# Paediatric Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): A Case Report With Varied Clinical Manifestations

**Authors:** Nur Ain Mohamad, Safinaz Mohd Khialdin, Nur Shahirah Amir Hamzah

PMC · DOI: 10.7759/cureus.85173 · Cureus · 2025-06-01

## TL;DR

This case report describes a young girl with MOGAD, highlighting varied pediatric symptoms and the importance of early diagnosis.

## Contribution

The paper presents a rare pediatric case of MOGAD with acute visual symptoms and atypical features.

## Key findings

- A three-year-old girl presented with bilateral optic neuritis and upper motor neuron signs.
- MRI showed bilateral optic neuritis with no spinal involvement, and anti-MOG antibodies were positive.
- Treatment with corticosteroids led to improved vision, emphasizing the need for early diagnosis in children.

## 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.

## Linked entities

- **Diseases:** acute disseminated encephalomyelitis (MONDO:0019383), optic neuritis (MONDO:0005885), transverse myelitis (MONDO:0021553)

## Full-text entities

- **Genes:** MOG (myelin oligodendrocyte glycoprotein) [NCBI Gene 4340] {aka BTN6, BTNL11, MOGIG2, NRCLP7}
- **Diseases:** reduced vision (MESH:D015354), afferent pupillary defect (MESH:D011681), optic neuritis (MESH:D009902), transverse myelitis (MESH:D009188), MOGAD (MESH:D003711), optic disc swelling (MESH:D010211), acute disseminated encephalomyelitis (MESH:D004673), autoimmune demyelinating condition (MESH:D020278)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12210090/full.md

## References

20 references — full list in the complete paper: https://tomesphere.com/paper/PMC12210090/full.md

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Source: https://tomesphere.com/paper/PMC12210090