Normality of colour vision in a compound heterozygous female carrying protan and deutan defects

Background: Inherited red‐green colour vision defects are quite common, affecting one in 12 males, but are less common in women, affecting about one in 250. Because red‐green defects are X‐linked, nearly 15 per cent of females are heterozygous carriers of red‐green colour deficiency. In addition, about one in 150 females are ‘double carriers’, where both of their X chromosomes have L/M gene arrays encoding a red‐green defect. If a woman carries the same type of colour vision defect on each X‐chromosome, she will be red‐green colour deficient, whereas if she carries opposing defects (protan versus deutan) on each X chromosome, she will have normal colour vision, owing to the process of X‐inactivation. These women are referred to as compound heterozygotes, though very few have been reported. Questions remain about whether the colour vision capacity of these women is comparable to that of ‘normal’ trichromats. Methods: We examined a compound heterozygote carrier of both protanopia and deuteranomaly. We also examined male members of her family representing both forms of red‐green defect carried by the female proband. Complete colour vision testing was done, including Rayleigh matches, pseudoisochromatic plates, unique hue measurements and 100‐Hue tests. Flicker‐photometric ERG estimates of L : M cone ratio were obtained, as were Medmont C100 settings. Results: Genetic analyses provided direct confirmation of compound heterozygosity. The compound heterozygote showed Schmidt's sign, consistent with an extreme skew in her L : M cone ratio and usually associated with protan carrier status. Conclusion: Apart from Schmidt's sign, we found the colour vision of the compound heterozygote to be indistinguishable from that of a normal trichromat.     

One of Australia's greatest cricketers was a protanope: a genetic detective story solved with the help of Schmidt's sign

Abnormal colour vision is under‐represented among first class cricketers (Goddard N and Coull B BMJ 1994; 309: 16841685) and interviews with cricketers, all of whom had a mild colour vision defect, suggest there may be times when they lose sight of the red cricket ball against green surrounds (Hams and Cole Clin Exp Optom 2005; 88: 176–180). It is possible that severe abnormal colour vision precludes playing cricket at its highest competitive level. It is known that Bill Ponsford, who played Test cricket from 1924 to 1934 and was one of Australia's greatest batsmen, had abnormal colour vision. We have diagnosed him to be a protanope by tracing the abnormal colour vision exhibited by some of his descendents. We used Schmidt's sign using the Medmont ClOO colour vision test to identify carriers of the protan gene to trace the protanopic gene to Ponsford with greater certainty. That such an accomplished batsman and highly regarded outfielder should have a severe colour vision deficiency suggests that abnormal colour vision might not be, or at least need not be, a handicap to playing cricket at the most competitive levels.     

The new Richmond HRR pseudoisochromatic test for colour vision is better than the Ishihara test

Aim: The Hardy‐Rand‐Rittler (HRR) pseudoisochromatic test for colour vision is highly regarded but has long been out of print. Richmond Products produced a new edition in 2002 that has been re‐engineered to rectify shortcomings of the original test. This study is a validation trial of the new test using a larger sample and different criteria of evaluation from those of the previously reported validation study. Methods: The Richmond HRR test was given to 100 consecutively presenting patients with abnormal colour vision and 50 patients with normal colour vision. Colour vision was diagnosed using the Ishihara test, the Farnsworth D15 test, the Medmont C‐100 test and the Type 1 Nagel anomaloscope. Results: The Richmond HRR test has a sensitivity of 1.00 and a specificity of 0.975 when the criterion for failing is two or more errors with the screening plates. Sensitivity and specificity become 0.98 and 1.0, respectively, when the fail criterion is three or more errors. Those with red‐green colour vision deficiency were correctly classified as protan or deutan on 86 per cent of occasions, with 11 per cent unclassified and three per cent incorrectly classified. All those graded as having a ‘mild’ defect by the Richmond HRR test passed the Farnsworth D15 test and had an anomaloscope range of 30 or less. Not all dichromats were classified as ‘strong’, which was one of the goals of the re‐engineering and those graded as ‘medium’ and ‘strong’ included dichromats and those who have a mild colour vision deficiency based on the results of the Farnsworth D15 test and the anomaloscope range. Conclusions: The test is as good as the Ishihara test for detection of the red‐green colour vision deficiencies but unlike the Ishihara, also has plates for the detection of the tritan defects. Its classification of protans and deutans is useful but the Medmont C‐100 test is better. Those graded as ‘mild’ by the Richmond HRR test can be regarded as having a mild colour vision defect but a ‘medium’ or ‘strong’ grading needs to be interpreted in conjunction with other tests such as the Farnsworth D15 and the anomaloscope. The Richmond HRR test could be the test of choice for clinicians who wish to use a single test for colour vision.     

