Subarachnoid Hemorrhage Patients Research Articles

Impact of Frailty Risk on Functional Outcome after Aneurysmal Subarachnoid Hemorrhage: A Historical Cohort Study.

We evaluated the utility of the Hospital Frailty Risk Score (HFRS) as a predictor of adverse events post-hospitalization in a retrospective analysis of patients undergoing neurosurgical procedures due to aneurysmal subarachnoid hemorrhage (SAH). This historical cohort study analyzed the data of patients hospitalized with aneurysmal SAH (n = 1,343) between April 2014 and August 2020 who were registered in the JMDC database. We used HFRS to classify the patients into the low-frailty risk group (HFRS < 5) and high-frailty risk group (HFRS ≥ 5). The primary outcome was a modified Rankin Scale (mRS) score of 0-2 points at discharge. Of 1,343 patients, 1,001 (74.5%) and 342 (25.5%) were in the low- and high-frailty risk groups, respectively. A high-frailty risk was negatively associated with a mRS score of 0-2 at discharge (high-frailty risk group: odds ratio 0.4; 95% confidence interval [CI]: 0.3-0.6) and home discharge (high-frailty risk group: odds ratio 0.5; 95% CI: 0.4-0.7). A high-frailty risk was negatively associated with Barthel Index gain (high-frailty risk group: coefficient -10.4, 95% CI: -14.7 to -6.2) and had a longer length of stay (high-frailty risk group: coefficient 8.4, 95% CI: 5.1-11.7). HFRS could predict adverse outcomes during hospitalization of aneurysmal SAH patients.

Complement Molecule C3a Exacerbates Early Brain Injury After Subarachnoid Hemorrhage by Inducing Neuroinflammation Through the C3aR-ERK-P2X7-NLRP3 Inflammasome Signaling Axis.

An important aspect of the pathophysiology of early brain damage (EBI) after subarachnoid hemorrhage (SAH) is inflammasome-mediated neuroinflammation. It has been demonstrated that C3aR activation exacerbates neuronal damage in a number of neurological disorders. This study aims to explore the role of C3a in activating the NLRP3 inflammasome and exacerbating neuroinflammation after SAH. Preprocessing of RNA-seq transcriptome datasets using bioinformatics analysis, and screening of differentially expressed genes between SAH patients and healthy individuals from the GEO database. Internal carotid artery puncture was performed to establish SAH models in rats and mice. SAH grading, neurological scoring, brain water content, behavioral analysis, and assessments using ELISA, Western blot, immunofluorescence, and immunohistochemistry were conducted. An in vitro model of SAH was induced in BV-2 cells treated with heme (200μM). The mechanism of C3a in post-SAH neuroinflammation was studied by interfering with and inhibiting C3aR. Results showed that the expression of C3aR was upregulated in the GEO dataset (serum of SAH patients) and identified as a key differential gene in SAH. Further, elevated levels of C3a were found in the cerebrospinal fluid of clinically collected SAH patients. In the cerebral cortex and/or serum of SAH rats, expression of C3a, IL-1β, IL-6, TNF-α, CD11b, and Ki67 were significantly increased, while IL-10 was significantly decreased. Correlation analysis revealed that C3a showed negative correlation with IL-10 and positive correlation with IL-1β, IL-6, TNF-α, CD11b, and Ki67. After stimulation with heme, protein levels of C3a increased in BV-2 cells. Interfering with C3aR significantly reduced LDH release, IL-1β secretion, Caspase1 activation, levels of NLRP3 expression and ASC oligomerization, and ATP release after heme stimulation in BV-2. Subsequently, the addition of inhibitors of ERK1/2 phosphorylation demonstrated that C3a promotes ATP efflux by activating ERK1/2 phosphorylation, thereby activating P2X7. Further addition of JNJ-55308942 (a P2X7R antagonist) revealed that C3a activated the NLRP3 inflammasome via P2X7. Finally, administering SB290157 (a C3aR inhibitor) in vivo effectively alleviated brain edema, reduced mortality, improved Garcia score, ameliorated motor dysfunction, and suppressed inflammation and NLRP3 inflammasome activation in mice after SAH. Overall, C3a exacerbates EBI-associated NLRP3 inflammasome and neuroinflammation via the C3aR-ERK-P2X7 pathway after SAH. Inhibiting C3aR may serve as a one possible treatment approach to alleviate SAH after EBI.

Uncovering SPP1+ Macrophage, Neutrophils and Their Related Diagnostic Biomarkers in Intracranial Aneurysm and Subarachnoid Hemorrhage.

