Longitudinal patterns of cortical thinning in multiple sclerosis. Issue 8 (17th February 2020)

• Record Type: Journal Article
• Authors: Tsagkas, Charidimos; Chakravarty, M. Mallar; Gaetano, Laura; Naegelin, Yvonne; Amann, Michael; Parmar, Katrin; Papadopoulou, Athina; Wuerfel, Jens; Kappos, Ludwig; Sprenger, Till; Magon, Stefano
• Is Part Of: Human brain mapping. Volume 41:Issue 8(2020)
• Page Start: 2198
• Page End: 2215
• Publication Date: 2020-02-17
• Subjects: atrophy -- biomarkers -- cortical thickness -- MRI -- multiple sclerosis -- T2 lesions; Brain mapping -- Periodicals; 611.81
• DOI: 10.1002/hbm.24940
• Languages: English
• ISSNs: 1065-9471

Abstract

Abstract: In multiple sclerosis (MS), cortical atrophy is correlated with clinical and neuropsychological measures. We aimed to examine the differences in the temporospatial evolution of cortical thickness (CTh) between MS‐subtypes and to study the association of CTh with T2‐weighted white matter lesions (T2LV) and clinical progression. Two hundred and forty‐three MS patients (180 relapsing–remitting [RRMS], 51 secondary‐progressive [SPMS], and 12 primary‐progressive [PPMS]) underwent annual clinical (incl. expanded disability status scale [EDSS]) and MRI‐examinations over 6 years. T2LV and CTh were measured. CTh did not differ between MS‐subgroups. Higher total T2LV was associated with extended bilateral CTh‐reduction on average, but did not correlate with CTh‐changes over time. In RRMS, CTh‐ and EDSS‐changes over time were negatively correlated in large bilateral prefrontal, frontal, parietal, temporal, and occipital areas. In SPMS, CTh was not associated with the EDSS. In PPMS, CTh‐ and EDSS‐changes over time were correlated in small clusters predominantly in left parietal areas. Increase of brain lesion load does not lead to an immediate CTh‐reduction. Although CTh did not differ between MS‐subtypes, a dissociation in the correlation between CTh‐ and EDSS‐changes over time between RRMS and progressive‐MS was shown, possibly underlining the contribution of subcortical pathology to clinical progression in progressive‐MS.