Cerebral edema after ischemic stroke: Pathophysiology and underlying mechanisms

Gu, Yuhang; Zhou, Chen; Piao, Zhe; Hu, Yuan; Jiang, Huimin; Wei, Huimin; Zhou, Yifan; Guo, Nan; Ji, Xunming

doi:10.3389/fnins.2022.988283

Cited by 41 publications

(25 citation statements)

References 153 publications

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“…Their median age was 71 [IQR 62-79] years and 45% were females. Baseline NIHSS was median 14 [8][9][10][11][12][13][14][15][16][17][18]. Time from last-seen-well to arrival was median 170 [73-347] minutes.…”

Section: Resultsmentioning

confidence: 99%

Recanalization status and temporal evolution of early ischemic changes following stroke thrombectomy

Virtanen,

Tomppo,

Georgiopoulos

et al. 2023

European Stroke Journal

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Introduction: Present-day computer tomography (CT) scanners have excellent spatial resolution and signal-to-noise ratio and are instrumental detecting early ischemic changes (EIC) in brain. We assessed the temporal changes of EIC based on the recanalization status after thrombectomy. Patients and methods: The cohort comprises consecutive patients with acute ischemic stroke in anterior circulation treated with thrombectomy in tertiary referral hospital. All baseline and follow-up scans were screened for any ischemic changes and further classified using Alberta Stroke Program Early CT Score (ASPECTS). Generalized linear mixed models were used to analyze the impact of recanalization status using modified Thrombolysis in Cerebral Infarction (mTICI) on temporal evolution of ischemic changes. Results: We included 614 patients with ICA, M1, or M2 occlusions. Median ASPECTS score was 9 (IQR 7–10) at baseline and 7 (5-8) at approximately 24 h. mTICI 3 was achieved in 207 (33.8%), 2B 241 (39.3%), 2A in 77 (12.6%), and 0–1 in 88 (14.3%) patients. Compared to patients with mTICI 3, those with mTICI 0–1 and 2A had less favorable temporal changes of ASPECTS ( p < 0.001). Effect of recanalization was noted in the cortical regions of ICA/M1 patients, but not in their deep structures or patients with M2 occlusions. All ischemic changes detected at baseline were also present at all follow-up images, regardless of the recanalization status. Conclusions: Temporal evolution of the ischemic changes and ASPECTS are related to the success of the recanalization therapy in cortical regions of ICA/M1 patients, but not in their deep brain structures or M2 patients. In none of the patients did EIC revert in any brain region after successful recanalization.

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Section: Resultsmentioning

confidence: 99%

Recanalization status and temporal evolution of early ischemic changes following stroke thrombectomy

Virtanen,

Tomppo,

Georgiopoulos

et al. 2023

European Stroke Journal

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“…These pathophysiological processes in ict severe damage upon neurons, glia, and endothelial cells, leading to irreversible neuronal injury [1,22]. The severity of IS correlates with factors such as the size of cerebral infarction, cerebral edema, and hemorrhagic transformation, all of which are linked to unfavorable outcomes in AIS [23][24][25].…”

Section: Discussionmentioning

confidence: 99%

Predictive Value of ICU Patients' Mortality Based on Serum Ionized Ca Rather Than Total Ca in Acute Ischemic Stroke: Insights from MIMIC-IV Database Analysis