Intracranial aneurysms (IA) frequently cause subarachnoid hemorrhage (SAH) and have poor prognosis. However, the molecular mechanisms and diagnostic biomarkers associated with IA and ruptured IA (rIA) remain poorly understood. In this study, single-cell and transcriptome datasets were obtained from the GEO database. The cell populations were annotated to identify potential pathogenic subpopulations, followed by intercellular communication, pseudotime, and SCENIC analyses. Proteome-wide and transcriptome-wide Mendelian randomization (MR) analyses were conducted to identify risk factors for IA and SAH. The major pathological changes and diagnostic biomarkers of IA and SAH were identified based on the transcriptome datasets. A clinical cohort was established to identify the diagnostic biomarkers and validate the results. Macrophages and neutrophils were predominantly increased in IA and rIA tissues, and neutrophils were markedly upregulated in the blood of SAH patients. SPP1+ Macrophage was progressively elevated in aneurysms, promoting vascular smooth muscle cell (VSMC) phenotypic transformation and collagen matrix remodeling through the SPP1 and TGF-β pathways. Furthermore, HIF1α regulon was enriched in SPP1+ Macrophage, mediating inflammation and metabolic reprogramming, which contributed to IA progression. Integrated MR analysis identified CD36 as a risk factor for both IA and SAH, and it has been recognized as an effective blood biomarker for SAH. Neutrophils and their related indicators have emerged as excellent biomarkers of SAH in clinical cohorts. This study highlighted the detrimental role of SPP1+ Macrophage in IA and SAH using single-cell sequencing and MR analyses. CD36 was identified as a risk factor for IA and SAH and was also an efficient blood biomarker for SAH. In a clinical cohort, neutrophils and related indicators were valuable for the early diagnosis of SAH.

Evaluation of revised UK-NEQAS CSF-xanthochromia method for subarachnoid hemorrhage: outcome data provide evidence for clinical value.

Subarachnoid haemorrhage (SAH) has a high morbidity and mortality and requires prompt diagnosis. In patients with negative findings on computed-tomogram of the brain (CT-Brain) cerebrospinal fluid (CSF)-xanthochromia is considered the test of choice if performed 12 h or more after symptom onset. We audited the accuracy, usefulness and timing of CSF-xanthochromia testing and the interpretation of equivocal CSF-xanthochromia findings. We also investigated mortality outcomes for defined subsets of patients. A retrospective audit of CSF-xanthochromia tests over 8 years was performed. The service uses the revised UK-NEQAS (United Kingdom National External Quality Assessment Service) method. We analysed 543 cases (F=299, median age 44yrs) with 19 cases (3.5 %) having SAH. Sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of CSF-xanthochromia testing were 100 , 98.1, 65.9, 100 % respectively (equivocal results were counted as positives). 280 cases (F=153, median age 43yrs) had LP performed more than 24 h after the onset of headache (median time to LP=72 h). The sensitivity and specificity of the CSF-xanthochromia were 100 and 97.4 % in this group with NPV 100 % and PPV 66.6 %. 183 (65.4 %) CSF- xanthochromia negative cases in this subgroup had follow up data and survived without SAH occurring in the 12months follow up. In this study, supported by follow up outcome data, we show that CSF-xanthochromia testing using the revised UK-NEQAS method is fit-for-purpose for the use as a second line test to exclude SAH in patients with negative CT-brain including delayed presentation more than 24 h after headache onset.

Prevention of deep vein thrombosis in patients with aneurysmal subarachnoid hemorrhage: a best practice implementation project

