Nontraumatic Subarachnoid Hemorrhage Research Articles

The Role of Long Non-Coding RNAs in Intracranial Aneurysms and Subarachnoid Hemorrhage.

Intracranial aneurysms (IAs) represent the most complex and relevant problem of modern neurology and neurosurgery. They serve as one of the main causes of non-traumatic subarachnoid hemorrhage (SAH), causing up to 85% of all cases of intracranial hemorrhage, which is associated with frequent disability and high mortality among patients. Unfortunately, the molecular mechanisms of the development and rupture of IAs are still under study. Long non-coding RNAs (lncRNAs) are non-coding RNAs that typically have a length of more than 200 nucleotides. It is known that lncRNAs regulate many processes, such as transcription, translation, cell differentiation, regulation of gene expression, and regulation of the cell cycle. In recent years, a lot of evidence has established their role in human diseases from oncology to cardiovascular disease. Recent studies have shown that lncRNAs may be involved in the pathogenesis of IAs. The study of lncRNAs and its targets in various pathological conditions of a person is a rapidly developing field, and it is likely that the knowledge obtained from these studies regarding the pathogenesis of intracranial aneurysms will have the potential to use lncRNAs in therapy, as well as in the diagnosis and prediction of high aneurysms risk of rupture.

Plasma brain natriuretic peptide level on admission predicts long-term outcome in patients with non-traumatic subarachnoid hemorrhage

IntroductionNon-traumatic subarachnoid hemorrhage (SAH) is a type of stroke that still has a high mortality rate. Some patients with SAH have electrocardiography (ECG) abnormalities or asymptomatic left ventricular apical ballooning, and requires intervention by cardiologists. However, the impact of cardiac abnormalities after SAH onset remains unclear. We investigated whether ECG abnormalities, myocardial damage, sympathetic nervous activity or echocardiographic left ventricular wall motion abnormalities (WMA) could provide additional risk stratification in patients with SAH. MethodsWe studied 118 SAH patients (78 women, age 63 ± 15) without a history of heart disease. Neurological grade (Hunt and Kosnik Grade) and clinical factors were evaluated. A standard 12-lead ECG, echocardiography and blood samples were obtained within 48 h after SAH onset. ECG abnormalities were defined as abnormal Q wave, ST elevation, giant T-wave inversion or QT prolongation. ResultsTwenty of 118 patients (17%) died during the follow-up (35 ± 31 months). Death was significantly associated with higher age (p < 0.0001), neurological grade (p < 0.0001), elevated BNP level (p < 0.0001), increased plasma norepinephrine levels (p < 0.0001) and WMA (p = 0.0070), while ECG abnormalities were not significantly associated. Neurological grade (p < 0.0001), age (p = 0.0047) and BNP (p = 0.0014, hazard ratio 1.0255 for each 1 pg/mL increase in BNP, 95%CI 1.0088 to 1.0499) were independently associated with death. Patients with BNP ≥ 96.6 had a higher risk of death (log- rank p < 0.0001). ConclusionPlasma BNP might provide an additional risk stratification in patients with non-traumatic SAH that requires intervention by cardiologists for both its prevention management after onset.

Impact of Ruptured Aneurysm Circulation on Mortality: A Nationwide Inpatient Sample Analysis

ObjectiveThis study investigates the effect of aneurysm circulation on mortality and patient outcomes after aneurysmal subarachnoid hemorrhage (SAH) within the United States. MethodsA retrospective cohort study was conducted using the Nationwide Inpatient Sample (NIS), a part of the Healthcare Cost and Utilization Project (HCUP), with ICD-10 codes for non-traumatic SAH between 2015-2016. Aneurysms were stratified as either anterior or posterior circulation. Multivariate logistic regression was used to find the impact of selected variables on the odds of mortality. ResultsThe NIS reported 1,892 cases of non-traumatic SAH within the study period that were predominantly anterior circulation (82.6%), female (68.6%), white (57.7%), with mean age of 59.07 years, and in-hospital mortality of 21.4%. Anterior circulation aneurysms were associated with lower severity of initial illness (p = 0.014) but higher likelihood of vasospasm (p = 0.0006) than those of the posterior circulation. In a multivariate logistic regression analysis, mortality was associated with posterior circulation aneurysms (OR: 1.42; CI 95% 1.005-20.10, p = 0.047), increasing age (OR: 1.035; 95% CI 1.022-1.049; p < 0.0001), and shorter hospital stays (OR: 0.7838; 95% CI 0.758-0.811; p < 0.0001). Smoking history (OR: 0.825; 95% CI 0.573-1.187, p > 0.05) and vasospasm (OR: 1.005; 95% CI 0.648-1.558; p > 0.05) were not significantly associated with higher odds of mortality. ConclusionsMortality following aneurysmal SAH is associated with posterior circulation aneurysms, and increasing age, but not smoking history or vasospasm. These findings may be useful for prognostication and counseling patients and families.

