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Updated: May 7, 2026

Myelin Oligodendrocyte Glycoprotein MOG35-55 Induced Experimental Autoimmune Encephalomyelitis EAE in C57BL/6 Mice
Published on: April 15, 2014
Paediatric Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): A Case Report With Varied
Nur Ain Mohamad1, Safinaz Mohd Khialdin1, Nur Shahirah Amir Hamzah1
1Ophthalmology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, MYS.
Abstract:
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an autoimmune demyelinating condition that can affect both the pediatric and adult populations. The initial phenotype for the pediatric group is different from the adult. Young children commonly present with acute disseminated encephalomyelitis followed by optic neuritis and/or transverse myelitis. Here we described the clinical presentation of a young girl diagnosed with MOGAD. A three-year-old girl presented with an acute onset of reduced vision in both eyes preceded by neurological symptoms two weeks prior. Bilateral vision was profoundly reduced, visual acuity (VA) with Cardiff at 50cm in both eyes was 6/96 with positive reverse afferent pupillary defect grade 3 in the left eye. Examination showed bilateral grade one optic disc swelling with upper motor neuron signs. Magnetic Resonance Imaging (MRI) Brain findings were consistent with bilateral optic neuritis with multiple areas of hyperintense lesions with area of enhancement. MRI Spine revealed no spine involvement. Serology analysis showed positive anti-MOG antibody. The patient was treated with high-dose intravenous corticosteroid. Her vision improved subsequently. There was limited knowledge on clinical phenotype and relapsing course in MOGAD, especially in the pediatric group. Knowing about variation in pediatric clinical presentation might guide ophthalmologists and pediatricians to reach an accurate diagnosis.
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