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BACKGROUND: Cerebral vasospasm (CV) is a feared complication which occurs after 20-40% of subarachnoid haemorrhage (SAH). It is standard practice to admit patients with SAH to intensive care for an extended period of resource-intensive monitoring. We used machine learning to predict CV requiring verapamil (CVRV) in the largest and only multi-center study to date. METHODS: Patients with SAH admitted to UCLA from 2013 to 2022 and a validation cohort from VUMC from 2018 to 2023 were included. For each patient, 172 unique intensive care unit (ICU) variables were extracted through the primary endpoint, namely first verapamil administration or no verapamil. At each institution, a light gradient boosting machine (LightGBM) was trained using five-fold cross validation to predict the primary endpoint at various hospitalization timepoints. FINDINGS: A total of 1750 patients were included from UCLA, 125 receiving verapamil. LightGBM achieved an area under the ROC (AUC) of 0.88 > 1 week in advance and ruled out 8% of non-verapamil patients with zero false negatives. Our models predicted no CVRV vs CVRV within three days vs CVRV after three days with AUCs = 0.88, 0.83, and 0.88, respectively. From VUMC, 1654 patients were included, 75 receiving verapamil. VUMC predictions averaged within 0.01 AUC points of UCLA predictions. INTERPRETATION: We present an accurate and early predictor of CVRV using machine learning with multi-center validation. This represents a significant step towards optimized clinical management and resource allocation in patients with SAH. FUNDING: Robert E. Freundlich is supported by National Center for Advancing Translational Sciences federal grant UL1TR002243 and National Heart, Lung, and Blood Institute federal grant K23HL148640; these funders did not play any role in this study. The National Institutes of Health supports Vanderbilt University Medical Center which indirectly supported these research efforts. Neither this study nor any other authors personally received financial support for the research presented in this manuscript. No support from pharmaceutical companies was received.

Background: Aneurysmal subarachnoid hemorrhage (aSAH) is a dreadful acute neurological condition with an overwhelmingly high rate of associated morbidities and mortality. Despite leaping advancement in neurosurgical techniques and imaging modalities, there is no substantiative improvement in the overall prognosis for aSAH. Cerebral vasospasm remains the predominant cause of associated morbidities. Human albumin has been used in different neurological conditions, including head trauma, intracerebral hemorrhages, and ischemic strokes, with favorable outcomes. However, its beneficial use in aSAH has not been sufficiently explored until recently a published systematic review by our team. In view of the scarcity of published data and lack of robust evidence, our group has designed the first-ever RCT to compare the use of human albumin-enhanced fluid management versus standard fluid therapy with crystalloids in patients with aSAH. Methods: This single-center open-label, prospective, parallel group randomized control trial will be conducted at Hamad General Hospital, Doha, Qatar, from August 2024 to July 2027. A sample size of 84 (42 in each arm) has been calculated to be sufficient to detect a clinically significant difference in the modified Rankin scale good score between two groups (human-albumin induced volume expansion therapy versus crystalloid only) for fluid management in aneurysmal subarachnoid hemorrhage patients. The primary outcome will be based on a dichotomized modified Rankin scale [good grades (0–2) and poor grades (3–6)], while the secondary outcome will include symptomatic vasospasm, transcranial Doppler velocities, and Pulse index Contour Cardiac Output (PiCCO) parameters. Discussion: The trial aims to provide firsthand evidence on the beneficial use of human albumin to achieve an optimal fluid management regime to explore its potential role in improving clinical outcomes in patients with aSAH. Trial registration: ClinicalTrials.gov NCT06548477. Registered on August 9, 2024. https://clinicaltrials.gov/search?term=NCT06548477. [ABSTRACT FROM AUTHOR]

Here, we present a photothermally triggered drug delivery nanosystem MoS2-NIMO-CHIT-SH, using the thiolated chitosan (CHIT-SH)-modified molybdenum disulfide (MoS2) nanosheets as near-infrared (NIR) photo-responsive carriers, loaded with the dihydropyridine calcium antagonist drug Nimodipine (NIMO). Although NIMO is used to treat stroke, migraine, Alzheimer's disease, cerebrovascular spasms, and hypertension, this drug is poorly water-soluble, with low bioavailability and lack of selectivity. Thus, there is an urgent need for a novel approach to creating NIMO formulations that are safe, effective, and have better solubility and bioavailability. To overcome these problems, we develop a cationic biopolymer functionalized MoS2 nanosheets as a photothermal drug carrier system to facilitate the NIR light-induced release of NIMO drugs. MoS2 nanosheets (<150 nm) as NIMO drug carriers are prepared through simple exfoliation of their bulk phase and then functionalized with CHIT-SH biopolymer to increase their physiological stability and biocompatibility. According to the results, MoS2-NIMO-CHIT-SH nanocomposites show strong NIR absorbance, which makes them a promising candidate for photothermal therapy. [ABSTRACT FROM AUTHOR]

Aneurysmal subarachnoid hemorrhage (SAH) involves a significant influx of blood into the cerebrospinal fluid, representing a severe form of stroke. Despite advancements in aneurysm closure and neuro-intensive care, outcomes remain impaired due to cerebral vasospasm and delayed cerebral ischemia (DCI). Previous pharmacological therapies have not successfully reduced DCI while improving overall outcomes. As a result, significant efforts are underway to better understand the cellular and molecular mechanisms involved. This review focuses on the activation and effects of immune cells after SAH and their interactions with neurotoxic and vasoactive substances as well as inflammatory mediators. Particular attention is given to clinical studies highlighting the roles of natural killer (NK) cells and regulatory T cells (Treg) cells. Alongside microglia, astrocytes, and oligodendrocytes, NK cells and Treg cells are key contributors to the inflammatory cascade following SAH. Their involvement in modulating the neuro-inflammatory response, vasospasm, and DCI underscores their potential as therapeutic targets and prognostic markers in the post-SAH recovery process. We conducted a systematic review on T cell- and natural killer cell-mediated inflammation and their roles in cerebral vasospasm and delayed cerebral ischemia. We conducted a meta-analysis to evaluate outcomes and mortality in studies focused on NK cell- and T cell-mediated mechanisms. [ABSTRACT FROM AUTHOR]

The article in Neurocritical Care discusses a case of a 60-year-old woman with Streptococcus pneumoniae bacterial meningitis who experienced a biphasic clinical trajectory, initially showing slow improvement but later deteriorating with marked cerebral infarcts. Follow-up MRI revealed progressive infarctions and vascular changes, challenging the understanding of vasculitis as a mechanism for strokes in meningitis patients. The detailed neuropathology findings suggest that vasculitis or thrombotic vasculopathy may not always explain secondary deterioration from cerebral infarction in such cases. The study highlights the complexity of cerebral infarcts in pneumococcal meningitis and the need for further research in this area. [Extracted from the article]

