Cases reported "Color Vision Defects"

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1/161. Complete sparing of high-contrast color input to motion perception in cortical color blindness.

    It is widely held that color and motion are processed by separate parallel pathways in the visual system, but this view is difficult to reconcile with the fact that motion can be detected in equiluminant stimuli that are defined by color alone. To examine the relationship between color and motion, we tested three patients who had lost their color vision following cortical damage (central achromatopsia). Despite their profound loss in the subjective experience of color and their inability to detect the motion of faint colors, all three subjects showed surprisingly strong responses to high-contrast, moving color stimuli--equal in all respects to the performance of subjects with normal color vision. The pathway from opponent-color detectors in the retina to the motion analysis areas must therefore be independent of the damaged color centers in the occipitotemporal area. It is probably also independent of the motion analysis area MT/V5, because the contribution of color to motion detection in these patients is much stronger than the color response of monkey area MT. ( info)

2/161. A locus for autosomal recessive achromatopsia on human chromosome 8q.

    Autosomal recessive achromatopsia is a rare disorder characterized by total absent color vision, nystagmus, photophobia, and visual impairment, frequently leading to 'legal blindness'. The primary defect is at the photoreceptor level, with retinal cones being absent or defective. The first locus for this disorder was mapped to chromosome 2q11. Here, we confirm the genetic mapping of a locus discovered in our studies of a kindred with Irish ancestry, but no known consanguinity, in which 5 of 12 children are affected. We have mapped the locus in this disorder in this family to chromosome 8q. Available data now narrow the region containing the putative gene to 1.2 cM. ( info)

3/161. Toxic optic neuropathy after concomitant use of melatonin, zoloft, and a high-protein diet.

    melatonin is a neuromodulating hormone found in the pineal gland and retina. It is involved in light-dark circadian rhythms and mediates retinal processes in a manner antagonistic to that of dopamine. Zoloft (sertraline) is an antidepressant drug that blocks the reuptake of serotonin at the neural synapse. serotonin is the natural precursor of melatonin. A 42-year-old woman sought treatment for visual acuity loss, dyschromatopsia, and altered light adaptation. Neuro-ophthalmologic examination was otherwise normal except for evolving bilateral cecocentral scotomas. She had taken Zoloft for 4 years and began a high-protein diet with melatonin supplementation 2 weeks before onset of visual symptoms. visual acuity and color vision improved within 2 months after melatonin and the high-protein diet were discontinued. Combined use of melatonin, Zoloft, and a high-protein diet may have resulted in melatonin/dopamine imbalance in the retina, manifesting as a toxic optic neuropathy. physicians and patients should be alerted to this potential drug interaction. ( info)

4/161. Hemianopic colour blindness.

    A man developed cortical blindness after cerebral infarction in the distribution of both posterior cerebral arteries. When he recovered from this condition, he was found to be colour blind in the left visual field, but not in the right. This unusual situation resulted in apparently contradictory performances on hemifield and free-field tasks of colour discrimination, naming, and recognition. The contradictions may be explained by interhemispheric competition between a hemisphere which could discriminate colours and a hemisphere which was colour blind. ( info)

5/161. Ocular manifestations of hypercupremia associated with multiple myeloma.

    Extensive copper infiltration of descemet membrane of the central cornea and of the anterior and posterior surfaces of the lens is associated with marked hypercupremia related to an abnormal immunoglobulin. observation of this spectrum of ophthalmic changes in an apparently well middle-aged woman heralded the diagnosis of a unique variety of multiple myeloma. ( info)

6/161. Binocular enhancement of color discrimination in a deutan.

    A 31-year-old white male deutan produced reliably different profiles when examined binocularly and monocularly with a Farnsworth-Munsell 100-hue test. Discrimination in the long wavelengths improved under the binocular conditions. Intensive testing yielded no information to account for the phenomenon. ( info)

7/161. 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. ( info)

8/161. Probable common origin of a hereditary fundus dystrophy (Sorsby's familial pseudoinflammatory macular dystrophy) in an English and Australian family.

    A genealogical link was established six generations back between a family living in england and australia, and one of the families reported originally by Sorsby et al (1949) as suffering from autosomal dominant inflammatory macular dystrophy (fundus dystrophy). The onset--in the fifth decade of life--and the progress of the condition, which usually ends in blindness, has been observed in a number of patients and the prodromal development of a colour vision deficiency in some of them confirmed. This defect is fundamentally different from the X-linked colour vision defects and merits further investigation. ( info)

9/161. X mapping in man: evidence against direct measurable linkage between ocular albinism and deutan colour blindness.

    A Newfoundland kindred in which ocular albinism and deutan colour blindness are segregating provides strong evidence against the loci for these two X-borne characters being within direct measurable distance of each other. ( info)

10/161. Unilateral colour vision defect resembling tritanopia.

    A case of unilateral tritan defect is described. Colour-naming experiments showed that the tritanopic eye could perceive multiple colour hues. Although the defect resembled congenital tritanopia, it was considered to be acquired secondary to retinal pathology. ( info)
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