PubMed Health⌕ Search

PubMed · 3310294

Acquired dyschromatopsias.

Abstract

Theories of color vision have been founded on behavioral observations of how the human eye distinguishes colors and mixtures of colors. Studies of congenital dyschromatopsias (inherited disorders of color vision) have been important to the development of these theories. Subsequent studies of acquired dyschromatopsias (disorders of color vision caused by disease) were understandably influenced by these concepts. Theories to explain the patterns of color vision impairment found in acquired diseases (for example, preferential hue discrimination defects) have stressed the likelihood of selective damage to specific components of the afferent visual system (photoreceptors, ganglion cells, synaptic elements, axons etc.). More recent evidence suggests, however, that impairment of color vision by diseases of the retina and optic nerve is commonly nonspecific, and not the result of selective impairment of individual neural mechanisms responsible for mediating color vision. Rather, the patterns of acquired dyschromatopsias often appear to be related to a physiologically heterogeneous distribution of color vision in the foveal and perifoveal visual field, coupled with a tendency for the visual field defects caused by acquired diseases to be unevenly distributed in these same areas.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

W M Hart. Acquired dyschromatopsias.. https://doi.org/10.1016/0039-6257(87)90070-1

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Diagnosing protan heterozygosity using the Medmont C-100 colour vision test.

BACKGROUND: A surprisingly high 15 per cent of women in Caucasian societies are carriers of the genes for abnormal colour vision but there is no clinical method to identify them. It has long been known that heterozygotes for the protan colour vision deficiencies can demonstrate a reduced luminous sensitivity to red light. This is known as Schmidt's sign, which is thought to arise from mosaicism (Lyonisation). The Medmont C-100 colour vision test measures relative spectral sensitivity using flicker photometry to differentiate protans and deutans. It should be able to diagnose Schmidt's sign. METHOD: We tested six known protan heterozygotes (four whose sons have a protan colour vision deficiency and two whose fathers are protan) with the Medmont C-100 test. RESULTS: All six heterozygotes made average settings of -1.75 or more negative at the Medmont C-100 test, settings which are at or beyond the boundary of the distribution of settings made by observers with normal colour vision. There have been two previous cases reported in the literature of protan heterozygotes, who made protan settings on the Medmont C-100 or its predecessor test, the OSCAR. We also tested six daughters of the known heterozygotes, 50 per cent of whom are likely to be heterozygotes. Four of the six (66 per cent) made protan settings on the Medmont C-100. The other two made normal 0.0 settings. CONCLUSION: We conclude that the Medmont C-100 can be used clinically to diagnose carriers of protan colour vision deficiency.

Color Perception Tests↗