Clinical and Experimental Optometry 81.6 November–December 1998 272 Colour vision in proliferative diabetes Mahon, Vingrys and Fleiszig OPTOMETRY C L I N I C A L A N D E X P E R I M E N T A L Early detection of eye disease is important to manage, treat and prevent visual loss. In this context, acquired colour vision losses are common 2 and can manifest char- acteristics similar to congenital defects. 2-6 Moreover, although many aspects of visual function can be affected by eye disease, colour vision changes often occur before the manifestation of other functional losses, such as alterations in visual acuity or visual fields. Colour vision is known to be affected in diabetes, 7-12 age-related maculopathy, 13-16 retinitis pigmentosa, 12 glaucoma, 17-21 optic neuropathies 22 and many other ocular diseases. Colour vision defects can manifest themselves as a generalised decrease of colour (hue) discrimination, as a specific loss of sensitivity for certain hues (for ex- ample, short wavelengths) or as a decrease in colour saturation processing (colours appear washed out). Because subtle hue or saturation losses may become apparent in the early stages of a disease process, they can allow for a more definitive and early diagnosis. 23 Elsewhere, we have developed a model that predicts large relative satu- Evidence for non-selective colour channel involvement in diabetic eyes especially after laser treatment Luke E Mahon* BOptom, MScOptom Algis J Vingrys BScOptom PhD FAAO Suzanne MJ Fleiszig* BScOptom PhD FAAO * School of Optometry and Program in Vision Science, University of California, Berkeley Visual Functions Laboratory, Department of Optometry and Vision Sciences, The University of Melbourne Accepted for publication: 9 February 1999 Purpose: We consider the hypothesis that proliferative diabetes produces selective loss of colour channels. We also consider the possibility that laser treatment for this condi- tion does not affect macula function. Methods: We tested for the possibility of a selective colour channel involvement in 35 eyes of 33 cases of proliferative diabetes by considering the outcomes of saturation and hue testing before and after pan-retinal photocoagulation (PRP). Saturation testing was achieved with the Sahlgren Saturation Test (SST) and hue testing was via the Farnsworth-Munsell 100 (FM100) hue test. Our results were compared to a recent model 1 that was developed to predict the saturation processing of diseased eyes. Results: All diabetic eyes with normal hue (FM100) scores passed the saturation test (SST). Most pre-treatment eyes (29 of 35 or 83 per cent) failed the FM100 hue test but only 16 of 35 (46 per cent) failed the saturation test. Following laser treatment, 97 per cent of eyes were abnormal on the FM100 hue test but only seven per cent failed the saturation test. Conclusion: Untreated diabetic eyes with proliferative retinopathy show losses of both hue and saturation processing. The nature of this relationship is consistent with that modelled assuming moderate and asymmetric non-selective losses in both chromatic and luminance channels. Laser treatment (PRP) appears to produce a paradoxical normalisation in saturation percepts in the presence of deteriorating hue scores. We find that this outcome is consistent with a more severe generalised reduction of sensi- tivity in both the chromatic and luminance processes and conclude that pan-retinal photocoagulation results in these unexpected macula changes. (Clin Exp Optom 1998; 81: 6: 272–279) Key words: colour vision, diabetes, hue tests, pan-retinal photocoagulation, saturation tests