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E. C. Zachi, M. F. Costa, A. Taub, D. F. Ventura; Color Vision Impairment Is Associated With Cognitive Deficits in Duchenne Muscular Dystrophy Patients. Invest. Ophthalmol. Vis. Sci. 2010;51(13):6302.
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Duchenne muscular dystrophy (DMD) has been associated with color vision losses and cognitive decrements. Since findings concerning interactions between these functions are still unknown we aim to examine the possibility of association between color vision impairment and cognitive deficits in patients with DMD.
20 DMD patients with age ranging from 11 to 26 years were tested. Color vision was evaluated using the Cambridge Color Test (CCT) using the Trivector protocol to measure discrimination thresholds in the protan, deutan and tritan color confusion axis (0.1977, 0.4689 u’v’ coordinates of the CIE 1976 color space). Cognitive performance was assessed using tests from the Cambridge Neuropsychological Test Automated Battery (CANTAB), including working memory examination (Spatial Span, SSP), spatial short term memory (Spatial Recognition Memory, SRM), short and long term visual memory (Pattern Recognition Memory, PRM), and perception and memory for complex stimuli presented simultaneously or after short interval (Delayed Matching to Sample, DMS). The participants had intellectual scores in the normal range according to the Wechsler Intelligence Scale or the Raven Matrices Test.
11 out of 20 patients had losses in the protan axis. These patients performed significantly worse on DMS scores in trials in which the sample and the choice patterns were shown simultaneously. Patients with protan losses, which in addition, had deutan losses (n=7) showed the same result and significantly lower scores on PRM delayed recall (main effects ANOVA, p<0.05).
visual perception was impaired in DMD patients with protan or deutan defects. Long term visual memory deficit was associated with combined (protan/deutan) defects. Color vision impairment in DMD may reflect selective parvocellular dysfunction since it is restricted to the red-green axis. In agreement with this, the visual memory losses detected were for detailed shapes with chromatic information, which are processed in ventral stream sites and receive parvocellular input, but not for stimuli which activate mainly the magnocellular pathway (SSP and SRM). There seems to be, therefore, an association between impairment in visual perception/visual memory performance and damage in parvocellular pathways, but not in magno pathways. Further analysis should clarify if these associations are found in non DMD individuals.
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