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Bilateral symmetry of disorders of vision is examined in 60 typical patients with retinitis pigmentosa. We observed a very high degree of interocular congruence in the patterns of both kinetic visual field defects and threshold profiles and in abnormalities of foveal colour discrimination and visual acuity. Abnormalities of foveal colour vision are highly correlated with the extent of visual field loss.
BACKGROUND: We considered whether the color discrimination of mild color defectives scoring < or = 100 is the same as that of normals. METHODS: We analyzed the FM 100-hue results of 126 normals and 94 congenital color defectives retrospectively by considering the Total Error Score (TES) and individual cap errors (error profiles). RESULTS: A TES of 100 passes 95% of normals and 24% of congenital color defectives. The error profiles of some of the mild defectives who pass show abnormal peaks along a red-green axis. An error > or = 5 in these regions is a good indicator of abnormal color discrimination. CONCLUSIONS: Some 30% of mild defectives (TES < or = 100) have limited hue discrimination in the red-green domain, so both the TES and error profiles need to be considered when providing vocational guidance.
A neuro-ophthalmologic examination, including fluorescein angiography and colour discrimination tests, was made of 15 workers (age range 30--65 years, mean 45.8 years) exposed to n-hexane (range of exposure 5--21 years) during vegetable oil extracting and adhesive bandage manufacturing. Visual acuity, visual fields, intraocular pressure, and biomicroscopical findings were normal. Ophthalmocopy revealed delicate macular changes in 11 or the 15 subjects. One subject had a history of central serous retinopathy in one eye. The macular changes consisted of an orange-like ophthalmoscopic appearance and a decreased macular lustre. Subtle defects of the pigment layer were present in the fluorescein angiography. Defective colour discrimination was found in 12 of the 15 subjects, one of whom had congenital deuteranopia. Colour defects were of the acquired type, mainly in the blue-yellow spectrum. Damage to the receptor lipids is suggested as the pathomechanism of the maculopathy found in this study.
All 3 children, 2 boys and 1 girl (the probands), in a family had high myopia and subnormal visual acuities. The boys had high myopia in both eyes, the girl had high myopia in 1 eye and low myopia in the other eye. Both of the boys had a protanomalous colour vision defect. The colour vision testing of the high myopic eye of the girl was not successful, the other eye had normal colour vision. In the electroretinogram examination, both cone and rod responses were decreased in 2 of the children. In the family study, results of an eye examination of 30 relatives were available. No other cases of high myopia or subnormal visual acuities were found. The father of the children, 1 of the paternal relatives, and 5 of the maternal relatives had low myopia. One maternal male cousin of the probands had a protanomalous colour vision defect. In the genealogical study, no relationship was found between the families of the father and the mother of the probands going back to the fifth generation. The heredity of this disorder is difficult to define. It could be autosomal dominant or recessive if the myopia only are taken into consideration. If the high myopias and cone dysfunction are considered to be parts of the same syndrome, the heredity could be x-chromosomal recessive or autosomal recessive.
A 70-year-old man with a history of hypertension and coronary artery disease suffered an abrupt loss of vision in June 1980. Neuro-ophthalmologic examination in August 1981 revealed 20/20+ acuity in both eyes, but quantitative perimetry disclosed a classic crossed-quadrant homonymous hemianopsia. This is known as the "checkerboard" visual field defect; a right upper quadrantanopsia as well as a left lower quadrantanopsia. A review of the eight previously reported cases is presented. A trial with "checkerboard" Fresnel prisms gave only a slight improvement in ambient field in this patient. The significance of that point is discussed. To our knowledge, this is the first patient with a "checkerboard" occipital lobe infarction pattern documented by computed tomography.
438 males and 369 females from four endogamous nomadic groups of the Yerukala viz. Suvvi, Badda, Uppu and Kunchapuri of Andhra Pradesh (India) were examined for red-green colour blindness using the 15th edition of Isihara's colour blindness chart. The absence of defective colour vision in the Badda Yerukala and very low frequencies among the other groups agree not only with the hypotheses of Post (1962) and Pickford (1963) concerning the operation of natural selection, but corroborates, too, the opinion of Malhotra (1978) that nomads by virtue of their life-style demand good colour vision.
Three sets of pseudoisochromatic plates were evaluated by photometry and colorimetry. The luminance contrast between the figure and background was measured and compared with a contrast detection threshold. The chromaticity coordinates of the figure and background were evaluated on the basis of how closely they approached a dichromatic line of confusion. The separation of the coordinates of the figure and background are a measure of the severity of the defect for which the plate tests. The plates were evaluated under both Macbeth (C) and tungsten (A) illuminants; two sets of plates were found to be better designed for tungsten illumination.
