Different brain activation patterns in dyslexic children: evidence from EEG power and coherence patterns for the double-deficit theory of dyslexia

QEEG and neuropsychological tests were used to investigate the underlying neural processes in dyslexia. A group of dyslexic children were compared with a matched control group from the Brain Resource International Database on measures of cognition and brain function (EEG and coherence). The dyslexic...

Full description

Saved in:
Bibliographic Details
Published inJournal of integrative neuroscience Vol. 6; no. 1; p. 175
Main Authors Arns, Martijn, Peters, Sylvia, Breteler, Rien, Verhoeven, Ludo
Format Journal Article
LanguageEnglish
Published England 01.03.2007
Subjects
Online AccessGet more information

Cover

Loading…
More Information
Summary:QEEG and neuropsychological tests were used to investigate the underlying neural processes in dyslexia. A group of dyslexic children were compared with a matched control group from the Brain Resource International Database on measures of cognition and brain function (EEG and coherence). The dyslexic group showed increased slow activity (Delta and Theta) in the frontal and right temporal regions of the brain. Beta-1 was specifically increased at F7. EEG coherence was increased in the frontal, central and temporal regions for all frequency bands. There was a symmetric increase in coherence for the lower frequency bands (Delta and Theta) and a specific right-temporocentral increase in coherence for the higher frequency bands (Alpha and Beta). Significant correlations were observed between subtests such as Rapid Naming Letters, Articulation, Spelling and Phoneme Deletion and EEG coherence profiles. The results support the double-deficit theory of dyslexia and demonstrate that the differences between the dyslexia and control group might reflect compensatory mechanisms. These findings point to a potential compensatory mechanism of brain function in dyslexia and helps to separate real dysfunction in dyslexia from acquired compensatory mechanisms.
ISSN:0219-6352
DOI:10.1142/S0219635207001404