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Background and purpose Visuospatial inattention (VSI) and language impairment ( LI) are often present early after stroke and associations with an unfavorable short-term functional outcome have been reported. The purpose of this study was to investigate whether a screening of VSI and LI as indicators of cortical symptoms early after stroke could predict long-term functional outcomes. Methods A consecutive cohort of 375 patients with ischemic stroke was assessed for the occurrence of VSI at a median of 7 days after admission (interquartile range, 1-5 days) using the Star Cancellation Test and for LI (within the first 7 days) with the language item in the Scandinavian Stroke Scale. Seven years later, functional outcomes were assessed by the modified Rankin scale and Frenchay Activities Index in 235 survivors without recurrent stroke. Relationships between baseline predictors and functional outcome at 7 years were analyzed with bivariate correlations and multiple categorical regressions with optimal scaling. Results The regression model significantly explained variance in the modified Rankin scale ( R2 = 0.435, P < 0.001) and identified VSI ( P = 0.001) and neurological deficits ( P < 0.001; Scandinavian Stroke Scale score without the language item) as the significant independent predictors. The model for Frenchay Activities Index was also significant ( R2 = 0.269, P < 0.001) with VSI ( P = 0.035) and neurological deficits ( P < 0.001) as significant independent predictors. Conclusions Visuospatial inattention at acute stroke has an independent impact on long-term functional outcomes. Early recognition may enable targeted rehabilitative interventions. [ABSTRACT FROM AUTHOR]

Background: Acute endotoxinemia elicits an early fibrinolytic response. This study analyzes the effects of the dose and duration of endotoxin infusion on arterial levels of tissue-type plasminogen activator (tPA) and pulmonary, mesenteric and hepatic plasma tPA fluxes.Methods: Pigs were randomized to receive an acute, high-dose (for 6 h, n=13, high ETX) or a prolonged, low-dose (for 18 h, n=18, low ETX) infusion of endotoxin or saline vehicle alone (for 18 h, n=14, control). All animals were fluid resuscitated to maintain a normodynamic circulation. Systemic and regional blood flows were measured and arterial, pulmonary arterial, portal and hepatic venous blood samples were analyzed to calculate regional net fluxes of tPA. Plasma tumor necrosis factor (TNF-alpha) levels were analyzed.Results: Mesenteric tPA release and hepatic uptake increased maximally at 1.5 h in ETX groups related to dose. Maximal mesenteric tPA release [high ETX 612 (138-1185) microg/min/kg, low ETX 72 (32-94) microg/min/kg, median+/-interquartile range] and hepatic tPA uptake [high ETX -1549 (-1134 to -2194) microg/min/kg, low ETX -153 (-105 to -307) microg/min/kg] correlated to TNF-alpha levels. Regional tPA fluxes returned to baseline levels at 6 h in both ETX groups and also remained low during sustained low ETX. No changes were observed in control animals.Conclusions: Endotoxemia induces an early increase in mesenteric tPA release and hepatic tPA uptake related to the severity of endotoxemia. The time patterns of changes in mesenteric and hepatic tPA fluxes are similar in acute high-dose endotoxemia and sustained low-dose endotoxemia. [ABSTRACT FROM AUTHOR]

Background and purpose Genome-wide association ( GWA) studies have identified a few risk loci for ischaemic stroke, but these variants explain only a small part of the genetic contribution to the disease. Coding variants associated with amino acid substitutions or premature termination of protein synthesis could have a large effect on disease risk. We performed an exome array analysis for ischaemic stroke. Methods Patients with ischaemic stroke ( n = 2385) and control subjects ( n = 6077) from three Swedish studies were genotyped with the Illumina HumanOmniExpressExome BeadChip. Single-variant association analysis and gene-based tests were performed of exome variants with minor allele frequency of < 5%. A separate GWA analysis was also performed, based on 700 000 genotyped common markers and subsequent imputation. Results No exome variant or gene was significantly associated with all ischaemic stroke after Bonferroni correction (all P > 1.8 × 10−6 for single-variant and >4.15 × 10−6 for gene-based analysis). The strongest association in single-variant analysis was found for a missense variant in the DNAH11 gene (rs143362381; P = 5.01 × 10−6). In gene-based tests, the strongest association was for the ZBTB20 gene ( P = 7.9 × 10−5). The GWA analysis showed that the sample was homogenous (median genomic inflation factor = 1.006). No genome-wide significant association with overall ischaemic stroke risk was found. However, previously reported associations for the PITX2 and ZFHX3 gene loci with cardioembolic stroke subtype were replicated ( P = 7 × 10−15 and 6 × 10−3). Conclusions This exome array analysis did not identify any single variants or genes reaching the pre-defined significance level for association with ischaemic stroke. Further studies on exome variants should be performed in even larger, well-defined and subtyped samples. [ABSTRACT FROM AUTHOR]

