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The ipsilateral hand (ILH) is impaired after unilateral stroke, but the underlying mechanisms remain unresolved. Based on the degeneracy theory of network connectivity that many connectivity patterns are functionally equivalent, we hypothesized that ILH impairment would result from the summation of microstructural white matter (WM) disruption in the motor network, with a task-related profile. We aimed to determine the WM disruption patterns associated with ILH impairment.This was a cross-sectional analysis of patients in the ISIS-HERMES Study with ILH and diffusion-MRI data collected 1 month post-stroke. Patients performed three tasks, the Purdue Pegboard Test (PPT), handgrip strength, and movement time. Fractional anisotropy (FA) derived from diffusion MRI was measured in 33 WM regions. We used linear regression models controlling for age, sex, and education to determine WM regions associated with ILH impairment.PPT was impaired in 42%, grip in 59%, and movement time in 24% of 29 included patients (mean age, 51.9 ± 10.5 years; 21 men). PPT was predicted by ipsilesional corticospinal tract (i-CST) (B = 17.95; p = 0.002) and superior longitudinal Fasciculus (i-SLF) (B = 20.52; p = 0.008); handgrip by i-CST (B = 109.58; p = 0.016) and contralesional anterior corona radiata (B = 42.69; p = 0.039); and movement time by the corpus callosum (B = - 1810.03; p = 0.003) i-SLF (B = - 917.45; p = 0.015), contralesional pons-CST (B = 1744.31; p = 0.016), and i-corticoreticulospinal pathway (B = - 380.54; p = 0.037).ILH impairment was associated with WM disruption to a combination of ipsilateral and contralesional tracts with a pattern influenced by task-related processes, supporting the degeneracy theory. We propose to integrate ILH assessment in rehabilitation programs and treatment interventions such as neuromodulation.

Ipsilateral hand (ILH) impairment is documented following motor stroke, but its impact on long-term outcome remains unknown. We assessed ILH impairment in subacute stroke and tested whether ILH impairment predicted long-term outcome.We performed a longitudinal study in 209 consecutive patients with unilateral stroke and sensorimotor deficit at admission. ILH impairment was evaluated using the Purdue Pegboard Test (PPT) and handgrip strength and defined as mild (z-score -1) or moderate (z-score -1.65). We used logistic regression (LR) to predict outcome assessed 9 (range, 7-12) months post-stroke with the modified Rankin scale (mRS) categorized into good (mRS ≤ 1) and poor outcome (mRS ≥ 2). For internal validation, LR-bootstrapping and cross-validation with LASSO and Random Forest were performed.ILH impairment assessed at 89.04 ± 45.82 days post-stroke was moderate in 10.53% (95% CI 6.7, 14.83) for PPT and 17.22% (95% CI 11.96, 22.49) for grip, and mild in 21.05% (95% CI 15.78, 26.79) for PPT and 35.89 (95% CI 29.67, 42.58) for grip. Good outcome was predicted by ILH-PPT (B = 1.03 [95% CI 0.39, 3.31]), ILH-grip (B = 1.16 [95% CI 0.54, 3.53]), low NIHSS-discharge (B = -1.57 [95% CI -4.0, -1.19]), and no depression (B = -0.62 [95% CI -1.63, -0.43]), accounting for stroke delay (B = -0.011 [95% CI -0.06, 0.01]). Model efficiency was 91.6% (AUC = 0.977; 95% CI 0.959, 0.996). LASSO and Random Forest methods provided similar results, confirming the LR model robustness.ILH impairment is frequent after motor stroke and predicts long-term outcome. We propose to integrate ILH impairment into rehabilitation programs to improve recovery and serve research interventions such as neuromodulation.

ObjectiveTo identify candidate biomarkers of walking recovery with motor tract integrity measurements using fractional anisotropy (FA) from the corticospinal tract (CST) and alternative motor pathways in patients with moderate to severe subacute stroke.MethodsWalking recovery was first assessed with generalized linear mixed model (GLMM) with repeated measures of walking scores (WS) over 2 years of follow-up in a longitudinal study of 29 patients with subacute ischemic stroke. Baseline FA measures from the ipsilesional and contralesional CST (i-CST and c-CST), cortico-reticulospinal pathway (i-CRP and c-CRP), and cerebellar peduncles were derived from a 60-direction diffusion MRI sequence on a 3T scanner. We performed correlation tests between WS and FA measures. Third, we investigated using GLMM whether motor tract integrity contributes to predict walking recovery.ResultsWe observed significant improvements of WS over time with a plateau reached at ≈6 months after stroke. WS significantly correlated with FA measures from i-CST, c-CST, i-CRP, and bilateral cerebellar peduncles. Walking recovery was predicted by FA measures from 3 tracts: i-CST, i-CRP, and contralesional superior cerebellar peduncle (c-SCP). Diffusion tensor imaging (DTI) predictors captured 80.5% of the unexplained variance of the model without DTI.ConclusionsWe identified i-CST and alternative motor-related tracts (namely i-CRP and c-SCP) as candidate biomarkers of walking recovery. The role of the SCP in walk recovery may rely on cerebellar nuclei projections to the thalamus, red nucleus, and reticular formation. Our findings suggest that a set of white matter tracts, part of subcortical motor networks, contribute to walking recovery in patients with moderate to severe stroke.

