Symposium: Clinical applications: hearing and speech disorders
Wednesday, Sep 9, 2015
12:00-13:00
Hörsaal 3

Atypical responses generated in MMN-paradigms as brain signatures of reading difficulties

Paavo Leppänen¹, Jarmo Hämäläinen, & Kaisa Lohvansuu

¹Department of Psychology, University of Jyväskylä, Unversity of Jyväskylä, Finland
paavo.ht.leppanen@jyu.fi

Deficits in phonological processing play a role in dyslexia, a disorder in learning to read. Relatively little is known, however, of early neurocognitive risk factors and their interaction with phonological deficits and later reading difficulties at school-age. Here I review and discuss brain signatures of dyslexia and its risk factors using brain event-related potentials (ERPs) generated in MMN-paradigms at infancy and childhood and their associations with later development. Jyväskylä Longitudinal Study of Dyslexia (JLD) at the University of Jyväskylä (Finland) shows that dyslexic children, diagnosed at school-age and who have familial risk background have atypical auditory/speech processing for various sound features, including non-speech and speech sounds, already at infancy. Atypical brain activation also persists in development until school-age, albeit with different response patterns. Infant brain responses also correlate to childhood language and pre-school age reading related skills, and reading and writing skills at school age up to the 8th grade. Similar findings from the large scale longitudinal Dutch Dyslexia Programme (DDP) show that infant brain responses to speech sound changes are related to familial risk for dyslexia and also predict later reading skills at school-age. Overall, such findings suggests developmental differences in the organization of the neural networks sub-serving auditory/ speech perception, with cascading effects on later reading related skills. However, the evidence also suggests that atypical basic processing skills alone are not likely a sufficient reason for dyslexia, but rather one endophenotype /risk factor. Challenges remain, therefore, for the individual identification of high risk children.