Occurrence and microstructural features of slowly expanding lesions on fingolimod or natalizumab treatment in multiple sclerosis. (September 2021)

• Record Type: Journal Article
• Authors: Preziosa, Paolo; Pagani, Elisabetta; Moiola, Lucia; Rodegher, Mariaemma; Filippi, Massimo; Rocca, Maria A
• Is Part Of: Multiple sclerosis. Volume 27:Number 10(2021)
• Page Start: 1520
• Page End: 1532
• Publication Date: 2021-09
• Subjects: Multiple sclerosis -- MRI -- disease-modifying drugs -- slowly expanding lesions -- chronic active lesions; Central nervous system -- Diseases -- Periodicals; Myelin sheath -- Diseases -- Periodicals; Inflammation -- Periodicals; Multiple sclerosis -- Periodicals; Central Nervous System Diseases -- Periodicals; Demyelinating Diseases -- Periodicals; Inflammation -- Periodicals; Multiple Sclerosis -- Periodicals; Système nerveux central -- Maladies -- Périodiques; Gaine de myéline -- Maladies -- Périodiques; Inflammation (Pathologie) -- Périodiques; Sclérose en plaques -- Périodiques; Electronic journals; 616.834005
• DOI: 10.1177/1352458520969105
• Languages: English
• ISSNs: 1352-4585

Abstract

Background: In multiple sclerosis (MS), up to 57% of white matter lesions are chronically active. These slowly expanding lesions (SELs) contribute to disability progression. Objective: The aim of this study is to compare fingolimod and natalizumab effects on progressive linearly enlarging lesions (i.e. SELs), a putative biomarker of smouldering inflammation. Methods: Relapsing-remitting MS patients starting fingolimod ( n = 24) or natalizumab ( n = 28) underwent 3T brain magnetic resonance imaging (MRI) at baseline, months 6, 12 and 24. SELs were identified among baseline-visible lesions showing ⩾ 12.5% of annual increase, calculated by linearly fitting the Jacobian of the nonlinear deformation field between timepoints obtained combining T 1 - and T 2 -weighted scans. SEL burden, magnetization transfer ratio (MTR) and T 1 signal intensity were compared using linear models. Results: The prevalences of fingolimod (75%) and natalizumab patients (46%) with ⩾ 1 SEL were not significantly different (adjusted- p = 0.08). Fingolimod group had higher SEL number and volume (adjusted- p ⩽ 0.047, not false discovery rate (FDR) survived). In both groups, SELs versus non-SELs showed lower MTR and T 1 signal intensity (adjusted- p ⩽ 0.01, FDR-survived). Longitudinally, non-SEL MTR increased in both treatment groups (adjusted- p ⩽ 0.005, FDR-survived). T 1 signal intensity decreased in SELs with both treatments (adjusted- p ⩽ 0.049, FDR-survived in fingolimod group) and increased in natalizumab non-SELs (adjusted- p = 0.03, FDR-survived). Conclusion: The effects of natalizumab and fingolimod on SEL occurrence seem modest, with natalizumab being slightly more effective. Both treatments may promote reparative mechanisms in stable or chronic inactive lesions.