Lacunar stroke is a common subtype of stroke, comprising 20%–25% of ischemic strokes, linking a number of clinical syndromes to occlusion of a single perforating artery (40–900 μm in diameter) resulting from vasculopathy characterized by lipohyalinosis, arteriolosclerosis, and microatheroma. Hypertension is the leading cause, along with atherosclerosis and other stroke risk factors.1-3 Lacunes may be described as small deep cerebral infarcts, 3–17 mm in maximum diameter, located in cerebral hemisphere and brainstem regions supplied by perforating arteries.4 The term lacune stems from the French literature in the 19th century to describe, based on anatomical examination, small cavities with liquefaction necrosis.

While motor recovery following mild stroke has been extensively studied with neuroimaging, mechanisms of recovery after moderate to severe strokes of the types that are often the focus for novel restorative therapies remain obscure. We used fMRI to: 1) characterize reorganization occurring after moderate to severe subacute stroke, 2) identify brain regions associated with motor recovery and 3) to test whether brain activity associated with passive movement measured in the subacute period could predict motor outcome six months later. Because many patients with large strokes involving sensorimotor regions cannot engage in voluntary movement, we used passive flexion-extension of the paretic wrist to compare 21 patients with subacute ischemic stroke to 24 healthy controls one month after stroke. Clinical motor outcome was assessed with Fugl-Meyer motor scores (motor-FMS) six months later. Multiple regression, with predictors including baseline (one-month) motor-FMS and sensorimotor network regional activity (ROI) measures, was used to determine optimal variable selection for motor outcome prediction. Sensorimotor network ROIs were derived from a meta-analysis of arm voluntary movement tasks. Bootstrapping with 1000 replications was used for internal model validation. During passive movement, both control and patient groups exhibited activity increases in multiple bilateral sensorimotor network regions, including the primary motor (MI), premotor and supplementary motor areas (SMA), cerebellar cortex, putamen, thalamus, insula, Brodmann area (BA) 44 and parietal operculum (OP1-OP4). Compared to controls, patients showed: 1) lower task-related activity in ipsilesional MI, SMA and contralesional cerebellum (lobules V-VI) and 2) higher activity in contralesional MI, superior temporal gyrus and OP1-OP4. Using multiple regression, we found that the combination of baseline motor-FMS, activity in ipsilesional MI (BA4a), putamen and ipsilesional OP1 predicted motor outcome measured 6 months later (adjusted-R2 = 0.85; bootstrap p, Highlights • Motor recovery after stroke can be robustly predicted using a passive task fMRI paradigm. • Sensorimotor network activity is decreased in moderate to severe stroke patients relative to healthy controls • Compensatory mechanisms in severe stroke involve both the dorsal (MI BA4a), and the ventral (OP1 and OP4) sensorimotor stream

Environmental factors contribute to the constitution and maintenance of the cognitive reserve and partially explain the variability of cognitive performance in older individuals. We assessed the role of leisure activities - social and individual - on the access to lexico-semantic representations evaluated through a task of object naming (ON). We hypothesize that compared to individual, social leisure activities explain better the ON performance in the older adults, which is explained by a mechanism of neural reserve. Our results in older adults indicate (a) a significant correlation between leisure social activities and the response time for ON, (b) a significant correlation between link the neural activity of the left superior and medial frontal (SmFG) for ON and leisure social activities. Interestingly, the activity of the left SmFG partially mediates the relationship between social activities and OD performance. We suggest that social leisure activities may contribute to maintain ON performances in healthy aging, through a neural reserve mechanism, in relation with left SmFG activity. This region is typically involved in the access to semantic representations, guided by the emotional state. These results open interesting perspectives on the role of social leisure activities on lexical production during aging.

