Literature DB >> 20006344

ADHD familial loading and abnormal EEG alpha asymmetry in children with ADHD.

T Sigi Hale1, Susan L Smalley, Jeff Dang, Grant Hanada, James Macion, James T McCracken, James J McGough, Sandra K Loo.   

Abstract

OBJECTIVE: Abnormal brain laterality (ABL) is indicated in ADHD. ADHD and brain laterality are heritable. Genetic factors contributing to lateralization of brain function may contribute to ADHD. If so, increased ADHD family loading should be associated with greater ABL. Previous studies have shown increased rightward alpha asymmetry in ADHD. We tested whether this was more pronounced in ADHD children with increased ADHD family loading.
METHODS: We compared EEG alpha asymmetry at rest and during the Conner's Continuous Performance Test (CPT) in ADHD children with and without ADHD affected parents, and replicated our findings in a second larger sample. The replication study additionally stratified the parent-affected sample by parental persistent versus non-persistent ADHD status, increased spatial resolution of EEG measures, and assessed low versus high-alpha.
RESULTS: Study-1: the parent-affected group showed increased rightward asymmetry across frontal and central regions and reduced rightward parietal asymmetry during an eyes closed (EC) condition, as well as increasing rightward parietal asymmetry with advancing age during the CPT. Study-2 replicated these findings and further delineated influences of low versus high-alpha, recording site, and effects of parental persistent versus non-persistent ADHD status.
CONCLUSION: Increased ADHD familial loading was associated with increased rightward frontal asymmetry. In contrast, increased rightward parietal asymmetry was associated with reduced ADHD family loading. Frontal results are consistent with an ADHD endophenotype. Parietal results suggest an ADHD adaptive trait prevalent with less ADHD family loading. Age effects indicate a unique developmental course among ADHD children whose parents have non-persistent ADHD. Copyright 2009 Elsevier Ltd. All rights reserved.

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Year:  2009        PMID: 20006344      PMCID: PMC2878884          DOI: 10.1016/j.jpsychires.2009.11.012

Source DB:  PubMed          Journal:  J Psychiatr Res        ISSN: 0022-3956            Impact factor:   4.791


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