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Behavioural changes after stroke might be explained by social cognition impairments. The aim of the present study was to investigate whether performances on social cognition tests (including emotion recognition, Theory of Mind (ToM), empathy and behaviour regulation) were associated with behavioural deficits (as measured by proxy ratings) in a group of patients with relatively mild stroke. Prospective cohort study in which 119 patients underwent neuropsychological assessment with tests for social cognition (emotion recognition, ToM, empathy, and behaviour regulation) 3-4 years post stroke. Test scores were compared with scores of 50 healthy controls. Behavioural problems were assessed with the Dysexecutive Questionnaire (DEX) self rating and proxy rating scales. Pearson correlations were used to determine the relationship between the social cognition measures and DEX scores. Patients performed significantly worse on emotion recognition, ToM and behaviour regulation tests than controls. Mean DEX-self score did not differ significantly from the mean DEX-proxy score. DEX-proxy ratings correlated with tests for emotion recognition, empathy, and behavioural regulation (lower scores on these items were associated with more problems on the DEX-proxy scale). Social cognition impairments are present in the long term after stroke, even in a group of mildly affected stroke patients. Most of these impairments also turned out to be associated with a broad range of behavioural problems as rated by proxies of the patients. This strengthens the proposal that social cognition impairments are part of the underlying mechanism of behavioural change. Since tests for social cognition can be administered in an early stage, this would allow for timely identification of patients at risk for behavioural problems in the long term.

End-of-life decisions after stroke should be guided by accurate estimates of the patient's prognosis. We assessed the accuracy of physicians' estimates regarding mortality, functional outcome, and quality of life in patients with severe stroke. Treating physicians predicted mortality, functional outcome (modified Rankin scale (mRS)), and quality of life (visual analogue scale (VAS)) at six months in patients with major disabling stroke who had a Barthel Index ≤6 (of 20) at day four. Unfavorable functional outcome was defined as mRS >3, non-satisfactory quality of life as VAS <60. Patients were followed-up at six months after stroke. We compared physicians' estimates with actual outcomes. Sixty patients were included, with a mean age of 72 years. Of fifteen patients who were predicted to die, one actually survived at six months (positive predictive value (PPV), 0.93; 95% CI, 0.66-0.99). Of thirty patients who survived, one was predicted to die (false positive rate (FPR), 0.03; 95%CI 0.00-0.20). Of forty-six patients who were predicted to have an unfavorable outcome, four had a favorable outcome (PPV, 0.93; 95% CI, 0.81-0.98; FPR, 0.30; 95% CI; 0.08-0.65). Prediction of non-satisfactory quality of life was less accurate (PPV, 0.63; 95% CI, 0.26-0.90; FPR, 0.18; 95% CI 0.05-0.44). In patients with severe stroke, treating physicians' estimation of the risk of mortality or unfavorable functional outcome at six months is relatively inaccurate. Prediction of quality of life is even more imprecise.

A genomewide association study indicates that a locus on chromosome 12 confers susceptibility (with a hazard ratio of approximately 1.3) to ischemic stroke. This locus is close to NINJ2, which encodes a cell adhesion molecule that shows increased expression on glia in response to nerve injury. A second gene near this locus influences blood pressure and hypertension. A genomewide association study indicates that a locus on chromosome 12 confers susceptibility (with a hazard ratio of approximately 1.3) to ischemic stroke. This locus is close to NINJ2, which encodes a cell adhesion molecule that shows increased expression on glia in response to nerve injury. Stroke is the leading neurologic cause of death and disability. 1 Twin and familial aggregation studies suggest that the risk of stroke has a substantial genetic component, 2 – 4 but the genes underlying this risk in the general population remain undetermined. Studies of candidate genes or studies that use classical linkage approaches have yielded inconsistent findings. 5 Genomewide association studies have uncovered previously unsuspected common variants underlying the risk of complex diseases such as diabetes 6 and coronary disease. 7 , 8 Two previous genomewide association studies of stroke were limited by a case–control design that is more susceptible to survival and selection biases than the . . .