IntroductionDeep vein thrombosis (DVT) is a common complication observed in aneurysmal subarachnoid hemorrhage (aSAH) patients, which significantly increases the survival risks and reduces the patient’s quality of life. However, preventive clinical measures for DVT have not been standardized; therefore, the scientific basis and effectiveness of these measures require further validation.ObjectiveThis study aims to employ evidence-based practices to effectively prevent the occurrence of DVT in aSAH patients.MethodsThis study was performed from June 2023 to March 2024 in the neurosurgical intensive care unit of a Grade III Class A general hospital in Nanchang, China. Furthermore, it was based on the healthcare model published by the Joanna Briggs Institute Library (JBI) in 2016, which emphasizes the use of previous evidence-based practices while considering appropriateness, feasibility, clinical significance, and validity. In this research study, 15 review indicators were developed, and baseline assessments on 47 nurses and 49 patients were conducted. Furthermore, factors promoting and obstructing implementation were analyzed, and targeted strategies to address these obstacles were formulated. Moreover, a follow-up audit was performed to identify best practices.ResultsThe baseline review results indicated that the incidence of DVT in aSAH patients was 16.3%. Furthermore, the implementation rates of six review indicators (1, 2, 4, 5, 8, 13) were all < 100.0%, with indicators 2, 5, and 8 indicating < 60.0% implementation rates. After the project implementation, a subsequent audit revealed that the best practice initiative yielded significant improvements compared to the baseline data. Moreover, the incidence of lower limb DVT in aSAH patients decreased from 16.3% before the evidence-based practices to 6.1% after their implementation. At the nursing level, the DVT prevention knowledge and practice questionnaire scores increased from 63.62 ± 11.48 to 74.77 ± 9.98 after the evidence-based practices (t = -5.03, p < .001). In addition, the implementation rates of the six review indicators improved to varying degrees after the implementation of evidence-based practices (p < .050).ConclusionsThis project implemented evidence-based practices and indicated a reduced incidence of lower limb DVT in patients with aSAH. Furthermore, this study improved the knowledge, provided evidence for DVT prevention for the neurosurgical ICU nurses, promoted the implementation rate of review indicators for DVT prevention, standardized the behavior of neurosurgical ICU nurses for preventing DVT in aSAH patients, and ensured the safety of patients.Trial registrationThis study has been registered at the EvidenceBased Nursing Center of Fudan University in China. Clinical trial number ER20230578.

Trajectory of mean platelet volume changes after aneurysmal subarachnoid hemorrhage in patients with or without delayed cerebral ischemia

The morbidity of aneurysmal subarachnoid hemorrhage (aSAH) remains high, particularly because of secondary cerebral lesions that significantly aggravate the primary lesions. The main type of secondary lesions is delayed cerebral ischemia (DCI), in which platelets (PLT) appear to play a key role. Mean platelet volume (MPV) is an indirect marker of platelet activation. We aimed to determine the individual trajectories of MPV over time in patients with and without DCI during the course of aSAH. This is a single-center, retrospective, longitudinal analysis of individual trajectories of MPV over time, in a cohort of aSAH patients included in the Prospective, Observational Registry of Patient with Subarachnoid Hemorrhage in Neurocritical Care Unit (ProReSHA). A mixed-effects linear regression model was used to compare the trajectories of MPV and MPV/PLT ratio between patients who developed a DCI and those who did not. A total of 3634 MPV values were collected in 587 patients. The analysis of MPV as a function of DCI occurrence showed a significant difference in the trajectory over time between patients with DCI and those without, with an estimate of 0.02 (95%CI 0.01, 0.04, p = 0.009). The analysis of the MPV/PLT ratio as a function of DCI occurrence and other covariates showed a significant difference in the trajectory over time only for patients with a modified Fisher score less than 3, with an estimate of -0.59 (95%CI: -0.94, -0.23, p = 0.001). The individual trajectories of MPV over time differ between patients with DCI and those without. However, MPV values vary greatly over time and between patients. Thus it does not appear as a reliable biomarker for stratifying patients based on their specific risk of developing DCI. ClinicalTrials.gov identifier: (NCT02890004), registered in August 2016.

Identifying Patients at Increased Risk for Poor Outcomes Among Poor-Grade Aneurysmal Subarachnoid Hemorrhage Patients: The IPOGRO Risk Model.

A subarachnoid hemorrhage due to an aneurysmal rupture (aSAH) is a serious condition with severe neurological consequences. The World Federation of Neurosurgical Societies (WFNS) classification is a reliable predictor of death and long-term disability in patients with aSAH. Poor-grade neurological conditions on admission in aSAH (PG-aSAH) are often linked to high mortality rates and unfavorable outcomes. However, more than one-third of patients with PG-aSAH may recover and have good functional outcomes if aggressive treatment is provided. We developed a risk model called Identifying POor GRade Outcomes (IPOGRO) to predict 6-month mRS outcomes in PG-aSAH patients as a secondary analysis of a previously published study. All consecutive patients in poor-grade neurological conditions (WFNS IV-V) admitted to our institute from 2010 to 2020 due to aSAH were considered. Clinical and neuroradiological parameters were employed in the univariable analysis to evaluate the relationship with a 6-month modified Rankin Scale (mRS). Then, a multivariable multinomial regression model was performed to predict 6-month outcomes. 149 patients with PG-aSAH were included. Most patients were surgically treated, with only 33.6% being endovascularly treated. The 6-month mRS score was significantly associated with clinical parameters on admission, such as lowered Glasgow Coma Scale (GCS), leukocytosis, hyperglycemia, raised Systolic Blood Pressure (SBP), greater Simplified Acute Physiology Score (SAPS II score), increased initial serum Lactic Acid (LA) levels, and the need for Norepinephrine (NE) administration. Neuroradiological parameters on the initial CT scan showed a significant association with a worsening 6-month mRS. The IPOGRO risk model analysis showed an association between a WFNS V on admission and a poor outcome (mRS 4-5), while raised SBP was associated with mortality. Our IPOGRO risk model indicates that PG-aSAH patients with higher SBP at admission had an increased risk of death at 6-month follow-up, whereas patients with WFNS grade V at admission had an increased risk of poor outcome but not mortality.