Dysphagia following non-traumatic subarachnoid haemorrhage: A prospective pilot study.

Whilst dysphagia is a commonly reported complication of stroke, it has received relatively little attention in the literature for patients following non-traumatic subarachnoid haemorrhage (SAH). To investigate dysphagia incidence, risk factors, clinical progression and recovery in patients following non-traumatic SAH. A prospective cohort study of 49 patients admitted to a tertiary neurosurgical referral unit with non-traumatic SAH over a 12-month period was conducted. Swallowing function was assessed by a speech-language pathologist within 72 h of medical stability and monitored throughout the acute inpatient admission. Dysphagia incidence was 16.33% (n = 8/49). Risk factors associated with dysphagia included; Glasgow Coma Scale (GCS) score on admission, need for intensive care unit (ICU) admission, length of ICU stay, need for intubation and ventilation, and hydrocephalus. Participants with dysphagia were admitted to hospital 1.9 times longer than those without dysphagia (p < 0.05) and were more likely to be transferred to another inpatient facility for ongoing care (p < 0.05). Dysphagia remained present at hospital discharge for over half (62.5%) of participants who developed this complication. Care pathways for patients admitted to hospital with non-traumatic SAH should include early screening for dysphagia risk. Further research using a larger prospective cohort is required to validate dysphagia incidence and risk factors in this patient cohort. What this paper adds What is already known on this subject Dysphagia is a negative complication following non-traumatic SAH, and can occur as a result of primary injury or secondary to treatment complications (e.g., intubation and ventilation, surgical intervention). However, limited evidence regarding its incidence, risk factors, clinical progression and recovery in a prospective cohort exists. What this paper adds to existing knowledge This study is the first to examine prospectively patients with non-traumatic SAH within 72 h of medical stability. It identifies dysphagia incidence, risk factors, clinical characteristics and recovery during the acute hospital admission for this patient cohort. What are the potential or actual clinical implications of this work? Early and regular screening for dysphagia in the presence of associated risk factors is essential for patients admitted with non-traumatic SAH. Speech-language pathologist resources in the neurocritical care context should be available to support the assessment and management of dysphagia in this cohort.

Incidence and case fatality of aneurysmal subarachnoid hemorrhage admitted to hospital between 2008 and 2014 in Norway

BackgroundTo provide age- and sex-specific incidence and case fatality rates for non-traumatic aneurysmal subarachnoid hemorrhage (aSAH) in Norway. We also studied time trends in incidence and case fatality, as well as predictors of death following aSAH.MethodsA nationwide study using discharge data for patients admitted with aSAH between 2008 and 2014.ResultsA total of 1732 patients with aSAH were included. The mean age was 60 years (SD 14) and 63% were females. Crude annual incidence was 5.7 per 100,000 person-years (95% CI 5.4–6.0) and was higher in females (6.3 per 100,000, 95% CI 5.9–6.7) compared with males (4.9 per 100,000, 95% CI 4.5–5.3). The annual decline in aSAH incidence was 3.2% per year (p = 0.007). The cumulative proportions of fatalities at days 30, 90, and 1 year were 22%, 25%, and 37%, respectively. The 30-day mortality rate did not change during the study period. Age (HR 0.7–2.2) and aneurysms in the posterior circulation (HR 1.7, 95% CI 1.3–2.3, p = 0.001) were associated with higher 30-day case fatality following aSAH, while aneurysm repair (HR 0.2, 95% CI 0.2–0.3, p < 0.001) was associated with lower risk.ConclusionsThe incidence of aSAH declined in Norway between 2008 and 2014. Case fatality following aSAH continues to be high, and the 30-day mortality during the study period was unchanged. Increasing age and aneurysms in the posterior circulation were associated with increased risk of death within 30 days following aSAH.

