Journal of Clinical Ophthalmology and Research

: 2021  |  Volume : 9  |  Issue : 3  |  Page : 99--102

Loss of visual function in diabetes mellitus

Sanaa Mohammed Konnakkodan, Valsa T Stephen, Rajeevan Palpoo 
 Department of Ophthalmology, Government Medical College, Kozhikode, Kerala, India

Correspondence Address:
Sanaa Mohammed Konnakkodan
22/325 B1 Mafaza, Vayalveede Parambe, Thiruvannur P.O, Calicut- 673 029, Kerala


Background: Diabetes mellitus being a well-known cause for peripheral neuropathy, this study aims to detect visual pathway dysfunction in diabetics using contrast sensitivity as a subjective measure and visual-evoked potential (VEP) as an objective measure of visual pathway function. Aims: To compare contrast sensitivity and VEP in patients with type 2 diabetes mellitus as compared with control and to find the correlation with glycemic level. Materials and Methodology: This was a comparative study conducted at a tertiary eye care center. After detailed ophthalmological evaluation, contrast sensitivity and VEP of 40 patients with diabetes (20 with retinopathy and 20 without retinopathy) were compared with suitable control. Data were analyzed using the SPSS (Statistical Product and Service Solutions) version 18 using the independent sample t-test and ANOVA. Results: There was reduction of mean contrast sensitivity in diabetics as compared to nondiabetics. Contrast sensitivity was better in diabetics without retinopathy as compared to diabetics with retinopathy. There was prolongation of P100 latencies and reduction of P100 amplitudes among diabetics as compared to non-diabetics and among those with diabetic retinopathy as compared to those with normal fundus. Reduced contrast sensitivity and reduction of P100 amplitudes were seen among those with poor glycemic control. Conclusion: There was evidence of reduction of contrast sensitivity and alteration of VEP in patients with diabetes even before reduction in visual acuity giving evidence of visual pathway dysfunction in diabetes mellitus. This may also be affected by the glycemic status of the patient.

How to cite this article:
Konnakkodan SM, Stephen VT, Palpoo R. Loss of visual function in diabetes mellitus.J Clin Ophthalmol Res 2021;9:99-102

How to cite this URL:
Konnakkodan SM, Stephen VT, Palpoo R. Loss of visual function in diabetes mellitus. J Clin Ophthalmol Res [serial online] 2021 [cited 2023 Jun 8 ];9:99-102
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Full Text

Globally, 422 million adults are diabetic as of 2016[1] which includes 62 million Indians.[2] Type 2 diabetes accounts for 85%–90% of these cases.[3] Diabetes increases risk of blindness by 25 times with 7%–29% of these patients developing diabetic retinopathy. Vision loss due to diabetes is largely attributed to diabetic retinopathy, early onset cataract, and glaucoma. However, not much emphasis has been placed on the loss of visual function in diabetes considering that a wide variety of disturbances affecting the central and peripheral nervous system either directly or indirectly are seen in diabetic patients. This study attempts to investigate this loss of visual function in diabetes both related to and independent of status of diabetic retinopathy. Visual pathway function is assessed in this study using contrast sensitivity as a subjective measure and visual evoked potential (VEP) as an objective measure. This study aims to compare VEP and contrast sensitivity in patients with diabetes mellitus as compared with control and to find out the correlation between glycemic level with VEP and contrast sensitivity.

 Materials and Methodology

This study was conducted at a tertiary eye care center after obtaining clearance from the ethics committee. The sample size was calculated using the following formula n = (2× (z1-σ/2 + z1-β) σ2)/d2.

