Cerebral Vasospasm In Patients Research Articles

Transcranial Doppler in the Detection of Cerebral Vasospasm After Subarachnoid Hemorrhage.

Background Transcranial Doppler (TCD) is a simple, noninvasive, nonionizing, portable technique but not widely practiced to detect cerebral vasospasm after subarachnoid hemorrhage (SAH). Objective The aim of this study was to assess the performance of TCD in the detection of cerebral vasospasm in patients with SAH considering CT angiography (CTA) as a gold standard. Methods and material This cross-sectional study included 50 patients with acute SAH admitted to the National Institute of Neurosciences & Hospital (NINS & H), Dhaka, Bangladesh, from February to June 2021. The neurological status, severity of SAH, and initial CT findings were recorded. All patients were screened for cerebral vasospasm with TCD on the 4th, 7th, 10th, and 14th days after the event. Screening of cerebral vasospasm by CTA was done on the 14th day of the event or earlier if TCD suggested vasospasm. Results The mean age of the participants was 51.4 ±13.4 years (mean ± SD), and females were predominant (N=29, 58%). CTA detected cerebral vasospasm in 18 (36%) participants, but TCD could detect it in only 13 (26%) cases. Among the participants who had no vasospasm by CTA, all but one were also found to have no vasospasm by TCD. The agreement between TCD and CTA in detecting cerebral vasospasm was significant (p<0.001, κ=0.726). TCD shows good specificity (96.9%) and positive predictive value (92.8%), but sensitivity (72.2%) and negative predictive value (81.6%) were comparatively lower. Overall, the diagnostic accuracy of TCD in detecting cerebral vasospasm was 88%. Conclusions Although compared to CTA, TCD is a highly specific but less sensitive tool in detecting vasospasm, TCD remains a reliable screening tool for detecting vasospasm following SAH.

Impact of human serum albumin level on symptomatic cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage.

To investigate the impact of human serum albumin (HSA) levels on symptomatic cerebral vasospasm (SCVS) in patients with aneurysmal subarachnoid hemorrhage (aSAH). We retrospectively reviewed the medical records. SCVS was defined as the development of a new neurological deterioration when the cause was considered to be ischemia attributable to vasospasm after other possible causes of worsening had been excluded. The aSAH patients were divided into two groups: those with SCVS (group 1) and those without SCVS (group 2). The HSA level data on the 1st, 2nd, and 3rd day after admission was collected. Multivariate logistical regression and receiver operating characteristic (ROC) analysis were performed to evaluate the ability of HSA level to predict the development of SCVS. A total of 270 patients were included in our study, of which 74 (27.4%) developed SCVS. The average and lowest HSA levels were lower in group 1 (P < 0.001). In univariate logistic regression, white blood cell count, neutrophil count, and average and lowest HSA levels were associated with SCVS. After adjustment for age, CT Fisher grade, Hunt-Hess grade, and WFNS grade, both the average and lowest HSA levels remained independent predictors of SCVS (P < 0.001). The CT Fisher grade was confirmed to be an independent predictor of SCVS across each model. ROC analysis revealed that the lowest HSA level was a better predictor for SCVS than average HSA level and CT Fisher grade. Clinicians are encouraged to measure HSA levels for the first 3 days after admission to predict the occurrence of SCVS after aSAH.

Cervical Ganglion Sympathectomy to Treat Cerebral Vasospasm in Subarachnoid Hemorrhage.

Delayed cerebral ischemia (DCI) is still a significant cause of death and disability after aneurysmal subarachnoid hemorrhage. Cerebral vasospasm represents one of the most reported mechanisms associated with DCI. The management of DCI-related vasospasm remains a significant challenge for clinicians; induced hypertension, intraarterial vasodilators, and/or intracranial vessel angioplasty-particularly in refractory or recurrent cases-are the most used therapies. Because an essential role in the pathophysiology of cerebral vasospasm has been attributed to the adrenergic sympathetic nerves, a "sympatholytic" intervention, consisting of a temporary interruption of the sympathetic pathways using local anesthetics, has been advocated to minimize the vascular narrowing and reverse the consequences of cerebral vasospasm on tissue perfusion. In this review, we have analyzed the existing literature on the block of the cervical ganglions, particularly the stellate ganglion, in managing refractory cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage. These findings could help clinicians to understand the potential role of such intervention and to develop future interventional trials in this setting.

