Abstract General Information

Title

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) with peripheral nervous system involvement: a case report

Case Report

Case presentation: GLF, male, 13 years old. The patient came for consultation in June 2020. At the age of three, he had a generalized tonic-clonic febrile seizure with post-ictal drowsiness. From then on, a difficulty in school learning was noticed. At the age of 7, he evolved with bilateral visual impairment with pain at eye mobilization. Two years later, he started with distal weakness and frequent falls. The patient presented with childish behavior for age. Mini-mental state exam: 22/30. He also presented flaccid tone and global hypotrophy associated with symmetrical tetraparesis predominantly crural. Deep tendon reflexes and cutaneous-plantar reflex were absent. Dysdiadochokinesia and dysmetria was evident. Distal hypopalesthesia was noticed. Visual acuity: 20/300 in the left eye and 20/200 in the right eye. Fundoscopy showed bilateral optic nerve atrophy. Considering the phenotype of presentation, it was measured the anti-MOG IgG, with a positive result, corroborating a diagnosis of Myelin oligodendrocyte glycoprotein antibody-associated disease with PNS involvement, manifested in our patient as polyradiculoneuropathy. Discussion: MOGAD is an immune-mediated demyelinating inflammatory disorder of the central nervous system predominantly affecting the optic nerves, brain, and spinal cord. Oligodendrocyte myelin glycoprotein is a protein on the surface of oligodendrocytes that has historically been considered as a potential antibody target in multiple sclerosis, until in 2007 it was described as a different disease phenotype. According to a database review (PUBMED), there are a few studies that corroborate the occurrence of peripheral impairment associated with MOGAD, present in 7% of MOGAD patients in an Australian cohort. There are some hypotheses to justify the concomitant central and peripheral demyelination processes. Final comments: The presence of central demyelination syndrome and PNS involvement may be associated with MOGAD and may respond to immunotherapy, and should not discourage the search for MOGAD in patients with an appropriate clinical setting.

Area

Clinical findings