BACKGROUND: Diffusion tensor imaging has been widely used to measure HIV effects on white matter microarchitecture. While many authors have reported reduced fractional anisotropy and increased mean diffusivity in HIV, quantitative inconsistencies across studies are numerous. PURPOSE: Our aim was to evaluate the consistency across studies of HIV effects on DTI measures and then examine the DTI reliability in a longitudinal seropositive cohort. DATA SOURCES: Published studies and investigators. STUDY SELECTION: The meta-analysis included 16 cross-sectional studies reporting fractional anisotropy and 12 studies reporting mean diffusivity in the corpus callosum. DATA ANALYSIS: Random-effects meta-analysis was used to estimate study standardized mean differences and heterogeneity. DTI longitudinal reliability was estimated in seropositive participants studied before and 3 and 6 months after beginning treatment. DATA SYNTHESIS: Meta-analysis revealed lower fractional anisotropy (standardized mean difference, −0.43; P 0.96. LIMITATIONS: Many studies pooled participants with varying treatments, ages, and disease durations. CONCLUSIONS: HIV effects on WM microstructure had substantial variations that could result from acquisition, processing, or cohort-selection differences. When acquisition parameters and processing were carefully controlled, the resulting DTI measures did not show high temporal variation. HIV effects on WM microstructure may be age-dependent. The high longitudinal reliability of DTI WM microstructure measures makes them promising disease-activity markers.

Background: Little is known about the relationship between hypercholesterolaemia and specific aetiological subtypes of brain infarction (BI). Methods: In a cross-sectional study of 492 pairs of patients with a BI proven by MRI and matched hospital controls, we determined the blood levels of triglycerides, total, HDL and LDL cholesterol, and apolipoprotein A1 and B, in the same centralized laboratory. We performed aetiological BI subtype classification. Results: Except for triglycerides, the risk of BI increased continuously with the lipid levels, without any heterogeneity between the main BI subtypes or the group on lipid-lowering therapy. The adjusted odds ratio per standard deviation in LDL cholesterol (0.93 mmol/l) was 1.74 (95% confidence interval, 1.02–2.98) in atherothrombotic strokes (n = 109) and 2.71 (95% confidence interval, 1.60–4.55) in lacunar strokes (n = 105). Eighty percent of patients were above the ATP-III guideline threshold LDL cholesterol of 2.59 mmol/l (100 mg/dl), with a major contribution of both atherothrombotic and lacunar stroke subtypes to this group. Conclusions: These findings suggest that blood lipids, particularly total and LDL cholesterol levels, are associated with all subtypes of BI, and that LDL above 2.59 mmol/l is highly prevalent.

While experimental studies in the monkey have shown that motor recovery after partial destruction of the hand motor cortex was based on adjacent motor reorganization, functional MRI (fMRI) studies with isolated primary motor cortical stroke have not yet been reported in humans. Based on experimental data, we designed a study to test if recovery after stroke within primary motor cortex (M1) was associated with reorganization within the surrounding motor cortex, i.e. the motor cortex was able to vicariate. Since motor recovery is time-dependent and might be inflected according to the tested task, the delay after stroke and two motor tasks were included in our design. We examined four patients with one ischaemic stroke limited to M1, and four sex- and age-matched healthy controls in a temporally balanced prospective longitudinal fMRI study over three sessions

Resume L’hypoglycemie est une cause de coma frequente et grave. Les indicateurs du pronostic, telles la severite de l’hypoglycemie et la duree du coma, sont peu nombreux et leur fiabilite est incertaine. Nous rapportons un cas de coma hypoglycemique associe a la presence d’hypersignaux en IRM de diffusion, suivie de l’installation rapide d’une atrophie cerebrale au niveau des memes aires. Ces constatations suggerent que l’IRM de diffusion serait un marqueur des lesions neuronales dans l’hypoglycemie et pourrait constituer un indicateur du pronostic.

Stroke is the second leading cause of death worldwide and the most common cause of severe disability. Neuroprotection and repair mechanisms supporting endogenous brain plasticity are often insufficient to allow complete recovery. While numerous neuroprotective drugs trials have failed to demonstrate benefits for patients, they have provided interesting translational research lessons related to neurorestorative therapy mechanisms in stroke. Stroke damage is not limited to neurons but involve all brain cell type including the extracellular matrix in a "glio-neurovascular niche". Targeting a range of host brain cells, biotherapies such as growth factors and therapeutic cells, currently hold great promise as a regenerative medical strategy for stroke. These techniques can promote both neuroprotection and delayed neural repair through neuro-synaptogenesis, angiogenesis, oligodendrogliogenesis, axonal sprouting and immunomodulatory effects. Their complex mechanisms of action are interdependent and vary according to the particular growth factor or grafted cell type. For example, while "peripheral" stem or stromal cells can provide paracrine trophic support, neural stem/progenitor cells (NSC) or mature neurons can act as more direct neural replacements. With a wide therapeutic time window after stroke, biotherapies could be used to treat many patients. However, guidelines for selecting the optimal time window, and the best delivery routes and doses are still debated and the answers may depend on the chosen product and its expected mechanism including early neuroprotection, delayed neural repair, trophic systemic transient effects or graft survival and integration. Currently, the great variety of growth factors, cell sources and cell therapy products form a therapeutic arsenal that is available for stroke treatment. Their effective clinical use will require prior careful considerations regarding safety (e.g. tumorgenicity, immunogenicity), potential efficacy, cell characterization, delivery route and in vivo biodistribution. Bone marrow-derived cell populations such as mesenchymal stromal/stem cells (MSC) or mononuclear cells (MNC), umbilical cord stem cells and NSC are most investigated notably in clinical trials. Finally, we discuss perspectives concerning potential novel biotherapies such as combinatorial approaches (growth factor combined with cell therapy, in vitro optimization of cell products, or co-transplantation) and the development of biomaterials, which could be used as injectable hydrogel scaffold matrices that could protect a cell graft or selectively deliver drugs and growth factors into the post-stroke cavity at chronic stages. Considering the remaining questions about the best procedure and the safety cautions, we can hope that future translational research about biotherapies will bring more efficient treatments that will decrease post-stroke disability for many patients.

Background and Purpose— Although neuroimaging studies have revealed specific patterns of reorganization in the sensorimotor control network after stroke, their role in recovery remains unsettled. To review the existing evidence systematically, we performed activation likelihood estimation meta-analysis of functional neuroimaging studies investigating upper limb movement-related brain activity after stroke. Methods— Twenty-four studies using sensorimotor tasks in standardized coordinates were included, totaling 255 patients and 145 healthy controls. Across the entire brain, we compared task-related activity patterns in good and poor recovery and assessed the magnitude of spatial shifts in sensorimotor activity in cortical motor areas after stroke. Results— When compared with healthy controls, patients showed higher activation likelihood estimation values in contralesional primary motor soon after stroke that abated with time, but were not related to motor outcome. The observed activity changes were consistent with restoration of typical interhemispheric balance. In contrast, activation likelihood estimation values in ipsilesional medial-premotor and primary motor cortex were associated with good outcome, reorganization that may reflect vicarious processes associated with ventral activity shifts from BA4a to 4p. In the anterior cerebellum, a novel finding was the association of poor recovery with increased vermal activity, possibly reflecting behaviorally inadequate compensatory strategies engaging the fastigio-thalamo-cortical and corticoreticulospinal systems. Conclusions— Activity in ipsilesional primary motor and medial-premotor cortices in chronic stroke signals good motor recovery, whereas cerebellar vermis activity signals poor recovery. Functional MRI may be useful in identifying recovery biomarkers.

Background and Purpose —Three major randomized controlled trials of streptokinase in acute ischemic stroke were curtailed because of safety concerns. The prospective Thrombolysis in Acute Stroke Pooling Project (TAS-PP) was established to examine the aggregate data to identify factors influencing the effect of streptokinase. Methods —Individual patient data from the Australian Streptokinase Trial (ASK), Multicentre Acute Stroke Trial-Europe (MAST-E), Multicentre Acute Stroke Trial-Italy (MAST-I), and Glasgow Trial (Glasgow) were pooled. Multivariate modeling determined the interaction between treatment effect and delay from symptom onset to treatment, predicted baseline risk, age, concomitant aspirin or heparin use, and the presence of early CT signs on the outcomes of 10-day death, death and disability, or death alone at 3 or 6 months. Results —Patients’ records were pooled (total 1292 patients; streptokinase, n=653, no streptokinase n=639). The subgroup analysis of treatment effect according to delay from symptoms to inclusion shows only a trend toward a better treatment effect with shorter delay, which is not statistically significant for any outcome. Heavier patients in MAST-E may have had a lower (non significant) risk from the fixed dose of 1.5 million units of streptokinase. Concomitant aspirin increased the excess mortality rates in streptokinase-treated patients (17% without aspirin versus 91% with aspirin, P =0.005). The presence of early CT scan signs did not increase the detrimental effect of streptokinase. Conclusions —Few factors influenced the response to streptokinase. However, earlier administration, lower doses of streptokinase, and avoidance of concomitant aspirin should be considered if further streptokinase trials in acute stroke are planned.

