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Background: Although disability is considered the main cause of low bone mineral density (BMD) in multiple sclerosis (MS), other factors related to the disease process or treatment could also be involved. The aim of this study was to assess whether patients with MS are more likely to develop low BMD (osteopenia or osteoporosis) than patients with the non-inflammatory neurological diseases Hereditary Spastic Paraplegia (HSP) and Hereditary Ataxia (HA)., Methods: We performed a case control study comparing BMD (spine, hip and total body) and biochemical measures of bone metabolism in 91 MS patients and 77 patients with HSP or HA, matched for age, gender and disability. Both patient groups had lived with the disease for at least 10 years., Results: In total 74.7% of the patients with MS and 75.3% of the patients with HSP or HA had osteopenia (-2.5 < T- score < -1.0) or osteoporosis (T- score ≤ -2.5) in one or more sites. Osteoporosis was more common in patients with MS than with HSP/HA (44.0 vs 20.8%, p =0.001). This difference was not significant after correction for confounders (p = 0.07), nor were any of the biochemical markers., Conclusion: Most patients with disabling neurological diseases like MS and HSP/HA develop osteopenia or osteoporosis. MS patients had osteoporosis more frequently than HA/HSP patients, though the difference was not significant after adjusting for confounders. Osteoporosis and bone health should be considered in all patients with both inflammatory and degenerative chronic neurological diseases.

Objectives: Over the past few decades, there has been an improvement in the rate of disability progression in multiple sclerosis (MS) patients, and most studies relate this evolvement to the introduction of disease-modifying therapies. However, several other factors have changed over this period, including access to MRI and newer diagnostic criteria. The aim of this study is to investigate changes in the natural course of MS over time in a near-complete and geographically well-defined population from the south-east of Norway. Methods: We examined disease progression and demographics over two decades and assessed the effect of disease-modifying therapies using linear mixed-effect models. Results: In a cohort of 2097 patients, we found a significant improvement in disability as measured by the Expanded Disability Status Scale (EDSS) stratified by age, and the improvement remained significant after adjusting for time on disease-modifying medications, gender and progressive MS at onset. The time from disease onset to EDSS 6 in the total cohort was 29.8 years (95% CI 28.5–31.1) and was significantly longer in patients diagnosed after 2006 compared to patients diagnosed before. There are significant differences between patient demographics, as well as time to EDSS 6, in the near-complete, geographically well-defined population compared to an additional cohort from the capital Oslo and its suburbs. Conclusion: The natural course of MS is improving, but the improvement seen in disease progression has multifaceted explanations. Our study underlines the importance of completeness of data, relevant timeframes and demographics when comparing different MS populations. Studies on incomplete populations should be interpreted with caution. [ABSTRACT FROM AUTHOR]

Abstract: High exposure to vitamin D may protect against development and progression of multiple sclerosis (MS), possibly through the immunomodulatory properties of its biologically active metabolite 1,25-dihydroxyvitamin D. So far, most studies on the possible mechanisms for vitamin D involvement in MS have focused on immune modulation outside the central nervous system (CNS). However, vitamin D may also interfere with the pathophysiology of MS within the CNS. In this review, the potential presence and functions of vitamin D in the inflamed and healthy CNS are explored. We discuss that vitamin D, vitamin D binding protein (DBP), the vitamin D receptor (VDR) and enzymes needed for metabolism (CYP27B1) are present in the CNS. Both VDR and CYP27B1 are expressed on a variety of cells, including neurons, glial cells, and invading lymphocytes. Additionally, vitamin D has been postulated to play a modulating role in several key-processes in MS pathophysiology, including inflammation, demyelination, axonal damage, and remyelination. We conclude that a local role of vitamin D in the inflamed CNS is likely and potentially relevant to MS. Future studies should further characterize the impact of vitamin D on the local disease process of MS in the CNS. [Copyright &y& Elsevier]