Background Patients with severe stroke often do not have the capacity to participate in discussions on treatment restrictions because of a reduced level of consciousness, aphasia, or another cognitive disorder. We assessed the role of advance directives and proxy opinions in the decision-making process of incapacitated patients. Methods Sixty patients with severe functional dependence (Barthel Index ≤6) at day four after ischemic stroke or intracerebral hemorrhage were included in a prospective two-center cohort study. The decision-making process with respect to treatment restrictions was assessed by means of a semi-structured questionnaire administered to the treating physician at the day of inclusion. Results Forty-nine patients (82%) did not have the capacity to participate in the decision-making process. In eight patients, there was no discussion on treatment restrictions and full care was installed. In 41 patients, the decision whether to install treatment restrictions was discussed with proxies. One patient had a written advance directive. In the remaining 40 patients, proxies based their opinion on previously expressed wishes of the patient (18 patients) or advised in the best interest of the patient (22 patients). In 36 of 41 patients, treatment restrictions were installed after agreement between physician and proxy. At six months, 23 of 49 patients had survived. In only three of them the decision on treatment restrictions was based on previously expressed wishes. Remarkably, two of these survivors could not recall any of their alleged previously expressed wishes. Conclusions Treatment restrictions were installed in the majority of incapacitated patients after stroke. Proxy opinions frequently served as the best way to respect the patients’ autonomy, but their accuracy remains unclear.

ObjectiveA substantial part of non-traumatic intracerebral haemorrhages (ICH) arises from a macrovascular cause, but there is little guidance on selection of patients for additional diagnostic work-up. We aimed to develop and externally validate a model for predicting the probability of a macrovascular cause in patients with non-traumatic ICH.MethodsThe DIagnostic AngioGRAphy to find vascular Malformations (DIAGRAM) study (n=298; 69 macrovascular cause; 23%) is a prospective, multicentre study assessing yield and accuracy of CT angiography (CTA), MRI/ magnetic resonance angiography (MRA) and intra-arterial catheter angiography in diagnosing macrovascular causes in patients with non-traumatic ICH. We considered prespecified patient and ICH characteristics in multivariable logistic regression analyses as predictors for a macrovascular cause. We combined independent predictors in a model, which we validated in an external cohort of 173 patients with ICH (78 macrovascular cause, 45%).ResultsIndependent predictors were younger age, lobar or posterior fossa (vs deep) location of ICH, and absence of small vessel disease (SVD). A model that combined these predictors showed good performance in the development data (c-statistic 0.83; 95% CI 0.78 to 0.88) and moderate performance in external validation (c-statistic 0.66; 95% CI 0.58 to 0.74). When CTA results were added, the c-statistic was excellent (0.91; 95% CI 0.88 to 0.94) and good after external validation (0.88; 95% CI 0.83 to 0.94). Predicted probabilities varied from 1% in patients aged 51–70 years with deep ICH and SVD, to more than 50% in patients aged 18–50 years with lobar or posterior fossa ICH without SVD.ConclusionThe DIAGRAM scores help to predict the probability of a macrovascular cause in patients with non-traumatic ICH based on age, ICH location, SVD and CTA.

Objectives The few voxel-wise lesion-symptom mapping (VLSM) studies aimed at identifying the anatomy of executive function are limited by the absence of a model and by small populations. Using Trail Making Test (TMT) and verbal fluency and a model of their architectures, our objective was to identify the key structures underlying two major executive processes, set-shifting and strategic word search. Methods We applied a validated VLSM analysis to harmonized cognitive and imaging data from 2009 ischemic stroke patients as a part of the Meta VCI Map consortium. All contrast analyses used an adjusted threshold with 2000 Freedman–Lane permutations ( p  ≤ 0.05). Results The TMT parts A and B were associated with structures involved in visual-spatial processing, the motor system, the frontal lobes, and their subcortical connections. Set-shifting depended on the left dorsomedial frontal region. Both semantic and phonemic fluency tests depended on verbal output abilities and processing speed with similar slopes in different languages. The strategic search process depended on Broca’s area, F2 and related tracts, temporal and deep regions. Lastly, the lesion map of set-shifting did not overlap with those of strategic word search processes. Interpretation Our results identify the anatomical substrates of two main executive processes, revealing that they represent only a specific subpart of previously reported structures. Finally, our results indicate that executive functions depend on several specific, anatomically separable executive processes mainly operating in various parts of the frontal lobes.

