Search

Background Methods Findings Conclusion A blood‐based biomarker that accurately reflects neuronal injury in acute ischemic stroke could be an easily accessible and cost‐effective complement to clinical and radiological evaluation. Here, we investigate whether plasma levels of the novel biomarker brain‐derived tau (BD‐tau) reflect cerebral infarct volumes and whether BD‐tau can improve clinical outcome prediction.The present study included 713 consecutive cases from two different hospital‐based cohorts, the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS) and SAHLSIS phase 2 (SAHLSIS2). Acute stroke severity was determined by the Scandinavian Stroke Scale converted to the National Institutes of Health stroke scale (NIHSS) in SAHLSIS and by the NIHSS in SAHLSIS2. All participants were assessed for functional outcome 3 months after stroke by the modified Rankin Scale, and 254 participants in SAHLSIS had quantitative neuroimaging available.Plasma BD‐tau concentrations and cerebral infarct volumes were highly correlated (ρ 0.72, p < 0.001). BD‐tau improved the prognostic accuracy of suffering an unfavorable outcome over age and stroke severity in the whole cohort. However, the gain in predictive power was dependent on stroke severity and infarct location. The largest improvement was observed for mild ischemic strokes (NIHSS <5; area under the curve [AUC] = 0.73 for age + NIHSS versus AUC = 0.84 with addition of BD‐tau; DeLong p 0.02), posterior circulation stroke (AUC = 0.75 vs. AUC = 0.84; DeLong p 0.06) and more specifically for infarcts in the brainstem/cerebellum (AUC = 0.74 vs. 0.87; DeLong p 0.009).Plasma BD‐tau can provide information on the extent of acute neuronal damage in ischemic stroke and adds prognostic value for outcome, especially for mild and posterior circulation strokes. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the influence of stroke lesions in predefined highly interconnected (rich‐club) brain regions on functional outcome post‐stroke, determine their spatial specificity and explore the effects of biological sex on their relevance. We analyzed MRI data recorded at index stroke and ~3‐months modified Rankin Scale (mRS) data from patients with acute ischemic stroke enrolled in the multisite MRI‐GENIE study. Spatially normalized structural stroke lesions were parcellated into 108 atlas‐defined bilateral (sub)cortical brain regions. Unfavorable outcome (mRS > 2) was modeled in a Bayesian logistic regression framework. Effects of individual brain regions were captured as two compound effects for (i) six bilateral rich club and (ii) all further non‐rich club regions. In spatial specificity analyses, we randomized the split into "rich club" and "non‐rich club" regions and compared the effect of the actual rich club regions to the distribution of effects from 1000 combinations of six random regions. In sex‐specific analyses, we introduced an additional hierarchical level in our model structure to compare male and female‐specific rich club effects. A total of 822 patients (age: 64.7[15.0], 39% women) were analyzed. Rich club regions had substantial relevance in explaining unfavorable functional outcome (mean of posterior distribution: 0.08, area under the curve: 0.8). In particular, the rich club‐combination had a higher relevance than 98.4% of random constellations. Rich club regions were substantially more important in explaining long‐term outcome in women than in men. All in all, lesions in rich club regions were associated with increased odds of unfavorable outcome. These effects were spatially specific and more pronounced in women. [ABSTRACT FROM AUTHOR]

Background: Post‐stroke fatigue (PSF) is common with great impact on quality of life. We explored predictive and cross‐sectionally correlated features in the long term after ischemic stroke. Methods: This study comprises 430 participants of the prospective Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS), aged 18–69 years at index stroke. Information on acute stroke severity and cardiovascular risk factors was collected at index stroke. After 7 years, PSF was assessed by the Daily Fatigue Impact Scale (D‐FIS). Cognitive, neurological, and functional outcomes, and symptoms of depression and anxiety, pain, insomnia, and physical activity were also assessed. Associations between baseline variables and PSF were analyzed by ordinal regression. Correlations between PSF and cross‐sectionally assessed variables, and between PSF and baseline variables, were analyzed with Spearman's or point‐biserial correlation for the whole sample and in sex‐stratified analyses. Results: At 7 years post‐stroke, 80% of the participants reported some impact of fatigue. Female sex and stroke severity were independently associated with PSF, whereas no associations were detected with baseline cardiovascular risk factors. In cross‐sectional analyses at 7 years, we found correlations between PSF and poor functional, neurological, and cognitive outcomes, as well as depressive symptoms, anxiety, insomnia, pain, and low physical activity (p <.001 throughout). The correlation with insomnia was stronger in women than in men (two‐way ANOVA interaction test, p =.03). Conclusions: Our findings confirm that PSF is common in the long term after ischemic stroke and show a complex interplay with sex and several other outcomes. Future studies should address causal relationships and interventions towards fatigue and coexisting features. [ABSTRACT FROM AUTHOR]

