Background and Purpose-Patients undergoing intra-arterial therapy (IAT) for acute ischemic stroke receive either general anesthesia (GA) or conscious sedation. GA may delay time to treatment, whereas conscious sedation may result in patient movement and compromise the safety of the procedure. We sought to determine whether there were differences in safety and outcomes in GA patients before initiation of IAT. Methods-A cohort of 980 patients at 12 stroke centers underwent IAT for acute stroke between 2005 and 2009. Only patients with anterior circulation strokes due to large-vessel occlusion were included in the study. A binary logistic-regression model was used to determine independent predictors of good outcome and death. Results-The mean age was 66Ϯ15 years and median National Institutes of Health Stroke Scale score was 17 (interquartile range, 13-20). The overall recanalization rate was 68% and the symptomatic hemorrhage rate was 9.2%. GA was used in 44% of patients with no differences in intracranial hemorrhage rates when compared with the conscious sedation group. The use of GA was associated with poorer neurologic outcome at 90 days (odds ratioϭ2.33; 95% CI, 1.63-3.44; PϽ0.0001) and higher mortality (odds ratioϭ1.68; 95% CI, 1.23-2.30; PϽ0.0001) compared with conscious sedation. Conclusions-Patients placed under GA during IAT for anterior circulation stroke appear to have a higher chance of poor neurologic outcome and mortality. There do not appear to be differences in hemorrhagic complications between the 2 groups. Future clinical trials with IAT can help elucidate the etiology of the differences in outcomes. (Stroke. 2010; 41:1175-1179.)

Background and purpose Endovascular techniques are frequently employed to treat large artery occlusion in acute ischemic stroke (AIS). We sought to determine the predictors and clinical impact of intracranial hemorrhage (ICH) after endovascular therapy. Methods Retrospective analysis of consecutive patients presenting to 13 high volume stroke centers with AIS due to proximal occlusion in the anterior circulation who underwent endovascular treatment within 8 h from symptom onset. Logistic regression was performed to determine the variables associated with ICH, hemorrhagic infarction (HI), and parenchymal hematomas (PHs), as well as 90 day poor outcome (modified Rankin Scale score ≥3) and mortality. Results There were a total of 363 ICHs (overall rate 32.3%; HI=267, 24%; PH=96, 8.5%) among the 1122 study patients (mean age 67±15 years; median National Institutes of Health Stroke Scale score 17 (IQR 13–20)). Independent predictors for HI included diabetes mellitus (OR 2.27, 95% CI (1.58 to 3.26), p<0.0001), preprocedure IV tissue plasminogen activator (tPA) (1.43 (1.03 to 2.08), p<0.037), Merci thrombectomy (1.47 (1.02 to 2.12), p<0.032), and longer time to puncture (1.001 (1.00 to 1.002), p<0.026). Patients with atrial fibrillation (1.61 (1.01 to 2.55), p<0.045) had a higher risk of PH while the use of IA tPA (0.57 (0.35 to 0.90), p<0.008) was associated with lower chances of PH. Both the presence of HI (2.23 (1.53 to 3.25), p<0.0001) and PH (6.24 (3.06 to 12.75), p<0.0001) were associated with poor functional outcomes; however, only PH was associated with higher mortality (3.53 (2.19 to 5.68), p<0.0001). Conclusions Greater understanding about the predictors and consequences of ICH post endovascular stroke therapy is essential to improve risk assessment, patient selection/clinical outcomes, and early prognostication. Our data suggest that patients with atrial fibrillation are particularly prone to severe ICH and question the ‘benign’ nature of HI suggested by earlier studies.

The PED represents a promising new endovascular technology for the treatment of cerebral aneurysms; however, as an investigational device, long-term follow-up data are sparse at this point. The etiology of the very late thrombosis of the PED construct in this case remains unknown; however, this report underscores the need for a continued, careful systematic evaluation and close long-term follow-up of treated patients.

