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Rationale Despite several large clinical trials assessing blood pressure lowering in acute stroke, equipoise remains particularly for ischemic stroke. The “Blood pressure in Acute Stroke Collaboration” commenced in the mid-1990s focussing on systematic reviews and meta-analysis of blood pressure lowering in acute stroke. From the start, Blood pressure in Acute Stroke Collaboration planned to assess safety and efficacy of blood pressure lowering in acute stroke using individual patient data. Aims To determine the optimal management of blood pressure in patients with acute stroke, including both intracerebral hemorrhage and ischemic stroke. Secondary aims are to assess which clinical and therapeutic factors may alter the optimal management of high blood pressure in patients with acute stroke and to assess the effect of vasoactive treatments on hemodynamic variables. Methods and design Individual patient data from randomized controlled trials of blood pressure management in participants with ischemic stroke and/or intracerebral hemorrhage enrolled during the ultra-acute (pre-hospital), hyper-acute (<6 h), acute (<48 h), and sub-acute (<168 h) phases of stroke. Study outcomes The primary effect variable will be functional outcome defined by the ordinal distribution of the modified Rankin Scale; analyses will also be carried out in pre-specified subgroups to assess the modifying effects of stroke-related and pre-stroke patient characteristics. Key secondary variables will include clinical, hemodynamic and neuroradiological variables; safety variables will comprise death and serious adverse events. Discussion Study questions will be addressed in stages, according to the protocol, before integrating these into a final overreaching analysis. We invite eligible trials to join the collaboration. [ABSTRACT FROM AUTHOR]

Background and purpose: Hydration status at the time of stroke has been acknowledged as an important determinant in early stroke recovery. However, the diagnosis of dehydration, or more accurately, a volume-contracted state, at the time of stroke is challenging since there are currently no consensus diagnostic criteria. In this systematic review, we gather the available evidence about diagnosis and treatment of dehydration after stroke.Methods: Studies of hospitalized ischemic stroke patients that reported rates of dehydration from January 1997 to March 2017 were screened for inclusion via a systematic search of PubMed, CINAHL, Cochrane, and Scopus using keywords hydration, dehydration, hemodilution, viscosity, volume status, and thirst.Results: Twenty-five studies of 8699 acute stroke patients were included. Nineteen studies reported on the diagnostic approach to dehydration. Findings are synthesized into four main categories of available research including studies that specify: (1) biological mechanisms using animal models to investigate the relationship between dehydration and stroke; (2) measures of dehydration in the acute human stroke population; (3) rehydration therapies after stroke; and (4) outcomes after stroke in dehydrated patients.Conclusions: We found considerable variation in terminology specific to hydration status, diagnostic approach to dehydration, and few prospective studies of treatment strategies with varying results. This review supports the need for consensus development of operational diagnostic criteria, standardization of language, and the opportunity for prospective study of rehydration strategies to impact outcome after stroke. [ABSTRACT FROM AUTHOR]

Background Communication between professionals, patients and families about palliative and end-of-life care after stroke is complex and there is a need for educational resources in this area. Methods To explore the key learning needs of healthcare professionals, a multidisciplinary, expert group developed a short electronic survey with open and closed questions, and then distributed it to six UK multiprofessional networks and two groups of local clinicians. Results A total of 599 healthcare professionals responded. Educational topics that were either definitely or probably needed were: ensuring consistent messages to families and patients (88%); resolving confiicts among family members (83%); handling unrealistic expectations (88%); involving families in discussions without them feeling responsible for decisions (82%); discussion of prognostic uncertainties (79%); likely mode of death (72%); and oral feeding for 'comfort' in patients at risk of aspiration (71%). The free-text responses (n = 489) and 82 'memorable' cases identified similar themes. Conclusion Key topics of unmet need for education in end-of-life care in stroke have been identified and these have infiuenced the content of an open access, web-based educational resource. [ABSTRACT FROM AUTHOR]

