January 2010
Volume 51, Issue 1
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Retina  |   January 2010
Correlation between Retinal Oscillatory Potentials and Retinal Vascular Caliber in Type 2 Diabetes
Author Affiliations & Notes
  • Chi D. Luu
    From the Centre for Eye Research Australia, University of Melbourne, Royal Victorian Eye and Ear Hospital, East Melbourne, Australia;
    the Singapore Eye Research Institute, Singapore;
  • Joshua A. Szental
    From the Centre for Eye Research Australia, University of Melbourne, Royal Victorian Eye and Ear Hospital, East Melbourne, Australia;
    The Alfred Hospital, Melbourne, Australia;
  • Shu-Yen Lee
    the Singapore Eye Research Institute, Singapore;
    the Singapore National Eye Centre, Singapore;
  • Raghavan Lavanya
    the Singapore Eye Research Institute, Singapore;
    the Singapore National Eye Centre, Singapore;
  • Tien Y. Wong
    From the Centre for Eye Research Australia, University of Melbourne, Royal Victorian Eye and Ear Hospital, East Melbourne, Australia;
    the Singapore Eye Research Institute, Singapore;
    the Singapore National Eye Centre, Singapore;
    the Department of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
  • Corresponding author: Chi D. Luu, Macular Research Unit, Centre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, Level 1, 32 Gisborne Street, East Melbourne, VIC 3002, Australia; cluu@unimelb.edu.au
Investigative Ophthalmology & Visual Science January 2010, Vol.51, 482-486. doi:10.1167/iovs.09-4069
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      Chi D. Luu, Joshua A. Szental, Shu-Yen Lee, Raghavan Lavanya, Tien Y. Wong; Correlation between Retinal Oscillatory Potentials and Retinal Vascular Caliber in Type 2 Diabetes. Invest. Ophthalmol. Vis. Sci. 2010;51(1):482-486. doi: 10.1167/iovs.09-4069.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose.: To assess retinal function in individuals with type 2 diabetes with no retinopathy or nonproliferative diabetic retinopathy (NPDR) and determine the relationship between retinal function and retinal vascular caliber.

Methods.: A full-field electroretinogram (ERG) and retinal vascular caliber measurements were performed in subjects with nonproliferative diabetic retinopathy (NPDR, n = 10), diabetic subjects without retinopathy (no-DR, n = 18), and normal control subjects (n = 18). The response amplitudes and implicit times of scotopic and photopic ERG and the retinal arteriolar and venular calibers were compared among the study groups. The relationships between ERG parameters and retinal vascular calibers were determined.

Results.: There were statistically significant differences between diabetic (no-DR and NPDR groups) and control subjects in the amplitudes and implicit times of rod-derived ERG responses, but not in the cone-derived ERG responses. All the oscillatory potential (OP) components (OP1–OP4) were significantly reduced in amplitude and increased in implicit time in the no-DR and NPDR groups. No significant difference was found in any of the ERG parameters between the no-DR and NPDR groups. Of all the ERG parameters examined, only OP4 amplitude correlated significantly with the retinal arteriolar caliber (r = −0.556, P = 0.006). None of the OP components correlated significantly with retinal venular caliber.

Conclusions.: Significant retinal dysfunction was demonstrated in all diabetic patients, even in those without clinically detectable retinopathy, with the rod system being predominantly affected. OP4 amplitude correlates with retinal arteriolar caliber in diabetic patients, suggesting a correlation between retinal neuronal dysfunction and microvasculature changes.

