ArticleEBioMedicine2019
Early blood-brain barrier dysfunction predicts neurological outcome following aneurysmal subarachnoid hemorrhage.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.
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Who cites it
50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 78 citations in OpenAlex.
- Prediction and Risk Assessment Models for Subarachnoid Hemorrhage: A Systematic Review on Case Studies.BioMed research international · 2022Pooled it
- Targeting High Mobility Group Box 1 in Subarachnoid Hemorrhage: A Systematic Review.International journal of molecular sciences · 2020Pooled it
- A narrative review of pathophysiology and therapeutic frontiers in early brain injury followed by aneurysm subarachnoid hemorrhage.Surgical neurology international · 2026Review
- Subarachnoid hemorrhage mediates human neocortical network, membrane potential, and action potential bursting via glutamate receptors.Communications biology · 2025Article
- Claudin proteins and hemorrhage severity in aneurysmal subarachnoid hemorrhage: Correlation with modified Fisher score but not functional outcome.Neurosurgical review · 2025Article
- Beyond the bleed: complications after aneurysmal subarachnoid hemorrhage. Pathophysiology, clinical implications, and management strategies: a review.Critical care (London, England) · 2025Review
- Restoring brain barriers: an innovative approach for treating neurological disorders.Fluids and barriers of the CNS · 2025Review
- Iron Hemostasis in Patients With Subarachnoid Hemorrhage and the Role of Early CSF Drainage.Neurology · 2025Review
- Relationship Between Systemic and Cerebral Microdialysate Glucose in Patients With Severe Acute Brain Injury-A Retrospective Study.Acta anaesthesiologica Scandinavica · 2025Observational
- Calcium/Calmodulin-Dependent Protein Kinase II β Regulates Autophagy Dependent Ferroptosis of Neurons after Cerebral Ischemic Injury by Activating the AREG/JUN/ELAVL1 Pathway.Neurochemical research · 2025Article
- Engineered endoplasmic reticulum-targeting nanodrugs with Piezo1 inhibition and promotion of cell uptake for subarachnoid hemorrhage inflammation repair.Journal of nanobiotechnology · 2025Article
- Modulation of the Immunological Milieu in Acute Aneurysmal Subarachnoid Hemorrhage: The Potential Role of Monocytes Through CXCL10 Secretion.Translational stroke research · 2025Article
- Pathophysiological mechanisms underlying early brain injury and delayed cerebral ischemia in the aftermath of aneurysmal subarachnoid hemorrhage: a comprehensive analysis.Frontiers in neurology · 2025Review
- NX210c drug candidate peptide strengthens mouse and human blood-brain barriers.Fluids and barriers of the CNS · 2024Article
- Activation of Piezo1 by intracranial hypertension induced neuronal apoptosis via activating hippo pathway.CNS neuroscience & therapeutics · 2024Article
- Early and delayed blood-brain barrier permeability predicts delayed cerebral ischemia and outcomes following aneurysmal subarachnoid hemorrhage.European radiology · 2024Article
- From spreading depolarization to blood-brain barrier dysfunction: navigating traumatic brain injury for novel diagnosis and therapy.Nature reviews. Neurology · 2024Review
- Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition.Acta biochimica et biophysica Sinica · 2024Article
- Subarachnoid hemorrhage-associated brain injury and neurobehavioral deficits are reversed with synthetic adropin treatment through sustained Ser1179 phosphorylation of endothelial nitric oxide synthase.Frontiers in stroke · 2024Article
- Narrative review of roles of astrocytes in subarachnoid hemorrhage.Annals of translational medicine · 2023Review
Corrections and comments
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Authors and funding
18 authors at 10 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDisease progression and delayed neurological complications are common after aneurysmal subarachnoid hemorrhage (aSAH). We explored the potential of quantitative blood-brain barrier (BBB) imaging to predict disease progression and neurological outcome.
methodsData were collected as part of the Co-Operative Studies of Brain Injury Depolarizations (COSBID). We analyzed retrospectively, blinded and semi-automatically magnetic resonance images from 124 aSAH patients scanned at 4 time points (24-48 h, 6-8 days, 12-15 days and 6-12 months) after the initial hemorrhage. Volume of brain with apparent pathology and/or BBB dysfunction (BBBD), subarachnoid space and lateral ventricles were measured. Neurological status on admission was assessed using the World Federation of Neurosurgical Societies and Rosen-Macdonald scores. Outcome at ≥6 months was assessed using the extended Glasgow outcome scale and disease course (progressive or non-progressive based on imaging-detected loss of normal brain tissue in consecutive scans). Logistic regression was used to define biomarkers that best predict outcomes. Receiver operating characteristic analysis was performed to assess accuracy of outcome prediction models.
findingsIn the present cohort, 63% of patients had progressive and 37% non-progressive disease course. Progressive course was associated with worse outcome at ≥6 months (sensitivity of 98% and specificity of 97%). Brain volume with BBBD was significantly larger in patients with progressive course already 24-48 h after admission (2.23 (1.23-3.17) folds, median with 95%CI), and persisted at all time points. The highest probability of a BBB-disrupted voxel to become pathological was found at a distance of ≤1 cm from the brain with apparent pathology (0·284 (0·122-0·594), p < 0·001, median with 95%CI). A multivariate logistic regression model revealed power for BBBD in combination with RMS at 24-48 h in predicting outcome (ROC area under the curve = 0·829, p < 0·001).
interpretationWe suggest that early identification of BBBD may serve as a key predictive biomarker for neurological outcome in aSAH. FUND: Dr. Dreier was supported by grants from the Deutsche Forschungsgemeinschaft (DFG) (DFG DR 323/5-1 and DFG DR 323/10-1), the Bundesministerium für Bildung und Forschung (BMBF) Center for Stroke Research Berlin 01 EO 0801 and FP7 no 602150 CENTER-TBI. Dr. Friedman was supported by grants from Israel Science Foundation and Canada Institute for Health Research (CIHR). Dr. Friedman was supported by grants from European Union's Seventh Framework Program (FP7/2007-2013; grant #602102).
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