Background and purpose: This cross‐sectional cohort study aims at investigating young ischaemic stroke survivors with good physical recovery 7 years post‐stroke in order to analyze the relation between late cognitive ability and employment. Methods: Consecutive ischaemic stroke survivors participating in the Sahlgrenska Academy Study on Ischemic Stroke, <55 years of age at stroke onset, and with no or minimal persisting neurological deficits corresponding to a score ≤2 on the National Institutes of Health Stroke Scale at long‐term follow‐up 7 years post‐stroke were included. At this follow‐up, the participants were assessed with respect to general cognitive function, processing speed, executive functions, cardiovascular risk factors, self‐reported employment, cognitive difficulties, fatigue, depressive symptoms, anxiety and physical function. Results: Seven years post‐stroke 112/142 (79%) had part‐time or full‐time work and 30/142 (21%) had full‐time disability pension or sick leave. Compared to those with full‐time disability pension or sick leave, participants with current employment demonstrated significantly better performance with respect to general cognitive function and processing speed, and significantly lower self‐ratings for cognitive difficulties, physical limitations, fatigue and depressed mood. Multivariable logistic regression selected self‐rated memory (odds ratio [OR] 2.61, 95% confidence interval [CI] 1.61–4.21), processing speed (OR 3.50, 95% CI 1.67–7.33) and self‐rated communication skills (OR 3.46, 95% CI 1.75–6.85) as most important correlates (area under the curve 0.83–0.87) of having current employment. Conclusion: This study indicates that cognitive dysfunction is an important contributor to long‐term work disability amongst young stroke survivors with good physical recovery. [ABSTRACT FROM AUTHOR]

Objectives: The cause of ischemic stroke remains unknown, cryptogenic, in 25% of young and middle‐aged patients. We hypothesized that if atherosclerosis is prominent in cryptogenic stroke, it would have a similar proinflammatory protein signature as large artery atherosclerosis (LAA) stroke. Materials & Methods: Blood was collected in the acute phase and after 3 months from cryptogenic (n = 162) and LAA (n = 73) stroke patients aged 18–69 years and once from age‐matched controls (n = 235). Cryptogenic stroke was divided into Framingham Risk Score (FRS) quartiles to compare low and high risk of atherosclerosis. Plasma concentrations of 25 proteins were analyzed using a Luminex multiplex assay. The discriminating properties were assessed with discriminant analysis and C‐statistics. Results: We identified proteins that separated cryptogenic and LAA stroke from controls (area under the curves, AUCs ≥ 0.85). For both subtypes, RANTES, IL‐4, and IFN‐γ contributed the most at both time points. These associations were independent of risk factors of atherosclerosis. We also identified proteins that separated cryptogenic strokes in the lowest quartile of FRS from those in the highest, and from LAA stroke (AUCs ≥ 0.76), and here eotaxin and MCP‐1 contributed the most. Conclusions: The protein signature separating cases from controls was different from the signature separating cryptogenic stroke with low risk of atherosclerosis from those with high risk and from LAA stroke. This suggests that increased RANTES, IL‐4, and IFN‐γ in stroke may not be primarily related to atherosclerosis, whereas increased eotaxin and MCP‐1 in cryptogenic stroke may be markers of occult atherosclerosis as the underlying cause. [ABSTRACT FROM AUTHOR]

Objectives: Studies on long‐term progression of white matter hyperintensities (WMH) after ischemic stroke are scarce. Here, we sought to investigate this progression and its predictors in a cohort presenting with ischemic stroke before 70 years of age. Materials and methods: Participants in the Sahlgrenska Academy Study on Ischemic Stroke who underwent magnetic resonance imaging (MRI) of the brain at index stroke were examined by MRI again after 7 years (n = 188, mean age 53 years at index stroke, 35% females). WMH at index stroke and progression were assessed according to Fazekas' grades and the WMH change scale. Stroke subtype was classified according to TOAST. Results: Marked WMH at index stroke were present in 20% of the participants and were significantly associated with age, hypertension, and subtype. Progression of WMH after 7 years was observed in 63% and 35% of the participants for subcortical and periventricular locations, respectively. Significant independent predictors of progression were age and marked WMH at baseline for both locations, whereas no significant associations were detected for vascular risk factors or subtype in multivariable analyses. In participants with no or only mild WMH at baseline, 20% showed marked WMH at follow‐up. Age and hypertension, but not subtype, were independently associated with this acquisition of marked WMH. Conclusions: Age and marked WMH at index stroke, but not stroke subtype, predicted long‐term WMH progression after ischemic stroke before 70 years of age, whereas age and hypertension predicted acquisition of marked WMH in those with no or only mild WMH at baseline. [ABSTRACT FROM AUTHOR]

Background: Systematic studies on increased muscle tone and spasticity late after ischemic stroke, without any selection, are limited. Therefore, we aimed to determine the prevalence of increased muscle tone, classical spasticity and contracture and predictors of increased muscle tone seven years after stroke. Methods: Consecutive patients with acute ischemic stroke <70 years of age (n = 411) were recruited to the Sahlgrenska Academy Study on Ischemic Stroke. Symptoms at index stroke were assessed using the Scandinavian Stroke Scale. Seven years after stroke, survivors (n = 358) were invited for follow‐up assessments, of whom 292 agreed to participate and 288 contributed data. Muscle tone according to the Modified Ashworth scale, classical spasticity, and contracture was assessed by a neurologist. The associations between increased muscle tone and characteristics at index stroke and recurrent strokes during follow‐up were investigated using logistic regression analysis. Results: Increased muscle tone was recognized in 99 participants (34%): 94 (33%) in the upper limbs, and 72 (25%) in the lower limbs. Classical spasticity was found in 51 participants (18%) and contracture in 26 (9%). Age (odds ratio [OR] 1.03 [95% confidence interval [CI] 1.00–1.06]), arm paresis (OR 1.76 [95% CI 1.40–2.2]), aphasia (OR 1.68 [95% CI 1.12–2.51]), and facial palsy (OR 2.12 [95% CI 1.10–4.07]) were independent predictors of increased muscle tone. Conclusions: One‐third of patients with ischemic stroke before 70 years of age showed increased muscle tone at 7‐year follow‐up. Half of them also had classical spasticity. Age, arm paresis, aphasia, and facial palsy at index stroke were predictors of increased muscle tone poststroke. [ABSTRACT FROM AUTHOR]