Acute systematic inflammatory response syndrome and serum biomarkers predict outcomes after subarachnoid hemorrhage

Subarachnoid hemorrhage (SAH) can trigger immune activation sufficient to induce systematic inflammatory response syndrome (SIRS). Serum inflammatory biomarkers and SIRS can predict a poor outcome. The relationship between surgical stress and inflammatory response is well known but described in few reports in the neurosurgical population. We aimed to ascertain whether postoperative SIRS and initial serum biomarkers were associated with outcomes and evaluate whether the postoperative SIRS score differed between those with clipping and coil embolization. We evaluated 87 patients hospitalized within 24 h from onset of nontraumatic SAH. Serum biomarkers, such as levels of C-reactive protein (CRP), white blood cells (WBC), and D-dimer, as well as stress index (SI: blood sugar/K ratio) were obtained at admission. SIRS scores 3 days after admission were derived by adding the number of variables meeting the standard criteria (heart rate [HR] >90, respiratory rate [RR] >20, temperature >38 °C or <36 °C, and WBC count <4000 or >12,000). Clinical variables were compared according to whether they were associated with poor outcomes. Coil embolization was performed in 30 patients and clipping in 57. WBC, SI, D-dimer levels, and SIRS scores were significantly higher in patients with poor-grade SAH and were associated with poor outcomes. SIRS scores were significantly higher with clipping than with coil embolization among patients with good-grade SAH without intracerebral hemorrhage. Acute SIRS and serum biomarkers predict outcomes after SAH. Moreover, our study suggests the influence of surgical invasion via clipping on SIRS after SAH.

Utility of the Hijdra Sum Score in Predicting Risk of Aneurysm in Patients With Subarachnoid Hemorrhage: A Single-Center Experience With 550 Patients.

Subarachnoid hemorrhage (SAH) is most commonly caused by a ruptured vascular lesion. A significant number of patients presenting with SAH have no identifiable cause despite extensive cerebrovascular imaging at presentation. Significant neurological morbidity or mortality can result from misdiagnosis of aneurysm. To generate a model to assist in predicting the risk of aneurysm in this patient population. We conducted a retrospective study of all patients aged≥18 yr admitted to a single center from March 2008 to March 2018 with nontraumatic SAH (n=550). Patient information was compared between those with and without aneurysm to identify potential predictors. Odds ratios obtained from a logistic regression model were converted into scores which were summed and tested for predictive ability. Female sex, higher modified Fisher or Hijdra score, nonperimesencephalic location, presence of intracerebral hemorrhage, World Federation of Neurosurgical Societies (WFNS) score≥3, need for cerebrospinal fluid diversion on admission, and history of tobacco use were all entered into multivariable analysis. Greater modified Fisher, greater Hijdra score, WFNS≥3, and hydrocephalus present on admission were significantly associated with the presence of an aneurysm. A model based on the Hijdra score and SAH location was generated and validated. We show for the first time that the Hijdra score, in addition to other factors, may assist in identifying patients at risk for aneurysm on cerebrovascular imaging. A simple scoring tool based on patient sex, SAH location, and SAH burden can assist in predicting the presence of an aneurysm in patients with nontraumatic SAH.

Isolated Bradycardia During Aneurysmal Clipping: Rebleed or Trigeminocardiac Reflex?