The prevalence of type 2 diabetes mellitus is rising rapidly worldwide. It is estimated that 380 million people will have this condition by 2025. 1 Diabetic retinopathy (DR) is the fifth leading cause of blindness worldwide and the leading cause of visual loss in adults of working age in industrialized countries. 1,2  
The retinal neurons and the retinal vasculature are both implicated in the pathogenesis of DR. 3,4 It is now known that the function of the neural components of the middle and inner retinal layers, detected by electroretinography (ERG), is altered in persons with diabetes before the development of retinopathy. Thus, the ERG has been shown to be a sensitive measure of early neuronal abnormalities, long before DR can be detected clinically. 5 The most common ERG abnormality in diabetic patients without retinopathy is a reduction in the amplitude and increase in the implicit time of the oscillatory potentials (OPs). 69 Other ERG abnormalities that have been observed in persons with diabetes without retinopathy include a reduction in the scotopic b-wave amplitude. 7,8,10  
Retinal vascular abnormalities are also implicated in the pathogenesis of DR. Studies have demonstrated that retinal arteriolar dysfunction, manifesting as dilatation, is present in diabetic patients without retinopathy 4,1113 and is associated with both the subsequent incidence of clinically detectable DR and with the progression of DR. 1416  
The relationship between retinal neuronal function and retinal vascular caliber in the early stages of diabetes is unknown. In this study, we investigated retinal neuronal function and the relationship between retinal function and retinal vascular caliber in diabetic subjects with and without early DR. 
Methods
Study subjects were recruited from the Diabetic Retinopathy Clinic at Singapore National Eye Centre and a population-based cohort study (the Singapore Indian Chinese Cohort Eye Study, an extension among Indian and Chinese participants from the Singapore Malay Eye Study), 17 which was being conducted at the Singapore Eye Research Institute. In addition to these two sources, normal control subjects were also recruited from volunteered staff and students of the Singapore National Eye Centre and Singapore Eye Research Institute (SERI). The study was approved by the Institutional Review Board of SERI and the research procedures adhered to the tenets of the Declaration of Helsinki. Written informed consent was obtained from all participants at enrollment. 
The subjects were subdivided into three study groups of normal control (group 1, control), subjects with diabetes and no clinically detectable retinopathy (group 2, no-DR), or subjects with nonproliferative (background) diabetic retinopathy (group 3, NPDR). All subjects in groups 2 and 3 had type 2 diabetes mellitus, which was diagnosed based on a combination of a physician-ascertained history of diabetes, use of diabetic medications, and fasting blood glucose levels. 
The level of retinopathy (no-DR or NPDR) was graded by study ophthalmologists who used slit lamp microscopy with 78-D lens and indirect ophthalmoscopy based on a modified Arlie House Classification of DR, as used in the Singapore Malay Eye Study. 18 Exclusion criteria were type 1 diabetes mellitus, proliferative DR, cataract (LOCS III score >2), high myopia (−6 D or greater), macular edema (as determined clinically or on optical coherence tomography or any ocular conditions other than NPDR. 
All subjects underwent ERG followed by digital color fundus photographs of both eyes. Assessment of the retinal function was performed with a full-field ERG. Pupils were dilated with tropicamide 1%, and the recordings were performed when the pupils were equally dilated to at least 7 mm. Both eyes were recorded simultaneously. The flash stimulus was delivered by a Ganzfeld stimulator (ColorDome; Diagnosys LLC, Lowell, MA). An electrophysiology system (Espion E2; Diagnosys LLC) was used for stimulus generation and data acquisition. The ERG was recorded using Dawson-Trick-Litzkow disposable fiber electrodes (DTL; Diagnosys LLC) 19 and complied with International Society for Clinical Electrophysiology of Vision (ISCEV) standards. 20 In brief, the recording protocol consisted of dark-adaptation for 20 minutes, after which scotopic ERG, maximum ERG, and dark-adapted oscillatory potentials (OPs) were recorded. After the dark-adapted ERGs, the eyes were light-adapted for 10 minutes, and the photopic ERG and 30-Hz flicker ERG were recorded. The outcome measures were the response amplitudes and implicit time of each ERG component. 
Measurements of the response amplitude were between baseline and trough for the a-wave and between peak and the preceding trough for the b-wave (Fig. 1). All implicit time measurements were taken between stimulus onset and the specific response. 
Digital color photographs of the fundus (ETDRS standard field 1, centered on the disc) were taken after the ERG using a nonmydriatic retinal camera (CD-DGi; Canon, Singapore) based on the standardized protocols. 18 Retinal vascular caliber (arteriolar and venular) was measured with a computer-based program according to a previously validated protocol. 14,21 In brief, all arterioles and venules coursing through an area one half to one disc diameter from the disc margin were measured and expressed as the central retinal artery and vein equivalents. These equivalents represented the average of projected calibers for the central retinal vessels. 
Kruskal-Wallis and Mann-Whitney U tests were used to estimate the level of significance for the difference in the ERG parameters among the study groups as appropriate. The results were evaluated without (P = 0.05) and with the Bonferroni correction for 23 ERG parameters (P = 0.05/23 = 0.0022) to minimize type I error associated with multiple independent ERG components examined. The Bonferroni correction assumes that all the ERG parameters tested are independent from one another; however, many of the ERG components were highly correlated such as the amplitudes of the maximum and photopic ERG a- and b-waves. As a result, the use of Bonferroni correction in these cases was likely to be an overcorrection. Pearson's correlation coefficient and multiple linear regression analysis were used to determine the relationship between ERG parameters and retinal vascular caliber. 
Results
A total of 42 subjects were recruited for the present study. The mean age of the control group was slightly younger than that of the no-DR and NPDR groups; however, the differences were not statistically significant (P = 0.074). A summary of demographic and clinical data of the participants is presented in Table 1. ERG and retinal vascular caliber data from only the right eye are presented, as results were similar in analysis of the left eye. Typical response waveforms of various ERG components from a normal subject are presented in Figure 1
Table 1.
 
Demographic and Clinical Data of the Study Subjects
Table 1.
 
Demographic and Clinical Data of the Study Subjects
Parameters Normal (Group 1) No DR (Group 2) NPDR (Group 3) P *
Sex (male/female) 10/8 9/5 6/4 N/A
Eyes studied (n) 18 14 10 N/A
Age (mean ± SD) 49.6 ± 17.6 58.2 ± 6.5 58.2 ± 12.1 0.074
LogMAR visual acuity (mean ± SD) 0.00 ± 0.00 0.01 ± 0.03 0.09 ± 0.11 <0.001
Figure 1.
 
Response waveforms of various ERG components. Double-headed arrows: response amplitude measurements.
Figure 1.
 
Response waveforms of various ERG components. Double-headed arrows: response amplitude measurements.
Initial screening of the ERG data showed that there were statistically significant (P < 0.05) differences between the diabetic (no-DR and NPDR groups) and normal control groups in scotopic ERG response amplitudes and implicit times, maximum ERG a- and b-wave implicit time, and in implicit times for photopic single-flash a-wave and 30-Hz flicker ERG (Table 2). All the OP components (OP1–OP4) were significantly reduced in amplitude and increased in implicit time in the no-DR and NPDR groups compared with that of the normal control subjects at the P = 0.05 level (Table 2). However, when we applied the Bonferroni correction and used a threshold significance level of P = 0.0022, rather than P = 0.05, the scotopic b-wave amplitude and implicit time, maximum ERG a-wave implicit time, amplitudes of OP1–OP4, implicit times of OP2, and the summed OP time were the only ERG parameters that remained significantly different between the study groups (Table 2). 
Table 2.
 
ERG Components for Normal Control, No-DR, and NPDR Groups
Table 2.
 