Background: Subarachnoid hemorrhage is a serious condition caused by ruptured intracranial aneurysms, resulting in severe disability mainly in young adults. Cerebral vasospasm is one of the most common complication of subarachnoid hemorrhage; thus, active prevention is key to improve the prognosis. The glycosylation of proteins is a critical quality attribute which is reportedly altered in patients diagnosed with acute ischemic stroke. In this study, we examined the N-glycosylation profile of serum glycoproteins in patients with subarachnoid hemorrhage without vasospasm compared to patients with vasospasm. Methods: The serum N-glycans were released by PNGase F (Peptide: N-glycosidase F) digestion and subsequently labeled by procainamide via reductive amination. The samples were analyzed by hydrophilic-interaction liquid chromatography after solid-phase extraction-based sample purification. Results: Besides the glycosylation pattern, we also investigated the biomarkers following subarachnoid hemorrhage. Multiple statistical analyses were performed in order to find significant differences and identify potential prediction factors of cerebral vasospasm. Significant differences were identified such as higher sialylation on bi-, tri-, and tetra-antennary structures in patients with subarachnoid hemorrhage and cerebral vasospasm. Conclusions: Our results suggest that glycosylation analysis can improve the identification of patients with cerebral vasospasm in combination with laboratory parameters. [ABSTRACT FROM AUTHOR]

Background: Subarachnoid hemorrhage (SAH) is characterized by intense central inflammation, leading to substantial post-hemorrhagic complications such as vasospasm and delayed cerebral ischemia. Given the anti-inflammatory effect of transcutaneous auricular vagus nerve stimulation (taVNS) and its ability to promote brain plasticity, taVNS has emerged as a promising therapeutic option for SAH patients. However, the effects of taVNS on cardiovascular dynamics in critically ill patients, like those with SAH, have not yet been investigated. Given the association between cardiac complications and elevated risk of poor clinical outcomes after SAH, it is essential to characterize the cardiovascular effects of taVNS to ensure this approach is safe in this fragile population. Therefore, this study assessed the impact of both acute and repetitive taVNS on cardiovascular function. Methods: In this randomized clinical trial, 24 SAH patients were assigned to either a taVNS treatment or a sham treatment group. During their stay in the intensive care unit, we monitored patient electrocardiogram readings and vital signs. We compared long-term changes in heart rate, heart rate variability (HRV), QT interval, and blood pressure between the two groups. Additionally, we assessed the effects of acute taVNS by comparing cardiovascular metrics before, during, and after the intervention. We also explored acute cardiovascular biomarkers in patients exhibiting clinical improvement. Results: We found that repetitive taVNS did not significantly alter heart rate, QT interval, blood pressure, or intracranial pressure (ICP). However, repetitive taVNS increased overall HRV and parasympathetic activity compared to the sham treatment. The increase in parasympathetic activity was most pronounced from 2 to 4 days after initial treatment (Cohen's d = 0.50). Acutely, taVNS increased heart rate, blood pressure, and peripheral perfusion index without affecting the corrected QT interval, ICP, or HRV. The acute post-treatment elevation in heart rate was more pronounced in patients who experienced a decrease of more than one point in their modified Rankin Score at the time of discharge. Conclusions: Our study found that taVNS treatment did not induce adverse cardiovascular effects, such as bradycardia or QT prolongation, supporting its development as a safe immunomodulatory treatment approach for SAH patients. The observed acute increase in heart rate after taVNS treatment may serve as a biomarker for SAH patients who could derive greater benefit from this treatment. [ABSTRACT FROM AUTHOR]

Aneurysmal subarachnoid hemorrhage (aSAH) is a common neurosurgical disorder with high morbidity and poor prognosis, and the associated delayed cerebral ischemia (DCI) is a key factor contributing to poor prognosis. Despite extensive research on the risk factors associated with DCI development, the evidence remains conflicting. Therefore, this meta-analysis of case-control studies aimed to investigate the risk factors for DCI occurrence during hospitalization in patients with aSAH. We systematically searched PubMed, Embase, Web of Science, and the Cochrane Central Register of Controlled Trials for eligible studies published before November 20, 2023. Two independent reviewers extracted relevant data from the included studies using a pre-established data extraction form. The primary outcome was DCI occurrence during hospitalization in patients with aSAH. A total of 42 studies involving 21,726 patients with aSAH were included. The pooled meta-analysis showed that female sex; Hunt-Hess, modified Fisher, and World Federation of Neurosurgical Societies scale scores of 4–5, 3–4, and 4–5, respectively; vasospasm; combined intraventricular hemorrhage; pre-existing hypertension; hydrocephalus; intracranial infections; and high white blood cell count on admission were independent risk factors for the development of postoperative DCIs in patients with aSAH. Patients with aSAH who have a Hunt-Hess scale score ≥4, a modified Fisher scale score ≥3, a WFNS scale score ≥4, intraventricular hemorrhage, pre-existing hypertension, cerebral vasospasm, a high white blood cell count on admission, intracranial infection, and female sex are at high risk of DCI and hence should be carefully monitored in the intensive care unit. [ABSTRACT FROM AUTHOR]

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Background Delayed cerebral ischemia (DCI) is one of the main contributors to poor clinical outcome after aneurysmal subarachnoid hemorrhage (SAH). Endovascular spasmolysis with intra-arterial nimodipine (IAN) may resolve angiographic vasospasm, but its effect on infarct prevention and clinical outcome is still unclear. We report the effect of IAN on infarction rates and functional outcome in a consecutive series of SAH patients. Methods To assess the effectiveness of IAN, we collected functional outcome data of all SAH patients referred to a single tertiary center since its availability (2011-2020). IAN was primarily reserved as a last tier option for DCI refractory to induced hypertension (iHTN). Functional outcome was assessed after 12 months according to the Glasgow Outcome Scale (GOS, favorable outcome = GOS4-5). Results Out of 376 consecutive SAH patients, 186 (49.5%) developed DCI. Thereof, a total of 96 (25.5%) patients remained unresponsive to iHTN and received IAN. DCI-related infarction was observed in 44 (45.8%) of IAN-treated patients with a median infarct volume of 111.6 mL (Q1: 51.6 to Q3: 245.7). Clinical outcome was available for 84 IAN-treated patients. Of those, a total of 40 (47.6%) patients reached a favorable outcome after 1 year. Interventional complications were observed in 9 (9.4%) of the IAN-treated patients. Conclusion Intra-arterial spasmolysis using nimodipine infusion was associated with low treatment specific complications. Despite presenting a subgroup of severely affected SAH patients, almost half of IAN-treated patients were able to lead an independent life after 1 year of follow-up. [ABSTRACT FROM AUTHOR]

