25591
The Impact of Stimulant Medication on EEG Alpha Power in Children with Autism Spectrum Disorder

Thursday, May 11, 2017: 5:30 PM-7:00 PM
Golden Gate Ballroom (Marriott Marquis Hotel)
A. Kresse1, L. A. Edwards2, J. W. Keller3, C. A. Nelson3, K. A. Pelphrey4 and S. J. Webb5, (1)Seattle Children's Research Institute, Seattle, WA, (2)Marcus Autism Center, Children's Healthcare of Atlanta and Emory University School of Medicine, Atlanta, GA, (3)Boston Children's Hospital, Boston, MA, (4)Yale University, New Haven, CT, (5)Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA
Background:  It has been estimated that 56% of children with autism spectrum disorder are taking at least one psychotropic medication (Mandell et al., 2008). These rates of medication use present a challenge for researchers studying brain activity in autism using EEG. For example, stimulants are one of the most commonly prescribed medications in autism, with approximately 22% of children taking some type of stimulant (Mandell et al., 2008). If children on medication are included in a study it may be impossible to differentiate brain responses due to medication from brain responses related to autism. However, if researchers choose to exclude individuals taking medications from their study, they could be eliminating a significant portion of children with autism, resulting in a limited and/or biased sample.

Objectives:  This study will leverage the large sample size of the ACE GENDAAR Project to investigate the potential impact of psychotropic medication on EEG alpha power. To parse out the different effects of medications and the behaviors they’re prescribed to treat, we will examine EEG alpha power and stimulant use in children with and without externalizing behaviors.

Methods:  High density EEG was collected while children with autism between the ages of 8 and 17 completed a resting task that alternated passively viewing screensaver-like videos (Eyes Open condition) and sitting with eyes closed (Eyes Closed condition). Movement and blink artifacts were rejected, and FFT was performed over clean segments. Average power across 8 – 12 hz for mid-posterior electrodes was calculated for each subject. High externalizing behaviors were characterized as a Child Behavioral Check List domain of Externalizing Problems score in the borderline or clinical range (T score > 59). Of children with autism 22 were reported as taking a stimulant (High Externalizing, n = 10; Low Externalizing, n = 12) and 79 were not on a stimulant (High Externalizing, n = 28; Low Externalizing, n = 51); the samples did not differ on age (p = .35) or IQ (p = .53).

Two-way ANOVAs were calculated to look at the effects of both Externalizing (high, low) and Stimulant Medication (Stimulant, No Stimulant) on mid-posterior alpha power for both Eyes Open and Eyes Closed conditions.

Results:  In the Eyes Open condition, there was a significant main effect of stimulant, F(1,98) = 4.55, p = .04; and on the Eyes Closed condition, there was a marginal main effect of stimulant, F(1, 95) = 2.95, p = .089). This suggests that regardless of externalizing levels, children who are currently taking stimulant medication have significantly higher mid-posterior alpha power compared to children who are not on stimulant medication.

Conclusions:  These findings indicate increased mid-posterior alpha power in children with autism who are taking a stimulant medication, and provide evidence for the importance of taking medication status into account during EEG analyses. Findings will be extended by looking at alpha power spectra in other regions, including frontal alpha and hemispheric differences in alpha power.