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Acute ischemic stroke (AIS) is among the leading causes of death and long-term disability. Intravenous tissue plasminogen activator has been the mainstay of acute therapy. Recently, several prospective randomized trials documented the value of endovascular revascularization in selected patients with large-vessel occlusion within the anterior circulation. This finding has led to a paradigm shift in the management of AIS, including wide adoption of noninvasive neuroimaging to assess vessel patency and tissue viability, with the supplemental and independent use of intravenous tissue plasminogen activator to improve clinical outcomes. In this article, we review the landmark studies on management of AIS and the current position on the diagnosis and management of AIS. The review also highlights the importance of early stabilization and prompt initiation of therapeutic interventions before, during, and after the diagnosis of AIS within and outside of the hospital.

Abstract Introduction: Acute ischemic stroke can occur in the setting of aortic dissection. Information concerning the utility of endovascular mechanical thrombectomy as an intervention for patients with aortic dissection who are experiencing an acute stroke due to large vessel occlusion is limited to a few case reports. Case series of patients presenting with this clinical situation are needed to further investigate the potential utility of this procedure when patients with acute ischemic stroke and aortic dissection are encountered. Case Presentation: We report a patient with a chronic Stanford type A aortic dissection with dissection extension into the left common carotid artery and left internal carotid artery who had a good clinical outcome following mechanical thrombectomy for a symptomatic middle cerebral artery occlusion. We also review other cases in which endovascular mechanical thrombectomy was conducted in patients with aortic dissection and acute ischemic stroke and discuss the potential risks and benefits of carotid artery stenting in this clinical situation. Conclusion: The rate of successful arterial recanalization in patients with aortic dissection, large vessel occlusion, and acute ischemic stroke treated with mechanical thrombectomy is high. The intervention has been associated with good neurological outcomes and a low rate of procedure-related complications. Additional case series are needed to help discern if our observations are present in a broader array of patients in order to identify which patients are most likely to benefit from mechanical thrombectomy.

Dysphagia may predispose stroke patients toward undernutrition and hydration. These comorbidities increase patient risks for reduced functional outcome and short-term mortality. Despite this impact, available information on relationships among dysphagia, nutrition, and hydration status in acute stroke is limited and conflicted. This study evaluated nutrition and hydration status in ischemic stroke patients with versus without clinically significant dysphagia at admission and at discharge from acute care. Sixty-seven patients admitted to the stroke unit in a tertiary-care hospital provided data for this study. On the day of hospital admission and upon discharge or at 7 days post admission, serum biochemical measures were obtained for nutrition (prealbumin) and hydration status (BUN/Cr). Clinical evaluation for dysphagia, nutrition status, and stroke severity were completed an average of 1.4 days following hospital admission. Dysphagia was identified in 37 % of the cohort. At admission 32 % of patients demonstrated malnutrition based on prealbumin levels and 53 % demonstrated evidence of dehydration based on BUN/Cr levels. No differences in nutrition status were attributed to dysphagia. Patients with dysphagia demonstrated significantly higher BUN/Cr levels (greater dehydration) than patients without dysphagia at admission and at discharge. Dehydration at both admission and discharge was associated with dysphagia, clinical nutrition status, and stroke severity. Results of this study support prior results indicating that dysphagia is not associated with poor nutrition status during the first week post stroke. Dehydration status is associated with dysphagia during this period. The results have implications for future confirmatory research and for clinical management of dysphagia in the acute stroke period.