AbstractThe most common cause of nontraumatic subarachnoid hemorrhage is the rupture of intracranial aneurysm. After initial bleed, the risk of rebleeding is highest in the early postictal period and this rebleed is strongly associated with poor neurological outcome. The major goal of anesthesia in these surgeries is to prevent the rebleed. If rebleeding occurs prior to the craniotomy, it results in the acute rise of intracranial pressure and usually presents as bradycardia and hypertension (Cushing’s reflex). Here we reported a case where rebleeding presented unusually as isolated bradycardia without associated hypertension and was mistaken as trigeminocardiac reflex. The surgeon was informed about the event and they planned to proceed. After craniotomy, despite all the efforts the brain was persistently tight and surgery could not be completed. Postoperative scan showed rebleeding and the patient died after a few days in ICU.We highlighted in this case report the fact that isolated transient bradycardia may also be the presentation of rebleed with closed cranial vault. It is not always necessary to see all the features of Cushing’s traid in every patient. If bradycardia occurs before the craniotomy, the surgeon should be notified, the severity of bleed should be assessed, and further management should be planned according to the severity of bleed.

Compressive myelopathy secondary to posthemorragic arachnoiditis: Case report and literature review

BackgroundSpinal arachnoiditis is an arachnoid inflammatory process frequently caused by infection or spinal surgery; there are different degrees of severity, including arachnoid thickening and severe adhesive lesions that can lead to the development of arachnoid cysts. Non-traumatic subarachnoid haemorrhage (ntSAH) is a relatively uncommon cause of arachnoiditis; further complication with spinal cord compression (SCC) is even more unusual. Methodwe describe a 70-year-old female, with SCC caused by arachnoid cysts. Her medical past history was relevant for an episode of ntSAH after rupture of a posterior communicating artery aneurysm, eight months prior to the onset of symptoms. We also present a literature review of previous published cases. Resultswe selected 23 articles with 24 case reports. A noticeable female predominance (11:1) was observed. It is more common between the fourth and fifth decades. The majority of cases (58 %) were secondary to aneurysmal SAH due to rupture of a posterior circulation aneurysm. The most common location of the cyst is in the cervicothoracic spine. The average time between the initial bleeding and symptom development is 3–6 months. The most frequently described treatment is laminectomy and marsupialization of the cyst, but reports show a high recurrence rate. ConclusionsntSAH is an uncommon aetiology of arachnoiditis and arachnoid cysts. SCC from arachnoid cysts secondary to ntSAH is exceptional. Treatment through laminectomy has a relatively high recurrence rate (33 %). We present different hypotheses to try to explain how the alteration of cerebrospinal fluid (CSF) dynamics after ntSAH can lead to arachnoid cyst development and SCC. Although the small number of cases included in the present series precludes us to draw definite conclusions, ventriculoperitoneal shunt (VPS) placement can be considered as an alternative treatment in the management of known ntSAH patients that present recurrent symptomatic arachnoid cysts.

Amantadine and Modafinil as Neurostimulants Following Acute Stroke: A Retrospective Study of Intensive Care Unit Patients.

Background/ObjectiveNeurostimulants may improve or accelerate cognitive and functional recovery after intracerebral hemorrhage (ICH), ischemic stroke (IS), or subarachnoid hemorrhage (SAH), but few studies have described their safety and effectiveness in the intensive care unit (ICU). The objective of this study was to describe amantadine and modafinil administration practices during acute stroke care starting in the ICU and to evaluate safety and effectiveness.MethodsConsecutive adult ICU patients treated with amantadine and/or modafinil following acute non-traumatic IS, ICH, or SAH were evaluated. Neurostimulant administration data were extracted from the electronic medication administration record, including medication (amantadine, modafinil, or both), starting dose, time from stroke to initiation, and whether the neurostimulant was continued at hospital discharge. Patients were considered responders if they met two of three criteria within 9 days of neurostimulant initiation: increase in Glasgow coma scale (GCS) score ≥ 3 points from pre-treatment baseline, improved wakefulness or participation documented in caregiver notes, or clinical improvement documented in physical or occupational therapy notes. Potential confounders of the effectiveness assessment and adverse drug effects were also recorded.ResultsA total of 87 patients were evaluable during the 3.7-year study period, including 41 (47%) with ICH, 29 (33%) with IS, and 17 (20%) with SAH. The initial neurostimulant administered was amantadine in 71 (82%) patients, modafinil in 13 (15%), or both in 3 (3%) patients. Neurostimulants were initiated a median of 7 (4.25, 12.75) days post-stroke (range 1–27 days) for somnolence (77%), not following commands (32%), lack of eye opening (28%), or low GCS (17%). The most common starting dose was 100 mg twice daily for both amantadine (86%) and modafinil (54%). Of the 79 patients included in the effectiveness evaluation, 42 (53%) were considered responders, including 34/62 (55%) receiving amantadine monotherapy and 8/24 (33%) receiving both amantadine and modafinil at the time they met the definition of a responder. No patient receiving modafinil monotherapy was considered a responder. The median time from initiation to response was 3 (2, 5) days. Responders were more frequently discharged home or to acute rehabilitation compared to non-responders (90% vs 62%, p = 0.006). Among survivors, 63/72 (88%) were prescribed a neurostimulant at hospital discharge. The most common potential adverse drug effect was sleep disruption (16%).ConclusionsNeurostimulant administration during acute stroke care may improve wakefulness. Future controlled studies with a neurostimulant administration protocol, prospective evaluation, and discretely defined response and safety criteria are needed to confirm these encouraging findings.Electronic supplementary materialThe online version of this article (10.1007/s12028-020-00986-4) contains supplementary material, which is available to authorized users.

