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      Clinical relevance of brain atrophy assessment in multiple sclerosis. Implications for its use in a clinical routine

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          Abstract

          Brain atrophy measurement in multiple sclerosis (MS) has become an important outcome for determining patients at risk for developing physical and cognitive disability.

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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--the plaque and its pathogenesis.

            Elliot M. Frohman, Michael K. Racke, Cedric Raine (2006)
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              Transected neurites, apoptotic neurons, and reduced inflammation in cortical multiple sclerosis lesions.

              J Peterson, L. Bo, S Mörk … (2001)
              Multiple Sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system that causes motor, sensory, and cognitive deficits. The present study characterized demyelinated lesions in the cerebral cortex of MS patients. One hundred twelve cortical lesions were identified in 110 tissue blocks from 50 MS patients. Three patterns of cortical demyelination were identified: Type I lesions were contiguous with subcortical white matter lesions; Type II lesions were small, confined to the cortex, and often perivascular; Type III lesions extended from the pial surface to cortical layer 3 or 4. Inflammation and neuronal pathology were studied in tissue from 8 and 7 patients, respectively. Compared to white matter lesions, cortical lesions contained 13 times fewer CD3-positive lymphocytes (195 vs 2,596/mm3 of tissue) and 6 times fewer CD68-positive microglia/macrophages (11,948 vs 67,956/mm3 of tissue). Transected neurites (both axons and dendrites) occurred at a density of 4,119/mm3 in active cortical lesions, 1,107/mm3 in chronic active cortical lesions, 25/mm3 in chronic inactive cortical lesions, 8/mm3 in myelinated MS cortex, and 1/mm3 in control cortex. In active and chronic active cortical lesions, activated microglia closely apposed and ensheathed apical dendrites, neurites, and neuronal perikarya. In addition, apoptotic neurons were increased significantly in demyelinated cortex compared to myelinated cortex. These data support the hypothesis that demyelination, axonal transection, dendritic transection, and apoptotic loss of neurons in the cerebral cortex contribute to neurological dysfunction in MS patients.
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                Author and article information

                Journal
                Title: Expert Review of Neurotherapeutics
                Abbreviated Title: Expert Review of Neurotherapeutics
                Publisher: Informa UK Limited
                ISSN (Print): 1473-7175
                ISSN (Electronic): 1744-8360
                Publication date Created: July 02 2016
                Publication date (Electronic): May 13 2016
                Publication date (Print): July 02 2016
                Volume: 16
                Issue: 7
                Pages: 777-793
                Affiliations
                [1 ] Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA
                [2 ] MR Imaging Clinical Translational Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA
                [3 ] Department of Neurology and Center of Clinical Neuroscience, Charles University in Prague, First Faculty of Medicine and General University Hospital, Prague, Czech Republic
                [4 ] Jacobs Multiple Sclerosis Center, Department of Neurology, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA
                [5 ] Department of Radiology, First Faculty of Medicine and General University Hospital, Charles University, Prague, Czech Republic
                [6 ] Sydney Neuroimaging Analysis Centre; Brain & Mind Centre, University of Sydney, Sydney, Australia
                [7 ] IRCCS ‘S.Maria Nascente’, Don Gnocchi Foundation, Milan, Italy
                Article
                DOI: 10.1080/14737175.2016.1181543
                PubMed ID: 27105209
                SO-VID: 08665362-2694-409b-83c2-a8d57db28333
                Copyright © © 2016
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