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Delayed cerebral ischemia (DCI) is a common and severe complication after subarachnoid hemorrhage (SAH). Logistic regression (LR) is the primary method to predict DCI, but it has low accuracy. This study assessed whether other machine learning (ML) models can predict DCI after SAH more accurately than conventional LR. PubMed, Embase, and Web of Science were systematically searched for studies directly comparing LR and other ML algorithms to forecast DCI in patients with SAH. Our main outcome was the accuracy measurement, represented by sensitivity, specificity, and area under the receiver operating characteristic. In the six studies included, comprising 1828 patients, about 28% (519) developed DCI. For LR models, the pooled sensitivity was 0.71 (95% confidence interval [CI] 0.57-0.84; p < 0.01) and the pooled specificity was 0.63 (95% CI 0.42-0.85; p < 0.01). For ML models, the pooled sensitivity was 0.74 (95% CI 0.61-0.86; p < 0.01) and the pooled specificity was 0.78 (95% CI 0.71-0.86; p = 0.02). Our results suggest that ML algorithms performed better than conventional LR at predicting DCI.Trial Registration: PROSPERO (International Prospective Register of Systematic Reviews) CRD42023441586; https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=441586.

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BACKGROUND: The VASOGRADE is a simple aneurysmal subarachnoid hemorrhage (aSAH) grading scale that combines the modified Fisher scale (mFisher) and the World Federation of Neurological Societies (WFNS) grading system, allowing the stratification of delayed cerebral ischemia (DCI) risk. However, the VASOGRADE accuracy in predicting functional outcomes is still to be determined. METHODS: We retrospectively evaluated a multiethnic cohort of consecutive patients with aSAH admitted to a high-volume center in Brazil from January 2016 to January 2019. Patients were classified according to the severity of the clinical presentation (WFNS), the amount of blood in the initial head computerized tomography (mFisher) scan, and the VASOGRADE (green, yellow, red). The primary outcome was to detect DCI-related cerebral infarction, and the secondary outcome was the functional outcome at hospital discharge according to the modified Rankin scale (mRs). Univariate and multivariate logistic regression models were employed. RESULTS: A total of 212 patients (71.7% female, mean age 52.7 ± 12.8) were included. Sixty-nine patients were classified as VASOGRADE-Green (32.5%), 98 patients as VASOGRADE-Yellow (46.9%), and 45 patients as VASOGRADE-Red (20.6%). DCI-related infarction was present in 39 patients (18.9%). The proportions of patients in the VASOGRADE-Green, VASOGRADE-Yellow, and VASOGRADE-Red categories with DCI-related infarction were 7.7, 61.5, and 30.8%, respectively. After a multivariable analysis including age, sex, aneurysm location, and the VASOGRADE classification as variables, both VASOGRADE-Yellow and VASOGRADE-Red were independently associated with DCI-related infarction (odds ratio [OR] 7.69, 95% confidence interval [CI] 2.13-27.8, and OR 8.07, 95% CI 2.03-32.11, respectively) and unfavorable outcome (OR 4.16, 95% CI 1.33-13.03, and OR 25.57, 95% CI 4.45-147.1, respectively). The VASOGRADE discrimination performance for DCI-related infarction (area under the receiver operating characteristic curve) was 0.67 ± 0.04 (95% CI 0.58-0.75; p = 0.001). VASOGRADE-Red had 97.5% specificity for predicting an unfavorable mRs score at discharge (95% CI 92.8-99.5%). Conversely, VASOGRADE-Green had an excellent specificity for predicting favorable outcome at discharge (mRs score 0-2, 95% CI 82.6-95.5%). CONCLUSIONS: In conclusion, in a multiethnic cohort of patients with aSAH, VASOGRADE-Green predicted the absence of DCI and good clinical outcome at discharge with very high specificity, and patients in this category might be selected for early intensive care unit (ICU) discharge, minimizing costs and medical complications associated with prolonged hospital stay. On the other hand, patients categorized as VASOGRADE-Yellow and VASOGRADE-Red were at the highest risk for DCI. They should, therefore, be selected as a priority for care in high-volume aSAH centers, being aggressively monitored for DCI at the ICU. Such stratification methods are crucial, especially in countries with low financial resources and high health care services demand.

