Perihematomal Edema After Intracerebral Hemorrhage: An Update on Pathogenesis, Risk Factors, and Therapeutic Advances

Chen, Yi-Hao; Chen, Shengpan; Chang, Jinyuan; Wei, Junji; Feng, Ming; Wang, Renzhi

doi:10.3389/fimmu.2021.740632

Cited by 64 publications

(65 citation statements)

References 132 publications

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“…Thrombin activation after ICH implies the vasculogenic edema formation associated with the destruction of endothelial cells and the BBB ( Wilkinson et al, 2018 ). Perihematomal edema (PHE), associated with a worse prognosis, has been recognized as an evident marker of SBI after ICH and a likely therapeutic pathophysiological target for attenuating SBI ( Brouwers and Greenberg, 2013 ; Bautista et al, 2021 ; Chen et al, 2021 ). Furthermore, it was displayed that intracranial hematoma expands to further and adjacent brain tissues through perivascular spaces, white matter tracts, and their perineurium ( Yin et al, 2013 ; Fu et al, 2021 ), particularly if ICH is combined with an intraventricular hemorrhage ( Bosche et al, 2020 ).…”

Section: Pathological Changes After Intracerebral Hemorrhagementioning

confidence: 99%

Mesenchymal Stem Cell Application and Its Therapeutic Mechanisms in Intracerebral Hemorrhage

Yang

Fan

Mazhar

et al. 2022

Front. Cell. Neurosci.

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Intracerebral hemorrhage (ICH), a common lethal subtype of stroke accounting for nearly 10–15% of the total stroke disease and affecting two million people worldwide, has a high mortality and disability rate and, thus, a major socioeconomic burden. However, there is no effective treatment available currently. The role of mesenchymal stem cells (MSCs) in regenerative medicine is well known owing to the simplicity of acquisition from various sources, low immunogenicity, adaptation to the autogenic and allogeneic systems, immunomodulation, self-recovery by secreting extracellular vesicles (EVs), regenerative repair, and antioxidative stress. MSC therapy provides an increasingly attractive therapeutic approach for ICH. Recently, the functions of MSCs such as neuroprotection, anti-inflammation, and improvement in synaptic plasticity have been widely researched in human and rodent models of ICH. MSC transplantation has been proven to improve ICH-induced injury, including the damage of nerve cells and oligodendrocytes, the activation of microglia and astrocytes, and the destruction of blood vessels. The improvement and recovery of neurological functions in rodent ICH models were demonstrated via the mechanisms such as neurogenesis, angiogenesis, anti-inflammation, anti-apoptosis, and synaptic plasticity. Here, we discuss the pathological mechanisms following ICH and the therapeutic mechanisms of MSC-based therapy to unravel new cues for future therapeutic strategies. Furthermore, some potential strategies for enhancing the therapeutic function of MSC transplantation have also been suggested.

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Section: Pathological Changes After Intracerebral Hemorrhagementioning

confidence: 99%

Mesenchymal Stem Cell Application and Its Therapeutic Mechanisms in Intracerebral Hemorrhage

Yang

Fan

Mazhar

et al. 2022

Front. Cell. Neurosci.

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“…The mechanisms underlying PHE formation differ across the various stages. Changes in PHE (<6 h) are mainly mediated by blood clot retraction and serum protein accumulation in surrounding parenchymatous tissues ( Ironside et al, 2019 ; Chen et al, 2021 ). We observed between-group differences in the PHE volume; however, it showed no statistical significance in the logistic regression model.…”

Section: Discussionmentioning

confidence: 99%

Development and Validation of a Clinical-Based Signature to Predict the 90-Day Functional Outcome for Spontaneous Intracerebral Hemorrhage

Huang

Wang

Zhang

et al. 2022

Front. Aging Neurosci.

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We aimed to develop and validate an objective and easy-to-use model for identifying patients with spontaneous intracerebral hemorrhage (ICH) who have a poor 90-day prognosis. This three-center retrospective study included a large cohort of 1,122 patients with ICH who presented within 6 h of symptom onset [training cohort, n = 835; internal validation cohort, n = 201; external validation cohort (center 2 and 3), n = 86]. We collected the patients’ baseline clinical, radiological, and laboratory data as well as the 90-day functional outcomes. Independent risk factors for prognosis were identified through univariate analysis and multivariate logistic regression analysis. A nomogram was developed to visualize the model results while a calibration curve was used to verify whether the predictive performance was satisfactorily consistent with the ideal curve. Finally, we used decision curves to assess the clinical utility of the model. At 90 days, 714 (63.6%) patients had a poor prognosis. Factors associated with prognosis included age, midline shift, intraventricular hemorrhage (IVH), subarachnoid hemorrhage (SAH), hypodensities, ICH volume, perihematomal edema (PHE) volume, temperature, systolic blood pressure, Glasgow Coma Scale (GCS) score, white blood cell (WBC), neutrophil, and neutrophil-lymphocyte ratio (NLR) (p < 0.05). Moreover, age, ICH volume, and GCS were identified as independent risk factors for prognosis. For identifying patients with poor prognosis, the model showed an area under the receiver operating characteristic curve of 0.874, 0.822, and 0.868 in the training cohort, internal validation, and external validation cohorts, respectively. The calibration curve revealed that the nomogram showed satisfactory calibration in the training and validation cohorts. Decision curve analysis showed the clinical utility of the nomogram. Taken together, the nomogram developed in this study could facilitate the individualized outcome prediction in patients with ICH.

