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Resting EEG effective connectivity at the sources in developmental dysphonetic dyslexia. Differences with non-specific reading delay

诵读困难 心理学 听力学 脑电图 颞上沟 颞中回 舌回 神经科学 阅读(过程) 功能磁共振成像 医学 政治学 法学
作者
Jorge Bosch‐Bayard,Katia Girini,R. Biscay,Pedro A. Valdés‐Sosa,Alan C. Evans,Giuseppe A. Chiarenza
出处
期刊:International Journal of Psychophysiology [Elsevier]
卷期号:153: 135-147 被引量:21
标识
DOI:10.1016/j.ijpsycho.2020.04.021
摘要

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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