Development and Validation of a Prechiasmatic Mouse Model of Subarachnoid Hemorrhage to Measure Long-Term Cognitive Deficits.

Controllable and reproducible animal models of aneurysmal subarachnoid hemorrhage (SAH) are crucial for the systematic study of the pathophysiology and treatment of this debilitating condition. However, current animal models have not been successful in replicating the pathology and disabilities seen in SAH patients, especially the long-term neurocognitive deficits that affect the survivor's quality of life. Therefore, there is an unmet need to develop experimental models that reliably replicate the long-term clinical ramifications of SAH - especially in mice where genetic manipulations are straightforward and readily available. To address this need, a standardized mouse SAH model is developed that reproducibly produced significant and trackable long-term cognitive deficits. SAH is induced by performing double blood injections into the prechiasmatic cistern - a simple modification to the well-characterized single prechiasmatic injection mouse model of SAH. Following SAH, mice recapitulated key characteristics of SAH patients, including cerebral edema measured by MRI - an indicator of early brain injury (EBI), neuroinflammation, apoptosis, and long-term cognitive impairment.This newly developed SAH mouse model is considered an ideal paradigm for investigating the complex SAH pathophysiology and identifying novel druggable therapeutic targets for treating SAH severity and SAH-associated long-term neurocognitive deficits in patients.

Significant individual variation in cardiac-cycle-linked cerebrospinal fluid production following subarachnoid hemorrhage

BackgroundSpontaneous subarachnoid hemorrhage (SAH) often results in altered cerebrospinal fluid (CSF) flow and secondary hydrocephalus, yet the mechanisms behind these phenomena remain poorly understood. This study aimed to elucidate the impact of SAH on individual CSF flow patterns and their association with secondary hydrocephalus.MethodsIn patients who had experienced SAH, changes in CSF flow were assessed using cardiac-gated phase-contrast magnetic resonance imaging (PC-MRI) at the Sylvian aqueduct and cranio-cervical junction (CCJ). Within these regions of interest, volumetric CSF flow was determined for every pixel and net CSF flow volume and direction calculated. The presence of acute or chronic hydrocephalus was deemed from ventriculomegaly and need of CSF diversion. For comparison, we included healthy subjects and patients examined for different CSF diseases.ResultsTwenty-four SAH patients were enrolled, revealing a heterogeneous array of CSF flow alterations at the Sylvian aqueduct. The cardiac-cycle-linked CSF net flow in Sylvian aqueduct differed from the traditional figures of ventricular CSF production about 0.30–0.40 mL/min. In 15 out of 24 patients (62.5%), net CSF flow was retrograde from the fourth to the third and lateral ventricles, while it was upward at the cranio-cervical junction in 2 out of 2 patients (100%). The diverse CSF flow metrics did not distinguish between individuals with acute or chronic secondary hydrocephalus. In comparison, 4/4 healthy subjects showed antegrade net CSF flow in the Sylvian aqueduct and net upward CSF flow in CCJ. These net CSF flow measures also showed interindividual variability among other patients with CSF diseases.ConclusionsThere is considerable inter-individual variation in net CSF flow rates following SAH. Net CSF flow in the Sylvian aqueduct differs markedly from the traditional ventricular CSF production rates of 0.30–0.40 mL/min in SAH patients, but less so in healthy subjects. Furthermore, the cardiac-cycle-linked net CSF flow rates in Sylvian aqueduct and CCJ suggest an important role of extra-ventricular CSF production.

