On the Relationship between Magnocellular Pathway and Automatic Attentional Orienting: Evidences from Developmental Dyslexia

Although developmental dyslexia (DD) is frequently associate to a linguistic deficit, the underlying neurobiological cause remains unclear. One prominent vision science hypothesis suggests a specific deficit in magnocellular (M) pathway in DD. However, a recent hypothesis proposes that M-deficits contribute to the etiology of phonological decoding ability (i.e., new word and nonword reading), impairing selectively the attentional orienting process onto letter string. Thus, a specific M-pathway impairment in association with an attentional orienting disorder in DD children with phonological decoding deficit was specifically predicted by this neurobiological hypothesis. In the present study we investigated the M-pathway and attentional orienting in 18 dyslexic (10 with phonological decoding deficit) and in 29 chronological age and IQ matched normally reading children by measuring dynamic stimuli sensibility (i.e., spatial frequency doubling illusion) and the time-course of automatic covert attention (i.e., target detection effect at different SOAs of a non-predictive and peripheral spatial cue), respectively. The results showed a specific deficit of the M-pathway task in dyslexic with phonological decoding deficit. More importantly, the same group of dyslexics with M-deficit presented a sluggish attentional orienting: attentional facilitation was present at longer cue-target SOAs compared with normal readers. These results highlight that a M-deficit linked to a parietal-attentional dysfunction might impair the phonological decoding mechanisms that are critical for reading acquisition.