Anti nmo anti mog9/13/2023 ![]() ![]() The initial clinical event in AQP4-NMOSD was unilateral ON ( N = 4), myelitis ( N = 3), bilateral ON ( N = 2), or simultaneous myelitis and ON ( N = 1). The two seronegative patients had their first clinical event, respectively, at 63 and 45 years. Median age at the first clinical event was 37.8 years in AQP4-NMOSD (range 14–73.7) and 27.7 years in MOGAD (range 9.8–39.5). Age at first clinical event significantly varied across groups (Kruskal–Wallis, χ 2(2) = 6.77, p = 0.033), showing earlier onset in MOGAD patients than in AQP4-NMOSD ( χ 2(1) = 4.18, p = 0.041). Here, we detail the clinical, biological and imaging phenotype of AQP4-NMOSD, MOGAD and SN-NMOSD patients diagnosed in the neuroimmunology unit of CHU Liège between 19. A reliable diagnosis is mandatory to ensure proper treatment and prognosis. ![]() The distinction between MS, AQP4-NMOSD, MOGAD and SN-NMOSD is essential but challenging due to overlapping clinical, biological and radiological features. Finally, patients with NMOSD, negative for both AQP4 and MOG antibodies, are now diagnosed as ‘seronegative NMOSD’ (SN-NMOSD). These disorders are now referred to as ‘MOG-associated disorders’ (MOGAD). The clinical phenotype of disorders with MOG-antibodies far exceeds neuromyelitis optica and includes uni- or bilateral, isolated or recurrent ON, myelitis with or without ON, ADEM, brainstem and supra-tentorial lesions. Antibodies against conformational MOG epitopes detected by cell-based assay (CBA) were later causally implicated in acute disseminated encephalomyelitis (ADEM) and NMOSD. Initially, MOG-antibodies were largely associated to several inflammatory diseases including MS, but the former western-blots and ELISA lacked specificity. It later appeared that only 80% patients with a NMOSD phenotype are seropositive for AQP4-antibodies: other cases are seronegative and a minority of them (20%) bear antibodies against MOG. This pleomorphic phenotype led to the concept of ‘NMO spectrum disorders’ (NMOSD). This objective biomarker allowed for a broadening of NMO phenotype to isolated myelitis without optic neuritis (ON) or even central nervous system (CNS) involvement without a spinal cord or optic nerve damage, e.g., area postrema syndrome. NMO was considered as a subtype of MS until the discovery of causal antibodies against AQP4 protein. In 1894, Eugène Devic reported atypical cases of multiple sclerosis (MS) characterized by an inflammatory lesion of both optic nerves and spinal cord, a condition which he dubbed ‘neuromyelitis optica’ (NMO). A better understanding of these diseases should encourage prompt biological screening and hasten proper diagnosis and treatment. Despite a fairly good visual outcome after MOG-associated ON, retinal nerve fibre layer (RNFL) thickness decreased, suggesting a fragility of the optic nerve toward further attacks.Īs observed in larger cohorts, our MOGAD and AQP4-NMOSD cases differ by clinical and prognostic features. MOG-associated ON mainly affected the anterior part of the optic nerve with a papilledema in 79.2% of cases. In total we counted 54 ON, with more ON per patient in MOGAD. Fifteen of our 20 patients encountered a relapsing course with 90% relapses in AQP4-NMOSD, 62.5% in MOGAD and 50% in seronegative group, and a mean period between first and second clinical event of 7.1 and 4.8 months for AQP4-NMOSD and MOGAD, respectively. In both groups, the first clinical event most often consisted of optic neuritis (ON), followed by isolated myelitis. Age at onset was 37.8 and 27.7 years old for AQP4-NMOSD and MOGAD respectively. (J Neuroinflammation 15:134, 2018) for MOGAD (MOG associated disorders), we retrospectively surveyed 10 AQP4-NMOSD, 8 MOGAD and 2 seronegative NMOSD, followed at the specialized neuroimmunology unit of the CHU Liège.įemale predominance was only observed in AQP4 group. (Neurology 85:177–189, 2015) criteria for NMOSD and on those more recently proposed by Jarius et al. To emphasize physio-pathological, clinical and prognosis differences between conditions causing serious and sometimes very similar clinical manifestations: anti-aquaporin-4 (AQP4) and anti-myelin oligodendrocyte glycoprotein (MOG) antibodies related diseases, and seronegative NMOSD (neuromyelitis optica spectrum disorders).īased on Wingerchuk et al. ![]()
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