Reply to ‘ ‘ Letter to the Editor : Independent patterns of damage within magno-, parvo-and koniocellular pathways in Parkinson ’ s disease (

We are thankful for the author’s interest in our work, and for his constructive comments. We do also find some of his intriguing speculations on a possible role of dopamine in retinal toxicity quite interesting. However, there are some factual and conceptual misunderstandings that we need to address. Although these are in most cases subtle inaccuracies, they are however critical regarding the main points. Despite these facts we would like to stress that we find that the commentary also contains many valid and interesting points. We do find concomitant impairment of multiple visual pathways in Parkinson’s disease and made clear in the paper that age-matching eliminates ageing as a between-group confound. It should also be understood, as a major point that was discussed in the paper, that it is also important to carefully exclude within each group disorders typical of aged groups, such as ocular hypertension (even in absence of glaucoma) and diabetes (even in absence of retinopathy). Our main point was that the external validity of any study becomes compromised if this is not taken into account, and we hope that this point has now become clear. The simple fact that we use an age-matched control population avoids age itself as a confound and is the methodological procedure of choice (Silva et al., 2005). It should also be understood that age-matching is not enough, and should be complemented with strict exclusion criteria, to prevent that subjects with subclinical disorders typical of that age group, such as ocular hypertension or diabetes, are included. These disorders may lead to achromatic and chromatic deficits that are completely unrelated to PD. The possibility that other medical conditions of old populations could influence in particular ‘tritan’ like measures in PD was also previously recognized by Birch et al. (1998), and discussed in our paper. Unfortunately, this paper is omitted from Gaynes’ comment. This omission is somewhat critical because this paper is a more recent update of an older paper (whose senior author and another author shared coauthorship in both) that is cited in the comment (Haug et al., 1995). The more recent paper should have been given weight, because it provides an improved and updated view that is much more consistent with our view (for details and more references, see below). The author discusses our findings in terms of a ‘single measurement’. This central point is however incorrect. Indeed, the author attempts to discuss ‘independent damage to visual pathways subsequent to PD by a single psychophysical measurement’. This represents a crucial misunderstanding because statistical independence can only be tested with at least two measurements. Actually the strength of our study is that we have obtained multiple test measures for distinct pathways: for each subject, 17 achromatic test thresholds were obtained in independent locations, 3 chromatic test thresholds were obtained along cone-isolating axes in colour space and eight chromatic colour test thresholds were still obtained along eight additional axes in colour space, to provide measures unbiased to cone spaces. This allowed for testing multiple visual processing pathways, using up to 28 distinct threshold measurements and not 1, as supposed by the author. It is also noteworthy to point out that all these measures were obtained in a random, interleaved manner, which allowed for simultaneous comparisons. Furthermore, it was possible to extract reliability criteria, such as false positives and false negatives.