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PubMed1987

Normal and defective colour vision in large field.

Colour vision is spatially organized. A light stimulus has to strike spectrally different photoreceptors, covering the center and surround of the receptive field of a colour opponent retinal ganglion cell. Otherwise, no colour opponent processing of signals will occur. Vice versa, spatial summation provided by a large field may compensate for weak opponency. This happens not only in congenital, but also in acquired colour vision defects, when opponency is weakened secondary to a reduced receptoral input. Large field colour vision in Daltonians. Large field red-green opponency is a common phenomenon in patients fitting into the criteria of protanopia and deuteranopia. The difference between small and large field colour vision can be demonstrated by the "projection anomaloscope". At a 30 degrees test field, many anopes behave like the respective anomalous observers. The majority of anopes appear to have some "forbidden cones" at their retinal disposal. So, anomaly and anopia share a common photochemical basis, i.e., the anomalous pigment. However, in anopes, the number of those anomalous cones is extremely small. Therefore, anopic observers usually need a very large amount of spatial summation to arrive at a well defined match of the projection anomaloscope. In protanopes the large field match in our experiments was always a protanomalous one, with the exception of one large field protanope. In deuteranopes, however, there was no such constant behaviour in large field matching. We found deuteranomalous matches as well as matches in the vicinity of the normal mid-match point. Contrary to this behaviour of anopes anomalous observers do not significantly alter their matching pattern irrespectively of whether small (1 degree) or large (30 degrees) test fields are used. So-called peripheral colour blindness of normal observer. Results of classical colour perimetry reveal a dichromatism of the intermediate and a monochromatism of the extreme retinal periphery of the normal observer. These results appear to contradict the common everyday experience of colour constancy throughout the visual field. But a threshold correlation of colour constancy at different retinal exentricities can be demonstrated by recording spectral increment thresholds with test field diameters increasing towards the retinal periphery. So, the colour blindness of the retinal periphery is merely an area phenomenon. It can be overcome by large field observation, rendering spatial summation. Congenital achromatopsia. Remnants of colour vision can be demonstrated in many achromats.(ABSTRACT TRUNCATED AT 400 WORDS)

Color Perception↗
PubMed1995

Selective cone dystrophy with protan genotype.

PURPOSE: To determine the functional defects in two male patients with progressive cone dystrophy and hybrid L-M cone pigment genes. METHODS: Clinical evaluation, standard electroretinography, and electrooculography were performed in two affected patients and two family members. Measurements of spectral sensitivity and transient tritanopia were made in both patients. RESULTS: In the patients, visual acuity varied between 20/50 and 20/100. The electroretinogram showed reduced flicker responses. When light adapted, a-wave amplitudes were borderline, but b-wave amplitudes were reduced severely. Electroretinography with chromatic stimuli showed a difference between well-preserved responses to green and markedly reduced responses to red stimuli. Spectral sensitivity measurement revealed a lack of L (long-wavelength sensitive; red) cone function and normal function of the S (short-wavelength sensitive; blue) and M (middle-wavelength sensitive; green) cones. Transient tritanopia was abnormal, indicating a severe disturbance of cone-cone interaction. CONCLUSIONS: Progressive cone dystrophy with predominant dysfunction of L cones exists in both patients. The cone dystrophy may be caused by a rearrangement of the X-chromosome pigment gene array that is associated with the deletion of L-cone sequences and the formation of hybrid L-M cone pigment genes. It cannot be excluded, however, that both patients have protanopia and that cone dystrophy developed because of other causes.

Adult↗
PubMed1994

[The history of research in color perception as a key to understanding various forms of congenital defects in red-green perception].