Abnormal colour vision is a handicap to playing cricket but not an insurmountable one

Background: Two studies have reported that abnormal colour vision is under‐represented among cricketers, presumably because cricketers with abnormal colour vision have difficulty seeing the red ball against the green grass of the cricket field and the green foliage around it. We have previously reported on the difficulties of five cricketers with abnormal colour vision but we have also reported that one of Australia’s finest cricketers was a protanope. This survey was undertaken to confirm the under‐representation of abnormal colour vision among cricketers and to ascertain whether those playing tend to be (1) those with a mild colour vision deficiency, (2) bowlers rather than batsman and (3) prefer to field close to the batsman rather than in the outfield. Methods: The colour vision of 293 members of seven Melbourne Premier cricket clubs was tested using the Ishihara test. Those who failed were examined further to confirm their abnormal colour vision, to assess its severity with the Farnsworth D15 test and to classify it as either protan or deutan using the Medmont C100 test. A questionnaire about cricketing ability and problems playing cricket was administered. Results: Twenty‐six (8.9 per cent) of the cricketers had abnormal colour vision, of whom six played in the First Grade (6.7 per cent of First Grade players). The proportion of cricketers with a severe deficiency was significantly less than expected for the First Grade players. There were only two protans. Bowlers were not over‐represented among the colour vision defective cricketers but those preferring to field close to the batsman were significantly over‐represented. Conclusion: Abnormal colour vision is a modest handicap to playing cricket, especially at the higher levels of the game. It may impede batting and the ability to field in the outfield.     

Colour blindness does not preclude fame as an artist: celebrated Australian artist Clifton Pugh was a protanope

Purpose: The aim was to make a posthumous diagnosis of the abnormal colour vision of the acclaimed artist Clifton Pugh and to analyse his use of colours to discern the strategies he used to overcome his limited colour perception. Methods: A pedigree of Pugh's family was constructed by searching public records. Pugh had no daughters but he had two older brothers, one of whom was still living. We tested the colour vision of this brother and one of his daughters and one of his grandsons. Three children of the other brother were questioned about the colour vision of their father and one daughter was tested for heterozygosity with the Medmont C100. Four observers with normal colour vision categorised the colours used by Pugh in a sample of 59 of his paintings. Protanopic transformations of some of these paintings were made using the Vischeck algorithms to gain an appreciation of how Pugh saw his own paintings. The validity of the transformations was tested by asking a protanope to report if the transformations looked the same as the normal colour images of 10 of Pugh's paintings. Results: Pugh's brother was a severe protan. His daughter showed Schmidt's sign and was a carrier of the protan gene and her son was a protanope. The oldest brother was reported as having normal colour vision. Therefore, it is almost certain that Clifton Pugh was a protanope. Pugh used all colours in his paintings but preferred to structure them on brown, black and blue or, for high key paintings, on cream or flesh colours. He used greens and purples sparingly. The protanopic Vischeck transformations did not always look the same as the normal colour image for the protanope observer. Conclusion: A severe colour vision deficiency does not preclude success as a painter. It is a handicap but there are strategies artists can use to overcome it.     

