Ⅰ. Introduction
Anisometropia or some differences in the refractive state of the two eyes is common in myopic patients. Myopic anisometropia is defined as a difference in myopic spherical equivalent (SE) refractive errors of 1.00 D or more between the two eyes of an individual.1) In non-amblyopic myopic anisometropes, no significant difference was observed in visual acuity and in total higher-order monochromatic aberrations between the two eyes.
In binocular vision most people have a dominant eye, even though each of two eyes provide equal vision. The dominant eye is not always the eye with better visual acuity. In myopic anisometropia, Wang et al.2) found no significant relation between ocular dominance and difference in SE power between dominant and non-dominant eye in myopic anisometropia of 1.0~1.75 D. However, in myopic anisometropia over SE 1.75 D group, the degree of myopia was significantly higher in non-dominant eyes than dominant eyes. Ocular dominance have tendency to prefer visual input from one eye or functional superiority and preferential use of one eye over the other.3) Ocular dominance plays a role in reading4) that dominant eye shows greater accommodative response during binocular viewing.5) Thus, it is assumed the non-dominant eye will be easier to suppress blur image than dominant eye3) that monovision success for presbyopia correction is that the imbalance of sensory dominance interfere with binocular visual function. Sensory dominance interference may lower the success of mono-vision for presbyopia correction.
During the binocular vision in anisometropia, Koh and Charman6) found that during binocular viewing, both eyes of anisometropia stimulated with unequal accommodative demand, that the eye which requires the least accommodative demand effort to maintain clear image and controls the accommodative response in both eyes7) that the retinal images of the two eye are not equal. Anisometropia also results in anisometropic aniseikonia that there are significant difference in perceived size of retinal images, however, human eyes recognize one clear image through the sensory fusion in visual cortex.8)
If blurry and anisometroic images are focused on the one retina, binocular rivalry of two different stimuli on to each eye, these stimuli compete for temporary perceptual dominance that these images of the two eyes cannot be fused and decreased quality of visual acuity, reduction of contrast sensitivity and stereopsis can be found.9) Uncorrected anisometropia can be lead to amblyopia in children because it inhibits sensory fusion and suppress the image of the one eye.10,11)
Numerous studies have used an intermittent stimulus presentation to evaluate the stages of processing associated with perceptual reversals using event-related potential (ERP) components.12) ERP is an electrical neuroimaging approach and is identical to the prestimulus EEG topography that reflects perceptual reversals during binocular rivalry.13)
ERP records stimulus which is related to visual perception. Human faces evoke a negative potential between 130 and 200 msec (N170) after onset of the facial stimulation that the N170 of ERP is thought to reflect the visual processing related to facial perception of human faces.14-16) It is different from visual evoked potential (VEP) which is used for the detection of basic visual response related to simple stimulus. There are many previous studies that explores the initial visual response in P100 using the VEP, however there was few study on the visual cognition in N170 using ERP.
Monovision is the correction of one eye with the required distance refractive power and the other eye with the required near refractive power to correct presbyopia. For many years, it was the most popular form of contact lens correction for presbyopia and pseudophakic monovision surgery.17,18) By making the refraction targets to distant for one eye and to near for another one, the patients would have both clear distant and near vision. This approach is based upon the principle that the visual system can alternate suppression between the two eyes when viewing is alternating between distance and near targets.
In this study, we investigated ERP changes of P100 and N170 to the facial expression stimuli at the intermediate distance in the induced anisometropia using plus-powered contact lenses to understand visual recognition responses in the anisometropia and monovision correction.
Ⅱ. Methods
1. Subjects
Fifteen volunteers were participated in this study. Exclusion criteria included spectacle-corrected visual acuity (VA) worse than 0.00 logMAR in each eye, myopia < 2.00 D, astigmatism > 0.75 D, anisometropia > 0.50 D, abnormal accommodative amplitude in their age, and any history of refractive or other ocular surgery. The study was approved by the Institutional Review Board (Ispaik-2017-04-002-003).
2. Procedure
1) Method of induced anisometropia
Dominant eye was determined by ‘hole in the card’ method. An anisometropia was induced using contact lenses with additional +1.00 and +2.00 D power over the refractive power in non-dominant eye. ERP was measured monocularly (dominant eyes, non-dominant eyes) and binocularly.
2) ERP recording
ERP was measured under the 100 lx illuminance condition and at 80 cm distance to record using computer. The ERP signals were recorded using a Neuroscan Synamps 2 (Compumedics, EI paso, TX, USA). Electrode impedance was maintained at < 5 kΩ. EEG data was recorded with a 0.1~100 Hz band pass filter at a sampling rate of 1,000 and 60 Hz noise was removed using a notch filter. The recorded EEG data were pre-processed using Scan 4.3 software (Compumedics). Horizontal eye movements and blink were removed in the pre-processing. Data were epoched from –200 ms before stimulus onset to 500 ms after stimulus onset. The epoches were subtracted from the average value of the pre-stimulus interval for the baseline correction.
