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Evidence for the late MMN as a neurophysiological endophenotype for dyslexia.

Neuhoff N, Bruder J, Bartling J, Warnke A, Remschmidt H, Müller-Myhsok B, Schulte-Körne G - PLoS ONE (2012)

Bottom Line: In total, 225 children were included in the study.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University of Munich, Munich, Germany.

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.

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Related in: MedlinePlus

MMN1, MMN2, and late MMN for all 3 groups.MMN1, MMN2, and late MMN for dyslexic children (black line), unaffected siblings (dashed line), and unrelated controls (dotted line) at the nine fronto-central electrodes, giving the timeframes for the MMN1 (84–188 ms), MMN2 (188–300 ms), and late MMN (300–700 ms).
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pone-0034909-g001: MMN1, MMN2, and late MMN for all 3 groups.MMN1, MMN2, and late MMN for dyslexic children (black line), unaffected siblings (dashed line), and unrelated controls (dotted line) at the nine fronto-central electrodes, giving the timeframes for the MMN1 (84–188 ms), MMN2 (188–300 ms), and late MMN (300–700 ms).

Mentions: The average accepted trials was 271 for deviant stimuli and 372 for standard stimuli. The lowest number of accepted trials for any proband was 47. Therefore, all children had an acceptable number of accepted trials and we did not exclude any children from the analysis. Difference waveforms (MMN curves) were calculated by subtracting the averaged standard from the averaged deviant AERP. Grand averages were generated over all subjects for each group separately. Based on the observed scalp topography of the MMN in the control group and on electrode choice in previous MMN studies, the following fronto-central electrodes were chosen for analysis: F3, F4, Fz, C3, C4, Cz, Fc3, Fc4, Fcz. This fronto-central region is also known to be of interest for auditory stimulus perception and processing [67] and these electrodes were also used for group comparisons between dyslexic probands and controls in former speech perception studies [18], [19]. The grand average wave forms (figure 1) revealed three MMN components: labelled MMN1, MMN2, and late MMN. For the analysis of these components the grand averages were tested against zero using running t-tests in order to determine which time windows differed significantly from zero for each component. The following three time windows were determined: MMN1 (84–188 ms), MMN2 (188–300 ms) and late MMN (300–700 ms). Mean MMN peak amplitude and mean MMN peak latency for MMN1 and MMN2 were calculated using these time windows. Because late MMN revealed a broad amplitude with no obvious peak the value of the area under the curve (µV *ms) was taken.


Evidence for the late MMN as a neurophysiological endophenotype for dyslexia.

Neuhoff N, Bruder J, Bartling J, Warnke A, Remschmidt H, Müller-Myhsok B, Schulte-Körne G - PLoS ONE (2012)

MMN1, MMN2, and late MMN for all 3 groups.MMN1, MMN2, and late MMN for dyslexic children (black line), unaffected siblings (dashed line), and unrelated controls (dotted line) at the nine fronto-central electrodes, giving the timeframes for the MMN1 (84–188 ms), MMN2 (188–300 ms), and late MMN (300–700 ms).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3351484&req=5

pone-0034909-g001: MMN1, MMN2, and late MMN for all 3 groups.MMN1, MMN2, and late MMN for dyslexic children (black line), unaffected siblings (dashed line), and unrelated controls (dotted line) at the nine fronto-central electrodes, giving the timeframes for the MMN1 (84–188 ms), MMN2 (188–300 ms), and late MMN (300–700 ms).
Mentions: The average accepted trials was 271 for deviant stimuli and 372 for standard stimuli. The lowest number of accepted trials for any proband was 47. Therefore, all children had an acceptable number of accepted trials and we did not exclude any children from the analysis. Difference waveforms (MMN curves) were calculated by subtracting the averaged standard from the averaged deviant AERP. Grand averages were generated over all subjects for each group separately. Based on the observed scalp topography of the MMN in the control group and on electrode choice in previous MMN studies, the following fronto-central electrodes were chosen for analysis: F3, F4, Fz, C3, C4, Cz, Fc3, Fc4, Fcz. This fronto-central region is also known to be of interest for auditory stimulus perception and processing [67] and these electrodes were also used for group comparisons between dyslexic probands and controls in former speech perception studies [18], [19]. The grand average wave forms (figure 1) revealed three MMN components: labelled MMN1, MMN2, and late MMN. For the analysis of these components the grand averages were tested against zero using running t-tests in order to determine which time windows differed significantly from zero for each component. The following three time windows were determined: MMN1 (84–188 ms), MMN2 (188–300 ms) and late MMN (300–700 ms). Mean MMN peak amplitude and mean MMN peak latency for MMN1 and MMN2 were calculated using these time windows. Because late MMN revealed a broad amplitude with no obvious peak the value of the area under the curve (µV *ms) was taken.

Bottom Line: In total, 225 children were included in the study.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University of Munich, Munich, Germany.

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.

Show MeSH
Related in: MedlinePlus