It is accurate to date the first scientific report about colour-deficiencies on 1777. Earlier descriptions may be followed up to the end of the 17th century. But usually it is only mentioned, that mistakes had happened. Huddart 1777, however, reported for the first time, that more than one person was involved in a family and that demonstrations of coloured ribbons helped to find out which colours became confounded. The famous self-observation of Dalton contains the assortment of individually combined silk-threads, which is an anticipation of subsequent arrangement-tests. Goethe developed a systematic arrangement-test of self-made small coloured targets with colours out of his own colour-wheel. A. Seebeck was the first who--using the spectrum for examination--found out that a special group of subjects showed a shortening of the spectrum at the red end. From this result Helmholtz concluded the existence of two types of red-green blindness. This new argument for the trichromatic organisation of our colourvision was the basis for the statement of the three types: protanopia, deuteranopia and tritanopia (v. Kries, A. König). Rayleigh later on succeeded in finding out anomalous trichromats following preparatory examinations of Maxwell. Nagel has the merit to have analysed protanomaly and deuteranomaly using the anomaloscope constructed by himself. Side by side with the spectral colour-tests pseudoisochromatic plates were developed for diagnostic purposes, at first thought out and introduced by Stilling and in the meantime used in many variations.

Color Perception Tests↗
PubMed2005

Progressive cone dystrophy with deutan genotype and phenotype.

PURPOSE: To study the electroretinographic signals originating in the long-wavelength-sensitive (L) and middle-wavelength-sensitive (M) cone pathways by means of large-field and multifocal cone type-specific electroretinograms (ERGs) in a patient with progressive cone dystrophy. METHODS: A 65-year-old male patient with colour vision disturbances (age at onset 10 years), loss of visual acuity (14 years), and central visual field defects (40 years) was investigated. Large-field flicker-ERG responses to stimuli that exclusively modulated the L-cones or the M-cones, or the two simultaneously (both in-phase and in counter-phase), were measured. Short-wavelength-sensitive (S) cones were not modulated. Multifocal ERGs (mfERGs) were also recorded, with a pattern-reversing display that modulated only the L- or the M-cones at equal cone contrasts and average quantal catches. Genetic analysis of L- and M-pigment genes was performed on genomic DNA isolated from peripheral venous blood. RESULTS: The patient showed a normal rod-driven ERG but reduced cone-driven electroretinographic amplitudes with normal implicit times in the International Society for Clinical Electrophysiology of Vision (ISCEV) standard ERG. The large-field flicker-ERG responses to pure L-cone modulation were significantly above noise level but were substantially reduced in comparison with both normal trichromatic subjects and (otherwise normal) deuteranopes. The L-cone driven electroretinographic implicit times and phases were within normal limits. The M-cone driven electroretinographic responses were not detectable. A model fit of all the L- and M-cone driven flicker-ERG data revealed that the responses were exclusively driven by the L-cones. Consistently, the cone type-specific mfERGs showed severely reduced but detectable responses to L-cone-isolating stimuli. The M-cone driven multifocal-ERG responses were undistinguishable from noise. The L- and M-pigment gene array consisted of only a single L-pigment gene. The complete coding sequence of this gene was determined and showed no abnormality. CONCLUSIONS: This patient exhibits a coincidence of progressive cone dystrophy and deuteranopia. The molecular genetic data of the L/M-pigment gene array is consistent with the deutan phenotype. It cannot be excluded that the rearrangement of the X-chromosome pigment gene array is responsible for the cone dystrophy in this patient. It is, however, suggested that the dichromacy and the cone dystrophy have different and independent genetic origins.

Aged↗
PubMed1983

Classical tritanopia.