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BACKGROUND: In aneurysmal subarachnoid hemorrhage (aSAH), one of the main determinants of prognosis is delayed cerebral ischemia (DCI). Transcranial Doppler (TCD) is used to monitor vasospasm and DCI. We aimed to better understand cerebral hemodynamics response to hypertension induction (HI) with norepinephrine (NE) and inotropic therapy with milrinone so that TCD can be a bedside tool in helping to guide DCI therapies. Our primary objective was to determine TCD blood flow velocity (BFV) kinetics during HI and inotropic therapy for DCI treatment. Secondly, we performed an analysis by treatment subgroups and evaluated clinical response to therapies. METHODS: We performed a prospective observational cohort study in a Brazilian high-volume center for aSAH. Patients with aSAH admitted between 2016 and 2018 who received NE or milrinone for DCI treatment were included. TCDs were performed before therapy initiation (t0) and 45 (t1) and 90 min (t2) from the onset of therapy. For each DCI event, we analyzed the highest mean flow velocity (MFV) and the mean MFV and compared their kinetics over time. The National Institutes of Health Stroke Scale was determined at t0, t1, and t2. RESULTS: Ninety-eight patients with aSAH were admitted during the study period. Twenty-one (21.4%) developed DCI, of whom six had DCI twice, leading to a total of 27 analyzed DCI events (12 treated with HI and 15 with milrinone). Patients treated with NE had their mean arterial pressure raised (85 mm Hg in t0, 112 mm Hg in t2 [p < 0.001]), whereas those treated with milrinone had a significant decrease in mean arterial pressure over treatment (94 mm Hg in t0, 88 mm Hg in t2 [p = 0.004]). Among all treated patients, there was a significant drop from t0 to t2 but not to t1 in the highest MFV and in the highest mean MFV. Among those treated with HI, there were no significant changes from t0 to t1 or t2 (highest MFV in t0 163.2 cm/s, in t1 172.9 cm/s [p = 0.27], and in t2 164 cm/s [p = 0.936]). Conversely, in those treated with milrinone, there was a significant decrease from t0 to t1 and to t2 (highest MFV in t0 197.1 cm/s, in t1 172.8 cm/s [p = 0.012], in t2 159 cm/s [p = 0.002]). Regarding clinical outcomes, we observed a significant improvement in mean National Institutes of Health Stroke Scale scores from 17 to 16 in t1 (p < 0.001) and to 15 in t2 (p = 0.002). CONCLUSIONS: BFV analyzed by TCD in patients with aSAH who developed DCI and were treated with milrinone or NE significantly decreased in a time-dependent way. Milrinone effectively decrease cerebral BFV, whereas NE do not. Clinical improvement was achieved with both treatment strategies.

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Ruptured intracranial aneurysms, as the leading cause of spontaneous subarachnoid hemorrhage (aSAH), represents an emergency with high morbi-mortality. The comprehension of the underlying pathology that involves inflammatory and immune responses, through the neutrophil-to-lymphocyte ratio (NLR), could help to predict complications such as delayed cerebral ischemia (DCI) or rebleeding and the functional outcome. Systematic review of English-based literature through PubMed and Biblioteca Vitural em Saúde (BVS) to find papers discussing the use of NLR in the aSAH setting. Area-under-curve (AUC) of receiver operating characteristics (ROC), cutoff value, sensitivity, and specificity were retrieved. From 53 articles included, 4 papers were evaluated after exclusion criteria. Rebleeding could be predicted with a NLR cutoff value of 9.88 (sensitivity 72.3%, specificity 63.3%). The mean cutoff value for DCI was 12.85, with sensitivity 66.3% and specificity 75.8%. Finally, a worse 3-month functional outcome could be predicted with a mean sensitivity of 73.3% and a mean specificity of 54%. NLR is a new issue in scientific community, especially neurosurgery. The current understanding points to a multifactorial process after aSAH that emerges as alterations on the NLR. As a measurement readily available and cost-effect after admission of the patient, its use signals that patients that need expedite surgical treatment or more aggressive treatment for vasospasm. As other medical subspecialties already use this ratio to predict outcomes, the literature reviewed by this paper constitute the earliest clues that higher NLR predicts re-bleeding, DCI, and functional outcome.

