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The Forced Choice Test (FCT) can be used to detect malingered loss of memory or sensory deficits. In this test, examinees are presented with two stimuli, one correct and one incorrect, in regards to a specific event or a perceptual discrimination task. The task is to select the correct answer alternative, or guess if it is unknown. Genuine impairment is associated with test scores that fall within chance performance. In contrast, malingered impairment is associated with purposeful avoidance of correct information, resulting in below chance performance. However, a substantial proportion of malingerers intentionally randomize their responses, and are missed by the test. Here we examine whether a ‘runs test’ and a ‘within test response ‘bias’ have diagnostic value to detect this intentional randomization. We instructed 73 examinees to malinger red/green blindness and subjected them to a FCT. For half of the examinees we manipulated the ambiguity between answer alternatives over the test trials in order to elicit a response bias. Compared to a sample of 10,000 cases of computer generated genuine performance, the runs test and response bias both detected malingered performance better than chance.

The digitization of aircraft cockpits places high demands on the colour vision of pilots. The present study investigates colour vision changes upon acute exposure to hypobaric hypoxia. The digital Waggoner Computerized Color Vision Test and the Waggoner D-15 were performed by 54 healthy volunteers in a decompression chamber. Respective altitude levels were sea level, 10,000 or 15,000 ft for exposure periods of 15 and 60 min, respectively. As for 60 min of exposure a significant decrease in colour perception was found between subjects at 15,000 ft as compared to the control group as well as between subjects at 15,000 ft as compared to subjects at 10,000 ft. No significant difference was found in the comparison within the 15,000 ft groups across time points pre-, peri-, and post-exposure. Thus, pilots appear to experience only minor colour vision impairment up to an exposure altitude of 15,000 ft over 60 min of exposure.

AimsTo examine the association between colour vision deficiency (CVD) and other ophthalmic disorders including amblyopia, strabismus and ametropia in a large population study.MethodsThe retrospective, cross-sectional study included 916 388 Israeli army male recruits who had their premilitary medical assessment at the age of 16–18 years from 2000 to 2020, analysing the prevalence of ophthalmic disorders including amblyopia, strabismus and ametropia in army recruits with CVD compared with all other recruits with normal colour vision. Demographic and socioeconomic data were also collected.ResultsThe prevalence of amblyopia (1.28% vs 0.71%, p<0.001), strabismus (1.09% vs 0.83%, p<0.001) and ametropia (moderate—less than 6.00 diopters, 35.05% vs 30.50%, p<0.001 and high—higher than 6.00 diopters, 3.18% vs 2.30%, p<0.001) were all higher among 28 001 (3.06%) army recruits with CVD compared with all other individuals with normal colour vision. CVD was more common in individuals with a higher socioeconomic status (high 3.15% vs low 2.93%, p<0.001) and varied according to recruits’ origin. It was most frequent in individuals whose mother was born in the former Soviet Union (4.98%) compared with other European countries (3.89%), North America (3.28%), Asia (2.78%) and Ethiopia (1.63%).ConclusionCVD is associated with an increased frequency of amblyopia, strabismus and ametropia, which can all impart vision difficulties besides colour vision impairment alone.

