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

• Published in: Multiple sclerosis Vol. 22; no. 6; p. 761
• Main Authors: Guttmann, Charles Rg, Rousset, Matthieu, Roch, Jean A, Hannoun, Salem, Durand-Dubief, Françoise, Belaroussi, Boubakeur, Cavallari, Michele, Rabilloud, Muriel, Sappey-Marinier, Dominique, Vukusic, Sandra, Cotton, François
• Format: Journal Article
• Language: English
• Published: England 01.05.2016
• Subjects: Adult; Disease Progression; Female; Humans; Longitudinal Studies; Magnetic Resonance Imaging - methods; Male; Middle Aged; Multiple Sclerosis, Relapsing-Remitting - diagnostic imaging; relapsing–remitting; Magnetic resonance imaging; multiple sclerosis; T2 lesions
• ISSN: 1477-0970
• DOI: 10.1177/1352458515600247

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. The purpose of this study was to characterize MS lesion occurrence and early evolution on high-resolution MRI acquired at weekly intervals. 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). 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. 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.