Ang-1 Inhibited Endoplasmic Reticulum Stress and Apoptosis of VECs in Rats with aSAH-induced CVS Through the Regulated PI3K/Akt Pathway.

To explore angiopoietin-1 (Ang-1) involved in cerebral vasospasm (CVS) after aneurysmal subarachnoid hemorrhage (aSAH) through its effect on endoplasmic reticulum stress (ERS) and apoptosis of vascular endothelial cells (VECs). CVS accounts for high morbidity and mortality of aSAH. Abnormal cellular physiological processes of VECs play a critical role in aSAH-induced CVS. In addition, Ang-1 is involved in regulating vascular structure and function. To study the role of Ang-1 played in CVS and the underlying mechanism. Blood samples of 130 aSAH patients were collected from 2016 to 2020 at West China Hospital of Sichuan University. A two-hemorrhage rodent model was employed to structure an aSAH-induced CVS rat model. Moreover, oxyHb was used to treat VECs to construct a CVS cell model in vitro. ELISA was used to measure the level of Ang-1 and HE staining to assess the rat's basilar arteries. Subsequently, CCK-8 was used to detect cell viability ability, and flow cytometry was used to test the cell apoptosis rate. Western blotting was used to determine the expression level of ERS marker and apoptosis-related proteins. There was an abnormally low expression of Ang-1 in CVS patients and CVS rats; besides, oxyHb treatment decreased Ang-1 in VECs in a concentration-dependent manner. Ang-1 treatment led to the thinner basilar artery wall and lumen circumference in CVS rats; moreover, in oxyHbtreated VECs, Ang-1 treatment inhibited ERS and apoptosis. In addition, the expression of p-PI3K and p-Akt in the CVS group decreased, while the expression of p53 in the CVS group increased. The expression of p-PI3K and p-Akt in 8 CVS rats negatively correlates with the expression of Ang- 1, but the correlation between p53 and Ang-1 was positive. Furthermore, the results suggested that Ang-1 suppressed ERS and apoptosis of VECs through the regulated PI3K/Akt/p53 pathway. Elevated Ang-1 inhibited p53-mediated ERS and apoptosis of VECs through the activated PI3K/Akt pathway; Ang-1 might be an attractive treatment strategy for CVS.

More is less: Effect of ICF-based early progressive mobilization on severe aneurysmal subarachnoid hemorrhage in the NICU.

Aneurysmal subarachnoid hemorrhage (aSAH) is a type of stroke that occurs due to a ruptured intracranial aneurysm. Although advanced therapies have been applied to treat aSAH, patients still suffer from functional impairment leading to prolonged stays in the NICU. The effect of early progressive mobilization as an intervention implemented in the ICU setting for critically ill patients remains unclear. This retrospective study evaluated ICF-based early progressive mobilization's validity, safety, and feasibility in severe aSAH patients. Sixty-eight patients with aSAH with Hunt-Hess grades III-IV were included. They were divided into two groups-progressive mobilization and passive movement. Patients in the progressive mobilization group received progressive ICF-based mobilization intervention, and those in the passive movement group received passive joint movement training. The incidence of pneumonia, duration of mechanical ventilation, length of NICU stay, and incidence of deep vein thrombosis were evaluated for validity. In contrast, the incidence of cerebral vasospasm, abnormally high ICP, and other safety events were assessed for safety. We also described the feasibility of the early mobilization initiation time and the rate of participation at each level for patients in the progressive mobilization group. The results showed that the incidence of pneumonia, duration of mechanical ventilation, and length of NICU stay were significantly lower among patients in the progressive mobilization group than in the passive movement group (P = 0.031, P = 0.004, P = 0.012), but the incidence of deep vein thrombosis did not significantly differ between the two groups. Regarding safety, patients in the progressive mobilization group had a lower incidence of cerebral vasospasm than those in the passive movement group. Considering the effect of an external ventricular drain on cerebral vasospasm (P = 0.015), we further analyzed those patients in the progressive mobilization group who had a lower incidence of cerebral vasospasm in patients who did not have an external ventricular drain (P = 0.011). Although we found 2 events of abnormally increased intracranial pressure in the progressive mobilization group, there was no abnormal decrease in cerebral perfusion pressure in the 2 events. In addition, among other safety events, there was no difference in the occurrence of adverse events between the two groups (P = 0.073), but the number of potential adverse events was higher in the progressive mobilization group (P = 0.001). Regarding feasibility, patients in the progressive mobilization group were commonly initiated 72 h after admission to the NICU, and 47.06% were in the third level of the mobilization protocol. We conclude that the ICF-based early progressive mobilization protocol is an effective and feasible intervention tool. For validity, more mobilization interventions might lead to less pneumonia, duration of mechanical ventilation and length of stay for patients with severe aSAH in the NICU, Moreover, it is necessary to pay attention over potential adverse events (especially line problems), although we did not find serious safety events.