Background and Purpose —Hemorrhagic transformation (HT) is the most critical complication of thrombolytics in clinical trials in acute stroke. The aim of this study was to determine the rates and the predictors of HT in the Multicenter Acute Stroke Trial–Europe (MAST-E) study. Methods —We performed a post hoc analysis of MAST-E data designed to assess the safety and efficacy of streptokinase administered intravenously within 6 hours of stroke onset. HT included all intracerebral hemorrhages and symptomatic hemorrhages (SHT) associated with clinical worsening. The predictors of HT and SHT were determined using multivariate modeling. Results —Among the 310 patients included, 159 patients had HT and 37 SHT (97 and 33 in the streptokinase group and 62 and 4 in the placebo group, respectively). Patients with SHT had significantly more atrial fibrillation, diabetes mellitus, no heparin use, streptokinase treatment, and early CT signs. In the multivariate analysis, HT was predicted by early CT signs and streptokinase treatment. SHT was predicted by diabetes mellitus, early CT signs, streptokinase treatment, and the interaction between streptokinase treatment and decreased level of consciousness. Among the streptokinase-treated patients, the same predictors remained. Conclusions —The relative risks of HT after streptokinase were in the same range in MAST-E as in other streptokinase and tPA trials. Early CT signs were strong predictors of both HT and SHT, stressing that these patients are at high risk of bleeding. In our study, the predictors of HT and SHT were similar to those of tPA trials in acute stroke.

A door-to-door population-based epidemiological study of the prevalence of migraine and headache in a sample of 3246 people older than 15 years of age was carried out in Cuzco, a high-altitude town in the Peruvian Andes, located at 3380 meters. Among the 3246 screened people, there were 172 cases of migraine and 930 cases of headache, yielding a crude 1-year prevalence of 5.3% for migraine (2.3% among men and 7.8% among women) and 28.7% for headache (17.5% among men and 38.2% among women). Our results suggest that migraine prevalence in Cuzco is close to that of other developing countries, whereas headache prevalence may be higher than in other developing countries. Multivariate logistic regression suggested that both migraine and headache were related to the female sex, age, and anxiety and/or depression. This study suggests that migraine is a relatively common disorder in Cuzco, but does not show any difference which could be significantly related to altitude. In contrast, our results suggest that headache may be more frequent at high altitude than at sea level.

The French healthcare system is organised according to a political, geographical and demographic framework. In France today, less than 20 hospitals have dedicated intensive care units for acute stroke patients. In the 1999 national survey, 94% of stroke patients were admitted to public hospitals, 35% were treated in neurological wards and 4% had access to an intensive care stroke unit. To improve the quality of care and resource utilisation, a national plan for stroke will be implemented at regional level during the next five-year plan. After a long period of status quo, many positive actions for stroke care have been initiated within a couple of years, based on the evidence of more effective stroke treatments, such as thrombolysis and the specialist care provided by stroke units.

Background: Survival may depend on the ability to efficiently identify threats signaled by the emotional content of facial expressions. While current neural models of facial emotion processing do not prominently feature the basal ganglia, evidence from clinical and functional imagi¬ng studies suggest involvement of the ventral striatum. Methods: To assess the specific role of the basal ganglia in emotion processing, we compared basic facial emotion identification in 23 young patients with a pure focal basal ganglia stroke (mean age 44.9 ± 11.6; 10 males) to 68 matched healthy controls (43.8 years ± 14.0; 27 males). We used quantitative MRI lesion analysis to assess the relationship between basal ganglia location and basic emotion identification. To assess whether facial emotion identification might be related to non-specific lesion effects, we also assessed a wide range of cognitive and motor abilities and screened participants for co-morbid conditions such as depression or anxiety. In addition, we assessed social behavior in terms of social adaptability and the ability to return to work. Results: (1) Basic emotion identification was impaired following focal lesions limited to the basal ganglia. (2) The identification impairment was limited to threat-related emotions, including anger, fear and disgust identification, suggesting a role for the basal ganglia in threat detection. These findings may reflect altered gating mechanisms for facial emotion displays conveying threat signals, with the basal ganglia selecting information relevant to safety. (3) We found that emotion identification impairments adversely affect social behavior, suggesting that emotion identification skills may be of substantial practical importance, and should be considered in the clinical assessment and rehabilitation of patients with basal ganglia lesions. Conclusions: Dorsolateral striatal lesions may affect threat-related emotion identification by disrupting limbic basal ganglia-thalamocortical loop functions associating threat detection with selection of appropriate escape or defensive actions that can preserve individual safety. From a clinical perspective, while the impact of emotion identification impairment on social behavior should be more thoroughly examined in further studies, the consequences of basal ganglia damage appear to be detectible at the individual level. Figure legend: Lesion overlap for patients with identification impairments for anger (red); fear (blue) disgust (green) and all threat emotion (yellow).