Jan Lovie‐Kitchin

Background: Colour vision deficiency (CVD) has a high prevalence and is often a handicap in everyday life. Those who have CVD will be better able to adapt and make more informed career choices, if they know about their deficiency. The fact that from 20 to 30 per cent of adults with abnormal colour vision do not know they have CVD suggests that colour vision is not tested as often as it should be. This may be because of practitioner uncertainty about which tests to use, how to interpret them and the advice that should be given to patients on the basis of the results. The purpose of this paper is to recommend tests for primary care assessment of colour vision and provide guidance on the advice that can be given to patients with CVD. Methods: The literature on colour vision tests and the relationship between the results of the tests and performance at practical colour tasks was reviewed. Results: The colour vision tests that are most suitable for primary care clinical practice are the Ishihara test, the Richmond HRR 4th edition 2002 test, the Medmont C‐100 test and the Farnsworth D15 test. These tests are quick to administer, give clear results and are easy to interpret. Tables are provided summarising how these tests should be interpreted, the advice that can be given to CVD patients on basis of the test results, and the occupations in which CVD is a handicap. Conclusion: Optometrists should test the colour vision of all new patients with the Ishihara and Richmond HRR (2002) tests. Those shown to have CVD should be assessed with the Medmont C‐100 test and the Farnsworth D15 test and given appropriate advice based on the test results.     

Search for coloured objects in natural surroundings by people with abnormal colour vision

Background: People with abnormal colour vision often report difficulty seeing coloured berries and flowers in foliage, which suggests they will have a diminished capacity for visual search when target objects are marked out by colour. There is very little experimental evidence of the effect of abnormal colour vision on visual search and none relating to search for objects in natural foliage. Method: We showed 79 subjects with abnormal colour vision (seven protanopes, 10 deuteranopes, 16 protanomals and 46 deuteranomals) and 20 subjects with normal colour vision photographs of natural scenes and asked them to locate clumps of red berries, to trace the length of a red string on grass and to name the season depicted in a photograph taken in the Autumn and the same scene photographed in the Summer. Colour vision was assessed using the Ishihara, the Medmont C100, the Farnsworth D15, the Richmond HRR and the Nagel anomaloscope. Results: All the subjects with abnormal colour vision located fewer clumps of red berries than those with normal colour vision. The subjects who failed the Farnsworth D15 performed significantly worse than those who passed but the distribution of scores in the two groups overlaps. The majority of subjects with abnormal colour vision could not trace the full length of the string: only 38 per cent of anomalous trichromats who passed the Farnsworth D15 test and three per cent of those who failed it were able to trace the full length of the string. Fifty‐five per cent of those classed as having a mild deficiency by the HRR test could trace the whole string. Most dichromats were unable to identify the Autumn season and those who did may have been assisted by guessing. Most (94 per cent) of those who passed the Farnsworth D15 test and all those classified as having a ‘mild’ deficiency by the HRR test could identify the season. Conclusions: All people with abnormal colour vision, even those with a very mild deficiency, have some degree of impairment of their ability to see coloured objects in natural surroundings. A pass at the Farnsworth D15 test or a ‘mild’ classification with the Richmond HRR test identifies those likely to have the least problems with visual search and identification tasks. The results have practical implications for the selection of personnel in occupations that involve visual search in natural terrain.     

Repeatability of the C‐100 colour vision test

Background: The C‐100 colour vision test has been shown to have a high validity for diagnosing the type of red‐green colour vision defect, however, there is little information on the repeatability of the test. This study examines the repeatability of the C‐100 in classifying the colour vision defect as either protan or deutan. Methods: The C‐100 was administered on two occasions to 58 subjects with congenital red‐green colour vision defects: The sessions were separated by a minimum period of 10 days. Results: The repeatability of the C‐100 was high with a kappa coefficient of agreement for diagnosis of 0.96. The few discrepancies were misclassifying protans as deutans. Conclusion: The C‐100 is a highly repeatable test in terms of separating protans from deutans. However, if a discrepancy occurs, it is more likely to be a protan misclassified as a deutan rather than vice versa.     