Neuroangiography: Review of Anatomy, Periprocedural Management, Technique, and Tips.

Neuroangiography (NA) is a minimally invasive procedure used to diagnose patients with neurovascular diseases. Noninvasive imaging has improved dramatically in recent years and is utilized more frequently; however, further evaluation with NA is still required in certain cases. NA indications include intracranial (cerebral aneurysms, arteriovenous malformations, dural arteriovenous fistula, cerebral vasculitis, cerebral vasospasm, ischemic stroke, nontraumatic subarachnoid hemorrhage, intracerebral hemorrhage, Moyamoya, vein of Galen malformation, intracranial tumors, and pseudotumor cerebri) and extracranial (internal and common carotid artery stenosis, vertebral artery stenosis, carotid artery blowout, vertebral artery blowout, epistaxis, oropharyngeal bleeding, and carotid body tumor) pathologies which can help with diagnosis and potential subsequent endovascular treatment. A thorough understanding of normal and variant cervical/cranial vascular anatomy is required. In addition, periprocedural management, catheter technique, equipment needed, and underlying disease pathology are paramount to successful and safe outcomes. This article will review basic neurovascular anatomy, periprocedural management, NA technique, and tips for safe and successful outcomes.

Vasopressor treatment and mortality following nontraumatic subarachnoid hemorrhage: a nationwide electronic health record analysis.

Subarachnoid hemorrhage (SAH) is a devastating cerebrovascular condition, not only due to the effect of initial hemorrhage, but also due to the complication of delayed cerebral ischemia (DCI). While hypertension facilitated by vasopressors is often initiated to prevent DCI, which vasopressor is most effective in improving outcomes is not known. The objective of this study was to determine associations between initial vasopressor choice and mortality in patients with nontraumatic SAH. The authors conducted a retrospective cohort study using a large, national electronic medical record data set from 2000-2014 to identify patients with a new diagnosis of nontraumatic SAH (based on ICD-9 codes) who were treated with the vasopressors dopamine, phenylephrine, or norepinephrine. The relationship between the initial choice of vasopressor therapy and the primary outcome, which was defined as in-hospital death or discharge to hospice care, was examined. In total, 2634 patients were identified with nontraumatic SAH who were treated with a vasopressor. In this cohort, the average age was 56.5 years, 63.9% were female, and 36.5% of patients developed the primary outcome. The incidence of the primary outcome was higher in those initially treated with either norepinephrine (47.6%) or dopamine (50.6%) than with phenylephrine (24.5%). After adjusting for possible confounders using propensity score methods, the adjusted OR of the primary outcome was higher with dopamine (OR 2.19, 95% CI 1.70-2.81) and norepinephrine (OR 2.24, 95% CI 1.80-2.80) compared with phenylephrine. Sensitivity analyses using different variable selection procedures, causal inference models, and machine-learning methods confirmed the main findings. In patients with nontraumatic SAH, phenylephrine was significantly associated with reduced mortality in SAH patients compared to dopamine or norepinephrine. Prospective randomized clinical studies are warranted to confirm this finding.

