Atypical Brianne Herlitzke, OD

INTRODUCTION • Clinical: • Myelin oligodendrocyte glycoprotein (MOG) is expressed in the central nervous Table 1: Summary of clinical exam ndings E xam Finding Right eye Left eye system (CNS) on the surface of the myelin sheath and the plasma membrane of Acuity cc HM w/eccentric viewing 20/80 oligodendrocytes. Pinhole acuity cc No pinhole improvement 20/60 Pupils Trace APD • MOG has been found to have a crucial role in oligodendrocyte maturation and Cornea Normal Normal recent research has found antibodies can be formed against these glycoproteins. Disc 3+ Optic disc edema 2+ Optic disc edem a • Although the frequency and relevance of these antibodies remains controversial, C/D ratio 0.0 0.35 presence of MOG antibodies in a patient does not indicate (MS), • Fundus Photography: the most commonly known form of demyelinating disease, is present. Rather, the MOG antibody is associated with acute disseminated encephalomyelitis, neuromyelitis optica, and longitudinally extensive transverse myelitis. • and retinal neuro-axonal damage has been found in MOG antibody associated demyelinating disease. • of optic neuritis include aerent pupillary defect (APD), decreased color vision, and/or visual eld defects. • Initial attack is treated aggressively with steroids. A rapid drop in the MOG-antibody is typically seen with steroid treatment. If the MOG antibody

persists or a relapse occurs, immune suppression may be utilized to prevent Lorem ipsum disease progression. 1a 1b

• Prognosis for visual outcome has been seen to be more favorable with Figure 1a: Posterior pole Zeiss photos right eye image on the left. Figure 1b: left eye image on the right MOG-associated disease when compared to other atypical demyelinating diseases. DISCUSSSION

• Eye care providers should consider MOG-IgG testing on patients with sudden vision CASE REPORT loss, signicant disk edema, or recurrent optic neuritis. • A 52-year-old female presented for central vision loss in the right eye followed by • Testing for the MOG-IgG antibody is important because it has been found that some vision loss in the left eye two days later. Mild with eye movements. No other MS can worsen rarer forms of demyelinating conditions. signicant medical or ocular history. • Early diagnosis and timely treatment is paramount to prevent sight threatening • Visual acuity was “hand motion” in the right eye and 20/80 in the left. There was a complications. trace right aerent pupillary defect. REFEERENCES • RNFL OCT illustrated optic head edema in each eye. Diuse vision loss in 1. Reindl, Markus, Franziska Di Pauli, et.al. “The Spectrum of MOG Autoantibody-Associated Demyelinating Diseases.” Nature each eye was seen with 24-2 HVF. MRI showed enhancements of the Reviews , vol. 9, no. 8, 2013, pp. 455–461., doi:10.1038/nrneurol.2013.118. 2. “Neurology and Neurosurgery.” Mayo Clinic, Mayo Foundation for Medical Education and Research, and sheath. results were normal opening pressure and www.mayoclinic.org/medical-professionals/neurology-neurosurgery/news/novel-mog-assay-aids-diagnosis-of-demyelinati composition. ng-diseases/mac-20430597. 3. Pache, Florence, and Hanna Zimmermann. “MOG-IgG in NMO and Related Disorders: a Multicenter Study of 50 Patients. • Laboratory testing was negative for aquaporin-4-IgG (AQP4) antibody and positive Part 4: Aerent Visual System Damage after Optic Neuritis in MOG-IgG-Seropositive versus AQP4-IgG-Seropositive for MOG antibody. Patients.” Journal of Neuroinammation, vol. 13, no. 1, 2016, doi:10.1186/s12974-016-0720-6. 4. Ehlers, Justis P., Chirag P. Shah, et.al. The Wills Eye Manual: Oce and Emergency Room Diagnosis and Treatment of Eye Disease. Publishers: Wolters Kluwer, 2010.