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Anterior EEG Asymmetry and the Modifier Model of Autism
Individual differences in the expression of autism complicate research on the nature and treatment of this disorder. In the Modifier Model of Autism (Mundy et al. 2007), we proposed that individual differences in autism may result not only from syndrome specific causal processes, but also from varia...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3134771/ https://www.ncbi.nlm.nih.gov/pubmed/21107671 http://dx.doi.org/10.1007/s10803-010-1138-0 |
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author | Burnette, Courtney P. Henderson, Heather A. Inge, Anne Pradella Zahka, Nicole E. Schwartz, Caley B. Mundy, Peter C. |
author_facet | Burnette, Courtney P. Henderson, Heather A. Inge, Anne Pradella Zahka, Nicole E. Schwartz, Caley B. Mundy, Peter C. |
author_sort | Burnette, Courtney P. |
collection | PubMed |
description | Individual differences in the expression of autism complicate research on the nature and treatment of this disorder. In the Modifier Model of Autism (Mundy et al. 2007), we proposed that individual differences in autism may result not only from syndrome specific causal processes, but also from variability in generic, non-syndrome specific modifier processes that affect the social and emotional development of all people. One study supporting this model found that measures of resting anterior EEG asymmetry, a measure reflecting complex brain processes associated with generic individual differences in approach and avoidance motivation, may help explain differences in the expression of autism in children without intellectual disabilities (Sutton et al. 2005). In the current study, we partially replicated the observation that children with autism who exhibited a pattern of left frontal EEG asymmetry tended to display milder levels of social symptoms, although in the current sample this pattern applied only to HFA children with relatively lower verbal IQs. New observations indicated that left frontal EEG asymmetry was also associated with retrospective parent reports of significantly later age of onset of symptoms, but also higher levels of self-reported outward expressions of anger as well as symptoms of obsessive compulsive disorder in school-age higher functioning children with ASD. Therefore, the results of this study provide a new and fully independent set of observations, which indicate that individual differences in anterior EEG asymmetry may significantly moderate the expression and developmental course of autism. This observation may have clinical implications for identifying meaningful diagnostic sub-groups among children with autism. |
format | Online Article Text |
id | pubmed-3134771 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-31347712011-08-24 Anterior EEG Asymmetry and the Modifier Model of Autism Burnette, Courtney P. Henderson, Heather A. Inge, Anne Pradella Zahka, Nicole E. Schwartz, Caley B. Mundy, Peter C. J Autism Dev Disord Original Paper Individual differences in the expression of autism complicate research on the nature and treatment of this disorder. In the Modifier Model of Autism (Mundy et al. 2007), we proposed that individual differences in autism may result not only from syndrome specific causal processes, but also from variability in generic, non-syndrome specific modifier processes that affect the social and emotional development of all people. One study supporting this model found that measures of resting anterior EEG asymmetry, a measure reflecting complex brain processes associated with generic individual differences in approach and avoidance motivation, may help explain differences in the expression of autism in children without intellectual disabilities (Sutton et al. 2005). In the current study, we partially replicated the observation that children with autism who exhibited a pattern of left frontal EEG asymmetry tended to display milder levels of social symptoms, although in the current sample this pattern applied only to HFA children with relatively lower verbal IQs. New observations indicated that left frontal EEG asymmetry was also associated with retrospective parent reports of significantly later age of onset of symptoms, but also higher levels of self-reported outward expressions of anger as well as symptoms of obsessive compulsive disorder in school-age higher functioning children with ASD. Therefore, the results of this study provide a new and fully independent set of observations, which indicate that individual differences in anterior EEG asymmetry may significantly moderate the expression and developmental course of autism. This observation may have clinical implications for identifying meaningful diagnostic sub-groups among children with autism. Springer US 2010-11-24 2011 /pmc/articles/PMC3134771/ /pubmed/21107671 http://dx.doi.org/10.1007/s10803-010-1138-0 Text en © The Author(s) 2010 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. |
spellingShingle | Original Paper Burnette, Courtney P. Henderson, Heather A. Inge, Anne Pradella Zahka, Nicole E. Schwartz, Caley B. Mundy, Peter C. Anterior EEG Asymmetry and the Modifier Model of Autism |
title | Anterior EEG Asymmetry and the Modifier Model of Autism |
title_full | Anterior EEG Asymmetry and the Modifier Model of Autism |
title_fullStr | Anterior EEG Asymmetry and the Modifier Model of Autism |
title_full_unstemmed | Anterior EEG Asymmetry and the Modifier Model of Autism |
title_short | Anterior EEG Asymmetry and the Modifier Model of Autism |
title_sort | anterior eeg asymmetry and the modifier model of autism |
topic | Original Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3134771/ https://www.ncbi.nlm.nih.gov/pubmed/21107671 http://dx.doi.org/10.1007/s10803-010-1138-0 |
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