A Rare Presentation of Myelin Oligodendrocyte Glycoprotein Antibody Disease With Peripheral Neuropathy in a Pediatric Patient

Keywords:
Myelin oligodendrocyte glycoprotein antibody disease (MOGAD); peripheral neuropathy; demyelination; pediatric neurology; autoimmune encephalomyelitis; central nervous system

Introduction:
Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD) is an idiopathic, demyelinating, inflammatory, and immune-mediated disease affecting the central nervous system (CNS). This disease causes damage to the brain, brainstem, optic nerve, and spinal cord [1].

Case Presentation:
The case we present is of a 7-year-old previously healthy girl who presented with acute flaccid paralysis following a viral prodrome. Her symptoms rapidly evolved, including cranial nerve involvement, bladder dysfunction, and bilateral progressive limb weakness. Imaging revealed patchy T2/FLAIR hyperintensities in the brainstem and spinal cord on brain and spine MRI. Serum myelin oligodendrocyte glycoprotein (MOG) antibodies were positive. Following the diagnosis, the patient was managed with high dose corticosteroids, intravenous immunoglobulins (IVIG), and physiotherapy. She recovered over the next few months, showing significant neurological improvement of the cranial nerve and limb weakness. However, during the recovery phase, she exhibited left upper limb-predominant weakness and distal weakness in the right lower limb. Neurological examination showed left ulnar clawing, right-sided foot drop, and sensory disturbances in the affected regions. The demonstrated left ulnar, bilateral peroneal, and tibial nerve involvement suggested multiple peripheral nerve involvement. Repeat imaging revealed resolution of the previous radiological findings. Repeat testing for serum MOG antibodies returned negative.

Discussion:
Myelin oligodendrocyte glycoprotein (MOG) is a protein found on the outer surface of the myelin sheath of nerves in the central nervous system. MOG is thought to play a role in myelin maturation and integrity. In MOGAD, the MOG protein is attacked by the immune system. MOGAD presenting symptoms include the following categories: optic neuritis, transverse myelitis, acute disseminated encephalomyelitis, and cerebral encephalitis [2]. MOGAD diagnostic criteria is by positive MOG-IgG antibodies in serological and cerebrospinal fluid tests in appropriate clinical settings [3]. This case is unique as the patient had a rare presentation of MOGAD with peripheral neuropathy. The limited number of reported cases with peripheral demyelination in MOGAD raises important questions about whether the disease may involve additional, unrecognized pathological mechanisms or represent a broader clinical spectrum than currently recognized.

Conclusion:
This case highlights the rare involvement of the peripheral nervous system in a purely central nervous system disorder like MOGAD. We postulate that this could be secondary to possible cross-reactivity between MOG antibodies and peripheral myelin components or a bystander immune activation affecting peripheral nerves. In these cases, combining IV Immunoglobulin with standard corticosteroid treatment may enhance clinical outcomes.

References:
[1] Zheng S. et al. (2024) Front. Immunol., 15, 1278867. [2] Li Y. et al. (2022) Front. Aging Neurosci., 14, 850743.
[3] Banwell B. et al. (2023) Lancet Neurol., 22(3), 268–282.

Biography:
We are year 6 undergraduate medical students aspiring to be future pediatricians. We are currently working on multiple pediatric related research projects and would love to present one of our unpublished projects as a poster. We are interested in studying the impact of early intervention, specifically in neurological illnesses in the pediatric population. We aim to improve and advance pediatric medicine through academic research, and we would love to spread the knowledge and collaborate with other pediatricians.

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