Ramanathan S, Mohammad S, Tantsis E, Nguyen TK, Merheb V, Victor Fung SC et al (2018) Clinical course, therapeutic responses and outcomes in relapsing MOG antibodyassociated demyelination. Rostásy K, Mader S, Hennes EM, Schanda K, Gredler V, Guenther A et al (2013) Persisting myelin oligodendrocyte glycoprotein antibodies in aquaporin4 antibody negative pediatric neuromyelitis optica. Hennes EM, Baumann M, Schanda K, Anlar B, Bajer-Kornek B, Blaschek A et al (2017) Prognostic relevance of MOG antibodies in children with an acquired demyelinating syndrome. Īrmangue T, Olive-Cirera G, Martinez-Hernadez E, Sepulveda M, Ruiz-Garcia R, Munoz-Batista M et al (2020) Associations of paediatric demyelinating and encephalitic syndromes with myelin oligodendrocyte glycoprotein antibodies: a multicentre observational study. Wynford-Thomas R, Jacob A, Tomassini V (2019) Neurological update: MOG-antibody disease. Jarius S, Paul F, Aktas O, Asgari N, Dale RC, de Seze J et al (2018) MOG encephalomyelitis: international recommendations on diagnosis and antibody testing. Waters P, Fadda G, Woodhall M, O’Mahony J, Brown RA, Castro DA et al (2019) Serial antimyelin oligodendrocyte glycoprotein antibody analyses and outcomes in children with demyelinating syndromes. There are various clinical phenotypes and MRI patterns, recognition of which may help in the determination of therapeutic strategies, and long-term prognosis.įernandez-Carbonell C, Vargas Lowy D, Musallam A et al (2016) Clinical and MRI phenotype of children with MOG antibodies. The Spectrum of MOG-associated disorders is wider affecting the brain (grey and white matter) and the meninges. Poor prognostic indicators included: (i) incomplete recovery from an acute attack, (b) brainstem syndrome, (c) ADEM with incomplete recovery, (d) MRI suggestive of leukodystrophy pattern, (e) severe ON, (f) ADEMON. ADEM was exclusively seen in pediatric patients. There was exclusive vomiting in 24.7% prior to onset of clinical syndrome, none of them had area postrema involvement. Among the 263 demyelinating episodes 45.8% were optic neuritis (ON), 22.8% were myelopathy, 17.1% were brainstem, 7.6% were acute demyelinating encephalomyelitis(ADEM), 4.2% were opticomyelopathy and 2.3% with cerebral manifestations. The study population consisted of 93 (M:F = 45:48) (Pediatric:40, Adult-onset:47, Late-onset:7) patients with a median age of 21 years. Description of the various clinical phenotypes, investigation profile, therapeutic response, differences between pediatric and adult-onset neurological disorders, determination of poor prognostic factors was done. MethodsĪll patients with MOGAD were included. We aimed to determine the frequency of MOG-associated disorders (MOGAD), its various clinical phenotypes, and imaging characteristics. Myelin oligodendrocyte glycoprotein (MOG) is an oligodendrocytopathy resulting in demyelination.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |