Article

Predictors and impact of early cerebral infarction after aneurysmal subarachnoid hemorrhage

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Abstract

Cerebral infarction is a frequent and serious complication of aneurysmal subarachnoid hemorrhage (SAH). This study aimed to identify independent predictors of the timing of cerebral infarction and clarify its impact on disease course and patients' outcome. All consecutive patients with SAH admitted to our institution from January 2005 to December 2012 were analyzed. Serial computed tomography (CT) scans were evaluated for cerebral infarctions. Demographic, clinical, laboratory and radiological data of patients during hospitalization as well as clinical follow-ups 6 months after SAH were recorded. Of the 632 analyzed patients, 320 (51%) developed cerebral infarction on CT scans. 136 patients (21.5%) with early cerebral infarction (occurring within 3 days after SAH) had a significantly higher risk of unfavorable outcome than patients with late infarction [odds ratio (OR) 2.94; P = 0.008], a higher in-hospital mortality (OR 3.14; P = 0.0002) and poorer clinical outcome after 6 months (OR 0.54; P < 0.0001). The rates of decompressive craniectomy (OR 1.96, P = 0.0265), tracheostomy (OR 1.87, P = 0.0446), the duration of intensive care unit stay and mechanical ventilation were significantly higher in patients with early infarction. In multivariate analysis, Hunt and Hess grades 4 and 5 (OR 2.06, P = 0.008), Fisher grades 3 and 4 (OR 3.99, P = 0.014), sustained elevations of intracranial pressure >20 mmHg (OR 5.95, P < 0.0001) and early vasospasm on diagnostic angiograms (OR 3.01, P = 0.008) were predictors of early cerebral infarction. Early cerebral infarction after SAH is associated with severe clinical course and unfavorable outcome and can be reliably predicted by poor initial clinical condition, thick subarachnoid clot, early angiographic vasospasm and sustained elevations of intracranial pressure. © 2015 EAN.

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... In fact, multiple early prognostic factors for mortality following aSAH, including in-hospital mortality, have already been reported, such as age, the Hunt-Hess scale, the World Federation of Neurosurgical Societies (WFNS) classification, Fisher and modified Fisher grades, aneurysm size and location, etc. [3][4][5][6][7][8][9][10]. Among them, Hunt-Hess and WFNS grades are the most commonly accepted predictors. ...
... Fisher and modified Fisher grades are the other two scales frequently utilized for the early prediction of mortality in aSAH patients. Regrettably, previous pertinent studies reveal that both of these two grades seemed to be more correlated with delayed cerebral ischemia than they are with mortality [5,6,12,13]. The other commonly mentioned predictors, such as age, aneurysm size, and location, have not consistently been found to be associated with aSAH mortality [3-7, 9, 10, 14]. ...
... p < 0.001), and the highest RPP sublevel (≥ 20,000) was shown to be related to an approximately 11-fold increased probability of in-hospital death (adjusted OR 11.07, 95% CI 4.52-27.14; p < 0.001), when compared with the reference RPP sublevel (10,(0)(1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)999). From the above, it can be seen that the risk of in-hospital mortality was increased in a stepwise fashion with either higher or lower RPP levels. ...
Article
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Early prediction of in-hospital mortality in aneurysmal subarachnoid hemorrhage (aSAH) is essential for the optimal management of these patients. Recently, a retrospective cohort observation has reported that the rate-pressure product (RPP, the product of systolic blood pressure and heart rate), an objective and easily calculated bedside index of cardiac hemodynamics, was predictively associated with in-hospital mortality following traumatic brain injury. We thus wondered whether this finding could also be generalized to aSAH patients. The current study aimed to examine the association of RPP at the time of emergency room (ER) admission with in-hospital mortality and its predictive performance among aSAH patients. We retrospectively included 515 aSAH patients who had been admitted to our ER between 2016 and 2020. Their baseline heart rate and systolic blood pressure at ER presentation were extracted for the calculation of the admission RPP. Meanwhile, we collected relevant clinical, laboratory, and neuroimaging data. Then, these data including the admission RPP were examined by univariate and multivariate analyses to identify independent predictors of hospital mortality. Eventually, continuous and ordinal variables were selected from those independent predictors, and the performance of these selected predictors was further evaluated and compared based on receiver operating characteristic (ROC) curve analyzes. We identified both low (< 10,000; adjusted odds ratio (OR) 3.49, 95% CI 1.93–6.29, p < 0.001) and high (> 15,000; adjusted OR 8.42, 95% CI 4.16–17.06, p < 0.001) RPP on ER admission to be independently associated with in-hospital mortality after aSAH. Furthermore, after centering the admission RPP by its median, the area under its ROC curve (0.761, 95% CI 0.722–0.798, p < 0.001) was found to be statistically superior to any of the other independent predictors included in the ROC analyzes (all p < 0.01). In light of the predictive superiority of the admission RPP, as well as its objectivity and easy accessibility, it is indeed a potentially more applicable predictor for in-hospital death in aSAH patients.
... EAVS has been reported to correlate with the functional outcome of SAH [6,7,9] , but the correlation between EAVS and delayed symptomatic vasospasm could not be proven [6] . Therefore, the possible mechanism underlying the clinical impact of EAVS is still controversial. ...
... Therefore, the severity of symptomatic vasospasm was judged upon the need for angioplasty and/or repetitive endovascular treatments. The detailed description of clinical management of SAH patients at our institution has already been reported previously [9][10][11] . ...
... All previous publications uniquely point to the high risk of poor functional outcome in patients developing EAVS after aneurysm rupture [6,7,9] . Furthermore, strong associations between EAVS with early [9] and delayed [6,11] cerebral infarctions could also be shown. ...
Article
Background: Cerebral vasospasm usually develops several days after subarachnoid hemorrhage (SAH) and is generally acknowledged as a strong outcome predictor. In contrast, much less is known about the nature and eventual consequences of early angiographic vasospasm (EAVS) seen on admission digital subtraction angiography (DSA). Therefore, we aimed at identifying the risk factors and clinical impact of EAVS after SAH. Methods: Five hundred and thirty-one SAH patients with admission DSA performed within 72 h after the bleeding event were selected from a comprehensive database containing all consecutive SAH patients treated at our institution between January 2005 and December 2012. Predictors of EAVS, as well as associations between EAVS and delayed vasospasm-related complications, and unfavorable outcome (defined as modified Rankin scale >3) were evaluated in univariate and multivariate analyses. Results: EAVS was seen on 60 DSAs (11.3%) and was independently correlated with delayed symptomatic vasospasm requiring intra-arterial spasmolysis (OR 5.24, p < 0.0001), angioplasty (OR 2.56, p = 0.015) and repetitive endovascular treatment (OR 4.71, p < 0.0001). EAVS also increased the risk for multiple versus single territorial infarction on the follow-up CT scan(s) (OR 2.04, p = 0.047) and independently predicted unfavorable outcome (OR 2.93, p = 0.008). The presence of radiographic signs suspicious for fibromuscular dysplasia were independently associated with the occurrence of EAVS (OR 2.98, p = 0.026) and the need for repetitive endovascular vasospasm treatment (OR 3.95, p = 0.019). Conclusions: In view of the strong correlation with delayed symptomatic vasospasm and its ischemic complications, EAVS can be considered an alerting signal for severe symptomatic vasospasm. Therefore, more attention should be paid to the presence of EAVS on admission DSA.
... 2,12 Additionally, their retrospective design precluded the inference of strong conclusions. 8,13 In the current study, we analyzed clinical features that were associated with early (24-48 hours after aneurysm repair) and delayed (6 weeks after aSAH) cerebral infarcts identified on computed tomography (CT) scans of patients enrolled in the CONSCIOUS-1 study (Clazosentan to Overcome Neurological Ischemia and Infarction Occurring After Subarachnoid Hemorrhage). 14 These data included patients who underwent neurosurgical clipping and endovascular ...
... Studies have often focused on cerebral infarction identified at long-term follow-up with imaging 3,12,[25][26][27] or have only identified infarcts on imaging in patients who became symptomatic and were subsequently imaged in hospital. 8,13 These strategies may significantly underestimate the incidence of both early and delayed infarction. The current study is the first to examine the frequency of early procedure-related and delayed cerebral infarction in a prospectively collected and protocol-driven data set and to directly compare differences between patients treated by clipping or coiling. ...
... The findings of the present report are supported by several previous studies that have shown that clipping is associated with early cerebral infarcts 2,8,12,25 and that early cerebral infarcts are associated with poor neurological outcomes. 2,12,13 In our study, 45% of patients had a CT-identified cerebral infarct after repair of a ruptured intracranial aneurysm, 18% of patients had an early infarct, 19% had a delayed infarct, and 9% had both early and delayed infarcts. Previous studies have demonstrated that after aSAH, 30% to 65% of patients will have a cerebral infarct identified on imaging at long-term follow-up. ...
Article
Background and Purpose Cerebral infarction after aneurysmal subarachnoid hemorrhage is a significant cause of substantial morbidity and mortality. Because early and delayed cerebral infarction after aneurysmal subarachnoid hemorrhage may be mediated by different processes, we evaluated whether aneurysm-securing methods contributed to infarcts and whether long-term outcomes differ between early and delayed infarcts. Methods A post hoc analysis of the CONSCIOUS-1 study (Clazosentan to Overcome Neurological Ischemia and Infarction Occurring After Subarachnoid Hemorrhage) was performed. Using multivariate logistic regression analysis and propensity matching, independent clinical risk factors associated with infarctions were identified, and the contribution of cerebral infarcts to long-term outcomes was evaluated. Results Within the cohort of 413 subjects, early infarcts were present in 76 subjects (18%), whereas delayed infarcts occurred in 79 subjects (19%), and 36 subjects (9%) had new infarctions that were present on both early and delayed imaging. Propensity score matching revealed a significantly higher proportion of early infarcts after clipping (odds ratio, 4.62; 95% confidence interval, 1.99-11.57; P=0.00012). Multivariate logistic regressions identified clipping as an independent risk factor for early cerebral infarction (odds ratio, 0.26; 95% confidence interval, 0.15-0.48; P<0.001), and angiographic vasospasm was an independent risk factor for delayed cerebral infarction (odds ratio, 1.79; 95% confidence interval, 1.03-3.13; P=0.039). Early infarcts were a significant independent risk factor for poor long-term outcomes at 3 months (odds ratio, 2.34; 95% confidence interval, 1.18-4.67; P=0.015). Conclusions Clipping is an independent risk factor for the development of early cerebral infarcts, whereas delayed cerebral infarcts are associated with angiographic vasospasm. Early cerebral infarcts are stronger predictors of worse outcome than delayed infarction. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT00111085.
... randomized controlled trials comparing icP to variables derived from other types of neuromonitoring techniques were preferred but also prospective or retrospective studies were considered and included if pertinent. We did the majority of the studies were retrospective [26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42] or prospective [43][44][45][46][47] single-center studies. No multicenter studies were identified. ...
... twenty-one articles were further assessed for eligibility. one study was selected through our secondary search in PubMed, one article was eligible from the cochrane research and three related articles were identified, for a total of 26 studies included in the final analy- studies: the glasgow coma scale (gcs), 27 the gos, 26-28, 30, 31, 43 the mrs, 35 the ni-Hss, 33 the sF-36, 43 Dci incidence, 27,29,[32][33][34][35] were alternatively used. Different thresholds for the definition of elevated ICP were used, varying from >20 mmHg, 26,27,32,33,35 >25 mmHg, 29-31 >30 mmHg, 28,33,42 up to >40mmHg (table iii). ...
... one study was selected through our secondary search in PubMed, one article was eligible from the cochrane research and three related articles were identified, for a total of 26 studies included in the final analy- studies: the glasgow coma scale (gcs), 27 the gos, 26-28, 30, 31, 43 the mrs, 35 the ni-Hss, 33 the sF-36, 43 Dci incidence, 27,29,[32][33][34][35] were alternatively used. Different thresholds for the definition of elevated ICP were used, varying from >20 mmHg, 26,27,32,33,35 >25 mmHg, 29-31 >30 mmHg, 28,33,42 up to >40mmHg (table iii). 33 The main findings of these studies are as follows: -poor-grade patients are more likely to have elevated icP values on admission. ...
Article
Full-text available
Background: Evidences supporting the use of ICP monitoring after aneurysmal subarachnoid hemorrhage (aSAH) are limited. The aim of our paper is to examine whether elevated intracranial pressure (ICP) and ICP-derived variables predict mortality and functional outcomes after aSAH. Methods: A systematic review of the literature was performed through PubMed and Cochrane databases up to June 2015. Population was restricted to aSAH patients requiring admission to the intensive care unit. ICP was included in the analysis as absolute value as well as variables derived from ICP monitoring (pressure reactivity index, ICP pulse wave amplitude, ICP-arterial blood pressure wave amplitude correlation and ICP variability). Outcomes included mortality, neurological recovery and delayed cerebral ischemia (DCI). Quality of evidence was rated using the GRADE system. Results: Twenty-six studies were examined. Due to heterogeneity in qualifying studies, a meta-analysis could not be generated. We found a correlation between elevated ICP and mortality. However, ICP absolute values were not independent predictors of long-term functional outcomes (low quality of evidence). A variable relationship between elevated ICP and DCI was found (very low quality of evidence). ICP-derived variables had higher accuracy than ICP absolute values in predicting functional outcomes (moderate quality of evidence). Conclusions: Elevated ICP was associated with higher mortality however absolute ICP values per se were not independent predictors of functional recovery. Variables derived from ICP monitoring are more accurate than ICP absolute values in predicting outcome. Given the absence of good quality data, additional large studies may help to better define the prognostic value of ICP after aSAH.
... All persons or their relatives gave their informed consent within written treatment contract on admission and therefore prior to their inclusion in the study. 5 ...
... Our SAH management policy has been described in previous publications. 5,6 After interdisciplinary decision, the aneurysms were treated by clipping or coiling. Posthemorrhagic hydrocephalus was treated with external ventricular drainage (EVD) that permitted continuous monitoring of intracranial pressure (ICP) in these patients. ...
... According to in-house treatment protocols, the cutoff for pathological ICP elevation was set at 20 mmHg. 5 Transcranial Doppler ultrasonography (TCD) was performed at least once daily for a period of three weeks. 6 Absolute mean flow velocities >160 cm/s for the anterior circulation were considered suspicious of clinically relevant cerebral vasospasm. ...
Article
Background: Intraventricular hemorrhage is known to complicate the course and outcome of aneurysmal subarachnoid hemorrhage. Aims: To identify independent risk factors for intraventricular hemorrhage development and its severity during aneurysm rupture. Methods: Six hundred and twenty-five subarachnoid hemorrhage patients treated at our institution between January 2005 and December 2012 were included. The severity of intraventricular hemorrhage was assessed according to the original Graeb score. Clinical and radiographic features of patients present at the bleeding event were tested as potential risk factors for intraventricular hemorrhage. The characteristics of intraventricular hemorrhage were correlated with the clinical course and outcome. Results: Intraventricular hemorrhage was present in 206 patients (33%) and was independently predicted by patient's age (p = 0.001, odds ratio (OR) = 1.02/year of age increase), aneurysm size (p = 0.031, OR = 1.05/mm increase), and location (p < 0.0001, OR = 3.2 for aneurysms of posterior circulation). The severity of intraventricular hemorrhage was predicted by aneurysm size (p = 0.023) and location (higher severity for aneurysms of anterior circulation, p = 0.01). The presence of intraventricular hemorrhage (p < 0.0001, OR = 4.1) and intraventricular hemorrhage severity of >3 points on the Graeb score (p = 0.029, OR = 3.4) was independently associated with poor outcome. Shunt dependency was associated only with the occurrence of intraventricular hemorrhage (p < 0.0001, OR = 2.8) while the severity of intraventricular hemorrhage influenced the timing of shunt placement (p = 0.0156). Conclusions: Increasing age, aneurysm size, and location in the posterior circulation are the main risk factors for occurrence of aneurysmal intraventricular hemorrhage, which is independently associated with poor outcome. The severity of intraventricular hemorrhage, however, is higher if the aneurysm is located in the anterior circulation and has impact on functional outcome, but not on shunt dependency.
... From a comprehensive database including all patients treated with non-traumatic SAH at the University Medical Center Freiburg between January 1 st 2005 and December 31 st 2012, we selected patients with acute NASAH. Results of patients with aneurysmal SAH (ASAH) have been reported previously [6]. The presently applied inclusion criteria for NASAH were: 1) diagnosis of SAH verified by computed tomography (CT) scan within 72 hours after clinical onset, or, in case of negative CT scan, by lumbar puncture; 2) absence of clinical and/or radiographic signs potentially indicative of a traumatic cause of SAH; 3) exclusion of underlying vascular lesions by means of CT-angiography (CTA) and complete (four vessel) digital subtraction angiography (DSA), according to our diagnostic algorithms that were previously described [7]. ...
... The neurological condition on admission measured by Hunt & Hess grade reflects the severity of the early brain injury and is known to be a fair predictor of morbidity and mortality after SAH [32]. Finally, the bleeding pattern arises from the severity of initial bleeding, an acknowledged precursor of multiple early and late complications of SAH [6,33]. Since cerebral vasospasm and infarction were not important predictors of functional outcome after NASAH, the impact of bleeding pattern on clinical outcome can be conditioned by the severity of early brain injury immediately after the bleeding event [34]. ...
... Comparison of population characteristics of patients with ASAH and NASAH.* -the detailed data of ASAH patients have been reported previously[6] † -acetylsalicylic acid or warfarin; § -mean values within 14 days after ictus; NS -not statistically significant. ...
Article
Contrary to aneurysmal bleeding, non-aneurysmal non-traumatic subarachnoid hemorrhage (NASAH) is rarely associated with unfavorable clinical outcome, cerebral infarction and vasospasm. We aimed to identify independent predictors for a poor clinical course and outcome after NASAH. All patients with NASAH treated at our institution between January 2005 and December 2012 were retrospectively analyzed. Collected demographic, clinical and radiographic variables were divided into primary (admission) and secondary (follow-up) parameters. Independent predictors of unfavorable outcome (defined as modified Rankin scale=3-6), cerebral infarction and development of vasospasm were identified. In addition, a risk score for the estimation of clinical outcome was designed. Out of population with 157 NASAH patients, unfavorable outcome was documented in 57 cases (36.3%) at discharge and in 17 cases (10.8%) after 6 months. Cerebral infarction(s) were found in 7 patients (4.3%). In multivariate analyses, higher age (≥65 years), poorer initial clinical condition measured by Hunt & Hess grade and diffuse basal bleeding pattern were independent outcome predictors and therefore included in the risk score (1-8 points). The risk score correlated with outcome at discharge (p<0.0001) and clinical improvement after 6 months (p=0.0238). A diffuse basal bleeding pattern predicted the detection of vasospasm by transcranial Doppler (p=0.001). Poor initial clinical condition (p=0.028) and vasospasm (p=0.031) were associated with the occurrence of cerebral infarction. NASAH patients with higher age, bad clinical condition on admission and diffuse bleeding pattern are prone to unfavorable outcome. The proposed risk score helps to identify patients with poor prognosis after NASAH.
... The study populations ranged from 38e632 patients. Four studies 15,16,20,22 used MRI and 6 13,14,[17][18][19]21 performed CT scans as the method of brain imaging. Seven studies 13-16,18,20,21 described functional outcomes, 4 12,13,15,20 described 3-month mortality, and 2 studies 16,19 described mortality on a different time frame. ...
... with 58.6% heterogeneity. Excluding the study with the most heterogeneity influence, 21 the RR is 1.94 (95% CI 1.61e2.33) with 20.6% heterogeneity. ...
... When the scan was performed before the aneurysm repair procedure, the RR was 2.59 (95% CI 2.23e3.01). Of the 4 studies, [14][15][16]21 which had brain imaging available before the repair procedure, 3 14-16 describe the infarction before any invasive procedure, even diagnostic angiography. Therefore the infarction came from the bleeding itself and not as a complication of surgery or angiography with endovascular aneurysm repair. ...
Article
Objective: Aneurysmal subarachnoid haemorrhage (aSAH) is an acute cerebrovascular event that leads to devastating consequences. Early brain infarction (EBI) develops very early, within the first 72 hours after bleeding, but may have a significant impact on long-term outcomes. The incidence and impact of EBI in the prognosis of aSAH remain uncertain. We performed a systematic review and meta-analysis to evaluate the incidence of EBI in patients with aSAH and determine the effect of EBI on mortality and functional outcomes. Methods: We performed a systematic review and meta-analysis. Inclusion criteria were: Studies that performed a brain imaging study up to 72 hours of haemorrhage; both computed tomography (CT) or magnetic resonance imaging (MRI); and included a description of the findings of the brain imaging study (whether an infarct was present or not). Results: Ten studies that met the criteria were included. The incidence of EBI was 17%. The risk ratio (RR) for 3-month mortality was 2.18 (95% CI 1.48 - 3.30). The overall RR for poor outcome was 2.26 (95% CI 1.75 - 2.93). Conclusions: EBI plays an important role in the outcome of patients with aSAH. Its significant impact could represent a new therapeutic frontier for improving outcomes of these patients.
... 1 Evidence suggests that the thick and diffuse blood distribution in cerebrospinal fluid (CSF) is the main risk factor of severe clinical course and poor outcome in SAH patients. 2,3 Blood components with secondary products (such as coagulation and degradation products) trigger a series of pathophysiological changes in both the acute and chronic stages after SAH. 4 Surgical interventions, such as lumbar drainage (LD) and external ventricular drainage (EVD), are widely used in the current clinical setting to facilitate bloody CSF clearance in SAH patients. However, the benefit remains limited and there is a risk of infection. ...