Poor expression of miR-195-5p can assist the diagnosis of cerebral vasospasm after subarachnoid hemorrhage and predict adverse outcomes.

Patients with spontaneous subarachnoid hemorrhage (SAH) may develop refractory arterial cerebral vasospasm (CVS), which is the leading cause of death in SAH patients. This study explored the clinical diagnostic value of serum miR-195-5p levels in CVS after SAH (SAH + CVS) and its relationship with the prognosis of SAH + CVS. A total of 110 patients with spontaneous SAH were divided into the SAH group (N=62) and SAH + CVS group (N=58), with 60 healthy subjects as controls. The clinical data of blood glucose, blood sodium fluctuation, and serum lactic acid were recorded. miR-195-5p serum level was detected by RT-qPCR and its diagnostic value on SAH + CVS was analyzed by receiver operating characteristic curve. Serum levels of PDGF/IL-6/ET-1 and their correlation with miR-195-5p were analyzed using RT-qPCR, enzyme-linked immunosorbent assay, and Pearson's method. The patient prognosis was evaluated by Glasgow Outcome Scale. The effect of miR-195-5p levels on adverse prognosis was analyzed by Kaplan-Meier method and Cox regression analysis. miR-195-5p was lowly expressed in the serum of SAH patients and lower in SAH + CVS patients. Serum miR-195-5p level assisted the diagnosis of SAH and SAH + CVS and was negatively correlated with PDGF/IL-6/ET-1 levels and was an independent risk factor together with ET-1 and blood glucose for SAH + CVS. miR-195-5p low expression predicted a higher cumulative incidence of adverse outcomes and was an independent predictor of adverse outcomes. Poor expression of miR-195-5p can assist the diagnosis of SAH + CVS and predict higher adverse outcomes.

Effect of early stellate ganglion block in cerebral vasospasm after aneurysmal subarachnoid hemorrhage (BLOCK-CVS): study protocol for a randomized controlled trial

IntroductionStellate ganglion block has been reported to expand cerebral vessels and alleviate vasospasm after aneurysmal subarachnoid hemorrhage. However, the causal relationship between early stellate ganglion block and cerebral vasospasm prevention has not yet been established. The purpose of this study was to explore the effectiveness and safety of early stellate ganglion block as a preventive treatment for cerebral vasospasm and delayed cerebral ischemia.Methods/designThis is a single-center, prospective, randomized, controlled, blinded endpoint assessment superiority trial. A total of 228 patients will be randomized within 48 h of aneurysmal subarachnoid hemorrhage onset in a 1:1 ratio into two groups, one group receiving an additional e-SGB and the other group receiving only a camouflaging action before anesthesia induction in the operating room. The primary outcome is the incidence of symptomatic vasospasm within 14 days after aSAH. Further safety and efficacy parameters include the incidence of radiographic vasospasm, new cerebral infarction, postoperative delirium, and complications up to 90 days after surgery; postoperative cerebral hemodynamics; Mini-Mental State Examination score; modified Rankin scale score; and all-cause mortality up to 90 days after surgery.DiscussionThis is a randomized controlled trial to explore the effectiveness and safety of early stellate ganglion block as a preventive treatment to reduce cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage. If the results are positive, it may provide a new direction for the prevention and treatment of cerebral vasospasm and delayed cerebral ischemia.Trial registrationThe study was registered on Clincaltrials.gov on December 13, 2020 (NCT04691271).