The TMEDIC is a safe and effective method to repair transtemporal meningoencephalocele obviating the need for a middle fossa craniotomy in certain cases.

ObjectiveTo summarize and classify the evidence for the use of endovascular techniques in the treatment of patients with acute ischemic stroke.MethodsRecommendations previously published by the American Heart Association (AHA) (Guidelines for the early management of adults with ischemic stroke (Circulation2007) and Scientific statement indications for the performance of intracranial endovascular neurointerventional procedures (Circulation2009)) were vetted and used as a foundation for the current process. Building on this foundation, a critical review of the literature was performed to evaluate evidence supporting the endovascular treatment of acute ischemic stroke. The assessment was based on guidelines for evidence based medicine proposed by the Stroke Council of the AHA and the University of Oxford, Centre for Evidence Based Medicine (CEBM). Procedural safety, technical efficacy and impact on patient outcomes were specifically examined.

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Medical management with combination aspirin and clopidogrel for 3 months and aggressive risk factor modification is the firstline therapy for patients with symptomatic ICAD. Endovascular angioplasty with or without stenting is a possible therapeutic option for selected patients with symptomatic ICAD. Further studies are necessary to define appropriate patient selection and the best therapeutic approach for various subsets of patients.

c Cystic fibrosis (CF) is characterized by an excessive neutrophilic inflammatory response within the airway as a result of defective cystic fibrosis transmembrane receptor (CFTR) expression and function. Interleukin-17A induces airway neutrophilia and mucin production associated with Pseudomonas aeruginosa colonization, which is associated with the pathophysiology of cystic fibrosis. The objectives of this study were to use the preclinical murine model of cystic fibrosis lung infection and inflammation to investigate the role of IL-17 in CF lung pathophysiology and explore therapeutic intervention with a focus on IL-17. Cftr-deficient mice (CF mice) and wild-type mice (WT mice) infected with P. aeruginosa had robust IL-17 production early in the infection associated with a persistent elevated inflammatory response. Intratracheal administration of IL-17 provoked a neutrophilic response in the airways of WT and CF animals which was similar to that observed with P. aeruginosa infection. The neutralization of IL-17 prior to infection significantly improved the outcomes in the CF mice, suggesting that IL-17 may be a therapeutic target. We demonstrate in this report that the pathophysiological contribution of IL-17 may be due to the induction of chemokines from the epithelium which is augmented by a deficiency of Cftr and ongoing inflammation. These studies demonstrate the in vivo contribution of IL-17 in cystic fibrosis lung disease and the therapeutic validity of attenuating IL-17 activity in cystic fibrosis. Cystic fibrosis (CF) lung disease is characterized by an exaggerated inflammatory response associated with the robust infiltration of neutrophils within the airways (1, 2). The etiology of this excessive inflammation remains to be elucidated. Many cytokines and small molecules have been shown to recruit neutrophils into the airway of individuals with CF, including interleukin-8 (IL-8) and leukotriene (LT) B4 (3-7). IL-17 has traditionally been identified to be a product of activated T lymphocytes and is critically important in the host lung response to infections caused by Gram-negative bacteria, including Pseudomonas aeruginosa (8,9). Experiments with IL-17 receptor knockout (KO) mice have demonstrated an increased susceptibility to Gram-negative bacterial pneumonia due to excessive neutrophil recruitment into the airways (10-13) and the upregulation of airway mucins, potentially contributing to inefficient mucociliary clearance (5,14).Increased concentrations of IL-17 have been associated with a wide range of inflammatory diseases, including rheumatoid arthritis (15, 16), inflammatory bowel disease (17), diabetes (18,19), cancer (20), and allergic asthma (21, 22). The utilization of neutralizing IL-17A antibodies in a mouse model of allergic asthma (23, 24) and lipopolysaccharide-induced inflammation (9, 25) demonstrated decreased airway neutrophilia, implicating IL-17 as a potential therapeutic target in asthma. IL-17 has also been associated with P. aeruginosa infections, linking it to not just the patholo...