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Abstract
Background: Myelin Oligodendrocyte Glycoprotein Antibody Associated Disease (MOGAD) is a relatively new and rare autoimmune disease that causes demyelination of the central nervous system. The pathogenicity of this disease is characterized by an immune reaction against myelin oligodendrocyte glycoprotein: a component of the myelin sheath that is also expressed on the surface of oligodendrocytes. The purpose of this glycoprotein is thought to be for construction and maintenance of myelin and cell to cell communication. The destruction of oligodendrocytes and myelin in the central nervous system affects the brain, spinal cord, and optic nerves, and can cause symptoms such as acute disseminated encephalomyelitis, transverse myelitis, and optic neuritis/vision loss. Multiple Sclerosis (MS) and Neuromyelitis Optica Spectrum Disorder associated with Anti-Aquaporin-4 (AQP4-NMOSD) can have similar presentations which can make a diagnosis of MOGAD difficult without a foundational education of the clinical and diagnostic differences between them. For example, MOGAD differs from AQP4-NMOSD in that it is characterized by inflammatory demyelination versus AQP4-NMOSD which is characterized by astrocytopathy. MOGAD also differs from MS in that MOGAD lesions are perivascular and consist of MOG-laden macrophages and CD4+ infiltration, whereas lesions in MS are also perivascular, but they consist of complement proteins, immunoglobulins, and CD8+ infiltration.
Case Report: We present a 38-year-old female who was hospitalized for acute onset bilateral ophthalmalgia. She described the pain as constant and pressure-like, 8/10, and worse with lateral gaze bilaterally. The ophthalmalgia was associated with unilateral headache ipsilateral to the side with the more severe ophthalmalgia and accompanied by photophobia. Two weeks later, the patient experienced an episode of blurry vision on the left side. The patient's vision continued to deteriorate significantly and her headache became more severe which prompted her to go to the ED. The patient’s vision changes included darkening of the visual field and increased blurriness.
Over the course of the patient’s hospital stay a series of studies were done. A CT of head and brain was unremarkable. An MRI brain wo/w contrast and an MRI face neck orbit wo/w contrast showed questionable minimally increased enhancement of the left optic nerve and the interpretation could not exclude optic neuritis. The patient then had a lumbar puncture analysis that had no significant findings. The patient was discharged after she regained some vision with a diagnosis of optic neuritis.
Two weeks later, the patient’s serum came positive for anti-MOG and the patient was diagnosed with MOGAD. She returned to the hospital for treatment with high-dose steroids.
Conclusion: This case illustrates a presentation of a rare autoimmune disease and how it can be mistaken for an isolated episode of optic neuritis or other diagnoses that have overlapping phenotypical symptoms such as MS or AQP4-NMOSD.
Presentation Type
Poster
Recommended Citation
Stein, Kirhyn A.; Garcia, Laura; Memon, Sobia; Guanajuato, Hernan; and Mora, Johanna, "A Presentation of Myelin Oligodendrocyte Glycoprotein Antibody Associated Disease (MOGAD) as Optic Neuritis" (2024). Research Colloquium. 4.
https://scholarworks.utrgv.edu/colloquium/2024/posters/4
A Presentation of Myelin Oligodendrocyte Glycoprotein Antibody Associated Disease (MOGAD) as Optic Neuritis
Background: Myelin Oligodendrocyte Glycoprotein Antibody Associated Disease (MOGAD) is a relatively new and rare autoimmune disease that causes demyelination of the central nervous system. The pathogenicity of this disease is characterized by an immune reaction against myelin oligodendrocyte glycoprotein: a component of the myelin sheath that is also expressed on the surface of oligodendrocytes. The purpose of this glycoprotein is thought to be for construction and maintenance of myelin and cell to cell communication. The destruction of oligodendrocytes and myelin in the central nervous system affects the brain, spinal cord, and optic nerves, and can cause symptoms such as acute disseminated encephalomyelitis, transverse myelitis, and optic neuritis/vision loss. Multiple Sclerosis (MS) and Neuromyelitis Optica Spectrum Disorder associated with Anti-Aquaporin-4 (AQP4-NMOSD) can have similar presentations which can make a diagnosis of MOGAD difficult without a foundational education of the clinical and diagnostic differences between them. For example, MOGAD differs from AQP4-NMOSD in that it is characterized by inflammatory demyelination versus AQP4-NMOSD which is characterized by astrocytopathy. MOGAD also differs from MS in that MOGAD lesions are perivascular and consist of MOG-laden macrophages and CD4+ infiltration, whereas lesions in MS are also perivascular, but they consist of complement proteins, immunoglobulins, and CD8+ infiltration.
Case Report: We present a 38-year-old female who was hospitalized for acute onset bilateral ophthalmalgia. She described the pain as constant and pressure-like, 8/10, and worse with lateral gaze bilaterally. The ophthalmalgia was associated with unilateral headache ipsilateral to the side with the more severe ophthalmalgia and accompanied by photophobia. Two weeks later, the patient experienced an episode of blurry vision on the left side. The patient's vision continued to deteriorate significantly and her headache became more severe which prompted her to go to the ED. The patient’s vision changes included darkening of the visual field and increased blurriness.
Over the course of the patient’s hospital stay a series of studies were done. A CT of head and brain was unremarkable. An MRI brain wo/w contrast and an MRI face neck orbit wo/w contrast showed questionable minimally increased enhancement of the left optic nerve and the interpretation could not exclude optic neuritis. The patient then had a lumbar puncture analysis that had no significant findings. The patient was discharged after she regained some vision with a diagnosis of optic neuritis.
Two weeks later, the patient’s serum came positive for anti-MOG and the patient was diagnosed with MOGAD. She returned to the hospital for treatment with high-dose steroids.
Conclusion: This case illustrates a presentation of a rare autoimmune disease and how it can be mistaken for an isolated episode of optic neuritis or other diagnoses that have overlapping phenotypical symptoms such as MS or AQP4-NMOSD.