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Background: Studies have suggested promising evidence that glial fibrillary acidic protein (GFAP) could be used as a blood biomarker to distinguish between ischaemic stroke (IS) and intracerebral haemorrhage (ICH) in acute stage. Objective: To determine the available evidence for GFAP as a blood biomarker for differentiating ICH from IS and stroke mimics using a meta-analysis approach. Methods: Search terms were used for literature search: ("STROKE" [Mesh] OR "BIOMARKER" [Title/Abstract] OR "GFAP" [Title/Abstract])] OR "SPECIFICITY" OR "SENSTIVITY" at various search engines like PubMed, Google scholar, Trip database, clinicaltrial.gov for articles from 1990 to April 2019 using filter 'human subjects'. Data were analysed using software STATA version 13. Results: A pooled analysis including 12 studies suggested that GFAP if used as a biomarker to differentiate between different types of strokes (ICH from IS and mimics) had a sensitivity of 78% (95% CI: 67–86%) and a specificity of 95% (95% CI: 88–98%). Positive likelihood ratio (LR) was 14.4 and negative LR was 0.23. SROC with prediction and confidence contours suggests promising area under the curve 0.93, 95% CI ranges from 0.90 to 0.95. Diagnostic odds ratio with 95% CI was observed 63 (31–125). Conclusion: Our meta-analysis suggests that GFAP has a promising diagnostic accuracy for the differentiation of ICH from IS and mimics. Further, phase II and phase III diagnostic test studies are required to validate the findings before using GFAP as a blood based biomarker for clinical use. Trial Registration: This study was registered in OSF registries 10.17605/OSF.IO/B9JP4 [ABSTRACT FROM AUTHOR]

Intermittent fasting (IF) is a diet with salutary effects on cognitive aging, Alzheimer's disease (AD), and stroke. IF restricts a number of nutrient components, including glucose. 2-deoxyglucose (2-DG), a glucose analog, can be used to mimic glucose restriction. 2-DG induced transcription of the pro-plasticity factor, Bdnf , in the brain without ketosis. Accordingly, 2-DG enhanced memory in an AD model (5xFAD) and functional recovery in an ischemic stroke model. 2-DG increased Bdnf transcription via reduced N-linked glycosylation, consequent ER stress, and activity of ATF4 at an enhancer of the Bdnf gene, as well as other regulatory regions of plasticity/regeneration (e.g., Creb5 , Cdc42bpa , Ppp3cc , and Atf3) genes. These findings demonstrate an unrecognized role for N-linked glycosylation as an adaptive sensor to reduced glucose availability. They further demonstrate that ER stress induced by 2-DG can, in the absence of ketosis, lead to the transcription of genes involved in plasticity and cognitive resilience as well as proteostasis. [Display omitted] • 2-deoxyglucose (2-DG), a glucose-restriction mimetic, drives Bdnf transcription • 2-DG reduces disability after ischemic stroke and improves cognition in AD • 2-DG inhibits N-glycosylation to induce ER stress, ATF4, and Bdnf transcription • N-glycosylation senses low glucose to drive adaptation to stroke and AD Intermittent fasting (IF) is a nutritional paradigm that forestalls cognitive aging, stroke disability, and Alzheimer's progression. How glucose restriction, an aspect of IF, contributes to IF-induced benefits is unclear. Here, we used 2-deoxyglucose to elucidate how low glucose engages an evolutionarily conserved ER stress response pathway to stimulate brain plasticity and treat stroke and AD. [ABSTRACT FROM AUTHOR]

