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Imaging Surrogates of Disease Activity in Neuromyelitis Optica Allow Distinction from Multiple Sclerosis
Authors:Lucy Matthews  Shannon Kolind  Alix Brazier  Maria Isabel Leite  Jonathan Brooks  Anthony Traboulsee  Mark Jenkinson  Heidi Johansen-Berg  Jacqueline Palace
Affiliation:1. Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom.; 2. Neurology Department, Oxford University Hospitals NHS Trust, Oxford, United Kingdom.; 3. Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada.; 4. Clinical Research and Imaging Centre (CRiCBristol), University of Bristol, Bristol, United Kingdom.; Medical University Vienna, Center for Brain Research, AUSTRIA,
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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