... The CSF circulation is severely disturbed in both acute and late phases after SAH, which directly leads to increased intracerebral pressure (ICP), decreased cerebral blood perfusion, brain oedema formation, and hydrocephalus. 7À10 The blood coagulation response to SAH in the subarachnoid space is considered the leading cause of CSF flow abnormalities, 2,3,8,9,11 which directly blocks the ventricular system and arachnoid granules with the resultant CSF retention and acute hydrocephalus. 12,13 The coagulation cascade leads to fibrin clotting and deposition in the subarachnoid space and perivascular space, which further blocks the CSFinterstitial fluid (ISF) exchange and induces cerebral vasospasm and the neuroinflammatory response. ...
Article
Full-text available
Background: Neuroinflammation and blood coagulation responses in cerebrospinal fluid (CSF) contribute to the poor outcome associated with subarachnoid haemorrhage (SAH). We explored the role of caspase-1-mediated inflammasome activation on extrinsic blood coagulation in CSF after SAH. Methods: Post-SAH proteomic changes and correlation between caspase-1 with extrinsic coagulation factors in human CSF after SAH were analysed. Time course and cell localisation of brain inflammasome and extrinsic coagulation proteins after SAH were explored in a rat SAH model. Pharmacological inhibition of caspase-1 via VX-765 was used to explore the role of caspase-1 in blood clearance and CSF circulation after SAH in rats. Primary astrocytes were used to evaluate the role of caspase-1 in haemoglobin-induced pyroptosis and tissue factor (TF) production/release. Findings: Neuroinflammation and blood coagulation activated after SAH in human CSF. The caspase-1 levels significantly correlated with the extrinsic coagulation factors. The activated caspase-1 and extrinsic coagulation initiator TF was increased on astrocytes after SAH in rats. VX-765 attenuated neurological deficits by accelerating CSF circulation and blood clearance through inhibiting pyroptotic neuroinflammation and TF-induced fibrin deposition in the short-term, and improved learning and memory capacity by preventing hippocampal neuronal loss and hydrocephalus in the long-term after SAH in rats. VX-765 reduced haemoglobin-induced pyroptosis and TF production/release in primary astrocytes. Interpretation: Inhibition of caspase-1 by VX-765 appears to be a potential treatment against neuroinflammation and blood coagulation in CSF after SAH. Funding: This study was supported by National Institutes of Health of United States of America, and National Natural Science Foundation of China.
... Spontaneous subarachnoid hemorrhage (SAH) is a neurological disease with high morbidity and mortality (De Vivo et al. 1998;Jabbarli et al. 2015;Nieuwkamp et al. 2009). SAH has an incidence of 4-5 cases/100,000 inhabitants/year (Nieuwkamp et al. 2009;Teunissen et al. 1996) and its mortality rate at 30 days is 40-45 %. ...
Conference Paper
Background Nearly 20% of patients who suffer a subarachnoid hemorrhage (SAH) present cognitive impairment even after a year of follow-up. In this sense, visuospatial and visuoperceptive domains have not been fully studied in these patients. Furthermore, they have been associated with the activity in the so-called mirror neuron system (MNS). Objective To analyze the pattern of brain activity with a MNS task-based functional magnetic resonance imaging (fMRI) study in SAH patients. Methods A complete neuropsychological assessment and fMRI study (with observation and execution conditions) were both performed in patients with a history of SAH registered in the database of the Hospital Universitario de Canarias. They must fulfill all the inclusion criteria for the study (less than 40 years old; SAH with Fisher score 1-3; no vasospasm or ischemia; minimum follow-up of one year). Results Twelve patients were completely neuropsychologically studied. Four of them presented visuospatial/visuoperceptive impairment. fMRI study demonstrated the presence of higher activity in MNS regions in these patients than in patients with normal visuospatial/visuoperceptive functions. Furthermore, there was a negative correlation between the test scores and the extent of activation in premotor regions of the studied patients. Conclusion SAH patients with visuospatial/visuoperceptive impairment present an increase of activity in the MNS regions. This may be associated with a subcortical dysfunction, leading to a disruption of neural activity and a less efficient behavior of this brain network.
... As the components of the score, poor initial clinical condition, the presence of IVH, location of the ruptured aneurysm in the posterior circulation and acute PHH requiring external CSF diversion are generally acknowledged as strong predictors of shunt dependency [4][5][6][7]9]. Early cerebral infarction on CT scan has already been recognized as a strong predictor of poor functional outcome and different late complications of SAH [16]. The crucial role of early cerebral infarction for the development of shunt dependency after SAH was also shown with the present data. ...
Article
Background and purpose: Acute hydrocephalus is an early and common complication of aneurysmal subarachnoid hemorrhage (SAH). However, considerably fewer patients develop chronic hydrocephalus requiring shunt placement. Our aim was to develop a risk score for early identification of patients with shunt dependency after SAH. Methods: Two hundred and forty-two SAH individuals who were treated in our institution between January 2008 and December 2013 and survived the initial impact were retrospectively analyzed. Clinical parameters within 72 h after the ictus were correlated with shunt dependency. Independent predictors were summarized into a new risk score which was validated in a subsequent SAH cohort treated between January and December 2014. Results: Seventy-five patients (31%) underwent shunt placement. Of 23 evaluated variables, only the following five showed independent associations with shunt dependency and were subsequently used to establish the Chronic Hydrocephalus Ensuing from SAH Score (CHESS, 0-8 points): Hunt and Hess grade ≥IV (1 point), location of the ruptured aneurysm in the posterior circulation (1 point), acute hydrocephalus (4 points), the presence of intraventricular hemorrhage (1 point) and early cerebral infarction on follow-up computed tomography scan (1 point). The CHESS showed strong correlation with shunt dependency (P = 0.0007) and could be successfully validated in both internal SAH cohorts tested. Patients scoring ≥6 CHESS points had significantly higher risk of shunt dependency (P < 0.0001) than other patients. Conclusion: The CHESS may become a valuable diagnostic tool for early estimation of shunt dependency after SAH. Further evaluation and external validation will be required in prospective studies.
... Pathognomic finding of hemosiderin deposition can be characterized as hypointensity on T2-weighted imaging (T2WI) MRI and gradient recalled echo T2-WI (GRE T2*WI) MRI. [11,13,18,20] There is accumulating evidence that three-dimensional T2 star-weighted angiography [12] may be superior to GRE T2*WI for the diagnosis of SS. [8,46] Previously, a case of intracranial dural arteriovenous fistula (dAVF) treated with open surgery and a spinal dAVF as a cause of symptomatic SS have been reported as the putative cause for SS of CNS. [6,38] We will describe the second and third cases of intracranial dAVF as the cause of symptomatic intracranial SS and successful treatment of SS-associated dAVF with endovascular embolization. ...
Article
Full-text available
Background: Superficial siderosis (SS) is the occult deposition of hemosiderin within the cerebral cortex due to repeat microhemorrhages within the central nervous system. The collection of hemosiderin within the pia and superficial cortical surface can lead to injury to the nervous tissue. The most common presentation is occult sensorineural hearing loss although many patients have been misdiagnosed with diseases such as multiple sclerosis and amyotrophic lateral sclerosis before being diagnosed with SS. Only one case report exists in the literature describing an intracranial dural arteriovenous fistula (dAVF) as the putative cause for SS. Case description: We describe two cases of SS caused by a dAVF. Both patients had a supratentorial, cortical lesion supplied by the middle meningeal artery with venous drainage into the superior sagittal sinus. In both patients, symptoms improved after endovascular embolization. The similar anatomic relationship of both dAVFs reported presents an interesting question about the pathogenesis of SS. Similar to the pathologic changes seen in the formation of intracranial arterial aneurysms; it would be possible that changes in the blood vessel lining and wall might predispose a patient to chronic, microhemorrhage resulting in SS. Conclusions: We describe the second and third cases of a dAVF as the cause of SS, and the first cases of successful treatment of SS-associated dAVF with endovascular embolization. As noninvasive imaging techniques become more sensitive and easily obtained, one must consider their limitations in detecting occult intracranial vascular malformations such as dAVF as a possible etiology for SS.
... Aneurysmal subarachnoid haemorrhage (SAH) remains a lifethreating disease with a mortality rate of up to 35% [30]. Rebleeding of the aneurysm, delayed cerebral ischaemia (DCI) and chronic hydrocephalus are well-studied complications resulting in increased mortality rates [14,15,30]. In addition, medical complications and systemic diseases affect the clinical course and outcome on the intensive care unit (ICU) [11]. ...
Article
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Hyperactive delirium (agitation) is a common complication in patients on intensive care units and can be assessed by the Richmond Agitation and Sedation Scale (RASS) in principle. However, the role of agitation in patients with aneurysmal subarachnoid haemorrhage (SAH) is poorly understood. We performed a retrospective analysis to identify risk factors for the development of a hyperactive delirium and its functional consequences for neurological outcome. Three hundred thirty-eight patients with SAH were screened in this study resulting in 212 patients which reached at least once a RASS of 0 and were eligible for further analysis. Clinical characteristics were analysed towards the occurrence of a hyperactive delirium. Neurological outcome at discharge and follow-up was assessed using the Glasgow Outcome Scale. Seventy-eight of 212 patients (36.8%) developed a hyperactive delirium; the duration ranged from 1 to 11 days. Multivariate regression revealed initial hydrocephalus (odds ratio (OR) 3.21 95% confidence interval (CI) [1.33–7.70]; p = 0.01), microsurgical clipping (OR 3.70 95%CI 1.71–8.01]; p = 0.001), male gender (OR 1.97 95%CI [1.05–3.85]; p = 0.047) and a higher Graeb score (OR 1.11 95%CI [1.00–1.22]; p = 0.043) to be significantly associated with the development of agitation. Medical history of psychiatric disorders, alcohol or nicotine abuse showed no correlation with agitation. Cox regression analysis revealed no significant influence of agitation towards unfavourable outcome at discharge or follow-up. We provide four independent risk factors for the development of agitation in SAH patients. Our study emphasizes the specific entity of agitation in patients with SAH and underscores its relevance in neurological patients.
... The initial clinical condition (i.e., the WFNS grade at admission) reflects the severity of the early brain injury after SAH. 34,35 Therefore, WFNS grade 5 presents the clinical consequence of a very severe early brain injury with frequently irreversible cerebral damage. For these conditions, DC has a considerably less potential to improve the outcome. ...
