Background Regularly updated data on stroke and its pathological types, including data on their incidence, prevalence, mortality, disability, risk factors, and epidemiological trends, are important for evidence-based stroke care planning and resource allocation. The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) aims to provide a standardised and comprehensive measurement of these metrics at global, regional, and national levels. MethodsWe applied GBD 2019 analytical tools to calculate stroke incidence, prevalence, mortality, disability-adjusted life-years (DALYs), and the population attributable fraction (PAF) of DALYs (with corresponding 95% uncertainty intervals [UIs]) associated with 19 risk factors, for 204 countries and territories from 1990 to 2019. These estimates were provided for ischaemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, and all strokes combined, and stratified by sex, age group, and World Bank country income level. FindingsIn 2019, there were 12•2 million (95% UI 11•0-13•6) incident cases of stroke, 101 million (93•2-111) prevalent cases of stroke, 143 million (133-153) DALYs due to stroke, and 6•55 million (6•00-7•02) deaths from stroke. Globally, stroke remained the second-leading cause of death (11•6% [10•8-12•2] of total deaths) and the third-leading cause of death and disability combined (5•7% [5•1-6•2] of total DALYs) in 2019. From 1990 to 2019, the absolute number of incident strokes increased by 70•0% (67•0-73•0), prevalent strokes increased by 85•0% (83•0-88•0), deaths from stroke increased by 43•0% (31•0-55•0), and DALYs due to stroke increased by 32•0% (22•0-42•0). During the same period, age-standardised rates of stroke incidence decreased by 17•0% (15•0-18•0), mortality decreased by 36•0% (31•0-42•0), prevalence decreased by 6•0% (5•0-7•0), and DALYs decreased by 36•0% (31•0-42•0). However, among people younger than 70 years, prevalence rates increased by 22•0% (21•0-24•0) and incidence rates increased by 15•0% (12•0-18•0). In 2019, the age-standardised stroke-related mortality rate was 3•6 (3•5-3•8) times higher in the World Bank low-income group than in the World Bank high-income group, and the age-standardised stroke-related DALY rate was 3•7 (3•5-3•9) times higher in the low-income group than the high-income group. Ischaemic stroke constituted 62•4% of all incident strokes in 2019 (7•63 million [6•57-8•96]), while intracerebral haemorrhage constituted 27•9% (3•41 million [2•97-3•91]) and subarachnoid haemorrhage constituted 9•7% (1•18 million [1•01-1•39]). In 2019, the five leading risk factors for stroke were high systolic blood pressure (contributing to 79•6 million [67•7-90•8] DALYs or 55•5% [48•2-62•0] of total stroke DALYs), high bodymass index (34•9 million [22•3-48•6] DALYs or 24•3% [15•7-33•2]), high fasting plasma glucose (28•9 million [19•8-41•5] DALYs or 20•2% [13•8-29•1]), ambient particulate matter pollution (28•7 million [23•4-33•4] DALYs or 20•1% [16•6-23•0]), and smoking (25•3 million [22•6-28•2] DALYs or 17•6% [16•4-19•0]...

The GUSS offers a quick and reliable method to identify stroke patients with dysphagia and aspiration risk. Such a graded assessment considers the pathophysiology of voluntary swallowing in a more differentiated fashion and provides less discomfort for those patients who can continue with their oral feeding routine for semisolid food while refraining from drinking fluids.

Post-stroke dementia (PSD) or post-stroke cognitive impairment (PSCI) may affect up to one third of stroke survivors. Various definitions of PSCI and PSD have been described. We propose PSD as a label for any dementia following stroke in temporal relation. Various tools are available to screen and assess cognition, with few PSD-specific instruments. Choice will depend on purpose of assessment, with differing instruments needed for brief screening (e.g., Montreal Cognitive Assessment) or diagnostic formulation (e.g., NINDS VCI battery). A comprehensive evaluation should include assessment of pre-stroke cognition (e.g., using Informant Questionnaire for Cognitive Decline in the Elderly), mood (e.g., using Hospital Anxiety and Depression Scale), and functional consequences of cognitive impairments (e.g., using modified Rankin Scale). A large number of biomarkers for PSD, including indicators for genetic polymorphisms, biomarkers in the cerebrospinal fluid and in the serum, inflammatory mediators, and peripheral microRNA profiles have been proposed. Currently, no specific biomarkers have been proven to robustly discriminate vulnerable patients (‘at risk brains’) from those with better prognosis or to discriminate Alzheimer’s disease dementia from PSD. Further, neuroimaging is an important diagnostic tool in PSD. The role of computerized tomography is limited to demonstrating type and location of the underlying primary lesion and indicating atrophy and severe white matter changes. Magnetic resonance imaging is the key neuroimaging modality and has high sensitivity and specificity for detecting pathological changes, including small vessel disease. Advanced multi-modal imaging includes diffusion tensor imaging for fiber tracking, by which changes in networks can be detected. Quantitative imaging of cerebral blood flow and metabolism by positron emission tomography can differentiate between vascular dementia and degenerative dementia and show the interaction between vascular and metabolic changes. Additionally, inflammatory changes after ischemia in the brain can be detected, which may play a role together with amyloid deposition in the development of PSD. Prevention of PSD can be achieved by prevention of stroke. As treatment strategies to inhibit the development and mitigate the course of PSD, lowering of blood pressure, statins, neuroprotective drugs, and anti-inflammatory agents have all been studied without convincing evidence of efficacy. Lifestyle interventions, physical activity, and cognitive training have been recently tested, but large controlled trials are still missing.

No abstract

The close relationship between stroke and dementia is an important health issue. Ischaemic stroke can facilitate the onset of vascular dementia as well as aggravate pre-existing cognitive decline. The onset of cognitive decline may become manifest immediately following the onset of ischaemic stroke, but often there is a delay in the development of cognitive decline after a stroke. This delay can be seen as a therapeutic time window allowing interventions to be applied to preserve cognition following stroke. Both neurodegenerative and vascular mechanisms are activated and probably result in overlapping processes within the neurovascular unit. This review focuses on the incidence and prevalence of cognitive decline following stroke, predisposing stroke aetiologies, pre-stroke decline, imaging factors and biomarkers. Outcomes are discussed in relation to timing of assessment and neuropsychological tests used for evaluation of cognitive decline in ischaemic stroke patients. Including such tests in routine evaluations of stroke patients after some weeks or months is recommended. Finally, an outlook on ongoing and planned intervention trials is added and some recommendations for future research are proposed.

No abstract

There is a discrepancy between theoretical stroke knowledge and the reaction in an acute situation. Help-seeking behaviour is more dependent on the perceived severity of symptoms than on symptom knowledge. Bystanders play an important role in the decision to call for help and should be included in stroke education. Education is effective and should be culturally adapted and presented in a social context. It is unclear which educational concept is best suited to enhance symptom recognition in the acute situation of stroke, especially in view of discrepancies between knowledge and action.

Most life history traits are positively influenced by body size, whereas disadvantages of large body size are poorly documented. To investigate presumed intrinsic costs of large size in the yellow dung fly (Scathophaga stercoraria; Diptera: Scathophagidae), we established two replicates each of three body size laboratory selection lines (small, control and large; selection on males only), and subjected flies of the resulting extended body size range to various abiotic stresses. Response to selection was symmetrical in the small and large lines (realized h2 = 0.16–0.18). After 24 generations of selection body size had changed by roughly 10%. Female size showed a correlated response to selection on male size, whereas sexual size dimorphism did not change. Development time also showed a correlated response as, similar to food limited flies, small line flies emerged earlier at smaller body size. At the lowest larval food limit possible, flies of all lines emerged at the same small body size after roughly the same development time; so overall phenotypic plasticity in body size and development time strongly increased following selection. Juvenile mortality increased markedly when food was extremely limited, large line flies showing highest mortality. Winter frost disproportionately killed large (line) flies because of their longer development times. Mortality at high temperatures was high but size‐selective effects were inconsistent. In all environments the larger males suffered more. Initial growth rate was higher for males and at unlimited food. Small line individuals of both sexes grew slowest at unlimited larval food but fastest at limited larval food, suggesting a physiological cost of fast growth. Overall, extension of the natural body size range by artificial selection revealed some otherwise cryptic intrinsic juvenile viability costs of large size, mediated by longer development or faster growth, but only in stressful environments.