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In this randomized trial involving patients who had moderate-to-severe acute ischemic stroke with proximal vessel occlusion and a small infarct core, endovascular treatment improved functional outcomes. Ischemic stroke is a devastating condition with a high burden of neurologic disability and death. As a systemic treatment, intravenous alteplase has been shown to be better than conservative care. 1 , 2 Among patients with a proximal vessel occlusion in the anterior circulation, 60 to 80% of patients die within 90 days after stroke onset or do not regain functional independence despite alteplase treatment. 3 , 4 The major reason for the limited efficacy of alteplase is the modest rate of early reperfusion among patients with a large-vessel occlusion. 5 , 6 Local treatment of large-vessel occlusion began with intraarterial delivery of thrombolytic drugs. 7 The . . .

Cryptogenic (of unknown cause) ischaemic strokes are now thought to comprise about 25% of all ischaemic strokes. Advances in imaging techniques and improved understanding of stroke pathophysiology have prompted a reassessment of cryptogenic stroke. There is persuasive evidence that most cryptogenic strokes are thromboembolic. The thrombus is thought to originate from any of several well established potential embolic sources, including minor-risk or covert cardiac sources, veins via paradoxical embolism, and non-occlusive atherosclerotic plaques in the aortic arch, cervical, or cerebral arteries. Accordingly, we propose that embolic strokes of undetermined source are a therapeutically relevant entity, which are defined as a non-lacunar brain infarct without proximal arterial stenosis or cardioembolic sources, with a clear indication for anticoagulation. Because emboli consist mainly of thrombus, anticoagulants are likely to reduce recurrent brain ischaemia more effectively than are antiplatelet drugs. Randomised trials testing direct-acting oral anticoagulants for secondary prevention of embolic strokes of undetermined source are warranted.

Minor cerebral ischemic events are associated with a higher risk of a future more serious illness. A 2007 study found that, before the era of urgent treatment, patients with transient ischemic attack (TIA) or minor stroke had an estimated risk of recurrent ischemic stroke in the next 90 days of 17%. However, urgent assessment and treatment of TIA or minor stroke can reduce this risk to 2%-3%. It is critical to understand that brain ischemia is a time-sensitive diagnosis that warrants time-sensitive action. As in the assessment of chest pain, clinical symptoms alone cannot be used to make a diagnosis; electrocardiography and serum troponin are used in conjunction with clinical symptoms to make the diagnosis and guide management. Similarly, clinical symptoms and urgent brain and neurovascular imaging are all needed to accurately assess TIA and minor stroke.

The purpose of this study was to investigate whether low cerebral blood flow (CBF) is associated with subsequent development of white matter hyperintensities (WMH). Patients were included from a longitudinal magnetic resonance (MR) imaging study of minor stroke/transient ischemic attack patients. Images were co-registered and new WMH at 18 months were identified by comparing follow-up imaging with baseline fluid-attenuated inversion recovery (FLAIR). Regions-of-interest (ROIs) were placed on FLAIR images in one of three categories: (1) WMH seen at both baseline and follow-up imaging, (2) new WMH seen only on follow-up imaging, and (3) regions of normal-appearing white matter at both time points. Registered CBF maps at baseline were used to measure CBF in the ROIs. A multivariable model was developed using mixed-effects logistic regression to determine the effect of baseline CBF on the development on new WMH. Forty patients were included. Mean age was 61 ± 11 years, 30% were female. Low baseline CBF, female sex, and presence of diabetes were independently associated with the presence of new WMH on follow-up imaging. The odds of having new WMH on follow-up imaging reduces by 0.61 (95% confidence interval = 0.57 to 0.65) for each 1 mL/100 g per minute increase in baseline CBF. We conclude that regions of white matter with low CBF develop new WMH on follow-up imaging.

Ninety-five TIA subjects and 51 non-TIA subjects were assessed using DTI and neuropsychological batteries. Fractional anisotropy (FA) and mean diffusivity (MD) maps were generated and measurements were collected from WM tracts. Adjusted mixed effects regression modelled the relationship between groups and DTI metrics. Transient ischemic attack subjects had a mean age of 67.9 ± 9.4 years, and non-TIA subjects had a mean age 64.9 ± 9.9 years. The TIA group exhibited higher MD values in the fornix (0.36 units, P < 0.001) and lower FA in the superior longitudinal fasciculus (SLF) (-0.29 units, P = 0.001), genu (-0.22 units, P = 0.016), and uncinate fasciculus (UF) (-0.26 units, P = 0.004). Compared to non-TIA subjects, subjects with TIA scored lower on the Addenbrooke's Cognitive Assessment-Revised (median score 95 vs 91, P = 0.01) but showed no differences in scores on the Montreal Cognitive Assessment (median 27 vs 26) or the Mini-Mental State Examination (median 30). TIA subjects had lower scores in memory (median 44 vs 52, P < 0.01) and processing speed (median 45 vs 62, P < 0.01) but not executive function, when compared to non-TIA subjects. Lower FA and higher MD in the fornix, SLF, and UF were associated with poorer performance on tests of visual memory and executive function but not verbal memory. Lower FA in the UF and fornix were related to higher timed scores on the TMT-B (P < 0.01), and higher SLF MD was related to higher scores on TMT-B (P < 0.01), confirming worse executive performance in the TIA group. DTI scans may be useful for detecting microstructural disease in TIA subjects before cognitive symptoms develop. DTI parameters, white matter hyperintensities, and vascular risk factors underly some of the altered neuropsychological measures in TIA subjects.