Background: Factor V Leiden is the most common genetic variation among the blood coagulation pathway which leads to prothrombotic state, therefore, is considered an important gene for understating the stroke mechanism. Aim: The aim of the present study is to determine the relationship between single nucleotide polymorphism at G1691A position of Factor V gene and risk of ischemic stroke (IS) in North Indian population. Materials and Methods: In a retrospective case–control study, 250 patients with IS and 250 age‑ and gender‑matched controls were enrolled in the period of October 2012 to September 2014 from in‑ and out‑patient department of Neurology, All India Institute of Medical Sciences, New Delhi, India. Deoxyribonucleic acid for each case and control was isolated from peripheral blood using phenol‑chloroform extraction method. Polymerase chain reaction‑restriction fragment length polymorphism method was used to determine the polymorphism. Data were analyzed using STATA Software Version 13. Results: The mean age of IS patient was 52.8 ± 12.5 years and in control group was 50.97 ± 12.7 years. Genotypic frequency distributions were in accordance with Hardy–Weinberg equilibrium in both cases and controls. As expected hypertension, diabetes, dyslipidemia, smoking, heavy alcohol intake, family history of stroke, and poor economic status were significantly associated with the risk of IS. Multivariate analysis revealed 5.17 times higher odds for developing the risk of large vessel subtype of IS in patients carrying Factor V Leiden G1691A gene variation as compared to control subjects (OR, 5.17; 95% CI, 1.32–20.3, P = 0.01). Conclusion: The present study suggests that Factor V Leiden G1691A polymorphism may be significantly associated with the risk of large vessel subtype of IS. Large sample size studies using prospective cohort designs are required to corroborate the present findings. [ABSTRACT FROM AUTHOR]

Previously published studies that have examined whether the three polymorphisms, G894T, T786C, and 4b/a in the endothelial nitric oxide synthase (eNOS) gene, are associated with ischemic stroke (IS) have reported conflicting results. Thus, we performed a meta-analysis to examine the potential association between these three single nucleotide polymorphisms (SNPs) of the eNOS gene and IS risk. A literature search was carried out for eligible candidate gene studies published before August 05, 2015 in the PubMed, Embase, and Google Scholar databases. The following combinations of main keywords were used in our study: ('endothelial nitric oxide synthase') or ('eNOS') and ('G894T, 4b/a, and T786C') and ('polymorphism') or ('polymorphisms') and ('Ischemic Stroke' or 'IS') and ('Cerebral Infarction' or 'CI') and ('genetic polymorphism' or 'single nucleotide polymorphisms' or 'SNP'). Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by using fixed or random effects model. Meta-regression analysis was used to investigate the potential sources of heterogeneity. Begg's funnel plots were used to explore the publication bias, and heterogeneity was assessed by I2 test. Twenty seven case-control studies involving 6733 cases and 7305 controls were analyzed in our meta-analysis. Significant association was observed for G894T (OR = 1.17; 95% CI: 1.08 to 1.28; P< 0.001) and 4b/a (OR = 1.25; 95% CI: 1.13 to 1.39; P < 0.001) whereas a non-significant association was observed for T786C (OR = 1.11; 95% CI: 0.98 to 1.26; P =0.109) eNOS gene polymorphisms and IS. Our meta-analysis establishes that the G894T and 4b/a polymorphisms of eNOS gene are significantly associated with the risk of IS. However, a non-significant association was found between T786C polymorphism of the eNOS gene and IS risk. Further prospective large epidemiological studies need to be done to confirm these findings. [ABSTRACT FROM AUTHOR]

Purpose: Lymphotoxin alpha (LTA), a proinflammatory cytokine, plays an important role in promoting atherosclerosis which is an independent risk factor for stroke. Recent genetic studies have suggested that polymorphisms in the LTA gene, which affect its expression and biological function, may contribute to the development of stroke. The aim of this case-control study was to determine the association between LTA (-252 A/G and -804 C/A) gene polymorphisms and risk of stroke.Methods: Genotyping was determined by using SNaPshot method for 250 ischemic stroke (IS) patients, 250 age and sex matched IS free controls, 100 intracerebral hemorrhage (ICH) patients and 100 age and sex matched ICH free controls. Conditional logistic regression analysis with adjusting multiple demographic and risk factor variables was used to calculate the strength of association between LTA (-252 A/G and -804 C/A) gene polymorphisms and risk of stroke. The linkage disequilibrium (LD) was analyzed by using HaploView 4.2 software.Results: The distribution of LTA (-252 A/G and -804 C/A) genotypes was consistent with Hardy–Weinberg equilibrium. Adjusted conditional logistic regression analysis showed no significant association between LTA (-252 A/G and -804 C/A) gene polymorphisms and risk of both IS and ICH. Based on Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification, a significant association between LTA -252 A/G gene polymorphism and small vessel disease subtype of IS under dominant model (OR, 2.06; 95% CI, 1.03–4.12;pvalue 0.04) with the risk of IS was observed. No LD was observed for both single nucleotide polymorphisms (SNPs) in north Indian population.Conclusion: Neither -252 G/A nor -804 C/A polymorphism of the LTA gene was found to be associated with overall stroke as well as any subtype of IS excluding SVD in North Indian population. [ABSTRACT FROM PUBLISHER]

Transforming growth factor-β1 (TGF-β1) is a multifunctional pro-inflammatory cytokine involved in inflammation and pathogenesis of cerebrovascular disease. As per our knowledge, there is no published study investigating the association between variations within the TGF-β1 gene polymorphisms and risk of intracerebral hemorrhage (ICH). The aim of this study was to investigate the association of the TGF-β1 gene (C509T, G800A and T869C) polymorphisms, and their haplotypes with the risk of ICH in North Indian population. 100 ICH patients and 100 age- and sex-matched controls were studied. Genotyping was performed using SNaPshot method. Conditional logistic regression analysis was used to calculate the strength of association between TGF-β1 gene polymorphisms and risk of ICH. Hypertension, diabetes, dyslipidemia, low socioeconomic status, smoking, physical activity were found to be associated with the risk of ICH. The distribution of C509T, G800A and T869C genotypes was consistent with Hardy-Weinberg Equilibrium (HWE) in the ICH and control group. Adjusted conditional logistic regression analysis showed an independent association of TGF-β1 G800A (OR 9.07; 95% CI 2.3-35.6; P = 0.002) and T869C (OR 5.1; 95 % CI 1.9-13.2; P = 0.001) with the risk of ICH under dominant model. Haplotype analysis showed that C509-G800-C869 and C509-A800-C869 haplotypes were significantly associated with the increased risk of ICH. C509T and T869C were in strong linkage disequilibrium (D' = 0.53, r(2) = 0.23). Our results suggest that TGF-β1 (G800A, T869C) gene polymorphisms and their haplotypes are significantly associated with the risk of ICH in North Indian population. Further prospective studies with large sample size are required for independent validation. Our findings could be helpful in identifying individuals at increased risk for developing ICH. [ABSTRACT FROM AUTHOR]

Stroke, a heterogeneous multifactorial disorder, is known to be a major cause of death and adult disability within both the developed and developing countries. Approximately 85% of stroke cases are ischemic, whereas the remaining 15% are hemorrhagic. It is caused by multiple genetic factors, environmental factors, and interactions among these factors. Several candidate genes have been found to be associated with ischemic stroke. The most extensively studied genes include those involved in hemostasis, inflammation, nitric oxide production, homocysteine and lipid metabolism, and rennin-angiotensin-aldosterone system. Combined linkage/association studies have demonstrated that genes encoding phosphodiesterase 4D (PDE4D) and arachidonate 5-lipoxygenase-activating protein (ALOX5AP) confer risk for stroke. Even though there is substantial evidence for the genetic basis of stroke as provided by the epidemiological data from twin- and family-based studies, the contribution of genetic factors identified till now is either not enough or very less to explain the entire spectrum of encountered phenomena associated with ischemic stroke. Till date, no genome-wide association studies (GWAS) have been carried out in India. We aim to extensively review the studies on candidate genes that may have potential applications in the early diagnosis, prevention, and treatment of ischemic stroke in the Indian population. This article further emphasizes the role of GWAS in ischemic stroke and the need for an extensive GWAS in the Indian population. [ABSTRACT FROM AUTHOR]

Modern definitions of epigenetics incorporate models for transient but biologically important changes in gene expression that are unrelated to DNA code but responsive to environmental changes such as injury-induced stress. In this scheme, changes in oxygen levels (hypoxia) and/or metabolic co-factors (iron deficiency or diminished 2-oxoglutarate levels) are transduced into broad genetic programs that return the cell and the organism to a homeostatic set point. Over the past two decades, exciting studies have identified a superfamily of iron-, oxygen-, and 2-oxoglutarate-dependent dioxygenases that sit in the nucleus as modulators of transcription factor stability, co-activator function, histone demethylases, and DNA demethylases. These studies have provided a concrete molecular scheme for how changes in metabolism observed in a host of neurological conditions, including stroke, traumatic brain injury, and Alzheimer׳s disease, could be transduced into adaptive gene expression to protect the nervous system. We will discuss these enzymes in this short review, focusing primarily on the ten eleven translocation (TET) DNA demethylases, the jumonji (JmJc) histone demethylases, and the oxygen-sensing prolyl hydroxylase domain enzymes (HIF PHDs). This article is part of a Special Issue entitled SI: Neuroprotection . [ABSTRACT FROM AUTHOR]

Background Stroke is a multi-factorial disease and influenced by both genetic and environmental factors. The purpose of the present case control study was to check the relationship between beta-2 adrenergic receptor (ADRB2) polymorphism and ischemic stroke in North Indian Population. Methods In a hospital based case control study, patients with ischemic stroke and control subjects from outpatient department and neurology ward of All India Institute of Medical Sciences New Delhi. Genotyping was performed by using Polymerase chain reaction-Restriction fragment length polymorphism. Frequency distributions of genotypes and alleles were compared between cases and controls using multivariate logistic regression. Results In this study, 224 patients and 224 age-and sex-matched control subjects were recruited. Mean age of cases and controls were 53.9 ± 13.4 and 53.6 ± 12.9 years respectively. Multivariate logistic regression analysis showed an independent association between Gln27Glu polymorphism and large vessel stroke (LVD) under a recessive model of inheritance (OR 3.9; 95% CI 1.3 to 11). An age-stratified analysis, suggested independent association between Gln27Glu polymorphism and ischemic stroke, large vessel disease and small vessel disease stroke who had onset of disease at an older age. Conclusions The findings of the present study suggest that Gln27Glu polymorphism of the ADRB2 gene may confer higher risk of large vessel disease stroke in a North Indian population. Prospective studies with larger sample size are required for independent validation. [ABSTRACT FROM AUTHOR]

Background: Several observational studies have reported the prevalence of cerebral microbleeds (CMBs) and their risk factors in an elderly population. Any information in this regard is currently lacking from India. Aim of this study was to estimate the prevalence, risk factors of CMBs, and association with cognition in an Indian urban population aged 50 years and above. Methods: Household surveys were conducted as part of ongoing Longitudinal Cognition and Aging Research on Population of the National Capital Region (LoCARPoN) study in areas of urban Delhi. Magnetic resonance imaging of the brain was performed in 2599 participants. Using standard neuropsychological battery, mean Z-scores for each domain (memory, executive, information) were derived. Binary and stepwise logistic regression models were used to determine associated risk factors for the presence of CMB and its association with cognitive domains. Results: The prevalence of CMBs was 14.42% (95% confidence interval [CI]: 13.06-15.73). Of these, 203 (7.81%) participants had single CMBs and 172 (6.61%) had multiple microbleeds (≥2). Higher prevalence was observed in older age (6070 years: odds ratio [OR]: 1.25 [95% CI: 0.93-1.67]; 70-80 years: OR: 2.05 [95% CI: 1.48-2.84]; ≥80 years: OR: 3.27 [95% CI: 1.97-5.44]) compared to individuals in the age group 50-60 years. History of stroke (OR: 2.97 [95% CI: 1.56-5.66]), hypertension (OR: 1.36 [95% CI: 1.05-1.75]), and smoking (OR: 1.43 [95% CI: 1.11-1.85]) was associated with at least one CMB. Multiple CMBs were associated with worse scores in memory and executive domains. Conclusion: Older age, hypertension, history of stroke, and history of smoking emerged as important risk factors for the presence of multiple CMBs. Follow-up study is required to determine implications of CMBs. [ABSTRACT FROM AUTHOR]

Background: Spontaneous intracerebral hemorrhage (SICH) accounts for 7.5%-30% of all strokes and carries higher morbidity and mortality. Raised blood urea nitrogen and creatinine ratio (BUNR) is a marker of dehydration and related to poor outcome in stroke patients. However, the ratio varies between 15 and 80 in different studies. The aim of the present study was to assess BUNR as an independent predictor of mortality and its sensitivity and specificity in predicting outcome in the SICH population.Materials and Methods: Patients above the age of 18 years with SICH who were admitted in the Department of Neurology at Sir Sunderlal Hospital, Banaras Hindu University between January 2018 and July 2020 were enrolled in the study and prospectively followed up. Demographic, clinical, radiological, and outcome parameters were recorded.Results: A total of 217 patients were included. Of these, 137 (63%) were males. Seventy-one patients died during the initial 30 days. Number of patients with intraventricular hemorrhage (IVH; P = 0.003), higher mean intracerebral hemorrhage (ICH) volume (P < 0.001) and midline shift (P = 0.021), and poor Glasgow Coma Scale (GCS) score (<9) (P = 0.040) was more in the group which did not survive. Mean level of urea was significantly lower among survivors than in those who died (P = 0.001). BUNR was also significantly higher in those who died than in those who survived (P = 0.001). BUNR with a cutoff value of 39.17 was significantly associated with mortality at 30 days with a sensitivity and specificity of 61.97% and 62.33%, respectively. On performing two different multivariable logistic studies, it was found that model B with BUNR ratio as a predictor of mortality out performed model A (without BUNR).Conclusions: The study showed that SICH was associated with significant mortality. Independent predictors of death at 30 days were lower GCS on admission, larger hematoma volume, and BUNR of more than 39.17. [ABSTRACT FROM AUTHOR]

Introduction: Genetic factors may play a role in the susceptibility of intracerebral hemorrhage (ICH). The present case-control study hypothesized that genetic polymorphisms in tumor necrosis factor- α (TNF-α) gene may affect the risk of ICH.Materials and Methods: In this study, we investigated the association of four single nucleotide polymorphisms (-308G/A, +488G/A, -857C/T, and -1031T/C) within TNF-α gene promoter and their haplotypes with the risk of ICH in a North Indian population. Genotyping was determined by using the SNaPshot method for 100 ICH patients and 100 age and sex-matched ICH-free controls. Conditional logistic regression analysis with adjusting multiple demographic and risk factor variables was used to calculate the strength of association between TNF-α gene polymorphisms and risk of ICH. Haplotypes were reconstructed using PHASE 2.0, and patterns of linkage disequilibrium (LD) analysis were performed using Haploview version 4.2 software.Results: TNF-α +488G/A gene polymorphism was found to be independently associated with the risk of ICH under dominant [GG + GA vs. AA] (OR = 3.1; 95% CI = 1.2-8.2; P = 0.001) and allelic [G vs. A] (OR = 2.2; 95% CI = 1.2-4.2; P = 0.007) models. However, no significant association between -308G/A, -857C/T, and -1031T/C gene polymorphisms and risk of ICH was observed. Haplotype analysis showed that 308A-488G-857C-1031T and 308G-488A-857T-1031T haplotypes were significantly associated with an increased risk of ICH. Strong LD was observed for + 488G/A and -857C/T TNF-α polymorphisms (D' = 0.72, r2= 0.01).Conclusion: Our findings suggest that the TNF-α +488G/A polymorphism may be an important risk factor for ICH, whereas -308G/A, -857C/T, and -1031T/C gene polymorphisms may not be associated with risk of ICH in North Indian population. [ABSTRACT FROM AUTHOR]

Background: Stroke is the second largest cause of mortality (WHO 2014) and long lasting disability worldwide. Many risk factors are associated with stroke, such as age, gender, chronic illnesses, cardiovascular disease, lifestyle, and smoking. With global industrialization, the roles of environmental contaminants and their association with stroke are still unclear and have attracted much more attention. Materials and Methods: We conducted a systematic review on the environmental toxic metal contaminants and the risk of ischemic stroke. A comprehensive literature search was carried out till June 30, 2021 from databases such as PubMed, Science Direct, Embase, and Scopus. The quality of all the articles which met our inclusion criteria was assessed using Newcastle--Ottawa scaling, and four eligible studies were included for our systematic review. Results: The serum and urine cadmium concentrations were positively associated with the risk of ischemic stroke. There was an inverse association of serum and urine concentrations of mercury (Hg), serum concentration of gold and cerium with ischemic stroke, and the serum and urine concentrations of lead (Pb) had no association with ischemic stroke risk. Conclusion: The study showed strong associations between heavy metals and ischemic stroke, but more studies are required to prove the associations. [ABSTRACT FROM AUTHOR]

Background: Interleukin-6 (IL-6), as one of the most typical pro-inflammatory and immunoregulatory cytokines, is believed to be associated with the genesis and maintenance of inflammatory response. Genetic association studies (GAS) that have investigated the association between Interleukin 6 (G174C and G572C) promoter gene polymorphisms and susceptibility to ischemic stroke (IS) which have produced contradictory and unconvincing results. Purpose: The aim of this meta-analysis is to provide a relatively comprehensive account of the association of IL-6 (G174C and G572C) polymorphisms with susceptibility to IS. Methods: A literature search was conducted using electronic database PubMed, Medline, and Trip database for all case-control studies investigating for association of IL-6 genetic polymorphisms with ischemic stroke published till August 30, 2014. The following combinations of main keywords were used: ('Interleukin- 6' or 'IL-6') and ('ischaemic stroke or 'cerebral infarction' or 'IS') and ('genetic polymorphism' or 'single nucleotide polymorphisms' or 'SNP'). Pooled Odds ratios (ORs) and 95% confidence intervals (CIs) were determined for IL-6 gene-disease association. Meta-analysis was carried out using Revman 5.3 software. Results: 16 case-control studies involving a total of 3,317 IS patients and 3,432 healthy controls for G174C polymorphism and 3 case-control studies with a total of 2,001 IS patients and 2,027 healthy controls for G572C IL-6 gene polymorphisms were included in a meta-analysis. For IL-6 G174C gene polymorphisms, no significant association was observed under dominant [GC + CC vs. GG: OR = 1.01, 95% CI: 0.77-1.34, P = 0. 92], recessive [CC vs. GG + GC: OR = 0.82, 95% CI: 0.40-1.70, P = 0. 59] and allelic model [C vs. G Allele: OR = 0.99, 95% CI: 0.74-1.31, P = 0. 93]. For IL-6 G572C, no significant association was observed under dominant [CC vs. GG + GC: OR = 0.99, 95% CI: 0.57-1.71, P = 0. 97], recessive [CC vs. GG + GC: OR = 0.93, 95% CI: 0.60-1.45, P = 0. 75] and allelic model [C vs. G Allele: OR = 0.95, 95% CI: 0.66-1.36, P = 0. 76]. Conclusion: This meta-analysis shows that IL-6 (G174C) and IL-6 (G572C) gene polymorphisms may not be associated with an increased susceptibility to IS. Further studies are required for confirmatory results. [ABSTRACT FROM AUTHOR]

Ferroptosis is a caspase-independent, iron-dependent form of regulated necrosis extant in traumatic brain injury, Huntington disease, and hemorrhagic stroke. It can be activated by cystine deprivation leading to glutathione depletion, the insufficiency of the antioxidant glutathione peroxidase-4, and the hemolysis products hemoglobin and hemin. A cardinal feature of ferroptosis is extracellular signal-regulated kinase (ERK)1/2 activation culminating in its translocation to the nucleus. We have previously confirmed that the mitogen-activated protein (MAP) kinase kinase (MEK) inhibitor U0126 inhibits persistent ERK1/2 phosphorylation and ferroptosis. Here, we show that hemin exposure, a model of secondary injury in brain hemorrhage and ferroptosis, activated ERK1/2 in mouse neurons. Accordingly, MEK inhibitor U0126 protected against hemin-induced ferroptosis. Unexpectedly, U0126 prevented hemin-induced ferroptosis independent of its ability to inhibit ERK1/2 signaling. In contrast to classical ferroptosis in neurons or cancer cells, chemically diverse inhibitors of MEK did not block hemin-induced ferroptosis, nor did the forced expression of the ERK-selective MAP kinase phosphatase (MKP)3. We conclude that hemin or hemoglobin-induced ferroptosis, unlike glutathione depletion, is ERK1/2-independent. Together with recent studies, our findings suggest the existence of a novel subtype of neuronal ferroptosis relevant to bleeding in the brain that is 5-lipoxygenase-dependent, ERK-independent, and transcription-independent. Remarkably, our unbiased phosphoproteome analysis revealed dramatic differences in phosphorylation induced by two ferroptosis subtypes. As U0126 also reduced cell death and improved functional recovery after hemorrhagic stroke in male mice, our analysis also provides a template on which to build a search for U0126's effects in a variant of neuronal ferroptosis. [ABSTRACT FROM AUTHOR]

Introduction: An increase in the common carotid artery intima‐media thickness (CCA‐IMT) is generally considered an early marker of atherosclerosis and is a well‐established predictor of cardiovascular disease (CVD). An association between changes in CCA‐IMT and risk of stroke has been reported but has conflicting findings. Objective: The present meta‐analysis was aimed to clarify the association between CCA‐IMT with the risk of stroke and its subtype by estimating pooled analysis of published literature. Methods: Comprehensive search for all published articles was performed in electronic databases including PubMed, Embase, Cochrane Library, Trip Databases, Worldwide Science, CINAHL and Google Scholar from 01 January 1950 to 30 April 2020. Results: In our meta‐analysis, a total of 19 studies, of which sixteen studies involving 3475 ischaemic stroke (IS) cases and 11 826 controls; six studies with 902 large vessel disease (LVD) and 548 small vessel disease (SVD) of IS subtypes; five studies with 228 intracerebral haemorrhage (ICH) and 1032 IS cases, were included. Our findings suggest a strong association between increased CCA‐IMT with risk of IS as compared to control subjects [SMD = 1.46, 95% CI = 0.90‐2.02]. However, there is an increased risk of LVD as compared to the SVD subtype of IS [SMD = 0.36, 95% CI = 0.19‐0.52] and more chance of occurrence of IS rather than ICH [SMD = 0.71, 95% CI = 0.28‐1.41]. Conclusions: Carotid intima thickness measurements are found to be associated with the risk of stroke along with its subtypes and may be used as a diagnostic marker for predicting the risk of stroke events. [ABSTRACT FROM AUTHOR]

Background: Correct diagnosis of stroke and its subtypes is pivotal in early stages for optimum treatment. Aims: The aim of this systematic review and meta-analysis is to summarize the published evidence on the potential of blood biomarkers in the diagnosis and differentiation of stroke subtypes. Methods: A literature search was conducted for papers published until 20 April 2020 in PubMed, EMBASE, Cochrane Library, TRIP, and Google Scholar databases to search for eligible studies investigating the role of blood biomarkers in diagnosing stroke. Quality assessment was done using modified Quality Assessment of Diagnostic Accuracy Studies questionnaire. Pooled standardized mean difference and 95% confidence intervals were calculated. Presence of heterogeneity among the included studies was investigated using the Cochran's Q statistic and I 2 metric tests. If I 2 was < 50% then a fixed-effect model was applied else a random-effect model was applied. Risk of bias was assessed using funnel plots and between-study heterogeneity was assessed using meta-regression and sensitivity analyses. Entire statistical analysis was conducted in STATA version 13.0. Results: A total of 40 studies including patients with 5001 ischemic strokes, 756 intracerebral hemorrhage, 554 stroke mimics, and 1774 healthy control subjects analyzing 25 biomarkers (within 24 h after symptoms onset/after the event) were included in our meta-analysis; 67.5% of studies had moderate evidence of quality. Brain natriuretic peptide, matrix metalloproteinase-9, and D-dimer significantly differentiated ischemic stroke from intracerebral hemorrhage, stroke mimics, and health control subjects (p < 0.05). Glial fibrillary acidic protein successfully differentiated ischemic stroke from intracerebral hemorrhage (standardized mean difference −1.04; 95% confidence interval −1.46 to −0.63) within 6 h. No studies were found to conduct a meta-analysis of blood biomarkers differentiating transient ischemic attack from healthy controls and stroke mimics. Conclusion: This meta-analysis highlights the potential of brain natriuretic peptide, matrix metalloproteinase-9, D-dimer, and glial fibrillary acidic protein as diagnostic biomarkers for stroke within 24 h. Results of our meta-analysis might serve as a platform for conducting further targeted proteomics studies and phase-III clinical trials. PROSPERO Registration ID: CRD42019139659. [ABSTRACT FROM AUTHOR]

Objective: Caregivers usually are not involved while planning the stroke survivor's medical and rehabilitation goals and interventions. This review aimed to identify the needs of stroke survivors as perceived by their caregivers. Design: A literature search from 2003 to 2014 was conducted using Medline, CINAHL, PsychINFO, and Google Scholar. Sixty-six studies were included. Most studies excluded did not encompass caregivers' perspectives. Four reviewers screened the titles, abstracts, and full texts of the articles for inclusion. The data extracted from these studies were synthetized into metathemes. Results: Fifty-two qualitative, ten quantitative survey, and four mixed-methods studies were included in the final synthesis. The studies came from 11 countries. The data synthesis produced following three metathemes: (a) body functional needs, including psychological function, physical function, cognitive function, and uncertainty related to function; (b) activity and participatory needs, including healthy lifestyle, physical activities, speech, independence, cognitive activities, and uncertainty related to activities and participation; and (c) environmental needs, encompassing support, services, safety, accommodation and accessibility, and uncertainty related to environmental factors. Conclusions: This scoping review identified a range of needs of stroke survivors as perceived by their caregivers. Incorporating the caregiver's preferences and values into clinical decisions may improve outcomes among stroke survivors. [ABSTRACT FROM AUTHOR]

In a developing country, where patient access to tertiary care is limited and most patients have to pay out of pocket, it is imperative for the physicians to practice evidence-based medicine. Reports on prescription details and surveys are not available. The aim of this study is to describe the prescribing patterns for various medications used in the treatment of stroke among the first contact physicians in North India; to estimate the proportion of patients being prescribed the non-recommended drugs and to determine any relationship between the economic status of the patient and the prescription pattern. Details of economic status, education level, type of stroke, type of hospital, qualification of treating physician and the number and nature of medications were noted from the prescriptions and patients. Two hundred and sixteen patients with ischemic stroke (71.3% males, average age 51.5 years) were included. Among poor patients,N= (36.8%) received any of the neuroprotective drugs including citicoline 19 (27.5%), piracetam 11(15.9%) and edaravone 2(2.9%). Both specialist and private hospitals are associated with higher prescription of “ineffective neuroprotective” drugs in both poor and rich patients. Reasons for overprescribing neuroprotective medications need to be studied and remedial measures need to be taken to practice evidence-based medicine. [ABSTRACT FROM AUTHOR]