A Longitudinal Study of Disability, Cognition and Gray Matter Atrophy in Early Multiple Sclerosis Patients According to Evidence of Disease Activity.
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). 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). 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. 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). 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.
Department of Neurology, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Gro O
GO
Nygaard
Department of Neurology, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Elisabeth G
EG
Celius
Department of Ophthalmology, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Sigrid A
SA
de Rodez Benavent
Department of Radiology, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Piotr
P
Sowa
Department of Neurology, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Marte W
MW
Gustavsen
Department of Psychology, University of Oslo, Oslo, Norway.
Anders M
AM
Fjell
Department of Psychology, University of Oslo, Oslo, Norway.
Nils I
NI
Landrø
Department of Psychology, University of Oslo, Oslo, Norway.
Kristine B
KB
Walhovd
Department of Neurology, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Hanne F
HF
Harbo
D000328:Adult; D001284:Atrophy / Q000473:pathology*; D001921:Brain / Q000473:pathology; D003071:Cognition / Q000502:physiology*; D004185:Disability Evaluation; D006233:Persons with Disabilities; D018450:Disease Progression; D005260:Female; D066128:Gray Matter / Q000473:pathology*; D006801:Humans; D008137:Longitudinal Studies; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D020529:Multiple Sclerosis, Relapsing-Remitting / Q000473:pathology*; D009413:Nerve Fibers, Myelinated / Q000473:pathology; D012008:Recurrence