TY - JOUR
T1 - Does the late positive component reflect successful reading acquisition? A longitudinal ERP study
AU - Wachinger, Christian
AU - Volkmer, Susanne
AU - Bublath, Katharina
AU - Bruder, Jennifer
AU - Bartling, Jürgen
AU - Schulte-Körne, Gerd
N1 - Publisher Copyright:
© 2017 The Author(s)
PY - 2018
Y1 - 2018
N2 - Developmental dyslexia is a reading disorder that is associated with deficits in phonological processing, where the exact neural basis for those processing deficits remains unclear. In particular, disagreement exists whether degraded phonological representations or an impaired access to the phonological representations causes these deficits. To investigate this question and to trace changes in neurophysiology during the process of reading acquisition, we designed a longitudinal study with event related potentials (ERPs) in children between kindergarten and second grade. We used an explicit word processing task to elicit the late positive component (LPC), which has been shown to reflect phonological processing. A brain-wide analysis of the LPC with an electrode-wise application of mixed effects models showed significantly attenuated amplitudes in the left temporo-parietal region in dyslexic children. Since these differences were only present in the word and not in the picture (i.e. control) condition, the attenuated amplitudes might reflect impaired access to the phonological representations of words. This was further confirmed by the longitudinal development, which showed a rapid increase in amplitude at the beginning of reading instruction and a decrease with continuing automatization, possibly pointing to a progression from grapheme-phoneme parsing to whole word reading. Our longitudinal study provides the first evidence that it is possible to detect neurophysiological differences in the LPC between children with dyslexia and control children in both preliterate and very early stages of reading acquisition, providing new insights about the neurophysiological development and a potential marker of later reading problems.
AB - Developmental dyslexia is a reading disorder that is associated with deficits in phonological processing, where the exact neural basis for those processing deficits remains unclear. In particular, disagreement exists whether degraded phonological representations or an impaired access to the phonological representations causes these deficits. To investigate this question and to trace changes in neurophysiology during the process of reading acquisition, we designed a longitudinal study with event related potentials (ERPs) in children between kindergarten and second grade. We used an explicit word processing task to elicit the late positive component (LPC), which has been shown to reflect phonological processing. A brain-wide analysis of the LPC with an electrode-wise application of mixed effects models showed significantly attenuated amplitudes in the left temporo-parietal region in dyslexic children. Since these differences were only present in the word and not in the picture (i.e. control) condition, the attenuated amplitudes might reflect impaired access to the phonological representations of words. This was further confirmed by the longitudinal development, which showed a rapid increase in amplitude at the beginning of reading instruction and a decrease with continuing automatization, possibly pointing to a progression from grapheme-phoneme parsing to whole word reading. Our longitudinal study provides the first evidence that it is possible to detect neurophysiological differences in the LPC between children with dyslexia and control children in both preliterate and very early stages of reading acquisition, providing new insights about the neurophysiological development and a potential marker of later reading problems.
KW - Brain development
KW - Dyslexia
KW - EEG
KW - Event-related potentials
KW - Longitudinal
UR - http://www.scopus.com/inward/record.url?scp=85032284688&partnerID=8YFLogxK
U2 - 10.1016/j.nicl.2017.10.014
DO - 10.1016/j.nicl.2017.10.014
M3 - Article
C2 - 29159040
AN - SCOPUS:85032284688
SN - 2213-1582
VL - 17
SP - 232
EP - 240
JO - NeuroImage: Clinical
JF - NeuroImage: Clinical
ER -