ERG Components for Normal Control, No-DR, and NPDR Groups
ERG Parameters Normal (n = 23 eyes) No-DR (n = 14 eyes) NPDR (n = 10 eyes) P *
Scotopic b-wave
    Amplitude 224.87 ± 57.42 169.68 ± 49.2 161.08 ± 55.50 0.001†
    Implicit time 104.52 ± 7.29 119.29 ± 7.48 117.70 ± 11.61 <0.001†
Maximal a-wave
    Amplitude 206.59 ± 60.39 181.75 ± 41.09 174.53 ± 33.84 0.318
    Implicit time 14.96 ± 0.93 16.43 ± 1.16 16.70 ± 1.25 <0.001†
Maximal b-wave
    Amplitude 294.68 ± 69.56 261.74 ± 52.88 253.70 ± 56.27 0.225
    Implicit time 52.83 ± 5.93 58.00 ± 5.04 56.80 ± 3.68 0.023
Maximal b-/a-wave amplitude ratio 1.45 ± 0.18 1.45 ± 0.14 1.48 ± 0.34 0.982
Dark-adapted OP
    OP1 amplitude 23.04 ± 6.96 15.42 ± 4.06 14.28 ± 3.91 <0.001†
    OP2 amplitude 37.84 ± 8.81 25.12 ± 7.37 20.36 ± 5.78 <0.001†
    OP3 amplitude 24.50 ± 8.95 12.09 ± 5.32 9.10 ± 5.57 <0.001†
    OP4 amplitude 11.97 ± 4.08 7.04 ± 3.08 4.16 ± 3.03 <0.001†
    OP1 implicit time 18.13 ± 0.76 18.91 ± 0.94 19.13 ± 0.84 0.015
    OP2 implicit time 24.44 ± 0.95 25.64 ± 0.81 26.00 ± 0.93 <0.001†
    OP3 implicit time 31.09 ± 0.90 32.55 ± 1.37 32.75 ± 1.28 0.002
    OP4 implicit time 38.17 ± 1.30 39.40 ± 1.51 39.57 ± 0.98 0.022
    SumOP time 111.83 ± 3.49 117.00 ± 3.56 116.86 ± 2.48 0.001†
Photopic a-wave
    Amplitude 22.22 ± 5.73 21.71 ± 3.87 22.25 ± 6.94 0.961
    Implicit time 16.32 ± 1.00 17.15 ± 0.80 17.13 ± 0.64 0.038
Photopic b-wave
    Amplitude 79.66 ± 20.19 70.44 ± 15.76 72.09 ± 18.79 0.493
    Implicit time 33.10 ± 1.48 34.15 ± 1.41 34.00 ± 0.76 0.091
Photopic b/a ratio 3.63 ± 0.66 3.30 ± 0.72 3.11 ± 0.47 0.216
30-Hz flicker
    Amplitude 62.75 ± 11.62 52.90 ± 12.54 56.78 ± 14.28 0.098
    Implicit time 29.53 ± 1.22 31.46 ± 1.51 30.88 ± 1.46 0.003
There was no significant difference between no-DR and NPDR group for response amplitudes or implicit times of any of the ERG parameters. The differences in OP amplitude and implicit time between no-DR and NPDR group were not statistically significant for any of the OPs (Fig. 2). 
Figure 2.
 
Response amplitude and implicit time of different OP components for each study group: 1, normal control; 2, no-DR group; and 3, NPDR. Error bars, 95% CI.
Figure 2.
 
Response amplitude and implicit time of different OP components for each study group: 1, normal control; 2, no-DR group; and 3, NPDR. Error bars, 95% CI.
There was no significant difference in retinal arteriolar caliber or retinal venular arteriolar caliber among the study groups. A summary of the retinal vascular caliber data is presented in Table 3
Table 3.
 
Retinal Vascular Calibers
Table 3.
 
Retinal Vascular Calibers
Control Group No-DR Group NPDR Group P *
Arteriolar caliber 72.12 ± 6.97 71.78 ± 6.09 75.76 ± 8.76 0.505
Venular caliber 84.53 ± 8.11 84.14 ± 10.90 87.83 ± 11.95 0.528
The relationships between retinal vascular caliber and various ERG parameters were determined in patients with diabetes. Retinal arteriolar caliber was significantly negatively (inversely) correlated with OP4 amplitude (r = −0.556, 95% confidence interval [CI], −0.792 to −0.175, P = 0.006) but not with other OP components (Fig. 3). However, retinal arteriolar caliber was not significantly correlated with OP4 amplitude in the control group (P = 0.5362). There was no significant association between retinal venular caliber and any of the OP components. None of the others ERG parameters, including the scotopic ERG b-wave amplitude, were significantly correlated with either retinal arteriolar caliber or retinal venular caliber. Multiple linear regression analyses were performed for OP amplitudes and retinal vessel calibers and a similar finding was obtained that only the OP4 amplitude was significantly associated with retinal arteriolar caliber (Table 4). 
Figure 3.
 
