Abstract
Motion perception deficits in dyslexia show a large intersubjective variability, partly reflecting genetic factors influencing brain architecture development. In previous work, we have demonstrated that dyslexic carriers of a mutation of the DCDC2 gene have a very strong impairment in motion perception. In the present study, we investigated structural white matter alterations associated with the poor motion perception in a cohort of twenty dyslexics with a subgroup carrying the DCDC2 gene deletion (DCDC2d+) and a subgroup without the risk variant (DCDC2d–). We observed significant deficits in motion contrast sensitivity and in motion direction discrimination accuracy at high contrast, stronger in the DCDC2d+ group. Both motion perception impairments correlated significantly with the fractional anisotropy in posterior ventral and dorsal tracts, including early visual pathways both along the optic radiation and in proximity of occipital cortex, MT and VWFA. However, the DCDC2d+ group showed stronger correlations between FA and motion perception impairments than the DCDC2d– group in early visual white matter bundles, including the optic radiations, and in ventral pathways located in the left inferior temporal cortex. Our results suggest that the DCDC2d+ group experiences higher vulnerability in visual motion processing even at early stages of visual analysis, which might represent a specific feature associated with the genotype and provide further neurobiological support to the visual-motion deficit account of dyslexia in a specific subpopulation.
Highlights
Dyslexia is a heritable neurodevelopmental condition, affecting between 3 and 15% of the population, characterized by a specific and persistent failure to acquire reading skills, despite normal intelligence and adequate educational opportunities (Peterson and Pennington 2015)
Typical subjects (Fig. 1a) had contrast threshold for direction discrimination around 0.003, while the DCDC2d+ subject of Fig. 1b had a threshold of 0.01 Michelson contrast which was three-fold higher
When pooling the data across all spatial frequencies (Fig. 1f), the deficit in motion sensitivity was significantly different from typicals in both dyslexic subject groups with a greater deficit of DCDC2d+ (t(16) = 3.29, p = 0.005) than DCDC2d– subjects (t(16) = 1.60, p = 0.013)
Summary
Dyslexia is a heritable neurodevelopmental condition, affecting between 3 and 15% of the population, characterized by a specific and persistent failure to acquire reading skills, despite normal intelligence and adequate educational opportunities (Peterson and Pennington 2015). Little consensus exists on whether dyslexics have impaired sensitivity to detect motion direction at low spatial frequencies, the optimal range for magnocellular processing, (up to 2 c/deg) (Martin and Lovegrove 1988; Cornelissen et al 1995) or whether the deficits are limited to motion direction of high spatial frequencies (Cornelissen 1993; Slaghuis and Ryan 1999; Stuart et al 2001). The observed deficits of coherence sensitivity of these stimuli in dyslexia are very small This may reflect the fact that the low spatial frequency information, that is prevailing in the RDK, is used to perform the task (Morrone et al 2008; Cicchini et al 2015). Measurements of motion direction coherence sensitivity, gauged with RDK stimuli, require rather long exposure times (typically above 500 ms), compared to contrast direction sensitivity (about 100 ms), implicating possible deficits in eye movements
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