The Benefits and Feasibility of External Lumbar Cerebrospinal Fluid Drainage for Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage: Meta-Analysis and Trial Sequential Analysis.

Cerebral vasospasm after aneurysmal subarachnoid hemorrhage is a main cause contributing to poor outcomes. Removal of blood from the subarachnoid may decrease development of cerebral vasospasm. The purpose of this study is to determine the effect of lumbar cerebrospinal fluid (CSF) drainage on cerebral vasospasm and related complications through meta-analysis and trial sequential analysis (TSA). A systematic search of the literature was performed. Case-control studies of the effects of external lumbar drainage in patients with subarachnoid hemorrhage were included. The association between lumbar drain and vasospasm, cerebral infarction, subsequent treatment, and mortality were evaluated. Eleven of 122 articles were included in the meta-analysis. Lumbar CSF drainage reduces occurrence of vasospasm and related complications. In meta-analysis, the pooled odds ratio for symptomatic vasospasm, cerebral infarct, endovascular treatment for vasospasm, and mortality was 0.40 (95% confidence interval [CI], 0.31-0.51; P= 0.00001), 0.47 (95% CI, 0.35-0.62; P < 0.0001), 0.29 (95% CI, 0.18-0.46; P < 0.0001), and 0.41, (95% CI, 0.23-0.74; P= 0.003), respectively, compared with the non-lumbar drainage group. In TSA, the cumulative Z line crossed α-spending boundaries and reached the required sample size in analysis of symptomatic vasospasm and endovascular treatment for vasospasm. Lumbar CSF drainage can decrease symptomatic vasospasm, cerebral infarction, subsequent endovascular treatment, and mortality. Through TSA, the accuracy and reliability of the effect of lumbar CSF drainage-related cerebral vasospasm and endovascular treatment are increased. Further studies of the association between lumbar drain and cerebral infarction and mortality are required to confirm the generalization of the results.

Transcranial Doppler Monitoring in Subarachnoid Hemorrhage

Cerebral vasospasm and delayed cerebral ischemia are common complications associated with subarachnoid hemorrhage (SAH) outcomes. Various modalities can be used to evaluate and detect cerebral vasospasm after SAH. Transcranial Doppler (TCD) ultrasonography can be used as an appropriate bedside dynamic monitoring tool to screen for the presence and progression of cerebral vasospasm in patients with SAH. This article briefly reviewed the severity of SAH and pathophysiology of vasospasm. In addition, information regarding the use of TCD for monitoring cerebral vasospasm, several variables measured by TCD to monitor vasospasm detection, and differentiating vasospasm from physiological conditions in the clinical setting following SAH were presented in this article.

Risk Factors for Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage: A Tertiary Care Center Experience

