A study of MRI cortical lesions in myelin oligodendrocyte glycoprotein antibody associated disease
ECTRIMS Online Library. Cortese R. 09/12/19; 279524; 246
Rosa Cortese
Rosa Cortese
Contributions
Abstract

Abstract: 246

Type: Free Communications

Abstract Category: Pathology and pathogenesis of MS - MRI and PET

R. Cortese1, L. Haider1,2, F. Prados1,3,4, A. Jacob5, A.T. Toosy1, W.J. Brownlee1, A. Trip1, R. Nicholas6, M. Yiannakas1, F. De Angelis1, L. Magnollay1, A. Bianchi1, Y. Hacohen1, F. Barkhof3,7,8, O. Ciccarelli1,7

1Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London, London, United Kingdom, 2Department of Biomedical Imaging and Image Guided Therapy, Medical University of Vienna, Vienna, Austria, 3Centre for Medical Imaging computing, Department of Medical Physics and Biomedical Engineering, University College of London, London, United Kingdom, 4Universitat Oberta de Catalunya, Barcelone, Spain, 5NMO Clinical Service at the Walton Centre, Liverpool, 6Division of Brain Sciences, Departement of Medicine, Imperial College London, 7National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research Centre, London, United Kingdom, 8Department of Radiology and Nuclear Medicine, MS Centre Amsterdam, VU Medical Centre, Amsterdam, The Netherlands

Background: Cortical lesions (CLs) are seen on MRI in relapsing-remitting multiple sclerosis (RRMS), while they are typically absent in aquaporin-4 (AQP4)-Ab neuromyelitis optica spectrum disorder (NMOSD). Although cortical involvement has been reported in MOG-Ab-positive patients with encephalopathy and seizures, it is unknown whether patients with MOG-Ab show silent cortical lesions on MRI.
Objective: To evaluate the occurrence of CLs in patients with MOG-Ab-associated disease.
Methods: We studied 24 consecutive patients with MOG-Ab-associated disease (none with history of encephalitis or seizures) (16 F, mean age: 37yrs. [±17], median EDSS: 2 [0-6.5]), 31 patients with RRMS (19 F, mean age: 45.7yrs. [±11.8], median EDSS: 2 [range: 1-7.5]), 29 AQP4-Ab-NMOSD (23 F, mean age: 48.9yrs. [±12.1], median EDSS: 2 [range: 1-7.5]) and 34 healthy controls (HC) (24 F, mean age: 34.7yrs. [±11.8]).
CLs were manually identified on phase sensitive inversion recovery (PSIR) sequences acquired at 3T MRI and classified as leukocortical (located within the cortex and adjacent juxtacortical white matter) or intracortical (located exclusively in the cortex, without involving the white matter or pial borders).
The presence of the CLs was based on the consensus between two independent readers who were blinded to the clinical data. In case of disagreement, a senior neuroradiologist reviewed the images.
Results: At least 1 CL was seen in 22/31 (71%) patients with RRMS (median: 1 [range: 0-14], mean: 2.39 [±3.14]), in 1/29 (0.03%) patients with AQP4-Ab NMOSD, in 1/24 (0.04%) patients with MOG-Ab and in 1/34 (0.03%) HC.
In RRMS, a total of 74 CLs was detected: 40 were leukocortical and 34 intracortical. The only CL seen in AQP4-Ab-NMOSD was intracortical, while the only CL seen in MOG-Ab associated disease was leukocortical. Similarly, the only lesion seen in the one HC was leukocortical.
Conclusions: The presence of cortical lesions on MRI outside an acute event points towards a diagnosis of multiple sclerosis rather than antibody-mediated diseases, when MOG-Ab-associated disease patients without seizures and encephalitis-like presentation are included.
Disclosure: RC, AJ, MY, FDA, LM, AB, YH report no disclosures.
LH was supported by an ESNR (European Society of Neuro-radiology) Research Fellow ship, the ECTRIMS-MAGNIMS Research Fellow ship and received funding from the Austrian MS society.
FP has a Non-clinical Guarantors of Brain Fellowship.
ATT has received honoraria/travel expenses from Biomedia, SSIF, Bayer, Biogen, Novartis, is UK PI for two MEDDAY clinical trials and has received research grants from MRC and ECTRIMS-MAGNIMS
WJB has received speaker fees from Merck Serono and Roche.
AT has received personal fees from Biogen, Merck Serono, Novartis, Roche and Teva, he is supported by the National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research Centre.
RN reports non-financial support from Roche, personal fees and non-financial support from Novartis, personal fees and non-financial support from Biogen, grants from UK MS Society.
FB serves as a consultant for Bayer Schering Pharma, Sanofi-Genzyme, Biogen Idec, Teva, Merck Serono, Novartis, Roche, IXICO, GeNeuro, Apitope Ltd. and Jansen Research.
OC is a consultant for Roche, Novartis, Biogen, Teva and Merck.

