Deferoxamine attenuates early brain injury after subarachnoid hemorrhage by inhibiting ferroptosis and preserving mitochondrial function and oxidative phosphorylation via Nrf2 signaling.

Ferroptosis mechanisms in early brain injury after subarachnoid hemorrhage.

Nimodipine and enoxaparin improve neurological outcomes and reduce cerebral edema by modulating glymphatic perivascular spaces in a rabbit model of subarachnoid hemorrhage.

Preadmission, admission, and post-discharge factors associated with impaired communication after hemorrhagic stroke.

We report the case of a 15-year-old male who died instantly after being struck in the right occipitoparietal region by an unconventional projectile-a "crystal ball"-during a public protest in Medellín, Colombia. The projectile was fired from a 37 or 40mm launcher modified with non-regulation ammunition. Autopsy findings, performed under the Minnesota Protocol, included cranial fracture, brain laceration, and subarachnoid hemorrhage. Although designed to be nonlethal, the improvised use of this kinetic ammunition converted it into a lethal weapon. This case highlights critical gaps in forensic analysis, legal oversight, and procedural protocols related to riot-control equipment and its misuse.

Ultrasensitive and multi-analyte detection of catecholamines in serum and cerebrospinal fluid using carboxyl-modified magnetic microspheres coupled with LC/MS.

Postpartum subarachnoid hemorrhage: A case report on the role of occupational therapy in parenting support and multidisciplinary collaboration

The prognosis for functional independence after aneurysmal subarachnoid hemorrhage (aSAH) relies largely on patients' initial clinical status, age, and extent of the bleeding. However, some patients have poor outcome despite initially being in good clinical condition. The aim of this study was to analyze factors related to unfavorable outcome in patients with good clinical grade (World Federation of Neurosurgical Societies I-III) immediately before aneurysm treatment. Prospectively gathered data of patients treated for aSAH in Sweden during the years 2014 to 2018 was analyzed. Preictal comorbidities, radiological findings, and aSAH-related and treatment-related adverse events (AEs) were analyzed using univariable and multivariable logistic regression. Outcome was assessed with Glasgow Outcome Scale Extended 1 year after the hemorrhage. One thousand thirty-seven patients were treated for aSAH, of whom 607 patients were in good clinical grade before aneurysm treatment. Clinical follow-up was obtained for 520 of these patients. At follow-up, 102 (20%) had an unfavorable outcome. Factors increasing the risk of unfavorable outcome in this subgroup were advanced age (odds ratio [OR] 1.05, 95% CI 1.03-1.07), hydrocephalus (OR 1.80, 95% CI 1.04-3.14), delayed ischemic neurological deficit (OR 3.43, 95% CI 1.96-6.00), and AEs during aneurysm occlusion (OR 2.38, 95% CI 1.30-4.38). Among patients with good clinical status (World Federation of Neurosurgical Societies I-III) before occlusion of the ruptured intracerebral aneurysm, 20% had unfavorable outcome after 1 year. Poor outcome was associated with age, complications resulting from the aSAH and AEs occurring during aneurysm occlusion.

Impact of time to endovascular securement on outcomes in aneurysmal subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) triggers robust neuroinflammatory responses that contribute to secondary brain injury, with microglia acting as central mediators; however, the upstream regulators governing microglial activation remain incompletely understood. To address this, we investigated the role of C-C chemokine receptor 5 (CCR5) using a murine endovascular perforation SAH model. Expression profiling revealed that CCR5 is rapidly upregulated after SAH, with prominent expression in microglia in the cortex and perilesional region. We then evaluated the therapeutic efficacy of pharmacological inhibition using the intranasal CCR5 antagonist maraviroc (MVC). MVC treatment successfully shifted microglia toward an anti-inflammatory phenotype and reduced pro-inflammatory cytokines. This inflammatory modulation attenuated brain edema, suppressed neuronal apoptosis, and significantly improved both early and long-term neurological outcomes. Furthermore, in vitro experiments confirmed that MVC reverses oxyhemoglobin-induced pro-inflammatory microglial polarization, indirectly protecting neurons from microglia-dependent injury. Collectively, these findings identify CCR5 as an important regulator of microglia-associated neuroinflammation after SAH and suggest that MVC exerts neuroprotection, at least in part, through modulation of the CCR5-related inflammatory microenvironment.