Objectives Cerebral vasospasm in subarachnoid hemorrhage (SAH) is associated with high morbidity and mortality. There is a lack of consensus on the risk factors leading to cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage (aSAH). In this retrospective study, our objective was to determine the association of risk factors for cerebral vasospasm aSAH. Methods A total of 259 charts of aSAH patients consecutively admitted to the surgical intensive care unit of Hamad General Hospital from January 2007 to December 2016 were reviewed and included. The patient's demographic data, including comorbidities like hypertension (HTN), was recorded. Variables of interest included measurements of the neurological deficit on admission, the severity of SAH, treatment modality, and the initial computerized tomography scan of the head for intraventricular hemorrhage, intracerebral hemorrhage, or hydrocephalus. Multivariate analysis and multiple logistic regression analyzed the relationship to identify the association of independent variables. Results Out of the 259 patients, 34% ( n = 87) suffered from cerebral vasospasm. The severity of SAH was associated with the development of cerebral vasospasm ( p < 0.05). The presence of HTN and neurological deficits on admission were associated with an increased risk of cerebral vasospasm ( p < 0.05, p < 0.01, respectively). Hydrocephalus requiring treatment using external ventricular drains decreased the risk of cerebral vasospasm ( p < 0.05). Intraventricular and intracerebral hemorrhage were not associated with cerebral vasospasm ( p = 0.25, p = 0.16). The endovascular treatment of cerebral aneurysms was associated with an increased risk of cerebral vasospasm ( p < 0.05). Conclusion Cerebral vasospasm is common among patients admitted with aSAH. It is significantly associated with the history of HTN, the neurological deficit on admission that corelates more strongly to the motor deficit on admission, the severity of hemorrhage (modified Fischer score), and endovascular treatment. External ventricular drainage was associated with a decrease in cerebral vasospasm. The present study's findings shed light on cerebral vasospasm's risk factors in the country and the region.

276 Bilirubin Oxidative Products as Predictive Biomarkers of Cerebral Vasospasm: A Pilot Study

OBJECTIVES/GOALS: Our aim is to understand the role bilirubin oxidation products play in the development of cerebral vasospasm in patients with subarachnoid hemorrhage. We aim to evaluate the time course of bilirubin, HO-1, and SOD1 in relation to the subsequent development of vasospasm in to establish predictors of vasospasm development. METHODS/STUDY POPULATION: Prospective cohort observational study involving collection of CSF samples of pts admitted to KU NeuroICU with SAH and placement of EVD. CSF will be extracted from the EVD of patients on the day of placement of the EVD, and then each subsequent day for a total of 10 days. Bilirubin concentration will be determined by means of spectrophotometry. HO-1 will be measured using a commercially available ELISA kit. Cu/Zn-Superoxide Dismutase will be measured using a commercially available ELISA kit. A review of patients chart will then be performed following discharge from hospital to determine if a diagnosis of vasospasm was made, details of the vasospasm (i.e. symptoms, severity), as well as to obtain demographic data and events occurring during patients admission that could confound statistical analysis. RESULTS/ANTICIPATED RESULTS: First: we will investigate the feasibility of collecting serial CSF samples and processing them for target analyte quantification. We predict that the protocol will yield quality data that will result in insight on the pathophysiology of cerebral vasospasm. Second: we will characterize the changes in target CSF bilirubin breakdown analytes over 10 days. From this we hypothesize that as bilirubin oxidation increases, the propensity for cerebral vasospasm will also increase. DISCUSSION/SIGNIFICANCE: If there is a clear correlation between formation of bilirubin and increase in HO-1, and SOD1, with the clinical signs of vasospasm, this could be used as a biomarker for not only identifying patients at risk for developing these complications but also a means to follow the effectiveness of potential therapies.

Leukocytosis and C-Reactive Protein May Predict Development of Secondary Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage.

