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    Imaging Surrogates of Disease Activity in Neuromyelitis Optica Allow Distinction from Multiple Sclerosis.

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    Author
    Matthews, L; Kolind, S; Brazier, A; Leite, MI; Brooks, J; Traboulsee, A; Jenkinson, M; Johansen-Berg, H; Palace, J
    Date
    2015
    Source Title
    PLoS One
    Publisher
    Public Library of Science (PLoS)
    University of Melbourne Author/s
    Jenkinson, Mark
    Affiliation
    Centre for Neuroscience
    Metadata
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    Document Type
    Journal Article
    Citations
    Matthews, L., Kolind, S., Brazier, A., Leite, M. I., Brooks, J., Traboulsee, A., Jenkinson, M., Johansen-Berg, H. & Palace, J. (2015). Imaging Surrogates of Disease Activity in Neuromyelitis Optica Allow Distinction from Multiple Sclerosis.. PLoS One, 10 (9), pp.e0137715-. https://doi.org/10.1371/journal.pone.0137715.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/253493
    DOI
    10.1371/journal.pone.0137715
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4575169
    Abstract
    Inflammatory demyelinating lesions of the central nervous system are a common feature of both neuromyelitis optica and multiple sclerosis. Despite this similarity, it is evident clinically that the accumulation of disability in patients with neuromyelitis optica is relapse related and that a progressive phase is very uncommon. This poses the question whether there is any pathological evidence of disease activity or neurodegeneration in neuromyelitis optica between relapses. To investigate this we conducted a longitudinal advanced MRI study of the brain and spinal cord in neuromyelitis optica patients, comparing to patients with multiple sclerosis and controls. We found both cross-sectional and longitudinal evidence of diffusely distributed neurodegenerative surrogates in the multiple sclerosis group (including thalamic atrophy, cervical cord atrophy and progressive widespread diffusion and myelin water imaging abnormalities in the normal appearing white matter) but not in those with neuromyelitis optica, where localised abnormalities in the optic radiations of those with severe visual impairment were noted. In addition, between relapses, there were no new silent brain lesions in the neuromyelitis optica group. These findings indicate that global central nervous system neurodegeneration is not a feature of neuromyelitis optica. The work also questions the theory that neurodegeneration in multiple sclerosis is a chronic sequela to prior inflammatory and demyelinating pathology, as this has not been found to be the case in neuromyelitis optica where the lesions are often more destructive.

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