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Updated: Dec 21, 2025

Infant Auditory Processing and Event-related Brain Oscillations
Published on: July 1, 2015
Resting EEG effective connectivity at the sources in developmental dysphonetic dyslexia. Differences with
Jorge Bosch-Bayard1, Katia Girini2, Rolando José Biscay3
1McGill Centre for Integrative Neuroscience (MCIN), Ludmer Centre for Neuroinformatics and Mental Health, Montreal Neurological Institute (MNI), McGill University, Montreal, Canada.
Abstract:
Previous studies conducted on subjects with dysphonetic dyslexia (DD) reported inefficient timing integration of information from various brain areas. This dysregulation has been referred as neuronal dyschronia or timing deficiency. The present study examines the effective brain connectivity in Dysphonetic Dyslexic subjects (DD) compared to a group of subjects with non-specific reading delay (NSRD). The hypothesis is that the timing defect should be reflected also in the effective connectivity and the subjects with developmental dyslexia have an altered information flow different from the group of children with non-specific reading delay. The quantitative EEG at the sources of 184 children with DD was compared with that of 43 children with NRSD. The Isolated Effective Coherence (iCoh) was calculated among 17 brain regions data driven selected. To assess statistical differences in the EEG connectivity between the two groups, a Linear Mixed Effect (LME) model was applied. Two very important areas perform as hubs in the information flow: one is the left calcarine sulcus, which is more active in the DD group. The second is the left rolandic operculum, which is more active in the NSRD group. In the DD group, the calcarine sulcus is sending information to the right postcentral gyrus, the left paracentral gyrus, the right angular gyrus and the right supplementary motor area. This flow of information occurs in almost all frequency bands, including delta and theta band. Slow connections may indicate less efficient or even pathological information flow. We consider this as a neurophysiological evidence of Boder's model of dyslexia.
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