Can we really ignore the treatment target of NEDA #ResearchSpeak #MSBlog #MSResearch
“In this relatively small study on MSers in Oslo, Norway, it is clear that MSers rendered NEDA (no evident disease activity) at 12 months on a DMT (disease-modifying therapy) do better than those who have EDA (evident disease activity). NEDA MSers had on average and improvement in their disability and less gray matter atrophy compared to MSers with EDA.”
“Please note the numbers (n = 72) and the follow-up (12 months) is very short. In addition, this study is not randomised, but open-label and hence there could be other factors that could explain the results. However, this data, and other data, supports the treatment principle of NEDA as a valid therapeutic target in MS. Put another way what would you like to be NEDA or EDA? If you are on a DMT and are not having annual MRI scans to look for subclinical relapses you should ask the question why not?”
Nygaard et al. A Longitudinal Study of Disability, Cognition and Gray Matter Atrophy in Early Multiple SclerosisPatients According to Evidence of Disease Activity. PLoS One. 2015;10:e0135974
Background: New treatment options may make “no evidence of disease activity” (NEDA: no relapses or disability progression and no new/enlarging MRI lesions, as opposed to “evidence of disease activity” (EDA) with at least one of the former), an achievable goal in relapsing-remitting multiple sclerosis(RRMS).
Objective: The objective of the present study was to determine whether early RRMS patients with EDA at one-year follow-up had different disability, cognition, treatment and gray matter (GM) atrophy rates from NEDA patients and healthy controls (HC).
Methods: RRMS patients (mean age 34 years, mean disease duration 2.2 years) were examined at baseline and one-year follow-up with neurological (n = 72), neuropsychological (n = 56) and structural MRI (n = 57) examinations. Matched HC (n = 61) were retested after three years.
Results: EDA was found in 46% of RRMS patients at follow-up. EDA patients used more first line and less second line disease modifying treatment than NEDA (p = 0.004). While the patients groups had similar disability levels at baseline, they differed in disability at follow-up (p = 0.010); EDA patients progressed (EDSS: 1.8-2.2, p = 0.010), while NEDA patients improved (EDSS: 2.0-1.7, p<0.001). Cognitive function was stable in both patient groups. Subcortical GM atrophy rates were higher in EDA patients than HC (p<0.001).
Conclusions: These results support the relevance of NEDA as outcome in RRMS and indicate that pathological neurodegeneration in RRMS mainly occur in patients with evidence of disease activity.