Multiple Sclerosis (MULT SCLER )

Publisher: SAGE Publications

Journal description

The journal focuses on the aetiology and pathogenesis of demyelinating and inflammatory diseases of the central nervous system and on the application of such studies to scientifically based therapy. The following research areas are of particular interest to the journal: Clinical neurology Myelin chemistry Neuroimaging Pathobiology of the blood/brain barrier Glial pathobiology/myelin repair Pathology Epidemiology Therapeutics Genetics Immunology Virology Psychology Rehabilitation.

Current impact factor: 4.86

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 4.863
2012 Impact Factor 4.472
2011 Impact Factor 4.255
2010 Impact Factor 4.23
2009 Impact Factor 3.279
2008 Impact Factor 3.312

Impact factor over time

Impact factor

Additional details

5-year impact 3.95
Cited half-life 4.60
Immediacy index 1.12
Eigenfactor 0.02
Article influence 1.17
Website Multiple Sclerosis website
Other titles Multiple sclerosis (Houndmills, Basingstoke, England: Online)
ISSN 1477-0970
OCLC 39932110
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

SAGE Publications

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors retain copyright
    • Pre-print on any website
    • Author's post-print on author's personal website, departmental website, institutional website or institutional repository
    • On other repositories including PubMed Central after 12 months embargo
    • Publisher copyright and source must be acknowledged
    • Publisher's version/PDF cannot be used
    • Post-print version with changes from referees comments can be used
    • "as published" final version with layout and copy-editing changes cannot be archived but can be used on secure institutional intranet
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Cognitive impairment is common in multiple sclerosis (MS) and may be subtle. The corpus callosum is essential for connectivity-demanding cognitive tasks and is significantly affected in MS, therefore it may serve as a marker for cognitive function. The objective of this paper is to longitudinally study the normalized corpus callosum area (nCCA) as a marker of cognitive function and disability in MS. Thirty-seven MS patients were followed from 1996 with follow-ups in 2004 and 2013. A healthy matched control group was recruited. The Expanded Disability Status Scale (EDSS) and Symbol Digit Modalities Test (SDMT) were assessed. The nCCA was measured on T2-weighted images. Volumetry was performed with FreeSurfer. Disease duration spanned five decades (1.6-46 years). Annual corpus callosal atrophy rate decreased with disease duration. nCCA was strongly correlated with SDMT (r = 0.793, p < 0.001) and moderately correlated with EDSS (r = -0.545, p < 0.001) after adjusting for disease duration, age and sex. The correlations of brain parenchymal fraction, white matter fraction, gray matter fraction and normalized lesion volume were less strong. The nCCA correlates well with physical and cognitive disability in time perspectives close to two decades, outperforming volumetric measurements. The nCCA is fast and could be feasible for clinical implementation where it may help identify patients in need of neuropsychological evaluation. © The Author(s), 2014.
    Multiple Sclerosis 12/2014;
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    ABSTRACT: Patients with multiple sclerosis (MS) almost always experience effects in the visual pathway; and thus, visual dysfunction is not only common but also highly relevant. The visual pathway represents a model of acute focal central nervous system (CNS) damage, through acute optic neuritis and retinal periphlebitis, as well as a model of chronic, diffuse CNS damage through chronic retinopathy and optic neuropathy. The optic pathway can be accurately evaluated in detail, due to the availability of highly sensitive imaging techniques (e.g. magnetic resonance imaging or optical coherent tomography) or electrophysiological tests (multifocal visual evoked potentials or electroretinography). These techniques allow the interactions between the different processes at play to be evaluated, such as inflammation, demyelination, axonal damage and neurodegeneration. Moreover, these features mean that the visual pathway can be used as a model to test new neuroprotective or regenerative therapies.
    Multiple Sclerosis 11/2014; 20(13):1678-1685.
  • Multiple Sclerosis 11/2014;
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    ABSTRACT: Background: Large population-based genome-wide association studies have identified several multiple sclerosis (MS) genetic risk variants, but the existing missing heritability warrants different strategies. Isolated populations offer an alternative way of searching for rare genetic variants and evaluating the possible role of consanguinity in the development of MS. Studies of consanguinity and MS risk have yielded conflicting results. Objectives: In this study we investigated the role of consanguinity on MS risk in the relatively isolated Faroe Islands, which have a presumed high level of inbreeding. Methods: A total of 29 cases and 28 matched controls were genotyped and assessed for inbreeding coefficients, number of runs of homozygosity (ROH) at different lengths and observed number of homozygotes as measures of relatedness. Parametric and non-parametric statistical models were applied. Results: Both cases and controls exhibited considerable relatedness demonstrated by very high inbreeding coefficients, large number of observed homozygotes and many long ROH. However, apart from the number of ROH ≥ 2.5 mega base pairs, no significant differences between the two groups were observed. Conclusions: Overall, no significant difference between cases and controls were found, indicating that consanguinity in itself does not appear to be an important risk factor for MS in the population of the Faroe Islands. Keywords:
