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This paper compares the performance of color defective patients on the Farnsworth Lantern test in both unlit and lit room conditions. We examined 18 dichromats and 33 anomalous trichromats, as diagnosed by the Mark I Nagel Anomaloscope. No statistically significant differences were found between their performance in the two conditions.
In retinitis pigmentosa patients the effect of cystoid macular edema on colour vision was studied. The occurrence of cystoid macular edema decreases with increasing colour vision defect. The mutual proportion of the main types of colour vision defects remains stable until visual acuity has dropped to 0.5; at lower VA levels the number of red-green defects increases. Neither the finding of a blue-yellow colour vision defect in FM100 Hue testing nor the appearance of anomaloscopic pseudoprotanomaly is influenced by cystoid macular edema. The authors conclude that cystoid macular edema in retinitis pigmentosa patients mainly affects visual acuity and not colour vision. They also noted a familial occurrence of cystoid macular edema.
Cone and rod functions of three blue cone monochromats (age 13-20, male) from three different families were investigated. In contrast to rod monochromats, they lack prominent nystagmus. Color matches as determined using the Nagel anomaloscope came close to those of rod monochromats but the green primary appeared slightly brighter to them. In color discrimination tests (Farnsworth-Munsell 100-hue and Panel D-15 desaturated), maximum confusion followed protan rather than scotopic axes. Measurements of spectral sensitivity revealed action spectra exclusively of blue sensitive cones, even under conditions that should isolate green- or red-sensitive cones. After 20 minutes of dark adaptation, rods determined the spectral sensitivity function. Transient tritanopia, which in normals results from the interaction between cones sensitive to short and long wavelengths, was completely absent in blue cone monochromats. Visual acuity (Snellen charts and contrast gratings) revealed values between 20/200 and 20/60. Recognition of high-spatial low-contrast gratings was improved by blue cut-off filters (Schott BG 28) and considerably worsened by yellow cut-off filters (Schott OG 510). Since alteration of visual acuity induced by cut-off filters was not found in rod monochromats, this two-filter test is a means of differentiating quickly between rod achromats and blue cone monochromats. As the mode of inheritance is autosomal recessive in rod achromats and x-linked recessive in blue cone monochromats, differential diagnosis is important for correct genetic counseling.
We evaluated 164 eyes of 87 patients with diabetes mellitus compared with 50 eyes from 25 healthy subjects as the control group. We compared 87 patients with diabetes mellitus (164 eyes) in relation to their duration of diabetes, fundus findings, visual acuity, and color vision defects. In all patients, color vision defects were determined using the Farnsworth-Munsell 100-hue test, and the total error score was established on the basis of age norms from subjects without diabetes. No color vision defect was detected in the control group. In the diabetic group, fundus degeneration and color vision defects were observed and correlated with the duration of diabetes. The dominant color defect was of the blue-yellow type.
Color vision abnormalities indicated by the Farnsworth-Munsell 100-hue Color Vision Tests (FM-100) were analyzed by computer to better characterize and group congenital and acquired color vision disorders and to help establish statistically significant diagnostic criteria. Standard evaluation of the FM-100 is by axis and error score calculations. A method has been established for computer-averaging many tests from patients with the same color abnormalities determined by history, standard FM-100 and Nagel anomaloscope. The computer calculated an average error score and standard deviation for each of the 85 color caps. Every time a new patient was evaluated for color vision abnormality, his score was compared with averaged tests with common diagnoses, by calculating distance scores. The averaged test with the lowest distance score consistently tended to coincide with the diagnosis. An analysis of 130 FM-100 color tests found technician-calculated error scores to be incorrect, although usually minor, in 40% of the tests. The computer-calculated axes agreed well with the technician's estimates. The distance scores predicted the diagnosis accurately 89% of the time. Many errors were due to the small number of protanopes averaged and inability to distinguish trichromats from dichromats.