Article
Objective: Decompressive craniectomy (DC) may become a life-saving measure for patients with subarachnoid hemorrhage (SAH). However, the benefit of early DC has not been shown yet. We aimed at identifying the clinical value of DC timing. Methods: We retrospectively analyzed 245 SAH patients who underwent DC between January 2003 and December 2015. The cohort was stratified into primary (at admission, n=171) and secondary DC (n=74). Moreover, primary DC was also subdivided into early (≤24 hours after ictus, n=120) and delayed (n=51) primary DC. Results: There was no difference between primary and secondary DC (65.5% and 74.3% respectively, p=0.1828) with regard to unfavorable outcome at 6 months post-SAH (defined as modified Rankin scale>3). However, individuals with early primary DC presented with significantly better functional outcome than the remaining cohort (p=0.014, OR=2.02) and even compared to the subgroup with delayed primary DC (p=0.023, OR=2.42). Among individuals with World Federation of Neurosurgical Societies Grade <5 at admission, the benefits of early DC were more impressive: lower rates of unfavorable outcome (p=0.003, OR=0.28), in-hospital mortality (p=0.031, OR=0.37) and cerebral infarctions (p=0.028, OR=0.38) on the follow-up computed tomography scans. Conclusion: Not the timing of DC indication (primary/secondary), but rather the actual time left between the ictus and DC is crucial for the functional improvement of SAH patients requiring DC. Especially, individuals without the signs of severe early brain injury strongly benefit from early DC.
... The different aspects of SAH management at our institution have already been elaborated on in our previous publications. [11][12][13][14] ...
Article
OBJECTIVE An asymmetry of the A 1 segments (A1SA) of the anterior cerebral arteries (ACAs) is an assumed risk factor for the development of anterior communicating artery aneurysms (ACoAAs). It is unknown whether A1SA is also clinically relevant after aneurysm rupture. The authors of this study investigated the impact of A1SA on the clinical course and outcome of patients with aneurysmal subarachnoid hemorrhage (SAH). METHODS The authors retrospectively analyzed data on consecutive SAH patients treated at their institution between January 2005 and December 2012. The occurrence and severity of cerebral infarctions in the ACA territories were evaluated on follow-up CT scans up to 6 weeks after SAH. Moreover, the risk for an unfavorable outcome (defined as > 3 points on the modified Rankin Scale) at 6 months after SAH was assessed. RESULTS A total of 594 patients were included in the final analysis. An A1SA was identified on digital subtraction angiography studies from 127 patients (21.4%) and was strongly associated with ACoAA (p < 0.0001, OR 13.7). An A1SA independently correlated with the occurrence of ACA infarction in patients with ACoAA (p = 0.047) and in those without an ACoAA (p = 0.015). Among patients undergoing ACoAA coiling, A1SA was independently associated with the severity of ACA infarction (p = 0.023) and unfavorable functional outcome (p = 0.045, OR = 2.4). CONCLUSIONS An A1SA is a common anatomical variation in SAH patients and is strongly associated with ACoAA. Moreover, the presence of A1SA independently increases the likelihood of ACA infarction. In SAH patients undergoing ACoAA coiling, A1SA carries the risk for severe ACA infarction and thus an unfavorable outcome. Clinical trial registration no.: DRKS00005486 ( http://www.drks.de/ )
... An assumed difference in occurrence rates of early cerebral infarction might explain the varied results. 14,15 The fact that Fisher grade was a relevant predictor for SDHC in our series is consistent with the results of a previous meta-analysis 28 but does not match the findings of another recent study. 14 The discrepancy is explained partially by the different scoring For the first time, increasing BNI scores were shown to be associated with increasing risk for the development of SDHC. ...
Article
OBJECTIVE Feasible clinical scores for predicting shunt-dependent hydrocephalus (SDHC) after aneurysmal subarachnoid hemorrhage (aSAH) are scarce. The chronic hydrocephalus ensuing from SAH score (CHESS) was introduced in 2015 and has a high predictive value for SDHC. Although this score is easy to calculate, several early clinical and radiological factors are required. The authors designed the retrospective analysis described here for external CHESS validation and determination of predictive values for the radiographic Barrow Neurological Institute (BNI) scoring system and a new simplified combined scoring system. METHODS Consecutive data of 314 patients with aSAH were retrospectively analyzed with respect to CHESS parameters and BNI score. A new score, the shunt dependency in aSAH (SDASH) score, was calculated from independent risk factors identified with multivariate analysis. RESULTS Two hundred twenty-five patients survived the initial phase after the hemorrhage, and 27.1% of these patients developed SDHC. The SDASH score was developed from results of multivariate analysis, which revealed acute hydrocephalus (aHP), a BNI score of ≥ 3, and a Hunt and Hess (HH) grade of ≥ 4 to be independent risk factors for SDHC (ORs 5.709 [aHP], 6.804 [BNI], and 4.122 [HH]; p < 0.001). All 3 SDHC scores tested (CHESS, BNI, and SDASH) reliably predicted chronic hydrocephalus (ORs 1.533 [CHESS], 2.021 [BNI], and 2.496 [SDASH]; p ≤ 0.001). Areas under the receiver operating curve (AUROC) for CHESS and SDASH were comparable (0.769 vs 0.785, respectively; p = 0.447), but the CHESS and SDASH scores were superior to the BNI grading system for predicting SDHC (BNI AUROC 0.649; p = 0.014 and 0.001, respectively). In contrast to CHESS and BNI scores, an increase in the SDASH score coincided with a monotonous increase in the risk of developing SDHC. CONCLUSIONS The newly developed SDASH score is a reliable tool for predicting SDHC. It contains fewer factors and is more intuitive than existing scores that were shown to predict SDHC. A prospective score evaluation is needed.
... In a recent study of 632 patients who were managed in a single center, predictors of early cerebral infarction were identified and included Hunt and Hess Grades IV and V (OR = 2.06, p = 0.008), Fisher Grades 3 and 4 (OR = 3.99, p = 0.014), sustained elevations of intracranial pressure > 20 mm Hg (OR 5.95, p < 0.0001), and early vasospasm on diagnostic angiography (OR 3.01, p = 0.008). 10 In a related paper, the authors reported a risk score for cerebral infarction (BEHAVIOR score) based on 7 independent predictors identified at multivariable analysis, including Fisher grade of SAH clot, patient age ≥ 55 years, Hunt and Hess grade, acute hydrocephalus requiring external CSF drainage, vasospasm on initial angiography, intracranial pressure greater than 20 mm Hg, and treatment of multiple aneurysms. 11 In addition, Kanamaru et al. recently published their post hoc analysis of predictors for cerebral infarction in 579 patients in the Prospective Registry of Subarachnoid Aneurysms Treatment (PRESAT). ...
Article
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OBJECTIVE In this study the authors sought to investigate the sex differences in the risk of delayed cerebral ischemia (DCI), delayed cerebral infarction, and the role of hormonal status. METHODS Ten studies included in the SAHIT (SAH International Trialists) repository were analyzed using a fitting logistic regression model. Heterogeneity between the studies was tested using I ² statistics, and the results were pooled using a random-effects model. Multivariable analysis was adjusted for the effects of neurological status and fixed effect of study. An additional model was examined in which women and men were split into groups according to an age cut point of 55 years, as a surrogate to define hormonal status. RESULTS A pooled cohort of 6713 patients was analyzed. The risk of DCI was statistically significantly higher in women than in men (OR 1.29, 95% CI 1.12–1.48); no difference was found with respect to cerebral infarction (OR 1.17, 95% CI 0.98–1.40). No difference was found in the risk of DCI when comparing women ≤ 55 and > 55 years (OR 0.87, 95% CI 0.74–1.02; p = 0.08) or when comparing men ≤ 55 and > 55 years (p = 0.38). Independent predictors of DCI were World Federation of Neurosurgical Societies (WFNS) grade, Fisher grade, age, and sex. Independent predictors of infarction included WFNS grade, Fisher grade, and aneurysm size. CONCLUSIONS Female sex is associated with a higher risk of DCI. Sex differences may play a role in the pathogenesis of DCI but are not associated with menopausal status. The predictors of DCI and cerebral infarction were identified in a very large cohort and reflect experience from multiple institutions.
... 16,18 In retrospect, the decision to initiate large randomized trials for ET-1 receptor antagonists was not supported by robust experimental data on clinically relevant outcomes. 14 Although angiographic vasospasm is a well-established predictor of cerebral ischemia/infarction in SAH, [19][20][21] its sensitivity and specificity (both approximately 70%) are far from optimal. 19 A meta-analysis of 55 experimental studies determined that the majority failed to assess whether ET-1 receptor antagonism changed cerebral blood flow (CBF) in SAH (only 3 of the 27 studies measured CBF); none of the studies investigated neurofunctional outcomes. ...
Article
Aneurysmal subarachnoid hemorrhage (SAH) is a devastating cerebral event that kills or debilitates the majority of those afflicted. The blood that spills into the subarachnoid space stimulates profound cerebral artery vasoconstriction and consequently, cerebral ischemia. Thus, once the initial bleeding in SAH is appropriately managed, the clinical focus shifts to maintaining/improving cerebral perfusion. However, current therapeutic interventions largely fail to improve clinical outcome, because they do not effectively restore normal cerebral artery function. This review discusses emerging evidence that perturbed cerebrovascular “myogenic reactivity,” a crucial microvascular process that potently dictates cerebral perfusion, is the critical element underlying cerebral ischemia in SAH. In fact, the myogenic mechanism could be the reason why many therapeutic interventions, including “Triple H” therapy, fail to deliver benefit to patients. Understanding the molecular basis for myogenic reactivity changes in SAH holds the key to develop more effective therapeutic interventions; indeed, promising recent advancements fuel optimism that vascular dysfunction in SAH can be corrected to improve outcome.
... The patients with good initial condition and benign clinical course who did not require EVD were considered not to have pathologic ICP elevations. 16 Any sustained ICP elevation requiring additional ICP management (conservative/surgical) in the time frame from EVD placement up to the patients' return to our ICU after the aneurysm treatment was included into the risk score. ...
Article
Cerebral infarction (CI) is a crucial complication of aneurysmal subarachnoid hemorrhage (SAH) associated with poor clinical outcome. We aimed at developing an early risk score for CI based on clinical characteristics available at the onset of SAH. Out of a database containing 632 consecutive patients with SAH admitted to our institution from January 2005 to December 2012, computed tomography (CT) scans up to day 42 after ictus were evaluated for CIs. Different parameters from admission up to aneurysm treatment were collected with subsequent construction of a risk score. Seven clinical characteristics were independently associated with CI and included in the Risk score (BEHAVIOR Score, 0 to 11 points): Blood on CT scan according to Fisher grade ⩾3 (1 point), Elderly patients (age ⩾55 years, 1 point), Hunt&Hess grade ⩾4 (1 point), Acute hydrocephalus requiring external liquor drainage (1 point), Vasospasm on initial angiogram (3 points), Intracranial pressure elevation >20 mm Hg (3 points), and treatment of multiple aneurysms ('Overtreatment', 1 point). The BEHAVIOR score showed high diagnostic accuracy with respect to the absolute risk for CI (area under curve=0.806, P<0.0001) and prediction of poor clinical outcome at discharge (P<0.0001) and after 6 months (P=0.0002). Further validation in other SAH cohorts is recommended.Journal of Cerebral Blood Flow & Metabolism advance online publication, 29 April 2015; doi:10.1038/jcbfm.2015.81.