Correlation between the OP amplitudes and retinal vascular calibers. Note that of all the OPs examined, only OP4 correlated significantly with retinal arteriolar caliber (r = −0.556, P = 0.006). None of the OPs correlated significantly with retinal venular caliber.
Figure 3.
 
Correlation between the OP amplitudes and retinal vascular calibers. Note that of all the OPs examined, only OP4 correlated significantly with retinal arteriolar caliber (r = −0.556, P = 0.006). None of the OPs correlated significantly with retinal venular caliber.
Table 4.
 
Multiple Linear Regression Analysis for OP Amplitudes and Retinal Vessel Calibers
Table 4.
 
Multiple Linear Regression Analysis for OP Amplitudes and Retinal Vessel Calibers
β Coefficients 95% CI for β P
Retinal arteriolar caliber
    OP1 amplitude 0.420 −0.401 to 1.240 0.296
    OP2 amplitude −0.070 −0.603 to 0.464 0.786
    OP3 amplitude 0.605 −0.356 to 1.565 0.202
    OP4 amplitude −1.686 −2.865 to −0.508 0.008
Retinal venular caliber
    OP1 amplitude −0.555 −2.078 to 0.967 0.442
    OP2 amplitude −0.224 −1.262 to 0.815 0.647
    OP3 amplitude 1.798 −0.213 to 3.809 0.075
    OP4 amplitude −2.837 −5.654 to 0.020 0.055
Discussions
The electrophysiological findings from the present study indicated that the rod system was predominantly affected in both the no-DR and NPDR groups. Both the response amplitude and implicit time were abnormal for rod-derived ERG responses, whereas, the cone-derived ERG responses were not significantly altered. These observations are consistent with previously published data. 610  
New observations from this study include a lack of significant differences in ERG responses between diabetic subjects with and without retinopathy (no-DR versus NPDR group), suggesting that there is a substantial retinal dysfunction in the early stages of diabetes. The difference in the OP amplitude between the no-DR and NPDR groups was minimal for OP1, and this difference increased progressively toward OP4. The retinal mechanism involved in this phenomenon is unclear and requires further investigation. It is possible that a significant difference in OP4 amplitude between no-DR and NPDR was not detected because of the small sample size. 
There have been no published data to our knowledge on the relationship between oscillatory potentials and retinal vascular caliber in diabetic retinopathy. Oscillatory potentials are low-amplitude oscillations (numbered OP1–OP4) superimposed on the ascending limb of the ERG b-wave. The OPs are thought to reflect the function of the inner retina and are sensitive to changes in retinal circulation. 9,22 Our data showed that there was a significant negative correlation between OP4 amplitude and retinal arteriolar caliber, but not other OP components, suggesting that OP4 could reflect early microvascular dysfunction. These findings also support the hypothesis that retinal arteriolar dilatation is a physiological indicator of microvascular dysfunction in diabetes. 15,23,24 It has also been shown that retinal venular dilatation occurs mainly in established DR, 24,25 which may explain the lack of correlation between the OP amplitude and retinal venular caliber in this study. 
It is believed that the OPs are derived from the activities, interactions, and biofeedback mechanisms of cells within the interplexiform layers of the retina. 9 Although the exact cellular contribution to each individual OP remains unknown, observations of the OPs in various retinal diseases indicated that individual OP may represent different cellular origin, and thus the OP responses are differentially affected in a diseased retina. 9,26,27 For example, in patients with the complete type of congenital stationary night blindness (CSNB), in which the ON-pathway is affected, the dark-adapted OP1 is well preserved but OP2, -3, and -4 are attenuated (Luu CD, unpublished clinical data, 2002). It has also been reported that OP2 and -3 of the suprathreshold photopic ERG are selectively absent in CSNB. 27 The results of our study suggest that OP4 may originate partly from retinal cells and mechanisms that are sensitive to microvascular changes. Further studies are necessary to enhance our understanding of the cellular contribution to OP4 and its association with retinal arteriolar caliber. 
We did not examine the relationship between the OP parameters and the retinal vascular caliber separately for each no-DR and NPDR group because of a small sample size. Nevertheless, there was no significant difference in the mean retinal arteriolar caliber between the no-DR and NPDR groups (P = 0.264). Thus, it is unlikely that the severity of retinopathy contributes to the association between OP4 and retinal arteriolar caliber. It is possible that retinal arteriolar dilatation is associated with physiological changes in the retina and that the OP4 parameter is sensitive to these changes. We plan to conduct a prospective study with a larger sample size to explore this relationship further. 
In summary, the results of this study indicate that there is a substantial retinal dysfunction in the early stages of diabetes, even in patients with no clinically detectable retinopathy, with the rod-derived ERG responses affected more than the cone-derived ERGs. The finding of a significant correlation between OP4 amplitude and retinal arteriolar caliber is novel and requires further studies to clarify the underlying pathophysiology and validate its clinical usefulness in predicting the development of DR. 
Footnotes
 Supported by Singapore National Medical Research Council (Pilot grant R491/40/2006) and the Biomedical Research Council (08/1/35/19/550).
Footnotes
 Disclosure: C.D. Luu, None; J.A. Szental, None; S.-Y. Lee, None; R. Lavanya, None; T.Y. Wong, None
The authors thank Liyu Chen, Mya Sandar, and Ryan E. K. Man for assistance in coordinating the study and data collection. 
References
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Figure 1.
 
