Abstract
Dyslexia affects 5–10% of school-aged children and is therefore one of the most common learning disorders. Research on auditory event related potentials (AERP), particularly the mismatch negativity (MMN) component, has revealed anomalies in individuals with dyslexia to speech stimuli. Furthermore, candidate genes for this disorder were found through molecular genetic studies. A current challenge for dyslexia research is to understand the interaction between molecular genetics and brain function, and to promote the identification of relevant endophenotypes for dyslexia. The present study examines MMN, a neurophysiological correlate of speech perception, and its potential as an endophenotype for dyslexia in three groups of children. The first group of children was clinically diagnosed with dyslexia, whereas the second group of children was comprised of their siblings who had average reading and spelling skills and were therefore “unaffected” despite having a genetic risk for dyslexia. The third group consisted of control children who were not related to the other groups and were also unaffected. In total, 225 children were included in the study. All children showed clear MMN activity to/da/−/ba/contrasts that could be separated into three distinct MMN components. Whilst the first two MMN components did not differentiate the groups, the late MMN component (300–700 ms) revealed significant group differences. The mean area of the late MMN was attenuated in both the dyslexic children and their unaffected siblings in comparison to the control children. This finding is indicative of analogous alterations of neurophysiological processes in children with dyslexia and those with a genetic risk for dyslexia, without a manifestation of the disorder. The present results therefore further suggest that the late MMN might be a potential endophenotype for dyslexia.
Highlights
Dyslexia is a specific disorder in learning to read and spell despite normal intelligence, adequate schooling, and no obvious sensory deficits [1]
This present study was conducted to obtain further insight on the significance of early and late mismatch negativity (MMN) elicited by differences in speech sounds as potential neurophysiological endophenotypes for dyslexia
We found three distinct MMN components of which the late MMN was reduced both in children with dyslexia and their unaffected siblings in comparison to control children
Summary
Dyslexia is a specific disorder in learning to read and spell despite normal intelligence, adequate schooling, and no obvious sensory deficits [1]. Aside from reading and spelling deficits, a number of neurophysiological studies have revealed altered auditory eventrelated potentials (AERP) in both children and adults with dyslexia when passively discriminating between two phonemes, such as/ da/and/ba/(for review see [4,5,6]). The MMN is a negative curve which is obtained by subtracting the AERP to a frequently presented standard stimulus from the AERP of an infrequently presented deviant stimulus. This negativity is registered at the fronto-central and central scalp electrodes, peaking around 150– 250 ms from change onset [6,7] and originates from sources in auditory and frontal cortices [6,8]. The MMN is an objective measurement of the speech discrimination ability, and is well-suited for studies in children; because active attention to the speech stimuli is not required [6]
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