Background and Purpose: MLC601 has been shown in preclinical studies to enhance neurorestorative mechanisms after stroke. The aim of this post hoc analysis was to assess whether combining MLC601 and rehabilitation has an effect on improving functional outcomes after stroke. Methods: Data from the CHInese Medicine NeuroAiD Efficacy on Stroke (CHIMES) and CHIMES-Extension (CHIMES-E) studies were analyzed. CHIMES-E was a 24-month follow-up study of subjects included in CHIMES, a multi-centre, double-blind placebo-controlled trial which randomized subjects with acute ischemic stroke, to either MLC601 or placebo for 3 months in addition to standard stroke treatment and rehabilitation. Subjects were stratified according to whether they received or did not receive persistent rehabilitation up to month (M)3 (non- randomized allocation) and by treatment group. The modified Rankin Scale (mRS) and Barthel Index were assessed at month (M) 3, M6, M12, M18, and M24. Results: Of 880 subjects in CHIMES-E, data on rehabilitation at M3 were available in 807 (91.7%, mean age 61.8 ± 11.3 years, 36% female). After adjusting for prognostic factors of poor outcome (age, sex, pre-stroke mRS, baseline National Institute of Health Stroke Scale, and stroke onset-to-study-treatment time), subjects who received persistent rehabilitation showed consistently higher treatment effect in favor of MLC601 for all time points on mRS 0–1 dichotomy analysis (ORs 1.85 at M3, 2.18 at M6, 2.42 at M12, 1.94 at M18, 1.87 at M24), mRS ordinal analysis (ORs 1.37 at M3, 1.40 at M6, 1.53 at M12, 1.50 at M18, 1.38 at M24), and BI ≥95 dichotomy analysis (ORs 1.39 at M3, 1.95 at M6, 1.56 at M12, 1.56 at M18, 1.46 at M24) compared to those who did not receive persistent rehabilitation. Conclusions: More subjects on MLC601 improved to functional independence compared to placebo among subjects receiving persistent rehabilitation up to M3. The larger treatment effect of MLC601 was sustained over 2 years which supports the hypothesis that MLC601 combined with rehabilitation might have beneficial and sustained effects on neuro-repair processes after stroke. There is a need for more data on the effect of combining rehabilitation programs with stroke recovery treatments. [ABSTRACT FROM AUTHOR]

Background: This study assessed the incidence and predictors of short-term stroke recurrence in ischemic stroke patients with active cancer, and elucidated whether cancer-associated hypercoagulation is related to early recurrent stroke. Methods: We retrospectively enrolled acute ischemic stroke patients with active cancer admitted to our hospital between 2006 and 2017. Active cancer was defined as diagnosis or treatment for any cancer within 12 months before stroke onset, known recurrent cancer or metastatic disease. The primary clinical outcome was recurrent ischemic stroke within 30 days. Results: One hundred ten acute ischemic stroke patients with active cancer (73 men, age 71.3 ± 10.1 years) were enrolled. Of those, recurrent stroke occurred in 12 patients (11%). When patients with and without recurrent stroke were compared, it was found that those with recurrent stroke had a higher incidence of pancreatic cancer (33 vs. 10%), systemic metastasis (75 vs. 39%), multiple vascular territory infarctions (MVTI; 83 vs. 40%), and higher -D-dimer levels (16.9 vs. 2.9 µg/mL). Multivariable logistic regression analysis showed that each factor mentioned above was not significantly associated with stroke recurrence independently, but high D-dimer (hDD) levels (≥10.4 µg/mL) and MVTI together were significantly associated with stroke recurrence (OR 6.20, 95% CI 1.42–30.7, p = 0.015). Conclusions: Ischemic stroke patients with active cancer faced a high risk of early recurrent stroke. The concurrence of hDD levels (≥10.4 µg/mL) and MVTI was an independent predictor of early recurrent stroke in active cancer patients. Our findings suggest that cancer-associated hypercoagulation increases the early recurrent stroke risk. [ABSTRACT FROM AUTHOR]

To assess hyperacute focal cerebral ischemia in rats on 3.0-Tesla diffusion-weighted imaging (DWI), we developed a novel voxel-wise lesion segmentation technique that overcomes intra- and inter-subject variation in apparent diffusion coefficient (ADC) distribution. Our novel technique involves the following: (1) intensity normalization including determination of the optimal type of region of interest (ROI) and its intra- and inter-subject validation, (2) verification of focal cerebral ischemic lesions at 1 h with gross and high-magnification light microscopy of hematoxylin-eosin (H&E) pathology, (3) voxel-wise segmentation on ADC with various thresholds, and (4) calculation of dice indices (DIs) to compare focal cerebral ischemic lesions at 1 h defined by ADC and matching H&E pathology. The best coefficient of variation was the mode of the left hemisphere after normalization using whole left hemispheric ROI, which showed lower intra- (2.54 ± 0.72%) and inter-subject (2.67 ± 0.70%) values than the original. Focal ischemic lesion at 1 h after middle cerebral artery occlusion (MCAO) was confirmed on both gross and microscopic H&E pathology. The 83 relative threshold of normalized ADC showed the highest mean DI (DI = 0.820 ± 0.075). We could evaluate hyperacute ischemic lesions at 1 h more reliably on 3-Tesla DWI in rat brains. [ABSTRACT FROM AUTHOR]

