Pediatric myelin oligodendrocyte glycoprotein antibody associated disease—Asymmetric papilledema and elevated ICP are two of the chameleons: A case report

Abstract

Background: Myelin oligodendrocyte glycoprotein antibody (MOGA) associated diseases are inflammatory immune-mediated demyelinating disorders with relapse potential involving the central nervous system. Multiple unusual clinical manifestations of those disorders were reported, making treatment decisions difficult.Case presentation: A healthy 12-year-old obese boy presented with headache and bilateral asymmetric papilledema. The patient had a negative medical history. His neurological and general examinations were unremarkable, his initial magnetic resonance imaging showed elevated intracranial pressure (ICP) only. A lumbar puncture revealed increased opening pressure and pleocytosis. The MOGA titer was 1:320. He needed acetazolamide and steroid therapy. After 2 months of medication, weight loss, exercise, the patient symptoms significantly improved, papilledema resolved, and visual function improved.Conclusion: MOGA-associated disorders have a variety of clinical features, so a high index of suspicion is required for their diagnosis. Papilledema and an elevated ICP are 2 of the chameleons of MOGA-associated disorders. MOGA test may be useful in patients with elevated ICP and inflammatory cerebrospinal fluid profiles. An investigation of the possible association between those disorders and high ICP is warranted.Abbreviations: ADEM = acute disseminated encephalomyelitis, CNS = central nervous system, CSF = cerebrospinal fluid, ICP = intracranial pressure, IIH = idiopathic intracranial hypertension, MOG = myelin oligodendrocyte glycoprotein, MOGA = myelin oligodendrocyte glycoprotein antibody, MRI = magnetic resonance imaging.

Myelin-oligodendrocyte glycoprotein associated optic neuritis: a case report

“…Extensive research has demonstrated that individuals maintaining MOG-IgG seropositivity throughout followup are at a higher likelihood of experiencing recurrence; hence, emphasizing the importance of early diagnosis, meticulous follow-up, and precise prognostic assessments. 8 The MOG protein's form and glycosylation are crucial for anti-MOG antibody recognition. 2 In a retrospective analysis involving 135 individuals with acute optic neuritis (ON), Hickman et al identified nine cases where aberrant MRI enhancement occurred in the intracranial optic nerve just anterior to the optic chiasm.…”

“…Investigating potential associations between MOGA-related diseases and elevated ICP is imperative for comprehensive clinical assessment. 8 The current absence of randomized controlled studies for MOGAD necessitates reliance on empirical treatment recommendations, often drawn from prior research. Highdose steroids, in line with their common use in other acquired inflammatory demyelinating diseases, serve as the primary first-line treatment for MOGA-related disorders.…”

Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: A Case Report

“…Over time, the presence of myelin oligodendrocyte glycoprotein (MOG)-autoantibodies in serum has grown to include various unique presentations, ranging from optic neuritis to encephalomyelitis [1]. The most common clinical manifestation of MOGAD is MOGAD-associated encephalitis, with optic neuritis being the second [2]. Of note, optic neuritis in MOGAD differs from MS as it tends to be bilateral and leads to severe visual deficits if left untreated [2].…”

“…The most common clinical manifestation of MOGAD is MOGAD-associated encephalitis, with optic neuritis being the second [2]. Of note, optic neuritis in MOGAD differs from MS as it tends to be bilateral and leads to severe visual deficits if left untreated [2].…”