Gene therapy in colour It is often assumed that critical periods exist for the development of vision and other neural capabilities and that they end prior to adolescence. For example, it might be expected that gene therapy in adults with congenital vision disorders would be impossible. But experiments in adult spider monkeys who are normally red–green colour blind show that it is possible to add a third photopigment (human opsin) into some of their retinal cells by gene therapy. The monkeys acquire a new dimension of colour vision as a result. Not only does this suggest a possible therapy for a common congenital visual defect in humans (clinical trials are now under way), but also it demonstrates the extreme neuroplasticity of visual processing and points to possible routes by which trichromatic vision evolved. Red–green colour blindness is the most common single locus genetic disorder. Gene therapy is now used in adult monkeys, colour blind since birth, to provide the receptoral basis for trichromatic colour vision. Despite the expectation from classic visual deprivation experiments that neural connections established during development are incapable of processing an input not present from birth, treated monkeys displayed trichromatic colour vision behaviour. Red–green colour blindness, which results from the absence of either the long- (L) or the middle- (M) wavelength-sensitive visual photopigments, is the most common single locus genetic disorder. Here we explore the possibility of curing colour blindness using gene therapy in experiments on adult monkeys that had been colour blind since birth. A third type of cone pigment was added to dichromatic retinas, providing the receptoral basis for trichromatic colour vision. This opened a new avenue to explore the requirements for establishing the neural circuits for a new dimension of colour sensation. Classic visual deprivation experiments 1 have led to the expectation that neural connections established during development would not appropriately process an input that was not present from birth. Therefore, it was believed that the treatment of congenital vision disorders would be ineffective unless administered to the very young. However, here we show that the addition of a third opsin in adult red–green colour-deficient primates was sufficient to produce trichromatic colour vision behaviour. Thus, trichromacy can arise from a single addition of a third cone class and it does not require an early developmental process. This provides a positive outlook for the potential of gene therapy to cure adult vision disorders.

To investigate the influence of color vision deficiency (CVD) on the ability of practicing optometrists to correctly identify lesions in digital color fundus photographs with and without the aid of a commercially available color vision remediation device. This study was conducted at the 2024 annual meeting of the American Academy of Optometry in Indianapolis, IN, USA. The color vision of each subject was assessed using the Konan ColorDx CCT-HD®. Individuals with a score <90 for any cone type were classified as having CVD. Each subject then attempted to correctly identify lesions in a series of 12 digital color fundus photographs. Subjects identified as having CVD repeated the photograph task while wearing EnChroma® indoor lenses. The quality of life (QoL) of each subject was evaluated using a modified version of the Color Blindness QoL survey. Fifty-five optometrists completed the study. Forty had normal color vision (CVN) and 15 had CVD. Four of 15 (27%) CVD optometrists were previously unaware of their CVD. Both age and CVD influenced the ability of optometrists to correctly identify lesions. Among CVN subjects, younger clinicians (<39 years) outperformed older ones (p = 0.001). However, among subjects with CVD, age did not significantly affect performance (p = 0.84). Compared across CVD status, younger clinicians with CVD performed worse than their normally sighted peers (p = 0.002) while CVD had little effect among older clinicians (p = 0.23). Performance did not improve with use of the EnChroma lenses. Approximately half (47%) of optometrists with CVD reported difficulties in their daily activities attributed to poor color perception. CVD and older age decreased the ability of optometrists to correctly identify lesions in fundus photographs. Performance did not improve with use of the EnChroma lenses. Our findings suggest that CVD may pose a disability to eye care providers. We endorse the recommendation that individuals entering medical practice undergo color vision testing and counseling if a deficiency is found.

The assessment of color vision is crucial in both fundamental visual research and clinical diagnosis. However, existing tools for color vision assessment are limited by various factors. This study introduces a novel, efficient method for color vision assessment, which is based on a continuous motion tracking task and a Kalman filter model. The effectiveness of this new method was evaluated by assessing the color vision of both color-deficient observers and normal controls. The results from both a small sample ( N  = 29, Experiment 1 ) and a large sample ( N  = 171, Experiment 2 ) showed that color-deficient observers could be perfectly identified within 20 s using the tracking performance. We also compared the new method with a traditional psychophysical detection task to examine the consistency of perceptual noise estimation between the two methods, and the results showed a moderate correlation (Pearson's r  = .59 ~ .64). The results also demonstrated that the new method could measure individuals’ contrast response functions of both red–green and blue–yellow colors (e.g., the L–M and S–(L + M) axes in DKL color space) in just a few minutes, showing much higher efficiency than traditional methods. All the findings from this study indicate that the continuous motion tracking method is a promising tool for both rapid screening of color vision deficiencies and fundamental research on color vision.