Minimum sample size was calculated as 19. For the purpose of the study, we selected 40 diabetics (20 with retinopathy and 20 without retinopathy) and 40 nondiabetics. Patients with a established diagnosis of type 2 diabetes mellitus referred to ophthalmology outpatient department for screening for the presence of diabetic retinopathy with duration of diabetes between 1 and 5 years and who were willing to participate in the study were included after obtaining informed consent. Patients with a history of cerebrovascular accidents, ocular comorbidities including relative afferent pupillary defect, disc edema, defective color vision, previous treatment for diabetic retinopathy including laser treatment and intravitreal injections, patients with clinically significant macular edema, and best-corrected visual acuity <20/60 were excluded from the study. Controls were selected from patients who attended ophthalmology outpatient department for refractive errors and prescription of glasses. All participants were evaluated in detail regarding diabetic status. As per the criteria defined by the American Diabetic Association, diabetes is diagnosed when fasting blood sugar (FBS) values are ≥126 mg%, 2 h postprandial blood sugar value was ≥200 mg% and glycated haemoglobin (HbA1c) ≥6.5%.[4] Among diabetics, FBS <126 mg% was taken as good recent glycemic control. The HbA1c test measures average blood sugar over the past 3 months. Mean HbA1c <6.5% was taken as good long term control. They were then subjected to a thorough ophthalmological examination including visual acuity and contrast sensitivity testing using Pelli Robson Contrast sensitivity charting. The chart consists of triplets. The contrast decreases from one triplet to the next. The log contrast sensitivity varies from 0.00 to 2.25. The subject's sensitivity is indicated by the finest triplet for which two of the three letters are named correctly. For pattern stimulation, the visual acuity of the participants was recorded and the subjects were optimally refracted for the viewing distance of the screen. A constant distance of 100 cm was maintained between the television screen and each subject. VEPs was recorded through pattern reversal stimulation with small checks (15') and large checks (60') using a checkerboard. Skin electrodes were used for recording VEPs. These include three scalp electrodes, i.e., frontal, occipital, and grounding. The aim is to achieve maximal stimulation of the foveal and parafoveal fibers at 75% contrast and a reversal rate of 1.2 Hz. An average of 100 sweeps of stimuli will be given to each eye per pattern used. The P100 latencies and amplitudes on testing with 60' check size was studied. Recording of ocular tension and fundus examination under mydriasis using 90 D lens was done. Diabetic retinopathy was graded using Early Treatment Diabetic Retinopathy Study classification into very mild, mild, moderate, severe, and very severe nonproliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopathy.[5] Data were analyzed using the SPSS (Statistical Product and Service Solutions) software version 18 SPSS is currently owned by International Business Machines Corporation (IBM) headquartered in Armonk, New York, United states of America. using independent sample t-test for comparison between groups and one-way ANOVA for multiple groups. P < 0.05 was considered statistically significant, whereas P > 0.05 was considered to be not statistically significant.


The sample population was age and sex matched. The mean age of diabetics was 55.5 years (37–74 years) and nondiabetics was 56.23 years (40–74 years). Male: female ratio in this study was 1:1 among both diabetics and nondiabetics.

Of the 40 diabetics, only 8 had an FBS <126 mg% and 12 patients had HbA1c values <6.5%.

Among the patients with diabetes, 21 eyes had findings of mild NPDR, 13 eyes had findings of moderate NPDR, and 6 eyes had findings of severe NPDR.

We found that contrast sensitivity was reduced in diabetic patients (1.1194 ± 0.19) when compared to nondiabetics (1.2937 ± 0.20) (P < 0.001). Analysis showed a reduction in mean contrast sensitivity values from 1.2937 ± 0.20 in nondiabetics to 1.2113 ± 0.22 in diabetics even prior to onset of retinopathy changes and worsened further with onset of retinopathy to 1.0275 ± 0.23(P < 0.001).On reanalysing with adjustment for vision as confounding factor the changes persisted. In group with 20/20–20/30 vision, the mean contrast sensitivity was 1.3095 ± 0.20 in nondiabetics (n*=74) as compared to 1.2090 ± 0.20 in diabetics (n* =50) (P = 0.006). Similar findings were observed in the group with 20/40–20/60 vision, the contrast sensitivity was 1.1000 ± 0.25 in nondiabetics (n* =6) as compared to 0.9700 ± 0.22 in diabetics (n* =30) (P = 0.182) (*n = number of eyes).

Glycemic control in the form of HbA1c seems to influence contrast sensitivity values with improvement of mean contrast sensitivity from 1.0848 ± 0.27 in those with HbA1c ≥6.5% as compared to 1.200 ± 0.14 in diabetics with HbA1c <6.5% (P = 0.046). Contrast sensitivity was 1.1813 ± 0.15 in those with FBS <126 mg/dl as compared to 1.1039 ± 0.26 in those with FBS ≥126 mg/dl (P = 0.246). On checking for correlation between contrast sensitivity and HbA1c, we got a Pearson coefficient value of − 0.343 showing negative correlation. This means that with increase in HbA1c values there is worsening of contrast sensitivity.

On comparing pattern reversal VEP among diabetics and nondiabetics [Table 1] the P100 latencies were prolonged in both right and left lobes and the P100 amplitudes were reduced in right and left lobe in diabetics when compared to nondiabetics.{Table 1}

The comparison of VEP between nondiabetics, diabetics without retinopathy, and diabetics with retinopathy [Table 1] showed a progressive increase in P100 latencies in right and left lobe and reduction of P100 amplitudes in right and left lobe as we move from nondiabetics to diabetics without retinopathy to diabetics with retinopathy.

