSAH) which results in delayed cerebral ischemia (DCI) and worsening of the outcome.MethodsThis study was performed on 41 aSAH patients diagnosed by non-contrast brain CT, CT angiography, and digital subtraction angiography followed by interventional aneurysmal embolization. Patients were followed up for 20 days by clinical assessment, EEG monitoring, and transcranial duplex studies (TCD) for early detection of vasospasm and DCI.ResultsThe most common ruptured aneurysmal sites were middle cerebral, anterior communicating, posterior communicating, terminal internal carotid, and anterior cerebral arteries respectively. The incidence of vasospasm was 36.8% of the included cases; 57% progressed to DCI while 43% passed a spontaneous regressive course. The most common arteries undergoing vasospasm were the MCA followed by the ACA, ICA, and lastly the basilar arteries. The mean time of vasospasm development as detected by EEG monitoring and/or TCD was 8.4 ± 2.8 days which was earlier than clinical signs by 12.5 ± 5.3 h in those progressed to DCI.ConclusionContinuous EEG monitoring and TCD are valuable methods for early detection of vasospasm and they allow for early therapeutic intervention before irreversible ischemic neurological deficits take place.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%

Vasospasm following aneurysmal subarachnoid hemorrhage: prediction, detection, and intervention

Nassar

Ghali

Bahnasy

et al. 2019

Egypt J Neurol Psychiatry Neurosurg

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“…Cerebral ischemia-reperfusion (I/R) injury is associated with a high incidence of morbidity and mortality (Yang et al, 2013). Clinical data indicate that global cerebral ischemia is a leading cause of mortality worldwide (Müller, et al, 2017;Von der Brelie et al, 2017;Aldakkan et al, 2017). Several mechanisms involve in the pathology of cerebral ischemia reperfusion damage including inflammation, cytotoxicity, oxidative stress, apoptosis and excitotoxicity (Gabriel-Salazar et al, 2018;Liu et al, 2018b;Paľa et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

MicroR-146 protects against rat ischemia-reperfusion injury by targeting NF-κB-mediated PI3K/AKT/mTOR signaling pathway

Wang

Liu²,

Shao

et al. 2022

Food Sci. Technol

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plays crucial roles in attenuating nerve injury during cerebral ischemia-reperfusion (I/R) injury. The purpose of this study was to investigate the neuroprotective effect of miR-146 against cerebral I/R injury. Rat model of cerebral I/R injury was established using 4-vessel occlusion and reperfusion. In this study, miR-146 expression was significantly decreased in neurons in cerebral I/R injury rat compared to sham group. In addition, miR-146+/+ significantly decreased inflammatory cytokines, oxidative stress, neuron cell apoptosis and the infarct size in cerebral I/R injury rats (p<0.05). Transfection of miR-146 reduced apoptosis, autophagy and autophagy-related proteins LC-3, Beclin-1 and increased p62 in the neuron cells compared to control group. Furthermore, overexpression of miR-146 was indicated to directly targeting NF-κB and activating PI3K/AKT/ mTOR expression in neuron cells. In conclusion, these findings suggested that miR-146 could protect against rat ischemiareperfusion injury by targeting NF-κB-mediated PI3K/AKT/mTOR signaling pathway, which offered a potential molecular for the treatment of cerebral I/R injury.

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“…10–12 Third, evidence shows that some SAH patients develop DCI without any angiographic evidence of large artery vasospasm. 13–15 Fourth, disappointing results were observed in two randomized, double-blind, placebo-controlled, phase III clinical trials using the endothelin A receptor antagonist, clazosentan – a powerful anti-vasospasm agent. In these trials, clazosentan significantly reduced large artery vasospasm, but failed to improve functional outcome or reduce mortality in SAH patients.…”

Section: Introductionmentioning

confidence: 99%

Microvascular platelet aggregation and thrombosis after subarachnoid hemorrhage: A review and synthesis

Clarke

Suggs

Diwan

et al. 2020

J Cereb Blood Flow Metab

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Delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (SAH) has been associated with numerous pathophysiological sequelae, including large artery vasospasm and microvascular thrombosis. The focus of this review is to provide an overview of experimental animal model studies and human autopsy studies that explore the temporal-spatial characterization and mechanism of microvascular platelet aggregation and thrombosis following SAH, as well as to critically assess experimental studies and clinical trials highlighting preventative therapeutic options against this highly morbid pathophysiological process. Upon review of the literature, we discovered that microvascular platelet aggregation and thrombosis occur after experimental SAH across multiple species and SAH induction techniques in a similar time frame to other components of DCI, occurring in the cerebral cortex and hippocampus across both hemispheres. We discuss the relationship of these findings to human autopsy studies. In the final section of this review, we highlight the important therapeutic options for targeting microvascular platelet aggregation and thrombosis, and emphasize why therapeutic targeting of this neurovascular pathology may improve patient care. We encourage ongoing research into the pathophysiology of SAH and DCI, especially in regard to microvascular platelet aggregation and thrombosis and the translation to randomized clinical trials.

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Predictors of Delayed Cerebral Ischemia in Patients with Aneurysmal Subarachnoid Hemorrhage with Asymptomatic Angiographic Vasospasm on Admission

Cited by 19 publications

References 22 publications

Vasospasm following aneurysmal subarachnoid hemorrhage: prediction, detection, and intervention

Vasospasm following aneurysmal subarachnoid hemorrhage: prediction, detection, and intervention

MicroR-146 protects against rat ischemia-reperfusion injury by targeting NF-κB-mediated PI3K/AKT/mTOR signaling pathway

Microvascular platelet aggregation and thrombosis after subarachnoid hemorrhage: A review and synthesis

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