Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan; Department of Education and Support for Regional Medicine, Tohoku University Hospital, Sendai, Japan.
Department of Ophthalmology, Tohoku University Graduate School of Medicine, Sendai, Japan; Department of Aging Vision Healthcare, Graduate School of Biomedical Engineering, Tohoku University, Sendai, Japan.
J Neurol Sci. 2022 Jun 15;437:120269. doi: 10.1016/j.jns.2022.120269. Epub 2022 Apr 22.
Retinal atrophy in the chronic phase of optic neuritis (ON) in anti-aquaporin-4 antibody (AQP4-Ab)-positive neuromyelitis optica spectrum disorder (NMOSD) and anti-myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) remains unclear.
Patients with these diseases were repeatedly evaluated using optical coherence tomography (OCT) for the circumpapillary retinal nerve fiber layer (cpRNFL) and macular ganglion cell complex (mGCC) in the ON-involved eyes during relapse-free period after the first ON episode before relapse. Optic MRI with short tau inversion recovery (STIR) sequences was further evaluated retrospectively.
Twelve patients with MOGAD (20 eyes with ON-involvement) and 14 with AQP4-Ab-positive NMOSD (16 eyes with ON-involvement) were enrolled. The progression of retinal atrophy ≥12 months after onset was observed in AQP4-Ab-positive NMOSD, but was not apparent in MOGAD. A decrease in retinal thickness by the same amount results in more severe visual impairment in AQP4-Ab-positive NMOSD. On optic MRI, the residual STIR hyperintensity in the optic nerves remained in the chronic phase in almost all eyes with ON in both diseases. Optic nerve atrophy occurred in all evaluated ON-involved eyes in AQP4-Ab-positive NMOSD, while it was observed in half of ON-involved eyes in MOGAD.
Progression of retinal atrophy in the chronic phase has been observed in patients with AQP4-Ab-positive NMOSD, while it remains uncertain in patients with MOGAD. The visual impairments upon similar levels of retinal atrophy would be worse in AQP4-Ab-positive NMOSD, possibly attributable in part to a higher incidence of optic nerve atrophy in this disease.
在水通道蛋白 4 抗体（AQP4-Ab）阳性视神经脊髓炎谱系疾病（NMOSD）和抗髓鞘少突胶质细胞糖蛋白抗体相关疾病（MOGAD）的慢性期视神经炎（ON）中，视网膜萎缩仍然不清楚。
在首次 ON 发作后无复发期间，对这些疾病的患者进行了多次评估，使用光学相干断层扫描（OCT）对 ON 受累眼的环周视网膜神经纤维层（cpRNFL）和黄斑神经节细胞复合体（mGCC）进行评估。此外，还回顾性地对短 tau 反转恢复（STIR）序列的视神经 MRI 进行了评估。
共纳入 12 例 MOGAD（20 只 ON 受累眼）和 14 例 AQP4-Ab 阳性 NMOSD（16 只 ON 受累眼）患者。AQP4-Ab 阳性 NMOSD 中观察到发病后≥12 个月视网膜萎缩进展，但 MOGAD 中未见明显进展。视网膜厚度减少相同量会导致 AQP4-Ab 阳性 NMOSD 患者的视力损害更严重。在视神经 MRI 上，两种疾病的大多数 ON 受累眼在慢性期仍存在视神经残留 STIR 高信号。AQP4-Ab 阳性 NMOSD 中所有评估的 ON 受累眼均发生视神经萎缩，而 MOGAD 中仅一半的 ON 受累眼发生视神经萎缩。
AQP4-Ab 阳性 NMOSD 患者在慢性期观察到视网膜萎缩进展，而 MOGAD 患者的情况尚不确定。在相似水平的视网膜萎缩时，AQP4-Ab 阳性 NMOSD 患者的视力损害会更严重，这可能部分归因于该疾病中视神经萎缩的发生率更高。
