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PubMed · 6972211

Congenital color blindness.

R D Gunkel
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Abstract

The term "color blind" is encountered frequently in areas pertaining to health, commerce, art, and entertainment, but in these cases it is generally not appropriate. Complete color blindness or achromasy is rare, but weakness or absence of discrimination to certain colors can be found in at least 8% of the male population. The most useful description of these color defects is in terms of hue and saturation, thresholds of which can be plotted as polar coordinates on a circular diagram. Plotting color thresholds with the chromagraph reveals more clearly than other clinical systems the true nature of color defects, as well as some inconsistencies in the traditional terminology and test methods. Fifty strongly color-defective subjects were tested by five different methods and the results compared. Normal values are also indicated.

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Color Perception TestsColor Vision DefectsHumansJournal Article

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BibTeXRIS

R D Gunkel. 1981. Congenital color blindness.. https://doi.org/10.1001/archopht.1981.03930011023008

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PubMed2005

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.

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