Overactivation of purinergic receptors during cerebral ischemia results in a massive release of neurotransmitters, including adenosine triphosphate (ATP), to the extracellular space which leads to cell death. Some hypothetical pathways of ATP release are large ion channels, such as calcium homeostasis modulator 1 (CALHM1), a membrane ion channel that can permeate ATP. Since this transmitter contributes to postischemic brain damage, we hypothesized that CALHM1 activation may be a relevant target to attenuate stroke injury. Here, we analyzed the contribution of CALHM1 to postanoxic depolarization after ischemia in cultured neurons and in cortical slices. We observed that the onset of postanoxic currents in neurons in those preparations was delayed after its blockade with ruthenium red or silencing of Calhm1 gene by short hairpin RNA, as well as in slices from CALHM1 knockout mice. Subsequently, we used transient middle cerebral artery occlusion and found that ruthenium red, a blocker of CALHM1, or the lack of CALHM1, substantially attenuated the motor symptoms and reduced significantly the infarct volume. These results show that CALHM1 channels mediate postanoxic depolarization in neurons and brain damage after ischemia. Therefore, targeting CALHM1 may have a high therapeutic potential for treating brain damage after ischemia. [ABSTRACT FROM AUTHOR]

The decision to perform decompressive hemicraniectomy (DHC) by default in malignant hemispheric stroke (MHS) remains controversial. Even under ideal conditions, DHC usually results in moderate to severe disability. The present study for the first time uses neuroimaging to identify independent outcome predictors in a prospective cohort of 96 MHS patients undergoing DHC. The primary outcome was functional status according to the modified Rankin Scale (mRS) at 12 months and categorized as favorable (mRS 0–3) or unfavorable (mRS 4–6). At 12 months, 19 patients (20%) reached favorable and 77 patients (80%) unfavorable outcome. The overall mean infarct volume was 328 ± 114 ml. Multivariable logistic regression identified age per year (OR 1.14, 95% CI 1.04–1.24; p = 0.005), infarct volume per cm3 (OR 1.012, 95% CI 1.003–1.022; p = 0.013), thalamic involvement (OR 8.65, 95% CI 1.04–72.15; p = 0.046) and postoperative pneumonia (OR 5.52, 95% CI 1.03–29.57; p = 0.046) as independent outcome predictors, which was confirmed by multivariable ordinal regression for age (p = 0.004) and infarct volume (p = 0.015). The infarct volume threshold for reasonable prediction of unfavorable outcome in our patients was 270 cm3, which in the future may help prognostication and development of clinical trials on DHC and outcome in MHS. [ABSTRACT FROM AUTHOR]

This document presents the consensus recommendations of the Hellenic Stroke Organization which can be of assistance to the treating stroke physicians. [ABSTRACT FROM AUTHOR]

Stroke-associated pneumonia is a frequent complication after stroke associated with poor outcome. Dysphagia is a known risk factor for stroke-associated pneumonia but accumulating evidence suggests that stroke induces an immunodepressive state increasing susceptibility for stroke-associated pneumonia. We aimed to confirm that stroke-induced immunodepression syndrome is associated with stroke-associated pneumonia independently from dysphagia by investigating the predictive properties of monocytic HLA-DR expression as a marker of immunodepression as well as biomarkers for inflammation (interleukin-6) and infection (lipopolysaccharide-binding protein). This was a prospective, multicenter study with 11 study sites in Germany and Spain, including 486 patients with acute ischemic stroke. Daily screening for stroke-associated pneumonia, dysphagia and biomarkers was performed. Frequency of stroke-associated pneumonia was 5.2%. Dysphagia and decreased monocytic HLA-DR were independent predictors for stroke-associated pneumonia in multivariable regression analysis. Proportion of pneumonia ranged between 0.9% in the higher monocytic HLA-DR quartile (≥21,876 mAb/cell) and 8.5% in the lower quartile (≤12,369 mAb/cell). In the presence of dysphagia, proportion of pneumonia increased to 5.9% and 18.8%, respectively. Patients without dysphagia and normal monocytic HLA-DR expression had no stroke-associated pneumonia risk. We demonstrate that dysphagia and stroke-induced immunodepression syndrome are independent risk factors for stroke-associated pneumonia. Screening for immunodepression and dysphagia might be useful for identifying patients at high risk for stroke-associated pneumonia. [ABSTRACT FROM AUTHOR]

