Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Color Vision”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,495 records · Page 83Linked to original sources
PubMed1984

Selective damage to chromatic mechanisms in neuro-ophthalmic diseases I. Review of published evidence.

Acquired color deficiencies may correspond to a general, non-selective loss of visual sensitivity. We summarise evidence for the opposite view that, in some cases, chromatic sensitivity can be more (or less) reduced than achromatic sensitivity. This evidence is based on: (1) Disproportion between chromatic and achromatic isopters; (2) Differential damage to red-green and blue-yellow color vision; (3) Detection static perimetry; (4) The foveal photochromatic interval; (5) The two color threshold technique; (6) Spectral sensitivity on a white background; (7) Single unit and histological studies of the retina and lateral geniculate nucleus; (8) Lesions of the prestriate color area; (9) Selective damage to achromatic processes. Possible problems of interpretation are considered and a new technique for comparing chromatic and achromatic sensitivity is briefly described.

Animals↗
PubMed1999

Selective color constancy deficits after circumscribed unilateral brain lesions.

The color of an object, when part of a complex scene, is determined not only by its spectral reflectance but also by the colors of all other objects in the scene (von Helmholtz, 1886; Ives, 1912; Land, 1959). By taking global color information into account, the visual system is able to maintain constancy of the color appearance of the object, despite large variations in the light incident on the retina arising from changes in the spectral content of the illuminating light (Hurlbert, 1998; Maloney, 1999). The neural basis of this color constancy is, however, poorly understood. Although there seems to be a prominent role for retinal, cone-specific adaptation mechanisms (von Kries, 1902; Pöppel, 1986; Foster and Nascimento, 1994), the contribution of cortical mechanisms to color constancy is still unclear (Land et al., 1983; D'Zmura and Lennie, 1986). We examined the color perception of 27 patients with defined unilateral lesions mainly located in the parieto-temporo-occipital and fronto-parieto-temporal cortex. With a battery of clinical and specially designed color vision tests we tried to detect and differentiate between possible deficits in central color processing. Our results show that color constancy can be selectively impaired after circumscribed unilateral lesions in parieto-temporal cortex of the left or right hemisphere. Five of 27 patients exhibited significant deficits in a color constancy task, but all of the 5 performed well in color discrimination or higher-level visual tasks, such as the association of colors with familiar objects. These results indicate that the computations underlying color constancy are mediated by specialized cortical circuitry, which is independent of the neural substrate for color discrimination and for assigning colors to objects.

Adaptation, Physiological↗
PubMed1983

Cone dystrophy, nyctalopia, and supernormal rod responses. A new retinal degeneration.

An unusual retinal degeneration considered to be inherited as an autosomal recessive trait occurred in two of four children in a Hispanic family. The abnormality causes a progressive and generalized loss of cone vision, including decreased acuity, decreased color vision, central scotomas to small test objects, photo-phobia, and a profound diminution of the cone-mediated electroretinographic (ERG) pattern. A loss of the foveal reflex and an increased granularity of the macula is seen funduscopically. In addition, there is a most unusual alteration of the rod system detectable in the rod-mediated ERG pattern. This rod response is supernormal in amplitude (greater than 1,000 microV, extrapolated), delayed in time course, and insensitive to dim stimuli, ie, the function relating response to light intensity has been drastically altered. The insensitivity to dim stimuli is accompanied by a mild nyctalopia. Some of these abnormalities could be caused by a defect in the retinal enzyme, cyclic nucleotide phosphodiesterase.

Adolescent↗