Sentinel seizure heralding Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease

• Published in: The Egyptian Journal of Neurology, Psychiatry and Neurosurgery Vol. 59; no. 1; pp. 31 - 4
• Main Authors: Das, Shambaditya, Pandit, Alak, Ray, Biman Kanti, Dubey, Souvik
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 09.03.2023; Springer Nature B.V; SpringerOpen
• Subjects: Antibodies; Case Report; Convulsions & seizures; Medical imaging; Medicine; Medicine & Public Health; MOG; Myelin oligodendrocyte glycoprotein antibody; Neuroimaging; Neurology; Neurosurgery; Presenting manifestation; Primary CNS demyelination; Psychiatry; Seizure; Presenting manifestation; Myelin oligodendrocyte glycoprotein antibody; Seizure; MOG; Primary CNS demyelination
• DOI: 10.1186/s41983-023-00632-8
• ISSN: 1110-1083

Background Isolated seizure as a manifestation of myelin oligodendrocyte antibody-associated disease (MOGAD) has rarely been reported previously. Case presentation A 16-year-old-male presented with single episode of left focal onset motor seizure with secondary generalization and impaired awareness, without any other focal neurological deficits. There was a history of right focal onset motor seizure with secondary generalized tonic–clonic seizure and impaired awareness 4 years ago. Neurological examination showed bilateral gaze evoked nystagmus. Brain imaging revealed bilateral superficial and deep white matter lesions including the corpus callosum. Anti-MOG antibody was positive. The patient received steroids and Rituximab therapy without any further recurrence of seizure or any neuro-deficits and gradual improvement in lesion burden in brain imaging. Conclusions This case of an adolescent boy with sole manifestation of episodes of focal seizures 4 years apart, finally diagnosed to be a case of MOGAD, not only boosts the evidence of establishing the possibility of MOG antibody-associated autoimmune epilepsy but also reinforces the importance of unexplained seizure as a clinical phenotype in MOGAD.