Montesano Giovanni, Ometto Giovanni, Higgins Bethany E, Das Radha, Graham Katie W, Chakravarthy Usha, McGuiness Bernadette, Young Ian S, Kee Frank, Wright David M, Crabb David P, Hogg Ruth E
Optometry and Visual Sciences, City, University of London, London, United Kingdom.
NIHR Biomedical Research Centre, Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology, London, United Kingdom.
Invest Ophthalmol Vis Sci. 2021 Mar 1;62(3):35. doi: 10.1167/iovs.62.3.35.
To provide structural and functional evidence of inner retinal loss in diabetes prior to vascular changes and interpret the structure-function relationship in the context of an established neural model.
Data from one eye of 505 participants (134 with diabetes and no clinically evident vascular alterations of the retina) were included in this analysis. The data were collected as part of a large population-based study. Functional tests included best-corrected visual acuity, Pelli-Robson contrast sensitivity, mesopic microperimetry, and frequency doubling technology perimetry (FDT). Macular optical coherence tomography volume scans were collected for all participants. To interpret the structure-function relationship in the context of a neural model, ganglion cell layer (GCL) thickness was converted to local ganglion cell (GC) counts.
The GCL and inner plexiform layer were significantly thinner in participants with diabetes (P < 0.05), with no significant differences in the macular retinal nerve fiber layer or the outer retina. All functional tests except microperimetry showed a significant loss in diabetic patients (P < 0.05). Both FDT and microperimetry showed a significant relationship with the GC count (P < 0.05), consistent with predictions from a neural model for partial summation conditions. However, the FDT captured additional significant damage (P = 0.03) unexplained by the structural loss.
Functional and structural measurements support early neuronal loss in diabetes. The structure-function relationship follows the predictions from an established neural model. Functional tests could be improved to operate in total summation conditions in the macula, becoming more sensitive to early loss.
在血管变化之前提供糖尿病患者视网膜内层损失的结构和功能证据,并在既定的神经模型背景下解释结构 - 功能关系。
本分析纳入了505名参与者一只眼睛的数据(134名患有糖尿病且视网膜无临床明显血管改变)。这些数据是作为一项大型基于人群的研究的一部分收集的。功能测试包括最佳矫正视力、佩利 - 罗布森对比敏感度、中视微视野检查和倍频技术视野检查(FDT)。为所有参与者收集黄斑光学相干断层扫描容积扫描。为了在神经模型背景下解释结构 - 功能关系,将神经节细胞层(GCL)厚度转换为局部神经节细胞(GC)计数。
糖尿病患者的GCL和内网状层明显更薄(P < 0.05),黄斑视网膜神经纤维层或外视网膜无显著差异。除微视野检查外,所有功能测试在糖尿病患者中均显示出显著损失(P < 0.05)。FDT和微视野检查均与GC计数显示出显著关系(P < 0.05),这与部分总和条件下神经模型的预测一致。然而,FDT捕捉到了结构损失无法解释的额外显著损伤(P = 0.03)。
功能和结构测量支持糖尿病早期神经元损失。结构 - 功能关系遵循既定神经模型的预测。功能测试可改进为在黄斑的总和条件下操作,对早期损失更敏感。