Subclinical MRI disease activity influences cognitive performance in @entity15 XXXX .

@entity1 @entity75 @entity73 @entity3780 @entity194 @entity2287 @entity15
BACKGROUND: The pathological mechanisms underlying @entity73 in @entity15 ( @entity15 ) are not yet fully understood and, in addition to demyelinating lesions and gray-matter @entity194 , subclinical disease activity may play a role. OBJECTIVE: To evaluate the contribution of asymptomatic @entity2287 -enhancing lesions to @entity73 along with gray-matter damage and @entity194 in @entity3780 ( @entity3780 ) @entity1 . METHODS: Forty-two treated @entity3780 and 30 controls were evaluated. MRI (3T) variables of interest were brain white-matter and cortical lesion load, cortical and deep gray-matter volumes, corpus callosum volume and presence of @entity2287 -enhancing lesions. Outcome variables included EDSS, @entity15 Functional Composite (MSFC) subtests and the Brief Repeatable Battery of Neuropsychological tests. @entity73 was classified as deficits in two or more cognitive subtests. Multivariate regression analyses assessed the contribution of MRI metrics to outcomes. RESULTS: @entity1 with @entity73 (45.2%) had more @entity75 and lower gray-matter and callosal volumes. @entity1 with subclinical MRI activity (15%) had worse cognitive performance. Clinical disability on MSFC was mainly associated with putaminal @entity194 . The main independent predictors for @entity73 were high burden of @entity75 and number of @entity2287 -enhancing lesions. CONCLUSIONS: @entity73 was especially related to high burden of @entity75 and subclinical disease activity. Cognitive studies in @entity15 should look over subclinical disease activity as a potential contributor to @entity73 .
