TL;DR: The 7-level, modified Rankin Scale (mRS) has several major strengths: it covers the entire range of functional outcomes from no symptoms to death, its categories are intuitive and easily grasped by both clinicians and patients, its concurrent validity is demonstrated by strong correlation with measures of stroke pathology and agreement with other stroke scales, and its use has demarcated effective and ineffective acute stroke therapies in trials with appropriately powered sample sizes.
Abstract: Who would have guessed that a scale introduced by Dr John Rankin in 1957 would become the primary outcome scale for almost all acute stroke trials?1 The Rankin Scale was modified to its current form by Charles Warlow and others as part of the UK-TIA (United Kingdom Transient Ischaemic Attack) trial in the 1980s,2 and its reproducibility was first examined by van Swieten et al, in 1988 (Table 1).3
View this table:
Table 1.
The Modified Rankin Scale (mRS)
There is no perfect stroke outcome scale. Regardless, the 7-level, modified Rankin Scale (mRS) has several major strengths: it covers the entire range of functional outcomes from no symptoms to death, its categories are intuitive and easily grasped by both clinicians and patients, its concurrent validity is demonstrated by strong correlation with measures of stroke pathology (eg, infarct volumes) and agreement with other stroke scales,4 and its use has demarcated effective and ineffective acute stroke therapies in trials with appropriately powered sample sizes. With a limited number of levels, the mRS may be less responsive to change than some other stroke scales; however, a single-point change on the mRS is clinically relevant.4
A limitation of the mRS has been the subjective determination between categories and the reproducibility of the score by examiners and patients.4 A systematic review and meta-analysis of studies describing interobserver variability of the mRS reports pooled reliability across 10 published studies (n=587 patients) of a κ=0.46 and a weighted κ of 0.90.5 Multimedia training and certification of examiners in the use of the mRS (http://rankinscale.org/), structured interviews and questionnaires,6–10 and centralized review of videotape assessments11 have sought to address these issues, but reproducibility remains a concern.
But the challenge for a trialist designing a new acute stroke trial is not whether …
TL;DR: This multispecialty statement provides a comprehensive review of the current evidence and gaps in current knowledge of the epidemiology, pathophysiology, outcomes, management, and prevention of PSD, and provides implications for clinical practice.
Abstract: Poststroke depression (PSD) is common, affecting approximately one third of stroke survivors at any one time after stroke. Individuals with PSD are at a higher risk for suboptimal recovery, recurre...
TL;DR: There is an important need to define better antithrombotic prophylaxis for this frequently occurring subtype of ischemic stroke, and Retrospective methods of available studies support a substantial rate of stroke recurrence during (mostly) antiplatelet therapy.
Abstract: Background and Purpose—Embolic stroke of undetermined source (ESUS) designates patients with nonlacunar cryptogenic ischemic strokes in whom embolism is the likely stroke mechanism. It has been hyp...
TL;DR: Treatment of stroke with tailored exosomes enriched with the miR-17–92 cluster increases neural plasticity and functional recovery after stroke, possibly via targeting phosphatase and tensin homolog to activate the PI3K/protein kinase B/mechanistic target of rapamycin/glycogen synthase kinase 3&bgr; signaling pathway.
Abstract: Background and Purpose—Multipotent mesenchymal stromal cell (MSC) harvested exosomes are hypothesized as the major paracrine effectors of MSCs. In vitro, the miR-17–92 cluster promotes oligodendrog...
TL;DR: It is proposed that ferroptosis or necroptotic signaling induced by lysed blood is sufficient to reach a threshold of death that leads to neuronal necrosis and that inhibition of either of these pathways can bring cells below that threshold to survival.
Abstract: Background and Purpose—Intracerebral hemorrhage leads to disability or death with few established treatments. Adverse outcomes after intracerebral hemorrhage result from irreversible damage to neur...
TL;DR: An overview of Symptomatic intracranial hemorrhage with a focus on pathophysiology and treatment is provided to establish treatments aimed at maintaining integrity of the blood-brain barrier in acute ischemic stroke based on inhibition of the underlying biochemical processes.
Abstract: Purpose— Symptomatic intracranial hemorrhage (sICH) is the most feared complication of intravenous thrombolytic therapy in acute ischemic stroke. Treatment of sICH is based on expert opinion and small case series, with the efficacy of such treatments not well established. This document aims to provide an overview of sICH with a focus on pathophysiology and treatment. Methods— A literature review was performed for randomized trials, prospective and retrospective studies, opinion papers, case series, and case reports on the definitions, epidemiology, risk factors, pathophysiology, treatment, and outcome of sICH. The document sections were divided among writing group members who performed the literature review, summarized the literature, and provided suggestions on the diagnosis and treatment of patients with sICH caused by systemic thrombolysis with alteplase. Several drafts were circulated among writing group members until a consensus was achieved. Results— sICH is an uncommon but severe complication of systemic thrombolysis in acute ischemic stroke. Prompt diagnosis and early correction of the coagulopathy after alteplase have remained the mainstay of treatment. Further research is required to establish treatments aimed at maintaining integrity of the blood-brain barrier in acute ischemic stroke based on inhibition of the underlying biochemical processes.
