Multiple sclerosis and related disorders · 2026
Characterizing spinal cord atrophy in multiple sclerosis patients without disease activity or brain atrophy progression.
СтатьяНаблюдательное исследованиеМногоцентровое исследованиеНазвание и аннотация: Перевод в очереди
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Yokote Hiroaki, Miyazaki Yusei, Fujimori Juichi, Adachi Saori, Toru Shuta, Niino Masaaki, Nakashima Ichiro, Miura Yoshiharu, Nishida Yoichiro, Misawa Sonoko
Аннотация
BACKGROUND: While spinal cord atrophy (SCA) is increasingly recognized as a contributor to disability in multiple sclerosis (MS), it is still unclear how spinal cord atrophy contributes to the clinical course of MS when brain atrophy is taken into account. This study aimed to characterize the longitudinal course and clinical correlates of SCA in MS patients without significant brain atrophy progression.
METHODS: In this multicenter, retrospective observational study, 120 MS patients with brain MRI data acquired approximately 2 years apart were enrolled. Brain and spinal cord atrophy were quantified using SIENA/X and JIM9, respectively. Patients were stratified by evidence of disease activity and brain atrophy to evaluate SCA progression independently of inflammatory activity.
RESULTS: Although 64.2% of patients achieved no evidence of disease activity (NEDA) -3 and 40.8% met NEDA-4 criteria, a non-negligible degree of the SCA (-0.791 ± 1.97% / year) as well as the brain volume loss (BVL) (-0.381 ± 0.553% / year) was observed. SCA correlated weakly with BVL but not with T2 lesion volume in the brain or clinical disease activity. Among patients who fulfilled the NEDA-4 criteria, those with greater rates of SCA unexpectedly exhibited significantly smaller brain T2 lesion volumes compared to those with lower atrophy rates (p = 0.041).
DISCUSSION: SCA may progress independently of brain inflammation or clinical activity, potentially reflecting "pure" neurodegenerative processes. Its evaluation may provide critical insight into disease progression in MS, particularly in clinically stable patients with minimal brain atrophy or lesion burden.
METHODS: In this multicenter, retrospective observational study, 120 MS patients with brain MRI data acquired approximately 2 years apart were enrolled. Brain and spinal cord atrophy were quantified using SIENA/X and JIM9, respectively. Patients were stratified by evidence of disease activity and brain atrophy to evaluate SCA progression independently of inflammatory activity.
RESULTS: Although 64.2% of patients achieved no evidence of disease activity (NEDA) -3 and 40.8% met NEDA-4 criteria, a non-negligible degree of the SCA (-0.791 ± 1.97% / year) as well as the brain volume loss (BVL) (-0.381 ± 0.553% / year) was observed. SCA correlated weakly with BVL but not with T2 lesion volume in the brain or clinical disease activity. Among patients who fulfilled the NEDA-4 criteria, those with greater rates of SCA unexpectedly exhibited significantly smaller brain T2 lesion volumes compared to those with lower atrophy rates (p = 0.041).
DISCUSSION: SCA may progress independently of brain inflammation or clinical activity, potentially reflecting "pure" neurodegenerative processes. Its evaluation may provide critical insight into disease progression in MS, particularly in clinically stable patients with minimal brain atrophy or lesion burden.