Zusammenfassung:
Objective: To obtain in-vivo evidence of early dynamics of multiple sclerosis (MS) lesions formation and changes that corticosteroids may induce.
Background: MRI showed that the development of MS lesions is dynamic and heterogeneous. Lesions grow outward from a central vein comprising disruption of the blood-brain-barrier (BBB) illustrated in the centrifugal enhancement proved by dynamic contrast–enhanced (DCE) MRI; in some of them, a substantial immune reaction at the edge of the lesion, opens the BBB in the capillaries mirrored as the centripetal enhancement by DCE. The latter, previously called ring-like, are associated with more severe tissue damage and may show a paramagnetic-rim, which persistency may represent failure of lesion repair and in later stages, smoldering lesions.
Design/Methods: Six relapsing patients were scanned in a General Electric 3.0 tesla scanner. T2-weighted, susceptibility-weighted, T1-weighted (before/after gadolinium), and DCE scans were acquired at baseline, days 5, 10 and 30 post-exacerbation. Half of the patients were infused with methylprednisolone 1000mg/5days, immediately after baseline MRI. For each enhancing-lesion, dynamic of enhancement, size, and phase appearance, were assessed at each time-point.
Results: Fifty-seven lesions were analyzed; centrifugal lesions (n=45) were smaller (4.5mm) than 15 centripetal ones (10.5 mm); eight centripetal showed a paramagnetic-rim. Three patients not treated with corticosteroids developed 19 lesions, 8/9(88%) at baseline were centrifugal (1 centripetal); at day 30, 7/9(70%) lesions were centripetal (2 centrifugal). Three patients treated with methylprednisolone had 38 lesions, 28/31(90%) at baseline were centrifugal (3 centripetal), most of enhancement transiently or definitely disappeared at second time-point. At day 30, 3/11 were centripetal (27%) (8 centrifugal).
Conclusions: Corticosteroids seem to be effective for closing transiently/definitely the BBB of most active lesions and notably for preventing the shift to centripetal enhancement, probably eluding the stronger immune reaction at the edge of the developing lesion. This may portend less chronic tissue damage.