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PubMed1983

Basic phenomena in acquired colour vision deficiency.

Acquired colour vision defects are directly related to the fixation mode: blue-yellow defects in foveolar fixation, blue-yellow or red-green defects in eccentric fixation. The primary localization of a disease can be retraced from the degree of cone damage. Optic nerve diseases essentially lack signs of cone damage. Processes at the level of the choriocapillaris/retinal pigment epithelium induce a non-selective receptor impairment. There are minor signs of cone damage. In cone dystrophies there is selective cone damage. Scotopization indicates a relatively well-preserved rod function.

Adolescent↗
PubMed1979

[Detection of dyschromatopsias and professional orientation].

Certain professions necessitate correct recognition of colour in their practice. Early defection of coloured vision abnormalities and professional orientation are therefore very important, especially as it is known that 8 % of the population presents a congenital dyschromatopsy of which one fourth (about 2 %) are serious dyschromatopsies which will prevent the practice of a certain number of professions.

Color Perception Tests↗
PubMed1978

Frequencies of different types of colour vision defects in the Netherlands.

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.

Adolescent↗
PubMed1993

Recent developments in certain X-linked genetic eye disorders.

Over the past few years, genetic diseases of the ocular system have become very active and fast-growing research areas in the vision field. The rapid development of the recombinant DNA techniques together with somatic cell genetics, during the last two decades has fueled this progress. As a result, many genetic disease genes have been localized in the human chromosome and several of them have been isolated and characterized. These and other studies have profoundly enriched our basic understanding of genetic eye disorders. Although gene replacement therapy, prenatal diagnosis and carrier detection have not been extensively tried for genetic eye diseases, such attempts will now be feasible. Molecular analyses made it clear that there are many challenging problems that need attention. This report highlights some of these initial developments, particularly on the X-linked major genetic eye diseases. In order to help the beginners and general audience, a brief description of the clinical pathology and the molecular probes used to locate the genetic defects of certain disorders are presented. Disorders are arranged according to their linkage from telomere to telomere on the chromosome to give a coherent structure. It is hoped that this information is useful and of general interest for the beginners, established investigators and ophthalmologists.

Cataract↗
PubMedDate not supplied

Hypertensive optic neuropathy.

In 1970 a 62-year-old physician with hypertensive vascular disease suffered a small infarction in the left optic disc, which left him with a subtle paracentral temporal visual field defect in that eye. In 1973 he had another separate and distinct episode in the same eye, which produced a dense lower nasal field defect. Careful Hruby lens examination of the disc under high magnification revealed focal arteriolar disease in the optic nerve head corresponding to the field defects, and fluorescein angiography confirmed these findings. The importance of differentiating ischemic optic neuropathy, hypertensive optic neuropathy, and temporal arteritis with optic nerve involvement is emphasized, and the therapy of each is discussed.

Color Vision Defects↗
PubMed1976

Colour vision deficiencies and haemophilia.

Our investigations have following results: In the Rath-von Verschuer family, which is so extraordinary that the authenticity sometimes had been doubted, we found that crossing overs which were present in 50% of the cases were shown by the combination of protan defect and haemophilia B. This corresponds exactly to the observation of Whittaker and co-workers, who starting from that fact, concluded that there was a remarkable distance between the protan gene and haemophilia B gene on the chromosome. The observation enlarges the number of pedigrees with the combination of protan defect and haemophilia B. At the same time, however, we are doubtful that there might be a probable preference for this combination. With regard to the question whether manifestation of protanopia and protanomaly in any given form could be influenced by an additional factor in the X-chromosome, our present investigations give no reliable data.

Color Vision Defects↗
PubMed1993

Modelling sensitivity losses in ocular disorders: colour vision anomalies following intense blue-light exposure in monkeys.

The effects of prolonged exposure to intense, short-wavelength light were studied in monkeys through the measurement of increment-threshold spectral sensitivity (ITSS) and threshold-versus-intensity (TVI) functions using a behavioural method. The long-term effect of intense blue-light exposure was to induce a short-wavelength (SW) sensitivity loss which did not depend on the intensity or chromatic composition of the adapting field. The TVI curves for short wavelength stimuli revealed an increase in test threshold without changes in field sensitivity. Since this SW sensitivity loss may generalize to characteristic colour vision defects found in many outer retinal diseases, models of acquired alterations of colour vision mechanisms are considered. These models describe probable changes in ITSS functions and TVI curves in diseases affecting the inner or outer retina as well as changes in dark adaptation.

Animals↗
PubMed1979

Bilateral symmetry of vision disorders in typical retinitis pigmentosa.

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.

Adolescent↗
PubMed1995

Scoring the Farnsworth-Munsell 100-hue for vocational guidance.

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.

Adult↗
PubMed1978

N-hexane maculopathy in industrial workers.

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.

Adult↗
PubMed1991

High myopia with cone dysfunction.

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.

Adolescent↗
PubMed1982

Crossed-quadrant homonymous hemianopsia. The "checkerboard" field defect.

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.

Aged↗
PubMed1993

Colour blindness and natural selection: studies in four nomadic tribal groups from Andhra Pradesh, India.

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.

Color Vision Defects↗
PubMed1983

Pseudoisochromatic plate design--Macbeth or tungsten illumination?

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.

Color Perception Tests↗
PubMedDate not supplied

Progressive human cone-rod dysfunction (dystrophy).

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.

Adolescent↗
PubMed1993

The Farnsworth-Munsell 100 hue test in the first episode of demyelinating optic neuritis.

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.

Adult↗
PubMed1993

Colour vision in retinitis pigmentosa. Influence of cystoid macular edema.

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.

Color Perception↗