Five affected males in the fifth generation of a large pedigree of X-chromosomal incomplete achromatopsia were tested. All had SWS cone function. A 19-year-old affected man was a classical blue cone monochromat on color matching and spectral sensitivity. A 16-year-old boy showed evidence of a long wavelength sensitive cone active in 8 degrees color matches. With a blue-green background, his cone spectral sensitivity function peaked near 550-560 nm. Three younger boys, aged 7-10 yrs were evaluated only with color matching. All showed evidence of long wavelength cone function with an 8 degree field and one showed long wavelength cones in 2 degree matches. An independent observation concerning the family was the finding that deuteranomaly was introduced in the third generation. The fourth generation women, all obligate carriers of X-linked achromatopsia, had a 0.5 chance to carry deuteranomaly. Neither carrier state per se is usually associated with expression of deuteranomaly. Three of the five tested expressed deuteranomaly. This finding of deuteranomaly in the carrier females might be a consequence of a double carrier state indicating association between the genes for deuteranomaly and X-linked achromatopsia.
A 24-year-old man acquired a color vision defect shortly after an accident in which he struck the back of his head. Results of the Farnsworth-Munsell 100-hue test showed that the patient had poor color discrimination in both eyes. His color matches on the Nagel anomaloscope suggested a red/green disturbance. Results from increment threshold testing demonstrated on absence of the blue mechanism. Results of field sensitivity measurements confirmed that foveal vision was mediated by the red or green mechanism. This case showed both similarities and differences to previously reported cases of acquired color vision defects secondary to cortical trauma.
PURPOSE: To describe a new test of color vision (cone-specific contrast sensitivity) and to evaluate its sensitivity in comparison to standard clinical tests. METHODS: Cone-specific colored letter charts were generated by computer and displayed on a color monitor. Each chart consists of colored letters that are most visible at the top but that gradually fade into a gray background. Cone contrast varies systematically on each chart so that letters are visible to only one cone type (L, M, or S cone). Cone-specific letter contrast sensitivity was measured in 30 color normals and 13 subjects with hereditary color deficiency. Values were compared to standard measures of color vision. RESULTS: In color normals, mean log contrast sensitivity was approximately the same on L-cone (1.84 +/- 0.08 log contrast sensitivity) and M-cone (1.87 +/- 0.08) tests but was reduced on the S-cone test (0.89 +/- 0.15) because of the fewer number of S-cones in the human retina. Subjects with red color deficiency showed significantly reduced contrast sensitivity on the L-cone test but normal performance on M- and S-cone tests. Subjects with green color deficiency showed decreased contrast sensitivity limited to the M-cone test. When standardized relative to variability, cone contrast sensitivity identified color deficiency unequivocally in all subjects, whereas FM 100 hue error scores detected 9 of 13 subjects with color deficiency. CONCLUSIONS: Cone-specific contrast sensitivity provides a quantitative measure of normal color vision and indicates both type and severity of color deficiency. It is useful for diagnosing hereditary color deficiency and for monitoring early color vision loss in ocular and systemic disease.
To the patient, the sudden onset of cerebral achromatopsia is like switching to black and white on a color TV. As a rule, the defect arises due to bilateral ischemic infarction in the inferior occipitotemporal region. Bilateral upper homonymous quadrantanopsias usually leave the macula more or less unimpaired, so that visual acuity is largely preserved. Prosopagnosia and loss of topographic memory are often associated with central achromatopsia. Investigations of color vision must include color-naming procedures and largefield tests in addition to the conventional methods. Color-naming tasks are indispensable in differentiating cerebral achromatopsia from the aphasic and disconnective types of color anomia. The authors' recommended strategy for investigating color vision relies on records of a case of cerebral achromatopsia obtained six months and two years, respectively, after the onset of symptoms. In addition to the above-mentioned procedures, spectral increment thresholds on white and colored backgrounds were determined. For the first time in cerebral achromatopsia, examinations with large-field spectral matches were performed using the projection anomaloscope. Large-field tests are indispensable for monitoring recovery in cases of central achromatopsia. In the author's patient, recovery of blue-green discrimination was far more complete than that of red-yellow-green discrimination, and for both conditions large-field color vision was far superior to small-field.
A computer-controlled test of colour vision is described, in which luminance noise and masking contours are used to ensure that the subject's responses depend on chromatic signals. The test avoids the need--common to most computer-controlled tests--to define equiluminance for the individual subject before the colour test itself can be administered. The test achieves a good separation of protan and deutan subjects and reveals the large range of chromatic sensibilities among anomalous trichromats. As a population, dichromats had higher thresholds on the tritan axis of the test than did normals. In an extension of the test, full discrimination ellipses were measured for normal and colour-deficient observers. The nature of anomalous trichromacy is discussed and the possibility is raised that hybrid genes, resulting from genetic recombination, may code for incorrectly labelled or functionally impaired molecules.
