ORCID Profile
0000-0002-5264-2588
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INSERM
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Publisher: SAGE Publications
Date: 04-07-2018
Abstract: Following middle cerebral artery (MCA) stroke, enhanced contralesional evoked responses have been consistently reported both in man and rodents as part of plastic processes thought to influence motor recovery. How early this marker of large-scale network reorganization develops has however been little addressed, yet has clinical relevance for rehabilitation strategies targeting plasticity. Previous work in mice has reported enhanced contralesional responses to unaffected-side forepaw stimulation as early as 45 min after MCA small branch occlusion. Using functional ultrasound imaging (fUSi) in anesthetized rats subjected to distal temporary MCA occlusion (MCAo), we assessed here (i) whether enhanced contralesional responses also occurred with unaffected-side whisker pad stimulation, and if so, how early after MCAo and (ii) the time course of this abnormal response during occlusion and after reperfusion. We replicate in a more proximal MCA occlusion model the earlier findings of ultra-early enhanced contralesional evoked responses. In addition, we document this phenomenon within minutes after MCAo, and its persistence throughout the entire 90-min occlusion as well as 90-min reperfusion periods studied. These findings suggest that plastic processes may start within minutes following MCAo in rodents. If replicated in man, they might have implications regarding how early plasticity-enhancing therapies can be initiated after stroke.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 03-2020
DOI: 10.1161/STROKEAHA.119.027268
Abstract: In randomized trials of symptomatic carotid endarterectomy, only modest benefit occurred in patients with moderate stenosis and important subgroups experienced no benefit. Carotid plaque 18 F-fluorodeoxyglucose uptake on positron emission tomography, reflecting inflammation, independently predicts recurrent stroke. We investigated if a risk score combining stenosis and plaque 18 F-fluorodeoxyglucose would improve the identification of early recurrent stroke. We derived the score in a prospective cohort study of recent ( days) non-severe (modified Rankin Scale score ≤3) stroke/transient ischemic attack. We derived the SCAIL (symptomatic carotid atheroma inflammation lumen-stenosis) score (range, 0–5) including 18 F-fluorodeoxyglucose standardized uptake values (SUV max g/mL, 0 points SUV max 2–2.99 g/mL, 1 point SUV max 3–3.99 g/mL, 2 points SUV max ≥4 g/mL, 3 points) and stenosis ( %, 0 points 50%–69%, 1 point ≥70%, 2 points). We validated the score in an independent pooled cohort of 2 studies. In the pooled cohorts, we investigated the SCAIL score to discriminate recurrent stroke after the index stroke/transient ischemic attack, after positron emission tomography-imaging, and in mild or moderate stenosis. In the derivation cohort (109 patients), recurrent stroke risk increased with increasing SCAIL score ( P =0.002, C statistic 0.71 [95% CI, 0.56–0.86]). The adjusted (age, sex, smoking, hypertension, diabetes mellitus, antiplatelets, and statins) hazard ratio per 1-point SCAIL increase was 2.4 (95% CI, 1.2–4.5, P =0.01). Findings were confirmed in the validation cohort (87 patients, adjusted hazard ratio, 2.9 [95% CI, 1.9–5], P .001 C statistic 0.77 [95% CI, 0.67–0.87]). The SCAIL score independently predicted recurrent stroke after positron emission tomography-imaging (adjusted hazard ratio, 4.52 [95% CI, 1.58–12.93], P =0.005). Compared with stenosis severity (C statistic, 0.63 [95% CI, 0.46–0.80]), prediction of post-positron emission tomography stroke recurrence was improved with the SCAIL score (C statistic, 0.82 [95% CI, 0.66–0.97], P =0.04). Findings were confirmed in mild or moderate stenosis (adjusted hazard ratio, 2.74 [95% CI, 1.39–5.39], P =0.004). The SCAIL score improved the identification of early recurrent stroke. Randomized trials are needed to test if a combined stenosis-inflammation strategy improves selection for carotid revascularization where benefit is currently uncertain.