A novel approach for propensity score matching and stratification for multiple treatments: Application to an electronic health record-derived study.

Currently, methods for conducting multiple treatment propensity scoring in the presence of high-dimensional covariate spaces that result from "big data" are lacking-the most prominent method relies on inverse probability treatment weighting (IPTW). However, IPTW only utilizes one element of the generalized propensity score (GPS) vector, which can lead to a loss of information and inadequate covariate balance in the presence of multiple treatments. This limitation motivates the development of a novel propensity score method that uses the entire GPS vector to establish a scalar balancing score that, when adjusted for, achieves covariate balance in the presence of potentially high-dimensional covariates. Specifically, the generalized propensity score cumulative distribution function (GPS-CDF) method is introduced. A one-parameter power function fits the CDF of the GPS vector and a resulting scalar balancing score is used for matching and/or stratification. Simulation results show superior performance of the new method compared to IPTW both in achieving covariate balance and estimating average treatment effects in the presence of multiple treatments. The proposed approach is applied to a study derived from electronic medical records to determine the causal relationship between three different vasopressors and mortality in patients with non-traumatic aneurysmal subarachnoid hemorrhage. Results suggest that the GPS-CDF method performs well when applied to large observational studies with multiple treatments that have large covariate spaces.

EEG Sleep Architecture as a Biomarker after Non-traumatic Subarachnoid Hemorrhage (2039)

EEG Sleep Architecture as a Biomarker after Non-traumatic Subarachnoid Hemorrhage (2039)

A Cohort Comparison Analysis of Fixed Pressure Ventriculoperitoneal Shunt Valves With Programmable Valves for Hydrocephalus Following Nontraumatic Subarachnoid Hemorrhage.

Hydrocephalus after nontraumatic subarachnoid hemorrhage (SAH) is a common sequela that may require the placement of ventriculoperitoneal shunts (VPS). Adjustable-pressure valves (APVs) are being widely used in this situation though more expensive than differential-pressure valves (DPVs). To compare outcomes between APV and DPV in SAH-induced hydrocephalus. We performed a retrospective chart review of patients with nontraumatic SAH who underwent VPS placement for the treatment of hydrocephalus after SAH, between July 2007 and December 2016. Patients were classified according to the type of valve (APV vs DPV). We evaluated factors that could predict the type of valve used, outcomes in VPS revision/replacement rate, and complications. A total of 66 patients underwent VPS placement who were equally distributed into the 2 groups of valves. VPS failure with the need for revision/replacement occurred in 13 (19.7%) cases. Ten (30.3%) patients with DPV had a VPS failure, while 3 (9.1%) patients with an APV had a similar failure with the need for revision/replacement (P=.03). VPS placement before discharge during the initial hospitalization (P=.02) was statistically significant associated with the use of a DPV, while the reason of external ventricular drain (EVD) failure (P=.03) was associated with the use of an APV. APVs had a lower rate of surgical revisions compared to DPVs. Early placement of VPS was associated with the use of a DPV. The need for EVD replacement due to EVD infection or malfunction was associated with higher rates of APV use.

Incidence of Cerebral Vasospasm and Delayed Cerebral Ischemia Following Non‐Traumatic Aneurysmal Subarachnoid Hemorrhage

