TY - JOUR
T1 - Contrasting the brain imaging features of MOG-antibody disease, with AQP4-antibody NMOSD and multiple sclerosis
AU - Messina, Silvia
AU - Mariano, Romina
AU - Roca-Fernandez, Adriana
AU - Cavey, Ana
AU - Jurynczyk, Maciej
AU - Leite, Maria Isabel
AU - Calabrese, Massimiliano
AU - Jenkinson, Mark
AU - Palace, Jacqueline
N1 - Funding Information:
The author(s) declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article: S.M. has received travel grants from Biogen, Novartis, Bayer, Merck, Almirall, Roche and honorarium for advisory work from Biogen. R.M. is undertaking graduate studies funded by the Rhodes Trust and the Oppenheimer Memorial Trust. A.R.-F. reports no disclosures. A.C. reports no disclosures. M.J. reports no disclosures. M.I.L. reported being involved in aquaporin 4 testing, receiving support from the National Health Service National Specialised Commissioning Group for Neuromyelitis Optica and the National Institute for Health Research Oxford Biomedical Research Centre, receiving speaking honoraria from Biogen Idec, and receiving travel grant from Novartis. J.P. is partly funded by highly specialised services to run a national congenital myasthenia service and a neuromyelitis service. She has received support for scientific meetings and honorariums for advisory work from Merck Serono, Biogen Idec, Novartis, Teva, Chugai Pharma and Bayer Schering, Alexion, Roche, Genzyme, MedImmune, EuroImmun, MedDay, Abide and ARGENX, and grants from Merck Serono, Novartis, Biogen Idec, Teva, Abide and Bayer Schering. Her hospital trust received funds for her role as clinical lead for the RSS, and she has received grants from the MS society and Guthie Jackson Foundation for research studies. M.C. has served on scientific advisory boards for Biogen Idec, Genzyme, Merck Serono, Novartis and Roche and has received grants from Genzyme, Merck Serono, Novartis and Roche and travel and/or speaker honoraria from Merck Serono, Roche, Biogen Idec, Novartis and Genzyme. M.J. receives royalties from licensing of FSL to non-academic, commercial parties.
PY - 2021
Y1 - 2021
N2 - BACKGROUND: Identifying magnetic resonance imaging (MRI) markers in myelin-oligodendrocytes-glycoprotein antibody-associated disease (MOGAD), neuromyelitis optica spectrum disorder-aquaporin-4 positive (NMOSD-AQP4) and multiple sclerosis (MS) is essential for establishing objective outcome measures.OBJECTIVES: To quantify imaging patterns of central nervous system (CNS) damage in MOGAD during the remission stage, and to compare it with NMOSD-AQP4 and MS.METHODS: 20 MOGAD, 19 NMOSD-AQP4, 18 MS in remission with brain or spinal cord involvement and 18 healthy controls (HC) were recruited. Volumetrics, lesions and cortical lesions, diffusion-imaging measures, were analysed.RESULTS: Deep grey matter volumes were lower in MOGAD (p = 0.02) and MS (p = 0.0001), compared to HC and were strongly correlated with current lesion volume (MOGAD R = -0.93, p < 0.001, MS R = -0.65, p = 0.0034). Cortical/juxtacortical lesions were seen in a minority of MOGAD, in a majority of MS and in none of NMOSD-AQP4. Non-lesional tissue fractional anisotropy (FA) was only reduced in MS (p = 0.01), although focal reductions were noted in NMOSD-AQP4, reflecting mainly optic nerve and corticospinal tract pathways.CONCLUSION: MOGAD patients are left with grey matter damage, and this may be related to persistent white matter lesions. NMOSD-AQP4 patients showed a relative sparing of deep grey matter volumes, but reduced non-lesional tissue FA. Observations from our study can be used to identify new markers of damage for future multicentre studies.
AB - BACKGROUND: Identifying magnetic resonance imaging (MRI) markers in myelin-oligodendrocytes-glycoprotein antibody-associated disease (MOGAD), neuromyelitis optica spectrum disorder-aquaporin-4 positive (NMOSD-AQP4) and multiple sclerosis (MS) is essential for establishing objective outcome measures.OBJECTIVES: To quantify imaging patterns of central nervous system (CNS) damage in MOGAD during the remission stage, and to compare it with NMOSD-AQP4 and MS.METHODS: 20 MOGAD, 19 NMOSD-AQP4, 18 MS in remission with brain or spinal cord involvement and 18 healthy controls (HC) were recruited. Volumetrics, lesions and cortical lesions, diffusion-imaging measures, were analysed.RESULTS: Deep grey matter volumes were lower in MOGAD (p = 0.02) and MS (p = 0.0001), compared to HC and were strongly correlated with current lesion volume (MOGAD R = -0.93, p < 0.001, MS R = -0.65, p = 0.0034). Cortical/juxtacortical lesions were seen in a minority of MOGAD, in a majority of MS and in none of NMOSD-AQP4. Non-lesional tissue fractional anisotropy (FA) was only reduced in MS (p = 0.01), although focal reductions were noted in NMOSD-AQP4, reflecting mainly optic nerve and corticospinal tract pathways.CONCLUSION: MOGAD patients are left with grey matter damage, and this may be related to persistent white matter lesions. NMOSD-AQP4 patients showed a relative sparing of deep grey matter volumes, but reduced non-lesional tissue FA. Observations from our study can be used to identify new markers of damage for future multicentre studies.
KW - MOG-Ab disease
KW - MRI
KW - Multiple sclerosis
KW - neuromyelitis optica with AQP4-Ab
KW - non-conventional MRI
UR - http://www.scopus.com/inward/record.url?scp=85106728764&partnerID=8YFLogxK
U2 - 10.1177/13524585211018987
DO - 10.1177/13524585211018987
M3 - Article
C2 - 34048323
JO - Multiple Sclerosis Journal
JF - Multiple Sclerosis Journal
SN - 1352-4585
ER -