Background and purpose The Coronary Artery Disease Genome-Wide Replication and Meta-Analysis Study (CARDIoGRAM) reported 25 single-nucleotide polymorphisms (SNPs) on 15 chromosomes to be associated with coronary artery disease ( CAD) risk. Because common vascular risk factors are shared between CAD and ischaemic stroke ( IS), these SNPs may also be related to IS overall or one or more of its pathogenetic subtypes. Methods We performed a candidate gene study comprising 3986 patients with IS and 2459 control subjects. The 25 CAD-associated SNPs reported by CARDIoGRAM were examined by allelic association analysis including logistic regression. Weighted and unweighted genetic risk scores ( GRSs) were also compiled and likewise analysed against IS. We furthermore considered the IS main subtypes large-vessel disease ( LVD), small-vessel disease and cardioembolic stroke [according to Trial of Org 10172 in Acute Stroke Treatment ( TOAST)] separately. Results SNP rs4977574 on chromosome 9p21.3 was associated with overall IS [odds ratio ( OR) = 1.12; 95% confidence interval ( CI): 1.04-1.20; P = 0.002] as well as LVD ( OR = 1.36; 95% CI: 1.13-1.64; P = 0.001). No other SNP was significantly associated with IS or any of its main subtypes. Analogously, the GRSs did not show any noticeable effect. Conclusions Besides the previously reported association with SNPs on chromosome 9p21, this study did not detect any significant association between IS and CAD-susceptible genetic variants. Also, GRSs compiled from these variants did not predict IS or any pathogenetic IS subtype, despite a total sample size of 6445 participants. [ABSTRACT FROM AUTHOR]

Objectives There are few studies on long-term outcome after ischemic stroke ( IS) for young and middle-aged stroke sufferers in relation to etiologic subtypes. Here, we report 2-year outcome in the Sahlgrenska Academy Study on Ischemic Stroke ( SAHLSIS). Materials and methods SAHLSIS comprises 600 patients with IS before the age of 70 years. Etiologic subtype of IS was classified according to Trial of Org 10172 in Acute Stroke Treatment ( TOAST). Recurrent vascular events and death were registered using several overlapping methods. Functional outcome was assessed according to the modified Rankin Scale (m RS). Results After 2 years, 55 (9.2%) patients had suffered a recurrent stroke, 15 (2.5%) had a transient ischemic attack ( TIA), 4 (0.7%) had a coronary event, and 24 (4.0%) had died. The number of recurrent stroke, TIA, and death differed significantly between etiologic stroke subtypes. The highest rates were observed in large-vessel disease ( LVD), whereas small-vessel disease and cryptogenic stroke showed the lowest recurrence and mortality rates. LVD was a significant predictor of the composite outcome (recurrent stroke, TIA, coronary event and/or death) independently of cardiovascular risk factors and stroke severity. Stroke subtype also predicted functional outcome 2 years after index stroke, but this association was not retained after adjustment for stroke severity. Conclusions In young and middle-aged stroke patients, stroke subtype predicts recurrent vascular events and/or death 2 years after index stroke independently of cardiovascular risk factors and stroke severity. Thus, it is important to take the etiologic subtype of IS in account when assessing the risk of recurrence both in the clinical setting and in future studies. [ABSTRACT FROM AUTHOR]

