Cortical hyperexcitability and sensitivity to discomfort glare

AbstractIt is well established that there are two main aspects to glare, the visual impairment and the discomfort, known as disability and discomfort glare, respectively. In contrast to the case of disability glare we understand very little about the underlying mechanisms or physiology of discomfort glare. This study attempts to elucidate the neural mechanisms involved using fMRI and glare sources with controlled levels of retinal illuminance. Prior to carrying out the fMRI experiment, we determined each participant's discomfort glare threshold. The participants were then divided into two groups of equal size based on their ranked sensitivity to discomfort glare, a low and high sensitivity group. In the fMRI experiment each participant was presented with three levels of glare intensity whilst simultaneously required to carry out a simple behavioral task. We compared BOLD responses between the two groups and found that the group more sensitive to glare had an increased response that was localized at three discrete, bilateral cortical locations: one in the cunei, one in the lingual gyri and one in the superior parietal lobules. This increased response was present for all light levels tested, whether or not they were intense enough to cause discomfort glare. Based on the results, we present the case that discomfort glare may be a response to hyperexcitability or saturation of visual neurons

Changes in color vision with decreasing light level: separating the effects of normal aging from disease.

The purpose of this study was to obtain additional information about the health of the retina (HR) by measuring the rate of loss of chromatic sensitivity with decreasing light level. The HR(index) is introduced to separate the effects of normal aging from early stage disease. For normal subjects the HR(index is largely independent of age (r(2)~0.1), but ~11% of clinically normal, asymptomatic, older subjects exhibit values below the 2σ limit. The HR(index provides a single number that captures how light level affects chromatic sensitivity irrespective of age and can be used to screen for preclinical signs of retinal disease

Understanding disability glare: light scatter and retinal illuminance as predictors of sensitivity to contrast

The presence of a bright light in the visual field has two main effects on the retinal image: reduced contrast and increased retinal illuminance due to scattered light; the latter can, under some conditions, lead to an improvement in retinal sensitivity. The combined effect remains poorly understood, particularly at low light levels. A psychophysical flicker-cancellation test was used to measure the amount and angular distribution of scattered light in the eye for 40 observers. Contrast thresholds were measured using a functional contrast sensitivity test. Pupil-plane glare-source illuminances (i.e. 0, 1.35, 19.21 lm/m2), eccentricities (5°, 10°, 15°), and background luminances (1, 2.6, 26 cd/m2) were investigated. Visual performance was better than predicted, based on loss of retinal image contrast caused by scattered light, particularly in the mesopic range. Prediction accuracy improved significantly when the expected increase in retinal sensitivity in the presence of scattered light was also incorporated in the model

The unseen color aftereffect of an unseen stimulus: Insight from blindsight into mechanisms of color afterimages

We show here that, in the absence of a direct geniculostriate input in human subjects, causing loss of sight in the visual half-field contralateral to the damage, the pupil responds selectively to chromatic modulation toward the long-wavelength (red) region of the spectrum locus even when the stimulus is isoluminant for both rods and cones and entirely restricted to the subjects’ “blind” hemifields. We also show that other colors are less or wholly ineffective. Nevertheless, red afterimages, generated by chromatic modulation toward the green region of the spectrum locus, also cause constrictions of the pupil even when green stimuli are themselves completely ineffective in the blind hemifield. Moreover, human subjects with damage to or loss of V1 are typically completely unaware of the stimulus that generates the aftereffect or of the aftereffect itself, both of which can be seen clearly in normal vision. The results show that pupillary responses can reveal the processing of color afterimages in the absence of primary visual cortex and in the absence of acknowledged awareness. This phenomenon is therefore a striking example of “blindsight” and makes possible the formulation of a model that predicts well the observed properties of color afterimages

Acuity and colour vision changes post intravitreal dexamethasone implant injection in patients with diabetic macular oedema - Fig 2

<p><b>CAD results before and after Ozurdex treatment in two subjects with diabetes (A- subject 11; B- subject 4).</b> Both subjects show significant improvement in chromatic sensitivity (i.e., smaller thresholds) post treatment. The grey, dotted lines show the colour limits imposed by the phosphors of the display. Subject B was unable to detect YB colour changes, even for the largest chromatic signals that are limited only by the phosphors of the display with no improvement post treatment. The RG thresholds, on the other hand, show significant improvement post-treatment.</p