The author has classified progressive human cone-rod dysfunction into primary and secondary types. The primary type, identified by early ERG cone and usually also rod abnormalities, was further subdivided into types 1 and 2 based on, amoung other distinguishing characteristics, the extent of associated retinal pigment epithelial defects. Secondary cone-rod dysfunction apparently results from disease initially affecting the retinal pigment epithelium. Initially normal ERG findings and the presence of flecks characterize this (type 3) progressive cone-rod dysfunction.
The Farnsworth-Munsell 100 hue test (F-M 100) was used to examine 30 patients with their first episode of unilateral demyelinating optic neuritis (DON) at presentation, after 6 weeks and after 6 months. Twelve patients satisfactorily completed the test with the affected eye at presentation. This number had increased to 23 by 6 weeks and to 27 by 6 months. No patient with a visual acuity of LogMAR 0.86 (Snellen equivalent approx 6/43) or worse, could complete the test. The mean total error score of affected eyes showed significant improvement at each subsequent examination but was always worse than the non-affected eyes. There was a significant correlation between total error scores and visual acuities of affected eyes at presentation and after 6 months. Fourteen patients recovered a visual acuity of LogMAR 0.0 (Snellen equivalent 6/6) or better but the total error scores of the affected eyes were significantly worse than the non-affected eyes (p = 0.017), indicating that defective colour vision is an indicator of a previous episode of DON despite the recovery of normal visual acuity. DON is reported to produce a red-green (Type II) axis of colour defect but individual F-M 100 polar diagrams were usually generally abnormal and did not show any predominance of recognisable axis of colour defect at any examination. Group averaging of the F-M 100 data from such a well-defined group of patients with acute DON revealed a significant bipolar abnormality in the tritan (blue-yellow) axis at presentation which was not demonstrated at the subsequent examinations or at any examination of the non-affected eyes.
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.
The responses of 455 male subjects on both editions of the City University Colour Vision Tests (City 1 and City 2) were recorded after the establishment of each subject's criterial status using the Nagel anomaloscope. Based on the Information Theory, each plate was assigned a contributory weighted score to the total test score. Using informational analysis, a cut-off point in test score separating normals and defectives was also determined for each test. This scoring system is an improvement on the existing (or manufacturer's) system. The analysis has also shown that the second edition (City 2) is a considerable improvement on the first (City 1). Despite this, even the improved City 2, like its origin, the D-15, is shown to be poorer than most of the commonly used PIC tests.
A method of color naming was used to determine the spectral locus for unique green (UG) as it was perceived by 20 color normals and 24 deuteranomalous trichromats. The loci for the normal group were distributed bimodally, as earlier investigators had reported, and a bimodal distribution was also found for the deuteranomalous group. In the latter group, UG was located at long wavelengths only by those who had been classified as mild deuteranomals according to several clinical criteria. Those who located UG at shorter wavelengths included individuals whose defects ranged from mild to severe. This result is discussed in the context of theories of deuteranomaly and is presented as further evidence for the existence of 2 types of deuteranomaly.