INTRODUCTION The main reasons for the unsatisfactory outcome of surgical treatment of patients with non-traumatic subarachnoid hemorrhage (SAH) due to ruptured cerebral aneurysms are vascular spasm (VS) and delayed cerebral ischemia. Lysis of blood clots in the subarachnoid space leads to the release of a large number of various vasoactive factors that stimulate cytotoxic, inflammatory reactions and oxidative stress, which may be one of the reasons for the development of VS and secondary ischemic brain damage.THE AIM OF THE STUDY Study of the dynamics of oxidative stress indicators and factors of endogenous vascular regulation in patients with non-traumatic SAH due to ruptured cerebral aneurysms.MATERIAL AND METHODS A total of 80 patients in the acute period of SAH due to ruptured cerebral aneurysms were treated and examined. The average age of the patients was 51.7 years. The control group (norm) included 25 practically healthy people, whose average age was 32.7±8.6 years. The study used the blood serum and cerebrospinal fluid of the patients. The study points were 0, 1, 3, and 7 days after the patient’s admission to the hospital. The severity of oxidative stress was assessed by the level of malonic dialdehyde (MDA) and total antioxidant activity of blood serum (TAA); vasotonic function of vascular endothelium by the content of stable metabolites of nitric oxide (NOx) and the concentration of angiotensin-converting enzyme (ACE). Biochemical studies were carried out on the biochemical analyzer “Olympus AU 2700” (Beckman Coulter, USA).RESULTS It was revealed that patients with SAH already had pronounced oxidative stress upon admission to the hospital (increased MDA level, decreased TAA level), which led to an imbalance in the endogenous regulation of vascular tone (decreased NOx level, increased ACE concentration) and increased by the 7th day after admission to the hospital. High lactate dehydrogenase (LDH) activity was observed, the peak of which was on the 7th day of observation. Determination of LDH activity may be promising as a biomarker of ischemic brain injury and a prognostic indicator of the development of an unfavorable outcome.CONCLUSIONS The obtained data indicate the need for a comprehensive approach to the treatment of patients with subarachnoid hemorrhage. The most relevant therapeutic goal is the removal of blood from the subarachnoid space of the brain to prevent increased oxidative stress and angiospasm.

Reversible cerebral vasoconstriction syndrome (RCVS) is a collective term used to describe pathological conditions with a similar clinical and radiological picture which is characterized by thunderclap headaches with a sudden onset and reversible segmental (multifocal) constriction of the cerebral arteries. The article is devoted to issues of terminology, genetic and clinical features of RSCV, and also discusses risk factors, differential diagnosis, complications and prognosis. Modern pathogenetic mechanisms and possible approaches to the treatment of this condition are presented.

Objective: Construction and validation of a predictive model for delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH) based on CT perfusion imaging parameters combined with serum nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2) and matrix metalloproteinase-9 (MMP-9). Methods: 227 aSAH patients were divided into DCI group after aSAH (n=68) and non-DCI group after aSAH (n=159) according to the occurrence of DCI. The risk factors were analyzed by multivariate Logistic regression analysis. The predictive value was verified by receiver operating characteristic (ROC) curve. Results: Compared with non-DCI group after aSAH, the proportion of Hunt-Hess grade 4-5 and cerebral vasospasm in DCI group after aSAH was significantly higher, the mean cerebral blood flow and cerebral blood volume in DCI group after aSAH were significantly lower, and the mean transit time, peak time and serum NOX2 and MMP-9 levels were significantly higher (all P<0.05). Mean cerebral blood flow, cerebral blood volume, mean transit time, peak time, NOX2 and MMP-9 were independent risk factors for DCI after aSAH (P<0.05). The area under the curve (AUC) of the prediction model based on CT perfusion imaging parameters combined with NOX2 and MMP-9 was 0.866, the specificity was 76.00%, and the sensitivity was 90.38%. Conclusion: The risk factors of DCI in aSAH patients include mean cerebral blood flow, cerebral blood volume, mean transit time, peak time, NOX2 and MMP-9, the model of CT perfusion imaging parameters combined with serum NOX2 and MMP-9 has high predictive value. [ABSTRACT FROM AUTHOR]

Purpose Subarachnoid hemorrhage (SAH) is a rare but life-threatening clinical event for pediatric patients. Cerebral vasospasm is a common complication of SAH that often leads to poor outcomes. This case report describes the use of dual intraventricular (IVT) vasodilators in a pediatric patient. Summary An 11-year-old male presented with traumatic diffuse SAH and cerebral vasospasm. Despite treatment with IVT nicardipine, intravenous (IV) milrinone by continuous infusion, enteral nimodipine, and intraarterial verapamil and milrinone given during digital subtraction angiography, transcranial Doppler (TCD) mean velocities continued to rise. IVT milrinone was then added to IVT nicardipine and IV milrinone. The combination of IVT nicardipine, IV milrinone, and rescue therapy with IVT milrinone was continued for a total of 7 days. TCD mean velocities decreased into the mild to moderate range within 2 days of the patient receiving this combined regimen and remained globally low thereafter. Conclusion This case illustrates the potential benefit of using dual IVT vasodilators to improve outcomes for pediatric patients with refractory cerebral vasospasm. [ABSTRACT FROM AUTHOR]

Reversible cerebral vasoconstriction syndrome (RCVS) is a relatively rare and underdiagnosed neurological condition that has similar clinical presentation to other neurological emergencies. Antidepressants such as selective serotonin reuptake inhibitors can be a secondary cause of RCVS. We present the case of a healthy young woman, with long term escitalopram use, who presented with bilateral neurological deficits and was found to have RCVS, whose symptoms improved remarkably after intra-arterial calcium channel blocker treatment. We discuss risk factors, theorized mechanisms, presentation, diagnostic tools, and management of RCVS. Our case should serve as a corollary for physicians to consider RCVS as a differential diagnosis for thunderclap headache, especially in patients with selective serotonin reuptake inhibitor use. [ABSTRACT FROM AUTHOR]

Purpose: The most common cause of cerebral vasospasm is subarachnoid hemorrhage, less frequently it occurs after trauma, infection, and tumor resection. Vasospasm in children is rare and has not been systematically investigated in posterior fossa surgery. Methods: The authors undertook a single-center retrospective study of all the pediatric patients who underwent surgery on the posterior fossa and presented with postoperative symptomatic vasospasm in the period from January 2018 to February 2024. Subsequently, a systematic literature review in accordance with the PRISMA guidelines was performed in the PubMed and Scopus databases to identify the published papers on symptomatic vasospasm after posterior fossa surgery in children. Results: Of the 178 patients who underwent surgery on the posterior fossa, only one patient was diagnosed with symptomatic diffuse vasospasm on postoperative day 21. The systematic literature review provided further 9 children. The underlying pathology comprised 8 intra-axial lesions with 4 medulloblastomas, 1 schwannoma in the medulla oblongata, 1 pilocytic astrocytoma, 1 primitive neuroectodermal tumor, and 1 arteriovenous malformation. The extra-axial lesions were 1 hypoglossal schwannoma and 1 oculomotor nerve schwannoma. Conclusion: Iatrogenic symptomatic vasospasm after posterior fossa surgery in children is a rare complication with an outcome ranging from complete recovery to the death of the patient. It is important for all staff involved in the care of patients undergoing surgery on the posterior fossa to be aware of this rare postoperative complication. The small number of patients affected does not allow a substantiated conclusion to be drawn about predictive risk factors. [ABSTRACT FROM AUTHOR]