Publisher: BMJ
Date: 11-2002
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 05-2016
DOI: 10.1161/STROKEAHA.115.012364
Abstract: The Stroke Imaging Research (STIR) group, the Imaging Working Group of StrokeNet, the American Society of Neuroradiology, and the Foundation of the American Society of Neuroradiology sponsored an imaging session and workshop during the Stroke Treatment Academy Industry Roundtable (STAIR) IX on October 5 to 6, 2015 in Washington, DC. The purpose of this roadmap was to focus on the role of imaging in future research and clinical trials. This forum brought together stroke neurologists, neuroradiologists, neuroimaging research scientists, members of the National Institute of Neurological Disorders and Stroke (NINDS), industry representatives, and members of the US Food and Drug Administration to discuss STIR priorities in the light of an unprecedented series of positive acute stroke endovascular therapy clinical trials. The imaging session summarized and compared the imaging components of the recent positive endovascular trials and proposed opportunities for pooled analyses. The imaging workshop developed consensus recommendations for optimal imaging methods for the acquisition and analysis of core, mismatch, and collaterals across multiple modalities, and also a standardized approach for measuring the final infarct volume in prospective clinical trials. Recent positive acute stroke endovascular clinical trials have demonstrated the added value of neurovascular imaging. The optimal imaging profile for endovascular treatment includes large vessel occlusion, smaller core, good collaterals, and large penumbra. However, equivalent definitions for the imaging profile parameters across modalities are needed, and a standardization effort is warranted, potentially leveraging the pooled data resulting from the recent positive endovascular trials.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 08-2017
DOI: 10.1161/STROKEAHA.116.012992
Abstract: We assessed whether the presence, number, and distribution of cerebral microbleeds (CMBs) on pre-intravenous thrombolysis MRI scans of acute ischemic stroke patients are associated with an increased risk of intracerebral hemorrhage (ICH) or poor functional outcome. We performed an in idual patient data meta-analysis, including prospective and retrospective studies of acute ischemic stroke treated with intravenous tissue-type plasminogen activator. Using multilevel mixed-effects logistic regression, we investigated associations of pre-treatment CMB presence, burden (1, 2–4, ≥5, and ), and presumed pathogenesis (cerebral amyloid angiopathy defined as strictly lobar CMBs and noncerebral amyloid angiopathy) with symptomatic ICH, parenchymal hematoma (within [parenchymal hemorrhage, PH] and remote from the ischemic area [remote parenchymal hemorrhage, PHr]), and poor 3- to 6-month functional outcome (modified Rankin score ). In 1973 patients from 8 centers, the crude prevalence of CMBs was 526 of 1973 (26.7%). A total of 77 of 1973 (3.9%) patients experienced symptomatic ICH, 210 of 1806 (11.6%) experienced PH, and 56 of 1720 (3.3%) experienced PHr. In adjusted analyses, patients with CMBs (compared with those without CMBs) had increased risk of PH (odds ratio: 1.50 95% confidence interval: 1.09–2.07 P =0.013) and PHr (odds ratio: 3.04 95% confidence interval: 1.73–5.35 P .001) but not symptomatic ICH. Both cerebral amyloid angiopathy and noncerebral amyloid angiopathy patterns of CMBs were associated with PH and PHr. Increasing CMB burden category was associated with the risk of symptomatic ICH ( P =0.014), PH ( P =0.013), and PHr ( P .00001). Five or more and CMBs independently predicted poor 3- to 6-month outcome (odds ratio: 1.85 95% confidence interval: 1.10–3.12 P =0.020 and odds ratio: 3.99 95% confidence interval: 1.55–10.22 P =0.004, respectively). Increasing CMB burden is associated with increased risk of ICH (including PHr) and poor 3- to 6-month functional outcome after intravenous thrombolysis for acute ischemic stroke.
Publisher: Elsevier BV
Date: 07-2008
DOI: 10.1016/J.EJVS.2008.02.006
Abstract: PET-FDG and USPIO-enhanced MRI are increasingly being used in depicting carotid atheroma inflammation--a risk factor for the high risk plaque. Their combined use has not been previously reported. Two patients presenting with stroke and identified with 50% carotid stenosis on duplex ultrasonography, underwent PET FDG and USPIO-enhanced MR imaging. Results were concordant and complementary suggesting that both techniques reflect similar metabolic processes. The selection of patients for carotid revascularisation has largely been based on the severity of luminal stenosis alone. The two imaging modalities, which identify inflammatory activity, may be potential surrogate risk markers in the selection of patients eligible for carotid surgery, if plaque inflammation can be correlated with risk of developing clinical symptoms.
