Children at risk for dyslexia show deficient left-hemispheric memory representations for new spoken word forms
Nora, A., Renvall, H., Ronimus, M., Kere, J., Lyytinen, H., & Salmelin, R. (2021). Children at risk for dyslexia show deficient left-hemispheric memory representations for new spoken word forms. NeuroImage, 229, Article 117739. https://doi.org/10.1016/j.neuroimage.2021.117739
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NeuroImageDate
2021Discipline
PsykologiaMonitieteinen aivotutkimuskeskusHyvinvoinnin tutkimuksen yhteisöPsychologyCentre for Interdisciplinary Brain ResearchSchool of WellbeingCopyright
© 2021 The Authors. Published by Elsevier Inc.
Developmental dyslexia is a specific learning disorder with impairments in reading and spelling acquisition. Apart from literacy problems, dyslexics show inefficient speech encoding and deficient novel word learning, with underlying problems in phonological processing and learning. These problems have been suggested to be related to deficient specialization of the left hemisphere for language processing. To examine this possibility, we tracked with magnetoencephalography (MEG) the activation of the bilateral temporal cortices during formation of neural memory traces for new spoken word forms in 7-8-year-old children with high familial dyslexia risk and in controls. The at-risk children improved equally to their peers in overt repetition of recurring new word forms, but were poorer in explicit recognition of the recurring word forms. Both groups showed reduced activation for the recurring word forms 400–1200 ms after word onset in the right auditory cortex, replicating the results of our previous study on typically developing children (Nora et al, 2017, Children show right-lateralized effects of spoken word-form learning. PLoS ONE 12(2): e0171034). However, only the control group consistently showed a similar reduction of activation for recurring word forms in the left temporal areas. The results highlight the importance of left-hemispheric phonological processing for efficient phonological representations and its disruption in dyslexia.
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This work was supported by the Academy of Finland (grant number 13332622 to AN, grant numbers 292552 and 315553 to RS, grant numbers 292493 and 311737 to HL, grant number 292573 to JK, and grant number 321460 to HR), Sigrid Jusélius Foundation (to RS), Finnish Cultural Foundation (to HR), and Emil Aaltonen Foundation (to AN).License
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