Background and purpose: Lateralized and non-lateralized impairments in visual attention have been identified as important components in patients with visuospatial neglect. This study investigated the course of these two phenomena across time in relation to neurological symptoms and functional outcome in a large consecutive and prospective stroke sample. Methods: A total of 375 consecutive stroke patients were divided into three groups (lateralized, non-lateralized or no visual inattention) acutely and 3 months post-stroke using the star cancellation test. Neurological impairments, localization of brain damage, asymmetry in clinical symptoms and functional outcome were assessed. Possible group differences were analysed, and stepwise logistic regressions were performed to examine the relative importance of predictors of functional dependency. Results: Participants with acute lateralized inattention differed ( P ≤ 0.05) from the other two groups by more often exhibiting severe neurological symptoms, functional dependency and persisting visual inattention. The regression analyses selected acute lateralized inattention as an important and independent predictor of functional dependency following right hemisphere damage, but not following left hemisphere damage. Conclusions: The results emphasize the prognostic value of lateralized inattention and the importance of separating lateralized and non-lateralized symptoms of visual inattention at the commencement of rehabilitation. [ABSTRACT FROM AUTHOR]

Aims: Myocardial ischemia remains a significant perioperative complication in coronary artery disease (CAD) patients. We hypothesized that noxious stimuli during major surgery are associated with an acute release of tissue-type plasminogen activator (t-PA) into the coronary circulation, and that this response is reduced by CAD. Methods and results: Two patient groups, with ( n=14) and without ( n=8) CAD, were studied during the initial phase of heart surgery. After retrograde great cardiac vein catheterizations during closed-chest conditions, coronary arterial–venous concentration gradients of t-PA and plasminogen activator inhibitor type-1 (PAI-1) were measured together with coronary blood flow measurements, allowing derivation of coronary net release rates. Pre-surgery atrial pacing, performed to evaluate the influence of increases in heart rate (+40 beats/min) and coronary blood flow (+80 ml/min), did not significantly alter coronary net release of t-PA or PAI-1 in either patient group. Sternotomy induced a prominent increase in coronary net release of both total and active t-PA in the non-CAD group. This response was considerably reduced in the CAD group. Conclusions: This study provides the first analysis of coronary t-PA release during major surgery and demonstrates a deficient local endothelial t-PA release in patients with CAD. This suggests a reduced local fibrinolytic capacity in CAD patients, which may explain the increased risk for coronary thrombosis in this patient group. [ABSTRACT FROM AUTHOR]

Tissue-type plasminogen activator (tPA) is a key mediator of fibrinolysis. Matching of pulmonary perfusion and ventilation is a critical denominator of oxygenation in acute lung injury (ALI). This study investigates pulmonary venoarterial plasma tPA gradients in association with acute ALI induced by bronchoalveolar lavage (BAL) and endotoxinemia (ETX). Twenty-one anaesthetized, ventilated pigs were allocated to control (CTRL, n=5), bronchoalveolar saline lavage (BAL, n=8) or infusion of Escherichia coli endotoxin (ETX, n=8). Total tPA was analyzed in plasma (ELISA calibrated for porcine tPA). The inflammatory response was assessed by TNFa levels (ELISA). All variables were assessed at baseline and 2 h following ALI. Bronchoalveolar lavage and ETX induced similar increases in pulmonary shunt whereas pulmonary vascular resistance was significantly more increased in ETX animals. Cardiac output remained stable in BAL animals but decreased in ETX animals. The pulmonary venoarterial tPA plasma gradient increased in ETX animals, yielding a positive pulmonary net flux of tPA, which was absent in BAL animals. TNFα levels increased in ETX, but not in BAL, animals. A significant correlation was observed between TNFα and tPA plasma levels in ETX animals. All variables remained unchanged in CTRL animals. Plasma changes of tPA levels support a pulmonary release of tPA in early experimental ALI induced by acute ETX but not lavage, and are related to the inflammatory response. Despite increased vascular fibrinolytic capacity in ETX animals, pulmonary dysfunction was not different from BAL animals. The results demonstrate the close relation between inflammation and coagulation in early ALI. [ABSTRACT FROM AUTHOR]

