DT MRI microstructural cortical lesion damage does not explain cognitive impairment in MS. (December 2017)

• Record Type: Journal Article
• Authors: Preziosa, Paolo; Pagani, Elisabetta; Morelli, Maria E; Copetti, Massimiliano; Martinelli, Vittorio; Pirro, Fiammetta; Falini, Andrea; Comi, Giancarlo; Filippi, Massimo; Rocca, Maria A
• Is Part Of: Multiple sclerosis. Volume 23:Number 14(2017)
• Page Start: 1918
• Page End: 1928
• Publication Date: 2017-12
• Subjects: Multiple sclerosis -- cortical lesions -- diffusion tensor -- MRI -- cognitive impairment; 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: 10.1177/1352458516689147
• Languages: English
• ISSNs: 1352-4585

Abstract

Objective: We combined double inversion recovery (DIR) and diffusion tensor (DT) magnetic resonance imaging (MRI) to quantify the severity of cortical lesion (CL) microstructural tissue abnormalities in a large cohort of relapse-onset multiple sclerosis (MS) patients and its contribution to cognitive dysfunction. Methods: DIR, DT, dual-echo, and three-dimensional (3D) T 1 -weighted scans were acquired from 149 MS patients and 40 controls. Cognitively impaired (CI) patients had ⩾2 abnormal neuropsychological tests. Diffusivity values in CLs, cortex, white matter (WM) lesions, and normal-appearing (NA) WM were assessed. Predictors of cognitive impairment were identified using a random forest analysis. Results: Compared to controls, MS patients had lower normalized brain volume (NBV), gray matter volume (GMV), WM volume, lower fractional anisotropy (FA), and higher mean diffusivity in cortex and normal-appearing white matter (NAWM). A total of 44 (29.5%) patients were CI. Compared to cognitively preserved (CP), CI patients had higher T 2 WM lesion volume (LV), lower NBV and GMV, and more severe diffusivity abnormalities in WM lesions, cortex, and NAWM. CL measures did not differ between CI and CP patients. Cortex FA, age, disease duration, T 2 WM LV, and GMV best predicted MS-related cognitive impairment (C-statistic = 0.88). Conclusion: "Diffuse" GM and NAWM damage and WM lesions, rather than intrinsic CL damage, contribute to cognitive impairment in MS.