Response waveforms of various ERG components. Double-headed arrows: response amplitude measurements.
Figure 1.
 
Response waveforms of various ERG components. Double-headed arrows: response amplitude measurements.
Figure 2.
 
Response amplitude and implicit time of different OP components for each study group: 1, normal control; 2, no-DR group; and 3, NPDR. Error bars, 95% CI.
Figure 2.
 
Response amplitude and implicit time of different OP components for each study group: 1, normal control; 2, no-DR group; and 3, NPDR. Error bars, 95% CI.
Figure 3.
 
Correlation between the OP amplitudes and retinal vascular calibers. Note that of all the OPs examined, only OP4 correlated significantly with retinal arteriolar caliber (r = −0.556, P = 0.006). None of the OPs correlated significantly with retinal venular caliber.
Figure 3.
 
Correlation between the OP amplitudes and retinal vascular calibers. Note that of all the OPs examined, only OP4 correlated significantly with retinal arteriolar caliber (r = −0.556, P = 0.006). None of the OPs correlated significantly with retinal venular caliber.
Table 1.
 
Demographic and Clinical Data of the Study Subjects
Table 1.
 
Demographic and Clinical Data of the Study Subjects
Parameters Normal (Group 1) No DR (Group 2) NPDR (Group 3) P *
Sex (male/female) 10/8 9/5 6/4 N/A
Eyes studied (n) 18 14 10 N/A
Age (mean ± SD) 49.6 ± 17.6 58.2 ± 6.5 58.2 ± 12.1 0.074
LogMAR visual acuity (mean ± SD) 0.00 ± 0.00 0.01 ± 0.03 0.09 ± 0.11 <0.001
Table 2.
 
ERG Components for Normal Control, No-DR, and NPDR Groups
Table 2.
 