3) Facial expression stimulation
To investigate the fusional and suppressional functions of facial perception in anisometropia, the stimuli used in this experiment were facial expression of neutral and sad using Eprime 2 program. Human face is the most distinguishable object in the visual response that facial expressions were used as visual stimuli. Among facial expressions, neutral and sad expressions are similar to each other and difficult to distinguish, so it was considered as suitable object for this study. The face stimulus size was 9.4 cm high and 7.5 cm wide. Stimulus presentation time is + target 100 ms, blank 500 ms, neutral/sad 500 ms, total 126 sample/cycle. Total experiment time was 5 minutes. When participants look at the neutral expression, they press the key number 1 and for the sad expression, they press the key number 2 to distinguish facial expressions between neutral and sad. In the ERP, P100 is related to the initial visual response related to Broadmann 17 area,16) and N170 is related to facial perception related to Broadmann 18 and 19 area,17) that we investigated the amplitudes and latency of P100, N170 in the induced anisometropia.
4) ERP analysis
The ERP signals were analyzed by program with Curry 7. The ERP signal graphs were extracted at –200 ms before stimulus onset and 500 ms after stimulus onset. Channels O1 and O2 were used for analysis of P100, and PO7, P7, PO8, and P8 channels were used for analysis of N170. P100 was extracted in 80 to 120 ms, and N170 was extracted ins 140 to 180 ms.
3. Statistic analysis
SPSS ver. 18 (SPSS Inc., Chicago, IL, USA) was used for the statistical analysis. The Shapiro-wilk test was used to perform a normality test. Repeated measurements were compared with the ANOVA test for recognizing cognition response about between normal and two types of induced anisometropia. Post-hoc analysis was performed using Bonferroni test.
Ⅲ. Results
1. Subjects
Fifteen volunteers with an average age of 26±1.60 years were participated in this study. Average spherical equivalent of participants was –3.61±1.06 D, anisometropia grade was 0.35±1.04 D (Table 1).
2. Monocular initial visual and face perception responses
1) P100 components
The P100 amplitude related to initial visual response of dominant eyes was 3.40±0.72 ㎶, and that of the non-dominant eyes was 4.05±0.80 ㎶ in the isometropia. The P100 components in the non-dominant eyes of induced 1.00 and 2.00 D were 4.57±0.69 ㎶, and 4.91±0.91 ㎶ respectively. The P100 amplitudes of dominant eyes was significantly smaller than non-dominant eyes, 1.00 and 2.00 D induced anisometropic eyes (F=4.04, p=0.010) (Table 2).
The P100 latency of dominant eyes, non-dominant eyes, 1.00 and 2.00 D induced anisometropic eyes were 105.10±3.70, 114.50±3.57, 106.77±4.64, and 107.40±3.92 ms respectively. The non-dominant eyes presented longer P100 latency than dominant, 1.00 and 2.00 D induced anisometropic eyes, however there are no significant difference among them (F=1.64, p=0.200) (Table 2).
2) N170 components
The N170 amplitudes of dominant eyes, non-dominant eyes, 1.00 and 2.00 D induced anisometropic eyes were –5.99±1.10, -5.42±1.09, -4.68±0.67, and –4.66±0.89 ㎶ respectively. The N170 amplitudes of dominant eye of isometropia presented greater value among them (F=3.01, p=0.040) (Table 3), and presented greater value than induced 1.00 and 2.00 D anisometropic eyes significantly (p=0.030 and p=0.270, respectively).
The N170 latency of dominant eyes, non-dominant eyes of 1.00 and 2.00 D induced anisometropic eyes were 159.02±3.19, 164.30±4.15, 165.42±5.05, and 162.93±4.34 ms respectively. The N170 latency of dominant eyes showed lower value than non-dominant eyes, 1.00 and 2.00 D induced anisometropic eyes, however there was no significant difference among the values (F=2.86, p=0.050) (Table 3).
3. Binocular initial visual and face perception responses
1) P100 components
The P100 amplitude of ERP of isometropia was 7.37±0.98 ㎶, and that of the 1.00 and 2.00 D induced anisometropia was 7.28±1.06 and 8.41± 0.93 ㎶ respectively and there was no significant difference among isometropia and two induced anisometropia (F=3.02, p=0.070) (Table 4) (Fig. 2).
The P100 latency of isometropia was 99.63±3.90 ms and that of 1.00 and 2.00 D induced anisometropia was 100.17±3.21 and 103.37±3.41 ms, and there was no among them (F=1.16, p=0.320) (Table 4) (Fig. 2).
2) N170 components
The amplitudes of N170 of isometropia, which is related to cognition response in facial perception, was –10.06±1.38 ㎶ and those of the 1.00 and 2.00 D induced anisometropia were –9.33±1.24 ㎶ and –8.23±1.19 ㎶. There was significantly difference between isometropia and induced anisometropia (F=5.20, p=0.010). N170 amplitude in the isometropia revealed greater than that of 1.00 and 2.00 D induced anisometropia, however, there was no significant difference in the N170 amplitude between 1.00 and 2.00 D induced anisometropia (p=0.540) (Table 5) (Fig. 3).