BackgroundInternational guidelines acknowledge the lack of subarachnoid hemorrhage (SAH) specific red blood cell transfusion thresholds. This study aimed to evaluate the efficacy and safety of red blood cell transfusion strategies in patients with SAH.MethodsWe systematically searched PubMed/MEDLINE, CENTRAL, EMBASE, and Google Scholar from inception to July 15, 2025. We included randomized controlled trials (RCTs) evaluating any transfusion strategy in SAH patients. Meta-analyses were conducted using random-effects models, and the certainty of evidence was assessed using the GRADE minimally contextualized approach. The protocol was registered in PROSPERO (CRD420251122925).ResultsThree RCTs comprising 966 participants were included. Two compared restrictive (hemoglobin threshold 7-8 g/dL) versus liberal (9-10 g/dL) transfusion strategies, and one compared a higher (≥11.5 g/dL) versus lower (≥10 g/dL) hemoglobin targets. A liberal transfusion strategy, compared with the restrictive approach, probably reduces unfavorable neurological outcomes (39.6% vs 45.5%; risk difference [RD]: -5 per 100; 95% CI: -10 to +1) and new cerebral ischemia (17.7% vs 22.9%; RD: -5 per 100; 95% CI: -11 to +2), while probably increasing hemoglobin levels (mean difference [MD]: +1.68 g/dL; 95% CI: +0.32 to +3.04), transfusion requirements (98.2% vs 37.7%; RD: +52 per 100; 95% CI: +24 to +92), and ICU length of stay (MD: +1.16 days; 95% CI: -0.11 to +2.42). It may also reduce the risk of cerebral vasospasm (30.0% vs 36.4%; RD: -5 per 100; 95% CI: -14 to +9), although the evidence is very uncertain. Evidence for higher versus lower hemoglobin targets (≥11.5 g/dL vs ≥10 g/dL) was very uncertain across all outcomes.ConclusionCompared with a restrictive strategy, a liberal transfusion approach in patients with SAH probably improves neurological outcomes and reduces cerebral ischemia. Evidence for higher hemoglobin targets remains very uncertain, underscoring the need for larger, high-quality trials to refine optimal transfusion thresholds.

Although several studies have examined the associations between apoptosis-related factors or growth factors and cardiovascular diseases, evidence on their prospective association with hemorrhagic stroke remains limited. We conducted a nested case-control study within the large cohort of the Circulatory Risk in Communities Study in Japan. A total of 98 cases (60 intracerebral hemorrhage and 38 subarachnoid hemorrhage; 34 men and 64 women, aged 35 to 83 years at baseline) were included, along with 196 controls matched by age, sex, community, and year of sample collection. We measured serum levels of the soluble form of Fas and insulin-like growth factor-I among cases and controls. The odds ratios of total hemorrhagic stroke and its subtypes were calculated using conditional logistic regression analyses. The median follow-up period from baseline to onset was 7.0 years. The multivariable odds ratios (95% confidence intervals) of total hemorrhagic stroke associated with a 1-standard deviation increment of soluble Fas (2.3 ng/mL) and insulin-like growth factor-I (40.5 ng/mL) were 0.93 (0.66-1.32) and 0.61 (0.41-0.89), respectively. The inverse association with insulin-like growth factor-I levels was similar for subarachnoid hemorrhage and intracerebral hemorrhage: the respective multivariable odds ratios were 0.53 (0.28-0.98) and 0.62 (0.37-1.04). The present study identified an inverse association between insulin-like growth factor-I levels and the risk of hemorrhagic stroke.