Background and Purpose: Vasospasm is a common iatrogenic event during mechanical thrombectomy (MT). In such circumstances, intra‐arterial nimodipine administration is occasionally considered. However, its use in the treatment of iatrogenic vasospasm during MT has been poorly studied. We investigated the impact of iatrogenic vasospasm treated with intra‐arterial nimodipine on outcomes after MT for large vessel occlusion stroke. Methods: We conducted a retrospective analysis of the multicenter observational registry Endovascular Treatment in Ischemic Stroke (ETIS). Consecutive patients treated with MT between January 2015 and December 2022 were included. Patients treated with medical treatment alone, without MT, were excluded. We also excluded patients who received another in situ vasodilator molecule during the procedure. Outcomes were compared according to the occurrence of cervical and/or intracranial arterial vasospasm requiring intraoperative use of in situ nimodipine based on operator's decision, using a propensity score approach. The primary outcome was a modified Rankin Scale (mRS) score of 0–2 at 90 days. Secondary outcomes included excellent outcome (mRS score 0–1), final recanalization, mortality, intracranial hemorrhage and procedural complications. Secondary analyses were performed according to the vasospasm location (intracranial or cervical). Results: Among 13,678 patients in the registry during the study period, 434 received intra‐arterial nimodipine for the treatment of MT‐related vasospasm. In the main analysis, comparable odds of favorable outcome were observed, whereas excellent outcome was significantly less frequent in the group with vasospasm requiring nimodipine (adjusted odds ratio [aOR] 0.78, 95% confidence interval [CI] 0.63–0.97). Perfect recanalization, defined as a final modified Thrombolysis In Cerebral Infarction score of 3 (aOR 0.63, 95% CI 0.42–0.93), was also rarer in the vasospasm group. Intracranial vasospasm treated with nimodipine was significantly associated with worse clinical outcome (aOR 0.64, 95% CI 0.45–0.92), in contrast to the cervical location (aOR 1.37, 95% CI 0.54–3.08). Conclusion: Arterial vasospasm occurring during the MT procedure and requiring intra‐arterial nimodipine administration was associated with worse outcomes, especially in case of intracranial vasospasm. Although this study cannot formally differentiate whether the negative consequences were due to the vasospasm itself, or nimodipine administration or both, there might be an important signal toward a substantial clinical impact of iatrogenic vasospasm during MT. [ABSTRACT FROM AUTHOR]

The article discusses the limitations of using transcranial Doppler (TCD) to screen for large vessel vasospasm (LVV) after aneurysmal subarachnoid hemorrhage (aSAH). While TCD is commonly used to identify LVV as a surrogate for delayed cerebral ischemia (DCI), the two are separate entities with different treatment responses. TCD's sensitivity in detecting LVV is limited, and technical factors further reduce its accuracy, potentially leading to unnecessary and harmful interventions for DCI. The article argues against routine TCD screening for LVV, emphasizing the need for more effective treatments and randomized controlled trials in managing aSAH. [Extracted from the article]

Cerebral vasospasm (CV) following subarachnoid hemorrhage (SAH) remains one of the leading causes of high mortality and poor outcomes. Understanding the risk factors associated with CV is pivotal to improving patients' outcomes. We conducted an extensive search for analytical observational studies that analyzed the correlation between various variables and the likelihood of CV development among adult patients with SAH (age ≥ 18 years). Five scholar databases were used, namely, PubMed, EBSCO, Web of Science, Science Direct, and Google Scholar. Relevant studies published between January 1st, 2016, and August 9th, 2023, were included. The Newcastle–Ottawa Scale was adopted to assess the risk of bias among included observational studies. A total of 33 studies met the inclusion criteria. Of the 24,958 patients with SAH who were identified, 6,761 patients had a subsequent CV (27.1%). Several statistically significant risk factors were reported across the literature. Younger age, female sex, smoking, alcohol intake, modified Fisher grade 3–4, higher Hunt and Hess grading, and the presence of multiple comorbidities (diabetes, hypertension, congestive heart failure, and history of stroke) were among the well-established risk factors for CV. Additionally, leukocytosis was consistently reported to be a significant predictor in multiple studies, providing compelling evidence for its association with CV. Even though single studies reported an association between CV and certain variables, further research is necessary to investigate the implications of these findings. These include arterial tortuosity, hypokalemia, potassium to glucose gradient, hypoalbuminemia, anemia, von Willebrand factor and vascular endothelial growth factor, use of desflurane, and hemodynamic stability. Overall, this systemic review provides a comprehensive summary of the current data that evaluates the potential risk factors for the development of CV after SAH. However, because of data heterogeneity, certain factors require further validation in their correlation with CV development. Larger-scale observational and clinical trials are mandatory to extensively investigate the significant predictors of CV to lay the scientific foundation for improving outcomes in susceptible patients with SAH. [ABSTRACT FROM AUTHOR]

Background: Temperature abnormalities are common after spontaneous subarachnoid hemorrhage (SAH). Here, we aimed to describe the evolution of temperature burden despite temperature control and to assess its impact on outcome parameters. Methods: This retrospective observational study of prospectively collected data included 375 consecutive patients with SAH admitted to the neurological intensive care unit between 2010 and 2022. Daily fever (defined as the area over the curve above 37.9 °C multiplied by hours with fever) and spontaneous hypothermia burden (< 36.0 °C) were calculated over the study period of 16 days. Generalized estimating equations were used to calculate risk factors for increased temperature burdens and the impact of temperature burden on outcome parameters after correction for predefined variables. Results: Patients had a median age of 58 years (interquartile range 49–68) and presented with a median Hunt & Hess score of 3 (interquartile range 2–5) on admission. Fever (temperature > 37.9 °C) was diagnosed in 283 of 375 (76%) patients during 14% of the monitored time. The average daily fever burden peaked between days 5 and 10 after admission. Higher Hunt & Hess score (p = 0.014), older age (p = 0.033), and pneumonia (p = 0.022) were independent factors associated with delayed fever burden between days 5 and 10. Increased fever burden was independently associated with poor 3-month functional outcome (modified Rankin Scale 3–6, p = 0.027), poor 12-month functional outcome (p = 0.020), and in-hospital mortality (p = 0.045), but not with the development of delayed cerebral ischemia (p = 0.660) or intensive care unit length of stay (p = 0.573). Spontaneous hypothermia was evident in the first three days in patients with a higher Hunt & Hess score (p < 0.001) and intraventricular hemorrhage (p = 0.047). Spontaneous hypothermia burden was not associated with poor 3-month outcome (p = 0.271). Conclusions: Early hypothermia was followed by fever after SAH. Increased fever time burden was associated with poor functional outcome after SAH and could be considered for neuroprognostication. [ABSTRACT FROM AUTHOR]

