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      Diagnostic criteria for multiple sclerosis: 2010 Revisions to the McDonald criteria

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          New evidence and consensus has led to further revision of the McDonald Criteria for diagnosis of multiple sclerosis. The use of imaging for demonstration of dissemination of central nervous system lesions in space and time has been simplified, and in some circumstances dissemination in space and time can be established by a single scan. These revisions simplify the Criteria, preserve their diagnostic sensitivity and specificity, address their applicability across populations, and may allow earlier diagnosis and more uniform and widespread use. Ann Neurol 2011

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          Anti-aquaporin-4 antibody is involved in the pathogenesis of NMO: a study on antibody titre.

          NMO-IgG is a disease-specific autoantibody for neuromyelitis optica (NMO) and its target antigen is aquaporin-4 (AQP4) water channel. Recently, we established a sensitive anti-AQP4 antibody assay using human AQP4-transfected cells, which appeared more sensitive than the original NMO-IgG assay. So far, there has been no large-scale study on anti-AQP4 antibody titre in NMO and related disorders. We tested 148 sera of patients with NMO, high-risk syndrome of NMO, multiple sclerosis (MS), clinically isolated syndrome suggestive of MS and miscellaneous diseases. We analysed the relation of anti-AQP4 antibody titres and clinical and laboratory parameters. The sensitivity of anti-AQP4 antibody assay was 91% (95% CI 79-100) for NMO and 85% (65-100) for high-risk syndrome, and the specificity was 100% (91-100) for NMO and high-risk syndrome, that is, none with the other disorders was positive. Among 21 anti-AQP4 antibody-positive cases whose NMO-IgG were tested, 15 were NMO-IgG-positive and 6 were NMO-IgG-negative. Higher anti-AQP4 antibody titres were associated with complete blindness and extensive or large cerebral lesions on MRI. The lengths of spinal cord lesions on MRI were positively correlated with the titres of anti-AQP4 antibody at the nadir of exacerbations. A few patients who had short (approx. one to two vertebral segments) spinal cord lesions on MRI were also seropositive with low anti-AQP4 antibody titres, but did have other clinical and MRI features of NMO. Anti-AQP4 antibody titres became lower after high-dose methylprednisolone, and a follow-up showed anti-AQP4 antibody titres remained low in relapse-free periods under immunosuppression. Cerebrospinal fluid (CSF)-anti-AQP4 antibody was detected when the serum-antibody titres exceeded 512x, at the ratio of 1 (CSF) to 500 (serum). Using a sensitive assay, the results of the present study suggest that NMO and high-risk syndrome may be essentially anti-AQP4 antibody-associated disorders, and that the anti-AQP4 antibody titres have significant clinical and immunological implications in NMO.
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            Consensus definitions proposed for pediatric multiple sclerosis and related disorders.

            The CNS inflammatory demyelinating disorders of childhood include both self-limited and lifelong conditions, which can be indistinguishable at the time of initial presentation. Clinical, biologic, and radiographic delineation of the various monophasic and chronic childhood demyelinating disorders requires an operational classification system to facilitate prospective research studies. The National Multiple Sclerosis Society (NMSS) organized an International Pediatric MS Study Group (Study Group) composed of adult and pediatric neurologists and experts in genetics, epidemiology, neuropsychology, nursing, and immunology. The group met several times to develop consensus definitions regarding the major CNS inflammatory demyelinating disorders of children and adolescents. Clinical definitions are proposed for pediatric multiple sclerosis (MS), acute disseminated encephalomyelitis (ADEM), recurrent ADEM, multiphasic ADEM, neuromyelitis optica, and clinically isolated syndrome. These definitions are considered operational and need to be tested in future research and modified accordingly. CNS inflammatory demyelinating disorders presenting in children and adolescents can be defined and distinguished. However, prospective research is necessary to determine the validity and utility of the proposed diagnostic categories.
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              Subpial demyelination in the cerebral cortex of multiple sclerosis patients.

              The extent and pattern of demyelination in the cerebral cortex was determined in 78 tissue blocks from the brains of 20 multiple sclerosis (MS) patients and 28 tissue blocks from 7 patients without neurological disease. Tissue blocks from 4 predetermined areas (cingulate gyrus, frontal, parietal, and temporal lobe) were studied, irrespective of macroscopically evident MS plaques. All tissue blocks contained cerebral cortex and periventricular and/or subcortical white matter. One hundred and nine demyelinating lesions were detected in the cerebral cortex, of which 92 (84.4%) were purely intracortical and 17 (15.6%) were lesions extending through both white and gray matter areas. In 5 of the 20 MS brains, subpial demyelination was extensive in the 4 widely spaced cortical areas studied, thus considered to represent a general cortical subpial demyelination. The percentage of demyelinated area was significantly higher in the cerebral cortex (mean 26.5%, median 14.1%) than in white matter (mean 6.5%, median 0%) (p = 0.001). Both gray and white matter demyelination was more prominent in the cingulate gyrus than in the other areas examined (p < 0.05). These results indicate that the cerebral cortex is likely to be a predilection site for MS lesions and identify general cortical subpial demyelination as a distinct pattern occurring in a significant subpopulation of MS patients.

                Author and article information

                Ann Neurol
                Annals of Neurology
                Wiley Subscription Services, Inc., A Wiley Company
                February 2011
                : 69
                : 2
                : 292-302
                [1 ]simpleDepartment of Neurology, Free University Amsterdam, the Netherlands
                [2 ]simpleScientific and Clinical Review Associates LLC New York, NY
                [3 ]simpleDivision of Neurology, Hospital for Sick Children Toronto, Ontario, Canada
                [4 ]simpleDepartment of Neurosciences, University Hospital Center Toulouse, France
                [5 ]simpleMellen Center for Multiple Sclerosis Treatment and Research, Cleveland Clinical Foundation Cleveland, OH
                [6 ]simpleNeuroimaging Research Unit, Division of Neuroscience, Scientific Institute and University Hospital San Raffaele Milan, Italy
                [7 ]simpleDepartment of Multiple Sclerosis Therapeutics, Tohoku University Graduate School of Medicine Sendai, Japan
                [8 ]simpleDepartment of Neurology, First Faculty of Medicine, Charles University Prague, Czech Republic
                [9 ]simpleSt Vincent's University Hospital Elm Park, Dublin, Ireland
                [10 ]simpleDepartments of Neurology and Biomedicine, University Hospital, Kantonsspital Basel, Switzerland
                [11 ]simpleCorrine Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Mount Sinai School of Medicine New York, NY
                [12 ]simpleClinical Neuroimmunology Unit, Multiple Sclerosis Center of Catalonia, University Hospital Vall d'Hebron Barcelona, Spain
                [13 ]simpleDivision of Neurology, St. Michael's Hospital, University of Toronto Toronto, Ontario, Canada
                [14 ]simpleDepartment of Neurology, University Hospital Lund, Sweden
                [15 ]simpleUniversity College London Institute of Neurology United Kingdom
                [16 ]simpleMultiple Sclerosis Center, University of California San Francisco, CA
                [17 ]simpleDepartment of Neurology, Mayo Clinic Rochester, MN
                [18 ]simpleDepartment of Neurology, University of Texas Health Sciences Center Houston, TX
                Author notes
                Address correspondence to Dr Polman, Department of Neurology, VU Medical Center Amsterdam, PO Box 7057, 1007 MB Amsterdam, the Netherlands. E-mail: ch.polman@
                Copyright © 2011 American Neurological Association

                Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.

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