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Results for “Color Vision Defects”

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PubMed1980

Results of colour vision tests in alcoholic and in mentally disordered subjects.

The responses at the Ishihara test, the Nagel anomaloscope, the standard Panel D--15 and the 100 hue test (with correction of the age effect) were recorded in 38 alcoholics in deprivation period (successively subdivided according to age, to abstinence duration and to liver condition) and in 32 subjects suffering from mental diseases (successively subdivided according to ethylic past, to age, to duration of the stay in the hospital and to activity). It is shown that alcoholism causes a diminution of the performance at the used colour vision tests and especially at the 100 hue test. The defect can be ascribed to psychical factors (chiefly in the cases of mental disease and in the younger people), but also to an acquired blue-yellow defectiveness of colour vision with a shift of the Rayleigh match to red (such a defectiveness can also be due to a liver damage and to some intoxications) and even to a Type II acquired red-green defectiveness of colour vision (possibly by tobacco or disulfiram intoxication). The defect due to alcohol itself soon disappears during desintoxication. The authors draw some practical conclusions.

Adult↗
PubMed1985

Probable autosomal dominant optic atrophy with hearing loss.

The seventh family manifesting an entity described as automosal dominant optic atrophy with hearing loss is reported here. This disorder shows great inter- and intrafamilial variation in the onset time and the degree of loss of both vision and hearing. Unlike autosomal dominant optic atrophy without hearing loss, it appears to be associated with a red-green (deutan) defect in color vision.

Adult↗
PubMed1998

M- and L-cones in early infancy: III. Comparison of genotypic and phenotypic markers of color vision in infants and adults.

Genetic analyses were performed on five male children (approximately 3 years), two suspect color-normals and three suspects for congenital color vision deficiencies. These classifications were based on visually-evoked potential (VEP) responses to M- and L-cone-isolating stimuli obtained in a previous study when each subject was either 4- or 8-weeks old. The present analyses were performed in a blind study to characterize the genotypes of these subjects. Four male adults with various color vision phenotypes were also tested as a control. DNA was isolated using a non-invasive technique followed by polymerase chain reaction (PCR) amplification and restriction enzyme analysis to examine the genomic DNA of each subject. The genetic analyses confirmed the VEP identification of two color defective infants, and were consistent with the diagnosis of two other infants as color normal. A third infant was predicted by VEP analysis to have a protan defect, but he did not have a gene array typically found in protan observers.

Child, Preschool↗
PubMed1979

A clinicopathologic study of autosomal dominant optic atrophy.

Of a family with 40 members, 12 had autosomal dominant optic atrophy. The affected members were aware of reduced vision from the first decade. Visual loss was moderate to severe, 6/12 (20/40) to 3/60 (10/200). The affected members showed similar centrocecal scotomata. Most affected patients had severe unclassified color defects. Electroretinography measurements were normal in all but one patient who had a small reduction in the scotopic response. The pathologic changes in a patient with autosomal dominant optic atrophy showed diffuse atrophy of the ganglion cell layer of the retina with a loss of myelin and nerve tissue within the optic nerves. We suggest that autosomal dominant atrophy is a primary degeneration of retinal ganglion cells.

Adult↗
PubMed1976

An acquired color defect of the opponent-color system.

An acquired unilateral color defect in a 22-year-old man has been investigated with standard clinical tests and by using techniques which, it is thought, test specifically for the sensitivity of the luminance and opponent-color systems. The spectral sensitivity of the defective left eye, using 1 degree 200 ms. test flashes on a white background, has a single broad peak at about 550 nm. and resembles the photopic luminosity curve; in contrast, the normal curve, measured in the same conditions, has three peaks at about 440, 520, and 600 nm. However, the subject's spectral sensitivity curve for detecting 20 Hz. flicker is quite normal and is similar to his curve for 200 ms. flashes. It has recently been proposed that the three peaks of the normal curve for 200 ms. flashes reflect the activity of the opponent-color system, whereas the single peak for flicker detection is related to the luminance system. The preceding observations may thus be interpreted in terms of a specific loss of the subject's opponent-color system and this would explain his poor color discrimination. His luminance system appears to be normal, and evidence is presented for the maintained function of red- and green-sensitive (but not blue-sensitive) cones. The spectral sensitivity of the subject's right eye is nearly normal, suggesting a precortical origin of the defect; however, there seems to be some abnormality in this eye, indicating a less developed form of the same defect.