Intracranial aneurysm (IA) is a common cerebral vascular malformation often leading to subarachnoid hemorrhage (SAH) with high mortality and disability rates. The molecular mechanisms underlying IA occurrence and rupture are poorly understood, highlighting the need for predictive molecular markers. Here, we employed bioinformatics and Mendelian randomization analysis to identify MICA and CYTH4 as molecular markers closely associated with arterial aneurysm rupture, offering new insights for IA prevention and treatment. We integrated five datasets (GSE15629, GSE26969, GSE54083, GSE13353, and GSE122897) to create a research cohort of 34 non-IA and 93 IA samples. Differential gene expression analysis was performed using single-cell sequencing data from IA mice, followed by KEGG enrichment analysis. Mendelian randomization analysis was conducted on two samples to determine the causal relationship between gene expression and IA risk. Receiver operating characteristic (ROC) and decision curve analysis (DCA) curves were constructed. We further conducted GSEA, immune microenvironment analysis, cell trajectory analysis, and intercellular communication research on single-cell data. Molecular biology experiments have confirmed that altered expression of MICA and CYTH4 can effectively regulate the proliferation of endothelial cells and their apoptosis under stress conditions. We identified 297 downregulated and 295 upregulated DEGs between IA and control groups. KEGG enrichment analysis implicated cytokines, NF-κB signaling, and TNF signaling in promoting IA onset, while cAMP signaling may inhibit it. Mendelian randomization analysis revealed MICA and CYTH4 as key genes related to IA prognosis, with CYTH4 as a risk factor, and MICA potentially protective. GSEA and GeneMANIA enrichment analysis indicated roles for CYTH4 and MICA in immune regulation of IA. Single-cell sequencing data linked CYTH4 to neutrophil degranulation during macrophage differentiation, with CellChat showing correlation between CYTH4 and CCL signaling. This study highlights MICA and CYTH4 as significant biomarkers for IA progression, particularly CYTH4's role in immune inflammatory response and prognosis. These findings contribute to understanding IA pathogenesis and advancing its diagnosis and treatment.

Mechanical thrombectomy (MT) is the standard of care for acute ischemic stroke due to large vessel occlusion. In Ecuador, no previous national data on MT outcomes have been reported, and, to our knowledge, there are no published series performed at high altitude. This was a retrospective, observational, descriptive study based on consecutive patients treated within a multicenter mechanical thrombectomy program in Quito, Ecuador, located at an altitude of ≈2,800 meters above sea level. Thirty-two patients treated between October 2023 and November 2024 were included. Baseline characteristics, procedural details, and 90-day functional outcomes were analyzed. The median age was 64 years [IQR 54-72], and the mean baseline NIHSS score was 18, decreasing to 7 at discharge. The median ASPECTS was 7. Intravenous thrombolysis was administered in 59.4% of patients, and general anesthesia was used in 84.4% of procedures. Successful reperfusion (TICI 2b-3) was achieved in 90.6% of patients, with complete reperfusion (TICI 3) in 62.5%. Neurological complications occurred in 9.4% (all asymptomatic subarachnoid hemorrhages), and 18.8% of patients required decompressive craniectomy (DC). At 90 days, 53.1% achieved functional independence (mRS 0-2). MT at high altitude (≈2,800m) in Ecuador is feasible, safe, and achieves outcomes comparable to international standards. Our study, the first multicenter experience of its kind in Ecuador, highlights a unique physiological risk for patients at this altitude: an elevated risk of cardiac pathologies as etiological factor, and increases susceptibility to severe cerebral edema requiring DC.

Post-stroke complications pose significant challenges in the management of stroke patients and are associated with adverse outcomes. The potential interplay and temporal sequence of stroke-associated pneumonia (SAP) and deep vein thrombosis (DVT) following stroke remain unclear. This study aimed to investigate the association between SAP and DVT and to elucidate temporal sequence of these complications after acute ischemic stroke (AIS), intracerebral hemorrhage (ICH), and subarachnoid hemorrhage (SAH). We conducted a study using the in-hospital Medical Complications after Acute Stroke (iMCAS) registry at Beijing Tiantan Hospital from 2014 to 2016. We documented the incidence of SAP and DVT and the time from stroke onset to diagnosis of each complication. A time-dependent Cox regression model was used to evaluate the association between SAP and DVT and the temporal sequence was compared across AIS, ICH, and SAH. A total of 1771 patients were included, comprising 1129 with AIS, 314 with ICH, and 328 with SAH. The incidence of SAP was higher than that of DVT in AIS (7.6% vs 1.9%), ICH (18.8% vs 5.7%) and SAH (16.8% vs 7.9%). SAP occurrence was significantly associated with subsequent DVT development (HR = 3.65, 95% CI: 2.08-6.40, P < 0.001). This association was also confirmed in AIS and ICH. The median time from stroke onset to SAP was 4 days (IQR: 2-6), and to DVT was 8 days (IQR: 5-12). SAP occurred significantly earlier than DVT in all stroke subtypes. SAP was significantly associated with an increased risk of subsequent DVT, with a consistent temporal sequence in which SAP preceded DVT.

