Kong Lingyao, Tan Xiaofeng, Wang Hang, Cao Le, Shi Ziyan, Zhang Nana, Kwapong William Robert, Wang Rui, Sun Dongren, Zhang Yangyang, Zhang Ying, Mou Zichao, Wang Xiaofei, Wu Bo, Zhou Hongyu
Department of Neurology, West China Hospital, Sichuan University, Guo Xuexiang 37, Chengdu, 610041, China.
State Key Laboratory of Oral Diseases and National Center for Stomatology and National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
J Neurol. 2025 Sep 2;272(9):606. doi: 10.1007/s00415-025-13350-3.
Emerging evidence suggests that subclinical visual pathway impairment might occur in neuromyelitis optica spectrum disorder (NMOSD) independently of optic neuritis (ON). This prospective longitudinal cohort study aims to characterize dynamic retinal neurodegeneration and microvascular alterations in NMOSD.
The quantitative parameters from swept-source optical coherence tomography (SS-OCT) and SS-OCT angiography (SS-OCTA) included the macular retinal nerve fiber layer (RNFL) thickness, ganglion cell-inner plexiform layer (GCIPL) thickness, superficial vascular complex (SVC) density, and deep vascular complex (DVC) density. Multivariable linear mixed-effects models adjusted for age, sex, treatment, follow-up time, and ON history were used to analyze correlations between SS-OCT/OCTA parameters and clinical features.
Cross-sectional analysis demonstrated significant reductions in the RNFL thickness (33.91 ± 8.90 vs. 38.88 ± 4.00 μm, p < 0.001), GCIPL thickness (54.89 ± 11.06 vs. 64.42 ± 5.28 μm, p < 0.001), and SVC density (38.17 ± 10.21% vs. 45.96 ± 3.83%, p < 0.001) in NMOSD patients versus healthy controls, along with reduced RNFL thickness (33.91 ± 8.90 μm vs. 36.22 ± 8.62 μm; p = 0.011) and SVC density (38.17 ± 10.21% vs. 40.66 ± 6.62%; p = 0.016) relative to patients with multiple sclerosis. Longitudinal analysis demonstrated a progressive decline in GCIPL thickness (- 0.18 µm/year, IQR: - 1.69 to 1.72 µm/year, p = 0.047), SVC density (- 1.11%/year, IQR:-2.90% to 0.87%/year, p = 0.003), and DVC density (- 1.88%/year, IQR: - 3.52% to 0.50%/year, p = 0.004) from baseline among clinically stable NMOSD patients. The annual degradation rate of GCIPL thickness showed significant inverse correlations with baseline logMAR visual acuity (p < 0.001), ON frequency (p < 0.001) and baseline EDSS scores (p = 0.039).
Our findings indicate that progressive retinal neurodegeneration and microvascular loss persist independently of clinical relapse, positioning SS-OCT/OCTA metrics as sensitive biomarkers for subclinical progression and supporting their integration into the framework of disease monitoring and treatment response assessment.
新出现的证据表明，视神经脊髓炎谱系障碍（NMOSD）可能独立于视神经炎（ON）发生亚临床视觉通路损伤。这项前瞻性纵向队列研究旨在描述NMOSD中动态视网膜神经变性和微血管改变的特征。
扫频光学相干断层扫描（SS-OCT）和SS-OCT血管造影（SS-OCTA）的定量参数包括黄斑区视网膜神经纤维层（RNFL）厚度、神经节细胞-内丛状层（GCIPL）厚度、浅表血管复合体（SVC）密度和深部血管复合体（DVC）密度。采用多变量线性混合效应模型，对年龄、性别、治疗、随访时间和ON病史进行校正，以分析SS-OCT/OCTA参数与临床特征之间的相关性。
横断面分析显示，与健康对照相比，NMOSD患者的RNFL厚度（33.91±8.90 vs. 38.88±4.00μm，p<0.001）、GCIPL厚度（54.89±11.06 vs. 64.42±5.28μm，p<0.001）和SVC密度（38.17±10.21% vs. 45.96±3.83%，p<0.001）显著降低，相对于多发性硬化症患者，RNFL厚度（33.91±8.90μm vs. 36.22±8.62μm；p=0.011）和SVC密度（38.17±10.21% vs. 40.66±6.62%；p=0.016）也降低。纵向分析显示，临床稳定的NMOSD患者从基线开始，GCIPL厚度（-0.18μm/年，IQR：-1.69至1.72μm/年，p=0.047）、SVC密度（-1.11%/年，IQR：-2.90%至0.87%/年，p=总论点：我们的研究结果表明，视网膜神经变性和微血管丢失的进展独立于临床复发，将SS-OCT/OCTA指标定位为亚临床进展的敏感生物标志物，并支持将其纳入疾病监测和治疗反应评估框架。0.003）和DVC密度（-1.88%/年，IQR：-3.52%至0.50%/年，p=0.004）逐渐下降。GCIPL厚度的年退化率与基线logMAR视力（p<0.001）、ON频率（p<0.001）和基线EDSS评分（p=0.039）呈显著负相关。
我们的研究结果表明，视网膜神经变性和微血管丢失的进展独立于临床复发，将SS-OCT/OCTA指标定位为亚临床进展的敏感生物标志物，并支持将其纳入疾病监测和治疗反应评估框架。