Intravenous thrombolysis is a standard of care treatment for patients with acute ischemic stroke. Tissue plasminogen activator (tPA) has been the main thrombolytic agent used since the publication of the seminal National Institutes of Neurological Disorders and Stroke trial in 1995. There is now mounting evidence to support the routine use of Tenecteplase (TNK) to treat acute ischemic stroke. TNK is a genetically modified tPA with higher fibrin specificity, longer half‐life, and reduced systemic coagulopathy. In this illustrated review, we compare the indications, doses, mechanisms of action, efficacy and safety of TNK and tPA. We provide an overview of published clinical trials studying TNK in acute ischemic stroke, including dose‐escalation studies and head‐to‐head comparisons with tPA. Finally, we summarize current acute stroke guideline recommendations and suggest treatment algorithms to manage the two main complications of intravenous thrombolysis: symptomatic intracerebral hemorrhage and angioedema.

ObjectiveTo evaluate the relationship between infarct pattern, inferred stroke mechanism and risk of recurrence in patients with ischaemic stroke. The question is clinically relevant to optimise secondary stroke prevention investigations and treatment.DesignWe conducted a retrospective analysis of the dabigatran treatment of acute stroke II (DATAS II) trial (ClinicalTrials.gove NCT NCT02295826), in which patients underwent diffusion-weighted imaging (DWI) at baseline and 30 days after randomisation to one of two antithrombotic therapies. Patients were classified as embolic, isolated small subcortical infarcts or transient ischaemic attack TIA (no infarct) at baseline and day 30. Stroke mechanism was determined by traditional and modified (based on DWI lesion findings) Trial of Org 10 172 in Acute Stroke Treatment (TOAST) criteria (DWI-TOAST).SettingMulticentre (6) tertiary acute stroke treatment hospitals.Participants305 adults with minor ischaemic stroke (National Institutes of Health Stroke Scale (NIHSS) score≤9).ResultsOf 305 patients, 148 had embolic pattern infarcts, 93 were isolated small subcortical infarcts and 64 had no infarct on baseline MRI (TIA). In the absence of DWI, TOAST classification indicated the mechanism was cryptogenic in 147 patients (48.2%), and small-vessel occlusion in 127 (41.6%). Using, DWI-TOAST, the number of cryptogenic strokes decreased to 123 (40.3%), and the number of small-vessel occlusion strokes increased to 151 (49.5%). Recurrent infarcts were seen in 13% of patients with an MRI-defined embolic infarct pattern and cryptogenic mechanism on DWI-TOAST. The relative risk of recurrent infarction in patients with undetermined aetiology was increased compared with other categories (standardised coefficient=1.0 (0.1, 1.9), p=0.029). The topography of recurrent infarcts was most often embolic (60.9%), but in 39.1% an isolated small subcortical infarct was seen.ConclusionsDefinitive identification of infarct topography with DWI has a significant impact on infarct mechanism classification. The variable relationship between baseline infarct patterns, clinical presentation and recurrent infarct distribution is a challenge to both the lacunar and embolic stroke of uncertain source (ESUS) concepts. Irrespective of aetiological classification, patients with MRI-defined cryptogenic embolic pattern infarcts are at high risk for recurrent events.Trial registration numberLinked to the DATAS II trial. ClinicalTrials.gov ID NCT02295826.

In 2016, 270 204 people in Canada (excluding Quebec) were admitted to hospital for heart conditions, stroke and vascular cognitive impairment, including 107 391 women and 162 813 men, of whom 91 524 died. This equates to 1 out of every 3 deaths in Canada and outpaces other diseases; 13% more people die of heart conditions, stroke or vascular cognitive impairment than die from all cancers combined. The benefits of acetylsalicylic acid (ASA) for secondary prevention of atherosclerotic cardiovascular disease are well established. In contrast, although low-dose ASA therapy for primary prevention of atherosclerotic cardiovascular disease was once commonly recommended, this practice is now being reconsidered in light of recent evidence. The use of ASA for prevention (primary and secondary) of vascular events has been a common practice in Canada and elsewhere for decades. Based on a reappraisal of the evidence in light of recent publications of large neutral trials, we now recommend that ASA no longer be routinely used for primary prevention in most individuals.