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          In patients presenting with a clinically isolated syndrome (CIS), magnetic resonance imaging (MRI) can support and substitute clinical information for multiple sclerosis (MS) diagnosis demonstrating disease dissemination in space (DIS) and time (DIT) and helping to rule out other conditions that can mimic MS. From their inclusion in the diagnostic work-up for MS in 2001, several modifications of MRI diagnostic criteria have been proposed, in the attempt to simplify lesion-count models for demonstrating DIS, change the timing of MRI scanning for demonstrating DIT, and increase the value of spinal cord imaging.

          Since the last update of these criteria, new data regarding the application of MRI for demonstrating DIS and DIT have become available and improvement in MRI technology has occurred. State-of-the-art MRI findings in these patients were discussed in a MAGNIMS workshop, the goal of which was to provide an evidence-based and expert-opinion consensus on diagnostic MRI criteria modifications.

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          Most cited references 97

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

          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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            International consensus diagnostic criteria for neuromyelitis optica spectrum disorders

            Neuromyelitis optica (NMO) is an inflammatory CNS syndrome distinct from multiple sclerosis (MS) that is associated with serum aquaporin-4 immunoglobulin G antibodies (AQP4-IgG). Prior NMO diagnostic criteria required optic nerve and spinal cord involvement but more restricted or more extensive CNS involvement may occur. The International Panel for NMO Diagnosis (IPND) was convened to develop revised diagnostic criteria using systematic literature reviews and electronic surveys to facilitate consensus. The new nomenclature defines the unifying term NMO spectrum disorders (NMOSD), which is stratified further by serologic testing (NMOSD with or without AQP4-IgG). The core clinical characteristics required for patients with NMOSD with AQP4-IgG include clinical syndromes or MRI findings related to optic nerve, spinal cord, area postrema, other brainstem, diencephalic, or cerebral presentations. More stringent clinical criteria, with additional neuroimaging findings, are required for diagnosis of NMOSD without AQP4-IgG or when serologic testing is unavailable. The IPND also proposed validation strategies and achieved consensus on pediatric NMOSD diagnosis and the concepts of monophasic NMOSD and opticospinal MS.
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              Transected neurites, apoptotic neurons, and reduced inflammation in cortical multiple sclerosis lesions.

              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.

                Author and article information

                Lancet Neurol
                Lancet Neurol
                The Lancet. Neurology
                5 February 2016
                26 January 2016
                March 2016
                01 March 2017
                : 15
                : 3
                : 292-303
                [1 ]Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy
                [2 ]Department of Neuroinflammation, Queen Square MS Centre, UCL Institute of Neurology, Queen Square, London, WC1N 3BG
                [3 ]National Institute for Health Research (NIHR), UCL/UCLH Biomedical Research Centre (BRC)
                [4 ]Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy
                [5 ]Division of Neurosciences, Queen’s medical centre campus, University of Nottingham, Nottingham, UK
                [6 ]Department of Neurology, University of Basel, Switzerland
                [7 ]Magnetic Resonance Unit, Department of Radiology (IDI), Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain
                [8 ]Centre d’Esclerosi Múltiple de Catalunya (Cemcat), Department of Neurology/Neuroimmunology, Hospital Universitari Vall d’Hebron; Universitat Autònoma de Barcelona; Barcelona, Spain
                [9 ]Department of Neurology, Glostrup Hospital and University of Copenhagen, Denmark
                [10 ]Department of Neurosciences, S. Camillo-Forlanini Hospital, Italy
                [11 ]Department of Clinical Neurology, University of Oxford Hospitals Trust, Oxford, UK
                [12 ]Translational Neuroradiology Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA
                [13 ]Division of Child Neurology, The Children’s Hospital of Philadelphia, Department of Neurology, Perelman School of Medicine, University of Pennsylvania
                [14 ]MS Centre Amsterdam, VU University Medical Centre, Netherlands
                Author notes
                Correspondence should be addressed to: Prof. Massimo Filippi, Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy. Telephone number: #39-02-26433033; Fax number: #39-02-26433031; filippi.massimo@ 123456hsr.it

                MAGNIMS Steering Committee: F. Barkhof, O. Ciccarelli, N. De Stefano, C. Enzinger, M. Filippi, J. Frederiksen, C. Gasperini, L. Kappos, J. Palace, M.A. Rocca, A. Rovira, J. Sastre-Garriga, T. Yousry, H. Vrenken.


                This manuscript version is made available under the CC BY-NC-ND 4.0 license.



                multiple sclerosis, magnetic resonance imaging, diagnosis, criteria


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