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      Leptomeningeal Contrast Enhancement Is Associated with Disability Progression and Grey Matter Atrophy in Multiple Sclerosis

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          Abstract

          Leptomeningeal contrast enhancement (LMCE) on magnetic resonance imaging (MRI) is a newly recognized possible biomarker in multiple sclerosis (MS), associated with MS progression and cortical atrophy. In this study, we aimed to assess the prevalence of LMCE foci and their impact on neurodegeneration and disability. Materials. 54 patients with MS were included in the study. LMCE were detected with a 3 Tesla scanner on postcontrast fluid-attenuated inversion-recovery (FLAIR) sequence. Expanded Disability Status Scale (EDSS) score, number of relapses during 5 years from MS onset, and number of contrast-enhancing lesions on T1 weighted MRI were counted. Results. LMCE was detected in 41% (22/54) of patients. LMCE-positive patients had longer disease duration ( p = 0,0098) and higher EDSS score ( p = 0,039), but not a higher relapse rate ( p = 0,091). No association of LMCE with higher frequency of contrast-enhancing lesions on T1-weighted images was detected ( p = 0,3842). Analysis of covariates, adjusted for age, sex, and disease duration, revealed a significant effect of LMCE on the cortex volume ( p = 0.043, F = 2.529), the total grey matter volume ( p = 0.043, F = 2.54), and total ventricular volume ( p = 0.039, F = 2.605). Conclusions. LMCE was shown to be an independent and significant biomarker of grey matter atrophy and disability in MS.

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          Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology.

          Roberta Magliozzi, Owain W Howell, Abhilash Vora … (2007)
          Intrathecal antibody production is a hallmark of multiple sclerosis and humoral immunity is thought to play an important role in the inflammatory response and development of demyelinated lesions. The presence of lymphoid follicle-like structures in the cerebral meninges of some multiple sclerosis patients indicates that B-cell maturation can be sustained locally within the CNS and contribute to the establishment of a compartmentalized humoral immune response. In this study we examined the distribution of ectopic B-cell follicles in multiple sclerosis cases with primary and secondary progressive clinical courses to determine their association with clinical and neuropathological features. A detailed immunohistochemical and morphometric analysis was performed on post-mortem brain tissue samples from 29 secondary progressive (SP) and 7 primary progressive (PP) multiple sclerosis cases. B-cell follicles were detected in the meninges entering the cerebral sulci of 41.4% of the SPMS cases, but not in PPMS cases. The SPMS cases with follicles significantly differed from those without with respect to a younger age at multiple sclerosis onset, irreversible disability and death and more pronounced demyelination, microglia activation and loss of neurites in the cerebral cortex. Cortical demyelination in these SPMS cases was also more severe than in PPMS cases. Notably, all meningeal B-cell follicles were found adjacent to large subpial cortical lesions, suggesting that soluble factors diffusing from these structures have a pathogenic role. These data support an immunopathogenetic mechanism whereby B-cell follicles developing in the multiple sclerosis meninges exacerbate the detrimental effects of humoral immunity with a subsequent major impact on the integrity of the cortical structures.
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            Cortical demyelination and diffuse white matter injury in multiple sclerosis.

            Alexandra Kutzelnigg, Claudia Lucchinetti, Christine Stadelmann … (2005)
            Focal demyelinated plaques in white matter, which are the hallmark of multiple sclerosis pathology, only partially explain the patient's clinical deficits. We thus analysed global brain pathology in multiple sclerosis, focusing on the normal-appearing white matter (NAWM) and the cortex. Autopsy tissue from 52 multiple sclerosis patients (acute, relapsing-remitting, primary and secondary progressive multiple sclerosis) and from 30 controls was analysed using quantitative morphological techniques. New and active focal inflammatory demyelinating lesions in the white matter were mainly present in patients with acute and relapsing multiple sclerosis, while diffuse injury of the NAWM and cortical demyelination were characteristic hallmarks of primary and secondary progressive multiple sclerosis. Cortical demyelination and injury of the NAWM, reflected by diffuse axonal injury with profound microglia activation, occurred on the background of a global inflammatory response in the whole brain and meninges. There was only a marginal correlation between focal lesion load in the white matter and diffuse white matter injury, or cortical pathology, respectively. Our data suggest that multiple sclerosis starts as a focal inflammatory disease of the CNS, which gives rise to circumscribed demyelinated plaques in the white matter. With chronicity, diffuse inflammation accumulates throughout the whole brain, and is associated with slowly progressive axonal injury in the NAWM and cortical demyelination.
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              Multiple Sclerosis Severity Score: using disability and disease duration to rate disease severity.

