Cortical sources of resting state EEG rhythms are abnormal in dyslexic children.

Objective: Previous studies have been inconclusive whether dominant resting state alpha rhythms differ in amplitude in dyslexic subjects when compared to control subjects, being these rhythms considered as a reflection of effective cortical neural synchronization and cognition. Here we used a validated EEG source estimation to test the hypothesis that resting state alpha rhythms are abnormal in dyslexic subjects and are related to reading deficits.
Methods: Eyes-closed resting state electroencephalographic (EEG) data were recorded in 26 dyslexics (12 males, mean age of 11 years ± 0.5 standard error of mean, SEM) and 11 age-matched normal control subjects (8 males, mean age of 11 years ± 0.7 SEM). EEG rhythms of interest, based on individual alpha frequency peak, were the following: about 2-4 Hz (delta), 4-6 Hz (theta), 6-8 Hz (alpha 1), 8-10 Hz (alpha 2), and 10-12 Hz (alpha 3). For the higher frequencies, we selected beta 1 (13-20 Hz), beta 2 (20-30 Hz), and gamma (30-40 Hz). Cortical EEG sources were estimated by low resolution electromagnetic tomography (LORETA). LORETA solutions were normalized across all voxels and frequencies.
Results: Compared to the control children, the dyslexics showed lower amplitude of parietal, occipital, and temporal alpha 2 and alpha 3 sources. In the dyslexics, some of these sources were correlated to reading time of pseudo-words (parietal alpha 2, r=-0.56, p=0.02; parietal alpha 3, r=-0.58, p=0.02; temporal alpha 3, r=-0.57, p=0.02); the higher the alpha power, the shorter the reading time.
Conclusions: Dyslexic children are characterized by limited abnormalities of resting state EEG rhythms as to topography (posterior regions) and frequency (alpha), which were related to phonological encoding (pseudo-words reading).
Significance: Dyslexia may be associated to some functional impairment of cortical neuronal synchronization mechanisms involved in the resting state condition.
(Copyright © 2012 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.)