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An Activation Likelihood Estimation Meta-Analysis of Social Cognition in Autism Spectrum Disorders

Thursday, 2 May 2013: 09:00-13:00
Banquet Hall (Kursaal Centre)
M. Patriquin1, L. Libero2 and R. K. Kana2, (1)Virginia Tech, Blacksburg, VA, (2)University of Alabama at Birmingham, Birmingham, AL

Recent perspectives on psychiatric diagnosis encourage researchers to seek objective and quantifiable markers of dysfunction (Montague et al., 2012). In autism spectrum disorders (ASD), broadly consistent findings have pointed to multiple brain regions, e.g., superior temporal sulcus (Kaiser et al., 2010) and fusiform face area (Spencer et al., 2011), associated with deficits in social cognition. These findings underscore the role of social brain structures by themselves and/or their functional connectivity (Kana, Libero, Moore, 2011) in the neuropathology of ASD. The present study set out to isolate the most critical components of social brain abnormality in individuals with ASD to gain further insight into their social deficits. 


The goal of this study was to identify common and consistent spatial locations in the brain, as spatial probability distributions, that underlie social cognition in ASD. 


This metaanalysis involved a systematic review of all functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) studies that utilized social cognition tasks (e.g., theory-of-mind, face processing, empathy, biological motion, self-other representation) in children and adults with and without ASD. Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) Statement guidelines, 37 studies were identified that used fMRI and PET techniques. Inclusion criteria were: 1) studies that contained a control and an ASD group of participants; 2) studies with control > autism comparison coordinates for activation reported; 3) studies that used PET or fMRI methods; and 4) studies that were published in English. Activation foci from studies meeting inclusion criteria (= 37) were subjected to a quantitative voxel-based meta-analysis using activation likelihood estimation (ALE; Laird et al., 2005; Laird, Lancaster, & Fox, 2008; Turkeltaub et al., 2002) in GingerALE. ALE maps are then obtained by computing the union of activation probabilities for each voxel.


Between-group comparisons showed that ASD participants had significantly reduced probability of activation, compared to controls, in areas consistently activated to social tasks: amygdala, superior temporal gyrus (STG), inferior frontal gyrus (IFG), insula, middle temporal gyrus (MTG), fusiform gyrus (FFA), anterior cingulate cortex (ACC), and angular gyrus (AG) (< 0.05, corrected for multiple comparisons using FDR). Some areas not commonly or primarily associated with social cognition tasks also demonstrated significantly higher likelihood of activation in controls relative to ASD: putamen, parahippocampal gryus, cerebellum, and thalamus. 


Results indicate significantly reduced engagement of key social brain areas in children and adults with ASD, including amygdala, STG, IFG, and FFA. Medial prefrontal cortex and orbitofrontal cortex, two additional areas considered to be part of the social brain network, were not found to be significantly reduced in ASD participants. The findings from this study synthesize results from existing neuroimaging data on social cognition in ASD, helping to elucidate the network of social brain regions perhaps responsible for the social impairment that is hallmark to ASD.

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