视神经炎
视神经
髓鞘少突胶质细胞糖蛋白
医学
髓鞘
眼科
神经纤维层
多发性硬化
病理
少突胶质细胞
髓鞘碱性蛋白
抗体
视神经脊髓炎
视网膜神经节细胞
视网膜
免疫学
实验性自身免疫性脑脊髓炎
作者
Stephanie L. Barnes,Yuyi You,Ting Shen,Todd A. Hardy,Clare L. Fraser,Stephen Reddel,Fabienne Brilot,Sudarshini Ramanathan,Alexander Klistorner,Con Yiannikas
标识
DOI:10.1177/20552173211063126
摘要
Optic neuritis (ON) occurs in immune-mediated disorders including multiple sclerosis (MS), aquaporin-4 antibody-positive (AQP4) neuromyelitis optica spectrum disorder (AQP4-NMOSD) and myelin oligodendrocyte glycoprotein (MOG) antibody-associated demyelination (MOGAD). Accurate determination of aetiology is critical for appropriate treatment and prognostication.To evaluate demyelination and axonal loss in MOG-ON to facilitate differentiation from MS-ON and AQP4-ON.15 MOGAD patients with previous ON (25 eyes) underwent multifocal visual evoked potential (mfVEP) recordings and optical coherence tomography scans. Comparison was made to previously reported MS patients (n = 67, 69 eyes) and AQP4-NMOSD patients (n = 15, 23 eyes) with prior ON and healthy controls (n = 37, 74 eyes).MOG-ON patients had less retinal nerve fibre layer (RNFL) loss than AQP4-ON patients (p < 0.05) and less mfVEP latency prolongation than MS-ON patients (p < 0.01). Number of ON episodes in MOGAD was associated with reduced RNFL thickness (global, p = 0.07; temporal, p < 0.001) and mfVEP amplitude (p < 0.001). There was no abnormality in non-ON eyes.Our study demonstrated a distinct pattern of damage in MOG-ON compared to AQP4-ON and MS-ON. ON in MOGAD produces less axonal loss than AQP4-NMOSD. Damage accumulates with relapses, supporting the role of maintenance immunosuppression to induce remission. Compared to MS, MOGAD causes less demyelination.
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