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“…The PHE expansion has been considered a novel neuroimaging marker of poor prognosis, and a recent study reviewed the impact of PHE on ICH prognosis ( 25 ). The pre-clinical research on magnetic resonance spectroscopy revealed that the recovery of N-acetylaspartate, choline, and creatine was faster in the PHE area than in the non-PHE area ( 31 ), suggesting that the PHE may provide a protective buffer against irreversible impairment.…”

Section: Discussionmentioning

confidence: 99%

“…In clinical practice, delayed PHE expansion is usually required to be identified for a patient who represents the unexpected appearance of intracranial hypertension in the recovery phase of ICH, and therapy targeted for PHE induced intracranial hypertension is needed. However, studies exclusively focusing on delayed perihematomal edema expansion (DPE) are to date very sparse as research on long course PHE is present with limitations and challenges: 1) there have not yet been any methods measuring the volume of PHE [manual/semiautomatic ( 21 , 22 )/automatic approach ( 23 , 24 )] being considered to be convenient and reliable, which limits obtaining the data of PHE volume from a large sample size; 2) growth course for PHE is long and variable among individuals ( 25 ); 3) currently no consensus exists regarding the definition of DPE. Peng et al.…”

Section: Introductionmentioning

confidence: 99%

Defining Delayed Perihematomal Edema Expansion in Intracerebral Hemorrhage: Segmentation, Time Course, Risk Factors and Clinical Outcome

et al. 2022

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We attempt to generate a definition of delayed perihematomal edema expansion (DPE) and analyze its time course, risk factors, and clinical outcomes. A multi-cohort data was derived from the Chinese Intracranial Hemorrhage Image Database (CICHID). A non-contrast computed tomography (NCCT) -based deep learning model was constructed for fully automated segmentation hematoma and perihematomal edema (PHE). Time course of hematoma and PHE evolution correlated to initial hematoma volume was volumetrically assessed. Predictive values for DPE were calculated through receiver operating characteristic curve analysis and were tested in an independent cohort. Logistic regression analysis was utilized to identify risk factors for DPE formation and poor outcomes. The test cohort’s Dice scores of lesion segmentation were 0.877 and 0.642 for hematoma and PHE, respectively. Overall, 1201 patients were enrolled for time-course analysis of ICH evolution. A total of 312 patients were further selected for DPE analysis. Time course analysis showed the growth peak of PHE approximately concentrates in 14 days after onset. The best cutoff for DPE to predict poor outcome was 3.34 mL of absolute PHE expansion from 4-7 days to 8-14 days (AUC=0.784, sensitivity=72.2%, specificity=81.2%), and 3.78 mL of absolute PHE expansion from 8-14 days to 15-21 days (AUC=0.682, sensitivity=59.3%, specificity=92.1%) in the derivation sample. Patients with DPE was associated with worse outcome (OR: 12.340, 95%CI: 6.378-23.873, P<0.01), and the larger initial hematoma volume (OR: 1.021, 95%CI: 1.000-1.043, P=0.049) was the significant risk factor for DPE formation. This study constructed a well-performance deep learning model for automatic segmentations of hematoma and PHE. A new definition of DPE was generated and is confirmed to be related to poor outcomes in ICH. Patients with larger initial hematoma volume have a higher risk of developing DPE formation.

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Perihematomal Edema After Intracerebral Hemorrhage: An Update on Pathogenesis, Risk Factors, and Therapeutic Advances

Cited by 64 publications

References 132 publications

Mesenchymal Stem Cell Application and Its Therapeutic Mechanisms in Intracerebral Hemorrhage

Mesenchymal Stem Cell Application and Its Therapeutic Mechanisms in Intracerebral Hemorrhage

Development and Validation of a Clinical-Based Signature to Predict the 90-Day Functional Outcome for Spontaneous Intracerebral Hemorrhage

Defining Delayed Perihematomal Edema Expansion in Intracerebral Hemorrhage: Segmentation, Time Course, Risk Factors and Clinical Outcome

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