TL;DR: In endovascular treatment for acute ischemic stroke, no difference was found between general anesthesia and conscious sedation in neurological outcome 3 months after stroke.
Abstract: Background and Purpose— Retrospective studies have found that patients receiving general anesthesia for endovascular treatment in acute ischemic stroke have worse neurological outcome compared with patients receiving conscious sedation. In this prospective randomized single-center study, we investigated the impact of anesthesia technique on neurological outcome in acute ischemic stroke patients.
Methods— Ninety patients receiving endovascular treatment for acute ischemic stroke in 2013 to 2016 were included and randomized to general anesthesia or conscious sedation. Difference in neurological outcome at 3 months, measured as modified Rankin Scale score, was analyzed (primary outcome) and early neurological improvement of National Institutes of Health Stroke Scale and cerebral infarction volume. Age, sex, comorbidities, admission National Institutes of Health Stroke Scale score, intraprocedural blood pressure, blood glucose, Paco2 and Pco2 modified Thrombolysis in Cerebral Ischemia score, and relevant time intervals were recorded.
Results— In the general anesthesia group 19 of 45 patients (42.2%) and in the conscious sedation group 18 of 45 patients (40.0%) achieved a modified Rankin Scale score ≤2 ( P =1.00) at 3 months, with no differences in intraoperative blood pressure decline from baseline ( P =0.57); blood glucose ( P =0.94); PaCO2 ( P =0.68); time intervals ( P =0.78); degree of successful recanalization, 91.1% versus 88.9% ( P =1.00); National Institutes of Health Stroke Scale score at 24 hours 8 (3–5) versus 9 (2–15; P =0.60); infarction volume, 20 (10–100) versus 20(10–54) mL ( P =0.53); and hospital mortality (13.3% in both groups; P =1.00).
Conclusions— In endovascular treatment for acute ischemic stroke, no difference was found between general anesthesia and conscious sedation in neurological outcome 3 months after stroke.
Clinical Trial Registration— URL: . Unique identifier: [NCT01872884][1].
[1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT01872884&atom=%2Fstrokeaha%2F48%2F6%2F1601.atom
TL;DR: The National Institutes of Health Stroke Scale (NIHSS) is the most widely used deficit rating scale in modern neurology: over 500 000 healthcare professionals have been certified to administer it using a web-based platform.
Abstract: The National Institutes of Health Stroke Scale (NIHSS) is the most widely used deficit rating scale in modern neurology: over 500 000 healthcare professionals have been certified to administer it using a web-based platform. Every clinical trial in vascular neurology—prevention, acute treatment, recovery—requires a severity assessment, and the NIHSS became the gold standard for stroke severity rating after the first successful trial in acute stroke therapy, the NINDS r-tPA (National Institute of Neurological Disorders and Stroke recombinant tissue-type plasminogen activator) for Acute Stroke Trial (the Trial).1 As part of the Trial, detailed and rigorous training/certification procedures were created for the NIHSS that facilitate wider use of the scale outside of research.2
Today, payers and regulators demand reportable data on patient outcomes, and such outcomes must be adjusted for baseline severity: the NIHSS has become the de facto metric for regulatory compliance. The Joint Commission, as part of its certification program for Primary Stroke Centers, now requires an NIHSS score within 12 hours of admission for all stroke patients; this assessment is to be done by a certified examiner.3,4 Federal agencies also require outcomes adjusted for baseline stroke severity—using the NIHSS.5 Despite widening regulatory requirements, considerable problems may arise in using the NIHSS in clinical practice because the scale was designed for research purposes.6 Given that the scale was not designed for such widespread—and determinative—application, anyone using (or mandating use of) the NIHSS must understand its development history, clinimetric properties, and its proper bedside administration.
During the late 1980s, several stroke-deficit rating scales were in use.7–10 For use in a National Institutes of Health–sponsored trial of naloxone for acute stroke, investigators combined scales that had been developed at the University of Cincinnati, Canadian neurological scale, the Edinburgh-2 coma scale, and the Oxbury …
TL;DR: Strong evidence is found that silent cerebrovascular disease is a common problem of aging and that silent brain infarcts and white matter hyperintensities are associated with future symptomatic stroke risk independently of other vascular risk factors.