Background: This study aims to investigate the effectiveness of mechanical thrombectomy compared with thrombolytic therapy in patients with acute stroke. Methods: This study is a systematic review on clinical studies, as the Cochrane library, PubMed, Google Scholar, Web of Science, and Embase databases were searched. The time span selected to retrieve articles is 1990 to 2017. The quality of the articles found was evaluated by the CONSORT checklist. Fixed effects and random effects models were employed for meta-analysis. Results were subject to sensitivity analysis in specified curtained interval, CMA (Comprehensive Meta-Analysis software): 2 software was used to carry out the meta-analysis task, and alpha was set to 5%. Results: The eight papers found met the inclusion criteria. Patients in mechanical thrombectomy group had a significantly higher improvement rate compared to the thrombolytic therapy group [OR 1.71 (1.182.48), P = 0.005]. There were no significant differences between mechanical thrombectomy and thrombolytic therapy groups regarding intracerebral hemorrhage ([OR 1.03 (0.71 - 1.49), P = 0.88]). Mechanical thrombectomy was more effective in reducing mortality rate of patients, however, this difference was not significant ([OR 0.84 (0.67 - 1.05), P = 0.12]). The effectiveness of mechanical thrombectomy is superior to thrombolytic therapy based on the improvement rate, 90-day mortality and symptoms of intracerebral hemorrhage OR: 2.23 (1.77 - 2.81), P < 0.00001; OR 0.79 (0.60 - 1.05), P = 0.10, and OR 1.02 (0.61 - 1.70), P = 0.95, respectively. Conclusions: Through some good criteria for selecting appropriate patients, mechanical thrombectomy can be superior to thrombolytic therapy in patients with acute stroke.

Crossed cerebellar diaschisis (CCD) is the phenomenon of hypoperfusion and hypometabolism of the contralateral cerebellar hemisphere caused by dysfunction of the related supratentorial region. Our aim was to analyze its influence on morphologic and functional outcome in acute ischemic stroke. Subjects with stroke caused by a large vessel occlusion of the anterior circulation were selected from an initial cohort of 1644 consecutive patients who underwent multiparametric CT including whole-brain CT perfusion. Two experienced readers evaluated the posterior fossa in terms of CCD absence (CCD-) or presence (CCDþ). A total of 156 patients formed the study cohort with 102 patients (65.4%) categorized as CCD- and 54 (34.6%) as CCDþ. In linear and logistic regression analyses, no significant association between CCD and final infarction volume (β=-0.440, p=0.972), discharge mRS≤2 (OR=1.897, p=0.320), or 90-day mRS≤2 (OR=0.531, p=0.492) was detected. CCDþ patients had larger supratentorial cerebral blood flow deficits (median: 164 ml vs. 115 ml; p=0.001) compared to CCD-patients. Regarding complications, CCD was associated with a higher rate of parenchymal hematomas (OR=4.793, p=0.035). In conclusion, CCD is frequently encountered in acute ischemic stroke caused by large vessel occlusion of the anterior circulation. CCD was associated with the occurrence of parenchymal hematoma in the ipsilateral cerebral infarction but did not prove to significantly influence patient outcome. [ABSTRACT FROM AUTHOR]

Purpose of Review: This study aims to describe the current state of telestroke clinical applications and policies, in addition to key technical and operational aspects of the telemedicine practice. Recent Findings: Delivery of telestroke services for neurovascular care expanded from the intravenous alteplase decision and administration in acute emergency department settings to a continuum of services in mobile and inpatient stroke units, intensive care units, virtual stroke clinics, rehabilitation, and clinical research. Telestroke cost-effectiveness is well established from multiple perspectives. Stroke centers, certification agencies, and national registries have made essential recommendations regarding telestroke quality measures monitoring and reporting. Summary: Telestroke continues to bring neurovascular expertise to resource-restricted areas with advanced virtual communication techniques, optimizing stroke care. Future research should aim at broadening telestroke technology applications, while improving quality and reducing the delivery-associated cost and resources. Comprehensive multidisciplinary virtual telestroke centers that cover all aspects of stroke management might become available in the future. [ABSTRACT FROM AUTHOR]

Phosphatidylinositol 3-kinases (PI3Ks) have recently been implicated in apoptosis and ischemic cell death. We tested the efficacy of early intervention with a peptide PI3K activator in focal cerebral ischemia. After determining the most effective dose (24 μg/kg) and time window (2 h after MCAO) of treatment, a total of 48 rats were subjected to middle cerebral artery occlusion (MCAO). Diffusion weighted MRI (DWI) was performed 1 h after MCAO and rats with lesion sizes within a predetermined range were randomized to either PI3K activator or vehicle treatment arms. Fluid attenuated inversion recovery (FLAIR) MRI, neurological function, western blots, and immunohistochemistry were blindly assessed. Initial DWI lesion volumes were nearly identical between two groups prior to treatment. However, FLAIR showed significantly smaller infarct volumes in the PI3K activator group compared with vehicle (146 ± 81 mm and 211 ± 96 mm, p = 0.045) at 48 h. The PI3K activator group also had better neurological function for up to 2 weeks. In addition, PI3K activator decreased the number of TUNEL-positive cells in the peri-infarct region compared with the control group. Western blot and immunohistochemistry showed increased expression of phosphorylated Akt (Ser473) and GSK-3β (Ser9) and decreased expression of cleaved caspase-9 and caspase-3. Our results suggest a neuroprotective role of early activation of PI3K in ischemic stroke. The use of DWI in the randomization of experimental groups may reduce bias. [ABSTRACT FROM AUTHOR]