There are few conclusive electroretinography (ERG) studies comparing the spectral characteristics in deutans and normals in contrast to protans and normals. The difficulties of research on deutans were thought to be due to problems in detecting the very slight differences in the spectral characteristics between deutans and normal subjects. To record monochromatic ERG responses accurately in deutans, our time-locked scanning method was improved as follows: We used 12 interference filters for stimulus lights with narrow half widths (4-6 nm) and wavelengths of peak transmission arranged at intervals of 10 nm between 520 nm and 600 nm. Each stimulus light was strictly adjusted to an equal energy and checked simultaneously with ERG recordings. Contact lens electrodes were reformed for comfortable fitting to subjects' corneas. The time interval between each stimulation was set at 300 msec and one scanning of all stimulations took only 3.9 sec. ERG bp-waves were recorded in congenital color blindness by scanning monochromatic light stimuli, and spectral responses obtained could be evaluated as a spectral pattern. Different spectral patterns of responses from those of normal subjects and shift of the peak in the spectral response curves were obtained for congenital color blind subjects. The maximal responses were recorded at around 540 nm in protans and at 570-580 nm in deutans under white adaptation. Differences in the response curves were not found between dichromats and anomalous trichromats. Moreover, selective chromatic adaptation disclosed the separate responses of green cone and red cone systems. In normal subjects the peak of the spectral response curves was shifted to around 540 nm by red adaptation and to around 580 nm by blue adaptation. The spectral patterns changed so that they looked like the patterns under white adaptation of protans and deutans, respectively. But in protans and deutans the same spectral response patterns and almost the same wavelengths of the peak in the spectral response curves as those obtained under white adaptation were recorded under chromatic adaptation. This method provides the possibility of differentiating between red and green color blind subjects and normal subjects by the ERG. Defects or marked abnormality in the red cone system in protans and the green cone system in deutans can also be detected. Monochromatic ERGs of deutans were recorded under more intense red adaptation.(ABSTRACT TRUNCATED AT 400 WORDS)
The findings are presented on the updated Kempster pedigree with Sorsby's fundus dystrophy. The study confirms the features described in other families: autosomal dominant inheritance with complete penetrance, loss of central vision due to subfoveal ingrowth of new vessels, and progressive peripheral chorioretinal atrophy. By contrast to other reports the family in the current study have peripheral retinal dysfunction, a deposit of a subretinal yellow material throughout the fundus and a tritan colour defect, all prior to the loss of central vision; in some patients there was loss of central vision from atrophic disease, rather than from ingrowth of subretinal new vessels; and, there was a different temporal progression of the central subretinal neovascular complex. These features suggest the possibility of genetic heterogeneity.
We report a 13-year-old male who complained of strabismus and low visual acuity in the right eye. Saccular aneurysms filled with dark-colored blood were noted in the upper nasal quadrant of the right fundus. Ishihara color plates and Lanthony's new color test revealed a red-green color defect. Cone response and 30-Hz flicker responses were nearly absent. Cavernous hemangioma of the retina is a rare vascular hamartoma; the associated findings show cone dysfunction concomitant with this peripheral lesion.
We measured the reflectance spectra for the 85 color caps of the Farnsworth-Munsell 100-hue test. Eigenvectors and eigenvalues of a correlation matrix of cone responses were computed, with the cone responses being determined from the 85 test caps, arranged in order (according to color) by means of a linear model. It is shown that the Farnsworth-Munsell 100-hue test can be simulated by use of eigenvectors of the cone responses. The eigenvectors can be interpreted as nonopponent signal and opponent color signals. The normal observer can determine the color of a cap by using two opponent color signals. For color-blind persons (dichromats) one or the other opponent signal is defective, and errors can occur during the test. The simulation results also suggest that eigenvectors can be used to predict results of arrangement tests similar to the Farnsworth-Munsell 100-hue test.
The recently introduced Holmes - Wright Type A and Type B lanterns and the Farnsworth lantern were administered to 100 observers with normal colour vision and 100 observers with defective colour vision. With the fail criteria adopted, all normals passed the Holmes - Wright Type A lantern and with one exception all normals passed the Farnsworth lantern. However, 8% of normals failed the more difficult Holmes - Wright Type B lantern. It is noted that the normals who fail this lantern test appear to do so not because of poor colour discrimination but because the coloured stimuli presented by the lantern have a point brilliance close to the average chromatic threshold. About one-third of the colour vision defective group passed the Farnsworth lantern and between 14 and 17% passed the Holmes - Wright Type A lantern depending on the test procedure used. Only two mild deuteranomals in the sample of 100 colour abnormal observers succeeded in passing the Holmes - Wright Type B lantern. Dichromats and severe anomalous trichromats fail all three lanterns so that those who pass are all mild anomalous trichromats. A significant proportion of protanomals pass the Farnsworth lantern and some protanomals pass the Holmes - Wright Type A lantern despite their reduced sensitivity to red light and correspondingly reduced signal range for red signals.
The Colour Vision Analyser was used for testing 98 persons of both sexes, aged from 10 to 70 years, and recognized as normal by means of pseudo-isochromatic plates and an anomaloscope. A drop of the saturation thresholds from yellow to green and from blue to purple was observed from the age of 40 years. The saturation thresholds from yellow to green was found lower in every age group than that from blue to purple. Congenital colour defects could be completely distinguished from normal subjects. As for the classification in types, those diagnosed as deutan by means of the anomaloscope were also diagnosed as deutan by the Analyser, however, there were, among those diagnosed as protan by the anomaloscope, some subjects who were diagnosed as deutan by the Analyser. Nearly all cases could be classified as anopia or anomaly.