Objective: Subarachnoid hemorrhage (SAH) is a life-threatening cerebrovascular condition that triggers a robust inflammatory response and cerebral vasospasm. This study aimed to evaluate the effects of anakinra, an interleukin-1 receptor antagonist, and tocilizumab, an interleukin-6 receptor antagonist, on inflammation and vasospasm in an experimental rat SAH model. Methods: Forty male Sprague Dawley rats (200–250 g) were randomly assigned to five groups: control, SAH, SAH + anakinra (ANA), SAH + tocilizumab (TCZ), and SAH + anakinra + tocilizumab (ANA+TCZ). SAH was induced by injecting non-heparinized arterial blood into the cisterna magna. Treatment groups received anakinra (50 mg/kg twice daily), tocilizumab (8 mg/kg once daily), or their combination for three days. Blood and cerebrospinal fluid (CSF) samples were analyzed for inflammatory markers (IL-1, IL-6, TNF-α, CRP), and histopathological evaluations were conducted to assess vasospasm and apoptosis. Results: SAH significantly increased pro-inflammatory cytokines (IL-1, IL-6, TNF-α, CRP) and fibrinogen levels in serum and CSF while reducing the basilar artery lumen diameter (p < 0.001). Anakinra and tocilizumab treatments significantly reduced inflammatory markers and vasospasm severity compared to the SAH group (p < 0.05). Combination therapy was more effective in reducing inflammation and vasospasm than either treatment alone (p < 0.05). Anakinra showed a stronger effect on IL-1 reduction, while tocilizumab was more effective in lowering IL-6 levels. The ANA+TCZ group exhibited a significant decrease in caspase activity, indicating reduced apoptosis (p < 0.05). Conclusions: Anakinra and tocilizumab effectively mitigated inflammation and vasospasm in an experimental SAH model, with combination therapy showing superior efficacy. These findings suggest that targeting both IL-1 and IL-6 pathways may be a promising therapeutic strategy for managing SAH complications. Further studies are warranted to evaluate long-term outcomes and clinical implications. [ABSTRACT FROM AUTHOR]

Objective To explore endovascular treatment for patients with blood blister-like aneurysms (BBA) of the internal carotid artery (ICA). Methods and Results A retrospective analysis of the clinical data of 25 patients with BBA of ICA admitted to The First Affiliated Hospital of Soochow University from January 2018 to January 2022 were conducted. All of them accepted endovascular treatment: 17 cases were treated with single-stent-assisted embolization, including 14 cases using Lvis stents and 3 cases using Enterprise stents; 4 cases were treated with double-stent-assisted embolization, all using Lvis stents; one case was treated with overlapping stent implantation, including 2 Lvis stents and one Enterprise stent; one case was treated with balloon -assisted embolization, and 2 cases were treated with Tubridge flow diverter. No aneurysm rupture occurred during the surgery. One patient had intra-stent thrombosis during the procedure, while other 24 patients showed smooth blood flow on postoperative immediate DSA. The Raymond classification showed that among the patients, there were 17 cases of grade I occlusion, 3 cases of grade II occlusion, and 5 cases of grade III occlusion. Postoperative complications included cerebral infarction (2 cases), cerebral vasospasm due to subarachnoid hemorrhage (one case), and hydrocephalus (2 cases). Six patients had aneurysm recurrence postoperatively (3 cases using a single Enterprise stent, one case using 2 Lvis stents, one case using Tubridge flow diverter, and one case using a balloon-assisted embolization), among whom 5 patients underwent repeat stent-assisted embolization treatment. And one patient still had recurrence after treatment but achieved cure by adjusting antiplatelet therapy regimen; one patient recovered by adjusting antiplatelet therapy regimen. At 12 months after surgery, the modified Rankin Scale (mRS) scores were as follows: 0 in 15 cases, 1 in 6 cases, 2 in 3 cases, and 6 in one case. The disability rate was 12% (3/25), and the mortality rate was 4% (1/25). Conclusions The degree of immediate postoperative occlusion is crucial for preventing aneurysm recurrence postoperatively. For recurrent BBA of ICA, adjustment of antiplatelet therapy should be considered first. [ABSTRACT FROM AUTHOR]

Background Vasospasm of the large cerebral arteries (CVS) after aneurysmatic subarachnoid hemorrhage (aSAH) reduces cerebral perfusion and causes delayed cerebral ischemia. Although endovascular spasmolysis shows convincing angiographic results, patients often do not improve in outcome. Delayed recognition of CVS contributes substantially to this effect. Therefore, this study aimed to confirm established and to identify unknown risk factors for CVS, which can be used for risk stratification. Methods In this monocentric, retrospective cohort study of 853 patients with aSAH, we compared demographics, clinical, and radiographic parameters at the time of aneurysm occlusion between patients who developed CVS and those who did not. Significant cohort differences were included as predictors in a multivariate analysis to address confounding. Logistic regression models were used to determine odds ratios (ORs) for the presence of CVS for each predictor. Results Of the 853 patients treated with aSAH, 304 (32%) developed CVS. In the univariable analysis, CVS was significantly associated with young age, female sex, aneurysm location, modified Fisher score, Barrow Neurological Institute (BNI) score, and surgical interventions. In the multivariable regression analysis, we identified BNI score (OR 1.33, 95% CI 1.11 to 1.58, p=0.002), decompressive craniectomy (OR 1.93, 95% CI 1.22 to 3.04, p=0.005), and aneurysm clipping (OR 2.22, 95% CI 1.50 to 3.29, p<0.001), as independent risk factors. Conclusions Young female patients with high BNI scores who undergo surgical interventions are more likely to develop CVS and should therefore be monitored most intensively after aneurysm occlusion. [ABSTRACT FROM AUTHOR]

Aneurysmal subarachnoid hemorrhage (aSAH) is often complicated by cerebral vasospasm (CVS) and delayed cerebral ischemia (DCI), which significantly impact patient outcomes. The study aimed to investigate the predictive value of systemic serum biomarker levels for CVS and DCI following aSAH. We retrospectively analyzed data for 450 aSAH patients admitted to University Hospital Düsseldorf between January 2011 and October 2021. Serum biomarkers were measured on admission. The occurrence of CVS and DCI was assessed based on clinical and radiological criteria. Multivariate logistic regression analysis was performed to determine the independent association of serum biomarkers with CVS and DCI. We compared the predictive values of various models using the area under the receiver operating characteristic curve. Of the 450 patients, 126 (28.0%) developed CVS, 123 (27.3%) developed DCI, and 62 (13.8%) developed co-occurring CVS and DCI. Patients with CVS, DCI, or both had significantly higher admission C-reactive protein (CRP) levels than those without these complications (P < 0.001). Elevated CRP levels were independently associated with an increased risk of CVS, DCI, and co-occurring CVS and DCI (P < 0.05). CRP demonstrated a higher predictive value for CVS (area under the curve [AUC]: 0.811) and co-occurring CVS and DCI (AUC: 0.802) compared to DCI alone (AUC: 0.690). Our findings suggest that admission systemic CRP levels can serve as a more valuable predictor for developing CVS than DCI following aSAH. Incorporating CRP into clinical assessments may aid in risk stratification and early intervention strategies for patients at high risk of these complications. [ABSTRACT FROM AUTHOR]

