Christoph Hüneke, David Ellenberger, Alexander Stahmann, Niklas Frahm
We found a markedly higher proportion of pwLOMS in the German population. The high proportion of progressive MS, faster achievement of EDSS milestones and higher conversion rate to SPMS indicate a relapse-independent disability pattern, suggesting a possible contribution of neurodegenerative mechanisms in LOMS.
BACKGROUND: The number of patients with late-onset multiple sclerosis (pwLOMS: initial MS symptoms after 50 years of age) is increasing. Therefore, we investigated pwLOMS compared with patients with adult-onset MS (pwAOMS) using epidemiologic, clinical and diagnostic comparative parameters.
METHODS: Using data from the German MS Register, pwLOMS (onset: ≥50 years) were compared with pwAOMS (onset: 18-34 years, 35-49 years). Following outcome measures were considered: time to reach the Expanded Disability Status Scale (EDSS) scores 3.0/6.0/7.0, time to transition from relapsing-remitting to secondary progressive MS (SPMS) and meeting the no evidence of disease activity-3 criteria two years after diagnosis. We used a multivariable Cox proportional-hazards model with several covariates (e.g., sex, symptoms at MS onset) for the analysis.
RESULTS: Overall, pwLOMS (N=814) showed a higher proportion of men and progressive MS, more frequent first motor symptoms and longer diagnostic delay, and reached the EDSS scores 3.0 and 6.0 faster than pwAOMS (N=5259). In pwLOMS, reaching EDSS=3.0 faster was more likely with initial motor/cerebellar/urinary tract system symptoms, while there was a lower risk of reaching the EDSS scores 3.0/6.0 with a delayed diagnosis. The risk of developing SPMS was higher in pwLOMS, which increased with the EDSS score within two years after disease onset.
CONCLUSION: We found a markedly higher proportion of pwLOMS in the German population. The high proportion of progressive MS, faster achievement of EDSS milestones and higher conversion rate to SPMS indicate a relapse-independent disability pattern, suggesting a possible contribution of neurodegenerative mechanisms in LOMS.