In a previous work, we empirically analysed the so-called “relevant colours” in paintings. These relevant colours describe the number of colours that stand out for an observer when glancing at a painting. On average, 19 relevant colours were identified, enabling reliable segmentation of colour images via a small palette of colours. The purpose of this study was to analyse how observers with different colour deficiencies (specifically, 11 deuteranopes, 11 protanopes, 3 deuteranomalous and 4 protanomalous observers) perceive the most representative colours in paintings. To achieve this, a set of painting images was presented to these observers. They were instructed to mark those areas within the image that contained a relevant colour via a mouse. The observers visually scanned the entire painting and selected pixels belonging to relevant chromatic areas. The study included 20 images from the Prado Museum in Madrid, Spain. The results revealed that, as expected, the average number of relevant colours identified by all observers was relatively small, consisting of only 9 colours. This number was lower than the average number of colours found for observers with normal colour vision in the earlier study and reveals that dichromatic observers experience a degradation in their mental impressions of the observed paintings. Nevertheless, the results indicate that there is almost no difference in the number of relevant colours obtained between the two types of colour vision deficiencies; deuteranopes seem to be able to use more relevant colours than protanopes need for the same painting (10 and 8 relevant colours, respectively). By analysing the segmentation of pictorial scenes with relevant colours identified for each painting as colour seeds, we inferred how colour-deficient observers perceive and communicate much of the critical chromatic content in a painting. Through maximizing communicative effectiveness and minimizing the cognitive load, our results assess the colour information retained by anomalous observers, indicating that they lose approximately 20% of the representational content compared with normal observers.

Primary congenital glaucoma is a rare disease that occurs in early birth and can lead to low vision. Evaluating affected children is challenging and there is a lack of studies regarding color vision in pediatric glaucoma patients. This cross-sectional study included 21 eyes of 13 children with primary congenital glaucoma who were assessed using the Farnsworth D-15 test to evaluate color vision discrimination and by spectral domain optical coherence tomography to measure retinal fiber layer thickness. Age, visual acuity, cup-to-disc ratio and spherical equivalent data were also collected. Global and sectional circumpapillary and macular retinal fiber layer thicknesses were measured and compared based on color vision test performance. Four eyes (19%) failed the color vision test with diffuse dyschromatopsia patterns. Only age showed statistical significance in color vision test performance. Global and sectional circumpapillary and macular retinal fiber layer thicknesses were similar between the color test outcomes dyschromatopsia and normal. While the color vision test could play a role in assessing children with primary congenital glaucoma, further studies are needed to correlate it with damage to retinal fiber layer thickness.

Achromatopsia is a hereditary form of day blindness caused by cone photoreceptor dysfunction. Affected patients suffer from congenital color blindness, photosensitivity, and low visual acuity. Mutations in the CNGA3 gene are a major cause of achromatopsia, and a sheep model of this disease was recently characterized by our group. Here, we report that unilateral subretinal delivery of an adeno-associated virus serotype 5 (AAV5) vector carrying either the mouse or the human intact CNGA3 gene under the control of the red/green opsin promoter results in long-term recovery of visual function in CNGA3-mutant sheep. Treated animals demonstrated shorter maze passage times and a reduced number of collisions with obstacles compared with their pretreatment status, with values close to those of unaffected sheep. This effect was abolished when the treated eye was patched. Electroretinography (ERG) showed marked improvement in cone function. Retinal expression of the transfected human and mouse CNGA3 genes at the mRNA level was shown by polymerase chain reaction (PCR), and cone-specific expression of CNGA3 protein was demonstrated by immunohistochemisrty. The rescue effect has so far been maintained for over 3 years in the first-treated animals, with no obvious ocular or systemic side effects. The results support future application of subretinal AAV5-mediated gene-augmentation therapy in CNGA3 achromatopsia patients.