![]() ![]() J Neurol Neurosurg Psychiatry 88(6):534–536. įujimori J, Takai Y, Nakashima I et al (2017) Bilateral frontal cortex encephalitis and paraparesis in a patient with anti-MOG antibodies. Hamid SHM, Whittam D, Saviour M et al (2018) Seizures and encephalitis in myelin oligodendrocyte glycoprotein IgG disease vs aquaporin 4 IgG disease. Ogawa R, Nakashima I, Takahashi T et al (2017) MOG antibody-positive, benign, unilateral, cerebral cortical encephalitis with epilepsy. J Neurol Neurosurg Psychiatry 89(2):127–137. Ramanathan S, Mohammad S, Tantsis E et al (2018) Clinical course, therapeutic responses and outcomes in relapsing MOG antibody-associated demyelination. Pandit L, Sato DK, Mustafa S et al (2016) Relapsing optic neuritis and isolated transverse myelitis are the predominant clinical phenotypes for patients with antibodies to myelin oligodendrocyte glycoprotein in India. Sato DK, Callegaro D, Lana-Peixoto MA et al (2014) Distinction between MOG antibody-positive and AQP4 antibody-positive NMO spectrum disorders. Kitley J, Waters P, Woodhall M et al (2014) Neuromyelitis optica spectrum disorders with aquaporin-4 and myelin-oligodendrocyte glycoprotein antibodies: a comparative study. ![]() Part 2: Epidemiology, clinical presentation, radiological and laboratory features, treatment responses, and long-term outcome. Jarius S, Ruprecht K, Kleiter I et al (2016) MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Kitley J, Woodhall M, Waters P et al (2012) Myelin-oligodendrocyte glycoprotein antibodies in adults with a neuromyelitis optica phenotype. Neurol Neuroimmunol Neuroinflamm 2(3):e89. Waters P, Woodhall M, O’Connor KC et al (2015) MOG cell-based assay detects non-MS patients with inflammatory neurologic disease. O’Connor KC, McLaughlin KA, De Jager PL et al (2007) Self-antigen tetramers discriminate between myelin autoantibodies to native or denatured protein. ConclusionĬurrent treatment of MOGAD is highly variable, indicating a need for consensus-based treatment guidelines, while awaiting definitive clinical trials. Regardless of monitoring results, 25.0% (13/52) would not stop MT. Treatment response is monitored by MRI (53.8% 28/52), optical coherence tomography (23.1% 12/52) and MOG antibody titres (36.5% 19/52). In children, IVIg is the preferred first line MT (54.5% 6/11). Commonly used first line MTs in adults are azathioprine (30.8%, 16/52), mycophenolate mofetil (25.0%, 13/52) and rituximab (17.3%, 9/52). Repeat MOG antibody status is used by 52.9% (27/51) to help decide on MT initiation. After an index event, 60% (31/51) usually start steroid-sparing maintenance therapy (MT) after ≥ 2 attacks 92.3% (48/52) would start MT. Following an acute attack, 55.8% (29/52) of respondents typically continue corticosteroids for ≥ 3 months though less commonly when treating children. 45.5% (5/11) of paediatric neurologists use IV immunoglobulin (IVIg) in preference to PE. If recovery is incomplete, 71.2% (37/52) proceed next to plasma exchange (PE). All treat acute attacks with high dose corticosteroids. Resultsįifty-two responses were received (response rate 60.5%) from 86 invited experts, comprising adult (78.8%, 41/52) and paediatric (21.2%, 11/52) neurologists in 22 countries. Neurologists worldwide with expertise in treating MOGAD participated in an online survey (February–April 2019). To survey the current global clinical practice of clinicians treating MOGAD. ![]() While monophasic and relapsing forms of myelin oligodendrocyte glycoprotein antibody associated disorders (MOGAD) are increasingly diagnosed world-wide, consensus on management is yet to be developed. Journal of Neurology volume 267, pages 3565–3577 ( 2020) Cite this article Treatment of MOG antibody associated disorders: results of an international survey ![]()
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