Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2012
Cortical sources of resting state EEG rhythms are abnormal in dyslexic children.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Babiloni Claudio, Stella Giacomo, Buffo Paola, Vecchio Fabrizio, Onorati Paolo, Muratori Chiara, Miano Silvia, Gheller Flavia, Antonaci Laura, Albertini Giorgio, Rossini Paolo M
Аннотация
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.
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.