![]() ![]() 6 Some patients complain of a headache around the eye or at the front of the head a few days before vision is affected. It is recurrent or bilateral/simultaneous in approximately 50% of all cases. Optic neuritis is the most common MOGAD presentation among adult patients. 1 2 5 Vision loss is usually temporary in some cases, it can be permanent and takes hours or days to happen and weeks to improve. Some people also report seeing flickering, flashing, or sparkles when moving their eyes. Vision loss from optic neuritis can present as loss of central or peripheral vision, colour, or visual acuity. Other symptoms include vision loss which can be either temporary or permanent depending on the nerve damage. 1 5 A common symptom of ON is eye pain, which can worsen when the eye moves. Optic neuritis (ON) is when the eye's optical nerve(s) becomes inflamed due to damage to the myelin surrounding the nerves in one or both eyes simultaneously. The most common presentation is Optic Neuritis (ON), followed by Transverse Myelitis (TM) and then Acute Disseminated Encephalomyelitis (ADEM). However, it is clear that anti-MOG-mediated disease has a diverging presentation consistent with lower rates of relapse, greater optic nerve involvement, a loss of female predominance, and better overall outcomes when compared to anti-AQP4 NMOSD.Symptoms of MOG Antibody disease can present differently from person to person. The serum anti-MOG antibody test has a reported specificity of 98.5% for anti-MOG associated disease (5).The exact distinction between anti-AQP4 and anti-MOG NMOSD is still being explored in the current literature. Limited studies suggest anti-MOG NMOSD may have a greater response to steroids than AQP4 NMOSD, thus prolonged steroid tapers are preferred (3,6) Further research into long-term therapy for relapse prevention with immunosuppression is needed to determine the best treatment course for anti-MOG NMOSD (8).Ĭonclusions: Clinicians should be suspicious of an autoimmune etiology after ruling out infectious causes in patients presenting with optic neuritis, progressive weakness, urinary retention, and imaging findings of extensive inflammation (3,4). The literature lacks evidence on the most effective treatments and relapse prevention for the disorder, particularly in pediatric patients due to the rarity of the disease (3).Patients with optic neuritis due to anti-MOG antibodies may have a more favorable outcome for vision than those who are anti-AQP4 seropositive (3,7). We present an interesting pediatric case of MOG antibody disease.Anti-MOG driven NMOSD has an emerging distinct clinical picture notable for greater optic nerve involvement, lower relapse rates, longitudinal lesions, and a greater occurrence in males when compared to classic NMOSD (2,3). Recent research has found antibodies against myelin oligodendrocyte glycoprotein (anti-MOG) which has a distinct clinical pattern in patients who are anti-AQP4 seronegative (2,3). The presumed pathogenesis of NMOSD is mostly due to autoantibodies against the aquaporin-4 channel (anti-AQP4 antibodies). He was discharged on a prolonged steroid taper and close follow up with neurology.ĭiscussion: Neuromyelitis Optica Spectrum Disorder (NMOSD) is an autoimmune demyelinating disease of the central nervous system (CNS) presenting with optic neuritis and transverse myelitis (1). He experienced return of strength in his lower extremities, improvement in assisted walking, and improvement of vision with treatment. He was treated with a consecutive course of high-dose IV methylprednisolone and plasmapheresis. Serum and CSF antibody testing showed no anti-AQP4 antibodies, but it was positive for the anti-MOG antibody in serum. Comprehensive infectious workup for HSV, enterovirus, Lyme, West Nile, syphilis, HIV, HTLV-1, and EBV was negative. Cerebrospinal fluid (CSF) analysis showed nucleated cells at 250, protein at 48, lymphocytes at 98, and glucose at 62. An MRI of the orbit, brain, and spine showed left optic neuritis and transverse myelitis extending from T9 to the conus medullaris. Case Presentation: A 17-year-old healthy male teenager presented with 2 weeks of bilateral lower extremity weakness with paresthesia, urinary retention, blindness of the left eye, left relative afferent pupillary defect, and retained deep tendon reflexes. ![]()
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