Volatile anesthetics have shown neuroprotective effects in preclinical studies, but clinical data on their use after aneurysmal subarachnoid hemorrhage (aSAH) are limited. This study aimed to analyze whether the use of volatile anesthetics for neurocritical care sedation affects the incidence of delayed cerebral ischemia (DCI), cerebral vasospasm (CVS), DCI-related infarction, or functional outcome. Data were retrospectively collected for ventilated aSAH patients (2016–2022), who received sedation for at least 180 hours. For comparative analysis, patients were assigned to a control and a study group according to the sedation used (intravenous vs. volatile sedation). Logistic regression analysis was performed to identify independent predictors of DCI, CVS, DCI-related infarction, and functional outcome. Ninety-nine patients with a median age of 58 years (interquartile range: 52–65 years) were included. Forty-seven patients (47%) received intravenous sedation, while 52 patients (53%) received (additional) volatile sedation with isoflurane (n = 30, 58%) or sevoflurane (n = 22, 42%) for a median duration of 169 hours (range: 5–298 hours). There were no significant differences between the 2 groups regarding the occurrence of DCI, angiographic CVS, DCI-related infarction, or functional outcome. In a multivariable logistic regression analysis, the use of volatile anesthetics had no impact on the incidence of DCI-related infarction or the patients' functional outcome. Volatile sedation in aSAH patients is not associated with the incidence of DCI, CVS, DCI-related infarction, or functional outcome. Although we could not demonstrate neuroprotective effects of volatile anesthetics, our results suggest that volatile sedation after aSAH has no negative effect on the patient's outcome. [ABSTRACT FROM AUTHOR]

Objective: Elevation of Troponin I (TnI) in spontaneous subarachnoid hemorrhage (SAH) patients is a well-known phenomenon and associated with cardiopulmonary complications and poor outcome. The present study was conducted to investigate the association of the TnI value on admission, and the occurrence of cerebral vasospam in SAH patients. Patients and Methods: A total of 142 patients with SAH, who were admitted to the neurosurgical intensive care unit (ICU) between December 2014 and January 2021 were evaluated. Blood samples were drawn on admission to determine TnI value. Each patient's demographic, radiological and medical data on admission, the modified Ranking Scale score at discharge as well as continuous measurements of transcranial Doppler sonography were analyzed. A maximum mean flow velocity (MMFV) > 120 cm/sec was defined as any vasospasm. These were stratified into severe vasospasms, which were defined as at least two measurements of MMFVs > 200 cm/sec or an increase of MMFV > 50 cm/sec/24 h over two consecutive days or a new neurological deterioration and mild vasospasm defined as MMFVs > 120 cm/sec in absence of severe vasospasm criteria. The total study population was dichotomized into patients with an initially elevated TnI (>0.05 µg/L) and without elevated TnI (≤0.05 μg/L). Results: A total of 52 patients (36.6%) had an elevated TnI level upon admission, which was significantly associated with lower GCS score (p < 0.001), higher WFNS score (p < 0.001) and higher Fisher grade (p = 0.01) on admission. In this context a higher rate of ischemic brain lesions (p = 0.02), a higher modified Rankin Scale score (p > 0.001) and increased mortality (p = 0.02) at discharge were observed in this group. In addition, TnI was identified as an independent predictor for the occurrence of any vasospasm and severe vasospasm. Conclusion: An initially elevated TnI level is an independent predictor for the occurrence of any and severe vasospasm in patients with SAH. [ABSTRACT FROM AUTHOR]

Subarachnoid hemorrhage (SAH) is a devastating type of stroke, leading to high mortality and morbidity rates. Cerebral vasospasm and delayed cerebral ischemia (DCI) are common complications following SAH that contribute significantly to the poor outcomes observed in these patients. Intrathecal (IT) nicardipine delivered via an existing external ventricular drain is an off‐label intervention that has been shown to be correlated with reduced DCI and improved patient outcomes. The current study aims to characterize the population pharmacokinetic (popPK) properties of intermittent IT nicardipine. Following informed consent, serial cerebrospinal fluid (CSF) samples were obtained from 16 SAH patients (50.4 ± 9.3 years old; 13 females) treated with IT nicardipine every 6 h (q6h, n = 8) or every 8 h (q8h, n = 8) for an average of 72 ± 21 doses. High‐performance liquid chromatography was used to quantify CSF concentration from each sample. Our popPK analysis showed that the CSF pharmacokinetics of IT nicardipine in the cohort was adequately described by a two‐compartment model with a lag time. Model parameter estimates were reliable (relative standard error <50%). Intracranial pressure influenced both the total clearance and the central volume of nicardipine (i.e., negative correlation, P <−.001). Calculated PK parameters were similar between q6h and q8h dosing regimens. Despite a small cohort of SAH patients, we successfully developed a popPK model to describe the nicardipine disposition kinetics in the CSF following IT administration. These findings may help inform future clinical trials designed to examine the optimal dosing of IT nicardipine. [ABSTRACT FROM AUTHOR]

Although endovascular management has been increasingly adopted for basilar apex aneurysms (BAAs), microsurgery still represents an amenable treatment option. In this case series, six female patients (median age: 46 years) with six saccular high-riding BAAs (50% ruptured) were included. The median neck size was 5.3 mm (range: 2.9–7.9), and the median length from base to dome was 7.25 mm (range: 5.2–11.4). Preoperative complications included hydrocephalus (22%) and rebleeding (22%). All patients underwent clipping with a pterional craniotomy with extension into the temporal bone base. Intraoperative aneurysm rupture occurred in one patient (17%). Postoperative complications occurred in two patients (34%), of which one died because of extensive cerebral vasospasm and hospital-acquired pneumonia. At the 6-month follow-up, all remaining patients had modified Rankin scale scores ≤ 2. Microsurgery remains a viable option for BAAs in limited-resource settings. Technical success depends on delicate tissue work, in-depth anatomical knowledge, and maneuverability in narrow corridors. [ABSTRACT FROM AUTHOR]

