title: Newborn brain event-related potentials revealing atypical processing of sound frequency and the subsequent association with later literacy skills in children with familial dyslexia.
abstract: The role played by an auditory-processing deficit in dyslexia has been debated for several decades. In a longitudinal study using brain event-related potentials (ERPs) we investigated 1) whether dyslexic children with familial risk background would show atypical pitch processing from birth and 2) how these newborn ERPs later relate to these same children's pre-reading cognitive skills and literacy outcomes. Auditory ERPs were measured at birth for tones varying in pitch and presented in an oddball paradigm (1100 Hz, 12%, and 1000 Hz, 88%). The brain responses of the typically reading control group children (TRC group, N=25) showed clear differentiation between the frequencies, while those of the group of reading disability with familial risk (RDFR, 8 children) and the group of typical readers with familial risk (TRFR, 14 children) did not differentiate between the tones. The ERPs of the latter two groups differed from those of the TRC group. However, the two risk groups also showed a differential hemispheric ERP pattern. Furthermore, newborn ERPs reflecting passive change detection were associated with phonological skills and letter knowledge prior to school age and with phoneme duration perception, reading speed (RS) and spelling accuracy in the 2nd grade of school. The early obligatory response was associated with more general pre-school language skills, as well as with RS and reading accuracy (RA). Results suggest that a proportion of dyslexic readers with familial risk background are affected by atypical auditory processing. This is already present at birth and also relates to pre-reading phonological processing and speech perception. These early differences in auditory processing could later affect phonological representations and reading development. However, atypical auditory processing is unlikely to suffice as a sole explanation for dyslexia but rather as one risk factor, dependent on the genetic profile of the child.
authors.affiliation: Department of Psychology, University of Jyväskylä, Jyväskylä, Finland. paavo.ht.leppanen@jyu.fi
authors.forename: Paavo H T
authors.initials: PH
authors.lastname: Leppänen
authors.forename: Jarmo A
authors.initials: JA
authors.lastname: Hämäläinen
authors.forename: Hanne K
authors.initials: HK
authors.lastname: Salminen
authors.forename: Kenneth M
authors.initials: KM
authors.lastname: Eklund
authors.forename: Tomi K
authors.initials: TK
authors.lastname: Guttorm
authors.forename: Kaisa
authors.initials: K
authors.lastname: Lohvansuu
authors.forename: Anne
authors.initials: A
authors.lastname: Puolakanaho
authors.forename: Heikki
authors.initials: H
authors.lastname: Lyytinen
mesh_terms: D000161:Acoustic Stimulation; D002648:Child; D002652:Child Behavior; D004410:Dyslexia / Q000235:genetics* / Q000523:psychology*; D004522:Educational Status; D004569:Electroencephalography; D005071:Evoked Potentials / Q000502:physiology*; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D007361:Intelligence Tests; D008137:Longitudinal Studies; D008297:Male; D010898:Pitch Perception / Q000502:physiology*; D011597:Psychomotor Performance / Q000502:physiology; D011932:Reading; D012044:Regression Analysis; D013067:Speech Perception / Q000502:physiology; D014825:Vocabulary