BackgroundLimited data exists on cognitive recovery in young stroke patients. We aimed to investigate the longitudinal course of cognitive performance during the first year after stroke at young age and identify predictors for cognitive recovery.MethodsWe conducted a multicentre prospective cohort study between 2013 and 2021, enrolling patients aged 18–49 years with first-ever ischaemic stroke. Cognitive assessments were performed within 6 months and after 1 year following the index event, covering seven cognitive domains. Composite Z-scores using normative data determined cognitive impairment (Z-score<−1.5). A Reliable Change Index (RCI) assessed cognitive recovery (RCI>1.96) or decline (RCI<−1.96).Results393 patients (median age 44.3 years, IQR 38.4–47.2) completed cognitive assessments with a median time interval of 403 days (IQR 364–474) between assessments. Based on RCI, a similar proportion of patients showed improvement and decline in each cognitive domain, while the majority exhibited no cognitive change. Among cognitively impaired patients at baseline, improvements were observed in processing speed (23.1%), visuoconstruction (40.1%) and executive functioning (20.0%). Younger age was associated with better cognitive recovery in visuoconstruction, and larger lesion volume was related to cognitive recovery in processing speed. No other predictors for cognitive recovery were identified.ConclusionsCognitive impairment remains prevalent in young stroke even 1 year after the event. Most patients showed no cognitive change, however, recovery may have occurred in the early weeks after stroke, which was not assessed in our study. Among initially cognitively impaired patients, cognitive recovery is observed in processing speed, visuoconstruction and executive functioning. It is still not possible to predict cognitive recovery in individual patients.

Due to their young age young stroke survivors have to cope with a dramatic impact on their life for the decades to come. We investigated the sex-specific very long-term functional outcome after transient ischemic attack (TIA) and ischemic stroke (IS) in adults aged 18–50 years. This study is part of a cohort study among 619 first-ever young ischemic stroke patients, admitted to our department between January 1, 1980 and November 1, 2010. Functional outcome was assessed during follow-up in 2009–2011 and in 2014–2015 with the modified Rankin Scale (mRS) and instrumental Activities of Daily Living scale (iADL). Risk factors for a poor functional outcome (mRS > 2 and iADL < 8) were calculated by logistic regression analysis. After a mean follow-up of 13.9 (SD 8.2) years, 24.5 % of TIA patients and 44.7 % of IS patients had a poor functional outcome (mRS > 2). When assessing the survivors, 15.2 % of TIA patients and 22.9 % of IS patients had a poor outcome as assessed by iADL. The strongest baseline predictors of poor outcome were female sex (OR 2.7, 95 % CI 1.5–5.0) and baseline NIHSS (OR 1.1, 95 % CI 1.1–1.2 per point increase). In conclusion, 14 years after an ischemic cerebrovascular event in young adults, one out of five IS survivors and one out of ten TIA survivors is still dependent in daily life, with a two to threefold higher risk of a poor outcome in women. This includes a period of life, during which important decisions regarding work and family life have to be made.