Carriers of APOE ɛ2 and ɛ4 have an increased risk of intracerebral haemorrhage (ICH) in lobar regions, presumably because of the effects of these gene variants on risk of cerebral amyloid angiopathy. We aimed to assess whether these variants also associate with severity of ICH, in terms of haematoma volume at presentation and subsequent outcome. We investigated the association of APOE ɛ2 and ɛ4 with ICH volume and outcomes in patients with primary ICH in three phases: a discovery phase of 865 individuals of European ancestry from the Genetics of Cerebral Hemorrhage on Anticoagulation study, and replication phases of 946 Europeans (replication 1) and 214 African-Americans (replication 2) from an additional six studies. We also assessed the association of APOE variants with ICH volume and outcomes in meta-analyses of results from all three phases, and the association of APOE ɛ4 with mortality in a further meta-analysis including data from previous reports. Admission ICH volume was quantified on CT scan. We assessed functional outcome (modified Rankin scale score 3–6) and mortality at 90 days. We used linear regression to establish the effect of genotype on haematoma volume and logistic regression to assess the effect on outcome from ICH. For patients with lobar ICH, carriers of the APOE ɛ2 allele had larger ICH volumes than did non-carriers in the discovery phase (p=2·5×10 −5), in both replication phases (p=0·008 in Europeans and p=0·016 in African-Americans), and in the meta-analysis (p=3·2×10 −8). In the meta-analysis, each copy of APOE ɛ2 increased haematoma size by a mean of 5·3 mL (95% CI 4·7–5·9; p=0·004). Carriers of APOE ɛ2 had increased mortality (odds ratio [OR] 1·50, 95% CI 1·23–1·82; p=2·45×10 −5) and poorer functional outcomes (modified Rankin scale score 3–6; 1·52, 1·25–1·85; p=1·74×10 −5) compared with non-carriers after lobar ICH. APOE ɛ4 was not associated with lobar ICH volume, functional outcome, or mortality in the discovery phase, replication phases, or meta-analysis of these three phases; in our further meta-analysis of 2194 patients, this variant did not increase risk of mortality (1·08, 0·86–1·36; p=0·52). APOE allele variants were not associated with deep ICH volume, functional outcome, or mortality. Vasculopathic changes associated with the APOE ɛ2 allele might have a role in the severity and clinical course of lobar ICH. Screening of patients who have ICH to identify the ɛ2 variant might allow identification of those at increased risk of mortality and poor functional outcomes. US National Institutes of Health-National Institute of Neurological Disorders and Stroke, Keane Stroke Genetics Research Fund, Edward and Maybeth Sonn Research Fund, and US National Center for Research Resources.

Despite evidence of a genetic role in stroke, the identification of common genetic risk factors for this devastating disorder remains problematic. We aimed to identify any common genetic variability exerting a moderate to large effect on risk of ischaemic stroke, and to generate publicly available genome-wide genotype data to facilitate others doing the same. We applied a genome-wide high-density single-nucleotide-polymorphism (SNP) genotyping approach to a cohort of samples with and without ischaemic stroke (n=278 and 275, respectively), and did an association analysis adjusted for known confounders in a final cohort of 249 cases and 268 controls. More than 400 000 unique SNPs were assayed. We produced more than 200 million genotypes in 553 unique participants. The raw genotypes of all the controls have been posted publicly in a previous study of Parkinson's disease. From this effort, results of genotype and allele association tests have been publicly posted for 88% of stroke patients who provided proper consent for public release. Preliminary analysis of these data did not reveal any single locus conferring a large effect on risk for ischaemic stroke. The data generated here comprise the first phase of a genome-wide association analysis in patients with stroke. Release of phase I results generated in these publicly available samples from each consenting individual makes this dataset a valuable resource for data-mining and augmentation.

While non-contrast head computed tomography is effective in detecting blood, it is not sensitive in diagnosing hyperacute ischemic stroke. One neuroradiologic marker for early thromboembolic occlusion of the distal middle cerebral artery is the middle cerebral artery “dot” sign. The “dot” seen on the typical axial plane represents a hyperdensity of the middle cerebral artery in the Sylvian fissure. A review of medical literature was conducted via PubMed utilizing search phrases “MCA,” “dot,” and “sign.” The review was limited to the intravenous tissue-type plasminogen activator era, 1996 and on. Articles were analyzed to determine the use of the sagittal plane of non-contrast head computed tomography to locate the middle cerebral artery “dot” sign. The search terms yielded 11 results which revealed that computed tomography reconstruction and sagittal planes were not used for detection of the middle cerebral artery “dot” signs. Our patient had no known past medical history. The initial non-contrast head computed tomography was read as having a hypodensity in the right insular region and a middle cerebral artery “dot” sign. Multiplanar reconstruction of the computed tomography demonstrated a hyperdense sagittal string-like appearance of the middle cerebral artery along the Sylvian fissure. Computed tomography angiography confirmed the M2 occlusion. This is the first report of using the head computed tomography sagittal plane for diagnosis of the middle cerebral artery “dot” sign. Incorporating multiplanar reconstruction and producing the sagittal plane may lead to a higher sensitivity of the middle cerebral artery “dot” sign. Further studies incorporating a patient cohort will be needed to determine how much the sagittal plane view augments predictive value of the middle cerebral artery “dot” sign.