Given the importance of neuronal plasticity in recovery from a stroke and the huge variability of recovery abilities in patients, we investigated neuronal activity in the acute phase to enhance information about the prognosis of recovery in the stabilized phase. We investigated the microstates in 47 patients who suffered a first-ever mono-lesional ischemic stroke in the middle cerebral artery territory and in 20 healthy control volunteers. Electroencephalographic (EEG) activity at rest with eyes closed was acquired between 2 and 10 days (T0) after ischemic attack. Objective criteria allowed for the selection of an optimal number of microstates. Clinical condition was quantified by the National Institute of Health Stroke Scale (NIHSS) both in acute (T0) and stabilized (T1, 5.4 ± 1.7 months) phases and Effective Recovery (ER) was calculated as (NIHSS(T1)-NIHSS(T0))/NIHSS(T0). The microstates A, B, C and D emerged as the most stable. In patients with a left lesion inducing a language impairment, microstate C topography differed from controls. Microstate D topography was different in patients with a right lesion inducing neglect symptoms. In patients, the C vs D microstate duration differed after both a left and a right lesion with respect to controls (C lower than D in left and D lower than C in right lesion). A preserved microstate B in acute phase correlated with a better effective recovery. A regression model indicated that the microstate B duration explained the 11% of ER variance. This first ever study of EEG microstates in acute stroke opens an interesting path to identify neuronal impairments with prognostic relevance, to develop enriched compensatory treatments to drive a better individual recovery. [ABSTRACT FROM AUTHOR]

Several clinical trials have recently proven the efficacy of mechanical thrombectomy for treating ischemic stroke, within a six-hour window for therapy. To move beyond treatment windows and toward personalized risk assessment, it is essential to accurately identify the extent of tissue-at-risk (“penumbra”). We introduce a fully automated method to estimate the penumbra volume using multimodal MRI (diffusion-weighted imaging, a T2w- and T1w contrast-enhanced sequence, and dynamic susceptibility contrast perfusion MRI). The method estimates tissue-at-risk by predicting tissue damage in the case of both persistent occlusion and of complete recanalization. When applied to 19 test cases with a thrombolysis in cerebral infarction grading of 1–2a, mean overestimation of final lesion volume was 30 ml, compared with 121 ml for manually corrected thresholding. Predicted tissue-at-risk volume was positively correlated with final lesion volume (p < 0.05). We conclude that prediction of tissue damage in the event of either persistent occlusion or immediate and complete recanalization, from spatial features derived from MRI, provides a substantial improvement beyond predefined thresholds. It may serve as an alternative method for identifying tissue-at-risk that may aid in treatment selection in ischemic stroke. [ABSTRACT FROM AUTHOR]

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Purpose/Aim: Data from chronic stroke studies have reported reduced blood flow and vascular endothelial function in the stroke-affected limb. It is unclear whether these differences are present early after stroke. First, we investigated whether vascular endothelial function in the stroke-affected limb would be different from healthy adults. Second, we examined whether between-limb differences in vascular endothelial function existed in the stroke-affected arm compared to the non-affected arm. Last, we tested whether reduced vascular endothelial function was related to pro-inflammatory markers that are present early after stroke. Materials and Methods: Vascular endothelial function was assessed by flow-mediated dilation (FMD) in the brachial artery within 72 h post-stroke. All participants withheld medications from midnight until after the procedure. Ultrasound scans and blood draws for pro-inflammatory markers occurred on the same day between 7:30 am and 9:00 am. Results: People with acute stroke had significantly lower FMD (4.2% ± 4.6%) than control participants (8.5% ± 5.2%, p = 0.037). Stroke participants had between-limb differences in FMD (4.2% ± 4.6% stroke-affected vs. 5.3% ± 4.4% non-affected, p = 0.02), whereas, the control participants did not. Of the pro-inflammatory markers, only vascular cell adhesion molecule-1(VCAM-1) had a significant relationship to FMD (stroke-affected limb, r = −0.62, p = 0.03; non-affected limb, r = −0.75, p = 0.005), but not tumor necrosis factor alpha nor interleukin-6. Conclusions: Vascular endothelial function is reduced starting in the early stage of stroke recovery. People with higher levels of VCAM-1 had a lower FMD response. [ABSTRACT FROM AUTHOR]

