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Pathologic scotopization: a shortened Nagel-II anomaloscopic micro-screw method.

A Pinckers
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Abstract

The Nagel-II micro-screw method uses eleven colour equations between 620 and 560 nm. The luminance settings are given and are based on the data of colour normal individuals. In the shortened version, intended to detect pathologic scotopization, it is ascertained at which position of the micro-screw the patient's colour adjustments drop beneath the level of 60 scale Units. A total of 64 patients was examined. 29 congenital colour defectives and 35 acquired colour defectives. With the shortened micro-screw method the patients can be divided into four groups: (1) a group without pathologic scotopization, which includes congenital protan defectives: (2) a group in which pathologic scotopization starts; (3) a group with evident pathologic scotopization, due to Stargardt's disease and other cone dystrophies; and (4) a group with complete pathologic scotopization, which includes the congenital achromats and the end-stages of the cone dystrophies.

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Color Perception TestsColor Vision DefectsFemaleHumansLightMaleRetinal Cone Photoreceptor CellsRetinal DegenerationJournal Article

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BibTeXRIS

A Pinckers. 1994. Pathologic scotopization: a shortened Nagel-II anomaloscopic micro-screw method.. https://doi.org/10.1007/bf01664933

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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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