Color vision impairment in Parkinson's disease.

Abstract

Acquired disturbances of color vision are a highly varied group of defects with frequent departures from established patterns. They can progress from normal trichromatism to anomalous trichromatism on to a dichromatic stage and to monochromatism where most color vision is lost, or they may be relatively stable [1]. A significant “modern effort” to present such conditions was published for first time in 1972 [2], attention was drawn in a significant account given 15 years later by Jaeger and Krastel emphasizing pharmaco-therapeutical effects [3]. Normally, dopaminergic neurons act in the outer and inner retina at multiple levels, producing alterations to the flow of visual information in a complex fashion. Dopamine is a chemical messenger for light adaptation, promoting the flow of information through cone circuits while diminishing that through rod circuits [4]. Color vision relies on the cone photoreceptor population and is therefore largely confined to the central retina. Because there is a segregation of color-specific information at the retinal into blue-yellow and red-green pathways, it is possible to use color discrimination tasks to assess cone and retinal ganglion cell subpopulations [4]. It has been reported that color vision is impaired in Parkinson’s disease (PD) [5] and some works have suggested that these disturbances to color vision affect predominantly the short-wave cone pathway [6]. Birch suggested that the acquired type three (tritan) defect at the retinal level as an early diagnostic sign of Parkinson’s ∗Correspondence to: Anna Piro, Neuroimaging Research Unit, IBFM-CNR, Germaneto, Catanzaro, Italy. Tel.: +393402529194; Fax: +39 0 9613695919; E-mail: anna.piro@cnr.it. disease [7]. We examined 49 PD Calabrian all male patients (age range, 50–85 years, mean age, 67 years) to avoid that genetic appearance of the “lionization” which can be present in the heterozygous females for color vision deficiency who mimic the vision of the normal females [8]. All patients underwent the L-DOPA doses subdivided into two different groups: 125–300 mg/day, low daily dose; 400–1000 mg/day, high daily dose. 25 age and sex matched controls showing a normal color vision, in comparison with the patients (chi square = 25.3, df = 1, p< 0.0005) were enrolled in comparison with 25/49 PD patients showing a defect of bleu/yellow axis. Controls did not show any PD signs, or other acquired ophthalmological disease. After informed consent, all patients, and controls had an examination by an ophthalmologist in order to rule a diabetic retinopathy, or a cataract, or an optic neuritis, or a senile maculopathy, or ocular fundus’ anomalies that could influence the color vision analysis. All PD patients who made more than 5 mistakes during their reading from the first 17 Ishihara plates were diagnosed as being color-blind, and this diagnosis was confirmed by their reading from the next four (numbers 18–21) Ishihara plates. The last four Ishihara plates (numbers 22–25) were utilized to define the type of color-blindness (the red or green colorbindness) and the grade of color-blindness: protanopy, the absence of red vision or protanomaly, the small deficiency of red color vision, and deuteranopy, the absence of green color vision or deuteranomaly, the small deficiency of green color vision [9]. PD colorblind patients were excluded from the analysis. So,