Literatura científica selecionada sobre o tema "Hyperintensités de la substance blanche"
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Artigos de revistas sobre o assunto "Hyperintensités de la substance blanche"
Peltier, J., B. Nicot, M. Baroncini, Y. Zunon-Kipré, A. Haidara, E. Havet, P. Foulon, C. Page, J. P. Lejeune e D. Le Gars. "Anatomie de la substance blanche périventriculaire". Neurochirurgie 57, n.º 4-6 (setembro de 2011): 151–55. http://dx.doi.org/10.1016/j.neuchi.2011.09.017.
Texto completo da fonteLabauge, P. "Génétique et maladies de la substance blanche". EMC - Neurologie 6, n.º 2 (janeiro de 2009): 1–8. http://dx.doi.org/10.1016/s0246-0378(09)50908-6.
Texto completo da fonteSchmitt, E. "Imagerie des pathologies de la substance blanche". Journal de Radiologie 90, n.º 10 (outubro de 2009): 1376. http://dx.doi.org/10.1016/s0221-0363(09)75427-7.
Texto completo da fonteAlamowitch, S. "Atteintes de la substance blanche et microbleeds". Pratique Neurologique - FMC 4, n.º 2 (abril de 2013): 79–86. http://dx.doi.org/10.1016/j.praneu.2013.01.012.
Texto completo da fonteMondot, L., S. Chanalet, S. Stolear, C. Lebrun-Frenay e B. Padovani. "NR-WP-30 IRM : La substance blanche simplifiee". Journal de Radiologie 90, n.º 10 (outubro de 2009): 1545. http://dx.doi.org/10.1016/s0221-0363(09)76048-2.
Texto completo da fontede Seze, J. "Les atteintes de la substance blanche d’origine dysimmunitaires". Pratique Neurologique - FMC 4, n.º 2 (abril de 2013): 73–75. http://dx.doi.org/10.1016/j.praneu.2013.01.006.
Texto completo da fonteDalloz, M. A., R. Debs, C. Bensa e S. Alamowitch. "Hypersignaux de la substance blanche révélant un pseudoxanthome élastique". Revue Neurologique 166, n.º 10 (outubro de 2010): 844–48. http://dx.doi.org/10.1016/j.neurol.2010.01.015.
Texto completo da fonteRodrigo, S., Y. Cointepas, L. Huwart, C. Oppenheim, C. Poupon, J. F. Méder e D. Frédy. "Radioanatomie des faisceaux de substance blanche en tenseur de diffusion". Journal de Radiologie 85, n.º 9 (setembro de 2004): 1344. http://dx.doi.org/10.1016/s0221-0363(04)77115-2.
Texto completo da fonteDurand-Birchenall, Julia, Claire Leclercq, Joël Daouk, Pauline Monet, Olivier Godefroy e Jean-Marc Bugnicourt. "Régression des anomalies de substance blanche après un AVC lacunaire". Revue Neurologique 168 (abril de 2012): A84. http://dx.doi.org/10.1016/j.neurol.2012.01.212.
Texto completo da fonteDietemann, J. L., C. Jacques, A. Bogorin, M. Abu Eid, M. Koob e G. Zöllner. "4306 IRM de la substance blanche normale et pathologique de l’adulte". Journal de Radiologie 85, n.º 9 (setembro de 2004): 1210. http://dx.doi.org/10.1016/s0221-0363(04)76681-0.
Texto completo da fonteTeses / dissertações sobre o assunto "Hyperintensités de la substance blanche"
Tran, Philippe. "Segmentation and characterization of cerebral white matter hyperintensities : application in individuals with multiple sclerosis and age-related pathologies". Electronic Thesis or Diss., Sorbonne université, 2022. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2022SORUS243.pdf.
Texto completo da fonteWhite matter hyperintensities (WMH) are more and more taken into account in the clinical monitoring of elderly subjects and/or dementia patients, and are crucial in patients with Multiple Sclerosis (MS). Automated methods have been proposed to better quantify these lesions on a large scale, in order to better understand the underlying mechanisms of these pathologies. However, to our knowledge, no automated method has reached consensus today for the segmentation of WMH, and no method has been validated on these two types of subjects. This thesis introduces several tools and their validations in order to better characterize WMH. First of all, WHASA-3D (Tran et al. 2022) is a new automated method for WMH segmentation adapted for 3D T2-FLAIR data and MS patients in a multicenter setting. It is a major improvement of WHASA (Samaille et al. 2012). WHASA-3D's performances are here compared with six state-of-the-art methods with their default parameters and optimized settings, when possible. Two extensions have then been developped to support the clinician for patient diagnosis and clinical monitoring. WHASA-Spatial is an extension for the automatic spatial characterization of WMH provided by WHASA-3D according to four classes (periventricular, infratentorial, juxtacortical/cortical, deep). The visual assessment on 104 MS subjects showed that the global classification was very satisfactory. Finally, WHASA-Longitudinal, is an extension that allows the automatic segmentation of new or enlarged lesions between two successive acquisitions. The performance of this method was satisfactory for volume agreement and a solution is proposed and needs to be investigated to improve new lesion count. These results need to be confirmed on a larger number of subjects
Djabelkhir, Jemmi Leila. "Prise en charge non pharmacologique des troubles cognitifs légers : effets différentiels d'un programme de stimulation cognitive informatisée selon la sévérité des hypersignaux de la substance blanche de patients MCI". Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB241.