Background and Objectives: Secondary cerebral vasospasm (CV) with subsequent delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH) remains an unpredictable pathology. The aim of this retrospective study was to investigate the association between inflammatory parameters, white blood cell (WBC) count, and C-reactive protein plasma levels (CRP) and the occurrence of secondary CV in patients with aSAH. Materials and Methods: The medical records of 201 Intensive Care Unit patients in Riga East University Hospital with aSAH were retrospectively reviewed in a 24-month period. WBC count and CRP values were observed at admission to the hospital and on the third day. According to the inclusion criteria, 117 (48 males) participants were enrolled for further analysis, with average age of 56 ± 15 years (mean ± SD). In total, secondary CV was diagnosed in 21.4% of cases, and DCI in 22.4% of cases. The patients were classified into three groups: SAH-CV group (n = 25), SAH-DCI group (n = 12), and SAH or control group (n = 80), for comparative analysis. Results: We found that SAH-CV patients demonstrated notably higher inflammatory parameters compared to controls: WBC 13.2 ± 3.3 × 109/L vs. 11.2 ± 3.7 × 109/L; p = 0.01 and CRP median 9.3 mg/L vs. 1.9 mg/L; p < 0.001, respectively. We found that the odds of developing CV increased by 5% for each CRP increase of 1 mg/L at admission (OR, 1.05; CI, 1.014–1.087; p = 0.006). Concomitantly, the odds increased by 16% for every rise in WBC count of 1 × 109/L (OR, 1.16; CI, 1.02–1.32; p = 0.02). WBC count was associated with the occurrence of CV with 96% sensitivity and 40% specificity, with a cut off level of 10.015 × 109/L and AUC 0.683; p = 0.006. CRP displayed 54% sensitivity and 90% specificity with a cut off value of 8.9 mg/L and AUC 0.751; p < 0.001. Moreover, higher values of inflammatory parameters at admission correlated with a longer stay in ICU (r = 0.3, p = 0.002 for WBC count and r = 0.305, p = 0.002 for CRP values), and poor outcome (death) was significantly associated with higher CRP values at admission and on the third day (16.1. vs. 2.2. and 57.4. vs. 11.1, p < 0.001, respectively). Higher mortality was detected in SAH-CV patients (32%) compared to controls (6.3%; p < 0.001). Conclusions: Inflammatory parameters such as WBC count and CRP values at admission might be helpful to predict the development of secondary CV.

Initiating Mobilization Is Not Associated with Symptomatic Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage: A Retrospective Multicenter Case-control Study.

The study aim was to investigate the association between initiating mobilization within 7 days after onset and symptomatic cerebral vasospasm (SCV) in patients with aneurysmal subarachnoid hemorrhage (aSAH). This was a retrospective multicenter case-control study in Japan. Patients with a diagnosis of aSAH who underwent physical therapy with/without occupational therapy were included and categorized into 2 groups according to the presence or absence of SCV. Initiating mobilization was defined as sitting on the bed edge (at least once, with/without assist, regardless of duration) within 7 days after aSAH onset. Cox proportional hazards regression analysis was performed to evaluate the association between initiating mobilization within 7 days after onset and SCV. The analysis included 510 patients. Among all included patients, 57 (11.2%) patients had SCV. In the univariate Cox proportional hazards regression analysis, initiating of mobilization was not associated with SCV (hazard ratio [HR] = 0.78; 95% confidence interval [CI] = 0.45-1.32). In the multivariate analysis, only the modified Fisher scale was significantly associated with SCV (HR = 26.23; 95% CI = 1.21-571.0). Initiating mobilization within 7 days after aSAH onset was not associated with SCV in patients with aSAH.

Impact of Stellate Ganglion Block in the Management of Cerebral Vasospasm: A Prospective Interventional Study.

Stellate ganglion block (SGB) causes blockage of sympathetic nerve activity, which may lead to intracerebral vessel dilatation and relieve cerebral vasospasm in patients of aneurysmal subarachnoid hemorrhage (aSAH). The aim of this study was to evaluate the efficacy and safety of SGB to relieve cerebral vasospasm on clinicoradiological parameters. We prospectively included 20 patients with clinical and angiographic evidence of vasospasm post aneurysmal clipping. Cerebral blood flow velocity and Lindegaard ratio were assessed using transcranial Doppler (TCD). Location of vasospasm, vessel diameter, vasospasm severity, parenchymal filling time, and venous sinus filling time were assessed on digital subtraction angiography (DSA). Patients received ultrasound-guided SGB with 10 mL of 0.5% bupivacaine on the ipsilateral side of the vasospasm. After 30 minutes, the neurological status, TCD, and DSA parameters were reevaluated. After SGB, there was statistically significant reduction in the middle cerebral artery (MCA) peak systolic velocity (P = 0.005), mean flow velocity (P = 0.025), and Lindegaard ratio (P = 0.022) on TCD. We observed significant dilatation in the mean vessel diameter measured at the mid-M1 segment of MCA (P = 0.003) and mid-A1 segment of ACA (P = 0.002) on DSA. The mean parenchymal filling time and mean venous sinus filling time decreased nonsignificantly after SGB (P = 0.163/0.104). Neurological improvement was observed in five (25%) patients. SGB has positive clinicoradiological influence in the management of cerebral vasospasm of large vessels. However, its effect on cerebral microvasculature is limited and needs a larger database for further analysis.