To derive the reperfusion index best predicting clinical outcome of ischemic stroke patients, we retrospectively analysed the acute and 24-h computed tomography perfusion data of 116 patients, collected from two centres equipped with whole-brain computed tomography perfusion. Reperfusion index was defined by the percentage of the ischemic region reperfused from acute to 24-h computed tomography perfusion. Recanalization was graded by arterial occlusive lesion system. Receiver operator characteristic analysis was performed to assess the prognostic value of reperfusion and recanalization in predicting good clinical outcome, defined as modified Rankin Score of 0-2 at 90 days. Among previous reported reperfusion measurements, reperfusion of the Tmax>6s region resulted in higher prognostic value than recanalization at predicting good clinical outcome (area under the curve = 0.88 and 0.74, respectively, p = 0.002). Successful reperfusion of the Tmax>6 s region (≥60%) had 89% sensitivity and 78% specificity in predicting good clinical outcome. A reperfusion index defined by Tmax>2s or by mean transit time>l45% had much lower area under the curve in comparison to Tmax>6 s measurement (p < 0.001 and p = 0.003, respectively), and had no significant difference to recanalization at predicting clinical outcome (p = 0.58 and 0.63, respectively). In conclusion, reperfusion index calculated by Tmax>6s is a stronger predictor of clinical outcome than recanalization or other reperfusion measures. [ABSTRACT FROM AUTHOR]

Objectives To examine the usefulness of including sodium (Na) levels as a criterion to the SOAR stroke score in predicting inpatient and 7-day mortality in stroke. Materials and Methods Data from the Norfolk and Norwich University Hospital Stroke & TIA register (2003-2015) were analysed. Univariate and then multivariate models controlling for SOAR variables were used to assess the association between admission sodium levels and inpatient and 7-day mortality. The prognostic ability of the SOAR and SOAR Na scores for mortality outcomes at both time points were then compared using the Area Under the Curve ( AUC) values from the Receiver Operating Characteristic curves. Results A total of 8493 cases were included (male=47.4%, mean (SD) 77.7 (11.6) years). Compared with normonatremia (135-145 mmol/L), hypernatraemia (>145 mmol/L) was associated with inpatient mortality and moderate (125-129 mmol/L) and severe hypontraemia (<125 mmol/L) with 7-day mortality after adjustment for stroke type, Oxfordshire Community Stroke Project classification, age, prestroke modified Rankin score and sex. The SOAR and SOAR-Na scores both performed well in predicting inpatient mortality with AUC values of .794 (.78-.81) and .796 (.78-.81), respectively. 7-day mortality showed similar results. Both scores were less predictive in those with chronic kidney disease ( CKD) and more so in those with hypoglycaemia. Conclusion The SOAR-Na did not perform considerably better than the SOAR stroke score. However, the performance of SOAR-Na in those with CKD and dysglycaemias requires further investigation. [ABSTRACT FROM AUTHOR]

Haemodynamic responses to spreading depolarizations (SDs) have an important role during the development of secondary brain damage. Characterization of the haemodynamic responses in larger brains, however, is difficult due to movement artefacts. Intrinsic optical signal (IOS) imaging, laser speckle flowmetry (LSF) and electrocorticography were performed in different configurations in three groups of in total 18 swine. SDs were elicited by topical application of KCl or occurred spontaneously after middle cerebral artery occlusion. Movement artefacts in IOS were compensated by an elastic registration algorithm during post-processing. Using movement-compensated IOS, we were able to differentiate between four components of optical changes, corresponding closely with haemodynamic variations measured by LSF. Compared with ECoG and LSF, our setup provides higher spatial and temporal resolution, as well as a better signalto-noise ratio. Using IOS alone, we could identify the different zones of infarction in a large gyrencephalic middle cerebral artery occlusion pig model. We strongly suggest movement-compensated IOS for the investigation of the role of haemodynamic responses to SDs during the development of secondary brain damage and in particular to examine the effect of potential therapeutic interventions in gyrencephalic brains. [ABSTRACT FROM AUTHOR]