Association between estimated pulse wave velocity and the risk of mortality in patients with subarachnoid hemorrhage: a retrospective cohort study based on the MIMIC database

BackgroundThe estimated pulse wave velocity (ePWV) is a recently developed, simple and useful tool to measure arterial stiffness and to predict long-term cardiovascular mortality. However, the association of ePWV with mortality risk in patients with subarachnoid hemorrhage (SAH) is unclear. Herein, this study aims to assess the potential prediction value of ePWV on short- and long-term mortality of SAH patients.MethodsData of adult patients with no traumatic SAH were extracted from the Medical Information Mart for Intensive Care (MIMIC) III and IV database in this retrospective cohort study. Weighted univariate and multivariable Cox regression analyses were used to explore the associations of ePWV levels with 30-day mortality and 1-year mortality in SAH patients. The evaluation indexes were hazard ratios (HRs) and 95% confidence intervals (CIs). In addition, subgroup analyses of age, the sequential organ failure assessment (SOFA) score, surgery, atrial fibrillation (AF), renal failure (RF), hepatic diseases, chronic obstructive pulmonary disease (COPD), sepsis, hypertension, and diabetes mellitus (DM) were also performed.ResultsAmong 1,481 eligible patients, 339 died within 30 days and 435 died within 1 year. After adjusting for covariates, ePWV ≥ 12.10 was associated with higher risk of both 30-day mortality (HR = 1.77, 95%CI: 1.17–2.67) and 1-year mortality (HR = 1.97, 95%CI: 1.36–2.85), compared to ePWV < 10.12. The receiver operator characteristic (ROC) curves showed that compared to single SOFA score, ePWV combined with SOFA score had a relative superior predictive performance on both 30-day mortality and 1-year mortality, with the area under the curves (AUCs) of 0.740 vs. 0.664 and 0.754 vs. 0.658. This positive relationship between ePWV and mortality risk was also found in age ≥ 65 years old, SOFA score < 2, non-surgery, non-hepatic diseases, non-COPD, non-hypertension, non-DM, and sepsis subgroups.ConclusionBaseline ePWV level may have potential prediction value on short- and long-term mortality in SAH patients. However, the application of ePWV in SAH prognosis needs further clarification.

Liberalization of the Systemic Glucose Management is Associated with a Reduced Frequency of Neuroglucopenia in Subarachnoid Hemorrhage Patients: An Observational Cohort Study.

Pathologically low brain glucose levels, referred to as neuroglucopenia, are associated with unfavorable outcomes in neurocritical care patients. We sought to investigate whether an increase in serum glucose levels would be associated with a reduction of neuroglucopenia. In this retrospective analysis of prospectively collected data, we included 55 consecutive patients with spontaneous subarachnoid hemorrhage who underwent cerebral microdialysis (CMD) monitoring. Neuroglucopenia was defined as CMD-glucose levels < 0.7mmol/l. We identified systemic glucose liberalization events, defined as a day with median serum glucose levels < 150mg/dl, followed by a day with median serum glucose levels > 150mg/dl, and compared concentrations of cerebral metabolites between these days. Unfavorable outcome was defined as modified Rankin Scale score ≥ 3 at 3 months after the bleeding. Episodes of neuroglucopenia were more frequent in patients with unfavorable outcome (19.8% [19.3-20.3%] vs. 10.9% [10.4-11.5%], p = 0.007). Sixty-nine systemic glucose liberalization events were identified in 40 patients. Blood glucose levels increased from 141.2 (138.7-143.6) mg/dl to 159.5 (157.0-162.2) mg/dl (p < 0.001), CMD-glucose levels increased from 1.44 (1.39-1.50) mmol/l to 1.68 (1.62-1.75) mmol/l (p = 0.001), and the frequency of neuroglucopenia decreased from 24.7% (22.9-26.5%) to 20.2% (18.7-21.8%) (p = 0.002) during these events. Liberalization was not associated with changes in CMD-lactate, CMD-pyruvate, CMD-lactate-to-pyruvate ratio, CMD-glutamate, or CMD-glycerol. In conclusion, the liberalization of serum glucose concentrations to levels between 150 and 180 mg/dl was associated with a significant reduction of neuroglucopenia.

Energy Expenditure in Critically Ill Patients with Aneurysmal Subarachnoid Hemorrhage, Intracerebral Hemorrhage, and Traumatic Brain Injury-A Prospective Observational Study.