Background: Infections are a common and serious threat to patients with acute ischemic stroke. The aim of this study was to assess the effect of infection on mortality and functional outcome at discharge and at 1 year. Methods: From a consecutive cohort study in 11 centers, the Netherlands Stroke Survey, we selected 521 patients with ischemic stroke admitted to hospital within 48 h of onset. Stroke-associated infection was defined as infection occurring within 7 days after admission. Poor outcome (modified Rankin score >2) was recorded at discharge and at 1 year. Results: Stroke-associated infection occurred in 78 patients (15%); 39 of these (7.5%) had pneumonia and 23 (4.4%) had urinary tract infection. Overall, 276 patients (53%) had a poor outcome at 1 year. Poor outcome was recorded in 69 patients with stroke-associated infection (88%), and 37 of the 78 patients with stroke-associated infection (47%) had died at 1 year. After adjustment for confounders, stroke-associated infection was associated with poor outcome at discharge [odds ratio (OR) 2.6, 95% confidence interval (CI) 1.0–6.7] and at 1 year (OR 3.8, 95% CI 1.8–8.9). Pneumonia had a stronger association with poor outcome at 1 year (OR 10, 95% CI 2.2–46). Conclusions: This study suggests that stroke-associated infection, in particular pneumonia, is independently associated with poor functional outcome after ischemic stroke.

Post-stroke cognitive impairment (PSCI) occurs in approximately half of people in the first year after stroke. Infarct location is a potential determinant of PSCI, but a comprehensive map of strategic infarct locations predictive of PSCI is unavailable. We aimed to identify infarct locations most strongly predictive of PSCI after acute ischaemic stroke and use this information to develop a prediction model. In this large-scale multicohort lesion-symptom mapping study, we pooled and harmonised individual patient data from 12 cohorts through the Meta-analyses on Strategic Lesion Locations for Vascular Cognitive Impairment using Lesion-Symptom Mapping (Meta VCI Map) consortium. The identified cohorts (as of Jan 1, 2019) comprised patients with acute symptomatic infarcts on CT or MRI (with available infarct segmentations) and a cognitive assessment up to 15 months after acute ischaemic stroke onset. PSCI was defined as performance lower than the fifth percentile of local normative data, on at least one cognitive domain on a multidomain neuropsychological assessment or on the Montreal Cognitive Assessment. Voxel-based lesion-symptom mapping (VLSM) was used to calculate voxel-wise odds ratios (ORs) for PSCI that were mapped onto a three-dimensional brain template to visualise PSCI risk per location. For the prediction model of PSCI risk, a location impact score on a 5-point scale was derived from the VLSM results on the basis of the mean voxel-wise coefficient (ln[OR]) within each patient's infarct. We did combined internal–external validation by leave-one-cohort-out cross-validation for all 12 cohorts using logistic regression. Predictive performance of a univariable model with only the location impact score was compared with a multivariable model with addition of other clinical PSCI predictors (age, sex, education, time interval between stroke onset and cognitive assessment, history of stroke, and total infarct volume). Testing of visual ratings was done by three clinicians, and accuracy, inter-rater reliability, and intra-rater reliability were assessed with Cohen's weighted kappa. In our sample of 2950 patients (mean age 66·8 years [SD 11·6]; 1157 [39·2%] women), 1286 (43·6%) had PSCI. We achieved high lesion coverage of the brain in our analyses (86·9%). Infarcts in the left frontotemporal lobes, left thalamus, and right parietal lobe were strongly associated with PSCI (after false discovery rate correction, q<0·01; voxel-wise ORs >20). On cross-validation, the location impact score showed good correspondence, based on visual assessment of goodness of fit, between predicted and observed risk of PSCI across cohorts after adjusting for cohort-specific PSCI occurrence. Cross-validations showed that the location impact score by itself had similar performance to the combined model with other PSCI predictors, while allowing for easy visual assessment. Therefore the univariable model with only the location impact score was selected as the final model. Correspondence between visual ratings and actual location impact score (Cohen's weighted kappa: range 0·88–0·92), inter-rater agreement (0·85–0·87), and intra-rater agreement (for a single rater, 0·95) were all high. To the best of our knowledge, this study provides the first comprehensive map of strategic infarct locations associated with risk of PSCI. A location impact score was derived from this map that robustly predicted PSCI across cohorts. Furthermore, we developed a quick and reliable visual rating scale that might in the future be applied by clinicians to identify individual patients at risk of PSCI. The Netherlands Organisation for Health Research and Development.