Long-term treatment was a shared patient decision; most were started on steroid sparing brokers such azathioprine and mycophenolic acid, although two patients preferred not to be on any treatment
February 23, 2022
Long-term treatment was a shared patient decision; most were started on steroid sparing brokers such azathioprine and mycophenolic acid, although two patients preferred not to be on any treatment. Traditionally, it was thought that MOG-Ab-positive cases carry a benign course and good prognosis. Disability Status Scale score at onset was 3.0 (range, 2.0C4.0). A monophasic course was noted in two (22.2%) patients, while the median number of relapse events was 3 (range 2C5) in 77.8% of the patients. Optic neuritis and transverse myelitis contributed equally as initial manifestations in three individuals (33%), while brainstem relapse was reported in two individuals (22%). The brain magnetic resonance imaging findings were compatible with McDonald’s 2010 dissemination in space criteria in three cases (33%). Short myelitis and an (H)-sign were each documented in one patient. Conclusion: The phenotypes of MOG Ab-positive cases exhibited overlapping features with MS and NMOSD. This obtaining highlights the importance of screening for anti-MOG in individuals with demyelinating symptoms, in concern of the possibility of false-positive MOG Ab results. Keywords: myelin oligodendrocyte glycoprotein, optic neuritis, neuromyelitis optica spectrum disorder, multiple sclerosis, transverse myelitis Introduction Myelin oligodendrocyte glycoprotein (MOG) is usually B-HT 920 2HCl a component of central nervous system (CNS) myelin. Antibodies against MOG have recently been acknowledged in a clinical syndrome that is likely a CNS demyelinating disorder individual from multiple sclerosis (MS), acute demyelinating encephalomyelitis (ADEM), and neuromyelitis optica spectrum disorder (NMOSD). Although MOG antibodies have been pointed out in the literature for the last 30 years, their role in demyelinating disease has not been fully elucidated and, to date, remains controversial (1, 2). In experimental allergic encephalomyelitis mouse models, MOG is the only CNS myelin autoantigen to cause both an encephalitogenic T cell-mediated inflammatory response and demyelination (3, 4). The significance of this is usually unclear, and the prevalence of MOG antibodies in MS remains undetermined. MOG antibodies have recently been linked to seronegative cases of NMOSD. Recent cohort studies have exhibited that 15C35% of seronegative NMOSD patients will test positive for MOG antibodies (5). The presence of MOG antibodies is not only described in seronegative cases of NMOSD (6); indeed, MOG antibody-positive cases have also been identified within a wider spectrum of demyelinating disorders. Recurrent optic neuritis, myelitis, brainstem encephalitis, and ADEM-like presentation such as encephalomyelitis have all been described in MOG-immunoglobulin (IgG)-positive patients (7C9). However, the clinical features of this CHK2 disease phenotype remain undetermined. We herein report the clinical presentation of a case series of B-HT 920 2HCl MOG-IgG-positive patients, not all of whom fulfill the NMOSD criteria, to be able to highlight the problems and top features of this condition. Case Explanation This research was authorized by the College or university of European Ontario’s (European) Health Technology Research Ethics Panel and written educated consent was from all individuals. All people who examined positive for anti-MOG in the London (Ontario) MS center were retrospectively evaluated. Data were acquired for age group at starting point, sex, first medical presentation, amount of relapses, disease program, and length. The neurological exam data included the Extended Disability Status Size (EDSS) rating at the original and last follow-up and mind and backbone B-HT 920 2HCl magnetic resonance imaging (MRI). Furthermore, data on serological tests and cerebrospinal liquid (CSF) evaluation including oligoclonal rings (OCB) were gathered if obtainable. Data on current and disease-modifying treatments (DMTs) had been also included. Nine MOG-IgG-positive instances were determined (Desk 1). Desk 1 Demographic, medical, and radiological features of individuals.
A52MBrainstem (vertigo)321Multiple periventricular and deep white matter lesionsN/A*3 OCBAZT**B29FBrainstem B-HT 920 2HCl (diplopia and ataxia)222Left optic nerve enhancementNormalNegativeMycophenolic acidC31FBrief myelitis232Multiple supratentorial and infratentorial lesionsMultiple cervical and thoracic section (2-3 vertebral measures)N/AWas on glatiramer acetate, discontinued and received no more treatmentD28MON***342Right optic nerve hyperintensity up to the chiasma and enhancementN/ANegativeMycophenolic acidE43FON442Right optic nerve hyperintensity, zero comparison enhancementNormalNegativeNo ataxia13 and treatmentF58FBladder.52Few subcortical hyperintensitiesNormalNegativeAZTG69FAbout42.53Juxtacortical, periventricular, and deep white matter even more pronounced in both occipital lobesNormalNegativeNo treatmentH34FTransverse myelitis12.intensive hyperintensity in the thoracic vertebral cordNegativeNo treatmentI35FLongitudinal transverse myelitis13 51NormalLongitudinally.52NormalLongitudinally extensive hyperintensity in the cervical spinal cordNegativeNo treatment Open up in another window *N/A, unavailable; **AZT, azathioprine; ***ON, optic neuritis; OCB, oligoclonal rings; EDSS, Expanded Impairment Status Size; MRI, magnetic resonance imaging; CSF, cerebrospinal liquid. Case A.