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. Myelin oligodendrocyte glycoprotein antibodies (MOG-IgG) associated diseases are a spectrum of central nervous system demyelinating disorders.

Anti mog antibody syndrome