Energy expenditure (EE) in patients with aneurysmal subarachnoid hemorrhage (SAH) may differ from other intracranial pathologies, such as intracerebral hemorrhage (ICH) or traumatic brain injury (TBI), due to an activation of the sympathetic nervous system. Indirect calorimetry (IC) is recommended, but is not always available. We study EE, catabolism, and metabolic stress in patients with SAH, TBI, ICH, and sepsis as controls. A prospective observational study was conducted in the intensive care units of the University Medical Center Hamburg-Eppendorf, Germany. IC was used to measure EE on days 2-3, 5-7, and 10-15 post-admission. Urinary catecholamines, metabolites, and urine urea were also measured. Statistical analysis included t-tests, Chi-square tests, and generalized mixed models. We included 110 patients-43 SAH patients (13 with the surgical securing of the aneurysm and 30 with coil embolization of the aneurysm), 22 TBI patients, 23 ICH patients, and 22 controls. The generalized linear mixed model analysis for groups and timepoints including age, height, and weight as covariates revealed a significantly lower EE at timepoint 1 for ICH versus SAH-interventional (p = 0.003) and versus the control (p = 0.004), as well as at timepoint 2 for ICH versus SAH-interventional (p = 0.002) and versus SAH-surgical (p = 0.013) with a lower EE in ICH patients. No significant differences between groups were found for EE at the other timepoints, or concerning urine urea and measurements of catecholamines in urine. In patients with SAH, ICH, and TBI, no meaningful differences in EE were detected compared to septic critically ill patients, except for a lower EE in ICH patients in the early phase.

Higher erythrocytes in cerebrospinal fluid on the first and seventh postoperative day: Associated with poor outcome in aneurysmal subarachnoid hemorrhage patients.

Aneurysmal subarachnoid hemorrhage is an acute cerebrovascular disease with high disability and mortality. We intended to explore the association between levels of erythrocytes in cerebrospinal fluid at different times of hemorrhage and the outcome of patients. One retrospective study including 216 patients with aneurysmal subarachnoid hemorrhage undergoing surgeries in the First Affiliated Hospital of Yangtze University from January 2020 to July 2023 was carried. The univariable analysis and multivariable logistic regression analysis were used for factors associated with poor outcome. The level of erythrocytes in cerebrospinal fluid on the 1st postoperative day in patients with poor outcome was 311 × 103/µL, significantly higher than patients with good outcome (108 × 103/µL), P < .001. The level of erythrocytes in cerebrospinal fluid on 7th postoperative day was 86.5 × 103/µL, also significantly higher than patients with good outcome (26.0 × 103/µL). The multivariable logistic regression analysis results showed that erythrocytes in cerebrospinal fluid on the 1st postoperative day (≥177 × 103/µL) and on the 7th postoperative day (≥53.5 × 103/µL) were possibly associated with poor outcome in aneurysmal subarachnoid hemorrhage patients. Treatment with tranexamic acid and continuous lumbar drainage did not result in a decrease of erythrocytes in cerebrospinal fluid. Higher erythrocytes in cerebrospinal fluid on the 1st and 7th postoperative days were associated with poor outcome in aneurysmal subarachnoid hemorrhage patients.

The impact of systolic blood pressure reduction on aneurysm re-bleeding in subarachnoid hemorrhage: A systematic review and meta-analysis

BackgroundPreventing early aneurysm rebleeding is crucial in the management of aneurysmal subarachnoid hemorrhage (SAH). Lowering systolic blood pressure (SBP) has been proposed as a potential strategy, but the evidence remains inconclusive. This systematic review and meta-analysis aimed to determine if a specific SBP target could reduce the risk of aneurysm rebleeding prior to treatment. MethodsElectronic databases were systematically searched for studies comparing SBP between SAH patients with and without aneurysm rebleeding before surgical treatment. Data on SBP values, patient characteristics, and rebleeding events were extracted. Meta-analyses were performed to pool mean SBP differences and odds ratios (ORs) for rebleeding at different SBP cut-offs. ResultsTen studies were included in the systematic review. Pooled data from the included studies showed that the mean SBP was higher in the rebleeding group (mean difference 5.89, 95 % CI 1.94 to 9.85). SBP ≤160 mmHg was associated with lower rebleeding risk (OR 0.30, 95 % CI 0.14 to 0.65). However, substantial heterogeneity and limitations in study designs and definitions were noted. ConclusionsThis meta-analysis suggests that SAH patients with rebleeding may present with higher SBP. However, the findings should be interpreted cautiously due to study limitations. Future prospective studies with standardized definitions and comprehensive data collection are needed to elucidate the complex relationship between blood pressure dynamics and rebleeding risk in SAH.

