Radiological differentiation of optic neuritis with myelin oligodendrocyte glycoprotein antibodies, aquaporin-4 antibodies, and multiple sclerosis

Ramanathan, Sudarshini; Prelog, Kristina; Barnes, Elizabeth H; Tantsis, Esther; Reddel, Stephen W.; Henderson, Andrew; Vucic, Steve; Gorman, Mark; Benson, Leslie; Alper, Gülay; Riney, Catherine J.; Barnett, Michael; Parratt, John; Hardy, Todd A.; Leventer, Richard J.; Merheb, Vera; Nosadini, Margherita; Fung, Victor S.C.; Brilot, Fabienne; Dale, Russell C.

doi:10.1177/1352458515593406

Cited by 317 publications

(319 citation statements)

References 32 publications

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“…Furthermore, 4.9% of children with MOG-ON had an optic chiasm lesion, indicating the MRI manifestation of MOG-ON can be longitudinally extensive. No differences were found in the MRI features of the AQP4-ON and MOG-ON groups, which is in contrast to the study by Ramanathan et al ,33 where MRI lesions in patients with MOG-ON tended to involve the anterior optic nerve segment and AQP4-ON lesions were in the posterior optic nerve segment.…”

Section: Discussioncontrasting

confidence: 99%

Clinical characteristics and prognosis of myelin oligodendrocyte glycoprotein antibody-seropositive paediatric optic neuritis in China

et al. 2018

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Section: Discussioncontrasting

confidence: 99%

Clinical characteristics and prognosis of myelin oligodendrocyte glycoprotein antibody-seropositive paediatric optic neuritis in China

et al. 2018

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“…This finding was consistent with previous reports that compared between MOG-ON (32.29±17.1 years old) and AQP4-ON (44.86±14.8 years old),8 MOG-ON (31 years old) and AQP4-ON (38 years old),10 MOG-ON (20±14 years old) and AQP4-ON (23±14 years old) 26. More than half (65%) of our patients with MOG-ON had a juvenile (<18 years) disease onset, which was more than those reported by previous study showing about 12.5%,9 50%10 or 16.7%13 of MOG-Ab-positive patients with demyelinating diseases began during juvenile period.…”

Section: Discussionsupporting

confidence: 93%

“…Bilateral ON and optic disc swelling were commonly observed in our Chinese MOG-ON cohort, which was corresponding with those patients with MOG-ON in various ethnic groups 26. However, previous reports indicated that most of the MOG-Ab-positive patients presented as monophasic disease or had less relapsing rate,8 9 which was different from the current study demonstrating both patients with MOG-ON and AQP4-ON had high recurrent episodes.…”

Section: Discussioncontrasting

confidence: 82%

Clinical features of demyelinating optic neuritis with seropositive myelin oligodendrocyte glycoprotein antibody in Chinese patients

et al. 2018

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“…1,2 There have only been 2 cases reported of large hemispheric or tumefactive lesions. 1,4 Our patient had a less common presentation with symptomatic large hemispheric tumefactive lesions, concurrent with the third episode of LETM, which is a core clinical characteristic for NMOSD. 3 Histopathology of active lesions from AQP4-seropositive patients with NMO showed inflammatory infiltrate with reduction or loss of GFAP-positive astrocytes, or astrocyte cytologic abnormalities.…”

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confidence: 89%

Inflammatory demyelination without astrocyte loss in MOG antibody–positive NMOSD

et al. 2016

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We report a patient with neuromyelitis optica spectrum disorder (NMOSD) with antibodies against myelin oligodendrocyte protein (MOG) and seronegative for aquaporin-4 (AQP4) presenting with relapsingremitting longitudinally extensive transverse myelitis (LETM) and cerebral tumefactive demyelinating lesions. Neuropathology showed active inflammatory demyelination with relative preservation of astrocytes.Case report. A 67-year-old woman with a history of hypothyroidism presented with 2 distinct symptomatic episodes of LETM. At initial presentation she had a T10 dissociated sensory level, sensory ataxia, and sphincter dysfunction, from which she recovered spontaneously. One month later, she presented with burning upper limb and thoracic pain, right lower limb weakness, and sphincter dysfunction. Initial spinal MRI showed a continuous T2-hyperintense central cord lesion from T2 to T9 with mild cord expansion and patchy enhancement; MRI 1 month later showed a new central cord T2 hyperintensity from C5 to T3 (figure, A and B). CSF examination was bland, with matched CSF/serum oligoclonal bands. AQP4 antibodies were negative. She made an almost complete recovery after 3 days of IV methylprednisolone, then oral prednisone 50 mg daily tapered over 5 weeks.Five months later, the patient presented to our institution with dysarthria and left facial weakness, rapidly progressing within 24 hours to left hemiparesis, lower limb flaccid paraparesis with extensor plantar responses, and a dissociated T10 sensory level. Brain MRI revealed 3 ill-defined white matter lesions in the right cerebral hemisphere (frontal corona radiata, posterior parietal lobe, and temporal pole), sparing the cortex, associated with extensive vasogenic edema, patchy enhancement, and peripheral concentric diffusion restriction. A few small lesions in the left hemispheric white matter and the right pons were also noted. Spinal MRI showed new T2 hyperintensity from T12 to the conus (figure, C-E). Visual evoked potentials were normal. Extensive blood investigations were normal or negative, including HIV and syphilis serology, serum angiotensin converting enzyme level, and vasculitic markers. Repeat testing for AQP4 antibodies was negative.Due to concerns of a neoplastic process, biopsy of the right frontal lesion was undertaken.Histology showed a sharply demarcated lesion, with macrophage-rich active inflammatory demyelination, with prominent loss of myelin, but relative preservation of axons (figure, Q-S). Immunostaining with glial fibrillary acid protein (GFAP) confirmed reactive astrocytes within and surrounding the lesion (figure J, O, and T). In the demyelinated white matter, there were dense perivascular cuffs of small T lymphocytes and fewer B lymphocytes. Immunostaining for SV40 (surrogate marker for JC virus infection) was negative.A cell-based assay using C-terminal-truncated human MOG later identified antibodies against full/ short-length MOG, including the more specific immunoglobulin G1 (IgG1) assay.1 After treatment with IV methylprednisolone, p...

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Radiological differentiation of optic neuritis with myelin oligodendrocyte glycoprotein antibodies, aquaporin-4 antibodies, and multiple sclerosis

Abstract: MOG-ON and AQP4-ON are more commonly bilateral and longitudinally extensive. MOG-ON tends to involve the anterior optic pathway, whereas AQP4-ON the posterior optic pathway.

Cited by 317 publications

References 32 publications

Clinical characteristics and prognosis of myelin oligodendrocyte glycoprotein antibody-seropositive paediatric optic neuritis in China

Clinical characteristics and prognosis of myelin oligodendrocyte glycoprotein antibody-seropositive paediatric optic neuritis in China

Clinical features of demyelinating optic neuritis with seropositive myelin oligodendrocyte glycoprotein antibody in Chinese patients

Inflammatory demyelination without astrocyte loss in MOG antibody–positive NMOSD

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