Summary Background Hemiplegia and hemiparesis are the most common deficits caused by stroke. A few small clinical trials suggest that fluoxetine enhances motor recovery but its clinical efficacy is unknown. We therefore aimed to investigate whether fluoxetine would enhance motor recovery if given soon after an ischaemic stroke to patients who have motor deficits. Methods In this double-blind, placebo-controlled trial, patients from nine stroke centres in France who had ischaemic stroke and hemiplegia or hemiparesis, had Fugl-Meyer motor scale (FMMS) scores of 55 or less, and were aged between 18 years and 85 years were eligible for inclusion. Patients were randomly assigned, using a computer random-number generator, in a 1:1 ratio to fluoxetine (20 mg once per day, orally) or placebo for 3 months starting 5–10 days after the onset of stroke. All patients had physiotherapy. The primary outcome measure was the change on the FMMS between day 0 and day 90 after the start of the study drug. Participants, carers, and physicians assessing the outcome were masked to group assignment. Analysis was of all patients for whom data were available (full analysis set). This trial is registered with ClinicalTrials.gov, number NCT00657163. Findings 118 patients were randomly assigned to fluoxetine (n=59) or placebo (n=59), and 113 were included in the analysis (57 in the fluoxetine group and 56 in the placebo group). Two patients died before day 90 and three withdrew from the study. FMMS improvement at day 90 was significantly greater in the fluoxetine group (adjusted mean 34·0 points [95% CI 29·7–38·4]) than in the placebo group (24·3 points [19·9–28·7]; p=0·003). The main adverse events in the fluoxetine and placebo groups were hyponatraemia (two [4%] vs two [4%]), transient digestive disorders including nausea, diarrhoea, and abdominal pain (14 [25%] vs six [11%]), hepatic enzyme disorders (five [9%] vs ten [18%]), psychiatric disorders (three [5%] vs four [7%]), insomnia (19 [33%] vs 20 [36%]), and partial seizure (one [ vs 0). Interpretation In patients with ischaemic stroke and moderate to severe motor deficit, the early prescription of fluoxetine with physiotherapy enhanced motor recovery after 3 months. Modulation of spontaneous brain plasticity by drugs is a promising pathway for treatment of patients with ischaemic stroke and moderate to severe motor deficit. Funding Public French National Programme for Clinical Research.

Background: Cognitive dysfunctioning (CDF) is an important issue in stroke, interfering with recovery and social dysfunctioning. We aimed to investigate the clinical and imaging correlates of CDF in patients with a first-ever subacute ischemic stroke and no dementia. Methods: We evaluated CDF 15 days after stroke in a prospective cohort of consecutive patients with a Mini Mental State Examination score ≧23 using a comprehensive neuropsychological battery. CDF was ranked into 3 categories according to Z scores calculated for each test and adjusted for age and education. CDF was analyzed in relation to stroke features. Imaging was assessed using MRI. An ordinal regression procedure was used to determine the clinical correlates of CDF and to compute probabilities. Results: Cognitive evaluation was achieved in 177 consecutive patients (age 50.0 ± 16.0 years). In bivariate analysis, CDF was associated with age, low level of education, depression, neurological deficit at day 15, stroke subtype, arterial territory and leukoaraiosis but not with stroke volume or location. The predictors of CDF were NIHSS score at day 15 (OR = 1.35; 95% CI = 1.05–1.73), middle cerebral artery infarct (OR = 2.96; 95% CI = 1.30–6.73), depression interacting with left stroke side (OR = 1.09; 95% CI = 1.03–1.15), and female gender interacting with high level of education (OR = 0.209; 95% CI = 0.085–0.514). Conclusions: Stroke features correlate with CDF in nondemented patients. These simple criteria may help to predict CDF at bedside in the subacute phase after stroke and to recommend a neuropsychological evaluation for patients’ management. Modeling CDF soon after stroke using simple neurological criteria may be a useful tool for designing clinical trials.

Background and Purpose— Determining cognitive dysfunctioning (CDF) after stroke is an important issue because it influences choices for management in terms of return to previous activities. Because previous research in subacute stroke has shown important variations in CDF rates, we aimed to describe the frequency and neuropsychological profile of CDF in subacute stroke outside dementia. We used a large battery of tests to screen any potentially hidden CDF. Methods— Patients with Mini-Mental State Examination scores ≥23 were prospectively and consecutively included 2 weeks after a first-ever ischemic brain infarct. Stroke features were based on MRI. Four domains were evaluated: instrumental and executive functions, episodic memory, and working memory (WM). Patients were scored using means and compared with education- and age-matched control subjects. Then we attributed Z-scores for each test and each domain. The most relevant cognitive tests characterizing CDF were determined using logistic regression. Results— Among 177 patients (mean age, 50.6 years), 91.5% failed in at least one cognitive domain. WM was the most impaired domain (87.6%) with executive functions (64.4%), episodic memory (64.4%), and instrumental functions (24.9%) being relatively preserved. CDF was associated with age, education, depression, neurological deficit, and leukoaraiosis in bivariate analysis. Using logistic regression, WM tests and age predicted CDF (Modified Paced Auditorial Serial Addition Test: OR=0.96 CI=0.93 to 0.98; Owen-spatial-WM: OR=1.07 CI=1.02 to 1.12; age: OR=0.96 CI=0.93 to 0.98). Conclusion— CDF appears to be almost constant, although underestimated, in subacute stroke. WM could reflect some hidden dysfunctioning, which may interfere with rehabilitation and return to work. Clinical routine may include WM tests in young patients with mild stroke.

International audience; BACKGROUND AND AIMS: Social functioning is impaired in approximately two-thirds of stroke patients of vocational age, even several months after a first ever mild to moderate stroke. The known predictors of social functioning are initial stroke severity, anxiety and depression, and the Mini-Mental State Evaluation, suggesting that cognitive deficits contribute to post-stroke social dysfunctioning. The aim of this study was to evaluate whether cognitive domains correlated with social functioning and to determine the cognitive predictors of social dysfunctioning. METHODS: 74 patients were prospectively included 6 months after a first ever stroke. National Institutes of Health Stroke Scale (NIHSS), modified Rankin scale, depression and anxiety were recorded. Social functioning was recorded using the Work and Social Adjustment Scale (WSAS). An extensive neuropsychological test battery explored general cognitive functioning, episodic memory, instrumental functions, executive functions and working memory. Univariate comparisons assessed the relationships between the neuropsychological tests and scores on the WSAS. Predicting factors for WSAS were determined using ordinal logistic regression. RESULTS: 52 patients (70%; 95% confidence interval 58% to 80%) complained of significant perturbations in work and social functioning. In univariate comparisons, general cognitive functioning, memory, instrumental functions, executive functions and working memory significantly correlated with social functioning. Working memory was the most affected domain. With multivariate modelling, the NIHSS at admission, Hospital Anxiety Depression scale and Owen's Spatial Working Memory test were independent predictors of WSAS. CONCLUSIONS: All cognitive domains were associated with social functioning, working memory being the main cognitive determinant. Our results suggest that cognitive impairment impacts on social dysfunctioning, which is known to be a component of quality of life.

International audience; BACKGROUND: With improvements in stroke treatments, the number of patients with dramatic recovery is increasing. However, many of them are still complaining of difficulties in returning to work and every day activities. The aim was to assess work and social dysfunctioning in patients with minor to moderate stroke and explore its contributing factors. METHODS: Consecutive patients were prospectively included at a median 7 months after a first-ever stroke. Scores on the Work and Social Adjustment Scale (WSAS), a generic self-reported scale for assessing social functioning, were correlated with scores on the National Institutes of Health Stroke Scale (NIHSS), activities of daily living, Hospital Anxiety and Depression scale (HAD) and MMSE, Iowa Scale of Personality Changes and return to work at 1 year. RESULTS: Among the 84 included patients (mean age 43.5 years), 57 (68%; 95% CI 57 to 78%) complained of significant perturbation of functioning attributed to stroke. WSAS was highly significantly related to modified Rankin scale, daily living activities, Iowa Scale of Personality Changes and return to work at 1 year. Using ordinal logistic regression, the contributors to WSAS were initial neurological severity (NIHSS at admission), HAD and MMSE. CONCLUSIONS: The study showed that up to 68% of our patients complained of significant work and social dysfunction due to stroke, despite a good clinical outcome. This self-estimation was correlated to external validation criteria, stressing the high burden of stroke from the patient's viewpoint. Moreover, when compared across diseases, social dysfunctioning after mild stroke was as important as in other major disabling diseases.

We report two patients aged 65 and 61 years, who presented a subacute dementia with normal CT scan without contrast injection. Angiography showed a dural arteriovenous malformation. The patients improved dramatically with treatment of the malformation. Dementia was characterised by frontal dysfunction, emotional disorders, mnesic and praxic impairment. This neuropsychological pattern suggests a profile of global dementia in the field of vascular dementia.

Introduction L’efficacite du facteur VII recombinant dans les hematomes cerebraux primitifs a recemment ete rapportee dans une etude de phase IIb, alors qu’il n’existait jusqu’alors aucune therapeutique specifique pour cette pathologie. Objectifs Evaluer en pratique clinique dans une unite neurovasculaire (UNV) la tolerance du facteur VII recombinant (FVIIr) chez des patients admis pour un hematome cerebral primitif. Methodes Les patients inclus etaient ceux admis dans l’UNV du CHU de Grenoble a partir de l’astreinte neurovasculaire pour un hematome primitif, repondant aux criteres d’inclusion de l’etude de Mayer et al, entre janvier 2005 et decembre 2006. Le traitement par FVIIr a ete administre dans les conditions de l’etude (delai Resultats 26 patients (âge moyen 59,2 ans) repondaient aux criteres d’inclusion. 12 ont recu un traitement par FVIIr. Le score NIHSS moyen a l’admission etait de 15,1 pour le groupe traite versus 15 pour le groupe non traite (p = 0,98). Le score NIHSS a la sortie etait de 10 pour le groupe traite contre 16,29 pour le groupe non traite (p = 0,18). 3 patients traites (25 p. 100) ont presente une complication thromboembolique veineuse versus 2 patients (14 p. 100) non traites (p = 0,42). Aucune complication arterielle n’est survenue. Discussion La difference de tolerance chez les patients traites par FVIIr n’est pas statistiquement significative. On remarque neanmoins pour 2 patients traites la survenue d’une complication thromboembolique veineuse moins de 48 h apres le debut des troubles. L’amelioration evaluee par le score NIHSS a la sortie des patients traites n’est pas non plus significative. Les resultats a 3 mois, non encore disponibles, seront presentes. Conclusion L’administration du FVIIr dans l’hematome cerebral de moins de 4 heures est bien toleree, mais pourrait exposer a un risque maladie thromboembolique veineuse precoce.

Background and Purpose We carried out a door-to-door survey on stroke prevalence at high altitude in Cuzco City, a town in the Peruvian Andes located 3380 m above sea level. Methods and Results Among the 3246 screened individuals over 15 years old, there were 21 cases of first-ever completed stroke, yielding a crude prevalence ratio of 6.47 per 1000 (95% confidence interval [CI], 3.71 to 8.93 per 1000). The age-adjusted to WHO population point prevalence ratio was 5.74 per 1000 (95% CI, 3.14 to 8.35 per 1000), and the age-adjusted to North American US population point prevalence ratio was 8.58 per 1000 (95% CI, 5.44 to 11.75 per 1000). Multivariate logistic regression analysis suggested that age, polycythemia, high consumption of alcohol, and area of residence were associated with stroke prevalence. Our results suggest that the stroke prevalence in the central areas of Cuzco with sedentary people having a relatively high standard of living was higher than that in the peripheral areas with people with a relatively lower standard of living and less sedentary activities (odds ratio, 5.8; 95% CI, 1.4 to 23). Conclusions The prevalence of stroke suggests that stroke may be a public health problem in developing countries. This study suggests the importance of environmental factors such as altitude and lifestyle in stroke occurrence. The role of these factors should be confirmed and taken into account in future stroke prevalence studies.

Cerebral venous sinus thrombosis is rare and can be promoted by various conditions. We report the case of cerebral venous thrombosis in a patient using androgens. A 31-year-old man using androgens for bodybuilding was admitted for headache and vomiting. He had cerebral venous sinus thrombosis, but extensive examinations did not reveal any known cause. We suggest that androgens may promote cerebral venous thrombosis. The mechanisms of venous thrombosis related to androgens may be platelet activation or an increase in coagulation factors. Because androgen use may be frequent and hidden in athletes, it may be an underestimated cause of cerebral venous sinus thrombosis in the young.

In clinical trials, assessing efficacy is based on validated scales, and the primary endpoint is usually based on a single scale. The aim of the review is to revisit the concepts and methods to design and analyze studies focused on restoration, recovery and or compensation. These studies are becoming more frequent with the development of restorative medicine. After discussing the definitions of recovery, we address the concept of recovery as the regain of lost capabilities, when the patient reaches a new equilibrium. Recovery is a dynamic process which assessment includes information from initial and final status, their difference, the difference between the final status of the patient and normality, and the speed of restoration. Finally, recovery can be assessed either for a specific function (focal restoration) or for a more global restoration. A single scale is not able to assess all the facets of a skill or a function, therefore complementary information should be collected and analyzed simultaneously to be tested in a single analysis. We are suggesting that recovery should be considered as a latent variable and therefore cannot be measured in pure form. We are also suggesting to customize the data collection and analysis according to the characteristics of the subjects, the mechanisms of action and consequences of the intervention. Moreover, recovery trials should benefit from latent variable analysis methods. Structural equation modeling is likely the best candidate for this approach applicable in pre-clinical and clinical studies.