Texto completo da fonteWhite matter hyper signals (WMH) were associated with executive and memory deficits and impairment of the cortical and subcortical frontal circuits. Their presence, in addition to amyloid deposition in many patients with Mild Cognitive Impairment (MCI), would increase the risk of conversion to Alzheimer's disease (AD). An important issues in the preclinical phase of MCI is to explore the potential of cognitive interventions to prevent cognitive decline and progression to AD. While WMH are increasingly considered as one of factors determining the heterogeneity of MCI patients, few studies have take into account their presence in cognitive interventions. The hypothesis that an intervention could induce differential effects according to the existence or not of WMH in MCI remains unexplored to our knowledge, and is at the heart of this work of thesis
Cognat, Emmanuel. "Lésions de la substance blanche dans la maladie CADASIL". Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC139/document.
Texto completo da fonteCADASIL is an autosomal dominant, hereditary, small vessel disease of the brain causing early and progressive white matter lesions. The histopathological characteristics of these lesions remain poorly known. The disease is caused by stereotyped mutations in the gene coding for the NOTCH3 receptor. One of CADASIL hallmarks is the presence in vessels of an abnormal accumulation of NOTCH3 extracellular domain (NOTCH3ECD). Data suggest that CADASIL pathophysiological process may be caused by a toxic effect resulting from NOTCH3ECD deposits, due to an abnormal recruitment of other extracellular matrix components. However, it has been shown that CADASIL mutations differentially affect Notch3 signaling, constitutively or progressively. The latter observations led scientists to propose the hypothesis that Notch3 loss of function may play an important role in CADASIL pathogenesis.We conducted a detailed white matter analysis in a CADASIL mouse model that overexpresses a Notch3 allele with the R169C/R170C mutation and that recapitulates the preclinical stages of the disease (TgPACNotch3R169C). In this model, we observed intramyelinic edema associated with myelin degradation / decompaction detectable by immunochemistry in the brain of mice as young as 6 months of age. Axonal integrity analysis in myelin lesions suggested that axonal loss may appear secondarily. A semi-quantitative method for the quantification of myelin debris has been developed.Next, we tested the hypothesis that Notch3 loss of function might play a key role in CADASIL pathophysiology. We first identified a set of genes that are sensitive to a reduction in Notch3 dosage by half. Quantification of these genes expression in both heterozygous and homozygous mice Knock-in for the R170C mutation showed that Notch3 activity was not lowered in this model. In addition, we analyzed the effect of a suppression of endogenous Notch3 copies on white matter lesions observed in TgPACNotch3R169C mice and observed no worsening of these lesions. Together these results suggest that hypomorphism is not a feature common to all CADASIL mutations, and that white matter lesions in CADASIL do no result from Notch3 loss of function.Finally, we studied the pathogenic effect of Timp3 and vitronectine accumulation, both proteins having been shown to accumulate with NOTCH3ECD early in the course of the disease. By the use of genetic interaction approaches (lowering and increase in Timp3 and vitronectine in TgPACNotch3R169C mice), we observed differential effects of the proteins on white matter lesions and cerebrovascular reactivity impairment. Indeed, vitronectine lowering improves white matter lesions without any effect on cerebrovascular reactivity while Timp3 diminution restores cerebrovascular reactivity without any effect on white matter lesions. These results provide proof of concept for the implication of TIMP3 and vitronectin excess in CADASIL pathogenesis and questions the dogma that make hypoperfusion the main determinant of white matter lesions in CADASIL
Samaille, Thomas. "Segmentation automatique des anomalies de la substance blanche du sujet âgé". Paris 6, 2013. http://www.theses.fr/2013PA066162.
Texto completo da fonteUszynski, Ivy. "Identification et caractérisation des faisceaux de substance blanche en IRM : développements précliniques". Thesis, Université Grenoble Alpes (ComUE), 2018. http://www.theses.fr/2018GREAY075/document.