The polk county screening tool screening for detecting subarachnoid hemorrhage

IntroductionThe subarachnoid space in the brain contains crucial blood vessels and cerebrospinal fluid. Aneurysms in these vessels can lead to subarachnoid hemorrhage (SAH), a serious stroke subtype with high morbidity and mortality rates. SAH treatment includes procedures like coiling and clipping, but these are available only at comprehensive stroke centers (CSCs), necessitating urgent diagnosis and transfer to specialized facilities.MethodsThis IRB-approved study was conducted by Polk County Fire Rescue (PCFR) in Florida. PCFR, serving an 850,000-person population, implemented a three-step SAH protocol. The protocol uses both Ottawa SAH criteria and recurring symptoms, such as new-onset seizures and high systolic blood pressure, that were identified by EMS. Acute management included administering labetalol, levetiracetam, and ondansetron.ResultsOf 2175 stroke patients, 80 screened positive for SAH and were eligible for transfer. Patients had a median age of 66, and 33% had an initial systolic BP over 220 mmHg. The interfacility transfer rate dropped from 12.9 to 3.6% after implementing the protocol.ConclusionThe PCFR protocol’s effectiveness suggests its potential for nationwide implementation. Early SAH recognition and prompt transfer to CSCs reduce complications and improve outcomes. Accurate field diagnosis by EMTs can prevent unnecessary transfers and enhance patient care. Future improvements may include portable diagnostic tools and enhanced EMT training to further improve SAH patients’ pre-hospital care.

Trial of the cerebral perfusion response to sodium nitrite infusion in patients with acute subarachnoid haemorrhage using arterial spin labelling MRI

Aneurysmal subarachnoid haemorrhage (SAH) is a devastating subset of stroke. One of the major determinants of outcome is an evolving multifactorial injury occurring in the first 72 hours, known as early brain injury. Reduced nitric oxide (NO) bioavailability and an associated disruption to cerebral perfusion is believed to play an important role in this process. We sought to explore this relationship, by examining the effect on cerebral perfusion of the in vivo manipulation of NO levels using an exogenous NO donor (sodium nitrite).We performed a double blind placebo controlled randomised experimental medicine study of the cerebral perfusion response to sodium nitrite infusion during the early brain injury period in 15 low grade (World Federation of Neurosurgeons grade 1–2) SAH patients. Patients were randomly assigned to receive sodium nitrite at 10 mcg/kg/min or saline placebo. Assessment occurred following endovascular aneurysm occlusion, mean time after ictus 66h (range 34–90h). Cerebral perfusion was quantified before infusion commencement and after 3 hours, using multi-post labelling delay (multi-PLD) vessel encoded pseudocontinuous arterial spin labelling (VEPCASL) magnetic resonance imaging (MRI).Administration of sodium nitrite was associated with a significant increase in average grey matter cerebral perfusion. Group level voxelwise analysis identified that increased perfusion occurred within regions of the brain known to exhibit enhanced vulnerability to injury. These findings highlight the role of impaired NO bioavailability in the pathophysiology of early brain injury.

Intracranial Aneurysms and Cerebral Small Vessel Disease: Is There an Association between Large- and Small-Artery Diseases?

Background/Objectives: Intracranial aneurysms (IAs) may be connected to interactions between large and small intracranial vessels. We aimed to investigate the association between IAs and cerebral small-vessel disease (CSVD) and assess CSVD impact on IA patient management. Methods: This retrospective study analyzed clinical data and MRI features of CSVD in 192 subarachnoid hemorrhage (SAH) patients: 136 with incidental IA, 147 with severe CSVD without SAH/IA, and 50 controls without SAH, IA, or severe CSVD. MRI assessments followed the Standards for Reporting Vascular Changes on Neuroimaging (STRIVE), with a total burden of small-vessel disease (TBSVD) score calculated. Statistical analyses included forward selection and binary logistic regression. Results: TBSVD differed significantly across groups (p < 0.001), except between SAH and IA groups (p = 0.8). Controls had the lowest TBSVD (1.00; 1.22 ± 0.996), followed by SAH (2.00; 2.08 ± 1.013) and IA groups (2.00; 2.04 ± 1.141), with the highest in the CSVD group (1.00; 1.22 ± 0.996). White-matter hyperintensity (WMH) patterns varied with IA rupture status (p = 0.044); type A was prevalent in SAH patients and type D in the IA group. Incorporating MRI CSVD features and TBSVD into risk assessments did not enhance IA prediction or outcome models. Conclusions: IA patients exhibit a higher CSVD burden than controls, suggesting a link between small and large intracranial vessels. WMH patterns distinguish between ruptured and unruptured IA patients, offering potential markers for IA rupture risk assessment and signaling a paradigm shift in understanding IAs and CSVD.