Background: Microcirculatory dysfunction and formation of microthrombi are common in sepsis as a result of a procoagulant state. A profibrinolytic change has however, been reported in early sepsis. This study investigates systemic and regional (pulmonary, preportal, hepatic, renal) fibrinolytic capacity as mirrored by fluxes of tissue-type plasminogen activator (t-PA) in response to acute endotoxemia and volume resuscitation.Methods: Eight anaesthetized, ventilated pigs (24-29 kg) were instrumented for systemic and regional haemodynamic monitoring. Aortic, pulmonary arterial, portal, hepatic and renal venous blood samples were collected. Following baseline stabilisation, Escherichia coli endotoxin was infused for 120 min. During the last 30 min of infusion, volume resuscitation was initiated targeting baseline cardiac output, and animals were observed for 3 h. Total tPA was analyzed by ELISA calibrated for porcine tPA. Net organ tPA fluxes were calculated based on in/outflowing plasma concentrations and regional blood flows.Results: Preportal release and hepatic extraction of tPA was observed at baseline. Pulmonary and renal net fluxes of tPA were not significantly different from zero. Endotoxemia increased plasma tPA levels in all investigated vascular beds. Preportal tPA release increased approximately 10-fold and hepatic extraction increased approximately 12-fold in non-resuscitated acute endotoxemia. No significant changes in pulmonary or renal tPA fluxes were observed. Volume resuscitation restored net fluxes to baseline values while plasma levels remained elevated approximately twofold compared with baseline.Conclusion: Acute endotoxemia induces a prompt, marked and regionally differentiated pro-fibrinolytic response that cannot be discerned based on systemic levels of circulating tPA and that was normalized during volume resuscitation. [ABSTRACT FROM AUTHOR]

Background: Tissue-type plasminogen activator (t-PA) is the key factor in initiating endogenous fibrinolysis in the vascular compartment. Regulated release of t-PA from endothelial stores is rapidly induced by several humoral factors as well as coagulation activation products. The aim of the present study was to test the hypothesis that regional myocardial ischemia induces regulated release of t-PA in the coronary vasculature in vivo . Methods: Healthy anesthetized (pentobarbital) pigs (n= 8) were studied before and after a 10-min left anterior descending region coronary artery occlusion (LAD). Coronary fluxes of lactate, total t-PA antigen (ELISA, detecting both complex bound and free fraction) and active t-PA (functional assay detecting biological free fraction) were determined at 1, 3, 5 and 10 min of reflow. Results: Coronary occlusion induced myocardial lactate production in all animals. Net coronary release of total t-PA, which was 21 ng/min during control, increased rapidly during reflow with a peak after only 1 min (136 ng/min), and returned to baseline within 3 min. Net release of active t-PA mirrored the overall net release response, but fell short of statistical significance. Conclusion: Data indicate a local myocardial profibrinolytic response following regional ischemia, which may serve as a prompt defence against coronary thromboembolic events. [ABSTRACT FROM AUTHOR]

Background: Tissue-type plasminogen activator (t-PA) is an endothelium derived key enzyme in the initiation of endogenous fibrinolysis. Acute regulated release of active t-PA occurs within minutes in response to threatening thrombotic vessel occlusion. The aim of this study was to investigate the impact of surgical stimulation on the kinetics of t-PA release in the coronary vascular bed in the pig. Methods: In anaesthetised pigs (n=16), arterio-venous concentration gradients of t-PA, and plasma flows (retrograde thermodilution) were obtained across the coronary vascular bed before (control) and at 1, 3, 5 and 10 min after sternotomy. Results: At control, no significant coronary net flux (release or uptake) of t-PA was observed, while sternotomy induced a rapid net release of total t-PA (132.6 ng · min-1), with an associated increase in active t-PA (93.6 ng · min-1). This response, evident already after 1 min, showed a peak at 5 min and returned towards baseline levels within 10 min. No concurrent alterations in aortic levels of active t-PA were found and haemodynamic variables were unaltered. Conclusion: The rapidly increasing and transient net coronary release of t-PA after sternotomy suggests that the endothelium actively promotes local endogenous fibrinolysis during surgery. Such events could reflect a dynamic responsiveness to protect the coronary circulation during stress. [ABSTRACT FROM AUTHOR]