Texto completo da fonteMagnetic resonance imaging (MRI) allows the observation of the major white matter fiber tracts in the brain. It can thus be used in many applications to have a better understanding of the development of healthy and pathological brains and to study the effect of potential therapeutic treatments. In order to observe these fibers, one must combine a today well-controlled MRI acquisition with a data processing procedure that is still under investigation for many research projects. To characterize those fibers whose diameters are only a few microns wide, the MRI spatial resolution must be raised beyond the spatial resolution of the acquisition. This super-resolution achievement can be obtained by combining biophysical models with several measures of the MRI signal. Together, one can gain access to axon diameter measures for example, as was done by Assaf in 2008 (AxCaliber approach). One of the interests of this measure is its correlation with the conduction velocity of the electric signals (Horowitz 2015). These methodological developments are mainly done in human research. However, many animal models are used to understand the healthy as well as the pathological brains. In the context of a collaboration between team UNIRS of NeuroSpin (Cyril Poupon) and team 5 of GIN (Grenoble Institute of Neuroscience) (Emmanuel Barbier), we have initiated the transfer for the mouse of the tools currently used for human
FAUQUETTE, ANNIE. "Maladie d'alzheimer : etude de la substance blanche en imagerie par resonance magnetique nucleaire". Lille 2, 1989. http://www.theses.fr/1989LIL2M175.
Texto completo da fonteCardoso, Marie-Céleste. "Implication du gène GFAP dans les pathologies humaines neurodégénératives de la substance blanche". Clermont-Ferrand 1, 2008. http://www.theses.fr/2008CLF1MM22.
Texto completo da fonteAmong genetic diseases involving the cerebral white matter or leukodystrophies, Alexander disease is characterized by an accumulation in astrocytes of diffuse eosinophilic cytoplasmic inclusions named Rosenthal fibers, with demyelination. The clinical spectrum and radiological characteristics of this disease are wider than initially described for early forms, adult forms being particularly heterogeneous. We have developed a diagnostic method, fast and inexpensive, based on DHPLC analysis of PCR products allowing the screening of GFAP mutations in a significant number of patients. We analyzed 42 families suspected of Alexander disease and identified 15 heterozygous missense mutations in 17 patients, 8 of which have never been described. The study of a large number of later forms led to redefine diagnostic criteria of juvenile and adult forms. Among our cohort of patients, 60% displayed no mutation of GFAP while clinical and radiological features of most of them do not differ from those of mutated patients. We have suspected the involvement of other GFAP molecular defects leading to overexpression : a copy number variation or a mutation in regulatory sequences. We analysed by QMPSF 177 patients affected by Alexander disease or undetermined leukodystrophy and identified neither duplication nor deletion of the 9 coding regions of GFAPα. We analysed by sequencing a 5'genomic region of GFAP in 58 patients displaying a phenotype consistent with Alexander disease and identified a total of 7 substitutions which functional consequences on transcription were tested in astrocytoma cells. Finally, 2 substitutions -1279C>T and 1313G>C reduced the in vitro transcriptional activity of the promoter. Finally we analyzed the specific coding sequences of 2 alternative isoforms GFAP ε and κ in 58 patients suspected of Alexander disease and identified a total of 8 variations including 2 amino acid substitutions : εp. Arg430Cys and εp. Arg430His. Functional tests in astroglioma cells have not provided arguments in favor of an intermediate filament disruption by direct interaction between these mutants and GFAPα. In conclusion we developed a molecular method for Alexander disease diagnostic suited for later forms analysis. We have excluded gene rearrangements as causative or aggravating factor and we do not obtained arguments in favor of GFAP ε and κ involvement. Two substitutions in the promoter sequence clearly reduce the in vitro transcriptional activity of this region. We have to confirm this inhibitory effect in vivo and demonstrate that the reduced expression is associated with Alexander phenotype
Koob, Mériam. "Etude de la substance blanche cérébrale de l'enfant par imagerie en tenseur de diffusion". Thesis, Strasbourg, 2012. http://www.theses.fr/2012STRAD005.
Texto completo da fonteDiffusion tensor imaging (DTI) is a diffusion-weighted imaging application that allows water motion quantification in any direction. This technique determines brain fiber direction in each voxel, and reconstructs indirectly white matter fibers tracts in 3D with tractography. Scalar DTI parameters, such as fractional anisotropy (FA) and apparent diffusion coefficient (ADC), provide a quantitative analysis of brain microstructure. DTI applications are numerous, especially in the study of brain development and white matter pathologies.First, we studied DTI in the fetus. For this, we implemented a processing method for fetal DTI images, and compiled it in a software, Baby brain Toolkit (BTK) (https://github.com/rousseau/fbrain). BTK was validated on normal cases, and then applied to a brain malformation model. We also studied a case of cytomegalovirus infection with DTI.We then investigated the utility of scalar DTI parameters in a rare leukodystrophy, Cockayne syndrome. DTI allows to diagnose Cockayne syndrome, to distinguish between clinical subtypes, and to understand its pathophysiology. We showed that Cockayne syndrome was a primitive hypomyelinating disorder, followed by a low grade secondary demyelination
Sakka, Laurent. "Evaluation d'un peptide de synthèse dans la réparation des lésions traumatiques de la substance blanche". Thesis, Clermont-Ferrand 1, 2015. http://www.theses.fr/2015CLF1S001/document.
