ArticleNeurocritical care2020
TNF-R1 Correlates with Cerebral Perfusion and Acute Ischemia Following Subarachnoid Hemorrhage.
Article in Neurocritical care, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Causal Relationships Between Gut Microbiota, Inflammatory Cells/Proteins, and Subarachnoid Hemorrhage: A Multi-omics Bidirectional Mendelian Randomization Study and Meta-analysis.Molecular neurobiology · 2024Pooled it
- Auricular vagus nerve stimulation for mitigation of inflammation and vasospasm in subarachnoid hemorrhage: a single-institution randomized controlled trial.Journal of neurosurgery · 2025Trial
- Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage.Neural regeneration research · 2024Review
- Interleukin-4 Modulates Neuroinflammation by Inducing Phenotypic Transformation of Microglia Following Subarachnoid Hemorrhage.Inflammation · 2024Article
- Article
- Intracranial Venous Alteration in Patients With Aneurysmal Subarachnoid Hemorrhage: Protocol for the Prospective and Observational SAH Multicenter Study (SMS).Frontiers in surgery · 2022Article
- Investigation of molecular regulation mechanism under the pathophysiology of subarachnoid hemorrhage.Open life sciences · 2021Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEarly cerebral hypoperfusion and ischemia occur after subarachnoid hemorrhage (SAH) and influence clinical prognosis. Pathophysiological mechanisms possibly involve inflammatory mediators. TNF-α has been associated with complications and prognosis after SAH. We investigated the relation of perfusion parameters and ischemic lesions, with levels of TNF-α main receptor, TNF-R1, after SAH, and their association with prognosis.
methodsWe included consecutive SAH patients admitted within the first 72 h of SAH onset. Blood samples were simultaneously collected from a peripheral vein and from the parent artery of the aneurysm. Levels of TNF-R1 were measured using ELISA (R&D Systems Inc., USA). CT perfusion and MRI studies were performed in the first 72 h. Correlation and logistic regression analysis were used to identify outcome predictors.
resultsWe analyzed 41 patients. Increased levels of TNF-R1 correlated with increased T
conclusionIncreased levels of TNF-R1 in arterial and venous blood correlate with worse cerebral perfusion and with increased burden of acute ischemic lesions in the first 72 h after SAH. Venous levels of TNF-R1 and DWI lesions were associated with poor outcome at 6 months. These results highlight the pathophysiological role of TNF-α pathways in SAH and suggest a possible role of combined imaging and laboratorial markers in determining prognosis in acute SAH.
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