Abstract: 246

Type: Free Communications

Abstract Category: Pathology and pathogenesis of MS - MRI and PET

R. Cortese1, L. Haider1,2, F. Prados1,3,4, A. Jacob5, A.T. Toosy1, W.J. Brownlee1, A. Trip1, R. Nicholas6, M. Yiannakas1, F. De Angelis1, L. Magnollay1, A. Bianchi1, Y. Hacohen1, F. Barkhof3,7,8, O. Ciccarelli1,7

1Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London, London, United Kingdom, 2Department of Biomedical Imaging and Image Guided Therapy, Medical University of Vienna, Vienna, Austria, 3Centre for Medical Imaging computing, Department of Medical Physics and Biomedical Engineering, University College of London, London, United Kingdom, 4Universitat Oberta de Catalunya, Barcelone, Spain, 5NMO Clinical Service at the Walton Centre, Liverpool, 6Division of Brain Sciences, Departement of Medicine, Imperial College London, 7National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research Centre, London, United Kingdom, 8Department of Radiology and Nuclear Medicine, MS Centre Amsterdam, VU Medical Centre, Amsterdam, The Netherlands

Background: Cortical lesions (CLs) are seen on MRI in relapsing-remitting multiple sclerosis (RRMS), while they are typically absent in aquaporin-4 (AQP4)-Ab neuromyelitis optica spectrum disorder (NMOSD). Although cortical involvement has been reported in MOG-Ab-positive patients with encephalopathy and seizures, it is unknown whether patients with MOG-Ab show silent cortical lesions on MRI.
Objective: To evaluate the occurrence of CLs in patients with MOG-Ab-associated disease.
Methods: We studied 24 consecutive patients with MOG-Ab-associated disease (none with history of encephalitis or seizures) (16 F, mean age: 37yrs. [±17], median EDSS: 2 [0-6.5]), 31 patients with RRMS (19 F, mean age: 45.7yrs. [±11.8], median EDSS: 2 [range: 1-7.5]), 29 AQP4-Ab-NMOSD (23 F, mean age: 48.9yrs. [±12.1], median EDSS: 2 [range: 1-7.5]) and 34 healthy controls (HC) (24 F, mean age: 34.7yrs. [±11.8]).
CLs were manually identified on phase sensitive inversion recovery (PSIR) sequences acquired at 3T MRI and classified as leukocortical (located within the cortex and adjacent juxtacortical white matter) or intracortical (located exclusively in the cortex, without involving the white matter or pial borders).
The presence of the CLs was based on the consensus between two independent readers who were blinded to the clinical data. In case of disagreement, a senior neuroradiologist reviewed the images.
Results: At least 1 CL was seen in 22/31 (71%) patients with RRMS (median: 1 [range: 0-14], mean: 2.39 [±3.14]), in 1/29 (0.03%) patients with AQP4-Ab NMOSD, in 1/24 (0.04%) patients with MOG-Ab and in 1/34 (0.03%) HC.
In RRMS, a total of 74 CLs was detected: 40 were leukocortical and 34 intracortical. The only CL seen in AQP4-Ab-NMOSD was intracortical, while the only CL seen in MOG-Ab associated disease was leukocortical. Similarly, the only lesion seen in the one HC was leukocortical.
Conclusions: The presence of cortical lesions on MRI outside an acute event points towards a diagnosis of multiple sclerosis rather than antibody-mediated diseases, when MOG-Ab-associated disease patients without seizures and encephalitis-like presentation are included.
Disclosure: RC, AJ, MY, FDA, LM, AB, YH report no disclosures.
LH was supported by an ESNR (European Society of Neuro-radiology) Research Fellow ship, the ECTRIMS-MAGNIMS Research Fellow ship and received funding from the Austrian MS society.
FP has a Non-clinical Guarantors of Brain Fellowship.
ATT has received honoraria/travel expenses from Biomedia, SSIF, Bayer, Biogen, Novartis, is UK PI for two MEDDAY clinical trials and has received research grants from MRC and ECTRIMS-MAGNIMS
WJB has received speaker fees from Merck Serono and Roche.
AT has received personal fees from Biogen, Merck Serono, Novartis, Roche and Teva, he is supported by the National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research Centre.
RN reports non-financial support from Roche, personal fees and non-financial support from Novartis, personal fees and non-financial support from Biogen, grants from UK MS Society.
FB serves as a consultant for Bayer Schering Pharma, Sanofi-Genzyme, Biogen Idec, Teva, Merck Serono, Novartis, Roche, IXICO, GeNeuro, Apitope Ltd. and Jansen Research.
OC is a consultant for Roche, Novartis, Biogen, Teva and Merck.

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