目的:急性黄斑神经视网膜病变(AMN)可引起健康年轻患者的突然发作和永久性暗点。对AMN患者的光学相干断层扫描(OCT)和OCT血管造影(OCTA)的分析可能会提供对疾病机制的见解。
方法:我们对1月1日在我们诊所就诊的连续SARS-Cov-2相关AMN患者进行了回顾性研究,2022年4月30日,2023年,症状发作后30天内。定量OCTA中AMN病变的视网膜血管面积密度(VAD),并与相邻组织对照(ATC)进行比较。对浅表血管丛(SVP)进行了量化,中间毛细血管丛(ICP),深毛细血管丛(DCP),脉络膜毛细血管(CC),和脉络膜.此外,分析了en面部OCT图像。
结果:确定了9名AMN患者,其中6个(4个女性,2男,平均年龄25岁)符合纳入标准,纳入本研究.从症状发作到OCTA的平均时间为14.3天。在任一视网膜层中都没有发现AMN和邻近组织之间的VAD差异(SVP,ICP,DCP)。相比之下,与ATC相比,CC中的VAD降低了27%(p=0.007),脉络膜VAD降低了41%(p=0.017)。对正面OCT的进一步分析可以表明,AMN中的特征红外低反射率是由感光体改变而不是内部视网膜层的变化引起的。
结论:我们的数据表明,脉络膜层的灌注不足是AMN的原因,而不是DCP的原因。这是当前文献中的主要假设。
OBJECTIVE: Acute macular neuroretinopathy (AMN) can cause sudden-onset and permanent scotoma in healthy young patients. Analysis of optical coherence tomography (OCT) and OCT angiography (OCTA) of AMN patients may provide insights into disease mechanism.
METHODS: We conducted a retrospective study of consecutive SARS-Cov-2-related AMN patients that presented in our clinic between Jan 1st, 2022, and April 30th, 2023, within 30 days of symptom onset. Retinal vessel area density (VAD) of AMN lesions in OCTA was quantified and compared to an adjacent tissue control (ATC). This quantification was performed for the superficial vascular plexus (SVP), the intermediate capillary plexus (ICP), the deep capillary plexus (DCP), the choriocapillaris (CC), and choroid. Furthermore, en face OCT images were analyzed.
RESULTS: Nine AMN patients were identified, 6 of these (4 female, 2 male, average age 25 years) fulfilled the inclusion criteria and were included into this study. Average time from symptom onset to OCTA was 14.3 days. No VAD differences between AMN and adjacent tissue were found in either retinal layer (SVP, ICP, DCP). In contrast, VAD in CC was reduced by 27% against the ATC (p = 0.007) and choroidal VAD was reduced by 41% (p = 0.017). Further analysis of en face OCT could show that the pathognomonic infrared hyporeflectivity in AMN is caused by photoreceptor alterations rather than changes in the inner retinal layers.
CONCLUSIONS: Our data suggests that a perfusion deficit in the choroidal layers is responsible for AMN rather than in the DCP, which is the predominant hypothesis in current literature.