Texto completo da fonteIn this work, we have studied the efficacy of a TSR-derived peptide in white matter repair. Neuroprotective properties were studied using two models of oxidative stress and apoptosis in vitro. NX210 increases cell viability after exposition to H2O2, one the main ROS that take part in the secondary lesion. Anti-oxidant action was mediated by the scavenger property of the molecule and the stimulation of signaling pathway. Anti-apoptotic action was assessed by measuring caspase 3/7 activity. NX210 inhibits caspase 3/7 activity according to a dose effect relation. Neurorepair was assessed using two separate rat models of spinal cord injury (SCI). In the model provided by section of both dorsal funiculi, NX210 stimulates early axonal growth that predominates on sensory fibers and displays a fasciculate organization. At the site of regrowth, neurofilaments were colocalized with laminin, a molecule involved in fasciculation and axonal guidance during embryogenesis. Clinical efficiency was assessed using a contusive model of SCI. Body weight was early and constantly increased in NX210 treated animals as compared to vehicle treated animals. Improvement in locomotor behavior was appraised with the open field tests. Path length was significantly increased while time spent in central cells was constantly decreased in NX210 treated animals. A BBB score above 14 only performed by NX210 treated animals was related to the restoration of coordination between forelimbs and hind limbs. Normalization of reflexes such as paw placement and toe spread in NX210 treated animals could becorrelated to the recovery of supraspinal control. The action on cell recruiting was assessed by immunohistochemistry using a rat model of corpus callosum section. The lesion was performed near the subventricular zone to study cell proliferation and migration from the stem cell niche to the site of injury. The lack of NeuN immunostaining confirmed the absence of neural cells recruitment. Myelin debris identified by MBP immunostaining were located at a distance from the site of injury. GFAP and NG2cells significantly more numerous in NX210 treated animals identified astrocyte and oligodendrocyte recruitment all around the lesion site
Maillard, Pauline. "Vieillissement et hypersignaux de la substance blanche : Détection automatique et application à l'analyse de grandes cohortes". Caen, 2008. http://www.theses.fr/2008CAEN2041.
Texto completo da fonteThe increase of life expectancy during the last century has led to a growing number of dementia cases in the aging population. This incidence has reinforced the importance of characterizing the mechanisms of the normal brain aging. Among them, White Matter Hyperintensities (WMH) are a strong marker of vascular diseases and explain, in parts, cognitive decline observed in individuals aged 65 years and over. We have developed an automated algorithm for the detection, quantification, localization and mapping WMH using T1-, T2- and PD- (proton density) weighted MRI. This algorithm was applied to the analysis of two large MRI databases: EVA (Etude du Vieillissement Artériel) and 3C (Etude des 3 Cités). The reliability of the whole procedure was assessed by the comparison of WMH load estimated with a conventional visual inspection approach and by investigating whether previously reported associations still hold with the WMH load detected by our algorithm. We finally tested the inter-centre reproducibility the method by comparing WMH distributions and loads in the two samples and its robustness to different MRI parameters. In order to apply to longitudinal data, the method has been optimized to study individually the emergence of new WMH between the two trials and the development of WMH already existing at baseline. This study suggested that load of deep WMH was constant between the two sessions, contrary to juxtaventricular or periventricular WMH underlying that dichotomization of WMH based on physiological determinants has an etiological relevance. The results also indicated that development of existing WMH was larger with age, particularly in men, contrary to the emergence of new WMH that kept constant with aging. This original approach offer new possibilities to investigate the aetiology of WMH, still largely unknown, and to make their cognitive and motor consequences on aging population clearer
Capítulos de livros sobre o assunto "Hyperintensités de la substance blanche"
Thines, L. "Anatomie cérébrale : substance blanche". In Atlas Interactif de Neuroanatomie Clinique, 39–45. Elsevier, 2016. http://dx.doi.org/10.1016/b978-2-294-74694-9.00004-9.
Texto completo da fonteDietemann, J. L., M. Koob, S. Kremer e A. Bogorin. "Pathologie de la substance blanche". In Neuro-Imagerie Diagnostique, 537–94. Elsevier, 2018. http://dx.doi.org/10.1016/b978-2-294-75394-7.00016-3.
Texto completo da fonteHausser-Hauw, Chantal. "Lésions vasculaires multiples de la substance blanche (maladie de Binswanger et CADASIL)". In Manuel d'EEG de l'adulte. Veille et sommeil, 271. Elsevier, 2007. http://dx.doi.org/10.1016/b978-2-294-07145-4.50063-5.
Texto completo da fonte