Abstract: Two decades of epidemiological research shows that silent cerebrovascular disease is common and is associated with future risk for stroke and dementia. It is the most common incidental finding on brain scans. To summarize evidence on the diagnosis and management of silent cerebrovascular disease to prevent stroke, the Stroke Council of the American Heart Association convened a writing committee to evaluate existing evidence, to discuss clinical considerations, and to offer suggestions for future research on stroke prevention in patients with 3 cardinal manifestations of silent cerebrovascular disease: silent brain infarcts, magnetic resonance imaging white matter hyperintensities of presumed vascular origin, and cerebral microbleeds. The writing committee found strong evidence that silent cerebrovascular disease is a common problem of aging and that silent brain infarcts and white matter hyperintensities are associated with future symptomatic stroke risk independently of other vascular risk factors. In patients with cerebral microbleeds, there was evidence of a modestly increased risk of symptomatic intracranial hemorrhage in patients treated with thrombolysis for acute ischemic stroke but little prospective evidence on the risk of symptomatic hemorrhage in patients on anticoagulation. There were no randomized controlled trials targeted specifically to participants with silent cerebrovascular disease to prevent stroke. Primary stroke prevention is indicated in patients with silent brain infarcts, white matter hyperintensities, or microbleeds. Adoption of standard terms and definitions for silent cerebrovascular disease, as provided by prior American Heart Association/American Stroke Association statements and by a consensus group, may facilitate diagnosis and communication of findings from radiologists to clinicians.
TL;DR: An initial definition of optimal brain health in adults is provided to provide the AHA/American Stroke Association with a foundation for a new strategic direction going forward in cardiovascular health promotion and disease prevention.
Abstract: Cognitive function is an important component of aging and predicts quality of life, functional independence, and risk of institutionalization. Advances in our understanding of the role of cardiovascular risks have shown them to be closely associated with cognitive impairment and dementia. Because many cardiovascular risks are modifiable, it may be possible to maintain brain health and to prevent dementia in later life. The purpose of this American Heart Association (AHA)/American Stroke Association presidential advisory is to provide an initial definition of optimal brain health in adults and guidance on how to maintain brain health. We identify metrics to define optimal brain health in adults based on inclusion of factors that could be measured, monitored, and modified. From these practical considerations, we identified 7 metrics to define optimal brain health in adults that originated from AHA’s Life’s Simple 7: 4 ideal health behaviors (nonsmoking, physical activity at goal levels, healthy diet consistent with current guideline levels, and body mass index 2 ) and 3 ideal health factors (untreated blood pressure
TL;DR: Brain arteriovenous malformations are a relatively uncommon but important cause of hemorrhagic stroke, especially in young adults, and implications for future research are described.
Abstract: Purpose—The aim of this statement is to review the current data and to make suggestions for the diagnosis and management of both ruptured and unruptured brain arteriovenous malformations. Methods—T...
TL;DR: Interestingly, FTY720 could reduce cognitive decline and ameliorate the disruption of WM integrity, a potential therapeutic drug targeting brain inflammation by skewing microglia toward M2 polarization after chronic cerebral hypoperfusion.
Abstract: Background and Purpose— White matter (WM) ischemic injury, a major neuropathological feature of cerebral small vessel diseases, is an important cause of vascular cognitive impairment in later life. The pathogenesis of demyelination after WM ischemic damage are often accompanied by microglial activation. Fingolimod (FTY720) was approved for the treatment of multiple sclerosis for its immunosuppression property. In this study, we evaluated the neuroprotective potential of FTY720 in a WM ischemia model. Methods— Chronic WM ischemic injury model was induced by bilateral carotid artery stenosis. Cognitive function, WM integrity, microglial activation, and potential pathway involved in microglial polarization were assessed after bilateral carotid artery stenosis. Results— Disruption of WM integrity was characterized by demyelination in the corpus callosum and disorganization of Ranvier nodes using Luxol fast blue staining, immunofluorescence staining, and electron microscopy. In addition, radial maze test demonstrated that working memory performance was decreased at 1-month post–bilateral carotid artery stenosis–induced injury. Interestingly, FTY720 could reduce cognitive decline and ameliorate the disruption of WM integrity. Mechanistically, cerebral hypoperfusion induced microglial activation, production of associated proinflammatory cytokines, and priming of microglial polarization toward the M1 phenotype, whereas FTY720 attenuated microglia-mediated neuroinflammation after WM ischemia and promoted oligodendrocytogenesis by shifting microglia toward M2 polarization. FTY720’s effect on microglial M2 polarization was largely suppressed by selective signal transducer and activator of transcription 3 (STAT3) blockade in vitro, revealing that FTY720-enabled shift of microglia from M1 to M2 polarization state was possibly mediated by STAT3 signaling. Conclusions— Our study suggested that FTY720 might be a potential therapeutic drug targeting brain inflammation by skewing microglia toward M2 polarization after chronic cerebral hypoperfusion.