Letter to the Editor Regarding “Clinical Characteristics as Predictors of Early and Delayed Cerebral Infarction in Aneurysmal Subarachnoid Hemorrhage Patients: A Meta-Analysis of 4527 Cases”

Letter to the Editor Regarding “Clinical Characteristics as Predictors of Early and Delayed Cerebral Infarction in Aneurysmal Subarachnoid Hemorrhage Patients: A Meta-Analysis of 4527 Cases”

The urotensin II receptor triggers an early meningeal response and a delayed macrophage-dependent vasospasm after subarachnoid hemorrhage in male mice

Subarachnoid hemorrhage (SAH) can be associated with neurological deficits and has profound consequences for mortality and morbidity. Cerebral vasospasm (CVS) and delayed cerebral ischemia affect neurological outcomes in SAH patients, but their mechanisms are not fully understood, and effective treatments are limited. Here, we report that urotensin II receptor UT plays a pivotal role in both early events and delayed mechanisms following SAH in male mice. Few days post-SAH, UT expression is triggered by blood or hemoglobin in the leptomeningeal compartment. UT contributes to perimeningeal glia limitans astrocyte reactivity, microvascular alterations and neuroinflammation independent of CNS-associated macrophages (CAMs). Later, CAM-dependent vascular inflammation and subsequent CVS develop, leading to cognitive dysfunction. In an SAH model using humanized UTh+/h+ male mice, we show that post-SAH CVS and behavioral deficits, mediated by UT through Gq/PLC/Ca2+ signaling, are prevented by UT antagonists. These results highlight the potential of targeting UT pathways to reduce early meningeal response and delayed cerebral ischemia in SAH patients.

High levels of blood lipid and glucose predict adverse prognosis in patients with aneurysmal subarachnoid hemorrhage

ObjectiveWe conducted a retrospective study on the prognostic factors of aneurysmal subarachnoid hemorrhage (aSAH) patients in the author's Hospital from January 2019 to May 2023. To discuss the association of the blood lipid and glucose levels of patients with the prognosis of aSAH, and verify that high blood lipid and glucose levels are important factors affecting adverse prognosis. MethodsAll patients with aSAH were collected as the case group, which was divided into two groups according to the modified Rankin Scores (mRS), the good prognosis group (Group A, mRS ＜ 3) and the adverse prognosis group (Group B,mRS ≥3). The clinical data of age, gender, accompanied chronic diseases (hypertension, diabetes), smoking, drinking, Glasgow Coma Scale (GCS), Hunt-Hess (H-H) grade, Modified Fisher grade, total cholesterol (TC) , triglyceride (TG) , high-density cholesterol lipoprotein (HDL-C) , low-density cholesterol lipoprotein (LDL-C) , blood glucose (BG) , responsible aneurysm diameter and location were recorded too. Correlations between blood lipid and glucose levels and Modified Fisher grade were assessed by the Spearman correlation analysis. The receiver operating characteristic (ROC) curve was utilized to evaluate the diagnostic efficacy. The effect of blood lipid and glucose levels on adverse prognosis was analyzed by Logistic regression models. ResultA total of 259 patients with aSAH were enrolled. The average age of all patients is (56.54 ± 10.52) years, including 96 males and 163 females. They were divided into Group A (n = 146) and Group B (n = 113). Univariate analysis results show that age, the levels of TC, TG, LDL-C, and BG were higher in Group B (P < 0.05). Besides, Group B had more severe GCS, H-H grade, and Modified Fisher grade than Group A, and a higher proportion of intracranial aneurysms with larger diameter (P < 0.05). Correlation analysis showed that TC, TG, LDL-C, and BG levels were positively correlated with Modified Fisher grade (P < 0.05) and H-H grade (P < 0.05). Multivariate logistic regression model analysis showed that high level of Modified Fisher grade (OR = 0.079, 95%CI: 0.027–0.230) , high level of H-H grade (OR = 0.204, 95%CI: 0.067–0.622) , TC (OR = 10.711, 95%CI: 2.457–46.700) , LDL-C (OR = 0.178, 95%CI: 0.039–0.823) and BG (OR = 1.273, 95%CI: 1.012–1.602) increased the risk of adverse prognosis. The AUC of “H-H grade”, “Modified Fisher grade”, “TC level”, “LDL-C level” and “BG level” was 0.822, 0.885, 0.860, 0.772, and 0.721, respectively, in the ROC curve. ConclusionModified Fisher grade, H-H grade, TC, LDL-C, and BG levels at admission were independent predictors of adverse prognosis of aSAH. Besides, TC, LDL-C, and BG levels were positively correlated with Modified Fisher grade and Hunt-Hess grade. What's more, high levels of TC, LDL-C, and BG combined with Modified Fisher grade and H-H grade can identify high-risk groups with adverse prognoses in aSAH patients.