TY - JOUR
T1 - Imaging surrogates of disease activity in neuromyelitis optica allow distinction from multiple sclerosis
AU - Matthews, Lucy
AU - Kolind, Shannon
AU - Brazier, Alix
AU - Leite, Maria Isabel
AU - Brooks, Jonathan
AU - Traboulsee, Anthony
AU - Jenkinson, Mark
AU - Johansen-Berg, Heidi
AU - Palace, Jacqueline
N1 - Funding Information:
Lucy Matthews has no relevant conflicts of interest. Shannon Kolind has received grants from Roche, personal fees from Roche, personal fees from Genzyme, personal fees from Serono, outside the submitted work. Alix Brazier has no relevant conflicts of interest. Maria Isabel Leite is involved in the AQP4 and MOG antibody testing, is supported by NHS National Specialised Commissioning Group for Neuromyelitis optica and by NIHR Oxford Biomedical Research Centre, and has received speaking honoraria from Biogen Idec, Japan, and travel and educational grant from Biogen Idec, UK. Dr. Traboulsee reports personal fees from Roche, personal fees from Teva Innovation, personal fees from EMD Serona, personal fees from Sanofi Genzyme, personal fees from Chugai Pharmaceuticals, personal fees from Medimmune, personal fees from Novartis, grants from Canadian Institute for Health Research, grants from Roche, grants from Sanofi Genzyme, outside the submitted work; Mark Jenkinson receives royalties from ISIS Innovation for FMRIB Software Library (FSL). Jonathan Brooks has no relevant conflicts of interest. Heidi Johansen-Berg receives royalties from Elsevier for edited volume Diffusion MRI. Jacqueline Palace has received support for scientific meetings and honoraria for advisory work from Merck Serono, Biogen Idec, Novartis, Teva, Chugai Pharma and Bayer Schering, and unrestricted grants from Merck Serono, Novartis, Biogen Idec and Bayer Schering. Her hospital trust receives funds for her role as clinical lead for the RSS, and she has received grants from the MS society for unrelated research studies. This does not alter the authors' adherence to PLOS ONE policies on sharing data and materials.
Funding Information:
Thank you to the NHS Highly Specialised Service for neuromyelitis optica from which the neuromyelitis optica patients were recruited. Thank you to our support staff at the John Radcliffe Hospital and Nuffield Department of Clinical Neurosciences, University of Oxford, including the radiographers and specialist nurses. Thank you to Prof Angela Vincent and Dr Mark Woodhall for antibody testing the patient cohort. This work was funded by an MRC fellowship to Dr Matthews (G0901996) and a postdoctoral fellowship from the MS Society of Canada to Dr Kolind. We are also grateful for support from the NIHR Oxford Biomedical Research Centre. Special thanks goes to the study subjects whom gave up their time for this research.
Publisher Copyright:
© 2015 Matthews et al.
PY - 2015/9/18
Y1 - 2015/9/18
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84946593873&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0137715
DO - 10.1371/journal.pone.0137715
M3 - Article
C2 - 26381510
AN - SCOPUS:84946593873
VL - 10
JO - PLoS One
JF - PLoS One
SN - 1932-6203
IS - 9
M1 - e0137715
ER -