BackgroundNon‐traumatic aneurysmal subarachnoid hemorrhage (aSAH), comprising ~ 3 percent of strokes, is one of the deadliest stroke subtypes with mortality reaching as high as 40 percent. This high rate of mortality is associated with delayed cerebral ischemia (DCI), likely due to cerebral vasospasm (CV). CV is characterized by progressive narrowing of cerebral arteries, diagnosed by neuroimaging, that occurs within 4–14 days of aSAH, and CV leads to DCI and infarction in ~ 25 percent of patients. While the etiology of CV remains unknown, autonomic nervous system dysfunction, specifically excessive sympathetic nervous system induced vasoconstriction, may play a role. The purpose of this study is to review clinical cases of aSAH from 2017–2019 from our local hospital and describe the frequency of aSAH, CV, and DCI for all cases.MethodsInstitutional review board approval was received from West Virginia University. We performed a retrospective chart review of all patients diagnosed with non‐traumatic aSAH from January 1, 2017 – October 1, 2019 (n= 156). The following variables were collected from the medical record: location of aneurysm, presence and location of SAH blood clot (Fisher grade), frequency and severity of CV‐diagnosed by angiography or transcranial doppler, frequency of DCI within 7 days of CV – diagnosed by CT or MRI. Frequencies of CV and DCI were compared between location of aneurysm. Other potentially confounding variables were also collected, including age, sex, cardiovascular risk factors, and treatment with an alpha‐1 antagonist at time of aSAH presentation. Statistical analysis was performed using IBM Statistics (Version 26). Frequencies were compared between groups using Fisher’s exact test, and correlations between variables were assessed by Spearman correlation. Binary logistic regression was used to identify factors that may predict incidence of CV. Statistical significance was determined at p &lt; 0.05.ResultsaSAH occurred in the anterior circulation in 71 percent of cases – middle cerebral artery (MCA) (23%), anterior cerebral artery (ACA) (20%), anterior communicating artery (20%), and internal carotid artery (ICA) (8%). CV occurred in 36 percent of all cases ‐ MCA (60%), ACA (26%) and ICA (12%). Hypertension was the only significant predictor associated with a higher incidence of CV (p=.032). Interestingly, the actual incidence of CV was not correlated with the expected incidence of CV predicted by Fisher grade (p=.656). CV led to DCI in 31 percent of cases, and there were no differences in DCI incidence compared between Fisher grade or vessel affected by CV.ConclusionsOur preliminary data provides a description of the incidence of CV and DCI following non‐traumatic aSAH at our institution. The observed incidence of CV and DCI are comparable to previously reported estimates; however, our results suggest that Fisher grade alone may not provide an accurate prediction for the incidence of CV, as the incidence of CV may vary across the cerebrovasculature. This study provides evocative evidence for further investigation into the factors that may contribute to CV and subsequent DCI. Upon validation, this information may be used by clinicians in the diagnosis and medical management of CV to prevent DCI and subsequently lower mortality associated with aSAH.

CT perfusion-guided endovascular treatment of symptomatic cerebral vasospasm in a patient with perimesencephalic non-aneurysmal subarachnoid hemorrhage

Symptomatic vasospasm represents an uncommon complication of perimesencephalic nonaneurysmal subarachnoid hemorrhage (SAH) which is a benign form of SAH without any recognizable source of bleeding accounting for about 15% of non-traumatic SAH [1,2].

Soluble ST2 Is Associated With New Epileptiform Abnormalities Following Nontraumatic Subarachnoid Hemorrhage.

Background and Purpose- We evaluated the association between 2 types of predictors of delayed cerebral ischemia after nontraumatic subarachnoid hemorrhage, including biomarkers of the innate immune response and neurophysiologic changes on continuous electroencephalography. Methods- We studied subarachnoid hemorrhage patients that had at least 72 hours of continuous electroencephalography and blood samples collected within the first 5 days of symptom onset. We measured inflammatory biomarkers previously associated with delayed cerebral ischemia and functional outcome, including soluble ST2 (sST2), IL-6 (interleukin-6), and CRP (C-reactive protein). Serial plasma samples and cerebrospinal fluid sST2 levels were available in a subgroup of patients. Neurophysiologic changes were categorized into new or worsening epileptiform abnormalities (EAs) or new background deterioration. The association of biomarkers with neurophysiologic changes were evaluated using the Wilcoxon rank-sum test. Plasma and cerebrospinal fluid sST2 were further examined longitudinally using repeated measures mixed-effects models. Results- Forty-six patients met inclusion criteria. Seventeen (37%) patients developed new or worsening EAs, 21 (46%) developed new background deterioration, and 8 (17%) developed neither. Early (day, 0-5) plasma sST2 levels were higher among patients with new or worsening EAs (median 115 ng/mL [interquartile range, 73.8-197]) versus those without (74.7 ng/mL [interquartile range, 44.8-102]; P=0.024). Plasma sST2 levels were similar between patients with or without new background deterioration. Repeated measures mixed-effects modeling that adjusted for admission risk factors showed that the association with new or worsening EAs remained independent for both plasma sST2 (β=0.41 [95% CI, 0.09-0.73]; P=0.01) and cerebrospinal fluid sST2 (β=0.97 [95% CI, 0.14-1.8]; P=0.021). IL-6 and CRP were not associated with new background deterioration or with new or worsening EAs. Conclusions- In patients admitted with subarachnoid hemorrhage, sST2 level was associated with new or worsening EAs but not new background deterioration. This association may identify a link between a specific innate immune response pathway and continuous electroencephalography abnormalities in the pathogenesis of secondary brain injury after subarachnoid hemorrhage.

