Local multifocal oscillatory potential abnormalities in diabetes and early diabetic retinopathy

Local multifocal oscillatory potential abnormalities in diabetes and early diabetic retinopathy
复制标题

DOI:
10.1167/iovs.04-0308
复制
发表时间:
2004-09-01
影响因子:
4.4
通讯作者:
Adams, AJ
Adams, AJ
中科院分区:
医学2区
文献类型:
--
作者:
Bearse, MA;Han, Y;Adams, AJ

文献摘要

被引文献

相似文献

目的。采用局部多焦视网膜电图振荡电位(mfOPs)分析新方法研究糖尿病和早期非增殖性糖尿病视网膜病变(NPDR)的视网膜功能障碍。对26例正常人、16例无视网膜病变的糖尿病患者和16例早期NPDR的糖尿病患者各检查一只眼。从中心45度处记录慢闪多焦视网膜电图(sf-mfERGs),并拍摄糖尿病眼立体眼底照片。从每个视网膜位置提取一阶(K1)、诱导一阶(K1i)和二阶(K2)响应分量,并将K1i和K2添加到Ks2中。来自35个连续区域的响应经过90至225 Hz的数字滤波以隔离mfOPs。计算mfOPs的信噪比(SNR),并将信噪比低于正常受试者的第5个百分位数定义为异常。在通过数字滤波隔离mfOPs之前,将K1i和K2分量组合成Ks2,提高了信噪比。平均Ks2和K1 mfOP信噪比分别在25%和19%的正常眼中异常,在62%的正常眼中均异常。局部Ks2和K1 mfOP异常的视网膜分布重叠,但存在差异。此外,局部Ks2 mfOP异常优先与含有NPDR的视网膜部位相关,而K1 mfOP异常则不相关。促进局部mfOPs产生的细胞受到糖尿病的影响,并在更大程度上受到早期NPDR的影响。结果表明,影响mfOPs的快速适应机制在含有NPDR的视网膜部位最为异常。
PURPOSE. To study retinal dysfunction in diabetes and early nonproliferative diabetic retinopathy (NPDR) using a new method to analyze local multifocal electroretinogram oscillatory potentials (mfOPs).METHODS. One eye of each of 26 normal subjects, 16 diabetic subjects without retinopathy (NoR), and 16 diabetic subjects with early NPDR was examined. Slow-flash multifocal electroretinograms (sf-mfERGs) were recorded from the central 45degrees, and stereo fundus photographs of the diabetic eyes were taken. The first-order (K1), induced first-order (K1i), and second-order (K2) response components were extracted from each retinal location, and K1i and K2 were added to create Ks2. Responses from 35 contiguous areas were digitally filtered 90 to 225 Hz to isolate the mfOPs. The signal-to-noise ratio (SNR) of the mfOPs was calculated, and abnormality was defined as SNR below the fifth percentile of the normal subjects.RESULTS. Combining the K1i and K2 components to form Ks2 before isolation of the mfOPs by digital filtering increased the SNR. Mean Ks2 and K1 mfOP SNRs were abnormal in 25% and 19% of the NoR eyes, respectively, and both were abnormal in 62% of the NPDR eyes. The retinal distributions of the local Ks2 and K1 mfOP abnormalities overlapped, but they differed. Furthermore, local Ks2 mfOP abnormalities were preferentially associated with retinal sites containing NPDR but K1 mfOP abnormalities were not.CONCLUSIONS. The cells that contribute to the generation of local mfOPs are affected by diabetes and, to a greater degree, by early NPDR. The results suggest that fast adaptive mechanisms influencing the mfOPs are most abnormal at retinal sites containing NPDR.