Abstract
The brain has specialized networks for processing of biological motion (BM) of socially relevant items. It is suggested that autism spectrum disorder (ASD) would reflect a dysfunctional parieto-frontal motion processing system, but previous perceptual studies on impaired BM sensitivity in children and adults with autism are inconclusive. Here, we explored brain signatures within the broader autism phenotype. Participants were selected into low (AQ < 11, mean=9.5) and high (AQ>21, mean =25.1) Autism Spectrum Quotient (AQ) groups. The participants observed a white fixation cross followed by 3s BM point-like movies (Giese lab)while MEG signals were recorded (Elektra TRIUX MEG system). Walkers were predominantly moving to the left or the right for each block of trials and participants gestured the number of stimuli for the minority direction at the end of each block. Brainstorm was used for analysis of evoked responses. During data pre-processing, several participants were removed because of extensive artefacts, with 11 in each of the High AQ and Low AQ groups analysed. The grand mean average MEFs for the Low AQ and High AQ groups were used for overall source localisation, using a minimum norm estimate (MNE). A pattern of posterior cortical activation was observed in primary cortex, in motion area (hMT+), in superior temporal sulcus (STS), and bilaterally in orbitofrontal cortex (OFC). “Scouts” were established at each location using a seed growing process across the tessellated cortical surface, allowing the evoked activity to be measured for each source for each participant. Connectivity was explored via Phase Transfer Entropy (PTE – available in Brainstorm) across the 8 scouts. It demonstrated greater occipital cortex to OFC connectivity of the Low AQ group cf the high AQ group, particularly for extended latencies in the range of 250–400 ms after stimulus appearance, supporting the behavioural findings.