TL;DR: Incidence of SICH after thrombectomy is higher in Asian patients with acute ischemic stroke, and Cardioembolic stroke, poor collateral circulation, delayed endovascular treatment, multiple passes with stent retriever device, lower pretreatment Alberta Stroke Program Early Computed Tomography Score, higher baseline neutrophil ratio may increase the risk of Sich.
Abstract: Background and Purpose—Symptomatic intracranial hemorrhage (SICH) pose a major safety concern for endovascular treatment of acute ischemic stroke. This study aimed to evaluate the risk and related ...
TL;DR: This document reviews the current status of telestroke and suggests measures for ongoing quality and outcome monitoring to improve performance and to enhance delivery of care.
Abstract: Purpose—Telestroke is one of the most frequently used and rapidly expanding applications of telemedicine, delivering much-needed stroke expertise to hospitals and patients. This document reviews th...
TL;DR: Patients, some with little experience using a smartphone, successfully used the technology and demonstrated a 50% improvement in adherence based on plasma drug concentration levels, and real-time monitoring has the potential to increase adherence and change behavior, particularly in patients on direct oral anticoagulant therapy.
Abstract: Background and Purpose— This study evaluated the use of an artificial intelligence platform on mobile devices in measuring and increasing medication adherence in stroke patients on anticoagulation therapy. The introduction of direct oral anticoagulants, while reducing the need for monitoring, have also placed pressure on patients to self-manage. Suboptimal adherence goes undetected as routine laboratory tests are not reliable indicators of adherence, placing patients at increased risk of stroke and bleeding. Methods— A randomized, parallel-group, 12-week study was conducted in adults (n=28) with recently diagnosed ischemic stroke receiving any anticoagulation. Patients were randomized to daily monitoring by the artificial intelligence platform (intervention) or to no daily monitoring (control). The artificial intelligence application visually identified the patient, the medication, and the confirmed ingestion. Adherence was measured by pill counts and plasma sampling in both groups. Results— For all patients (n=28), mean (SD) age was 57 years (13.2 years) and 53.6% were women. Mean (SD) cumulative adherence based on the artificial intelligence platform was 90.5% (7.5%). Plasma drug concentration levels indicated that adherence was 100% (15 of 15) and 50% (6 of 12) in the intervention and control groups, respectively. Conclusions— Patients, some with little experience using a smartphone, successfully used the technology and demonstrated a 50% improvement in adherence based on plasma drug concentration levels. For patients receiving direct oral anticoagulants, absolute improvement increased to 67%. Real-time monitoring has the potential to increase adherence and change behavior, particularly in patients on direct oral anticoagulant therapy. Clinical Trial Registration— URL: http://www.clinicaltrials.gov. Unique identifier: NCT02599259.
TL;DR: The results support the current guidelines of offering intravenous thrombolysis to eligible patients even if they are being considered for mechanical thrombectomy, and demonstrate that MT+IVT patients had better functional outcomes, lower mortality, higher rate of successful recanalization, requiring lower number of device passes, and equal odds of symptomatic intracerebral hemorrhage compared with MT−IVt patients.
Abstract: Background and Purpose— Whether prior intravenous thrombolysis provides any additional benefits to the patients undergoing mechanical thrombectomy for large vessel, acute ischemic stroke remains unclear. Methods— We conducted a meta-analysis of 13 studies obtained through PubMed and EMBASE database searches to determine whether functional outcome (modified Rankin Scale) at 90 days, successful recanalization rate, and symptomatic intracerebral hemorrhage rate differed between patients who underwent mechanical thrombectomy with (MT+IVT) and without (MT−IVT) pre-treatment with intravenous thrombolysis. Results— MT+IVT patients compared with MT−IVT patients had better functional outcomes (modified Rankin Scale score, 0–2; summary odds ratio [OR], 1.27 [95% confidence interval (CI), 1.05–1.55]; P =0.02; n=1769/1174), lower mortality (OR, 0.71 [95% CI, 0.55–0.91]; P =0.006; n=1774/1202), and higher rate of successful recanalization (OR, 1.46 [95% CI, 1.09–1.96]; P =0.01; n=1652/1216) without having increased odds of symptomatic intracerebral hemorrhage (OR, 1.11 [95% CI, 0.69–1.77]; P =0.67; n=1471/1143). A greater number of MT+IVT patients required ≤2 passes with a neurothrombectomy device to achieve successful recanalization (OR, 2.06 [95% CI, 1.37–3.10]; P =0.0005; n=316/231). Conclusions— Our results demonstrated that MT+IVT patients had better functional outcomes, lower mortality, higher rate of successful recanalization, requiring lower number of device passes, and equal odds of symptomatic intracerebral hemorrhage compared with MT−IVT patients. The results support the current guidelines of offering intravenous thrombolysis to eligible patients even if they are being considered for mechanical thrombectomy. Because the data are compiled from studies where the 2 groups differed based on eligibility for intravenous thrombolysis, randomized trials are necessary to accurately evaluate the added value of intravenous thrombolysis in patients treated with mechanical thrombectomy.
TL;DR: The authors describe the pathophysiology, classification, mode of presentation, imaging characteristics, natural history, and therapeutic armamentarium for intracranial dAVFs.
Abstract: Intracranial dural arteriovenous fistulae (dAVFs) are typified by pathological anastomoses between meningeal arteries and dural venous sinuses or cortical veins. These fistulae frequently reside within the dural leaflets surrounding a venous sinus, characteristically at the transverse-sigmoid junction but also at the cavernous sinus (CS), superior sagittal sinus, anterior cranial fossa, tentorium, and other locations. dAVFs are distinguished from their pial counterparts (eg, arteriovenous malformations) by their arterial supply from vessels that perfuse the dura mater and lack of a parenchymal nidus.1 dAVFs are rare lesions, accounting for 10% to 15% of all intracranial vascular malformations: 6% of supratentorial and 35% of infratentorial vascular malformations.2 Most frequently, dAVFs affect patients in their middle-to-later years of life (eg, 50–60 years of age).3 Less commonly, dAVFs occur in younger age groups, including children. There is neither a clear sex predilection nor genetic component to these lesions. Clinical manifestations vary widely and depend on both the hemodynamic properties and location of the fistula. Multiple classification systems have been proposed in an effort to predict which dAVFs are at high risk for new neurological events. Most of these schemes stratify risk based on angiographic appearance of the dAVFs, in particular involvement of a venous sinus and presence or absence of retrograde cortical venous drainage (CVD). Other schemes combine angiographic appearance with mode of presentation, given the impact symptoms related to intracerebral hemorrhage (ICH) and nonhemorrhagic neurological deficits (NHND) have on dAVF natural history.4–6
In the following review and synthesis, the authors describe the pathophysiology, classification, mode of presentation, imaging characteristics, natural history, and therapeutic armamentarium for intracranial dAVFs. Particular attention will be given to recent evidence that certain clinical and angiographic features of dAVFs can be used to help stratify risk of future ICH and NHND in an effort …
TL;DR: Patients with LVO who experience rapid infarct growth as fast progressors are referred to, and a significant number of patients maintain a small ischemic core and significant salvageable tissue beyond 6 hours and up to several days after persistent LVO.
Abstract: Approximately 40% of acute ischemic strokes are caused by proximal intracranial large vessel occlusion (LVO) and are associated with the worst clinical outcomes.1 Early reperfusion with IV tPA (tissue-type plasminogen activator) and intra-arterial thrombectomy leads to reduced final infarct volumes, lower disability rates, and improved cognitive function after anterior circulation LVO.2–6 However, most stroke patients with LVO remain untreated because they present beyond the conventional time windows for acute reperfusion therapies.7,8 Therefore, a growing paradigm has been to transition to a therapeutic window that is tailored to each patient’s individual pathophysiology or brain tissue window rather than a standardized time window.9,10 The principle of pathophysiology-based reperfusion therapy is built on the fundamental concept of a dynamic interrelation between the ischemic core (tissue that is already infarcted) and the ischemic penumbra (physiologically impaired but potentially salvageable tissue).11–13 After arterial occlusion, there can be temporal growth of the ischemic core into the penumbral area that is modulated by collateral blood flow, the key element setting the pace of the ischemic process.14 Infarct growth is thought to progress at different speeds across individuals because patients with occlusion of the proximal middle cerebral artery (MCA) or internal carotid artery (ICA) terminus present with widely variable stroke volumes independently of time after symptom onset.15–18 We refer to patients with LVO who experience rapid infarct growth as fast progressors. These patients have failing collaterals and a large ischemic core despite presenting early within 6 hours of stroke onset. Conversely, a significant number of patients maintain a small ischemic core and significant salvageable tissue beyond 6 hours and up to several days after persistent LVO.17,19 The latter patients are slow progressors because they maintain good collaterals and …
TL;DR: The island sign is a reliable CT imaging marker that independently predicts hematoma expansion and poor outcome in patients with ICH and may serve as a potential marker for therapeutic intervention.
Abstract: Background and Purpose— The aim of the study was to investigate the usefulness of the computed tomography (CT) island sign for predicting early hematoma growth and poor functional outcome. Methods— We included patients with spontaneous intracerebral hemorrhage (ICH) who had undergone baseline CT within 6 hours after ICH symptom onset in our hospital between July 2011 and September 2016. Two readers independently assessed the presence of the island sign on the admission noncontrast CT scan. Multivariable logistic regression analysis was used to analyze the association between the presence of the island sign on noncontrast admission CT and early hematoma growth and functional outcome. Results— A total of 252 patients who met the inclusion criteria were analyzed. Among them, 41 (16.3%) patients had the island sign on baseline noncontrast CT scans. In addition, the island sign was observed in 38 of 85 patients (44.7%) with hematoma growth. Multivariate logistic regression analysis demonstrated that the time to baseline CT scan, initial hematoma volume, and the presence of the island sign on baseline CT scan independently predicted early hematoma growth. The sensitivity of the island sign for predicting hematoma expansion was 44.7%, specificity 98.2%, positive predictive value 92.7%, and negative predictive value 77.7%. After adjusting for the patients’ age, baseline Glasgow Coma Scale score, presence of intraventricular hemorrhage, presence of subarachnoid hemorrhage, admission systolic blood pressure, baseline ICH volume, and infratentorial location, the presence of the island sign (odds ratio, 3.51; 95% confidence interval, 1.26–9.81; P =0.017) remained an independent predictor of poor outcome in patients with ICH. Conclusions— The island sign is a reliable CT imaging marker that independently predicts hematoma expansion and poor outcome in patients with ICH. The noncontrast CT island sign may serve as a potential marker for therapeutic intervention.
TL;DR: The 6-minute walk test was better able to discriminate among home, limited community, and full community ambulators than comfortable gait speed, andGait speed values commonly used to distinguish between home and community walkers may overestimate walking activity.
Abstract: Background and Purpose—Walking ability poststroke is commonly assessed using gait speed categories developed by Perry et al. The purpose of this study was to reexamine factors that predict home and...
TL;DR: The findings indicate that H19 promotes neuroinflammation by driving HDAC1-dependent M1 microglial polarization, suggesting a novel H19-based diagnosis and therapy for ischemic stroke.
Abstract: Background and Purpose—Long noncoding RNA H19 is repressed after birth, but can be induced by hypoxia. We aim to investigate the impact on and underlying mechanism of H19 induction after ischemic s...
TL;DR: Modifiable risk factors previously established in older populations also account for a large part of stroke in younger adults, with 4 risk factors explaining almost 80% of stroke risk.
Abstract: Background and Purpose— As stroke in young adults is assumed to have different etiologies and risk factors than in older populations, the aim of this study was to examine the contribution of established potentially modifiable cardiovascular risk factors to the burden of stroke in young adults. Methods— A German nationwide case–control study based on patients enrolled in the SIFAP1 study (Stroke In Young Fabry Patients) 2007 to 2010 and controls from the population-based GEDA study (German Health Update) 2009 to 2010 was performed. Cases were 2125 consecutive patients aged 18 to 55 years with acute first-ever stroke from 26 clinical stroke centers; controls (age- and sex-matched, n=8500, without previous stroke) were from a nationwide community sample. Adjusted population-attributable risks of 8 risk factors (hypertension, hyperlipidemia, diabetes mellitus, coronary heart disease, smoking, heavy episodic alcohol consumption, low physical activity, and obesity) and their combinations for all stroke, ischemic stroke, and primary intracerebral hemorrhage were calculated. Results— Low physical activity and hypertension were the most important risk factors, accounting for 59.7% (95% confidence interval, 56.3–63.2) and 27.1% (95% confidence interval, 23.6–30.6) of all strokes, respectively. All 8 risk factors combined explained 78.9% (95% confidence interval, 76.3–81.4) of all strokes. Population-attributable risks of all risk factors were similar for all ischemic stroke subtypes. Population-attributable risks of most risk factors were higher in older age groups and in men. Conclusions— Modifiable risk factors previously established in older populations also account for a large part of stroke in younger adults, with 4 risk factors explaining almost 80% of stroke risk. Clinical Trial Registration— URL: http://www.clinicaltrials.gov. Unique identifier: NCT00414583.
TL;DR: This meta-analysis confirms the main findings of the randomized controlled trials of dabigatran, rivaroxaban, and apixaban in the real-world setting and strengthens their validity.
Abstract: Background and Purpose— Evidence from the real-world setting complements evidence coming from randomized controlled trials. We aimed to summarize all available evidence from high-quality real-world observational studies about efficacy and safety of nonvitamin-K oral anticoagulants compared with vitamin-K antagonists in patients with atrial fibrillation. Methods— We searched PubMed and Web of Science until January 7, 2017 for observational nationwide or health insurance databases reporting matched or adjusted results comparing nonvitamin-K oral anticoagulants versus vitamin-K antagonists in patients with atrial fibrillation. Outcomes assessed included ischemic stroke, ischemic stroke or systemic embolism, any stroke or systemic embolism, myocardial infarction, intracranial hemorrhage, major hemorrhage, gastrointestinal hemorrhage, and death. Results— In 28 included studies of dabigatran, rivaroxaban, and apixaban compared with vitamin-K antagonists, all 3 nonvitamin-K oral anticoagulants were associated with a large reduction of intracranial hemorrhage (apixaban hazard ratio [HR], 0.45; 95% confidence interval [CI], 0.31–0.63; dabigatran HR, 0.42; 95% CI, 0.37–0.49; rivaroxaban HR, 0.64; 95% CI, 0.47–0.86); similar rates of ischemic stroke and ischemic stroke or systemic embolism (apixaban HR, 1.05; 95% CI, 0.75–1.19 and HR, 1.08; 95% CI, 0.95–1.22 / dabigatran HR, 0.96; 95% CI, 0.80–1.16 and HR, 1.17; 95% CI, 0.92–1.50 / rivaroxaban HR, 0.89; 95% CI, 0.76–1.04 and HR, 0.73; 95% CI, 0.52–1.04, respectively); apixaban and dabigatran with lower mortality (HR, 0.65; 95% CI, 0.56–0.75 and HR, 0.63; 95% CI, 0.53–0.75, respectively); apixaban with fewer gastrointestinal (HR, 0.63; 95% CI, 0.42–0.95) and major hemorrhages (HR, 0.55; 95% CI, 0.48–0.63); dabigatran and rivaroxaban with more gastrointestinal hemorrhages (HR, 1.20; 95% CI, 1.06–1.36 and HR, 1.24; 95% CI, 1.08–1.41, respectively); dabigatran and rivaroxaban with similar rate of myocardial infarction (HR, 0.96; 95% CI, 0.77–1.21 and HR, 1.02; 95% CI, 0.54–1.89, respectively). Conclusions— This meta-analysis confirms the main findings of the randomized controlled trials of dabigatran, rivaroxaban, and apixaban in the real-world setting and, hence, strengthens their validity.
TL;DR: Histological thrombus features vary significantly according to the underlying cause and may help to differentiate between cardioembolic and noncardioembolic stroke, and supports the hypothesis that most cryptogenic strokes have a cardioEmbolic cause.
Abstract: Background and Purpose— The introduction of stent retrievers allows for a complete extraction and histological analysis of human thrombi. Ischemic stroke is a major health issue, and differentiation of underlying causes is highly relevant to prevent recurrent stroke. Therefore, histopathologic analysis of the embolic clots after removal may provide valuable information about underlying pathologies. This study analyzes histological clot composition and aims to identify specific patterns that might help to distinguish causes of ischemic stroke. Methods— Patients with occlusion of the carotid-T or middle cerebral artery who underwent thrombectomy at our university medical center between December 2013 and February 2016 were included. Samples were histologically analyzed (hematoxylin and eosin, Elastica van Gieson, and Prussian blue), additionally immunohistochemistry for CD3, CD20, and CD68/KiM1P was performed. These data, along with additional clinical and interventional parameters, were compared for different stroke subtypes, as defined by the TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification. Results— One hundred eighty-seven patients were included, of these, in 77 patients, cardioembolic; in 46 patients, noncardioembolic; and in 64 patients, cryptogenic pathogenesis was determined. Cardioembolic thrombi had higher proportions of fibrin/platelets ( P =0.027), less erythrocytes ( P =0.005), and more leucocytes ( P =0.026) than noncardioembolic thrombi. We observed a strong overlap of cryptogenic strokes and cardioembolic strokes concerning thrombus histology. The immunohistochemical parameters CD3, CD20, and CD68/KiM1P showed no statistically noticeable differences between stroke subtypes. Conclusions— Histological thrombus features vary significantly according to the underlying cause and may help to differentiate between cardioembolic and noncardioembolic stroke. In addition, our study supports the hypothesis that most cryptogenic strokes have a cardioembolic cause.
TL;DR: The findings demonstrate the therapeutic potential of a BCI-driven neurorehabilitation approach using the unaffected hemisphere in this uncontrolled sample of chronic stroke survivors and demonstrate thatBCI- driven neurore rehabilitation can be effectively delivered in the home environment, thus increasing the probability of future clinical translation.
Abstract: Background and Purpose— There are few effective therapies to achieve functional recovery from motor-related disabilities affecting the upper limb after stroke This feasibility study tested whether a powered exoskeleton driven by a brain–computer interface (BCI), using neural activity from the unaffected cortical hemisphere, could affect motor recovery in chronic hemiparetic stroke survivors This novel system was designed and configured for a home-based setting to test the feasibility of BCI-driven neurorehabilitation in outpatient environments
Methods— Ten chronic hemiparetic stroke survivors with moderate-to-severe upper-limb motor impairment (mean Action Research Arm Test=134) used a powered exoskeleton that opened and closed the affected hand using spectral power from electroencephalographic signals from the unaffected hemisphere associated with imagined hand movements of the paretic limb Patients used the system at home for 12 weeks Motor function was evaluated before, during, and after the treatment
Results— Across patients, our BCI-driven approach resulted in a statistically significant average increase of 62 points in the Action Research Arm Test This behavioral improvement significantly correlated with improvements in BCI control Secondary outcomes of grasp strength, Motricity Index, and the Canadian Occupational Performance Measure also significantly improved
Conclusions— The findings demonstrate the therapeutic potential of a BCI-driven neurorehabilitation approach using the unaffected hemisphere in this uncontrolled sample of chronic stroke survivors They also demonstrate that BCI-driven neurorehabilitation can be effectively delivered in the home environment, thus increasing the probability of future clinical translation
Clinical Trial Registration— URL: Unique identifier: [NCT02552368][1]
[1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT02552368&atom=%2Fstrokeaha%2Fearly%2F2017%2F05%2F26%2FSTROKEAHA116016304atom
TL;DR: In observational studies, reinstitution of anticoagulation after ICH was associated with a lower risk of thromboembolic complications and a similar risk of ICH recurrence, and Randomized clinical trials are needed to determine the true risk–benefit profile of antICOagulation resumption after I CH.
Abstract: Background and Purpose— The safety and efficacy of restarting anticoagulation therapy after intracranial hemorrhage (ICH) remain unclear. We performed a systematic review and meta-analysis to summarize the associations of anticoagulation resumption with the subsequent risk of ICH recurrence and thromboembolism.
Methods— We searched published medical literature to identify cohort studies involving adults with anticoagulation-associated ICH. Our predictor variable was resumption of anticoagulation. Outcome measures were thromboembolic events (stroke and myocardial infarction) and recurrence of ICH. After assessing study heterogeneity and publication bias, we performed a meta-analysis using random-effects models to assess the strength of association between anticoagulation resumption and our outcomes.
Results— Eight studies were eligible for inclusion in the meta-analysis, with 5306 ICH patients. Almost all studies evaluated anticoagulation with vitamin K antagonists. Reinitiation of anticoagulation was associated with a significantly lower risk of thromboembolic complications (pooled relative risk, 0.34; 95% confidence interval, 0.25–0.45; Q =5.12, P for heterogeneity=0.28). There was no evidence of increased risk of recurrent ICH after reinstatement of anticoagulation therapy, although there was significant heterogeneity among included studies (pooled relative risk, 1.01; 95% confidence interval, 0.58–1.77; Q =24.68, P for heterogeneity <0.001). No significant publication bias was detected in our analyses.
Conclusions— In observational studies, reinstitution of anticoagulation after ICH was associated with a lower risk of thromboembolic complications and a similar risk of ICH recurrence. Randomized clinical trials are needed to determine the true risk–benefit profile of anticoagulation resumption after ICH.
TL;DR: Higher recent and higher cumulative intake of artificially sweetened soft drinks were associated with an increased risk of ischemic stroke, all-cause dementia, and Alzheimer’s disease dementia.
Abstract: Background and Purpose—Sugar- and artificially-sweetened beverage intake have been linked to cardiometabolic risk factors, which increase the risk of cerebrovascular disease and dementia. We examin...
TL;DR: Of patients with ischemic stroke with deficits potentially amenable to acute intervention, 14% are not identified using FAST, suggesting the inclusion of gait/leg and visual symptoms leads to a reduction in missed strokes.
Abstract: Background and Purpose—The FAST algorithm (Face, Arm, Speech, Time) helps identify persons having an acute stroke. We determined the proportion of patients with acute ischemic stroke not captured b...
TL;DR: Carotid web is associated with high recurrent stroke/TIA risk, despite antithrombotic use, and is amenable to carotid stenting in a cohort of patients with strokes from symptomatic Carotid webs.
Abstract: Background and Purpose—Carotid webs have been increasingly recognized as a cause of recurrent stroke, but evidence remains scarce. We aim to report the clinical outcomes and first series of carotid...