![]() ![]() Routine blood parameters, including complete hemogram, liver function test, renal function test, and serum blood glucose level, were normal. VA: visual acuity, CSF: cerebrospinal fluid, VEP: visual evoked potential, SSEP: somato sensory evoked potential, BAER: brain stem auditory response, MOG: myelin oligodendrocyte glycoprotein, NMO: neuromyelitis optica, CSCT: central sensory conduction time LFT: liver function tests Walking without support, hand incoordination improved, able to maintain daily life activities with minimal help, diplopia improved.ģ months: Walk with walker aid, urine incontinentģ months: Improved, mild spasticity of limbs Vision improved in both eye-finger counting from 3 meters distance bilaterallyīoth lower limbs having antigravity movement IV methylprednisolone 1 gm daily for five days followed by oral prednisolone 30 mg daily IV methylprednisolone 1 gm daily for five days followed by oral prednisolone 40 mg/day IV methylprednisolone 1 gm daily for five days followed by oral prednisolone 40 mg daily Multiple T2 & FLAIR hyperintense and contrast enhancing lesion in pons, medulla, cerebellum and left frontal white matter region. Cauda equina nerve roots are thickened and enhancement on post contrast. Swelling of cord at conus, T2 hyperintense signal in most of cross section of cord up to 3 cm, patchy enhancement on post contrast. Bilateral 6th cranial nerve palsy, left LMN facial palsy, hand incoordination +, gait: ataxic Sensation loss below umbilical level, bladder catheterized and stool incontinenceīilateral optic disc margin: blurred. VA: Right eye: finger counting from 1 meterīilateral lower limb motor power (MRC) 1/5 with weakness of lower truncal muscles. Neurological examination (abnormal findings) IV Methyl prednisolone 500 mg x five days Treatment received before admission to our Institute Undergone caesarian section at term for fetal distress under spinal anesthesia, postoperative day one noticed paraplegiaįever for six days one week prior to neurological deficitĪcute, right followed by left. Gait ataxia, slurred speech, horizontal diplopia (bilateral) We present three cases of MOG-IgG positive patients with bilateral optic neuritis, conus cauda syndrome, and pontine demyelination mimicking Chronic Lymphocytic Inflammation with Pontine Perivascular Enhancement Responsive to Steroids (CLIPPERS).īilateral lower limb weakness, bladder and bowel involvement 4 Involvement of conus and caudal nerve roots are rare involvement in MOG antibody associated diseases. 2, 3 MOG involves rhombencephalon especially pontine white matter tract, while NMOSD has predilection around the periventricular Aquaporin channels. NMOSD and MOG associated diseases share common involvement pattern of optic nerve and cervico-dorsal myelitis. 1, 2 Recurrence of illness, specific antibody positivity, and response to immunotherapy favors diagnosis. Clinical differentiations from multiple sclerosis, neuromyelitis spectrum disorder (NMOSD) with or without Aquaporin antibody (AQP4-Ab), are very narrow. All rights reserved.Myelin oligodendrocyte glycoprotein antibodies (MOG-IgG) associated diseases are a spectrum of central nervous system demyelinating disorders. In this review, we examine the history of the MOG antibody and its relevance to demyelinating disease, as well as compare the clinical, radiographic and serological profiles of patients with MOG antibody with patients with AQP4 antibody.Ĭopyright © 2018 Elsevier B.V. MOG antibody disease has thus recently emerged as a distinct entity carved out of the patient population diagnosed with NMOSD. In recent studies around the world where MOG testing is available, up to 42% of NMOSD patients who test seronegative for the AQP4 antibody test positive for MOG antibodies. In addition, acute disseminated encephalomyelitis (ADEM) is a well-recognized phenotype of MOG antibody disease in children. Clinically, the disease resembles neuromyelitis optica spectrum disorders in the predilection for relapses of optic neuritis and transverse myelitis. MOG is a glycoprotein expressed on the outer membrane of myelin and solely found within the central nervous system, including in the brain, optic nerves and spinal cord. MOG antibody disease is an autoimmune disease of the central nervous system associated with a serological antibody against MOG, myelin oligodendrocyte glycoprotein. ![]()
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