International Meeting for Autism Research: Neural Activation In Response to Sensory Stimuli In Adolescents and Children with and without ASD

Neural Activation In Response to Sensory Stimuli In Adolescents and Children with and without ASD

Friday, May 13, 2011
Elizabeth Ballroom E-F and Lirenta Foyer Level 2 (Manchester Grand Hyatt)
11:00 AM
S. A. Green1, D. Shirinyan2, N. L. Colich2, J. D. Rudie2, M. Dapretto3 and S. Y. Bookheimer3, (1)Psychology, University of California, Los Angeles, Los Angeles, CA, (2)Brain Mapping Center, University of California, Los Angeles, Los Angeles, CA, (3)Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, CA
Background: Children with ASD often exhibit sensory over-responsivity (SOR), which may cause them to react negatively to sensory stimuli such as noisy or visually stimulating environments (Liss et al., 2006).  Rates of SOR are over five times higher in children with ASD than in the typically developing (TD) children (e.g., Baranek et al., 2006; Ben-Sasson et al., 2007) and SOR is associated with increased functional impairment in children with ASD (e.g., Liss et al., 2006; Pfeiffer et al., 2005).  Theories about the neural basis of SOR include abnormal sensory gating in the thalamus (Hardan et al., 2008), and disruption of normal activation and processing by the limbic system, including the amygdala (Hitoglou et al., 2010; Waterhouse et al., 1996).  However, the neural bases for SOR are still unknown, and as of yet no functional MRI (fMRI) studies of SOR have been conducted in children with ASD.

Objectives: The purpose of this study was to examine differences in brain response to mildly aversive sensory stimuli in children with ASD and TD children.

Methods: Participants were 11 children and adolescents with ASD and 11 TD controls, between 8-17 years.  During fMRI, participants were presented with mildly aversive auditory (white noise) and visual (a continually rotating color wheel) stimuli.  Each stimulus trial was 3 seconds long and consisted of either the auditory stimulus, visual stimulus, or both. Each trial type was presented 12 times.  After the fMRI scan, participants were asked to rate on a scale from 1-10 how much each trial type bothered them and how much they wanted each trial type to stop.  Participants’ mothers rated their symptoms of SOR with the Sensory Profile (Dunn, 1999) and Sensory Over-Responsivity Inventory (Schoen et al., 2008). 

Results: The ASD group was rated as having significantly higher symptoms of SOR than the TD group.  During the fMRI task, both groups showed significant activity in visual and auditory cortices. However, during the visual task, the ASD group showed significantly more activation in the lateral geniculate nucleus of the thalamus and downstream primary and secondary visual cortex.  During the auditory task, the ASD group showed significantly more activation in the amygdala and auditory cortex.

Conclusions: Findings suggest that children with ASD exhibit hyperactivation of the thalamus and amygdala while processing mildly aversive sensory stimuli.  A lack of inhibition and/or habituation of these areas may lead to hyperactivity of the sensory cortical areas and may thus be more likely to lead to a sense of overstimulation  These findings support theories that SOR is related to abnormal thalamus and amygdala activity and that there may be a bottom up abnormality in primary sensory modulation.

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