ArticleJournal of neuroinflammation2024
Cerebrospinal fluid markers of neuroinflammation and coagulation in severe cerebral edema and chronic hydrocephalus after subarachnoid hemorrhage: a prospective study.
Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Risk factors for the development of hydrocephalus in traumatic brain injury: a systematic review and meta-analysis.Neurosurgical review · 2025Pooled it
- Downregulation of Lgals3 Alleviates Inflammatory Response and Apoptosis in a Mouse Model of Cerebral Ischemia/Reperfusion Injury.Brain and behavior · 2026Article
- Impaired Glymphatic-Meningeal Lymphatic Function in Patients with Spontaneous Subarachnoid Hemorrhage.Translational stroke research · 2026Article
- Brain Lymphatic Dysfunction in Subarachnoid Hemorrhage: Pathophysiology and Clinical Implications.Biomolecules · 2026Review
- Longitudinal in vivo imaging of dynamic immune-vascular responses to meningeal cerebrovascular injury.Journal of neuroinflammation · 2026Article
- Inflammation in Idiopathic Intracranial Hypertension: An Immunometabolic Mechanistic Framework and Clinical Implications.CNS neuroscience & therapeutics · 2026Review
- A Bedside Coagulation-Platelet Tipping Point for Mortality in Nontraumatic Subarachnoid Hemorrhage.Journal of multidisciplinary healthcare · 2026Article
- The role of glymphatic system in brain injury after subarachnoid hemorrhage.Frontiers in immunology · 2026Review
- Article
- The neurobiological regulatory mechanism of brain edema.Frontiers in cellular neuroscience · 2026Review
- Elevated ApoC3 levels in cerebrospinal fluid predict poor outcomes in patients with aneurysmal subarachnoid hemorrhage.Experimental biology and medicine (Maywood, N.J.) · 2026Article
- Characterizing CSF inflammatory proteomics in pediatric post-hemorrhagic hydrocephalus and Anti-NMDAR encephalitis.Journal of neuroinflammation · 2025Article
- Live longitudinal imaging of meningeal cerebrovascular injury and its sequelae in adult zebrafish.bioRxiv : the preprint server for biology · 2025Article
- Review
- Role of serum magnesium in post-aneurysmal subarachnoid hemorrhagic hydrocephalus.Acute and critical care · 2025Article
- Mendelian randomization suggests a causal relationship between cerebrospinal fluid metabolites and intracranial aneurysms.Neurosurgical review · 2025Article
- Prediction of functional outcomes in aneurysmal subarachnoid hemorrhage using pre-/postoperative noncontrast CT within 3 days of admission.NPJ digital medicine · 2025Article
- Association between international normalized ratio-to-albumin ratio and mortality in critically ill patients with gastrointestinal bleeding: a retrospective MIMIC-IV database study.BMC gastroenterology · 2025Article
- Spatiotemporal dynamic changes of meningeal microenvironment influence meningeal lymphatic function following subarachnoid hemorrhage: from inflammatory response to tissue remodeling.Journal of neuroinflammation · 2025Article
- SIRPα modulates microglial efferocytosis and neuroinflammation following experimental subarachnoid hemorrhage via the SHP1/STAT6 axis.Journal of neuroinflammation · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
backgroundEarly severe cerebral edema and chronic hydrocephalus are the primary cause of poor prognosis in patients with subarachnoid hemorrhage (SAH). This study investigated the role of cerebrospinal fluid (CSF) inflammatory cytokines and coagulation factors in the development of severe cerebral edema and chronic hydrocephalus in patients with SAH.
methodsPatients with SAH enrolled in this study were categorized into mild and severe cerebral edema groups based on the Subarachnoid Hemorrhage Early Brain Edema Score at admission. During long-term follow-up, patients were further classified into hydrocephalus and non-hydrocephalus groups. CSF samples were collected within 48 h post-SAH, and levels of inflammatory cytokines and coagulation factors were measured. Univariate and multivariate logistic regression analyses were performed to identify independent factors associated with severe cerebral edema and chronic hydrocephalus. The correlation between inflammatory cytokines and coagulation factors was further investigated and validated in a mouse model of SAH.
resultsSeventy-two patients were enrolled in the study. Factors from the extrinsic coagulation pathway and inflammatory cytokines were associated with both severe cerebral edema and chronic hydrocephalus. Coagulation products thrombin-antithrombin complexes (TAT) and fibrin, as well as inflammatory cytokines IL-1β, IL-2, IL-5, IL-7, and IL-4, were independently associated with severe cerebral edema. Additionally, Factor VII, fibrin, IL-2, IL-5, IL-12, TNF-α, and CCL-4 were independently associated with chronic hydrocephalus. A positive correlation between extrinsic coagulation factors and inflammatory cytokines was observed. In the SAH mouse model, tissue plasminogen activator was shown to alleviate neuroinflammation and cerebral edema, potentially by restoring glymphatic-meningeal lymphatic function.
conclusionsElevated levels of inflammatory cytokines and extrinsic coagulation pathway factors in the CSF are associated with the development of early severe cerebral edema and chronic hydrocephalus following SAH. These factors are interrelated and may contribute to post-SAH glymphatic-meningeal lymphatic dysfunction.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.