There are no conclusive data regarding the association between dyslipidemia and the risk of ischemic stroke (IS). Clinical investigations have primarily focused on the association between elevated levels of low-density lipoprotein cholesterol and low levels of high-density lipoprotein cholesterol as stroke risk factors. Much less scientific attention has been aimed at elevated levels of triglycerides. Consequently the potential role of hypertriglyceridemia as an independent risk factor for IS remains controversial. However, accumulating evidence has shown that hypertriglyceridemia is associated with pathophysiological processes such as endothelial dysfunction, atherosclerosis and the production of a prothrombotic state, which could contribute to IS risk. The aim of this review is to critically analyze the contribution of hypertriglyceridemia to the occurrence of IS.

Iron from haemolysed blood is implicated in secondary injury after intracerebral haemorrhage. We aimed to assess the safety of the iron chelator deferoxamine mesylate in patients with intracerebral haemorrhage and to establish whether the drug merits investigation in a phase 3 trial. We did a multicentre, futility-design, randomised, placebo-controlled, double-blind, phase 2 trial at 40 hospitals in Canada and the USA. Adults aged 18–80 years with primary, spontaneous, supratentorial intracerebral haemorrhage were randomly assigned (1:1) to receive deferoxamine mesylate (32 mg/kg per day) or placebo (saline) infusions for 3 consecutive days within 24 h of haemorrhage onset. Randomisation was done via a web-based trial-management system centrally in real time, and treatment allocation was concealed from both participants and investigators. The primary outcome was good clinical outcome, which was defined as a modified Rankin Scale score of 0–2 at day 90. We did a futility analysis: if the 90% upper confidence bound of the absolute risk difference between the two groups in the proportion of participants with a good clinical outcome was less than 12% in favour of deferoxamine mesylate, then to move to a phase 3 efficacy trial would be futile. Primary outcome and safety data were analysed in the modified intention-to-treat population, comprising only participants in whom the study infusions were initiated. This trial is registered with ClinicalTrials.gov, number NCT02175225, and is completed. We recruited 294 participants between Nov 23, 2014, and Nov 10, 2017. The modified intention-to-treat population consisted of 144 patients assigned to the deferoxamine mesylate group and 147 assigned to the placebo group. At day 90, among patients with available data for the primary outcome, 48 (34%) of 140 participants in the deferoxamine mesylate group, and 47 (33%) of 143 patients in the placebo group, had modified Rankin Scale scores of 0–2 (adjusted absolute risk difference 0·6% [90% upper confidence bound 6·8%]). By day 90, 70 serious adverse events were reported in 39 (27%) of 144 patients in the deferoxamine mesylate group, and 78 serious adverse events were reported in 49 (33%) of 147 patients in the placebo group. Ten (7%) participants in the deferoxamine mesylate and 11 (7%) in the placebo group died. None of the deaths were judged to be treatment related. Deferoxamine mesylate was safe. However, the primary result showed that further study of the efficacy of deferoxamine mesylate with anticipation that the drug would significantly improve the chance of good clinical outcome (ie, mRS score of 0–2) at day 90 would be futile. US National Institutes of Health and US National Institute of Neurological Disorders and Stroke.

President Obama has announced that the detention facility at Guantánamo Bay will be closed by January 22, 2010. He has also said that at least some of the detainees facing criminal prosecution will be tried in military commissions. The system of military commissions established by President Bush after the 9/11 attacks, as well as the one which Congress enacted in 2006 following the Supreme Court's Hamdan decision, were widely criticized as being unproductive and not meeting international legal standards. The Congress has, very recently, revised the rules and procedures for military commissions to make them fair, effective and much more like those used for courts-martial. This article compares and contrasts trials in revised military commissions with trials in federal district courts. It concludes that a combination of both forums would best serve the President, and that military commissions are still a prudent option for prosecuting some detainees where there are security and admissibility of evidence concerns. [PUBLICATION ABSTRACT]