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Article Dans Une Revue Multiple Sclerosis Journal Année : 2016

Multiple sclerosis lesion formation and early evolution revisited: A weekly high-resolution magnetic resonance imaging study

Muriel Rabilloud
Sandra Vukusic
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Résumé

Background:Several magnetic resonance imaging (MRI) studies investigated the evolution of multiple sclerosis (MS) lesions to understand the pathophysiological mechanisms leading to blood-brain barrier breakdown and lesion formation. Only a few assessed the early natural history of MS lesions using short-interval longitudinal MRI.Objective:The purpose of this study was to characterize MS lesion occurrence and early evolution on high-resolution MRI acquired at weekly intervals.Methods:Active lesions were characterized on 3D fluid attenuation inversion recovery (FLAIR) and gadolinium-enhanced 3D T1-weighted MRI performed weekly (seven weeks) on five untreated patients with relapsing–remitting MS (RRMS).Results:Active lesions (n=212) were detected in all patients. All showed contrast-enhancement on at least one time-point. Most new lesions (83.5%) were visible on FLAIR and post-contrast T1-weighted images at first detection; 11.2% showed activity on FLAIR images, one or more weeks before the appearance of contrast-enhancement; 12.5% enhanced before being apparent on FLAIR.Conclusion:Blood brain barrier disruption is a constant step in the natural history of active MS lesions, but does not always constitute the initial event. These findings are consistent with the existence of a subpopulation of lesions with an ‘inside-out’ genesis, where neurodegenerative processes might precede microglial activation, and a subsequent adaptive immune response.

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Imagerie
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hal-01597144 , version 1 (28-09-2017)

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Charles R G Guttmann, Matthieu Rousset, Jean-Amédée Roch, Salem Hannoun, Françoise Durand-Dubief, et al.. Multiple sclerosis lesion formation and early evolution revisited: A weekly high-resolution magnetic resonance imaging study. Multiple Sclerosis Journal, 2016, 22 (6), pp.761 - 769. ⟨10.1177/1352458515600247⟩. ⟨hal-01597144⟩
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