... In addition, onset age of this disease is becoming increasingly younger (5). Cerebral infarction is currently the most common type of cerebrovascular disease with a high rate of disability and recurrence (6). Fu et al (7) reported that mortality rate of cerebral infarction patients has reached 28%, and the recurrence rate was as high as 45%. ...
Article
Full-text available
Therapeutic efficacy of the use of oral atorvas­tatin in the treatment of patients with aspiration pneumonia complicated with cerebral infarction was investigated. Three hundred and fourteen cerebral infarction patients complicated with aspiration pneumonia who were admitted to the emer­gency department of Beijing Chaoyang Hospital Jingxi Branch from May 2015 to July 2017 were retrospectively analyzed. Among them, 160 patients who took atorvastatin were treated as observation group, and the remaining 154 patients were the control group. Patients were given basic treatment after diagnosis, and atorvastatin was also used for patients in the observation group. Venous blood was extracted to detect blood lipids and inflammatory cytokines. Patients were followed up for a period of six months, and the mortality was recorded. After treatment, blood lipid function and inflam­matory factors in both groups were significantly improved (P<0.05). Hospital stay in the observation group (86.88%) was significantly shorter than that in the control group (76.33%) (P<0.01). After treatment, levels of TC, LDL, TG and CRP in the observation group (86.25%) were significantly lower than those in the control group (76.32%) (P=0.01). However, after treatment, level of HDL-C in the observation group (11.88%) was significantly higher than that in the control group (23.38%) (P=0.01). After treatment, levels of IL-6, IL-8 and TNF-α in the observation group were significantly lower than those in the control group (P<0.01). Total effective rate in the observation group was significantly higher than that of the control group (P=0.01). Total death rate in the obser­vation group was significantly lower than that in the control group (P=0.02). In conclusion, atorvastatin is effective in the treatment of cerebral infarction patients complicated with aspiration pneumonia.
... Aneurysmal subarachnoid hemorrhage (SAH) is a devastating type of stroke with high morbidity and mortality [1]. Common complications after the initial bleed include early brain injury (EBI), symptomatic vasospasm, and brain edema [2]. Consequently, brain swelling results in increased intracranial pressure (ICP), which increases the risk of cerebral ischemia due to a reduction of cerebral perfusion pressure [3,4]. ...
Article
Full-text available
Objective The severity of early brain edema after aneurysm rupture was reported to be strongly associated with the risk of poor outcome after aneurysmal subarachnoid hemorrhage (SAH). Using the recently developed SEBES (Subarachnoid Hemorrhage Early Brain Edema Score), we analyzed the predictors of early brain edema and its impact on the complications related to intracranial pressure (ICP) increase after SAH and poor outcome. Methods All consecutive SAH cases treated between January 2003 and June 2016 with assessable SEBES were included (n=745). Data on demographic characteristics, previous medical history, initial severity of SAH, need for conservative ICP treatment and decompressive craniectomy, the occurrence of cerebral infarctions and unfavorable outcome at 6 months (mRS>2) were collected. Univariable and multivariable analyses were performed. Results Younger age (<55 years, adjusted odds ratio [aOR]=3.16, 95% confidence interval [CI]=2.28-4.38), female sex (aOR=1.64, 95% CI=1.16-2.31), poor initial clinical condition (WFNS=4-5, aOR= 1.74, 95% CI=1.23-2.46), presence of intracerebral hemorrhage (aOR=1.63, 95% CI=1.12-2.36), hypothyroidism (aOR=0.60, 95% CI=0.37-0.98) and renal comorbidity (aOR=0.29, 95% CI=0.11-0.78) were independently associated with the SEBES (scores 3-4). There was an independent association between the SEBES=3-4 and the need for conservative ICP treatment (aOR=2.43, 95% CI=1.73-3.42), decompressive craniectomy (aOR=2.68, 95% CI=1.84-3.89), development of cerebral infarcts (aOR=2.24, 95% CI=1.53-3.29) and unfavorable outcome (aOR=1.48, 95% CI=1.0-2.17). Conclusions The SEBES is a reliable predictor of ICP-related complications and poor outcome of SAH. Our findings highlight the need for further research of the impact of patients’ demographic characteristics and comorbidities on the severity of early brain edema after SAH.
... Our results are consistent with findings from previous studies showing an association between CA derangement and cerebral infarction, as DCI outcome [18,19]. As previously reported in other investigations [42][43][44][45], we also found that cerebral infarction was associated with an unfavorable long-term outcome. In our study, worse initial clinical severity as evaluated by APACHE II physiological sub-score at admission was also associated with unfavorable long-term outcome. ...
Article
Background Cerebral autoregulation (CA) impairment after aneurysmal subarachnoid hemorrhage (SAH) has been associated with delayed cerebral ischemia and an unfavorable outcome. We investigated whether the early transient hyperemic response test (THRT), a transcranial Doppler (TCD)-based CA evaluation method, can predict functional outcome 6 months after aneurysmal SAH. Methods This is a prospective observational study of all aneurysmal SAH patients consecutively admitted to a single center between January 2016 and February 2017. CA was evaluated within 72 h of hemorrhage by THRT, which describes the changes in cerebral blood flow velocity after a brief compression of the ipsilateral common carotid artery. CA was considered to be preserved when an increase ≥ 9% of baseline systolic velocity was present. According to the modified Rankin Scale (mRS: 4–6), the primary outcome was unfavorable 6 months after hemorrhage. Secondary outcomes included cerebral infarction, vasospasm on TCD, and an unfavorable outcome at hospital discharge. Results Forty patients were included (mean age = 54 ± 12 years, 70% females). CA was impaired in 19 patients (47.5%) and preserved in 21 (52.5%). Impaired CA patients were older (59 ± 13 vs. 50 ± 9, p = 0.012), showed worse neurological conditions (Hunt&Hess 4 or 5–47.4% vs. 9.5%, p = 0.012), and clinical initial condition (APACHE II physiological score—12 [5.57–13] vs. 3.5 [3, 4, 5], p = 0.001). Fourteen patients in the impaired CA group and one patient in the preserved CA group progressed to an unfavorable outcome (73.7% vs. 4.7%, p = 0.0001). The impaired CA group more frequently developed cerebral infarction than the preserved CA group (36.8% vs. 0%, p = 0.003, respectively). After multivariate analysis, impaired CA (OR 5.15 95% CI 1.43–51.99, p = 0.033) and the APACHE II physiological score (OR 1.67, 95% CI 1.01–2.76, p = 0.046) were independently associated with an unfavorable outcome. Conclusions Early CA impairment detected by TCD and admission APACHE II physiological score independently predicted an unfavorable outcome after SAH.
... The mechanisms underlying CVS remain unclear; it may be multifactorial and involve a complicated pathological process. Potential causes of CVS are as follows: 1. mechanical stimulation such as damage, compression or stretching of the blood vessels during surgery, leading to the blood owing into the subarachnoid space and subsequent occurrence of CVS occurs [17]; 2. vascular wall injury caused by compression of the vascular wall and vascular wall malnutrition [18]; 3. damage caused by the oxidation of hemoglobin to methemoglobin and release of oxygen free radicals [19]; 4. constriction of the blood vessels caused by vasoactive substances [20]; 5. increased intracranial pressure, the overdose of dehydration drugs and insu cient supply of blood volume [21]; and 6. in ammation and immune reactions of blood vessel walls [7,22,23]. The common nal pathway arising from all the above factors stated is a change in the permeability of smooth muscle cells in the blood vessels, an increase in calcium in ux and release of calcium ion from intracellular calcium stores, leading to an overload of free calcium in the cytosol [24]. ...
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Background Cerebral vasospasm (CVS) is a serious neurosurgical complication. This retrospective study was performed to analyze if nimodipine can improve prognosis and reduces ischemia secondary to delayed CVS after intracranial tumor surgery. Methods Retrospective analysis of 94 patients with an anterior cranial fossa tumor and underwent intracranial tumor surgery was performed, with 42 cases treated with normal saline and 52 cases treated with nimodipine solution. Transcranial Doppler ultrasonography was used to measure velocity in the middle cerebral artery (MCA) and distal extracranial internal carotid artery (eICA). An examination was conducted 1 day before surgery and 1, 3, 5, 7, and 14 days after surgery. Follow-up was performed using the Glasgow Outcome Scale (GOS) 3 months after discharge. Results We showed that in the nimodipine group, CVS occurred in 13 (25%) patients who did not have CVS in the first three days after operation; nine patients had CVS between 4 and 7 days, and 4 had CVS between 8 and 14 days. In the normal saline group, nineteen (45%) patients had CVS, 3 presented with CVS within 3 days, 11 between 4–7 days and 5 between 8–14 days. A significant difference in the occurrence of CVS was observed between the two groups. Preoperative and postoperative MCA velocities were compared, revealing a significant change in the normal saline group (P < 0.05) but not in the nimodipine group. Furthermore, significant differences in the outcome were observed between the two groups at the 3-month follow-up (P < 0.05). Conclusions Nimodipine markedly improves prognosis and significantly reduces ischemia secondary to delayed CVS after intracranial tumor surgery, as well as the risks of mortality and morbidity.
... The mechanisms underlying CVS remain unclear; it may be multifactorial and involve a complicated pathological process. Potential causes of CVS are as follows: 1. mechanical stimulation such as damage, compression or stretching of the blood vessels during surgery, leading to the blood owing into the subarachnoid space and subsequent occurrence of CVS occurs [17]; 2. vascular wall injury caused by compression of the vascular wall and vascular wall malnutrition [18]; 3. damage caused by the oxidation of hemoglobin to methemoglobin and release of oxygen free radicals [19]; 4. constriction of the blood vessels caused by vasoactive substances [20]; 5. increased intracranial pressure, the overdose of dehydration drugs and insu cient supply of blood volume [21]; and 6. in ammation and immune reactions of blood vessel walls [6,22,23]. The common nal pathway arising from all the above factors stated is a change in the permeability of smooth muscle cells in the blood vessels, an increase in calcium in ux and release of calcium ion from intracellular calcium stores, leading to an overload of free calcium in the cytosol [24]. ...