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Aneurysmal subarachnoid hemorrhage (SAH) is a sub-type of hemorrhagic stroke associated with the highest rates of mortality and long-term neurological disabilities. Despite the improvement in the management of SAH patients and the reduction in case fatality in the last decades, disability and mortality remain high in this population. Brain injury can occur immediately and in the first days after SAH. This early brain injury can be due to physical effects on the brain such as increased intracranial pressure, herniations, intracerebral, intraventricular hemorrhage, and hydrocephalus. After the first 3 days, angiographic cerebral vasospasm (ACV) is a common neurological complication that in severe cases can lead to delayed cerebral ischemia and cerebral infarction. Consequently, the prevention and treatment of ACV continue to be a major goal. However, most treatments for ACV are vasodilators since ACV is due to arterial vasoconstriction. Other targets also have included those directed at the underlying biochemical mechanisms of brain injury such as inflammation and either independently or as a consequence, cerebral microthrombosis, cortical spreading ischemia, blood-brain barrier breakdown, and cerebral ischemia. Unfortunately, no pharmacologic treatment directed at these processes has yet shown efficacy in SAH. Enteral nimodipine and the endovascular treatment of the culprit aneurysm, remain the only treatment options supported by evidence from randomized clinical trials to improve patients' outcome. Currently, there is no intervention directly developed and approved to target neuroinflammation after SAH. The goal of this review is to provide an overview on anti-inflammatory drugs tested after aneurysmal SAH.

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Spreading depolarization in cerebral cortex is associated with swelling of neurons, distortion of dendritic spines, massive ion translocation with a large change of the slow electrical potential, and silencing of brain electrical activity. The term spreading depression represents a wave of spontaneous activity of the electrocorticogram that propagates through contiguous cerebral gray matter at a characteristic velocity. Spreading depression is a consequence of cortical spreading depolarization. Therefore, spreading depolarization is not always accompanied by spreading depression and the terms are not synonymous.

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INTRODUCTION: Aneurysmal subarachnoid hemorrhage (aSAH) represents 3% of all strokes in the US. When the patient survives it can lead to permanent incapacity especially if the patient develops vasospasm. The vasospasm is a multifactorial disorder and can lead to delayed cerebral ischemia (DCI). Most of the drugs tested to treat vasospasm failed to improve outcome and the only exception is nimodipine. AREAS COVERED: In this review, the authors describe the multifactorial process of vasospasm leading DCI after aSAH, discussing the treatments available based on the past and latest researches. EXPERT OPINION: Nimodipine is the only FDA-approved medication with neuroprotective effect and able to improve outcomes after aSAH. Understanding nimodipine trials is mandatory to understand and criticize all the drug trials published until now. The mechanism to vasospasm is multifactorial and not completely understood and all the other attempts to find a better medication could not prove superior results. Newton and PEGylated Carboxyhemoglobin Bovine can be potentially effective to prevent vasospasm but we still need more data and large studies. Future research should investigate newer drugs, as well as the combination of multiple drugs therapy and the association with blood evacuation techniques.

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Spreading depolarization in cerebral cortex is associated with swelling of neurons, distortion of dendritic spines, massive ion translocation with a large change of the slow electrical potential, and silencing of brain electrical activity. The term spreading depression represents a wave of spontaneous activity of the electrocorticogram that propagates through contiguous cerebral gray matter at a characteristic velocity. Spreading depression is a consequence of cortical spreading depolarization. Therefore, spreading depolarization is not always accompanied by spreading depression and the terms are not synonymous.

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