Syndrome d encéphalopathie postérieure réversible et Magnésium (à propos de 57 cas)

Le syndrome d encéphalopathie postérieure réversible a été défini en 1996 par l association de signes cliniques et radiologiques. Les étiologies principales sont l encéphalopathie hypertensive, l éclampsie et les immunosuppresseurs. Nous avons mené une étude rétrospective multicentrique de 57 cas de PRES de 2000 à 2009 en analysant les données cliniques, radiologiques et biologiques (magnésémie plasmatique). 57 cas de PRES chez 56 patients (43 femmes, 13 hommes, âge moyen 41 ans) ont été étudiés . Les trois principales étiologies sont les traitements immunosuppresseurs (n=16), les encéphalopathies hypertensives (n=13) et l éclampsie (n=10). Les signes cliniques retrouvés sont : céphalées (74%), troubles de conscience (74%), convulsions (70%), troubles visuels (46%) et hypertension artérielle (75%). En imagerie, au delà des lésions postérieures classiques, on retrouve : une atteinte frontale (63,1%), cérébelleuse (28%), des noyaux gris centraux (17,5%), du tronc cérébral (5,2%), un œdème cytotoxique (16%), un vasospasme (14,2%), une hémorragie (21%). Ces caractéristiques clinico-radiologiques sont similaires aux données de la littérature. Une hypomagnésémie est observée dans 83,8% des cas où le dosage plasmatique était disponible, quelque soit le contexte étiologique. L hypomagnésémie est aiguë, contemporaine de l épisode neurologique (0,65 en moyenne contre 0.9 à distance). L hypomagnésemie aiguë serait un facteur de risque commun aux différentes étiologies jusqu alors évoquées dans le PRES. Le sulfate de magnésium constituerait le traitement de choix. Des études ultérieures sont nécessaires pour valider les résultats de notre étude.PARIS6-Bibl.Pitié-Salpêtrie (751132101) / SudocSudocFranceF

Imaging central nervous system myelin by positron emission tomography in multiple sclerosis using [methyl-¹¹C]-2-(4'-methylaminophenyl)- 6-hydroxybenzothiazole.

International audienceOBJECTIVE: Imaging of myelin tracts in vivo would greatly improve the monitoring of demyelinating diseases such as multiple sclerosis (MS). To date, no imaging technique specifically targets demyelination and remyelination. Recently, amyloid markers related to Congo red have been shown to bind to central nervous system (CNS) myelin. Here we questioned whether the thioflavine-T derivative 2-(4'-methylaminophenyl)-6-hydroxybenzothiazole (PIB), which also binds to amyloid plaques, could serve as a myelin marker. METHODS: PIB fixation to myelin was studied by fluorescence in the normal and dysmyelinating mouse brain, as well as in the postmortem brain of MS patients. Positron emission tomography (PET) experiments were conducted using [¹¹C]PIB in baboons and in a proof of concept clinical study in 2 MS patients. RESULTS: Applied directly on tissue sections or after intraperitoneal injection, PIB stained CNS myelin, and the decrease in the level of fixation paralleled the amount of myelin loss in a dysmyelinating mutant. In normally myelinated areas of postmortem MS brain, demyelinated and remyelinated lesions were clearly distinguishable by the differential intensity of labeling observed with PIB. PET using intravenously injected radiolabeled [¹¹C]PIB imaged CNS myelin in baboons and humans. In MS patients, the dynamic analysis of PET acquisitions allowed quantitative assessment of demyelination. INTERPRETATION: PIB could be used as an imaging marker to quantify myelin loss and repair in demyelinating diseases

Dynamic imaging of individual remyelination profiles in multiple sclerosis

International audienceBackground: Quantitative in vivo imaging of myelin loss and repair in patients with multiple sclerosis (MS) is essential to understand the pathogenesis of the disease and to evaluate promyelinating therapies. Selectively binding myelin in the central nervous system white matter, [11C]PIB can be used as a positron emission tomography (PET) tracer to explore myelin dynamics in MS.Methods: Patients with active relapsing-remitting MS (n=20) and healthy controls (n=8) were included in a longitudinal trial combining PET with [11C]PIB and magnetic resonance imaging. Voxel-wise maps of [11C]PIB distribution volume ratio, reflecting myelin content, were derived. Three dynamic indices were calculated for each patient: the global index of myelin content change; the index of demyelination; and the index of remyelination.Results: At baseline, there was a progressive reduction in [11C]PIB binding from the normal-appearing white matter to MS lesions, reflecting a decline in myelin content. White matter lesions were characterized by a centripetal decrease in the tracer binding at the voxel level. During follow-up, high between-patient variability was found for all indices of myelin content change. Dynamic remyelination was inversely correlated with clinical disability (p=0.006 and beta-coefficient=-0.67 with the Expanded Disability Status Scale; p=0.003 and beta-coefficient=-0.68 with the MS Severity Scale), whereas no significant clinical correlation was found for the demyelination index.Conclusions: [11C]PIB PET allows quantification of myelin dynamics in MS and enables stratification of patients depending on their individual remyelination potential, which significantly correlates with clinical disability. This technique should be considered to assess novel promyelinating drugs. This article is protected by copyright. All rights reserved