Publisher: SAGE Publications
Date: 20-03-2018
Abstract: Obstetrical analgesia remains a matter of controversy because of the fear of neurotoxicity of local anesthetics on demyelinated fibers or their potential relationship with subsequent relapses. To assess the impact of neuraxial analgesia on the risk of relapse during the first 3 months post-partum, with a focus on women who experienced relapses during pregnancy. We analyzed data of women followed-up prospectively during their pregnancies and at least 3 months post-partum, collected in the Pregnancy in Multiple Sclerosis (PRIMS) and Prevention of Post-Partum Relapses with Progestin and Estradiol in Multiple Sclerosis (POPARTMUS) studies between 1992–1995 and 2005–2012, respectively. The association of neuraxial analgesia with the occurrence of a post-partum relapse was estimated by logistic regression analysis. A total of 389 women were included, 215 from PRIMS and 174 from POPARTMUS. In total, 156 women (40%) had neuraxial analgesia. Overall, 24% experienced a relapse during pregnancy and 25% in the 3 months post-partum. Women with a pregnancy relapse were more likely to have a post-partum relapse (odds ratio (OR) = 1.83, p = 0.02), independently of the use of neuraxial analgesia. There was no association between neuraxial analgesia and post-partum relapse (OR = 1.08, p = 0.78). Neuraxial analgesia was not associated with an increased risk of post-partum relapses, whatever multiple sclerosis (MS) activity during pregnancy.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 26-07-2017
DOI: 10.1212/WNL.0000000000004259
Abstract: We evaluated recurrent intracerebral hemorrhage (ICH) risk in ICH survivors, stratified by the presence, distribution, and number of cerebral microbleeds (CMBs) on MRI (i.e., the presumed causal underlying small vessel disease and its severity). This was a meta-analysis of prospective cohorts following ICH, with blood-sensitive brain MRI soon after ICH. We estimated annualized recurrent symptomatic ICH rates for each study and compared pooled odds ratios (ORs) of recurrent ICH by CMB presence/absence and presumed etiology based on CMB distribution (strictly lobar CMBs related to probable or possible cerebral amyloid angiopathy [CAA] vs non-CAA) and burden (1, 2–4, 5–10, and CMBs), using random effects models. We pooled data from 10 studies including 1,306 patients: 325 with CAA-related and 981 CAA-unrelated ICH. The annual recurrent ICH risk was higher in CAA-related ICH vs CAA-unrelated ICH (7.4%, 95% confidence interval [CI] 3.2–12.6 vs 1.1%, 95% CI 0.5–1.7 per year, respectively p = 0.01). In CAA-related ICH, multiple baseline CMBs (versus none) were associated with ICH recurrence during follow-up (range 1–3 years): OR 3.1 (95% CI 1.4–6.8 p = 0.006), 4.3 (95% CI 1.8–10.3 p = 0.001), and 3.4 (95% CI 1.4–8.3 p = 0.007) for 2–4, 5–10, and CMBs, respectively. In CAA-unrelated ICH, only CMBs (versus none) were associated with recurrent ICH (OR 5.6, 95% CI 2.1–15 p = 0.001). The presence of 1 CMB (versus none) was not associated with recurrent ICH in CAA-related or CAA-unrelated cohorts. CMB burden and distribution on MRI identify subgroups of ICH survivors with higher ICH recurrence risk, which may help to predict ICH prognosis with relevance for clinical practice and treatment trials.
Publisher: Elsevier BV
Date: 03-2009
Publisher: SAGE Publications
Date: 27-03-2017
Abstract: Collaterals 2016 (third International Symposium on Collaterals to the Brain) was a multidisciplinary scientific conference focused on collateral circulation in acute ischemic stroke. Decisive challenges include generalizability of optimal triage and selection paradigms based on collateral status for definitive treatment of acute ischemic stroke, rapid dissemination of expert methods, and the urgent need to leverage networking opportunities for stroke science related to the hemodynamics of collaterals. The collaterome, or in idual capacity to offset ischemia in the brain, and determination of a favorable collateral profile have become pivotal factors in consideration of the precision medicine of stroke decision-making. The conference convened over 50 invited faculty from around the world to connect on-site participants at a state-of-the-art facility with remote audiences in more than 22 countries and regions. The 2½-day program was structured into 40-min sessions devoted to key issues in translating the collaterome in acute stroke therapy across the globe. This unique forum of expertise emphasized the timely impact of collaterals on a monumental scale, encouraging maximal participation, rapid diffusion and added value of a erse networking resource. The meeting format established a model geographical framework and innovative videoconferencing platform for future scientific conferences.