1. A subject who has suffered from central serous chorio-retinopathy in his left eye noticed differences in the colour of a given light as perceived by each eye alone. Standard screening tests (colour order and colour matching) indicated a tritan defect in the left eye; the right eye was normal on these tests.2. The subject was dichromatic in his left eye, trichromatic in his right. The left-eye distimulus colour-matching functions, spectral luminosity, and wave-length discrimination functions were indistinguishable from corresponding data for congenital tritanopia. Comparable right-eye data were normal.3. Spectral dichromatic colour matches were invariant under changes of intensity and under addition of a common light to both halves of the field. (Grassmann's laws of linearity are satisfied.)4. Increment threshold versus intensity (t.v.i.) curves for a blue (481.9 nm) test on a yellow background yielded the normal three branches (for Pi(4)(mu), Pi(1)(mu) and Pi(3)(mu) respectively) in the trichromatic eye. In the dichromatic eye a single mechanism was found. It had the field sensitivity of Pi(4)(mu) whether measured with the blue, or with a violet (429.5 nm) test. No trace of Pi(3)(mu) or Pi(1)(mu) was ever discovered in the tritanopic eye. Both are normal in the trichromatic eye.5. The field sensitivities of Pi(4), Pi(5) and Pi(3) of the normal eye are well fitted by linear combinations of the spectral colour-matching functions of the trichromatic eye. Pi(4) and Pi(5) of the dichromatic eye are well fitted by linear combinations of the tritanopic matching functions.6. Colour matches made by the trichromatic eye do not match when viewed by the tritanopic eye, almost certainly because the ocular media of the two eyes have wave-length-dependent differences in absorption. For the largest difference (430 nm) the trichromatic eye transmits about 2.2 times more light than its fellow. When allowance is made for these differences, the field sensitivities of Pi(4) and Pi(5) of the two eyes do not differ. The field sensitivities of Pi(4) and Pi(5) of the normal eye, on the other hand, differ significantly from those of the average spectra obtained on four normal trichromats by Stiles, in a way that cannot be attributed to differences in transmittance of ocular media.7. It is concluded that classical (or acquired) tritanopia is not distinguishable in its manifestations from congenital tritanopia; furthermore, tritanopia can be regarded as a reduced form of normal trichromacy, once allowances are made for absorption of the ocular media and for variations among normal trichromats.8. Despite extensive search no evidence could be uncovered which might exclude the hypothesis that the colour vision in tritanopia depends exclusively upon absorption in only two foveal cone pigments, one long-wave-absorbing and one medium-wave-absorbing.

Adult↗
PubMed1977

Involutional diabetic retinopathy.

The end-stage or involutional phase of proliferative diabetic retinopathy may result in stabilization of vision for long periods of time. However, the clinical resemblance to the progressive tapetoretinal degenerations suggests that marked functional impairment of the retina is present in such eyes. We studied 19 eyes with involutional retinopathy to document the status of the retinal function. Studies included fluorescein angiography, visual field examination, dark adaptation testing, color vision testing, electro-oculography and electroretinography (ERG). The results indicated marked functional abnormalities in all eyes. The ERG tracings showed uniformly subnormal responses and delayed implicit times, similar to those of dominantly inherited retinal pigment degeneration, and indicative of a progressive retinal disorder. In two patients, color vision testing showed defects similar to those seen in inherited tritanopia; and in the remaining patients, defects were indicative of an acquired blue-yellow dyschomatopsia.

Adaptation, Ocular↗
PubMed2001

Impact of color blindness on recognition of blood in body fluids.

BACKGROUND: Color blindness is a common hereditary X-linked disorder. OBJECTIVE: To investigate whether color blindness affects the ability to detect the presence of blood in body fluids. METHODS: Ten color-blind subjects and 20 sex- and age-matched control subjects were shown 94 photographs of stool, urine, or sputum. Frank blood was present in 57 (61%) of the photographs. Surveys were done to determine if board-certified internists had ever considered whether color blindness would affect detection of blood and whether an inquiry on color blindness was included in their standard medical interview. RESULTS: Color-blind subjects were significantly less able to identify correctly whether pictures of body fluids showed blood compared with non-color-blind controls (P =.001); the lowest rate of correct identifications occurred with pictures of stool (median of 26 [70%] of 37 for color-blind subjects vs 36.5 [99%] of 37 for controls; P<.001). The more severely color-blind subjects were significantly less accurate than those with less severe color deficiency (P =.009). Only 2 (10%) of the 21 physicians had ever considered the possibility that color blindness might affect the ability of patients to detect blood, and none routinely asked their patients about color blindness. CONCLUSIONS: Color blindness impairs recognition of blood in body fluids. Color-blind individuals and their health care providers need to be made aware of this limitation.

Adult↗
PubMed2002

Progressive worsening of spatial and chromatic processing deficits in Parkinson disease.