ERG Components for Normal Control, No-DR, and NPDR Groups
ERG Parameters Normal (n = 23 eyes) No-DR (n = 14 eyes) NPDR (n = 10 eyes) P *
Scotopic b-wave
    Amplitude 224.87 ± 57.42 169.68 ± 49.2 161.08 ± 55.50 0.001†
    Implicit time 104.52 ± 7.29 119.29 ± 7.48 117.70 ± 11.61 <0.001†
Maximal a-wave
    Amplitude 206.59 ± 60.39 181.75 ± 41.09 174.53 ± 33.84 0.318
    Implicit time 14.96 ± 0.93 16.43 ± 1.16 16.70 ± 1.25 <0.001†
Maximal b-wave
    Amplitude 294.68 ± 69.56 261.74 ± 52.88 253.70 ± 56.27 0.225
    Implicit time 52.83 ± 5.93 58.00 ± 5.04 56.80 ± 3.68 0.023
Maximal b-/a-wave amplitude ratio 1.45 ± 0.18 1.45 ± 0.14 1.48 ± 0.34 0.982
Dark-adapted OP
    OP1 amplitude 23.04 ± 6.96 15.42 ± 4.06 14.28 ± 3.91 <0.001†
    OP2 amplitude 37.84 ± 8.81 25.12 ± 7.37 20.36 ± 5.78 <0.001†
    OP3 amplitude 24.50 ± 8.95 12.09 ± 5.32 9.10 ± 5.57 <0.001†
    OP4 amplitude 11.97 ± 4.08 7.04 ± 3.08 4.16 ± 3.03 <0.001†
    OP1 implicit time 18.13 ± 0.76 18.91 ± 0.94 19.13 ± 0.84 0.015
    OP2 implicit time 24.44 ± 0.95 25.64 ± 0.81 26.00 ± 0.93 <0.001†
    OP3 implicit time 31.09 ± 0.90 32.55 ± 1.37 32.75 ± 1.28 0.002
    OP4 implicit time 38.17 ± 1.30 39.40 ± 1.51 39.57 ± 0.98 0.022
    SumOP time 111.83 ± 3.49 117.00 ± 3.56 116.86 ± 2.48 0.001†
Photopic a-wave
    Amplitude 22.22 ± 5.73 21.71 ± 3.87 22.25 ± 6.94 0.961
    Implicit time 16.32 ± 1.00 17.15 ± 0.80 17.13 ± 0.64 0.038
Photopic b-wave
    Amplitude 79.66 ± 20.19 70.44 ± 15.76 72.09 ± 18.79 0.493
    Implicit time 33.10 ± 1.48 34.15 ± 1.41 34.00 ± 0.76 0.091
Photopic b/a ratio 3.63 ± 0.66 3.30 ± 0.72 3.11 ± 0.47 0.216
30-Hz flicker
    Amplitude 62.75 ± 11.62 52.90 ± 12.54 56.78 ± 14.28 0.098
    Implicit time 29.53 ± 1.22 31.46 ± 1.51 30.88 ± 1.46 0.003
Table 3.
 
Retinal Vascular Calibers
Table 3.
 
Retinal Vascular Calibers
Control Group No-DR Group NPDR Group P *
Arteriolar caliber 72.12 ± 6.97 71.78 ± 6.09 75.76 ± 8.76 0.505
Venular caliber 84.53 ± 8.11 84.14 ± 10.90 87.83 ± 11.95 0.528
Table 4.
 
Multiple Linear Regression Analysis for OP Amplitudes and Retinal Vessel Calibers
Table 4.
 
Multiple Linear Regression Analysis for OP Amplitudes and Retinal Vessel Calibers
β Coefficients 95% CI for β P
Retinal arteriolar caliber
    OP1 amplitude 0.420 −0.401 to 1.240 0.296
    OP2 amplitude −0.070 −0.603 to 0.464 0.786
    OP3 amplitude 0.605 −0.356 to 1.565 0.202
    OP4 amplitude −1.686 −2.865 to −0.508 0.008
Retinal venular caliber
    OP1 amplitude −0.555 −2.078 to 0.967 0.442
    OP2 amplitude −0.224 −1.262 to 0.815 0.647
    OP3 amplitude 1.798 −0.213 to 3.809 0.075
    OP4 amplitude −2.837 −5.654 to 0.020 0.055
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