TY - JOUR
T1 - Reply to
T2 - Visual magnocellular deficits in dyslexia
AU - Amitay, Sygal
AU - Ben-Yehudah, Gal
AU - Banai, Karen
AU - Ahissar, Merav
PY - 2003/9/1
Y1 - 2003/9/1
N2 - The hypothesis of a mild magnocellular deficit in a large number of dyslexics has been challenged many times in the past. In fact, there have been more studies that failed to verify its predictions than those that successfully did. For example, a recent review by Skottun (2000) describes many studies that failed to verify the theory’s main prediction that dyslexics will have poor contrast sensitivity for sinusoidal gratings of high temporal frequency and low spatial frequency. Still, we decided to perform a systematic evaluation of this magnocellular hypothesis. We chose to do so because we found the magnocellular hypothesis very appealing. Its main merit was in relating a plethora of complex and seemingly unrelated phenomena to a single deficient mechanism, and, within the visual system, to a concrete anatomical pathway. As such, this hypothesis yielded specific predictions that could be assessed with many different methodologies. To our disappointment, when we assessed its predictions with a relatively large sample population (n = 60; 30 dyslexics and 30 controls) and with a broad range of psychophysical tasks, these predictions were not confirmed.
AB - The hypothesis of a mild magnocellular deficit in a large number of dyslexics has been challenged many times in the past. In fact, there have been more studies that failed to verify its predictions than those that successfully did. For example, a recent review by Skottun (2000) describes many studies that failed to verify the theory’s main prediction that dyslexics will have poor contrast sensitivity for sinusoidal gratings of high temporal frequency and low spatial frequency. Still, we decided to perform a systematic evaluation of this magnocellular hypothesis. We chose to do so because we found the magnocellular hypothesis very appealing. Its main merit was in relating a plethora of complex and seemingly unrelated phenomena to a single deficient mechanism, and, within the visual system, to a concrete anatomical pathway. As such, this hypothesis yielded specific predictions that could be assessed with many different methodologies. To our disappointment, when we assessed its predictions with a relatively large sample population (n = 60; 30 dyslexics and 30 controls) and with a broad range of psychophysical tasks, these predictions were not confirmed.
U2 - 10.1093/brain/awg218
DO - 10.1093/brain/awg218
M3 - Article
SN - 0006-8950
VL - 126
SP - E3
JO - Brain
JF - Brain
IS - 9
ER -