Psychophysical evidence for impaired Magno, Parvo, and Konio-cellular pathways in dyslexic children
Khazar Ahmadi MS 1, Hamid Reza Pouretemad PhD 2, Jahangir Esfandiari BS 3, Ahmad Yoonessi PhD 4, Ali Yoonessi MD, PhD 5
1 Department of Psychology, Shahid Beheshti University, Tehran, Iran
2 Department of Psychology; Tehran-Oxford Neurodevelopmental Center, Institute for Cognitive and Brain Sciences, Shahid Beheshti University, Tehran, Iran
3 Neuropsychology Lab, Institute for Cognitive Science Studies, Tehran, Iran
4 Depatment of Ophthalmology, McGill Vision Research, McGill University, Montreal, QC, Canada
5 Neuropsychology Lab, Institute for Cognitive Science Studies; Department of Neuroscience, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
Hamid Reza Pouretemad
Department of Psychology, Shahid Beheshti University, Evin, 1983969411, Tehran
Source of Support: None, Conflict of Interest: None
Purpose: Dyslexia is one of the most common learning disabilities affecting millions of people worldwide. Although exact causes of dyslexia are not well-known, a deficit in the magnocellular pathway may play a role. We examined possible deficiency of magnocellular, as compared to parvocellular and koniocellular pathway function by measuring luminance and color perception.
Methods: Visual stimuli consisted of a series of natural images, divided into layers of luminance, red-green and blue-yellow, which probed magnocellular, parvocellular, and koniocellular pathways, respectively. Thirteen children with dyslexia and 13 sex- and age- matched controls performed three psychophysical tasks. In the first task, subjects were instructed to match the contrast of luminance (magno) and red-green (parvo) images to that of the blue-yellow (konio) images. In the second task, subjects detected the isoluminant point of red-green images to probe parvocellular pathway. In the third task, temporal processing was assessed by measuring reaction time and percentage of correct responses in an identification task using four categories of images, activating all three pathways.
Results: The dyslexic group had significantly elevated luminance and color contrast thresholds and higher isoluminant point ratio in comparison to the control group. Furthermore, they had significantly less correct responses than the control group for the blue-yellow images.
Conclusion: We may suggest that dyslexic subjects might suffer from both magnocellular and parvocellular deficits. Moreover, our results show partial impairment of the koniocellular pathway. Thus, dyslexia might be associated with deficits in all three visual pathways.