MRI and clinical features of myelin oligodendrocyte glycoprotein (MOG)-antibody disease may overlap with those of other inflammatory demyelinating conditions posing diagnostic challenges, especially in non-acute phases and when serologic testing for MOG antibodies is unavailable or shows uncertain results. We aimed to identify MRI and clinical markers that differentiate non-acute MOG-antibody disease from aquaporin 4 (AQP4)-antibody neuromyelitis optica spectrum disorder and relapsing remitting multiple sclerosis, guiding in the identification of patients with MOG-antibody disease in clinical practice. In this cross-sectional retrospective study, data from 16 MAGNIMS centres were included. Data collection and analyses were conducted from 2019 to 2021. Inclusion criteria were: diagnosis of MOG-antibody disease; AQP4-neuromyelitis optica spectrum disorder and multiple sclerosis; brain and cord MRI at least 6 months from relapse; and Expanded Disability Status Scale (EDSS) score on the day of MRI. Brain white matter T2 lesions, T1-hypointense lesions, cortical and cord lesions were identified. Random forest models were constructed to classify patients as MOG-antibody disease/AQP4-neuromyelitis optica spectrum disorder/multiple sclerosis; a leave one out cross-validation procedure assessed the performance of the models. Based on the best discriminators between diseases, we proposed a guide to target investigations for MOG-antibody disease. One hundred and sixty-two patients with MOG-antibody disease [99 females, mean age: 41 (±14) years, median EDSS: 2 (0-7.5)], 162 with AQP4-neuromyelitis optica spectrum disorder [132 females, mean age: 51 (±14) years, median EDSS: 3.5 (0-8)], 189 with multiple sclerosis (132 females, mean age: 40 (±10) years, median EDSS: 2 (0-8)] and 152 healthy controls (91 females) were studied. In young patients (<34 years), with low disability (EDSS < 3), the absence of Dawson's fingers, temporal lobe lesions and longitudinally extensive lesions in the cervical cord pointed towards a diagnosis of MOG-antibody disease instead of the other two diseases (accuracy: 76%, sensitivity: 81%, specificity: 84%, P < 0.001). In these non-acute patients, the number of brain lesions < 6 predicted MOG-antibody disease versus multiple sclerosis (accuracy: 83%, sensitivity: 82%, specificity: 83%, P < 0.001). An EDSS < 3 and the absence of longitudinally extensive lesions in the cervical cord predicted MOG-antibody disease versus AQP4-neuromyelitis optica spectrum disorder (accuracy: 76%, sensitivity: 89%, specificity: 62%, P < 0.001). A workflow with sequential tests and supporting features is proposed to guide better identification of patients with MOG-antibody disease. Adult patients with non-acute MOG-antibody disease showed distinctive clinical and MRI features when compared to AQP4-neuromyelitis optica spectrum disorder and multiple sclerosis. A careful inspection of the morphology of brain and cord lesions together with clinical information can guide further analyses towards the diagnosis of MOG-antibody disease in clinical practice.
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http://dx.doi.org/10.1093/brain/awac480 | DOI Listing |
Neurol Neuroimmunol Neuroinflamm
January 2025
Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland.
Background And Objectives: In patients with myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD), acute disease activity is generally identified through medical history, neurologic examination, and imaging. However, these may be insufficient for detecting disease activity in specific conditions. This study aimed to investigate the dynamics of serum neurofilament light chain (sNfL) and serum glial fibrillary acidic protein (sGFAP) after clinical attacks and to assess their utility in discriminating attacks from remission in patients with MOGAD.
View Article and Find Full Text PDFRinsho Shinkeigaku
December 2024
Department of Neurology and Stroke Treatment, Kyoto First Red Cross Hospital.
A 49-year-old female was admitted to our hospital due to acute-onset dysarthria and unstable gait. Brain MR diffusion weighted imaging revealed high signal intensities in the midbrain. Brain tumors, abscess and demyelinating lesions was suspected firstly as etiology of the lesion and antibiotics and antiviral drug were started under consulting with the neurosurgeon about brain biopsy.
View Article and Find Full Text PDFbioRxiv
December 2024
Neuroscience Unit, University Hospital Center of Quebec - Laval University, Quebec City, Quebec, Canada.
Autoantibodies contribute to many autoimmune diseases, yet there is no approved therapy to neutralize them selectively. A popular mouse model, experimental autoimmune encephalomyelitis (EAE), could serve to develop such a therapy, provided we can better understand the nature and importance of the autoantibodies involved. Here we report the discovery of autoantibody-secreting extrafollicular plasmablasts in EAE induced with specific myelin oligodendrocyte glycoprotein (MOG) antigens.
View Article and Find Full Text PDFMult Scler J Exp Transl Clin
December 2024
Department of Neurology, Tokyo Women's Medical University, Tokyo, Japan.
Background: Few studies have examined B cells among patients with anti-myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD), including brain pathology.
Objective: To describe cases of tumefactive MOGAD with B-cell dominant central nervous system (CNS) infiltration.
Methods: In this study, we reviewed three cases with clinical and brain histopathological features with tumefactive MOGAD.
BMC Neurol
December 2024
King Abdullah International Medical Research Center, Riyadh, Saudi Arabia.
Background: Although pediatric optic neuritis (PON) is a rare condition, current advancements in its diagnosis, investigation, and treatment suggest that a more precise risk assessment is necessary given the history of irreversible damage and functional degeneration of the optic nerve. Additionally, after further investigations and/or new neurological events, the initial diagnosis is revised.
Aim: To report clinical profile, management and outcome of different demyelinating disease phenotypes of pediatric optic neuritis (PON) in individuals under the age of 18 years in a tertiary center in the Kingdom of Saudi Arabia (KSA).
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