Most studies on sensory extinction have focused on selected patients with subacute and chronic right hemisphere lesions. In studies conducted on acute stroke patients, risk factors and time course were not evaluated. Our aim was to determine the prevalence, risk factors, and time course of sensory extinction in the acute stroke setting. Consecutive patients with acute stroke were tested for tactile, visual, auditory, and auditory-tactile cross-modal extinction, as well as for peripersonal visuospatial neglect (PVN). Tests were repeated at 2, 7, 15, 30, and 90 days after initial examination. A multivariable logistic regression analysis was performed to test the association between sensory extinction and demographic and clinical risk factors. Seventy-three patients (38.4% women) were recruited: 64 with ischemic stroke and nine with haemorrhagic stroke. Mean age was 62.3 years (95% CI 58.8-65.7), mean NIHSS score was 1.6 (95% CI 1.2-2.1), and mean time to first examination was 4.1 days (95% CI 3.5-4.8). The overall prevalence of all subtypes of sensory extinction was 13.7% (95% CI 6.8-23.8). Tactile extinction was the most frequent subtype with a prevalence of 8.2% (95% CI 3.1-17.0). No extinction was found beyond 15 days after the first examination. After adjustment for age, sex, lesion side, type of stroke, time to first examination and stroke severity, a lesion volume ≥2 mL (adjusted OR = 38.88, p = 0.04), and presence of PVN (adjusted OR = 24.27, p = 0.04) were independent predictors of sensory extinction. The insula, the putamen, and the pallidum were the brain regions most frequently involved in patients with sensory extinction. Extinction is a rare and transient phenomenon in patients with minor stroke. The presence of PVN and lesion volume ≥2 mL are independent predictors of sensory extinction in acute stroke. [ABSTRACT FROM AUTHOR]

Objective: This study was done to assess the safety and efficacy of aspirin in the initial treatment and secondary prevention of acute stroke of undetermined or presumed ischemic etiology. Background: The use of aspirin for the initial treatment of acute stroke of unknown etiology in low-resource settings is often challenged by the lack of diagnostic brain imaging to confirm specific stroke type and guide treatment. Aspirin use carries a potential risk of causing or exacerbating cerebral hemorrhage which can be fatal or disabling. Hence, in developing countries only 3.8% of acute stroke patients take antiplatelet compared to 53.1% in high income countries. Methods: A systematic review of literature from the Cochrane library, Medline, Scopus and Google Scholar was done. Studies 1) involving patients with acute stroke of undetermined or presumed ischemic etiology, 2) involving the use of aspirin in the initial treatment and/or secondary prevention of acute stroke of unknown or presumed ischemic etiology, and 3) comparing aspirin to a control or other antiplatelet agent (s), were selected for the review. Results: There was homogeneity of results in support of aspirin use for the initial treatment and secondary prevention of acute stroke of unknown etiology. The studies showed significant reduction in in-hospital mortality, disability, stroke recurrence and risk of hemorrhagic stroke with the use of aspirin. Conclusion: Available evidence supported the use of aspirin for the initial treatment and secondary prevention of acute stroke of unknown or presumed ischemic etiology in resource-constrained settings, where brain imaging is unavailable to confirm stroke type. [ABSTRACT FROM AUTHOR]

We have characterized both acute and long-term vascular and metabolic effects of unilateral common carotid artery occlusion in mice by in vivo magnetic resonance imaging and positron emission tomography. This common carotid artery occlusion model induces chronic cerebral hypoperfusion and is therefore relevant to both preclinical stroke studies, where it serves as a control condition for a commonly used mouse model of ischemic stroke, and neurodegeneration, as chronic hypoperfusion is causative to cognitive decline. By using perfusion magnetic resonance imaging, we demonstrate that under isoflurane anesthesia, cerebral perfusion levels recover gradually over one month. This recovery is paralleled by an increase in lumen diameter and altered tortuosity of the contralateral internal carotid artery at one year post-ligation as derived from magnetic resonance angiography data. Under urethane/a-chloralose anesthesia, no acute perfusion differences are observed, but the vascular response capacity to hypercapnia is found to be compromised. These hemispheric perfusion alterations are confirmed by water [15O]-H2O positron emission tomography. Glucose metabolism ([18F]-FDG positron emission tomography) or white matter organization (diffusion-weighted magnetic resonance imaging) did not show any significant alterations. In conclusion, permanent unilateral common carotid artery occlusion results in acute and long-term vascular remodeling, which may have immediate consequences for animal models of stroke but also vascular dementia. [ABSTRACT FROM AUTHOR]

Background and purpose Elevated heart rate ( HR) is associated with worse outcomes in patients with cardiovascular disease. Its predictive value in acute stroke patients is less well established. We investigated the effects of HR on admission in acute ischaemic stroke patients. Methods Using the Virtual International Stroke Trials Archive ( VISTA) database, the association between HR in acute stroke patients without atrial fibrillation and the pre-defined composite end-point of (recurrent) ischaemic stroke, transient ischaemic attack ( TIA), myocardial infarction ( MI) and vascular death within 90 days was analysed. Pre-defined secondary outcomes were the composite end-point components and any death, decompensated heart failure and degree of functional dependence according to the modified Rankin Scale after 90 days. HR was analysed as a categorical variable (quartiles). Results In all, 5606 patients were available for analysis (mean National Institutes of Health Stroke Scale 13; mean age 67 years; mean HR 77 bpm; 44% female) amongst whom the composite end-point occurred in 620 patients (11.1%). Higher HR was not associated with the composite end-point. The frequencies of secondary outcomes were 3.2% recurrent stroke ( n = 179), 0.6% TIA ( n = 35), 1.8% MI ( n = 100), 6.8% vascular death ( n = 384), 15.0% any death ( n = 841) and 2.2% decompensated heart failure ( n = 124). Patients in the highest quartile ( HR> 86 bpm) were at increased risk for any death [adjusted hazard ratio (95% confidence interval) 1.40 (1.11-1.75)], decompensated heart failure [adjusted hazard ratio 2.20 (1.11-4.37)] and worse modified Rankin Scale [adjusted odds ratio 1.29 (1.14-1.52)]. Conclusions In acute stroke patients, higher HR (>86 bpm) is linked to mortality, heart failure and higher degree of dependence after 90 days but not to recurrent stroke, TIA or MI. [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate the safety and efficacy of multimodal reperfusion therapy (MMRT) for tandem internal carotid artery and middle cerebral arterial (TIM) occlusions. Cases of TIM occlusion were collected and retrospectively reviewed. The analyzed objects included etiology, sites of tandem occlusion, collateral flow, location and size of infarcts. Combined with mechanical recanalization techniques and its complications, the National Institute of Health Stroke Scale (NIHSS) score and imaging data that was derived pre- and post-procedure were further contrasted. The study enrolled six patients with TIM occlusions. The mean NIHSS score on admission was 17 (range 13–20) and the median time from puncture to recanalization was 141 min (range 60–230). The substantial recanalization rate (Thrombolysis in Cerebral Infarction 2b or 3) was 83.3% and no symptomatic intracerebral hemorrhage was observed. The mean NIHSS score after three days was 14 (range 10–19) and 9 (range 3–17) following discharge. However, one patient died of pulmonary infection one month after discharge. For the five patients who survived, the modified Rankin Scale was evaluated at three months, with scores of 3, 1, 3, 5 and 3, respectively. It is concluded that endovascular therapy for acute TIM occlusions are complex, MMRT may be relatively safe and effective. [ABSTRACT FROM PUBLISHER]

Stroke disrupts the brain's vascular supply, not only within but also outside areas of infarction. We investigated temporal delays (lag) in resting state functional magnetic resonance imaging signals in 130 stroke patients scanned two weeks, three months and 12 months post stroke onset. Thirty controls were scanned twice at an interval of three months. Hemodynamic lag was determined using cross-correlation with the global gray matter signal. Behavioral performance in multiple domains was assessed in all patients. Regional cerebral blood flow and carotid patency were assessed in subsets of the cohort using arterial spin labeling and carotid Doppler ultrasonography. Significant hemodynamic lag was observed in 30% of stroke patients sub-acutely. Approximately 10% of patients showed lag at one-year post-stroke. Hemodynamic lag corresponded to gross aberrancy in functional connectivity measures, performance deficits in multiple domains and local and global perfusion deficits. Correcting for lag partially normalized abnormalities in measured functional connectivity. Yet post-stroke FC-behavior relationships in the motor and attention systems persisted even after hemodynamic delays were corrected. Resting state fMRI can reliably identify areas of hemodynamic delay following stroke. Our data reveal that hemodynamic delay is common sub-acutely, alters functional connectivity, and may be of clinical importance. [ABSTRACT FROM AUTHOR]

The first paper of the series on the treatment of patients with vascular comorbidity (VC) is focused on the role and therapeutic potential of the correction of free radical processes (FRP) as pathogenetic factors of multifocal vascular pathology. Aim. To analyse the effects of VC on the incidence and outcomes of cerebral stroke (S), in order to create therapeutic algorithms of FRP correction. Material and methods. This prospective study included 634 S patients. The following factors were analysed: pre-stroke disability due to various VC variants; VC effects on the clinical course, as well as in-hospital and post-discharge outcomes; and FRP specifics in various VC variants. Results. VC was registered in 97% of S patients; in 45,3%, it resulted in pre-stroke disability. FRP parameters, reflecting the progression of tissue energy deficiency, differed significantly in patients with coronary heart disease, myocardial infarction, atrial fibrillation, and diabetes mellitus. Based on these findings, the therapeutic algorithms for effective energy deficiency correction have been created. Conclusion. The analysis of pre- and post-stroke disability and prevention of repeat events in cardiovascular patients has demonstrated the need for a more active implementation of modern multidisciplinary preventive programs.