• Alfredo Damasceno, Benito Pereira Damasceno, and Fernando Cendes.
• Department of Neurology, University of Campinas (UNICAMP), Campinas, Brazil. Electronic address: alfredodamasceno@hotmail.com.
• Mult Scler Relat Disord. 2015 Mar 1; 4 (2): 137-43.

BackgroundThe pathological mechanisms underlying cognitive dysfunction in multiple sclerosis (MS) are not yet fully understood and, in addition to demyelinating lesions and gray-matter atrophy, subclinical disease activity may play a role.ObjectiveTo evaluate the contribution of asymptomatic gadolinium-enhancing lesions to cognitive dysfunction along with gray-matter damage and callosal atrophy in relapsing-remitting MS (RRMS) patients.MethodsForty-two treated RRMS 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 gadolinium-enhancing lesions. Outcome variables included EDSS, MS Functional Composite (MSFC) subtests and the Brief Repeatable Battery of Neuropsychological tests. Cognitive dysfunction was classified as deficits in two or more cognitive subtests. Multivariate regression analyses assessed the contribution of MRI metrics to outcomes.ResultsPatients with cognitive impairment (45.2%) had more cortical lesions and lower gray-matter and callosal volumes. Patients with subclinical MRI activity (15%) had worse cognitive performance. Clinical disability on MSFC was mainly associated with putaminal atrophy. The main independent predictors for cognitive deficits were high burden of cortical lesions and number of gadolinium-enhancing lesions.ConclusionsCognitive dysfunction was especially related to high burden of cortical lesions and subclinical disease activity. Cognitive studies in MS should look over subclinical disease activity as a potential contributor to cognitive impairment.Copyright © 2015 Elsevier B.V. All rights reserved.

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