12/26/2023 0 Comments Optic neuritis anti mog![]() 8 Now a days fingolimod is considered as another option in treating patients of optic neuritis and OPN.In a study of 11 million people in the UK, optic neuritis (all causes) was found to have an incidence of 3.7 per 100 000 person-years. 8 The most common side effects of fingolimod are headache, diarrhea, nausea, abdominal pain and fatigue. Fingolimod (sphingosine-1-phosphate receptor modulator) is an immunomodular drug, mostly used to reduce rate of relapses in multiple sclerosis (MS). Recently, immunomodulator therapy like IV immunoglobulin, IFN β1 has come up with better outcome in chronic and recurrent cases. Steroid pulse systemic therapy followed by oral steroid is the mainstay in OPN, though recurrence is common. In recent MRI technique of fat suppression in with Gadolinium-DTPA contrast enhancement provide the best images of the optic nerve sheath, as well as the optic nerve. MRI is preferred diagnostic modality for OPN showing perineural enhancement called “tram-track” sign on axial view and “doughnut” sign on coronal view. 6 In our case we also propose MOG antibody as possible causative factor in OPN. recently reported a male patient with anti-MOG antibody positive OPN, who had peripheral visual impairment. It has been proposed that MOG causes inflammation of optic nerve and this extend to nerve sheath also which show as optic nerve sheath enhancement in MRI. So role of MOG antibody in OPN is controversial. Though optic nerve sheath is equivalent to meninges, it does not express MOG. 4 Oligodendrocyte cells of meninges express MOG. MOG is autoantibody acting against myelin oligodendrocyte glycoprotein and is well grooved biomarker of autoimmune inflammatory optic nerve pathologies. 1 Purvin et al reported 2 patients with abduction deficits out of 14 diagnosed OPN cases similar case were reported by Joo young et al. It may have idiopathic or an underlying systemic inflammatory causes. 1 Its presentation mimics optic neuritis. OPN is defined as a form of idiopathic orbital inflammatory disease, which target specific tissue in the optic nerve sheath. Chances of recurrence were clearly explained to the patient. Two months after the therapy, patient’s vision improved to 6/9 in both eyes with resolving disc edema and lateral rectus function. The neurologist diagnosed him as a case of MOG positive bilateral optic perineuritis and advised pulse dose Methylprednisolone therapy followed by oral steroid and Tablet Fingolimod. On redoing the MRI, the radiologist suspected the subtle perineural enhancement ( Figure 3) secondary to be optic perineuritis and hence was referred to a neurologist. The patient was advised an atypical optic neuritis panel of investigation, where he turned out to be MOG antibody positive. ![]() Three months after the first episode, patient reported again when he developed both eyes mild blurring of vision with drop in vision to 6/60 along with right eye lateral rectus palsy. ( Figure 2) An MRI was advised which was reported to have mild perineural enhancement, unfortunately the patient was lost to follow up after that. He responded well to therapy and improved to 6/12 and 6/9 in right and left eyes respectively with resolution of disc edema. On basis of these findings, he was suspected to have bilateral optic neuritis and was treated with pulse dose Methylprednisolone followed by oral steroids. ![]() On fundus examination both eyes showed significant disc edema (right eye more than left eye)( Figure 1). The best corrected visual acuity of right eye was perception of light and left eye was 1/60 and the intraocular pressures were 12 and 14mmhg respectively. A 25 year old male, chronic smoker presented with sudden diminution of vision and painful ocular movements in both eyes since 3 days. ![]()
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