Publisher: SAGE Publications
Date: 02-2008
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 09-2013
Publisher: SAGE Publications
Date: 18-01-2016
Abstract: For the STroke Imaging Research (STIR) and VISTA-Imaging Investigators The purpose of this study was to collect precise information on the typical imaging decisions given specific clinical acute stroke scenarios. Stroke centers worldwide were surveyed regarding typical imaging used to work up representative acute stroke patients, make treatment decisions, and willingness to enroll in clinical trials. STroke Imaging Research and Virtual International Stroke Trials Archive-Imaging circulated an online survey of clinical case vignettes through its website, the websites of national professional societies from multiple countries as well as through email distribution lists from STroke Imaging Research and participating societies. Survey responders were asked to select the typical imaging work-up for each clinical vignette presented. Actual images were not presented to the survey responders. Instead, the survey then displayed several types of imaging findings offered by the imaging strategy, and the responders selected the appropriate therapy and whether to enroll into a clinical trial considering time from onset, clinical presentation, and imaging findings. A follow-up survey focusing on 6 h from onset was conducted after the release of the positive endovascular trials. We received 548 responses from 35 countries including 282 in idual centers 78% of the centers originating from Australia, Brazil, France, Germany, Spain, United Kingdom, and United States. The specific onset windows presented influenced the type of imaging work-up selected more than the clinical scenario. Magnetic Resonance Imaging usage (27–28%) was substantial, in particular for wake-up stroke. Following the release of the positive trials, selection of perfusion imaging significantly increased for imaging strategy. Usage of vascular or perfusion imaging by Computed Tomography or Magnetic Resonance Imaging beyond just parenchymal imaging was the primary work-up (62–87%) across all clinical vignettes and time windows. Perfusion imaging with Computed Tomography or Magnetic Resonance Imaging was associated with increased probability of enrollment into clinical trials for 0–3 h. Following the release of the positive endovascular trials, selection of endovascular only treatment for 6 h increased across all clinical vignettes.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 02-2004
DOI: 10.1097/00019052-200402000-00011
Abstract: Imaging the penumbra is essential, not only to identify patients who might benefit from thrombolysis, but also to further understanding of the ischaemic process, thereby potentially revealing new opportunities for therapeutic intervention. Here we review recent imaging studies of the acute stroke process. Perfusion-computed tomography and computed tomography angiography enable assessment of the haemodynamic status and site of occlusion, leading to their promising use in guiding thrombolysis. The magnetic resonance concept of the diffusion-perfusion 'mismatch' being representative of penumbra appears to be an oversimplification. The mapping of simple variables such as time-to-peak might not directly reveal true penumbral perfusion levels. Also, lesions seen with diffusion-weighted imaging may be reversible as a result of early reperfusion. This reversal with subsequent normalization may represent selective neuronal damage. Late secondary injury, as indicated by the reappearance of the diffusion-weighted imaging lesion, has recently been documented the mechanisms are unknown but form potential targets for future therapies. Despite these caveats, diffusion-weighted imaging-perfusion-weighted imaging remains the most useful approach to map the pathophysiology of stroke in the clinical setting. Acute/subacute flumazenil positron emission tomography studies are being used as markers of neuronal integrity to help shed further light on infarction thresholds, and potentially document selective neuronal loss. F-labelled fluoromisonidazole positron emission tomography imaging of brain hypoxia documents the temporal and spatial progression of the penumbra. The goal of understanding the complex process that is acute ischaemia in stroke, and subsequently the development of therapeutic strategies, continues to be advanced by imaging the penumbra in novel ways.
Publisher: SAGE Publications
Date: 12-09-2019
Abstract: The Boston criteria are used worldwide for the in vivo diagnosis of cerebral amyloid angiopathy and are the basis for clinical decision-making and research in the field. Given substantial advances in cerebral amyloid angiopathy's clinical aspects and MRI biomarkers, we designed a multicenter study within the International cerebral amyloid angiopathy Association aimed at further validating the diagnostic accuracy of the Boston and potentially improving and updating them. We aim to derive and validate an updated “version 2.0” of the Boston criteria across the spectrum of cerebral amyloid angiopathy-related presentations and MRI biomarkers. Participating centers with suitable available data (see Methods) were identified from existing collaborations and an open invitation to the International Cerebral Amyloid Angiopathy Association emailing list. Our study s le will include: (1) a derivation cohort – Massachusetts General Hospital (MGH), Boston cases from inception to 2012 (∼150 patients) (2) temporal external validation cohort – MGH, Boston cases from 2012 to 2018 (∼100 patients) and (3) geographical external validation cohort – non-Boston cases (∼85 patients). Multicenter collaborative study. We will collect and analyze data from patients' age ≥ 50 with any potential sporadic cerebral amyloid angiopathy-related clinical presentations (spontaneous intracerebral hemorrhage, transient focal neurological episodes and cognitive impairment), available brain MRI (“index test”), and histopathologic assessment for cerebral amyloid angiopathy (“reference standard” for diagnosis). Trained raters will assess MRI for all prespecified hemorrhagic and non-hemorrhagic small vessel disease markers of interest, according to validated criteria and a prespecified protocol, masked to clinical and histopathologic features. Brain tissue s les will be rated for cerebral amyloid angiopathy, defined as Vonsattel grade ≥2 for whole brain autopsies and ≥1 for cortical biopsies or hematoma evacuation. Based on our estimated available s le size, we will undertake pre-specified cohort splitting as above. We will: (a) pre-specify variables and statistical cut-offs (b) examine univariable and multivariable associations and (c) then assess classification measures (sensitivity, specificity etc.) for each MRI biomarker in idually, in relation to the cerebral amyloid angiopathy diagnosis reference standard on neuropathology in a derivation cohort. The MRI biomarkers strongly associated with cerebral amyloid angiopathy diagnosis will be selected for inclusion in provisional (probable and possible cerebral amyloid angiopathy) Boston criteria v2.0 and validated using appropriate metrics and models. Boston criteria v2.0 for clinical cerebral amyloid angiopathy diagnosis. This work aims to potentially update and improve the diagnostic test accuracy of the Boston criteria for cerebral amyloid angiopathy and to provide wider validation of the criteria in a large s le. We envision that this work will meet the needs of clinicians and investigators and help accelerate progress towards better treatment of cerebral amyloid angiopathy.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 05-2008
DOI: 10.1161/STROKEAHA.107.512319
Abstract: The recent “Advanced Neuroimaging for Acute Stroke Treatment” meeting on September 7 and 8, 2007 in Washington DC, brought together stroke neurologists, neuroradiologists, emergency physicians, neuroimaging research scientists, members of the National Institute of Neurological Disorders and Stroke (NINDS), the National Institute of Biomedical Imaging and Bioengineering (NIBIB), industry representatives, and members of the US Food and Drug Administration (FDA) to discuss the role of advanced neuroimaging in acute stroke treatment. The goals of the meeting were to assess state-of-the-art practice in terms of acute stroke imaging research and to propose specific recommendations regarding: (1) the standardization of perfusion and penumbral imaging techniques, (2) the validation of the accuracy and clinical utility of imaging markers of the ischemic penumbra, (3) the validation of imaging biomarkers relevant to clinical outcomes, and (4) the creation of a central repository to achieve these goals. The present article summarizes these recommendations and examines practical steps to achieve them.
Publisher: Oxford University Press (OUP)
Date: 25-08-2010
DOI: 10.1093/BRAIN/AWQ187
Abstract: β-Amyloid deposition is one of the main hallmarks of Alzheimer's disease thought to eventually cause neuronal death. Post-mortem and neuroimaging studies have consistently reported cases with documented normal cognition despite high β-amyloid burden. It is of great interest to understand what differentiates these particular subjects from those without β-amyloid deposition or with both β-amyloid deposition and cognitive deficits, i.e. what allows these subjects to resist the damage of the pathological lesions. [¹¹C]Pittsburgh compound B positron emission tomography and magnetic resonance brain scans were obtained in 149 participants including healthy controls and patients with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease. Magnetic resonance data were compared between high versus low-[11C]Pittsburgh compound B cases, and between high-[¹¹C]Pittsburgh compound B cases with versus those without cognitive deficits. Larger temporal (including hippoc al) grey matter volume, associated with better episodic memory performance, was found in high- versus low-[¹¹C]Pittsburgh compound B healthy controls. The same finding was obtained using different [¹¹C]Pittsburgh compound B thresholds, correcting [¹¹C]Pittsburgh compound B data for partial averaging, using age, education, Mini-Mental State Examination, apolipoprotein E4 and sex-matched subs les, and using manual hippoc al delineation instead of voxel-based analysis. By contrast, in participants with subjective cognitive impairment, significant grey matter atrophy was found in high-[¹¹C]Pittsburgh compound B cases compared to low-[¹¹C]Pittsburgh compound B cases, as well as in high-[¹¹C]Pittsburgh compound B cases with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease compared to high-[¹¹C]Pittsburgh compound B healthy controls. Larger grey matter volume in high-[¹¹C]Pittsburgh compound B healthy controls may reflect either a tissue reactive response to β-amyloid or a combination of higher 'brain reserve' and under-representation of subjects with standard/low temporal volume in the high-[¹¹C]Pittsburgh compound B healthy controls. Our complementary analyses tend to support the latter hypotheses. Overall, our findings suggest that the deleterious effects of β-amyloid on cognition may be delayed in those subjects with larger brain (temporal) volume.
No related grants have been discovered for jean-claude baron.