Values of blood copeptin level as a marker of unfavorable forecast in subarachnoid haemorrhage of the brain of atraumatic origin

Objective – to evaluate of diagnostic informativeness of сopeptin serum values in determining the risk of complications in patients with subarachnoid hemorrhage.Materials and methods. A prospective cohort study of 82 patients (40 men and 42 women) with spontaneous (non-traumatic) subarachnoid hemorrhage (SAH) from the age of 23 to 72 years (average age – (49,6 ±1,3) year) was conducted.Results. Complications were recorded in 31 (74.20 %) patients with a serum level of copeptin ≥ 0.605 ng/ml on the third day of the SAH, which was in 9.49 times higher (95 % CI 3.60–24.80, р ˂0.0001) than in patients with a serum level of copeptin &lt; 0.605 ng/ml. When determining the cumulative risk of developing complications of SAH, the values ​​of positive and negative predictive values ​​of serum levels of copeptin on third day of SAH were 74.19 % and 92.20 % respectively, the accuracy of prediction (the sum of correctly classified observations) was 85.39 %.Conclusions. ROC-analysis suggests that the serum level of copeptin on third day of SAH ≥ 0.605 ng/ml is characterized by an optimal ratio of sensitivity and specificity in assessing the cumulative risk of developing such SAH complications as secondary ischemia combined with cerebral angiospasm.

Soluble vascular endothelial-cadherin in CSF after subarachnoid hemorrhage.

To determine if CSF and plasma levels of soluble vascular endothelial (sVE)-cadherin are associated with functional outcome after subarachnoid hemorrhage (SAH) and to investigate sVE-cadherin effects on microglia. Serial CSF and plasma were collected from prospectively enrolled patients with nontraumatic SAH from a ruptured aneurysm in the anterior circulation and who required an external ventricular drain for clinical indications. Patients with normal-pressure hydrocephalus without SAH served as controls. For prospective assessment of long-term outcomes at 3 and 6 months after SAH, modified Rankin Scale scores (mRS) were obtained and dichotomized into good (mRS ≤ 2) vs poor (mRS > 2) outcome groups. For SAH severity, Hunt and Hess grade was assessed. Association of CSF sVE-cadherin levels with long-term outcomes, HH grade, and CSF tumor necrosis factor (TNF)-α levels were evaluated. sVE-cadherin effects on microglia were also studied. sVE-cadherin levels in CSF, but not in plasma, were higher in patients with SAH and were associated with higher clinical severity and higher CSF TNF-α levels. Patients with SAH with higher CSF sVE-cadherin levels over time were more likely to develop worse functional outcome at 3 months after SAH. Incubation of cultured microglia with sVE-cadherin resulted in increased inducible nitric oxide synthase, interleukin-1β, reactive oxygen species, cell soma size, and metabolic activity, consistent with microglia activation. Microinjection of sVE-cadherin fragments into mouse brain results in an increased number of microglia surrounding the injection site, compared to injection of denatured vascular endothelial-cadherin fragments. These results support the existence of a novel pathway by which sVE-cadherin, released from injured endothelium after SAH, can shift microglia into a more proinflammatory phenotype and contribute to neuroinflammation and poor outcome in SAH.