Wu,

Li,

et al. 2024

Preprint

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Background While serum Ca has proven to be a reliable predictor of mortality across various diseases, its connection with the clinical outcomes of ischemic stroke (IS) remains inconclusive. Our research aimed to explore the relationships between serum total Ca (tCa) and serum ionized Ca (iCa) and mortality among acute IS (AIS) patients. Methods We gathered data from 1773 AIS patients in the Medical Information Mart for Intensive Care Database IV, including baseline demographic data, comorbidities, vital signs, laboratory-based data, and scoring systems. Endpoints for the study encompassed 30-d, 90-d, and 365-d all-cause mortalities. Employing restricted cubic spline Cox regression, we explored potential nonlinear relationships between admission serum iCa and tCa levels and mortality. Participants were categorized into four groups based on serum iCa and tCa quartiles. Multivariable Cox regression analysis was then conducted to evaluate the independent association of iCa and tCa quartiles with all-cause mortality. Results The restricted cubic spline revealed a U-shaped association between iCa and 30-d and 90-d mortality (P < 0.05), while the relationship between iCa and 365-d mortality was linear (P < 0.05). After adjusting for confounders, multivariable Cox analysis demonstrated that the lowest serum iCa level quartile was independently associated with increased risks of 30-d, 90-d, and 365-d mortality. Similarly, the highest serum iCa level quartile was independently associated with increased risks of 30-d and 90-d mortality, but not 365-d mortality. Notably, serum tCa level showed no association with increased risks of 30-d, 90-d, and 365-d mortality. Conclusions Our findings suggest that serum iCa, rather than tCa, is linked to ischemic stroke prognosis. Both high and low serum iCa levels are associated with poor short-term prognosis, while only low serum iCa is associated with poor long-term prognosis in AIS patients.

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“…In certain situation, this effect can excessively increase the BBB permeability, allowing different molecules to permeate and subsequently undergo metabolic transformations in the brain tissue, with the formation of pathological deposits that can initiate degenerative processes and neuronal death. Simultaneously, ionic, osmotic and vasogenic cerebral edema can occur, which can also have a detrimental effect on the structure and function of the CNS [ 36 ]. nNOS may play a major role in BBB disruption [ 37 ].…”

Section: Introductionmentioning

confidence: 99%

“…It has been suggested that the burst of both eNOS and nNOS, following acute cerebral ischemia, mediates the increase in NO production. The consequence is the occurrence of vasogenic cerebral edema with brain tissue damage [ 36 ]. The production of NO occurs in two waves, the first of which is characterized by the transient increase in NO synthesis, and the second one by an increased synthesis of NO that lasts up to 4–7 days.…”

Section: Introductionmentioning

confidence: 99%

Nitric Oxide/Nitric Oxide Synthase System in the Pathogenesis of Neurodegenerative Disorders—An Overview

et al. 2023

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Nitric oxide, a ubiquitous molecule found throughout the natural world, is a key molecule implicated in many central and benefic molecular pathways and has a well-established role in the function of the central nervous system, as numerous studies have previously shown. Dysregulation of its metabolism, mainly the upregulation of nitric oxide production, has been proposed as a trigger and/or aggravator for many neurological affections. Increasing evidence supports the implication of this molecule in prevalent neurodegenerative diseases, such as Parkinson’s disease, Alzheimer’s disease, or amyotrophic lateral sclerosis. The mechanisms proposed for its neurotoxicity mainly center around the increased quantities of nitric oxide that are produced in the brain, their cause, and, most importantly, the pathological metabolic cascades created. These cascades lead to the formation of neuronal toxic substances that impair the neurons’ function and structure on multiple levels. The purpose of this review is to present the main causes of increased pathological production, as well as the most important pathophysiological mechanisms triggered by nitric oxide, mechanisms that could help explain a part of the complex picture of neurodegenerative diseases and help develop targeted therapies.

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Cerebral edema after ischemic stroke: Pathophysiology and underlying mechanisms

Cited by 41 publications

References 153 publications

Recanalization status and temporal evolution of early ischemic changes following stroke thrombectomy

Recanalization status and temporal evolution of early ischemic changes following stroke thrombectomy

Predictive Value of ICU Patients' Mortality Based on Serum Ionized Ca Rather Than Total Ca in Acute Ischemic Stroke: Insights from MIMIC-IV Database Analysis

Nitric Oxide/Nitric Oxide Synthase System in the Pathogenesis of Neurodegenerative Disorders—An Overview

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