The latency of N170 component of isometropia was 148±2.26 ms and those of 1.00 and 2.00 D of induced anisometropia was 150.55±2.35 and 152.32±2.42 ms. There was significant difference between isometropia and induced anisometropia and in the 1.00 and 2.00 D induced anisometropia, there was significant difference between them (F=6.29, p=0.010) (Table 5) (Fig. 3).
Ⅳ. Discussion
In this study, we investigated visual recognition responses related to facial expressions in the induced anisometropia. In the isometropic eyes, the P100 which is related with the initial visual response, amplitude of non-dominant eye was stronger than the non-dominant eye. The amplitude and latency in N170 component which is related to visual recognition response, the amplitude of non-dominant eye was weaker in non-dominant eye than dominant eye. Wang et al.19) reported the P100 amplitude and latency of dominant eyes revealed larger and longer than non-dominant eyes, however in this study P100 amplitude of dominant eyes was weaker and no difference in the latency.
In the induced anisometropic eyes (1.00 and 2.00 D), the P100 amplitudes were stronger compared with isometropic dominant eye, and no difference in the latencies. The N170 amplitudes were weaker compared with isometropic dominant eye, and no difference in the latencies. From these results the initial visual responses in the 1.00 and 2.00 D anisometropic non-dominant eyes were stronger than dominant eyes monocularly, and those results could suggest blurred images of 1.00 and 2.00 D induced anisometropic eye can be recognized as a noise and response strongly in the brain.
In binocular condition of in the 1.00 and 2.00 D anisometropic eyes, the P100 amplitudes and latencies were not different with the isometropic eyes. The N170 amplitude an latency of 1.00 and 2.00 D anisometropic eyes were weaker and longer than isometropic eyes. And as the amount of anisometropia was larger, the amount of N170 amplitude was weaker and the amount of latency was longer. These results were different from those of previous studies. Katsumi et al.20) found as the level of aniseikonia increased, P100 amplitude and latency were smaller and longer. Plainis et al.21) reported the P100 amplitude and latency of 1.00 and 2.00 D induced anisometropia were smaller and longer than normal eyes in VEP. We thought it is because of the method of inducing anisometropia. In the previous studies, an anisometropia was induced with spectacle glasses that larger induced anisekonia can be occurred, which reduce the amplitude value. Lew et al.22) reported 1.89 and 3.17% of aniseikonia was induced in the 1.00 and 2.00 D anisometropia respectively. Thus, in the 2.00 D anisometropia, participants accepted the stronger stimuli because of the different size of images. In our study we used contact lenses to induce anisometropia because it did not affect on aniseikonia significantly that the initial visual responses could be stronger in anisometropic eyes. In the binocular fusion it is thought that defocused image of one eye could be suppressed or fused through sensory fusion, which shows a cognition response similar to isometropic eyes. However, the visual signal may be weakened and it could take more time to recognize in the brain. And in the 2.00 D anisometropic eyes presented a stronger initial visual response, however showed weaker and longer response in recognition response than 1.00 D anisometropic eyes. It is thought that in the 2.00 D anisometropic eyes, the initial visual response is strong because it is difficult to recognize blurred images in the brain, and also it is difficult to recognize the object because of imperfect binocular summation that the recognition related visual stimulus appears weakly.
Studies on anisometropia have difficulties in recruiting subjects, and therefore there aren't many studies on induced anisometropia. Anisometropia also result in anisometropic aniseikonia that causes different retinal image size. Moreover, aniseikonia causes abnormal binocular function such as decreased quality of visual acuity and stereopsis. We found the weaker stimulus and longer response in recognition response with 1.00 and 2.00 D anisometopic eyes that decreased visual acuity and stereopsis could be occurred in eyes with monovision correction. Monovision contact lenses with 1.00~2.00D addition are prescribed to facilitate near works for early presbyopia and could be prescribed for young adults with lack of accommodative function. Monovision is a prescription that cause anisometroic state in both eye that recognition response of monovision could be similar with an induced anisometopia.
Up to now, there was no study of visual recognition response about facial perception in anisometropia using ERP. So, this study is meaningful not only help to understand recognition response of anisometropia, but also helpful for the visual response of monovision. We suggest for the success of monovision, it would be good to prescribe the addition powers less than 2.00 D. This study is expected to be a reference for the theoretical background related to the visual recognition response of anisometropia and also provide information on the prescribe monovision correction for the accomodative deficiency.
Ⅴ. Conclusion
It was found that the induced anisometropic non-dominant eyes had a stronger initial visual response and had a weaker recognition response than the dominant eye in the monocular state. However, in the binocular vision induced anisometropia had a weaker stimuli and took more time to recognize in the brain. And the amount of anisometropia was larger, the amount of N170 amplitude was weaker and the amount of latency was longer.