    Multiple Sclerosis 11/2014;
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    ABSTRACT: Cognitive impairment affects half of the multiple sclerosis (MS) patient population and is an important contributor to patients' daily activities. Most cognitive impairment studies in MS are, however, cross-sectional or/and focused on the early disease stages.OBJECTIVE: We aim to assess the time course of decline of different cognitive domains.METHODS: We collected neuropsychological data on 514 MS patients to construct Kaplan-Meier survival curves of the tests included in the Neuropsychological Screening Battery for MS (NSBMS) and the Symbol Digit Modalities Test (SDMT). Cox-proportional hazard models were constructed to examine the influence of MS onset type, age at onset, gender, depression and level of education on the time course, expressed as age or disease.RESULTS: Survival curves of tests focusing on information processing speed (IPS) declined significantly faster than tests with less specific demands of IPS. Median age for pathological decline was 56.2 years (95% CI: 54.4-58.2) on the SDMT and 63.9 years (95% CI: 60-66.9) on the CLTR, a memory task.CONCLUSION: In conclusion, IPS is the cognitive domain not only most widely affected by MS but it is also the first cognitive deficit to emerge in MS.
    Multiple Sclerosis 07/2014;
  • Multiple Sclerosis 05/2014;
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    ABSTRACT: There is accumulating data suggesting an association between serum lipids, apolipoproteins and disability in multiple sclerosis (MS). To investigate the associations between serum lipids, apolipoproteins and disability in MS. A cohort of 178 participants with clinically-definite MS in southern Tasmania, Australia were prospectively followed from 2002 - 2005, and serum samples were obtained at study entry and at each biannual review, to measure lipid profile and apolipoprotein levels. Associations with disability and annual change in disability were evaluated using linear regression and multilevel mixed-effects linear regression. In the unadjusted analyses, nearly all lipid-related variables were positively associated with Expanded Disability Status Scale (EDSS). After adjustment for confounders, total cholesterol (TC) (p = 0.037), apolipoprotein B (ApoB) (p = 0.003), and the apolipoprotein B to apolipoprotein A-I ratio (ApoB/ApoA-I ratio) (p = 0.018) were independently associated with a higher EDSS. Higher body mass index (BMI) was also independently associated with higher EDSS (p = 0.013). With the progression analysis, the total cholesterol to high density lipoprotein (HDL) ratio (TC/HDL ratio) (p = 0.029) was prospectively associated with subsequent change in EDSS. In this prospective population-based cohort study, an adverse lipid profile was associated with high levels of MS disability and disease progression. Improving serum lipids may be beneficial for MS patients, to potentially improve clinical outcomes and vascular comorbidities.
    Multiple Sclerosis 05/2014;
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    ABSTRACT: Neuromyelitis optica (NMO), or Devic's disease, is a rare demyelinating disorder of the central nervous system that has a predilection for the optic nerve and spinal cord. Magnetic resonance imaging (MRI) is required to diagnose NMO. Longitudinally extensive transverse myelitis is NMO's imaging hallmark and the presence of a brain MRI that is not diagnostic of multiple sclerosis (MS) also remains part of the diagnostic criteria. It is increasingly recognised that MS and NMO brain imaging can, however, have similar appearances but differences do exist: hypothalamic, periaqueductal grey and area postrema lesions implicate NMO whilst cortical, U-fibre or Dawson's finger lesions are suggestive of MS. The timing of image acquisition, age, ethnicity and aquaporin-4 antibody status are all likely to alter the findings at MRI. This review therefore aims to overview and update the reader on NMO imaging, to provide clinically relevant guidance for diagnosing NMO and differentiating it from MS in order to guide management, and to highlight recent research insights.
    Multiple Sclerosis 05/2014;
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    ABSTRACT: Interleukin-7 (IL-7) is a non-redundant cytokine for T-cell development and survival. The IL-7 signaling pathway has been genetically and functionally associated with several autoimmune diseases including multiple sclerosis (MS). The objective of this paper is to elucidate the effect of the widely used immunomodulatory MS therapy interferon beta (IFNβ) on IL-7 homeostasis. Swedish MS patients were screened for IL-7 concentration in serum and blood cell counts. IL-7 receptor alpha chain (IL-7Rα) expression was determined by semi-quantitative real-time polymerase chain reaction (PCR) and flow cytometry. IFNβ treatment led to significantly increased serum IL-7 levels (mean: 17 pg/ml) compared with healthy controls (mean: 7.6 pg/ml) and natalizumab-treated patients (mean: 5.3 pg/ml). In vitro and in vivo, peripheral blood leukocytes showed decreased IL-7Rα expression and IL-7 consumption upon IFNβ exposure, suggesting that their IL-7 responsiveness is impaired during treatment. MS patients undergoing IFNβ treatment have increased serum IL-7 levels and decreased IL-7 consumption. Given IL-7's important role in T-cell immunity, this relationship may be highly relevant for IFNβ's treatment efficacy.