The luminance fall in anomaloscope examination: clinical examples

PURPOSE: The evaluation of the anomaloscope slope quotient in patients with acquired colour vision deficiency. METHODS: Two patients with Stargardt's disease in combination with protanomaly and deuteranomaly, respectively, were selected and also 3 patients with a presumed dominant optic atrophy of the protan type. The anomaloscope examination was performed according to the Linksz procedure. The luminance fall was calculated as the slope quotient SQ:Y units luminance fall per X units width of the matching range. RESULTS: The SQ of the 2 Stargardt patients was steeper than the SQ of congenital colour vision defectives, especially at the red end of the anomaloscope green-red mixture scale, indicating pathologic scotopization superimposed on the congenital deficiency. In optic atrophy of the protan type the SQ was flatter than in congenital deficiency, indicating that this deficiency has nothing to do with congenital protan deficiency. CONCLUSION: Calculation of the slope quotient SQ is helpful for the diagnosis of acquired colour vision deficiency, especially when the subject also has a congenital colour vision deficiency or is supposed to have such a deficiency.     

Does the Farnsworth D15 test predict the ability to name colours?

Background: The Farnsworth D15 test is designed to categorise colour vision deficiency as severe or moderate. The level of difficulty of the test was set so that those who passed it should be able to recognise surface colour codes, such as those used for electrical wiring. The test is widely used to provide advice to patients with abnormal colour vision and is often used for occupational selection when reliable recognition of surface colour codes is required. However, there has been only one previous study of the correlation between performance at the D15 test and the naming of surface colour codes and there has been no study of whether a person who passes the D15 can reliably name surface colours. Methods: One hundred and two people aged 11 to 65 years with abnormal colour vision were recruited from consecutively presenting optometric patients and were asked to name the colours of fabric, paint and cotton thread samples. There were 10 colours in each class of material and the samples were presented in a large (five to 10 degree angular subtense) and small size (2.5 deg and a single thread). The errors made were compared to those made by an age‐matched control group of equal size with normal colour vision. Results: The correlations between the Farnsworth D15 colour confusion index and colour naming errors were 0.62 for the large stimuli and 0.73 for the small stimuli. Its sensitivity and specificity identifymg those who made more errors than the worst performing colour normal person were 0.80 and 0.69 (large stimuli) and 0.75 and 0.71 (small stimuli). A Nagel anomaloscope range of less than 35 scale units provides essentially the same sensitivity and specificity. Conclusions: About 40 per cent of those with abnormal colour vision can name the main colours correctly under good visibility conditions. The D15 test is an imperfect predictor of those who can name surface colour codes correctly but it does provide useful information for general counselling. It is not suitable as a single test for occupational selection because it will pass 20 per cent who cannot name surface colours correctly and fail 30 per cent who can. In occupations in which recognition of surface colour codes is of critical importance, it may be best not to select people with abnormal colour vision because of the lack of a colour vision test that is a perfect predictor of the ability to recognise surface colours.     

Colour vision defects in asymptomatic carriers of the Leber's hereditary optic neuropathy (LHON) mtDNA 11778 mutation from a large Brazilian LHON pedigree: a case-control study