Background: Endothelium-derived tissue-type plasminogen activator, t-PA, is the key enzyme in the initiation of endogenous thrombolysis. Plasma levels of t-PA increase in response to sympatho-adrenergic activation. In the mesenteric vascular bed an increased norepinephrine spillover has been observed during positive end-expiratory pressure ventilation, PEEP. This experimental study examines the effects of PEEP-induced alterations on regional release rates and systemic levels of t-PA in vivo.Methods: The protocol included measurements of arterio-venous concentration gradients of t-PA and the respective plasma flow across the pulmonary, coronary, hepatic and preportal vascular beds, in pigs, during zero-PEEP and at 2, 4 and 10 min after the application of a PEEP of 10 cm H2O. Both total plasma t-PA antigen (ELISA with a porcine t-PA standard) and active t-PA (spectrophotometric functional assay) were determined.Results: During zero-PEEP, a high preportal basal net release and hepatic net uptake of total t-PA was observed. With PEEP, the magnitude of the preportal net release of t-PA was markedly enhanced (+24+/-5%), as was hepatic net uptake (+21+/-8%), simultaneously to a significant decrease in liver plasma flow (-30+/-2%). PEEP-induced alterations in active t-PA mirrored those observed in total t-PA. No significant net fluxes of total or active t-PA were observed across the coronary or the pulmonary vascular beds.Conclusions: Clinically used levels of PEEP induce increases in net release of endothelially derived t-PA within preportal organs. The application of PEEP is associated with increased systemic levels of total and active t-PA, in spite of a simultaneous increase in hepatic net uptake, indicating that the preportal vascular bed can not account for the systemic t-PA response. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate whether we could replicate a recent finding of an association between genetic variants on chromosome 9p21 and the ischaemic stroke (IS) subtype large-vessel disease (LVD). The Sahlgrenska Academy Study on Ischemic Stroke comprises 844 patients with IS, who suffered IS before reaching the age of 70, and 668 healthy controls. IS subtype was defined according to the TOAST criteria, and 111 patients were categorized as LVD. Seven single-nucleotide polymorphisms (SNPs) on 9p21 were analyzed. Functional outcome was assessed 3 months after IS using the modified Rankin scale. The SNP rs7857345 showed a significant association with the subtype LVD independent of traditional vascular risk factors. In addition, an association between rs7857345 and functional outcome after LVD was observed. In this relatively young sample of patients with IS, genetic variation on 9p21 is associated with LVD. [ABSTRACT FROM AUTHOR]

Background and purpose: The aim of this study was to investigate whether genetic variation at the third complement component ( C3) locus is associated with ischaemic stroke (IS). Methods: The Sahlgrenska Academy Study on Ischaemic Stroke comprises 844 patients with IS, and 668 healthy controls. Sixteen SNPs were analyzed. Results: Two SNPs, rs2277984 and rs3745565, showed a significant association with overall IS. The SNP rs2277984 also showed association with the IS subtype cryptogenic stroke. These associations were independent of hypertension, diabetes, and smoking. The independent association between rs3745565 and overall IS withstands correction for multiple testing. Conclusion: In this sample of patients with IS, genetic variation in C3 is associated with IS. [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., (© 2022 The Authors. Acta Neurologica Scandinavica published by John Wiley & Sons Ltd.)

Objectives: Motor problems are well-described neurological deficits that occur commonly after an infratentorial ischemic stroke. However, the brain stem and cerebellum are also part of the neural interconnections responsible for cognition, emotions, and behavioral responses. We lack studies on long-term cognitive outcomes and patient employment after an infratentorial stroke. In the present study, we described and compared long-term poststroke cognitive outcomes and employment between patients that experienced infratentorial and supratentorial ischemic strokes., Materials and Methods: We included consecutive patients that experienced an acute ischemic stroke at ≤58 years of age. Patients were classified according to the stroke location. At seven years poststroke, surviving participants were assessed for neurological deficits (National Institutes of Health Stroke Scale [NIHSS]), functional outcome (modified Rankin Scale [mRS]), cognitive function Barrow Neurological Institute Screen (BNIS), and employment., Results: Among 141 participants, 25 (18%) had infratentorial and 116 (82%) had supratentorial strokes. At the 7-year poststroke follow-up, there was no significant difference in BNIS total scores; with a median of 43 (IQR 40.5-46) and 41 (IQR 38-46) in the infratentorial and supratentorial groups, respectively. This result indicated that cognitive dysfunction occurred frequently in both groups. Similar employment rates were observed in the infratentorial (48%) and supratentorial (55%) groups. Both groups had a median NIHSS score of 0 and a median mRS score of 2 at the 7-year follow-up., Conclusion: Patients who survived an infratentorial or supratentorial ischemic stroke had similar rates of long-term cognitive dysfunction and difficulties in returning and/or remaining at work., (© 2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

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., (© 2020 The Authors. Acta Neurologica Scandinavica published by John Wiley & Sons Ltd.)

Objectives: Vascular endothelial growth factor (VEGF) acts in angiogenesis and neuroprotection, although the beneficial effects on experimental ischemic stroke (IS) have not been replicated in clinical studies. We investigated serum VEGF (s-VEGF) in the acute stage (baseline) and 3 months post-stroke in relation to stroke severity and functional outcome., Methods: The s-VEGF and serum high-sensitivity C-reactive protein (hs-CRP) concentrations were measured in patients enrolled in the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS) at the acute time-point (median 4 days, N = 492, 36% female; mean age, 57 years) and at 3 months post-stroke (N = 469). Baseline stroke severity was classified according to the National Institutes of Health Stroke Scale (NIHSS), and functional outcomes (3 months and 2 years) were evaluated using the modified Rankin Scale (mRS), dichotomized into good (mRS 0-2), and poor (mRS 3-6) outcomes. Multivariable logistic regression analyses were adjusted for covariates., Results: The baseline s-VEGF did not correlate with stroke severity but correlated moderately with hs-CRP (r = .17, P < .001). The baseline s-VEGF was 39.8% higher in total anterior cerebral infarctions than in lacunar cerebral infarctions. In binary logistic regression analysis, associations with 3-month functional outcome were non-significant. However, an association between the 3-month s-VEGF and poor 2-year outcome withstood adjustments for age, sex, cardiovascular covariates, and stroke severity (per 10-fold increase in s-VEGF, odds ratio [OR], 2.56, 95% confidence interval [CI] 1.12-5.82) or hs-CRP (OR 2.53, CI 1.15-5.55)., Conclusions: High 3-month s-VEGF is independently associated with poor 2-year functional outcome but not with 3-month outcome., (© 2020 The Authors. Acta Neurologica Scandinavica published by John Wiley & Sons Ltd.)

Objective: Lateralized inattention is a typical sign of neglect and related to poor functional outcome. Knowledge of the long-term course of this phenomenon is limited. The purpose of this study was to investigate presence and predictors for signs of lateralized inattention 7 years after stroke., Methods: From a cohort of acute ischemic stroke patients, aged 18-69 years (n = 297), a consecutive series of 188 survivors without recurrent stroke at follow-up 7 years later were included. Within the first week after stroke onset, stroke severity was assessed according to the Scandinavian Stroke Scale. Target omissions, asymmetry of omissions, and perceptual speed according to Star- and Letter Cancellation Tests were also assessed. Presence of lateralized inattention at the 7-year follow-up was investigated with the Star- and Letter Cancellation Tests and with the neglect item in the National Institutes of Health Stroke Scale., Results: At the follow-up, 22 (11.7%) participants had lateralized inattention and the multivariable regression showed that independent significant baseline predictors were total omissions in target cancellations (P < .001) and inferior baseline performance on visual processing speed (P = .008)., Conclusion: About one of ten individuals exhibited signs of lateralized inattention 7 years after stroke. Baseline performance in perceptual processing speed and target omissions independently predicted presence of late signs of lateralized inattention. This is the first time processing speed is recognized as a significant predictor of lateralized inattention several years after the stroke incidence, indicating that the longitudinal course of processing speed following stroke is a critical subject for future research., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

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., (© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

To study haematological effects of emotional stress, blood samples were obtained from 29 healthy, normotensive, non-smoking males aged 20-34 years before, during and after 10 min of mental arithmetic. There were significant increases in peripheral blood cell count, haemoglobin concentration, and haematocrit in response to mental stress. Parallel to these changes significant increases in heart rate, and systolic and diastolic blood pressure were observed. The relative increments of leucocyte (8%) and platelet (3.5%) count were significantly higher than the increase in haemoglobin concentration (2%). There was a significant positive correlation between the blood pressure increase and the mobilization of leucocytes, whereas the increase in erythrocyte count, haemoglobin concentration, and haematocrit showed significant positive correlations with heart rate reactivity. It is concluded that mental stress causes an increase in leucocyte and platelet count that could not solely be accounted for by the concurrent haemoconcentration.