Preprint
Full-text available
Background:Cerebral vasospasm (CVS) is a serious neurosurgical complication. This retrospective study was performed to analyze if nimodipine can improve prognosis and reduces ischemia secondary to delayed CVS after intracranial tumor surgery. Methods:Retrospective analysis of 94 patients with an anterior cranial fossa tumor and underwent intracranial tumor surgery was performed, with 42 cases treated with normal saline and 52 cases treated with nimodipine solution. Transcranial Doppler ultrasonography was used to measure velocity in the middle cerebral artery (MCA) and the distal extracranial internal carotid artery (eICA). An examination was conducted 1 day before surgery and 1, 3, 5, 7, and 14 days after surgery. Follow-up was performed using the Glasgow Outcome Scale (GOS) 3 months after discharge. Results:We showed that in the nimodipine group, CVS occurred in 13 (25%) patients who did not have CVS in the first three days after operation; nine patients had CVS between 4 and 7 days, and 4 had CVS between 8 and 14 days. In the normal saline group, nineteen (45%) patients had CVS, 3 presented with CVS within 3 days, 11 between 4-7 days and 5 between 8-14 days. A significant difference in the occurrence of CVS was observed between the two groups. Preoperative and postoperative the MCA velocities were compared, revealing a significant change in the normal saline group (P < 0.05) but not in the nimodipine group. Furthermore, significant differences in the outcome were observed between the two groups at the 3-month follow-up (P < 0.05). Conclusions:Nimodipine markedly improves prognosis and significantly reduces ischemia secondary to delayed CVS after intracranial tumor surgery, as well as the risks of mortality and morbidity.
... [11][12][13][14] Clinical vasospasm is more frequent in poor-grade SAH patients; however, some studies could not demonstrate a significant relationship with outcome up to the individualized collateral flow of patients. [15,16] Our analysis of patient and clinical characteristics according to the outcome group showed significant group differences in age, neurological status (Hunt and Hess grade), and aneurysm size. Patients in the favorable outcome group were younger, had smaller aneurysms, and lower Hunt and Hess grade. ...
Article
Objective: The objective of the study was to evaluate the outcome and related factors in patients with aneurysmal subarachnoid hemorrhage (aSAH). Materials and methods: Clinical data of 221 patients who were diagnosed with spontaneous SAH due to ruptured intracranial aneurysm and surgically treated at Vajira Hospital between January 2013 and May 2016 were retrospectively reviewed. Patient and aneurysm characteristics, clinical status at presentation, treatment, and status at discharge and 1 year after discharge were recorded. Outcomes 1 year after surgery were assessed using the Glasgow Outcome Scale (GOS). Patients were divided into two groups according to the GOS score: the favorable outcome group (GOS scores 4 and 5) and unfavorable outcome group (GOS scores 1-3). Results: Among the 221 study patients, 158 were classified in the favorable outcome group and 63 in the unfavorable outcome group. Patient age, Hunt and Hess grade, aneurysm size, use of Vitamin C solution irrigation in the subarachnoid space, and GOS score 1 year after surgery significantly differed between the two groups. Conclusions: Numerous factors analyzed in this study were significantly associated with 1-year outcome in surgically treated aSAH patients, including subarachnoid Vitamin C irrigation. Further study of subarachnoid Vitamin C irrigation is warranted.
... In fact, DC remains mostly an ultima ratio against intractable intracranial hypertension, which is basically the consequence of severe early brain injury and secondary ischemic complications after SAH. At the same time, these causal processes evoking DC are also acknowledged as strong outcome predictors of SAH (Jabbarli et al., 2015a;Jabbarli et al., 2015b). As noted in a recent meta-analysis on DC in SAH (Alotaibi et al., 2017), due to the lack of robust control groups, the effect of DC on functional outcomes versus that of other interventions for refractory intracranial hypertension is still unknown. ...
Article
Full-text available
The prognosis of patients with aneurysmal subarachnoid haemorrhage requiring decompressive craniectomy is usually poor. Proper selection and early performing of decompressive craniectomy might improve the patients' outcome. We aimed at developing a risk score for prediction of decompressive craniectomy after aneurysmal subarachnoid haemorrhage. All consecutive aneurysmal subarachnoid haemorrhage cases treated at the University Hospital of Essen between January 2003 and June 2016 (test cohort) and the University Medical Center Freiburg between January 2005 and December 2012 (validation cohort) were eligible for this study. Various parameters collected within 72 h after aneurysmal subarachnoid haemorrhage were evaluated through univariate and multivariate analyses to predict separately primary (PrimDC) and secondary decompressive craniectomy (SecDC). The final analysis included 1376 patients. The constructed risk score included the following parameters: intracerebral ('Parenchymal') haemorrhage (1 point), 'Rapid' vasospasm on angiography (1 point), Early cerebral infarction (1 point), aneurysm Sac > 5 mm (1 point), clipping (' S urgery', 1 point), age U nder 55 years (2 points), Hunt and Hess grade ≥ 4 ('Reduced consciousness', 1 point) and External ventricular drain (1 point). The PRESSURE score (0-9 points) showed high diagnostic accuracy for the prediction of PrimDC and SecDC in the test (area under the curve = 0.842/0.818) and validation cohorts (area under the curve = 0.903/0.823), respectively. 63.7% of the patients scoring ≥6 points required decompressive craniectomy (versus 12% for the PRESSURE < 6 points, P < 0.0001). In the subgroup of the patients with the PRESSURE ≥6 points and absence of dilated/fixed pupils, PrimDC within 24 h after aneurysmal subarachnoid haemorrhage was independently associated with lower risk of unfavourable outcome (modified Rankin Scale >3 at 6 months) than in individuals with later or no decompressive craniectomy (P < 0.0001). Our risk score was successfully validated as reliable predictor of decompressive craniectomy after aneurysmal subarachnoid haemorrhage. The PRESSURE score might present a background for a prospective randomized clinical trial addressing the utility of early prophylactic decompressive craniectomy in aneurysmal subarachnoid haemorrhage.
... The mechanisms underlying CVS remain unclear; it may be multifactorial and involve a complicated pathological process. Potential causes of CVS are as follows: 1. mechanical stimulation such as damage, compression or stretching of the blood vessels during surgery, leading to the blood owing into the subarachnoid space and subsequent occurrence of CVS occurs [17]; 2. vascular wall injury caused by compression of the vascular wall and vascular wall malnutrition [18]; 3. damage caused by the oxidation of hemoglobin to methemoglobin and release of oxygen free radicals [19]; 4. constriction of the blood vessels caused by vasoactive substances [20]; 5. increased intracranial pressure, the overdose of dehydration drugs and insu cient supply of blood volume [21]; and 6. in ammation and immune reactions of blood vessel walls [6,22,23]. The common nal pathway arising from all the above factors stated is a change in the permeability of smooth muscle cells in the blood vessels, an increase in calcium in ux and release of calcium ion from intracellular calcium stores, leading to an overload of free calcium in the cytosol [24]. ...
Preprint
Full-text available
Background:Cerebral vasospasm (CVS) is a serious neurosurgical complication. This retrospective study was performed to analyze if nimodipine can improve prognosis and reduces ischemia secondary to delayed CVS after intracranial tumor surgery. Methods:Retrospective analysis of 94 patients with an anterior cranial fossa tumor and underwent intracranial tumor surgery was performed, with 42 cases treated with normal saline and 52 cases treated with nimodipine solution. Transcranial Doppler ultrasonography was used to measure velocity in the middle cerebral artery (MCA) and the distal extracranial internal carotid artery (eICA). An examination was conducted 1 day before surgery and 1, 3, 5, 7, and 14 days after surgery. Follow-up was performed using the Glasgow Outcome Scale (GOS) 3 months after discharge. Results:We showed that in the nimodipine group, CVS occurred in 13 (25%) patients who did not have CVS in the first three days after operation; nine patients had CVS between 4 and 7 days, and 4 had CVS between 8 and 14 days. In the normal saline group, nineteen (45%) patients had CVS, 3 presented with CVS within 3 days, 11 between 4-7 days and 5 between 8-14 days. A significant difference in the occurrence of CVS was observed between the two groups. Preoperative and postoperative the MCA velocities were compared, revealing a significant change in the normal saline group (P < 0.05) but not in the nimodipine group. Furthermore, significant differences in the outcome were observed between the two groups at the 3-month follow-up (P < 0.05). Conclusions:Nimodipine markedly improves prognosis and significantly reduces ischemia secondary to delayed CVS after intracranial tumor surgery, as well as the risks of mortality and morbidity.
Article
One of the challenges in bringing new therapeutic agents (since nimodipine) in for the treatment of cerebral ischemia associated with aneurysmal subarachnoid hemorrhage (aSAH) is the incongruence in therapeutic benefit observed between phase II and subsequent phase III clinical trials. Therefore, identifying areas for improvement in the methodology and interpretation of results is necessary to increase the value of phase II trials. We performed a systematic review of phase II trials that continued into phase III trials, evaluating a therapeutic agent for the treatment of cerebral ischemia associated with aSAH. We followed the Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines for systematic reviews, and review was based on a peer-reviewed protocol (International Prospective Register of Systematic Reviews no. 222965). A total of nine phase III trials involving 7,088 patients were performed based on eight phase II trials involving 1558 patients. The following therapeutic agents were evaluated in the selected phase II and phase III trials: intravenous tirilazad, intravenous nicardipine, intravenous clazosentan, intravenous magnesium, oral statins, and intraventricular nimodipine. Shortcomings in several design elements of the phase II aSAH trials were identified that may explain the incongruence between phase II and phase III trial results. We suggest the consideration of the following strategies to improve phase II design: increased focus on the selection of surrogate markers of efficacy, selection of the optimal dose and timing of intervention, adjustment for exaggerated estimate of treatment effect in sample size calculations, use of prespecified go/no-go criteria using futility design, use of multicenter design, enrichment of the study population, use of concurrent control or placebo group, and use of innovative trial designs such as seamless phase II to III design. Modifying the design of phase II trials on the basis of lessons learned from previous phase II and phase III trial combinations is necessary to plan more effective phase III trials.
Article
The authors sought to evaluate whether initial intracranial pressure was associated with functional outcomes following aneurysmal subarachnoid hemorrhage. This retrospective analysis consisted of 54 consecutive patients with aneurysmal subarachnoid hemorrhage and acute symptomatic hydrocephalus requiring emergent placement of an external ventricular drain. Patient demographics, clinical data, intracranial pressure parameters, and radiographic imaging were collected. Functional outcomes were evaluated at 3 months using the modified Rankin Scale and dichotomized as favorable (modified Rankin Scale 0–2) or unfavorable (modified Rankin Scale 3–6). Univariate and multivariate logistic regression analyses were performed to investigate parameters independently associated with functional outcomes. In an adjusted multivariate logistic regression model, initial intracranial pressure (OR: 1.371, 95% CI: 1.119–1.679; p = 0.002) was found to be an independent predictor of unfavorable functional outcomes at 3 months. Receiver operating characteristic curve analysis for the prediction of unfavorable functional outcomes demonstrated that initial intracranial pressure exhibited an acceptable area under the curve (AUC = 0.901, 95% CI: 0.818–0.985; p < 0.001). The optimal predictive threshold to distinguish between favorable and unfavorable functional outcomes was identified at an initial intracranial pressure of 25 mmHg.
Thesis
1.1 Hintergrund und Ziele Aufgrund der alternden Bevölkerung steigen die Fallzahlen aneurysmatischer subarachnoidaler Blutungen (aSAB) der älteren Patienten (Alter ≥ 65 Jahre) stetig an. Die Therapie mittels minimalinvasiver Coilembolisation steht sowohl bei rupturierten als auch nicht rupturierten Aneurysmen älterer Patienten im Vordergrund, sie ist technisch jedoch nicht immer möglich. Die Frage ist allerdings, ob das Clipping über eine Trepanation im erhöhten Lebensalter eine gleichwertige Behandlungsalternative darstellt. Diese retrospektive Studie vergleicht klinische und radiologische Parameter sowie das klinische Outcome nach der offenen Aneurysmaklippung zwischen jüngeren Patienten mit denen von über 65 Jährigen. 1.2 Methoden In dieser retrospektiven Single Center Studie der Universitätsklinik Erlangen wurden 347 Patienten (107 männlich, 240 weiblich; Durchschnittsalter 53,2 Jahre ± 11,4, Spanne 16-83 Jahre) in einem Zeitraum von 7 Jahren aufgrund inzidenteller und rupturierter akuter Aneurysmen analysiert. Die Kontrollgruppe (n=290) bestand in Patienten, die das 65. Lebensjahr noch nicht erreicht hatten, darunter 197 Frauen und 93 Männer, mit einem Durchschnittsalter von 49,7±8,8 (Median: 50,0; Variationsbreite: 16-64). Die Altersgruppe der älteren Patienten (n=57) bestand aus zum Zeitpunkt der Einlieferung 65 Jahre oder älterer Patienten (14 männlich, 43 weiblich; Durchschnittsalter: 70,9±4,4 Jahre, Altersmedian: 70,0, Variationsbreite: 65-83 Jahre). Innerhalb der älteren Patientenkohorte wurden mittels chirurgischem Aneurysmaclipping 26 Patienten nach akuter subarachnoidaler Blutung und 28 Patienten aufgrund inzidenteller Aneurysmen operiert. In der Kontrollgruppe wurden 146 Patienten nach akuter Blutung und 104 zur präventiven Versorgung inzidenteller Aneurysmen mittels Clipping versorgt. Klinische Einschätzung und radiologisches Ausmaß der SAB sowie klinisches Outcome wurden anhand des Hunt und Hess Klassifikation, der Fisher-CT-Klassifikation sowie dem Glasgow Outcome Wert (GOS Klassifikation) verglichen. 1.3 Ergebnisse Nach erfolgter klinischer Aufnahme wurden die Patienten anhand der Hunt und Hess Klassifizierung (Grad 1-5; leichte Kopfschmerzen und Meningismus bis hin zu Koma und Dezerebrationszeichen) eingeteilt. Es zeigte sich kein signifikanter Unterschied zwischen den Werten älterer SAB Patienten und der Kontrollgruppe (3,0 vs 2,4) nach akuter Blutung (p=0.067). Es ließ sich unabhängig von der Altersgruppe ein gegengerichteter Zusammenhang mit dem GOS-Wert nach akuter SAB feststellen. Je schlechter die Einteilung im Hunt und Hess Score ausfiel (Annäherung an Grad=5), desto niedriger waren die Werte des GOS (Annäherung an Grad=1) (p<0,001 r=-0,431), das heißt, desto schlechter war das klinische Outcome der betroffenen Patienten. Es konnte gefolgert werden, dass der klinische Zustand der Patienten zum Zeitpunkt der Einlieferung maßgeblich für deren spätere Prognose war. Zudem ließ sich kein signifikanter Unterschied des Fisher-CT-Scores zwischen den beiden Altersgruppen (3,1 versus 3,1) ermitteln (p=0.574). Somit war die im CT sichtbar ausgetretene subarachnoidale Blutmenge von ähnlichem Ausmaß. Doch auch hier zeigte sich insgesamt ein altersunabhängiger, gegengerichteter Zusammenhang zwischen der Fisher-CT-Einteilung sowie dem zu erwartenden klinischen Outcome nach akuter SAB. Je höher die Einstufung im Fisher-CT-Score war, das heißt, je mehr Blut vorhanden war, desto schlechter waren die Werte beim GOS und ungünstiger die individuelle Prognose (p<0.001, r=-0,268). Ohne weitere Signifikanz stellte sich die Aneurysmagröße im Vergleich beider Altersgruppen dar (rupturierte Aneurysmen älterer Patienten 6,1mm; inzidentelle Aneurysmen älterer Patienten 6,4mm versus rupturierte Aneurysmen der Kontrollgruppe 6,7mm und inzidentelle Aneurysmen der Kontrollgruppe 6,2mm; p=0.440). Somit waren die technischen Herausforderungen in beiden Gruppen gleich. In den meisten Fällen präsentierten sich akut blutende Aneurysmen der Kontrollgruppe an der A. communicans anterior (Kontrollgruppe: n=75; 42,6%), hingegen zeigten sich rupturierte Aneurysmen der älteren Patienten überwiegend an der A. cerebri media (n=12; 41,4%) und nur zu 24,1% (n=7) an der A. communicans anterior (p=0.119). Innerhalb der Kontrollgruppe handelte es sich bei inzidentellen Gefäßaussackungen gehäuft um Aneurysmen der A. cerebri media (n=54;47,4%) sowie bei den älteren Patienten um Aneurysmen der A. communicans anterior (n=13; 46,4%) (p=0.111). Diese Unterschiede innerhalb der Altersgruppen waren nicht signifikant. Sowohl bei akuten SAB Patienten als auch bei inzidentellen Aneurysmen konnte kein signifikanter Zusammenhang zwischen dem Alter und der Lokalisation nachgewiesen werden. Das Alter der Patienten hatte nach akuter SAB signifikante Auswirkung auf das zu erwartende Outcome (p<0.001). In der Kontrollgruppe betrug der durchschnittliche GOS-Wert nach akuter SAB 4,14±1,16 (Median: 5,00), wohingegen der durchschnittliche GOS-Wert nach akuter SAB der älteren Patientenkohorte bei 3,03±1,43 (Median: 3,00) lag. Je älter die Patienten bei einsetzender Blutung waren, desto schlechter deren Prognose. Nach Clipping inzidenteller Aneurysmen wurde das Outcome älterer Patienten mit einem durchschnittlichen GOS-Wert von 4,5±0,8 (Median: 5,0; Variationsbreite: 2-5) bemessen. Im Vergleich dazu lag der GOS-Wert der jüngeren Patientengruppe bei 4,8±0,4 (Median: 5,0; Variationsbreite: 4-5) nach Clipping inzidenteller Aneurysmen. 1.4 Schlussfolgerung Entsprechend der neurologischen Verfassung zum Zeitpunkt der Einlieferung und nach computertomographischer Bildgebung ließen sich unabhängig vom Alter erste Aussagen über das Outcome nach SAB treffen. Je schlechter die neurologische Verfassung der Patienten und je größer die gefundene Blutmenge im CT war, desto schlechter war die zu erwartende Prognose. Zudem zeigte der ermittelte Glasgow Outcome Scale bei chirurgischer Versorgung mittels Clippings akuter Aneurysmen älterer Patienten signifikant schlechtere Ergebnisse als bei identischer Versorgung jüngerer Patienten. Davon abzuleiten war das steigende Alter bei akuter SAB als ein Indikator einer ungünstigeren Prognose. Hingegen ließ sich kein signifikanter Unterschied beider Altersklassen hinsichtlich des Outcomes nach operativer Versorgung inzidenteller Aneurysmen nachweisen. Das Outcome nach chirurgischem Clipping inzidenteller Aneurysmen war in beiden Altersgruppen gleich gut. Somit spielte das Alter der Patienten in der präventiven Versorgung blander Gefäßaussackungen nur eine untergeordnete Rolle und folglich ist bei älteren Patienten – wenn eine Coilembolisation nicht möglich ist – auch die Operation eine gute Behandlungsalternative. Nur in der Gruppe der älteren Patienten nach rupturierten Aneurysmen mit akuter Subarachnoidalblutung zeigte sich ein signifikanter Unterschied mit schlechterem Outcome gegenüber der jüngeren Gruppe, was am Ehesten der Multimorbidität älterer Patienten geschuldet scheint. In dieser Patientengruppe ist die minimalinvasive Coilembolisation in jedem Fall, wenn möglich, vorzuziehen.
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Delayed vasospasm that develops 3-7 days after aneurysmal subarachnoid hemorrhage (SAH) has traditionally been considered the most important determinant of delayed ischemic injury and poor outcome. Consequently, most therapies against delayed ischemic injury are directed towards reducing the incidence of vasospasm. The clinical trials based on this strategy, however, have so far claimed limited success; the incidence of vasospasm is reduced without reduction in delayed ischemic injury or improvement in the long-term outcome. This fact has shifted research interest to the early brain injury (first 72 h) evoked by SAH. In recent years, several pathological mechanisms that activate within minutes after the initial bleed and lead to early brain injury are identified. In addition, it is found that many of these mechanisms evolve with time and participate in the pathogenesis of delayed ischemic injury and poor outcome. Therefore, a therapy or therapies focused on these early mechanisms may not only prevent the early brain injury but may also help reduce the intensity of later developing neurological complications. This manuscript reviews the pathological mechanisms of early brain injury after SAH and summarizes the status of current therapies.
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Identifying ischemic lesions after subarachnoid hemorrhage (SAH) is important because the appearance of these lesions on follow-up imaging correlates with a poor outcome. The effect of ischemic lesions seen on computed tomography (CT) scans during the first days of treatment remains unknown, however. In 156 patients with SAH, clinical course and outcome, as well as the appearance of ischemic lesions on serial CT scans, were prospectively monitored for 3 months. At 3 months after SAH, magnetic resonance imaging was performed to detect permanent lesions that had not been visible on CT. Of the 53 patients with no lesions on any of the follow-up CT scans, four (8%) had a poor outcome. Of the 52 patients with a new hypodense lesion on the first postoperative day CT, 23 (44%) had a poor outcome. Among the remaining 51 patients with a lesion appearing later than the first postoperative morning, 10 (20%) had a poor outcome (p < 0.001). After adjusting for patient age; clinical condition on admission; amounts of subarachnoid, intracerebral, and intraventricular blood; and plasma glucose and D-dimer levels, a hypodense lesion on CT on the first postoperative morning was an independent predictor of poor outcome after SAH (odds ratio 7.27, 95% confidence interval 1.54-34.37, p < 0.05). A new hypodense lesion on early postoperative CT seems to be an independent risk factor for poor outcome after SAH, and this early lesion development may be more detrimental to clinical outcome than a later lesion occurrence.
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The long-standing concept that delayed cerebral infarction after aneurysmal subarachnoid hemorrhage results exclusively from large artery vasospasm recently has been challenged. We used data from the CONSCIOUS-1 trial to determine the relationship between angiographic vasospasm and cerebral infarction after subarachnoid hemorrhage. We performed a post hoc exploratory analysis of the CONSCIOUS-1 data. All patients underwent catheter angiography before treatment and 9±2 days after subarachnoid hemorrhage. CT was performed before and after aneurysm treatment, and 6 weeks after subarachnoid hemorrhage. Angiograms and CT scans were assessed by centralized blinded review. Angiographic vasospasm was classified as none/mild (0%-33% decrease in arterial diameter), moderate (34%-66%), or severe (≥67%). Infarctions were categorized as secondary to angiographic vasospasm, other, or unknown causes. Logistic regression was conducted to determine factors associated with infarction. Complete data were available for 381 of 413 patients (92%). Angiographic vasospasm was none/mild in 209 (55%) patients, moderate in 118 (31%), and severe in 54 (14%). Infarcts developed in 6 (3%) of 209 with no/mild, 12 (10%) of 118 patients with moderate, and 25 (46%) of 54 patients with severe vasospasm. Multivariate analysis found a strong association between angiographic vasospasm and cerebral infarction (OR, 9.3; 95% CI, 3.7-23.4). The significant association persisted after adjusting for admission neurological grade and aneurysm size. Method of aneurysm treatment was not associated with a significant difference in frequency of infarction. A strong association exists between angiographic vasospasm and cerebral infarction. Efforts directed at further reducing angiographic vasospasm are warranted.
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Interobserver agreement for the assessment of handicap in stroke patients was investigated in a group of 10 senior neurologists and 24 residents from two centers. One hundred patients were separately interviewed by two physicians in different combinations. The degree of handicap was recorded by each observer on the modified Rankin scale, which has six grades (0-5). The agreement rates were corrected for chance (kappa statistics). Both physicians agreed on the degree of handicap in 65 patients; they differed by one grade in 32 patients and by two grades in 3 patients. Kappa for all pairwise observations was 0.56; the value for weighted kappa (with quadratic disagreement weights) was 0.91. Our results confirm the value of the modified Rankin scale in the assessment of handicap in stroke patients; nevertheless, further improvements are possible.
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Sixty-eight patients with intraventricular hemorrhage (IVH) diagnosed by computed tomography (CT) were reviewed retrospectively to determine the etiology and prognosis, relationship to delayed hydrocephalus, and effect on neurological outcome. The most common causes were a ruptured aneurysm, trauma, and hypertensive hemorrhage. Ruptured aneurysms of the anterior communicating artery can often be predicted from the nonenhanced CT scan. The total mortality rate was 50%; however, 21% of patients returned to normal or had only mild disability. Patients in whom no cause was identified had a better prognosis. Delayed hydrocephalus was related to the effects of subarachnoid hemorrhage rather than obstruction of the ventricular system by blood. IVH per se is seldom a major factor in the neurological outcome.
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In 47 cases of verified ruptured saccular aneurysm, we investigated the relationship of the amount and distribution of subarachnoid blood detected by computerized tomography to the later development of cerebral vasospasm. When the subarachnoid blood was not detected or was distributed diffusely, severe vasospasm was almost never encounters (1 of 18 cases). In the presence of subarachnoid blood clots larger than 5 X 3 mm (measured on the reproduced images) or layers of blood 1 mm or more thick in fissures and vertical cisterns, severe spasm followed almost invariably (23 of 24 cases). There was an almost exact correspondence between the site of the major subarachnoid blood clots and the location of severe vasospasm. Every patient with severe vasospasm manifested delayed symptoms and signs. Excellent correlation existed between the particular artery in vasospasm and the delayed clinical syndrome. Severe vasospasm involved the anterior cerebral artery in 20 cases and the middle cerebral artery in only 14. As the grading system used is partly subjective, the findings should be regarded as preliminary. The results, if confirmed, indicate that blood localized in the subarachnoid space in sufficient amount at specific sites is the only important etiological factor in vasospasm. It should be possible to identify patients in jeopardy from vasospasm and institute early preventive measures. (Neurosurgery, 6: 1--9, 1980)
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Hemorrhage volume is a powerful predictor of 30-day mortality after spontaneous intracerebral hemorrhage (ICH). We compared a bedside method of measuring CT ICH volume with measurements made by computer-assisted planimetric image analysis. The formula ABC/2 was used, where A is the greatest hemorrhage diameter by CT, B is the diameter 90 degrees to A, and C is the approximate number of CT slices with hemorrhage multiplied by the slice thickness. The ICH volumes for 118 patients were evaluated in a mean of 38 seconds and correlated with planimetric measurements (R2 = 9.6). Interrater and intrarater reliability were excellent, with an intraclass correlation of .99 for both. We conclude that ICH volume can be accurately estimated in less than 1 minute with the simple formula ABC/2.
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Clinical and radiologic predictors of cerebral infarction occurrence and location after aneurysmal subarachnoid hemorrhage have been seldom studied. We evaluated all patients admitted to our hospital with aneurysmal subarachnoid hemorrhage between 1998 and 2000. Cerebral infarction was defined as a new hypodensity located in a vascular distribution on computed tomography (CT) scan. Fifty-seven of 143 patients (40%) developed a cerebral infarction. On univariate analysis, occurrence of cerebral infarction was associated with a worse World Federation of Neurological Surgeons grade (P=0.01), use of ventriculostomy catheter (P=0.01), preoperative vasospasm (P=0.03), surgical clipping (P=0.02), symptomatic vasospasm (P<0.01), and vasospasm on transcranial Doppler ultrasonography (TCD) or repeat angiogram (P<0.01). On multivariable analysis, only presence of symptoms ascribed to vasospasm (P<0.01) and evidence of vasospasm on TCD or angiogram predicted cerebral infarction (P<0.01). TCD and angiogram agreed on the diagnosis of vasospasm in 73% of cases (95% CI, 63% to 81%), but the diagnostic accuracy of this combination of tests was suboptimal for the prediction of cerebral infarction occurrence (sensitivity, 0.72; specificity, 0.68; positive predictive value, 0.67; negative predictive value, 0.72). Location of the cerebral infarction on delayed CT was predicted by neurological symptoms in 74%, by aneurysm location in 77%, and by angiographic vasospasm in 67%. Evidence of vasospasm on TCD and angiogram is predictive of cerebral infarction on CT scan but sensitivity and specificity are suboptimal. Cerebral infarction location cannot be predicted in one quarter to one third of patients by any of the studied clinical or radiological variables.
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Early vasospasm (EVSP), defined here as arterial narrowing seen on diagnostic angiography within the first 48 hours of aneurysmal rupture, is a rarely reported and poorly defined phenomenon in patients with subarachnoid hemorrhage (SAH). The purpose of this study was to characterize EVSP in a large database of such patients. We analyzed the relationship of EVSP to clinical characteristics, in-hospital complications, and outcome at 3 months among 3478 patients entered into 4 prospective, randomized, double-blind, placebo-controlled trials of tirilazad conducted in neurosurgical centers around the world between 1991 and 1997. Three hundred thirty-nine (10%) of 3478 patients had EVSP. EVSP was significantly more likely in patients with poor neurological grade on admission, history of SAH, intracerebral hematoma, larger aneurysm, thick SAH on cranial computed tomography, and intraventricular hemorrhage. EVSP was not associated with delayed cerebral vasospasm. After adjustment for differences in admission characteristics, EVSP was associated with cerebral infarction (adjusted odds ratios [OR]=1.51; 95% CI, 1.18 to 1.94; P=0.001), neurological worsening (OR=1.41; 95% CI, 1.10 to 1.81; P=0.007), and unfavorable outcome (OR=1.51; 95% CI, 1.15 to 2.00; P=0.003). In addition, there was a trend for patients with increasingly severe EVSP to have unfavorable outcome (OR=1.84 for mild and OR=2.66 for moderate/severe EVSP). EVSP was seen in 10% of SAH patients and was predictive of cerebral infarction and neurological worsening as well as unfavorable outcome at 3 months. EVSP was not associated with late vasospasm. EVSP may be as important as delayed vasospasm in predicting complications and long-term morbidity in SAH patients.
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Cerebral infarction would be expected to be associated with poor outcome after aneurysmal subarachnoid hemorrhage (SAH), although there are few data on which to base this assumption. The goals of this study were to determine the impact of cerebral infarction on outcome and to examine predictors of infarction in these patients. Univariate and multivariable statistical methods were used to examine the impact of cerebral infarction on the Glasgow Outcome Scale score 3 months after SAH among 3567 patients entered into four prospective, randomized, double-blind, placebo-controlled trials of tirilazad conducted in neurosurgical centers around the world between 1991 and 1997. Patient demographics, clinical variables, radiographic characteristics, and treatment variables associated with cerebral infarction were also determined by the same methods. Seven hundred and seven (26%) out of 2741 patients with complete data had cerebral infarction on computed tomographic scans 6 weeks after SAH. Multivariable logistic regression showed that cerebral infarction increased the odds of unfavorable outcome by a factor of 5.4 (adjusted odds ratio, 5.4; 95% confidence interval, 4.2-6.8; P < 0.0001), which was a higher odds ratio than all other factors associated with outcome. The proportion of explained variance in outcome was also highest for cerebral infarction and accounted for 39% of the explained variance. Multivariable analysis found that cerebral infarction was significantly associated with increasing patient age, worse neurological grade on admission, history of hypertension or diabetes mellitus, larger aneurysm, use of prophylactically or therapeutically induced hypertension, temperature more than 38 degrees C 8 days after SAH, and symptomatic vasospasm. Cerebral infarction was strongly associated with poor outcome after aneurysmal SAH. The most important potentially treatable factor associated with infarction was symptomatic vasospasm.
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Cerebral infarction is a common complication of aneurysmal subarachnoid hemorrhage (SAH), but usually occurs several days after onset as a complication of vasospasm or aneurysm repair. The frequency, causes, and clinical impact of acute infarction associated with the primary hemorrhage are poorly understood. We evaluated the presence of cerebral infarction on admission CT in 487 patients admitted within 3 days of SAH onset to our center between July 1996 and September 2002. Infarctions due to angiography or treatment complications were rigorously excluded. Outcome at 3 months was assessed with the modified Rankin Scale. A total of 17 patients (3%) had acute infarction on admission CT; eight had solitary and nine had multiple infarcts. Solitary infarcts usually appeared in the vascular territory distal to the ruptured aneurysm, whereas multiple infarcts tended to be territorial and symmetric. Global cerebral edema (P < 0.001), coma on presentation (P = 0.001), intraventricular hemorrhage (P = 0.002), elevated APACHE-II physiological subscores (P = 0.026) and loss of consciousness at onset (P = 0.029) were associated with early cerebral infarction. Mortality (P = 0.003) and death or moderate-to-severe disability (mRS 4-6, P = 0.01) occurred more frequently in the early cerebral infarction group. Early cerebral infarction on CT is a rare but devastating complication of acute SAH. The observed associations with coma, global cerebral edema, intraventricular hemorrhage, and loss of consciousness at onset suggest that intracranial circulatory arrest may play a role in the pathogenesis of this disorder.