The Benign Form of Multiple Sclerosis. A Study Based on 241 Cases Seen Within Three Years of Onset and Followed Up Until the Tenth Year or More of the Disease

McAlpine, Douglas

doi:10.1093/brain/84.2.186

Cited by 169 publications

(65 citation statements)

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“…It is uncertain whether MS is a single disease or whether the varying clinical patterns, for example, the relapsing and progressive forms, represent distinct entities (Noseworthy, 1999). In some MS patients (10-20%), the course of the disease can be classified as benign as they do not develop the characteristic disabilities (McAlpine, 1961;Ramsaransing et al, 2001). Plaques of demyelination, with perivascular inflammation and destruction of oligodendroglia, preceded by violation of the bloodbrain barrier (BBB), are scattered throughout the white matter of the CNS.…”

Section: Introductionmentioning

confidence: 99%

Multiple sclerosis and vitamin D: an update

et al. 2004

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MS is a chronic, immune-mediated inflammatory and neurodegenerative disease of the central nervous system (CNS), with an etiology that is not yet fully understood. The prevalence of MS is highest where environmental supplies of vitamin D are lowest. It is well recognized that the active hormonal form of vitamin D, 1,25-dihydroxyvitamin D (1,25-(OH) 2 D), is a natural immunoregulator with anti-inflammatory action. The mechanism by which vitamin D nutrition is thought to influence MS involves paracrine or autocrine metabolism of 25OHD by cells expressing the enzyme 1a-OHase in peripheral tissues involved in immune and neural function. Administration of the active metabolite 1,25-(OH) 2 D in mice and rats with experimental allergic encephalomyelitis (EAE, an animal model of MS) not only prevented, but also reduced disease activity. 1,25-(OH) 2 D alters dendritic cell and T-cell function and regulates macrophages in EAE. Interestingly, 1,25-(OH) 2 D is thought to be operating on CNS constituent cells as well. Vitamin D deficiency is caused by insufficient sunlight exposure or low dietary vitamin D 3 intake. Subtle defects in vitamin D metabolism, including genetic polymorphisms related to vitamin D, might possibly be involved as well. Optimal 25OHD serum concentrations, throughout the year, may be beneficial for patients with MS, both to obtain immune-mediated suppression of disease activity, and also to decrease disease-related complications, including increased bone resorption, fractures, and muscle weakness.

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Section: Introductionmentioning

confidence: 99%

Multiple sclerosis and vitamin D: an update

et al. 2004

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“…The disability was measured according to the EGS [1] , an ambulatory scale derived from the McAlpine classification [25] and from the EDSS scale [2] . EDMUS scores range from 0 (no neurological abnormality) to 10 (death from MS), with nine intermediary steps (see Appendix 1).…”

Section: Datamentioning

confidence: 99%

“…Some studies have identified prognostic factors for MS progression. An older age at MS onset ( 1 40 years old), not presenting optic neuritis as the initial symptom of MS (compared to neurological long tract impairment) and a primary progressive MS at onset, are all associated with a worse evolution [6][7][8][9][10][11][12][13][14][15][16] . The degree of recovery after the first relapse, the time to a second relapse, and the number of exacerbations during the first 5 years after MS onset also predict the disability evolution [1][2][3][4][5][6]17] .…”

Section: Introductionmentioning

confidence: 99%

Disability Evolution in Multiple Sclerosis: How to Deal with Missing Transition Times in the Markov Model?

et al. 2007

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Markov modeling of disability progression in multiple sclerosis requires knowledge of all times of transitions from a given level of disability to the next level, but such data are often missing. We address methodological challenges due to partly missing transition times. To estimate the effects of prognostic factors on the risk of transitions between three consecutive disability levels, two methods were used to deal with missing data. Listwise deletion limited the analysis to subjects with complete data. Multiple imputation of missing data revealed that data were missing at random (MAR mechanism) and imputed the missing transition times from the Weibull model. The results were then compared with the full data set with the actual times established through chart review. Multiple imputation estimates were systematically closer to those from the full data set than the listwise deletion estimates.

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“…The site affected and, therefore, individual symptoms in any episode do correlate with prognosis and dis ability. Relapses characterised by cerebellar involvement or weakness are much more likely to lead to permanent disability with time, whereas recur rent visual or sensory symptoms are reliably associated with a benign course, almost irrespective of their frequency [7], But the most important factor influencing the course of MS is age of onset; disability is more likely in older-onset cases [1,6], Disappointingly, the various immunological investigations described in patients with MS only provide clues to the pathogenesis of the disease and not its prognosis. Despite occasional claims to the contrary, there is no overall evidence that rates of IgG syn thesis, HLA phenotypes and changes in number of lymphocyte subpopula tions can be used to predict the clinical course in groups of patients or individuals with established MS or the response to treatment [1,8], New therapeutic ideas in patients with MS will therefore need to be tested clinically under scientific conditions which are sufficiently rigorous to establish whether or not each strategy is worth pursuing.…”

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confidence: 99%