Obesity, body adiposity, and intracranial aneurysms: A narrative review of clinical evidence beyond body mass index.

Differential impact of treatment timing on clinical outcomes after endovascular management of ruptured intracranial aneurysms across circulation locations.

Aneurysmal subarachnoid hemorrhage remains a devastating condition with persistently high rates of early mortality and disability. While numerous prognostic models exist, the prognostic relevance of metabolic dysfunction in aneurysmal subarachnoid hemorrhage remains uncertain. We retrospectively analyzed 60 consecutive patients with subarachnoid hemorrhage admitted between 2022 and 2024. Metabolic syndrome and its components-including impaired glucose tolerance, insulin resistance, hypertension, dyslipidemia, and obesity-were evaluated within 24 hours of admission. The primary endpoint was poor functional outcome at discharge (modified Rankin Scale 3-6). Secondary endpoints included in-hospital complications and mortality. In adjusted ridge-penalized logistic regression analyses, impaired glucose tolerance (adjusted odds ratio 4.93, 95% confidence interval 1.39-17.4, p = 0.014) and World Federation of Neurological Surgeons grade ≥3 (adjusted odds ratio 5.12, 95% confidence interval 1.62-16.18, p = 0.006) independently predicted poor outcome. Insulin resistance was independently associated with in-hospital complications (adjusted odds ratio 4.05, 95% confidence interval 1.15-14.3, p = 0.030). Mortality was independently predicted by age (adjusted odds ratio 1.06, 95% confidence interval 1.01-1.12, p = 0.032), World Federation of Neurological Surgeons grade ≥3, and impaired glucose tolerance. The composite metabolic syndrome variable was not an independent predictor of any outcome. In conclusion, specific metabolic abnormalities- impaired glucose tolerance, insulin resistance, and hypertension-rather than metabolic syndrome appear to drive early prognosis after subarachnoid hemorrhage. Early metabolic profiling and individualized glucose control may help identify patients at risk and guide future interventional studies.

Intracranial hypertension is a life-threatening complication of acute brain injuries such as traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), or intracerebral hemorrhage (ICH). In low-income and middle-income countries (LMICs), limited resources can delay timely neurocritical interventions. Smartphone-based quantitative pupillometry offers a scalable solution for early detection of elevated intracranial pressure (ICP). Here, we assessed its ability to (1) detect raised optic nerve sheath diameter (ONSD), a noninvasive surrogate for elevated ICP, and (2) classify severe TBI. Thirty-eight Nepali ICU patients with TBI (n=16), SAH (n=10), or ICH (n=12) underwent daily sonographic ONSD and pupillary light reflex (PLR) assessments through the PupilScreen app (Apertur Inc., Seattle, WA) over 7 days. Machine learning classifiers were trained on PLR features to detect elevated ONSD (>6.0mm). To identify severe TBI (Glasgow Coma Scale [GCS] ≤8 on admission), classifiers were trained on PLR features, ONSD, or both. For ONSD >6.0mm, a random forest model achieved an AUC of 0.66, with a sensitivity of 0.31 and specificity of 0.80. For identifying severe TBI, the optimal classifier was a random forest model incorporating ONSD and a subset of PLR metrics, with a sensitivity of 0.93, specificity of 1.00, and AUC of 0.96. In this pilot study, smartphone-based pupillometry showed modest ability for detecting elevated ONSD. However, its high performance in severe TBI classification warrants further evaluation. Larger, multicenter studies evaluating triage utility in prehospital and resource-limited settings are warranted to validate and extend these findings.

Visualizing Non-linear Prognosis: A Vital Tool for Shared Decision-making in Aneurysmal Subarachnoid Hemorrhage.