Early Fevers and Elevated Neutrophil-to-Lymphocyte Ratio are Associated with Repeat Endovascular Interventions for Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage.

Patients with aneurysmal subarachnoid hemorrhage (aSAH) may develop refractory arterial cerebral vasospasm requiring multiple endovascular interventions. The aim of our study is to evaluate variables associated with need for repeat endovascular treatments in refractory vasospasm and to identify differences in outcomes following one versus multiple treatments. We retrospectively reviewed patients treated for aSAH between 2017 and 2020 at two tertiary care centers. We included patients who underwent treatment (intraarterial infusion of vasodilatory agents or mechanical angioplasty) for radiographically diagnosed vasospasm in our analysis. Patients were divided into those who underwent single treatment versus those who underwent multiple endovascular treatments for vasospasm. Of the total 418 patients with aSAH, 151 (45.9%) underwent endovascular intervention for vasospasm. Of 151 patients, 95 (62.9%) underwent a single treatment and 56 (37.1%) underwent two or more treatments. Patients were more likely to undergo multiple endovascular treatments if they had a Hunt-Hess score > 2 (odds ratio [OR] 5.10 [95% confidence interval (CI) 1.82-15.84]; p = 0.003), a neutrophil-to-lymphocyte ratio > 8.0 (OR 3.19 [95% CI 1.40-7.62]; p = 0.028), and more than two fevers within the first 5days of admission (OR 7.03 [95% CI 2.68-20.94]; p < 0.001). Patients with multiple treatments had poorer outcomes, including increased length of stay, delayed cerebral ischemia, in-hospital complications, and higher modified Rankin scores at discharge. A Hunt-Hess score > 2, a neutrophil-to-lymphocyte ratio > 8.0, and early fevers may be predictive of need for multiple endovascular interventions in refractory cerebral vasospasm after aSAH. These patients have poorer functional outcomes at discharge and higher rates of in-hospital complications.

Efficacy and prognosis following combined cinepazaide maleate/nimodipine therapy in cerebral vasospasm patients after hemorrhage

Purpose: To investigate the efficacy and prognosis following treatment of cerebral vasospasm (CVS) patients with a combination of cinnarizide maleate and nimodipine after subarachnoid hemorrhage (SAH).Methods: Eighty-eight patients with CVS after SAH were selected and divided into control group (CG) and study group (EG), each with 44 patients (n = 44). Patients in CG were treated with intravenous infusion of cinnarizide maleate, while those in EG received intravenous infusion of cinnarizide maleate together, and their clinical efficacy and prognosis were compared.Results: Compared with CG, total treatment effectiveness (response) in EG was significantly higher, while levels of inflammatory factors were lower (p &lt; 0.05). Serum protein levels of S100 β and ET-1, and MCA blood flow velocity in EG were notably lower (p &lt; 0.05), but GCS scores were highercompared with CG (p &lt; 0.05). The NIHSS scores were lower and BI indices were higher in EG than in CG (p &lt; 0.05).Conclusion: Treatment of CVS patients after SAH using a combination of cinnarizide maleate and nimodipine effectively reduces the levels of inflammatory factors, improves quality of prognosis, and relieves symptoms of CVS, when compared with administration of cinnarizide maleate only. Therefore, the combination treatment is recommended for the management of CVS after SAH.