CONTEXT: Impairments of color discrimination (CD) and contrast sensitivity are established signs of Parkinson disease (PD), but their temporal evolution has not been studied. OBJECTIVE: To determine whether there is progressive, longitudinal deterioration of color discrimination (CD) and contrast sensitivity (CS) in PD. DESIGN: A prospective study. SETTING: Tertiary care center-based sample of PD patients without dementia with normal visual acuity (Snellen fraction >0.6 in the best eye). MAIN OUTCOME MEASURES: With a mean +/- SD interval of 19.8 +/- 2.8 months, the following tests were applied twice in 28 patients: the Lanthony D15 test and the Farnsworth Munsell 100 Hue test as tests of CD and the monocular and binocular Pelli-Robson test and the binocular Vistech tables as tests of CS. RESULTS: There was deterioration of both CD (Farnsworth Munsell 100 hue test: P =.002) and CS (binocular Vistech test at a spatial frequency of 6 cycles per degree, P<.001). Both deficits correlated with age, and the chromatic deficit additionally correlated with higher impairment of motor function (Unified Parkinson's Disease Rating Scale motor section, P =.04) and activities of daily life (Unified Parkinson's Disease Rating Scale activities of daily living section, P =.006). Patients with the highest pathologic psychiatric rating score (Brief Psychiatric Rating Scale) performed worse on both CS (P =.02) and CD (P =.01) at the second examination. CONCLUSIONS: Impairments of CD and CS in PD are progressive over time. Visual deficits may influence overall motor function and lead to enhanced motor impairment.

Aged↗
PubMed1999

Clinical characterization and linkage analysis of a family with congenital X-linked nystagmus and deuteranomaly.

OBJECTIVES: To identify a congenital nystagmus locus on the X chromosome and to characterize the phenotype of a 4-generation family affected with congenital nystagmus and color deficiency. METHODS: Sixty-five patients underwent an eye examination, including evaluation for the presence of nystagmus and color vision abnormalities. Affected patients and obligate carriers of the congenital nystagmus mutation were genotyped with short tandem repeat polymorphisms located on the X chromosome, and these data were subjected to linkage analysis. RESULTS: Fourteen patients were affected with a horizontal, conjugate, congenital nystagmus. All examined patients had a visual acuity of 20/60 or better. There were no associated ocular or systemic findings except that 18 of the family members had deficient red-green color vision, which was classified as deuteranomaly (the most common form of anomalous trichromacy). Five patients exhibited nystagmus and deuteranomaly. Significant linkage was demonstrated between the nystagmus phenotype and 11 markers from Xq. The maximum lod score was 4.84 (theta = 0) and was obtained with marker DXS8041. Analysis of recombinants defined the disease interval to lie between markers ATA59C05 and DXS1192 (a 5.4-centimorgan region). The proximity of this locus to the red-green opsin gene cluster (11 centimorgans more telomeric) explains the frequent coexistence of nystagmus and color vision deficiency in this family. CONCLUSIONS: We have identified the genetic locus of the X-linked congenital nystagmus gene in this family. The critical interval in this report is less than half the size of the previously described nystagmus locus. These findings will aid in identifying the gene responsible for this condition.

Chromosome Mapping↗
PubMed2000

Selective loss of S-cones in diabetic retinopathy.

OBJECTIVE: To determine whether selective cone loss could explain the acquired tritan-like color confusion found in diabetic retinopathy. METHODS: Terminal deoxynucleotidyl transferase-mediated biotin-deoxyuridine triphosphate nick end labeling (TUNEL) was employed on paraffin sections of retinas from 5 donors with diabetic retinopathy. For quantitative analysis, postmortem retinas were obtained from 13 human donors; 7 from patients with various durations and stages of diabetic retinopathy (4 background, 3 proliferative) and 6 controls. Enzyme histochemical analysis for carbonic anhydrase (CA) was used to distinguish L/M-cones (positive for CA) from S-cones (negative for CA). Cone topography was determined by sampling 360 degrees from 0.1 to 1.5 mm of foveal eccentricity and along the horizontal meridians from 1.5 to 15.0 mm. RESULTS: Rare cells in both the inner and outer nuclear layers of the diabetic eyes were positively labeled with the TUNEL method. The CA staining revealed incomplete and patchy losses of S-cones that were limited to the diabetic retinas. Statistically significant reduction in the density of S-cones was found at nearly all foveal eccentricities from 0.1 mm to 15.0 mm. This was not the case for the L/M-cones. On average, for all locations, the percentage of S-cones compared with L/M-cones was decreased by 21.0% +/- 3.4% with respect to the controls. CONCLUSION: The S-cones selectively die in diabetic retinopathy. CLINICAL RELEVANCE: Selective loss of S-cones may contribute to the tritan-like color vision deficit seen in patients with diabetic retinopathy.

Adult↗