AIMS: To determine if asymptomatic carriers from a previously identified large pedigree of the Leber's hereditary optic neuropathy (LHON) 11778 mtDNA mutation have colour vision deficits. METHODS: As part of a comprehensive analysis of over 200 members of a large Brazilian LHON pedigree spanning seven generations, colour vision tests were obtained from 91 members. Colour vision was tested one eye at a time using the Farnsworth-Munsell 100 (FM-100) hue colour vision test. The test was administered under uniform conditions, taking into account: ambient light levels, daylight colour temperature of 6700 kelvin, and neutral uniform background. Tests were scored using the FM-100 MS-Excel computer scoring program. Defects were determined and categorised as tritan, deutan, or protan. Categorisation of each dyschromatopsia was based on review of demonstrated axis computer generated plots and age adjusted error scores which coincided with Verriest 95% confidence intervals. Only the axis with the greatest magnitude error score was used to classify the defect. 55 of the 91 test subjects were LHON mtDNA 11778 J haplotype mutation carriers, proved by mtDNA analysis. The remaining 36 subjects were age matched non-blood relatives (off pedigree), who served as controls. RESULTS: 27 of 55 carriers (49.10%) were shown to have colour vision defects in one or both eyes. 13 of the 27 (48%) abnormal tests in the carrier group were tritan defects and the remaining 14 (52%) were deutan defects. Nine of the 27 (33%) abnormals in the carrier group were identified as having bilateral defects. Six of these were deutan, and the remaining three were tritan dyschromatopsias. Only six of the 36 (16.66%) age matched controls were found to have any type of dyschromatopsia. Five (83.3%) of these were deutan defects. The remaining one was a tritan defect. The difference between the two groups using a chi(2) test with one degree of freedom was statistically significant with a p value less that 0.001. CONCLUSIONS: Until now, LHON has always been characterised by a sudden, devastating vision loss. Asymptomatic carriers, those without vision loss, were considered unaffected by the disease. It now appears that asymptomatic carriers of the LHON mutation are affected by colour vision defects and may manifest other subtle, yet chronic, changes.     

Using clinical tests of colour vision to predict the ability of colour vision deficient patients to name surface colours

PURPOSE: To determine the predictive power of commonly used tests for abnormal colour vision to identify patients who can or cannot name surface colours without error. METHODS: The colour vision of 99 subjects with colour vision deficiency (CVD) was assessed using the Ishihara, the Richmond HRR (2002), the Farnsworth D15, the Medmont C100 and the Nagel anomaloscope. They named 10 surface colours (red, orange, brown, yellow, green, blue, purple, white, grey and black), which were presented in two shapes (lines and dots) and three sizes. The surface colours were also named by an age-matched group of 20 subjects with normal colour vision. The performance of the clinical tests to predict the CVD subjects who made no colour naming errors and those who made errors is expressed in terms of the predictive value of a pass P((P)) and the predictive value of a fail P((F)). RESULTS: The P((P)) values of the tests were between 0.59 and 0.70 and P((F)) values were between 0.77 and 1.00. CONCLUSIONS: A 'mild' classification with the Richmond HRR test, especially if no more than two errors are made on the HRR diagnostic plates, identifies patients with abnormal colour vision who are able to name surface colour codes without error or only the occasional error. A pass of the Farnsworth D15 test identifies patients who will make no or few (up to 6%) errors with a 10 colour code, but who will be able to name the colours of a seven colour code that does not include orange, brown and purple. If protans are excluded, the predictive value for a pass P((P)) for the Farnsworth D15 is improved from 0.59 to 0.70. The anomaloscope is not an especially good predictor of those who can recognise surface colour codes. However, an anomaloscope range >35 units identifies those who have difficulty in recognising surface colour codes, as does a fail at the Farnsworth D15 test.     

Anomaloscope examination: scotopization (the luminance fall).

PURPOSE: The evaluation of a criterion for the detection of pathologic scotopization in routine anomaloscope examination. METHODS: Fifty congenital protan subjects, 50 congenital deutan subjects, 30 autosomal recessive congenital achromats, and 25 (44 eyes) acquired type I red-green defective subjects were selected. The anomaloscope examination was according to the Linksz procedure. The luminance fall was calculated as the slope quotient SQ: Y units luminance fall per X units width of the matching range. RESULTS: The mean SQ was -0.01 for congenital deutan subjects, -0.40 for congenital protan subjects and -1.30 for congenital achromats. There was no overlap between the three groups. Pathologic scotopization was found in 98% of the eyes presenting with an acquired type I colour vision defect. CONCLUSION: Calculation of the slope quotient SQ is helpful for the detection of pathologic scotopization in acquired colour vision deficiency.     

Errors reading the Ishihara pseudoisochromatic plates made by observers with normal colour vision

Background: Ishihara pseudoisochromatic plates are one of the best screening tools for red‐green colour vision deficiencies. Although a majority of persons with normal colour vision read all plates correctly, a significant proportion makes mistakes. The purpose of this study was to obtain results for normal trichromats reading the Ishihara plates and analyse the misreading responses to seek clinical implications. Methods: A sample of 249 (161 female) was tested with the Ishihara pseudoisochromatic plates. The number and nature of errors were recorded and typical errors, those that observers with abnormal colour vision were expected to make, were distinguished from other kinds of error. Results: Out of 249 normal trichromats, 111 individuals (45 per cent) misread at least one plate. Females made up to six total errors and males up to five total errors. When only typical errors were counted, all the normal trichromats made two or fewer errors. There was no significant gender difference for either total or typical errors. Conclusion: It is suggested that clinicians count only typical errors when administering the Ishihara test. Using a criterion of no more than two typical errors for a diagnosis of normal colour vision could improve the specificity and sensitivity of the test.     

Protan colour vision deficiency and road accidents

Background : Protans are precluded from holding a commercial driver's licence in Australia because they have a substantially reduced ability to see red lights and have more road accidents involving signal lights. This exclusion has been in place since 1994 but is likely to be abandoned following a current review of medical standards for commercial drivers. This paper reviews the level of risk of road accidents due to protan colour vision deficiency. It also addresses the question of whether it is fair to regard all protans as having a higher risk of road accident because some protans might have a sensitivity to red light that is as good as that of some people with normal colour vision. Methods : Data of two studies by Verriest and co‐workers are re‐analysed to estimate the degree of overlap of the protan and colour normal distributions of sensitivity to red light. Results : Field trial data show that protans have a very reduced visual range for red signals compared to colour normal observers but there is considerable variability among both classes of observers and the distributions do overlap. However, some variability is due to differences in observers' choices of a detection criterion, their speed of response and the measurement method. A laboratory study of the spectral sensitivity of protan and colour normal subjects that largely removes these sources' variability shows that all protans have a sensitivity to red light that is less than that of the least sensitive colour normal. Conclusion : It is reasonable to conclude that all protans, regardless of the severity of their defect, have a lesser ability to see red signals than colour vision normal observers and for that reason will have a higher risk of road accident.     

The C-100:a new dichotomiser of colour vision defectives

This paper evaluates a new instrument (C-100) which employs flicker photometry or silent substitution to determine the type of colour vision defect (protan or deutan). Specifically, this study addresses the unit's capacity to: 1. detect colour vision defects; 2. differentiate protans from deutans; and 3. produce reliable measurements under different viewing conditions. We find that an average of five readings enables protans to be clearly separated from deutans in all cases (p < 0.0001), but that the distinction between these groups and normals is less clear. Dichromats are not distinguished from anomalous trichromats, so the instrument cannot be used as an index of severity. The results are shown to be robust to most of the test conditions likely to be encountered during normal clinical use. A clinical protocol is suggested that utilises the C-100 for classification of colour defective observers. It is concluded that normal, and some anomalous, trichromat settings are performed using flicker photometry, whereas dichromatic observers appear to utilise silent substitution.     

Clinical use of the City University Test (2nd Edition)

The City University test (TCU test) aims to identify people with significant colour deficiency and to classify the type of defect. 222 people with congenital red-green colour deficiency, diagnosed with the Nagel anomaloscope, were examined with the TCU lest (2nd Edition), All deuteranopes and 44% of deuteranomalous trichromats failed the TCU test. Deutans who failed could be subdivided into two categories of severity depending on whether errors were made on five or more plates. 96% of protanopes and 26% of protanomalous trichromats failed. Protans made fewer errors than deutans and subcategories of severity could not be distinguished according to the number of errors made. The Farnsworth D15 test was found to be more effective than the TCU test in identifying significant protan colour deficiency. Detection and classification rates varied on all the plates of the TCU test. Mixed protan and deutan classification errors were made by 61% of subjects with the majority result correct in 80%. The most efficient plates are identified and recommendations are made for the optimum use of the TCU test in clinical practice.     

Impairment of colour contrast sensitivity and neuroretinal dysfunction in patients with symptomatic HIV infection or AIDS.