              R H S R Roxburgh, S. R. Seaman, T Masterman … (2005)
              There is no consensus method for determining progression of disability in patients with multiple sclerosis (MS) when each patient has had only a single assessment in the course of the disease. Using data from two large longitudinal databases, the authors tested whether cross-sectional disability assessments are representative of disease severity as a whole. An algorithm, the Multiple Sclerosis Severity Score (MSSS), which relates scores on the Expanded Disability Status Scale (EDSS) to the distribution of disability in patients with comparable disease durations, was devised and then applied to a collection of 9,892 patients from 11 countries to create the Global MSSS. In order to compare different methods of detecting such effects the authors simulated the effects of a genetic factor on disability. Cross-sectional EDSS measurements made after the first year were representative of overall disease severity. The MSSS was more powerful than the other methods the authors tested for detecting different rates of disease progression. The Multiple Sclerosis Severity Score (MSSS) is a powerful method for comparing disease progression using single assessment data. The Global MSSS can be used as a reference table for future disability comparisons. While useful for comparing groups of patients, disease fluctuation precludes its use as a predictor of future disability in an individual.
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                Author and article information

                Contributors
                Gleb Makshakov:
                ORCID: http://orcid.org/0000-0001-6831-0441
                Journal
                Journal ID (nlm-ta): Neurol Res Int
                Journal ID (iso-abbrev): Neurol Res Int
                Journal ID (publisher-id): NRI
                Title: Neurology Research International
                Publisher: Hindawi
                ISSN (Print): 2090-1852
                ISSN (Electronic): 2090-1860
                Publication date (Print): 2017
                Publication date (Electronic): 2 October 2017
                Volume: 2017
                Electronic Location Identifier: 8652463
                Affiliations
                1SBIH City Clinical Hospital No. 31, City Center of MS and Autoimmune Diseases, St. Petersburg, Russia
                2Neurology Department, FSBEI HE I.P. Pavlov SPbSMU MOH Russia, St. Petersburg, Russia
                3Institute of Human Brain of the Russian Academy of Sciences, St. Petersburg, Russia
                4Center for Molecular Medicine, Laboratory of Autoimmune Diagnostics, FSBEI HE I.P. Pavlov SPbSMU MOH Russia, St. Petersburg, Russia
                5Department of Clinical Pharmacology and EBM, FSBEI HE I.P. Pavlov SPbSMU MOH Russia, St. Petersburg, Russia
                6Department of Pharmacoepidemiology and Biostatistics, FSBEI HE I.P. Pavlov SPbSMU MOH Russia, St. Petersburg, Russia
                7Institute of Experimental Medicine, St. Petersburg, Russia
                Author notes

                Academic Editor: Changiz Geula

                Author information
                http://orcid.org/0000-0001-6831-0441
                http://orcid.org/0000-0002-4998-3699
                Article
                DOI: 10.1155/2017/8652463
                PMC ID: 5643086
                PubMed ID: 29291134
                SO-VID: d2e93986-aacf-441e-b0b7-0e5d5097eaeb
                Copyright © Copyright © 2017 Gleb Makshakov et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 1 May 2017
                Date revision received : 7 August 2017
                Date accepted : 24 August 2017
                Funding
                Funded by: Russian Science Foundation
                Award ID: 16-15-10203
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Neurology
                Data availability:
                ScienceOpen disciplines: Neurology

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