This study aimed to investigate the effects of glaucoma on the perception of the contrast of visible, suprathreshold stimuli. Consistent with previous studies, contrast detection thresholds were increased in the glaucoma group within visual field defects relative to age-similar controls.
13,17 However, the perception of suprathreshold contrast was similar between the control and glaucoma groups, particularly in the more suprathreshold higher reference contrast condition. This unaltered perception of suprathreshold stimulus contrast for participants with glaucoma was present both within and outside of visual field defects as measured by perimetry. These results provide further evidence that common depictions of what glaucoma patients see, such as “black tunnel” effects and grayed-out regions, do not accurately represent the perception of scenes by people with glaucoma.
2,3 Further, the unaltered perception of suprathreshold contrast may be a factor in the lack of symptoms experienced by many people with early glaucoma, despite significant sensitivity loss measurable by perimetry.
Our finding of spatial frequency independent, near-veridical perception of suprathreshold contrast in healthy vision is consistent with previous literature where it has been termed “contrast constancy.”
6–10,27 Although the neural mechanisms underpinning contrast constancy are undetermined, a number of mechanisms have been hypothesized.
6,7,10 First, it has been widely proposed that a number of independent channels tuned to different spatial frequencies exist within the visual system to deconstruct and interpret the image.
4,28–30 Georgeson and Sullivan proposed that changes in contrast gain within these channels under suprathreshold conditions could compensate for the attenuation in sensitivity to high and low spatial frequencies at threshold, thus equalizing the visual system's response to suprathreshold stimuli of varying spatial frequencies.
6 Swanson et al.
10 extended this concept further by developing a model that could predict contrast matching data from contrast thresholds using a small number of medium bandwidth mechanisms tuned to differing spatial frequencies. The model demonstrated that the visual system's response to varying spatial frequencies could be normalized by adjusting the slope of the contrast transfer function (contrast gain) of individual mechanisms within the model.
10 Brady and Field,
7 however, proposed an alternative model that assumes contrast gain remains constant across spatial frequency channels under suprathreshold viewing conditions. Brady and Field suggested that contrast constancy is a result of the visual system's response to the signal alone rather than detection thresholds that are affected by the signal to noise ratio.
7 Brady and Field proposed that higher spatial frequency channels respond to noise more than mid-range spatial frequency channels, resulting in a reduced signal-to-noise ratio and increasing detection thresholds for high spatial frequency stimuli.
7 However, their empirical data show contrast constancy as soon as stimuli are suprathreshold, which is inconsistent with other literature showing a gradual flattening of contrast matching functions with increasing suprathreshold contrast.
6,10,27,31
The results of this study suggest that the mechanisms underlying contrast constancy in the healthy visual system may be intact in glaucoma and able to compensate for pathologic loss of sensitivity. Alternatively, or additionally, further mechanisms may aid compensation for sensitivity loss. It is possible that loss of sensitivity may be accompanied by decreased perceptual surround suppression via alterations to the gain and/or inhibition of downstream visual mechanisms. This may enable an overall perceptual response broadly similar to the predisease state to be maintained despite the decreased sensory input and, combined with existing contrast constancy mechanisms, may be one possible explanation for the present findings. A recent study has investigated two measures of lateral inhibition in the relatively intact central visual field of people with advanced glaucoma, finding no difference from healthy controls.
32 One of their measures, the difference in log contrast sensitivity between 1 and 4 c/deg can also be tested in our data. On this measure we also found no differences between any of the groups (
P = 0.92, linear mixed model), suggesting that there is no change in lateral inhibition between glaucoma within or outside visual field defects and healthy participants. Further research is needed to explore the mechanisms underlying suprathreshold contrast perception in glaucoma.
The results of this study are consistent with previous studies investigating suprathreshold contrast perception in other disorders of the visual system, including amblyopia
9 and nystagmus.
33 In people with atrophic AMD, exudative AMD, and juvenile macular degeneration, Mei et al.
31 found that, despite a flattening of the contrast matching functions, there was still a significant difference in contrast matching data between controls and those with maculopathy, although not as large as the difference between detection thresholds. This finding may be explained by not testing participants with maculopathy sufficiently far above threshold to reach contrast constancy; the highest contrast tested was 0.56, and all observers were assessed at the same contrast levels despite the maculopathy group having increased detection thresholds, relative to controls.
31
Because our everyday visual environment is dominated by suprathreshold contrast, the findings of this study provide some insight into the everyday visual experience of people with glaucoma. However, there are several reasons why our results should be interpreted with caution when considering everyday vision. First, participants were tested monocularly; thus, we are unable to comment on the effects of binocular interactions or the compensation for visual field defects in one eye by relatively intact corresponding visual field in the fellow eye. Further assessment of vision in glaucoma under binocular viewing conditions would be valuable in furthering our understanding of the daily visual experience of those with glaucoma. Second, we used simple Gabor stimuli to enable precise control of stimulus parameters, such as spatial frequency, contrast, and eccentricity. However, findings using these stimuli may not accurately reflect vision under complex natural viewing conditions. Studies have shown that the visual system responds differently to complex stimuli and natural scenes compared with simple stimuli,
34 so further work investigating apparent contrast in natural scenes in glaucoma may be valuable. Finally, a further potential limitation of the present study is that the contrast-matching paradigm used assumes that participants’ central vision was normal, but we did not measure foveal contrast sensitivity directly using the Gabor stimulus. Some studies have shown changes to central vision in early glaucoma.
35 Changes to contrast perception in central vision cannot explain our results, however, because apparent contrast of stimuli both within and outside of visual field defects, where contrast detection thresholds were markedly different, was close to veridical (
Figs. 3b and
4). Decreased apparent contrast of the central stimulus, if present, could only explain the contrast matches in one, but not both, visual field regions.
The results of this study do not imply that people with glaucoma do not experience visual impairment. Whatever the mechanism of the unaltered suprathreshold contrast perception observed herein, there is no mechanism that could compensate for a total loss of retinal input. Thus, when all retinal ganglion cells signaling a region of visual field are lost, that area becomes blind. Related, we were unable to test most participants with glaucoma within their visual field defect at four times the detection threshold reference contrast with the 4 c/deg stimulus. This was because detection thresholds for this stimulus were elevated beyond 25% contrast; thus, the appropriate reference contrast (>100%) could not be produced. A contrast detection threshold of 25% in this study was approximately four times the mean normal contrast detection threshold for the medium spatial frequencies. In clinical perimetry, a detection threshold four times higher than normal equates to a loss of 6 dB. Although the detection thresholds measured in this study are not directly comparable with perimetric thresholds owing to differences in the stimulus and its presentation, it is clear that many more advanced glaucomatous visual field defects would cause contrast detection thresholds to be increased beyond 25% contrast. Therefore, although our results are consistent with early glaucoma being asymptomatic, they are also compatible with more advanced glaucoma causing visual impairment.
This study has demonstrated that people with glaucoma perceive the contrast of visible, suprathreshold Gabor stimuli similarly to age-similar healthy observers despite decreased contrast sensitivity. This finding is consistent both within and outside of clinically measured visual field defects. The results suggest active or passive compensation for reduced sensory input in the damaged visual system that normalizes responses to suprathreshold contrast, possibly similarly to the mechanisms of contrast constancy in normal vision. The results also provide further evidence for the inaccuracy of common depictions of vision with glaucoma that show black or gray areas obscuring scenes. Further research is required to explore these mechanisms and to better understand the daily perceptual experience of people with glaucoma.