Ophthalmic and neurological complications are frequent findings in patients with AIDS. Little is known about neuroretinal dysfunction in patients with HIV infection. The purpose of this study was to measure and evaluate colour vision in patients with HIV infection or AIDS. Colour contrast sensitivity tests were performed on 75 patients (150 eyes) in different stages of HIV infection. A highly sensitive computer graphics system was used to measure tritan, deutan, and protan colour contrast thresholds. Patients were classified into three clinical groups: (a) asymptomatic HIV infection, (b) lymphadenopathy syndrome or AIDS-related complex, and (c) AIDS. Overall, tritan (p < 0.0001), deutan (p = 0.003), and protan (p = 0.009) colour contrast sensitivities were significantly impaired in patients with HIV infection compared with normal controls. Colour thresholds in patients with asymptomatic HIV infection (mean tritan threshold: 4.33; deutan: 4.41; protan: 3.97) were not impaired compared with normal controls. Colour vision was slightly impaired in patients with lymphadenopathy syndrome or AIDS-related complex (tritan: 6.25 (p < 0.0001); deutan: 4.99 (p = 0.02); protan: 4.45 (p = 0.05)). In patients with AIDS the impairment was even more marked (tritan: 7.66 (p < 0.0001); deutan: 5.15 (p < 0.0009); protan: 4.63 (p = 0.004)). Analysis of covariance controlling for age demonstrated a close association between impairment of tritan colour contrast sensitivity and progression of HIV disease (p < 0.0001). Following Köllner''s rule, our study suggests that neuroretinal dysfunction occurs in patients with symptomatic HIV infection or AIDS. This is emphasised by the finding that the relative impairment in tritan vision compared with deutan/protan vision might reflect the difference in the number of cones or receptive fields. Measurement of tritan colour contrast sensitivity appears to be an appropriate and easily applicable method to detect early neuroretinal dysfunction in patients with HIV disease.     

Orienteers with poor colour vision require more than cunning running

Background: Highly detailed colour coded maps are used in the sport of orienteering to enable competitors to navigate from one check point to another and to provide guidance on the nature of the terrain to be traversed. The colours are defined by the International Orienteering Foundation (IOF) and are said to have been chosen so they will not be confused by competitors who have abnormal colour vision. However, there are anecdotal reports that individuals with colour vision defects do have problems with the colour coding. Method: A Minolta Spectrophotometer CM‐503i was used to measure the CIE x,y chromaticity co‐ordinates and the reflectances of the standard colours recommended by the IOF for the colour coding of orienteering maps, as well as the colours on two maps used in orienteering events. Results: Four pairs of IOF standard colours are likely to be confused by protan observers and four pairs by deutan observers. There were three pairs of colours likely to be confused by both deutan and protan observers on one of the competition maps and one pair likely to be confused by protan observers on the other map. Some of the colours on the actual competition maps differed noticeably from the standard IOF colours. Discussion: Orienteers with more severe forms of abnormal colour vision are likely to be disadvantaged by their inability to differentiate some colours used on orienteering maps. The IOF should choose different colours that are less likely to be confused or should employ a redundant code (such as a pattern or texture). There is need for better quality control of the colours of competition maps to ensure they do conform to the IOF standard colours.     

Vision evaluation in people with Down's syndrome

We tested the colour vision of 72 people with Down's syndrome using the Ishihara test and an anomaloscope. We found that 13 of the subjects, 6 males and 7 females, had defective colour vision according to Pickford's classification. In monocular vision 10 eyes were protan (five simple, three extreme and two deviant), one eye was simple deuteranomalous and the remaining eyes were normal: in binocular vision four of the subjects were protan (two simple and two deviant), two subjects were deutan (one simple and one deviant) and the rest were normal. Many of our subjects had lens opacities, strabismus, nystagmus, hypermetropia, high myopia and astigmatism, confirming literature reports. The contrast sensitivity function measured with the VCTS test showed a considerable toss of low-frequency sensitivity in our subjects compared to a normal population, which was more marked in the more severely impaired subjects.