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No evidence of disease activity in multiple sclerosis: Implications on cognition and brain atrophy

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Background: The concept of no evidence of disease activity (NEDA) has emerged as an important outcome measure for multiple sclerosis (MS). However, it is not known if maintaining NEDA has a positive impact on cognition or brain atrophy. Objective: To evaluate NEDA status after two years, addressing its implications on cognition and brain atrophy. Methods: Forty-two relapsing–remitting MS patients and 30 controls underwent MRI (3T) and cognitive evaluation (BRB-N). Forty patients performed additional evaluations, after 12 and 24 months. NEDA was defined as the absence of clinical (relapses/disability progression) and MRI activity (new T2/gadolinium-enhancing lesions). Repeated measures and multivariate analyses were performed to assess the contribution of NEDA criteria to GM atrophy. Results: After two years, 30.8% of the cohort had NEDA. From these, 58.3% still had worsening in ⩾2 cognitive domains. Patients with MRI activity had more cortical thinning and slightly more thalamus volume decrease. Absence of new/enlarging T2 lesions was the only predictor of cortical thinning, subcortical GM and thalamic atrophy rates. Conclusions: NEDA status was achieved in a small proportion of our cohort, and did not preclude cognitive deterioration. Absence of MRI activity and especially of new/enlarging T2 lesions was associated with less cortical and subcortical GM atrophy.
Title: No evidence of disease activity in multiple sclerosis: Implications on cognition and brain atrophy
Description:
Background: The concept of no evidence of disease activity (NEDA) has emerged as an important outcome measure for multiple sclerosis (MS).
However, it is not known if maintaining NEDA has a positive impact on cognition or brain atrophy.
Objective: To evaluate NEDA status after two years, addressing its implications on cognition and brain atrophy.
Methods: Forty-two relapsing–remitting MS patients and 30 controls underwent MRI (3T) and cognitive evaluation (BRB-N).
Forty patients performed additional evaluations, after 12 and 24 months.
NEDA was defined as the absence of clinical (relapses/disability progression) and MRI activity (new T2/gadolinium-enhancing lesions).
Repeated measures and multivariate analyses were performed to assess the contribution of NEDA criteria to GM atrophy.
Results: After two years, 30.
8% of the cohort had NEDA.
From these, 58.
3% still had worsening in ⩾2 cognitive domains.
Patients with MRI activity had more cortical thinning and slightly more thalamus volume decrease.
Absence of new/enlarging T2 lesions was the only predictor of cortical thinning, subcortical GM and thalamic atrophy rates.
Conclusions: NEDA status was achieved in a small proportion of our cohort, and did not preclude cognitive deterioration.
Absence of MRI activity and especially of new/enlarging T2 lesions was associated with less cortical and subcortical GM atrophy.

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