Background Delayed cerebral ischemia (DCI) is usually caused by cerebral vasospasm (CVS). To detect DCI and CVS, a cranial computed tomography (CT) scan will be performed, but cervical vessels are not necessarily displayed. Methods A 63-year-old female patient who suffered from aneurysmal subarachnoid hemorrhage (SAH) was treated at the authors' institution. After an initially unremarkable clinical course, she developed aphasia on day 11. CT angiography (CTA) and perfusion imaging revealed significant hypoperfusion of the left hemisphere. In addition, the CTA showed a subtotal stenosis of the internal carotid artery (ICA) at the level of the petrous segment, suspicious for a dissection. This was not detectable angiographically in the final control of the intervention and was also not clinically evident until day 11. Results Cerebral perfusion as well as the clinical symptoms normalized rapidly after stent reconstruction of the ICA. Conclusion Even though CVS is the most common cause of hypoperfusion in patients after an SAH, a peri-interventional dissection can also lead to relevant stenosis and thus to a disturbed cerebral perfusion and corresponding neurologic deficits. The time delay between the intervention and the clinical and CTA manifestation in our case is remarkable. [ABSTRACT FROM AUTHOR]

The article discusses a case of reversible peripheral vestibular deficit in a patient with vestibular migraine, highlighting the occurrence of peripheral vestibular dysfunction during acute migraine attacks. Topics include clinical presentation and diagnostic testing, the reversible nature of vestibular injury, and potential mechanisms like vasospasm or neurogenic inflammation causing vestibular symptoms.

The article discusses the rehabilitation outcomes following acute subarachnoid hemorrhage (SAH) and the impact of early functional predictors and complications on these outcomes. A retrospective cohort study was conducted on patients with non-traumatic acute SAH undergoing rehabilitation. The study found that inpatient rehabilitation significantly improved functional independence, with most patients being discharged home. Complications during rehabilitation and their effects on discharge function were highlighted, emphasizing the need for effective prevention and management strategies. The study also identified factors such as motor weakness, dysphagia, and medical complications as predictors of poorer rehabilitation outcomes. [Extracted from the article]

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Background and Purpose Methods Results Conclusions Prognostication in patients with spontaneous subarachnoid hemorrhage (SAH) can be challenging. The aim of this study was to assess whether cerebrospinal fluid (CSF) red blood cell (RBC) count and total protein (TP) concentration are associated with SAH prognosis.Patients with SAH treated at the neurological intensive care unit (ICU) in Innsbruck were included in this real‐world, observational study. Longitudinal CSF samples were collected as part of routine diagnostics. RBC count and CSF TP at the time of admission (RBCfirst, TPfirst), in Week 1 (RBCDays1–7, TPDays1–7), Week 2 (RBCDays8–14, TPDays8–14), and Week 3 or thereafter (RBCDay>14, TPDay>14), the highest detected value (RBChighest, TPhighest), as well as the RBC count adjusted for disease duration (RBCadjusted) were assessed. Primary outcomes were good functional outcome after 3 months, defined as modified Rankin scale score ≤2 and ICU survival.A total of 183 SAH patients with a female predominance (69%), a median (interquartile range [IQR]) age of 60 (50–70) years and median (IQR) Hunt and Hess score of 4 (3–5) were included. Multivariable analyses revealed that lower values of RBCfirst, RBCadjusted, RBChighest, TPfirst and TPhighest were associated with good functional outcome and hospital survival. Lower TP concentrations in Weeks 1, 2 and 3 were associated with good functional outcome, and in Weeks 1 and 2 with ICU survival. Early RBC measurements (Week 1) were associated with good functional outcome and ICU survival.Low CSF RBC counts and TP concentrations were associated with good functional outcome and ICU survival in a real‐world cohort of SAH patients requiring external ventricular drainage. [ABSTRACT FROM AUTHOR]

Early brain injury is the leading cause of poor outcomes in spontaneous subarachnoid hemorrhage (sSAH). Plasma D-dimer levels and acute cerebral ischemia have been highlighted as relevant findings in early brain injury; however, their correlation has not been substantially investigated. This retrospective, single-center cohort study was conducted at a tertiary emergency medical center from January 2004 to June 2022. Consecutive patients with sSAH who presented within 12 hours of ictus and underwent magnetic resonance imaging within 3 days were included. We assessed the correlation of plasma D-dimer levels with acute ischemic lesions detected on the diffusion-weighted imageing and the clinical characteristics. Among 402 eligible patients (mean age, 63.5 years; 62.7% women; median time from onset to arrival, 45.5 minutes), 140 (34.8%) had acute ischemic lesions. Higher plasma D-dimer levels linearly correlated with worse neurological grades, more severe SAH on initial computed tomography, acute ischemic lesions, and poor outcomes, except for patients with neurogenic stunned myocardium. In the multivariate analysis, acute ischemic lesions were significantly associated with worse neurological grades, higher plasma D-dimer levels, bilateral loss of light reaction, and advanced age. The receiver operating characteristic curve analysis showed D-dimer levels as excellent predictors for acute ischemic lesions (area under the curve, 0.897; cut-off value, 5.7 μg/mL; P < 0.0001) and unfavorable outcomes (area under the curve, 0.786; cut-off value, 4.0 μg/mL; P < 0.0001). High plasma D-dimer levels correlated with the appearance of acute ischemic lesions on diffusion-weighted imaging and were dose-dependently associated with worse neurological grades, more severe hemorrhage, and worse outcomes. [Display omitted] [ABSTRACT FROM AUTHOR]

Reversible cerebral vasoconstriction syndrome (RCVS) is a rare but significant cause of intracranial arteriopathy and stroke in young adults. The syndrome encompasses a spectrum of disorders radiologically characterized by reversible narrowing and dilation of intracranial arteries, often triggered by vasoactive drugs or the postpartum period. The hallmark clinical feature of RCVS is thunderclap headache with or without other neurological signs. Though endothelial dysfunction and sympathetic hyperactivation are hypothesized to be key mechanisms, the exact pathogenesis of RCVS is still unclear. RCVS's diagnosis could be challenging, since vasospasm proceeds centripetally, initially involving distal small pial and cortical arteries, and angiographic studies, especially brain magnetic resonance angiography (MRA) and computed tomography angiography (CTA), may miss it in the early phase of the disease, while early signs such as vascular hyperintensities may be visible on T2/FLAIR sequences before vasospasm onset. Catheter angiography is the gold standard and it could be used to assess vasospasm reversibility post-intra-arterial vasodilator administration. Treatment is mainly symptomatic, and nimodipine is the most commonly administered therapy, given orally or intra-arterially in severe cases. Since many aspects of RCVS remain partially known, further research is needed to better understand the complex pathophysiology of this unique clinical condition and to optimize specific management strategies. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Clazosentan, an endothelin receptor antagonist, is used to prevent delayed neurological deterioration in patients with subarachnoid hemorrhage due to ruptured cerebral aneurysms. However, fluid management presents challenges. This single-center case series presents the findings from eight patients undergoing fluid management using transpulmonary thermodilution while receiving clazosentan. The median age of the patients was 49 years (interquartile range: 45.5–63.5), and four (50 %) were male. The median World Federation of Neurosurgical Societies classification was 5 (interquartile range: 2–5), and the median Fisher classification was 3 (interquartile range: 3). During clazosentan treatment, the median global end-diastolic volume index based on transpulmonary thermodilution remained at 715.5 ml/m2 (interquartile range: 643–788). No ischemic neurological deficits, bilateral pulmonary edema, and pleural effusion were observed. Strict fluid management using transpulmonary thermodilution might prevent the complications associated with clazosentan.