Analysis of risk factors correlated with angiographic vasospasm in patients with aneurysmal subarachnoid hemorrhage using explainable predictive modeling

Cerebral vasospasm (CAV) is a major complication of aneurysmal subarachnoid hemorrhage (aSAH) in patients with ruptured intracranial aneurysm. Explainable artificial intelligence (XAI) was used to analyze the contribution of risk factors on the development of CAV. We obtained data about patients (n = 343) treated for aSAH in our hospital. Predictive factors including age, aneurysm size, Hunt and Hess grade, and modified Fisher grade were used as input to analyze the contribution and correlation of factors correlated with CAV using a random forest regressor. An analysis conducted using an XAI model showed that aneurysm size (27.6%) was most significantly associated with the development of CAV, followed by age (20.7%) and Glasgow coma scale score (7.1%). In some patients with an estimated artificial intelligence-selected CAV value of 51%, the important risk factors were aneurysm size (9.1 mm) and location, and hypertension is also considered a major influencing factor. We could predict that Fisher grade 3 contributed to 20.3%, and the group using Antiplatelet contributed to 12.2% which is expected to lower cerebral CAV compared to the Control group (16.9%). The accuracy rate of the XAI system was 85.5% (area under the curve = 0.88). Using the modeling, aneurysm size and age were quantitatively analyzed and were found to be significantly associated with CAV in patients with aSAH. Hence, XAI modeling techniques can be used to analyze factors correlated with CAV by schematizing prediction results in some patients. Moreover, poor Fisher grade and use of postoperative antiplatelet agent are important factors for prediction of CAV.

Vitamin D as a modifiable risk factor, predictor, and theoretical therapeutic agent for vasospasm in spontaneous subarachnoid hemorrhage.

Delayed deterioration associated with cerebral vasospasm (CVS) is a feared complication after spontaneous subarachnoid hemorrhage (SAH) and is one of the leading causes of death in patients with intracranial hemorrhage. The pathophysiology of vasospasm is complex and not fully understood, involving multiple inflammatory pathways in addition to vasoconstriction induced ischemia. Current treatment with anti-inflammatory or vasodilatory medications has been met with limited success and has not led to a decrease in vasospastic associated mortality prompting continued investigation of potential treatment options. The active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25-VitD3), is a hormone with downstream effects that induce anti-inflammatory pathways, promote nitric oxide (NO) induced vasodilation, and lead to neuroprotective-gene expression, which may be useful in mitigating the vascular pathogenesis associated with CVS. A high prevalence of vitamin D deficiency has been identified in patients admitted with SAH. Low vitamin D levels in patients, as determined by time of year, has also been correlated to an increased incidence and severity of CVS. Further, the therapeutic usefulness of 1,25-VitD3 has been demonstrated in animal models leading to a decreased incidence of CVS but has yet to be thoroughly investigated in human studies. In this review, we will discuss the findings that suggest the potential of utilizing vitamin D as a predictive indicator, method of prevention, and or treatment option for CVS in patients following spontaneous SAH.

Clinical Efficacy of Shenmai Injection in the Treatment of Cerebral Vasospasm after Ruptured Aneurysm Surgery

Objective: To investigate the therapeutic effect of Shenmai Injection on postoperative cerebral vasospasm in patients with ruptured aneurysms. Methods: Seventy patients undergoing craniotomy for ruptured aneurysms in our hospital were selected as study subjects and randomly divided into control (n = 33) and research (n = 37) groups, they were treated with nimodipine and nimodipine combined with Shenmai injection after operation. The blood flow velocity in the middle cerebral artery (MCA) before and at 1, 3, 7, 11 and 14 days after surgery and the incidence of cerebral vasospasm during these days were compared, and the GCS scores at 14 days postoperatively and GOS scores at 6 months postoperatively were compared between the two groups. Results: There were no statistically significant differences in the occurrence of cerebral vasospasm, GCS or GOS scores between the two groups (P > 0.05), but the period of postoperative cerebral vasospasm in the study group was significantly shorter than that in the control group. Conclusion: Shenmai injection has the effect of shortening the cycle of occurrence of cerebral vasospasm after the operation of ruptured aneurysms, promoting patients to recover as early as possible and reducing their physical and mental burden.

In Reply to the Letter to the Editor Regarding “Intra-arterial Dantrolene for Refractory Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage”

In Reply to the Letter to the Editor Regarding “Intra-arterial Dantrolene for Refractory Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage”