Dataset Information

Peripheral glucose levels and cognitive outcome after ischemic stroke-Results from the Munich Stroke Cohort.

ABSTRACT:

Introduction

The relationship between glucose metabolism and stroke outcome is likely to be complex. We examined whether there is a linear or non-linear relationship between glucose measures in the acute phase of stroke and post-stroke cognition, and whether altered glucose metabolism at different time intervals (long- and short-term before stroke, acute phase) is associated with cognitive outcome.

Patients and methods

In all, 664 consecutively recruited patients with acute ischemic stroke and without pre-stroke dementia were included in this prospective observational study. Blood samples were taken at admission and fasting on the first morning after stroke. Duration of diabetes was assessed by interview. Cognitive outcome was assessed by the Telephone Interview for Cognitive Status 3 months post-stroke. Dose-response analyses were used to investigate non-linearity. Regression analyses were stratified by diabetes status and adjusted for relevant confounders.

Results

Cognitive status was testable in 422 patients (81 with diabetes). There was a non-linear relationship between both admission and fasting glucose levels and cognitive outcome. Lower glucose values were significantly associated with lower Telephone Interview for Cognitive Status scores 3 months post-stroke in patients without diabetes with a similar trend in diabetic patients. There was an inverse association between duration of diabetes and Telephone Interview for Cognitive Status scores (linear regression: -0.10 (95% confidence interval: -0.17 to -0.02) per year increase of diabetes duration), whereas HbA_1c was not related to cognitive outcome. Results were supported by sensitivity analyses accounting for attrition.

Conclusion

Lower glucose levels in the acute phase of stroke are associated with worse cognitive outcome but the relationship is non-linear. Long-term abnormalities in glucose metabolism are also related to poor outcome but this is not the case for shorter term abnormalities. Altered glucose levels at different stages of stroke may affect stroke outcome through different pathways.

SUBMITTER: Zietemann V

PROVIDER: S-EPMC6301221 | biostudies-literature | 2016 Mar

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Peripheral glucose levels and cognitive outcome after ischemic stroke-Results from the Munich Stroke Cohort.

Zietemann Vera V Wollenweber Frank Arne FA Bayer-Karpinska Anna A Biessels Geert Jan GJ Dichgans Martin M

European stroke journal 20160301 1

<h4>Introduction</h4>The relationship between glucose metabolism and stroke outcome is likely to be complex. We examined whether there is a linear or non-linear relationship between glucose measures in the acute phase of stroke and post-stroke cognition, and whether altered glucose metabolism at different time intervals (long- and short-term before stroke, acute phase) is associated with cognitive outcome.<h4>Patients and methods</h4>In all, 664 consecutively recruited patients with acute ischem ...[more]

PMID: 31008267

Similar Datasets

Project description:ObjectiveHyperglycemia is a common comorbidity for ischemic stroke and is associated with worsened neurological outcomes. Platelets are central mediators of ischemic stroke and hyperglycemia mediates platelet hyperactivity. In this study, we investigated the contribution of platelet glucose metabolism to ischemic stroke.MethodsMice lacking both Glut1 and Glut3 specifically in platelets (DKO) and their littermate controls (WT) were subjected to 1-hour transient middle cerebral artery occlusion under normoglycemic and streptozotocin-induced hyperglycemic conditions after which stroke outcomes, platelet activation, and platelet-neutrophil aggregate (PNA) formation were examined.ResultsUnder normoglycemic conditions, DKO mice were protected from ischemic stroke with smaller brain infarct volumes and improved cerebral blood flow. In addition, DKO mice had reduced platelet activation, PNA, and cerebral neutrophil recruitment after stroke. Hyperglycemia significantly increased infarct size and cerebral Evans blue extravasation and worsened neurological outcomes and cerebral blood flow in both WT and DKO mice, abolishing the protective effect witnessed under normoglycemic conditions. Flow cytometric analysis after stroke demonstrated increased platelet activation and neutrophil trafficking to the brain, independent of platelet glucose metabolism. Finally, platelets from healthy DKO mice were unable to become procoagulant upon dual agonist stimulation. Conversely, hyperglycemia increased platelet mitochondrial reactive oxygen species production which potentiated procoagulant platelet formation in WT mice and restored procoagulant platelet formation in DKO mice.ConclusionHyperglycemia aggravates ischemic stroke outcome independent of platelet glucose uptake. Furthermore, we demonstrated that hyperglycemia primes procoagulant platelet formation. This underlines the therapeutic potential for strategies targeting procoagulant platelet formation for the treatment of acute ischemic stroke.

Project description:The impact of reperfusion therapies on cognition has been poorly explored and little knowledge exists. We explored the influence of endovascular treatment (EVT) on cognitive outcome in patients with anterior circulation ischemic stroke. Patients presenting with ischemic stroke due to anterior large vessel occlusion who underwent intravenous thrombolysis (IVT) alone or EVT plus IVT were recruited. Cognitive abilities were evaluated at 6 months from stroke through a neuropsychological test battery. A total of 88 patients with a mean age of 66.3 ± 12.9 years were included, of which 38 treated with IVT alone and 50 with IVT plus EVT. Compared to patients treated with IVT alone, patients who received EVT plus IVT performed significantly better at the neuropsychological tests exploring executive functions, attention, abstract reasoning, visuospatial ability, visual and verbal and memory. At multivariable regression analysis, the EVT was independently associated with the 6-month cognitive performance after the adjustment for age, sex, admission National Institutes of Health Stroke Scale score, systolic blood pressure, glucose level, Alberta Stroke Program Early CT score, side of stroke, site of occlusion, and Back Depression Inventory score [Stroop Test Word Reading: adjβ = 13.99, 95% confidence interval (CI) 8.47-19.50, p < 0.001; Stroop Test Colour Naming: adjβ = 6.63, 95% CI 2.46-10.81, p = 0.002; Trail Making Test-A: adjβ = - 92.98, 95% CI - 153.76 to - 32.20, p = 0.003; Trail Making Test-B: adjβ = - 181.12, 95% CI - 266.09 to - 96.15; p < 0.001; Digit Span Test Forward: adjβ = 1.44, 95% CI 0.77-2.10, p < 0.001; Digit Span Test Backward: adjβ = 1.10, 95% CI 0.42-1.77, p = 0.002; Coloured Progressive Matrices: adjβ = 5.82, 95% CI 2.71-8.93, p < 0.001; Rey Complex Figure Test-Copy: adjβ = 6.02, 95% CI 2.74-9.30, p < 0.001; Rey Complex Figure Test-Immediate recall: adjβ = 6.00, 95% CI 2.34-9.66, p = 0.002; Rey Complex Figure Test-Delayed recall: adjβ = 5.73, 95% CI 1.95-9.51, p = 0.003; Rey Auditory Verbal Learning Test-Immediate recall: adjβ = 12.60, 95% CI 6.69-18.52, p < 0.001; Rey Auditory Verbal Learning Test-Delayed recall: adjβ = 1.85, 95% CI 0.24-3.45, p = 0.025]. Patients treated with EVT plus IVT had better cognitive performance than patients treated with IVT alone at 6 months from anterior circulation ischemic stroke.

Project description:Background: Ischemic stroke causes increased blood-brain barrier permeability and release of markers of axonal damage and inflammation. To investigate diagnostic and prognostic roles of neurofilament light chain (NF-L), we assessed levels of NF-L, S100B, interleukin-6 (IL-6), E-selectin, vascular endothelial growth factor-A (VEGF-A), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in patients with acute ischemic stroke or transient ischemic attack (TIA) and healthy controls. Methods: We studied neurofilament (NF) expression in 2 cases of human postmortem ischemic stroke, representing infarcts aged 3- to >7-days. In a prospective study, we measured plasma NF-L and inflammatory markers <8 h of symptom onset and at 72 h in acute ischemic stroke (n = 31), TIA (n = 9), and healthy controls (n = 29). We assessed whether NF-L, S100B, and IL-6 were associated with clinical severity on admission (Scandinavian Stroke Scale, SSS), diagnosis of ischemic stroke vs. TIA, and functional outcome at 3 months (modified Rankin Scale, mRS). Results: NF expression increased in ischemic neurons and in the infarcted brain parenchyma after stroke. Plasma NF-L levels were higher in stroke patients than in TIA patients and healthy controls, but IL-6 levels were similar. Higher acute NF-L levels were associated with lower SSS scores at admission and higher mRS scores at 3 months. No correlation was observed between NF-L and S100B, NF-L and IL-6, nor between S100B or IL-6 and SSS or mRS. Compared to controls, stroke patients had significantly higher VEGF-A and VCAM-1 at <8 h that remained elevated at 72 h, with significantly higher VEGF-A at <8 h; ICAM-1 was significantly increased at <8 h, while S100B and E-selectin were unchanged. Conclusions: Plasma NF-L levels, but not IL-6 and S100B, were significant predictors of clinical severity on admission and functional outcome at 3 months. Plasma NF-L is a promising biomarker of functional outcome after ischemic stroke.

Project description:The protective role of microRNA (miR)-135b in cerebral neurons has been previously identified. However, to the best of our knowledge, the involvement of miR-135b in acute ischemic stroke has yet to be elucidated. The present study aimed to investigate the expression profile of miR-135b in peripheral blood obtained from patients with acute ischemic stroke. A total of 76 patients with acute ischemic stroke were selected as the case group, which included 33 cases of aorta atheromatous plague, 19 cases of cardioembolism, 16 cases of small arterial occlusion and 8 cases with unknown causes. In addition, 60 healthy subjects were selected as the control group. Reverse transcription-quantitative PCR was used to measure the expression of miR-135b in the peripheral blood of the patients. The National Institutes of Health Stroke Scale (NIHSS) score was used to evaluate the severity of acute ischemic stroke. The relationship between miR-135b levels and acute stroke was subsequently analyzed. The expression of miR-135b in the peripheral blood of the case group was found to be significantly higher compared with that in the control group. By contrast, the expression levels of miR-135b in the case group did not differ significantly between the different etiology types of acute ischemic stroke. In addition, a significant positive correlation was observed between levels of miR-135b expression and NIHSS scores. Further analysis demonstrated that hypertension, hyperglycemia, platelet count, international normalized ratio and miR-135b were risk factors for acute ischemic stroke. Based on bioinformatics analysis, a conserved binding site for miR-135b was identified in the 3'-untranslated region of the transient receptor potential cation channel subfamily C member 6 (TRPC6). Dual luciferase reporter and western blot analysis showed that TRPC6 was a target gene of miR-135b. In conclusion, data from the present study suggest that elevated expression of miR-135b in the peripheral blood of patients with acute ischemic stroke is closely associated with disease severity.

Dataset Information

Peripheral glucose levels and cognitive outcome after ischemic stroke-Results from the Munich Stroke Cohort.

Introduction

Patients and methods

Results

Conclusion

Publications

Peripheral glucose levels and cognitive outcome after ischemic stroke-Results from the Munich Stroke Cohort.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets