Yet, all 21 patients had clinical and radiological findings previously described in MOG-antibody associated demyelination disease supporting the high specificity of the IgG1-CBA.
Seven IgG1-seropositive patients were seronegative for one or both IgG-CBAs. We then retested all sera of our 426 patients with the other two most popular MOG-CBAs for total IgG (a live-cell and a commercial fixed-cell CBAs). Their phenotypes were: 8 optic neuritis, 3 myelitis, 3 neuromyelitis optica, 2 encephalomyelitis, 2 autoimmune encephalitis and 3 atypical MS. Clinical, serological and radiological data were available and analyzed for the 21 seropositive patients out of the 426 patients of our clinics. 41 patients, versus 0 controls were seropositive.
We screened sera from 1300 Greek patients (including 426 patients referred by our 8 clinics) suspected for anti-MOG syndrome, and 120 controls with the live-cell MOG-CBA for IgG1-antibodies. We aimed to analyze the clinical and radiological features of patients with anti-MOG IgG1-antibodies detected with a live-cell CBA and to compare the three most popular MOG-CBAs. However, a universally accepted CBA has not been adopted yet. IgG antibodies to myelin oligodendrocyte glycoprotein (MOG) detected by cell based assays (CBA) have been identified in a constantly expanding spectrum of CNS demyelinating disorders. of Molecular Neurobiology and Immunology, Hellenic Pasteur Institute, 127, Vas. 12 Tzartos NeuroDiagnostics, 3, Eslin str., Athens 11523, Greece Lab.10 Neurology Clinic, Venizeleio General Hospital, Knossos Ave, Heraklion 714 09, Greece.9 Neurology Department, Henry Dunant Hospital, Athens, Greece.8 Neurology Department, General Hospital of Nikaia, 3, Andrea Petrou Mandouvalou, Athens 184 54, Greece.7 Neurology Department, University Hospital of Patras, Rίo 265 04, Greece.6 Saint Luke's Hospital, Panorama, Thessaloniki 552 36, Greece.5 2nd Neurology Department, University Hospital of Thessaloniki "AHEPA", Thessaloniki, Greece.4 Neurology Department, University Hospital of Ioannina, Ioannina, Greece.3 1st Department of Neurology, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, 72-74, Vas.Electronic address: 2 Tzartos NeuroDiagnostics, 3, Eslin str., Athens 11523, Greece Department of Biochemistry and Biotechnology, University of Thessaly, Larissa, Greece. Sofias Ave, Athens 11528, Greece Tzartos NeuroDiagnostics, 3, Eslin str., Athens 11523, Greece. 1 1st Department of Neurology, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, 72-74, Vas.4 Furthermore, MOGAD lesions in the brain can look like lesions seen in those with ADEM. 4 MOG antibody disease optic neuritis seems to predominantly affect the retrobulbar region, while AQP-4-associated optic neuritis is found intracranially. MRI findings are similar to those with MS and NMOSD, but there may be some differences. There appears to be no overlap between individuals with anti-MOG positivity and AQP-4 positivity, although there have been some isolated cases reported using the older ELISA assay. 2 Those with persistent detection of anti-MOG may be more likely to have a relapsing rather than monophasic disease course. Unlike anti-AQP4 antibodies, anti-MOG antibodies may decrease over time, and may not be detectable early in the disease process or during remission, and this is especially the case for MOG antibody disease associated ADEM. 2 CSF analysis from a lumbar puncture may show increased white blood cell counts in some patients during a relapse, and oligoclonal bands are not usually found. Only cell-based assays are considered reliable for the diagnosis of MOGAD because of the improved specificity over older ELISA tests. There are blood tests that can test for MOG antibodies. 2022 Rare Neuroimmune Disorders Symposium.
COVID-19 and Rare Neuroimmune Disorders.
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