    Multiple Sclerosis 05/2014;
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    ABSTRACT: Patients with multiple sclerosis (MS) lose brain volume (BV) faster than healthy individuals. Our purpose, within the 12-month phase 3 TRANSFORMS study, was to examine the effect of treatment on BV loss in patient subgroups, establish correlations between baseline normalized BV (NBV) and baseline disease parameters, to identify variables predictive of baseline NBV and on-study percentage BV change (PBVC), and to establish correlations between on-study PBVC and on-study efficacy outcomes. Patients received fingolimod 0.5 mg or 1.25 mg, or intramuscular (IM) interferon β-1a (IFNβ-1a) for 12 months. The effect of treatment on PBVC was examined in patient demographic, disease and magnetic resonance imaging (MRI) characteristic subgroups. Pearson's correlation analyses and a stepwise linear regression model were used to identify variables predictive of NBV and PBVC. Fingolimod reduced BV loss over 12 months versus IFNβ-1a IM in all patient subgroups assessed, including individuals with or without gadolinium (Gd)-enhancing lesions at baseline. Baseline T1 hypointense lesion volume had the strongest correlation with baseline NBV. Baseline Gd-enhancing T1 lesion count was most predictive of change in PBVC over 12 months. Our results improve understanding of the contributions of different baseline demographic, clinical and MRI characteristics to NBV, including factors that may be predictive of future BV loss.
    Multiple Sclerosis 05/2014;
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    ABSTRACT: The use of natalizumab has likely been limited by its association with progressive multifocal leukoencephalopathy (PML), an infection caused by the human polyomavirus John Cunningham (JC). Three factors were recently identified that contribute to the overall risk of natalizumab-associated PML: (1) Positive serostatus for anti-JCV antibodies, (2) prior use of immunosuppressants, and (3) duration of natalizumab therapy. This risk stratification algorithm has not led to a reduction in the incidence of PML in natalizumab-treated patients with multiple sclerosis between April 2010 and February 2014. This observation may appear perplexing, as treatment duration and JCV serostatus are modifiable risk factors. Potential reasons for the lack of success of companion diagnostics that determine the overall risk of natalizumab-associated PML are discussed.
    Multiple Sclerosis 05/2014;
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    ABSTRACT: Microglia, a unique type of myeloid cell, play a key role in the inflammation-mediated neurodegeneration occurring during both acute and chronic stages of multiple sclerosis (MS). These highly specialized cells trigger neurotoxic pathways, producing pro-inflammatory cytokines, reactive oxygen and nitrogen species and proteolytic enzymes, causing progressive neurodegeneration. Microglia have also been associated with development of cortical lesions in progressive MS, as well as with alterations of synaptic transmission in experimental autoimmune encephalomyelitis (EAE). However, they also play an important role in the promotion of neuroprotection, downregulation of inflammation, and stimulation of tissue repair. Notably, microglia undergo changes in morphology and function with normal aging, resulting in a decline of their ability to repair central nervous system damage, making axons and neurons more vulnerable with age. Modulation of microglial activation for therapeutic purposes must consider suppressing deleterious effects of these cells, while simultaneously preserving their protective functions.
    Multiple Sclerosis 05/2014;
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    ABSTRACT: The majority of patients with multiple sclerosis (MS) present with spinal cord pathology. Spinal cord atrophy is thought to be a marker of disease severity, but in long-disease duration its relation to brain pathology and clinical disability is largely unknown. Our aim was to investigate mean upper cervical cord area (MUCCA) in patients with long-standing MS and assess its relation to brain magnetic resonance imaging (MRI) measures and clinical disability. MUCCA was measured in 196 MS patients and 55 healthy controls using 3DT1-weighted cervical images obtained at 3T MRI. Clinical disability was measured using the Expanded Disability Status Scale (EDSS), Nine-Hole-Peg test (9-HPT), and 25 feet Timed Walk Test (TWT). Stepwise linear regression was performed to assess the association between MUCCA and MRI measures, and between MUCCA and clinical disability. MUCCA was smaller (mean 11.7%) in MS patients compared with healthy controls (72.56±9.82 and 82.24±7.80 mm(2) respectively; p<0.001), most prominently in male patients. MUCCA was associated with normalized brain volume, and number of cervical cord lesions. MUCCA was independently associated with EDSS, TWT, and 9-HPT. MUCCA was reduced in MS patients compared with healthy controls. It provides a relevant marker for clinical disability in long-standing disease, independent of other MRI measures.
    Multiple Sclerosis 05/2014;
  • Multiple Sclerosis 05/2014;