Early detection of congenital color vision defects is desirable, but school screening studies have been stymied by lack of a suitable test. We evaluated a new color vision test, the APT-5, for use by volunteer screeners in schools and preschools. The screeners tested 1794 children, ages 3 to 13 years, and found the APT-5 easy to use with young children ages 5 years and up. Children who failed the screening were recruited for diagnostic color vision testing; for the children ages 5 to 13 years, 56% of those who failed the screening were successfully recruited. Data analysis indicated that the false-positive rate in this age group was 1% to 2%, and that for boys in this age group the positive predictive value was 71% to 81%. Retest data indicated that most false-positives were not due to the test itself, but to other factors in the school screening situation. Two thirds of all children scored as abnormal by anomaloscopy were simple deuteranomalous, indicating that the APT-5 effectively identified even mild color defects. The results of this trial indicate that the APT-5 is suitable for school color vision screening of children ages 5 years and up.
The unilateral tritanope described in the previous paper (Alpern, Kitahara & Krantz, 1983) was able to match every narrow-band light presented to his tritanopic eye with lights from a tristimulus colorimeter viewed in the adjacent field by the normal eye. In two regions of the spectrum (called isochromes) physically identical lights appeared identical to the observer's two eyes. One isochrome was close to 'blue' for the normal eye, the other was in the long-wave spectral region seen by the normal eye predominantly as 'red'. Between these isochromes the normal eye required less than spectral purity to match, dropping to near zero purity at 560-570 nm. A mixture of the two isochromes that appeared purple to the normal eye appeared neutral to the tritanopic eye. Hence dichoptic matches grossly violate Grassmann's additivity law. For the normal eye colour naming conformed to typical normal results. For the tritanopic eye the results were coherent with those found by dichoptic matching: the spectrum was divided into two regions by the achromatic neutral band. To the short-wave side, only the colour names 'blue' and 'white' were ever used. To the long-wave side the predominant colour names were 'red' and 'white' with some 'yellow'. Spectral lights appeared neither 'red-blue' nor greenish. Surrounding the test with an annulus either 430 nm, 650 nm, or a mixture of these, fails to induce any greenish appearance, although the achromatic band shifted in the expected directions. It is concluded that there must be exactly three functionally independent, essentially non-linear central codes for colour perception, and that these codes are different from those suggested in existing theories of colour perception.
Two different population samples in Holland--one consisting of 1,093 boys from a technical school and the other of 493 male and 416 female students--were analysed for the presence of red-green colour vision defects. A total percentage of 7.3 for the male population was found. Based on the combined results of the Ishihara and HRR pseudoisochromatic plates, the Farnsworth 15-hue test and the anomaloscope, a subdivision of the deuteranomalous individuals into 3 subgroups is made. It is suggested that the differences between these groups may be genetic in nature and that the actual number of different genetic entities may still be greater.