Adult↗
PubMedDate not supplied

Color vision screening and viewing conditions: the problem of misdiagnosis.

The most popular techniques for assessing color vision, the pseudoisochromatic tests, have been found to differ widely in their sensitivity to changes in viewing conditions. A significant number of color-normal subjects will be misdiagnosed as color defective by some of the standard tests with even relatively minor variations from standardized viewing conditions. These results appear to have strong implications for the use of the tests in many applied settings which precise control over viewing conditions is difficult. In particular, as the consequences of a misdiagnosis become very serious, the tests must be used with special caution. If we were to recommend one test for use, our findings point to the Ishihara, which appears impervious to variation in viewing conditions.

Color Perception Tests↗
PubMed2000

A controlled study of vigabatrin and visual abnormalities.

AIMS: To assess the visual function in epileptic patients who have received vigabatrin; to compare this with the visual function in similar epileptic patients who have never received vigabatrin; to investigate whether the severity of visual field defect (VFD) is related to the dose of vigabatrin; to consider other factors that may correlate with the severity of VFD. METHODS: 21 consecutive patients who had taken vigabatrin at some time in their lives were enrolled from the epilepsy clinic of the Royal Shrewsbury Hospital and were compared with a group of 11 otherwise similar patients with epilepsy who had never received vigabatrin. One patient taking vigabatrin was excluded from the study because her visual field results were unreliable because of multi-infarct dementia. 15 patients were taking vigabatrin at the time of the study (VC), the other five had taken vigabatrin some time in the past (VP). Each patient underwent static perimetry using either the two point or the three point full field 120 screening program on the Humphrey visual field analyser, followed by an ophthalmic examination to rule out ocular causes for VFDs. The visual fields from each patient were then analysed using a method devised to convert the VFD into percentage defect in both eyes. In patients with known cerebral pathology that may affect the visual pathway, only the unaffected homonymous hemifield was used. RESULTS: Nine of 20 (45%) patients in the vigabatrin group (VC and VP) complained of blurring of vision compared with two of 11 (18%) controls. Four patients (20%) in the vigabatrin group described flickering lights compared with one control (9%). None had a posterior vitreous detachment. Three of 30 (7.5%) eyes in the VC group had distant visual acuity of 6/12 or worse compared with three of 22 (9%) controls and five of 30 (16.7%) had near visual acuity worse than N6 compared with one of 22 (4.5%) in the control group. A mean of 1.73 Ishihara plates were misread in VC patients compared with 0.2 in the VP group and 0.18 in the controls. 11 of 15 (73.3%) patients in the VC group had greater than 10% VFDs as opposed to one of 11 (9.1%) controls (chi(2) test, p=0. 002). In 12 of 15 (80%) VC patients the percentage VFD was greater in the nasal hemifields than the temporal hemifields compared with six of 11 (54.5%) controls. Significant correlation was found between the severity of VFD and the total dose of vigabatrin ingested for the 20 patients exposed to vigabatrin (VC and VP: Spearman correlation coefficient=0.525; p=0.002), for the 15 patients taking vigabatrin at the time of examination (VC: Spearman correlation coefficient=0.568; p=0.002). CONCLUSION: This pilot study suggested that epileptic patients taking vigabatrin are at much higher risk of developing VFDs compared with epileptic patients on other antiepileptic drugs. The total ingested dose of vigabatrin correlated significantly with the severity of VFDs especially in those patients who had not stopped taking vigabatrin. In our group we found that those who had taken a total dose of 1500 g or more of vigabatrin were at risk of developing significant visual field defects.

Adult↗
PubMed1976

A family with congenital deutan and tritan defects.

A family has been found with deuteranopia and a tritan defect which is not sex-linked. It is proposed that there is also an autosomal dominant gene for tritan defects showing variable expressivity.

Adolescent↗