Cerebral vasospasm (CVS), a serious complication following subarachnoid hemorrhage, is associated with high rates of mortality and disability. Emerging evidence suggests that abnormal miRNA and mRNA are involved in the development of CVS. This study aims to identify essential miRNA-mRNA regulatory pairs that contribute to CVS pathogenesis. We compared the differences between spasm and non-spasm groups after cerebral hemorrhage, identifying 183 differentially expressed genes (DEGs) and 19 differentially expressed miRNAs (DEMs) related to cerebral vasospasm from the GEO database. Further functional enrichment and KEGG analysis revealed that these DEGs were enriched in several terms and pathways, including the PI3K/AKT/mTOR signaling pathway, oxidative phosphorylation pathway, RNA degradation, and folate biosynthesis signaling pathway. By employing the degree scores method for each gene, we identified the top 10 genes and developed a protein-protein interaction (PPI) network. Additionally, we discovered 19 DEMs associated with CVS and integrated them with mRNA dataset analysis to construct a miRNA-mRNA network, which comprised 8 functionally differentially expressed DEMs and 6 target mRNAs. Experimental validation confirmed the significant regulatory roles of four miRNAs (Let-7a-5p, miR-24-3p, miR-29-3p, and miR-132-3p) and two mRNAs (CDK6 and SLC2A1) in the pathogenesis of CVS. In conclusion, this comprehensive study identifies pivotal miRNAs and their target mRNAs associated with CVS through an integrated bioinformatics analysis of miRNA-mRNA co-expression networks. This approach elucidates the intricate molecular mechanisms underlying CVS and uncovers potential therapeutic targets, thereby providing a valuable foundation for refining and optimizing future treatment strategies.

Abstract Cerebral vasospasm (CVS) is an important contributor to delayed cerebral ischemia following aneurysmal subarachnoid hemorrhage (aSAH), leading to high morbidity and long-term disability. While several microRNAs (miRNAs) have been implicated in vasospasm, the underlying mechanisms for CVS remain poorly understood. Our study aims to identify miRNAs that may contribute to the development of CVS. Whole-blood samples were obtained during or outside of vasospasm from aSAH patients whose maximal vasospasm was moderate or severe. MiRNAs were isolated from serial whole-blood samples, and miRNA sequencing was performed. Differentially expressed miRNAs were identified and the expression levels in patients’ samples were verified using real-time qPCR. The biological functions of identified miRNA were evaluated in human brain endothelial cells (HBECs). MiRNA profiling revealed significant upregulation of miR-148b-3p in patients during CVS. We demonstrated that miR-148b-3p directly targeted and decreased the expression of ROCK1, affecting cell proliferation, migration, and invasion of HBECs through the ROCK-LIMK-Cofilin pathway. We propose that the upregulation of miRNA-148b-3p plays a role in the development of CVS by regulating actin cytoskeletal dynamics in HBECs, which is crucial for vascular function. Our study highlights miR-148b-3p as a potential diagnostic marker as well as therapeutic target for CVS following aSAH.

Abstract Cerebral vasospasm is determined as a temporary narrowing of cerebral arteries a few days after an aneurysmal subarachnoid hemorrhage. The onset of this vascular event usually evolves with new neurological deficits or progression of ischemic areas. The success of interventions to treat or revert this condition is not satisfying. In addition to cerebral vasospasm, early brain injury plays an important role as a contributor to subarachnoid hemorrhage’s mortality. In this sense, stellate ganglion block appears as an alternative to reduce sympathetic system’s activation, one of the main pathophysiological mechanisms involved in brain injury. Over the past few years, there is growing evidence that stellate ganglion block can contribute to decline patient morbidity from subarachnoid hemorrhage. Is it time to include this procedure as a standard treatment after aneurysm rupture?

Arcanobacterium haemolyticum, found as normal flora in healthy individuals, is an unusual culprit for pharyngitis and sinusitis in young adults, rarely leading to severe infections. Here, we present a singular case involving a 19-year-old immunocompetent male who experienced complications arising from A haemolyticum sinusitis, leading to orbital and intracranial sinogenic complications. The patient developed severe cerebral vasospasm with delayed cerebral ischemia, necessitating aggressive management encompassing daily catheter-directed intra-arterial infusions, surgical source control, and maximal medical therapy.This case explores the challenging diagnostic and management aspects associated with cerebral artery vasospasm secondary to bacterial meningoencephalitis. The abrupt neurological decline in such patients presents a dilemma in recognizing the occurrence of cerebral vasospasm versus the progression of meningoencephalitis. By utilizing computed tomography brain perfusion scans, we were able to identify delayed cerebral ischemia due to cerebral vasospasm, acknowledging that this modality was not used to identify classical territorial stroke infarcts. This decision was made based on the understanding of the potential for bacterial-induced cerebral vasospasm to involve both hemispheres.

Cerebral vasospasm (CVS) is an important contributor to delayed cerebral ischemia following aneurysmal subarachnoid hemorrhage (aSAH), leading to high morbidity and long-term disability. While several microRNAs (miRNAs) have been implicated in vasospasm, the underlying mechanisms for CVS remain poorly understood. Our study aims to identify miRNAs that may contribute to the development of CVS. Whole-blood samples were obtained during or outside of vasospasm from aSAH patients whose maximal vasospasm was moderate or severe. MiRNAs were isolated from serial whole-blood samples, and miRNA sequencing was performed. Differentially expressed miRNAs were identified and the expression levels in patients' samples were verified using real-time qPCR. The biological functions of identified miRNA were evaluated in human brain endothelial cells (HBECs). MiRNA profiling revealed significant upregulation of miR-148b-3p in patients during CVS. We demonstrated that miR-148b-3p directly targeted and decreased the expression of ROCK1, affecting cell proliferation, migration, and invasion of HBECs through the ROCK-LIMK-Cofilin pathway. We propose that the upregulation of miRNA-148b-3p plays a role in the development of CVS by regulating actin cytoskeletal dynamics in HBECs, which is crucial for vascular function. Our study highlights miR-148b-3p as a potential diagnostic marker as well as therapeutic target for CVS following aSAH. [ABSTRACT FROM AUTHOR]

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. "In subarachnoid hemorrhage (SAH), therapies are limited and clinical outcomes remain disappointing. The authors show a contribution of the urotensin II system in microvascular changes, vasospasm, neuroinflammation and cognitive deficits post-SAH, primarily through meningeal cells and border-associated macrophages [ABSTRACT FROM AUTHOR]