Farnsworth's standard D15 and L'Anthony's desaturated D15 panel tests were administered to 99 congenital red-green color defective subjects. The results were analyzed in three ways: (1) by summing the color differences between adjacent caps according to Bowman, (2) by averaging color difference vectors (CDV) according to Vingrys and King-Smith, and (3) by visually inspecting and counting the crossings. The Bowman measure was highly correlated with one of the CDV measures but provides less information regarding a cap arrangement. The desaturated D15 test can be expected to misclassify 5% of dichromats by type (protan/deutan) compared to a type misclassification rate of less than 0.1% for the D15 panel test. The correct diagnostic rates for type were 45% for the standard D15 test and 58% for the desaturated D15 test. However, the improvement in correct diagnostic rate for the latter test was accompanied by an increase in the misdiagnostic rate from 2 to 10%. The main value of the desaturated D15 test in congenital color vision diagnosis would seem to be in providing classification of those subjects who pass the standard D15 test. Quantitative scoring of the tests provides a good estimate of severity of defect. Visual inspection provides a similar diagnostic rate to CDV analysis, but has a lower type misdiagnostic rate at the desaturated D15 test and is more likely to be correct when the two methods disagree. We suggest that quantitative scoring techniques are of limited benefit for the clinical diagnosis of congenital color vision defects but that they are of use in clinical trials or for the monitoring of changes in color vision over time.(ABSTRACT TRUNCATED AT 250 WORDS)
To the patient, the sudden onset of cerebral achromatopsia is like switching to black and white on a color TV. As a rule, the defect arises due to bilateral ischemic infarction in the inferior occipitotemporal region. Bilateral upper homonymous quadrantanopsias usually leave the macula more or less unimpaired, so that visual acuity is largely preserved. Prosopagnosia and loss of topographic memory are often associated with central achromatopsia. Investigations of color vision must include color-naming procedures and large-field tests in addition to the conventional methods. Color-naming tasks are indispensable in differentiating cerebral achromatopsia from the aphasic and disconnective types of color anomia. The authors' recommended strategy for investigating color vision relies on records of a case of cerebral achromatopsia obtained six months and two years, respectively, after the onset of symptoms. In addition to the above-mentioned procedures, spectral increment thresholds on white and colored backgrounds were determined. For the first time in cerebral achromatopsia, examinations with large-field spectral matches were performed using the projection anomaloscope. Large-field tests are indispensable for monitoring recovery in cases of central achromatopsia. In the author's patient, recovery of blue-green discrimination was far more complete than that of red-yellow-green discrimination, and for both conditions large-field color vision was far superior to small-field.
AIM: To determine if the City University Tritan Test is a useful addition to visual function assessment in rural communities in northern Nigeria. METHODS: The study was a cross sectional survey. The participants were 8394 people, aged 5 years and over, living in 37 rural communities, mesoendemic and nonendemic for onchocerciasis, in Kaduna State in northern Nigeria. The main outcome measures were the detection of a defect in blue-yellow colour vision by two criteria: (1) failure with the City University tritan screening plates; (2) failure with the City University grading plates to identify severe tritan defects. RESULTS: 91% of those aged 10 years and above could perform the test. Below this age, there were difficulties in comprehension. The test showed good inter- and intraobserver agreement. After adjustment for confounders the odds of failing the screening plates were significantly increased in the presence of optic atrophy or glaucoma (3.55 (2.48-5.08) and 15.9 (4.22-60.2) respectively). There was a greater increase in the adjusted odds of failing the grading plates in the presence of optic atrophy or glaucoma (5.30 (2.97-9.45) and 8.87 (1.61-48.7) respectively). Cataract had a smaller effect on the screening plates, adjusted odds 1.63 (0.95-2.80). CONCLUSION: Blue-yellow colour vision testing is a useful addition to visual function assessment in those aged 10 years and above in rural northern Nigeria, particularly in the detection of optic nerve disease.
Colour difference vector analysis provides useful and meaningful information in scoring the Farnsworth-Munsell (FM) 100-hue test. However, the FM 100-hue test is limited in its ability to diagnose type and severity of congenital colour vision defect. Type classification for all subjects is incorrect in 21% of cases, and for deuteranomals the misclassification rate is 38%. Visual inspection of the plots yields a similar misclassification rate and classification of plots with few errors (under 180) is generally less reliable. The FM 100-hue test has a limited ability to separate dichromats from anomalous trichromats. A test protocol based on joint D15 and FM 100-hue tests should pass 36% of anomalous trichromats and 26% of all colour defectives yet fail all dichromatic observers. We conclude that administering the FM 100-hue test is of less value than a combination of D15 panels (Standard D15 and L'Anthony's desaturated D15) in the clinical diagnosis of congenital colour defective observers. Our results for the FM 100-hue panel are similar to those reported previously by other investigators.
I shall discuss the nature of the sensation of colour and the reason for our colour vision, leading on to the existence of defects in that sense. I will consider the different kinds of such defects and the arguments for the use of particular tests in varying circumstances. I report the result of a recent survey of the value of a careers advisory service for "colour blind" school children seen between 1965 and 1977 (primarily red-green blind). This leads to examples of the value of these tests in genetics, and in the early diagnosis of disease or toxicity. I shall also describe the various modifications I have made to the 100-hue test, with its eventual automation both for computation and recording. Finally, the recommendations I make for future progress cover routine examination, both on starting primary education and on entering secondary education, analysis of the colour task at work, and the adoption of an enlightened system of colour coding.