While the majority of patients will present with positive antibody titers, the antibody titer may fluctuate resulting in testing becoming negative then turning positive again. Most studies have found that among patients with ON, the MOG antibody is detected in approximately 15% of patients, which is more frequent than that of AQP4 antibody, which is seen in 2% of cases. In contrast, multiple sclerosis ON and AQP4-IgG positive ON are generally seen in females in their second decade and fourth decade, respectively. MOG-IgG positive optic neuritis is generally seen in children or young adults, classically peaking around the third decade with an equal preponderance between females and males. Thus, despite the clinical overlap between these three entities, it is crucial to appreciate that they are separate diseases with differing pathophysiology, clinical course, and most importantly, different treatments. Most importantly, recent advances have categorized MOG-IgG associated disorders (MOGADs) as distict from both multiple sclerosis and aquaporin-4 (AQP4)-IgG-positive associated disorders. However, recent studies have found optic neuritis (ON) to be its predominant phenotype in both the pediatric and adult populations. Myelin oligodendrocyte glycoprotein (MOG)-IgG was initially thought of as a marker of multiple sclerosis and acute disseminated encephalomyelitis (ADEM) in children. Marked elevation and distortion of the optic nerve head leading to artifactual thickening of the retinal nerve fiber layer and ganglion cell layer OU.īiomarkers have changed the paradigm for characterizing and correctly diagnosing CNS inflammatory and demyelinating diseases.Optical Coherence Tomography (Figure 4).Left eye (left image) demonstrates complete loss of the I2e isopter, marked constriction of the I3e with small island remaining nasally, and a dense cecocentral scotoma with complete loss of the V4e.Right eye (right image) demonstrates complete loss of the I1e isopter, marked constriction of the I2e with only a small island remaining nasally, and a dense cecocentral scotoma with complete loss of the V4e.Myelin Oligodendrocyte Glycoprotein (MOG) Ab: positive 1:1000.Neuromyeltis optica (NMO) /Aquaporin-4-IgG Ab: negative.Meningitis/encephalitis panel: negative for bacterial and viral agents.Pink, hazy, no xanthochromia, total protein: 22, glucose: 73, RBC: 1000, total nucleated cells: 8 (0 neutrophils, 7 lymphocytes), opening pressure 26cm Lumbar puncture w/ cytology and opening pressure:. Bartonella henselae IgG/IgM titer: negative.Anti-neutrophil cytoplasmic antibody: negative.Anti-double stranded DNA quantitative: 6 (ref 0-4 IU/mL).Anti-double stranded DNA qualitative: indeterminant.MRI cervical, thoracic, lumbar spine: normal.(Figure 2) MRI brain and orbits w/ and w/o contrast: enhancement and enlargement of intraorbital segments of optic nerves, left > right.Intracranial mass with obstructive hydrocephalus and compression of anterior visual pathway.Cup-to-disc: no cup noted in either optic nerve.OS: Grade II disc edema, no pallor, no hemorrhages, no exudates.OD: Grade I disc edema, no pallor, no hemorrhages, no exudates.Iris: Normal architecture, pharmacologically dilated OU.
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