Recent control of diabetes seems to influence VEP with a reduction of P100 amplitudes among those with FBS ≥126 mg/dl as opposed to those with FBS <126 mg/dl [Table 2].{Table 2}

HbA1c values had an influence on VEP with reduction of P100 amplitude among those with HbA1c values ≥6.5% as compared to those with values <6.5% though the findings were not statistically significant [Table 2].


In our study, we found that contrast sensitivity was reduced in diabetic patients when compared to nondiabetics and there was reduction of contrast sensitivity in diabetics without retinopathy which reduced further in diabetics with retinopathy changes. This was similar to the findings in the study by Stavrou and Wood et al.[6] and Beszédesová et al.[7]

We found that poor glycemic control produces a reduction of contrast sensitivity which was similar to the findings in a study by Misra et al.[8] In this study, the authors suggested that the pathogenesis behind the reduction of contrast sensitivity in diabetics was the involvement of the ganglion cells causing changes in retinal function secondary to carbohydrate metabolism alteration rather than a microvascular complication. On the other hand, Stravou and Wood[6] believe both metabolic and vascular changes to be involved in the reduction of contrast sensitivity in diabetic patients with little or no diabetic retinopathy.

According to Dosso et al.,[9] retinal parenchyma is very susceptible to the modification of carbohydrate metabolism which might explain the effects of glycemic control on contrast sensitivity.

We found a reduction in contrast sensitivity even when the vision was normal or minimally affected. According to Misra et al.,[8] this dissociation of contrast sensitivity and visual acuity suggests that the measurement of contrast sensitivity discloses visual functions that are different from those that underlie visual acuity. With the added advantage of it being a noninvasive functional test, measurement of contrast sensitivity has been found to be useful in detecting the early effects of diabetes mellitus on neural activity. Furthermore, Nasralah et al.[10] have suggested that contrast sensitivity appears to be a more sensitive test of retinal function compared to visual acuity.

Our study demonstrated increased latencies and reduced amplitudes in diabetics as compared to nondiabetics. In a study by Algan et al.,[11] P100 wave latency was found to be significantly longer in diabetic patients as compared to normal controls. Similar study by Chopra et al.[12] found that there was significantly prolonged N70 and P100 latencies in diabetic patients and found a significant correlation between the delay in the P100 latency and the duration of the disease. This study concluded that abnormality of VEP can be used for the early diagnosis of central neuropathy.

Similar study by Gayathri et al.[13] found prolongation of P100 and N75 latencies and a decrease in amplitude of VEP in the diabetes mellitus group, when compared with the control group. The participants with poor metabolic control showed an increase in latencies, when compared with the participants having good metabolic control. It was observed that there was a prolongation in VEP latencies and reduction in amplitude in diabetic group as the duration increased.

The impact of duration of diabetes mellitus on VEP latencies and amplitudes could not be analysed in our study as our sample population were all early onset diabetics with duration since detection of diabetes <5 years.

Abnormal VEP in diabetes mellitus may be due to structural damage to myelinated optic nerve fibers or retinal ganglion cells as suggested by the findings of Eswaradass and Kalidoss[14] Hence, VEP is a noninvasive and sensitive screening tool for detecting early neurological involvement in diabetes mellitus.

Karlica et al.[15] concluded that the progressive increases in VEP latency values was a direct sign of retinal ganglion cell damage, that takes place even before the first ophthalmoscopically detectable signs of diabetic retinopathy arise. They concluded that, VEP can be considered as a valid method for detecting prediabetic retinopathy, which could contribute greatly to the prevention of diabetic retinopathy complications.

Dolu et al.[16] concluded that evoked potentials are useful as an investigational method in establishing neuropathy developing in the central nervous system. Their study evaluated various electrophysiological tests in 51 patients with type 2 diabetes.


Our study found changes in contrast sensitivity and VEPs in diabetics which point to the presence of visual pathway dysfunction in diabetes mellitus which occurred even before the development of diabetic retinopathy or overt signs of neuropathy. These changes were found to occur even when visual acuity was normal which points to the importance of detailed evaluation of diabetics complaining of visual distress who seem to be otherwise normal on ophthalmic evaluation. The reduction of contrast sensitivity with elevated HbA1c values stresses the need for strict glycemic control to prevent loss of visual function in diabetes.

This study hence points to the hidden burden of subtle dysfunction of the central nervous system which may explain unexplained visual loss in diabetic patients. An understanding of the extent and mechanisms of damage to the central nervous system in diabetes is a frontier for further research in the same.

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Conflicts of interest

There are no conflicts of interest.


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