No abstract

Individuals with autism are impaired in the recognition of fear, which may be due to their reduced tendency to look at the eyes. Here we investigated another potential perceptual and social consequence of reduced eye fixation. The eye region of the face is critical for identifying genuine, or sincere, smiles. We therefore investigated this ability in adults with autism. We used eye-tracking to measure gaze behaviour to faces displaying posed and genuine smiles. Adults with autism were impaired on the posed/genuine smile task and looked at the eyes significantly less than did controls. Also, within the autism group, task performance correlated with social interaction ability. We conclude that reduced eye contact in autism leads to reduced ability to discriminate genuine from posed smiles with downstream effects on social interaction.

By testing the facial fear-recognition ability of 341 men in the general population, we show that 8.8% have deficits akin to those seen with acquired amygdala damage. Using psychological tests and functional magnetic resonance imaging (fMRI) we tested the hypothesis that poor fear recognition would predict deficits in other domains of social cognition and, in response to socially relevant stimuli, abnormal activation in brain regions that putatively reflect engagement of the "social brain." On tests of "theory of mind" ability, 25 "low fear scorers" (LFS) performed significantly worse than 25 age-and IQ-matched "normal (good) fear scorers" (NFS). In fMRI, we compared evoked activity during a gender judgement task to neutral faces portraying different head and eye gaze orientations in 12 NFS and 12 LFS subjects. Despite identical between-group accuracy in gender discrimination, LFS demonstrated significantly reduced activation in amygdala, fusiform gyrus, and anterior superior temporal cortices when viewing faces with direct versus averted gaze. In a functional connectivity analysis, NFS show enhanced connectivity between the amygdala and anterior temporal cortex in the context of direct gaze; this enhanced coupling is absent in LFS. We suggest that important individual differences in social cognitive skills are expressed within the healthy male population, which appear to have a basis in a compromised neural system that underpins social information processing.

Using an attentional blink paradigm, we show that the typical enhancement of perception for emotionally arousing events is significantly reduced in Asperger's syndrome (AS) at short inter-target intervals. Control experiments demonstrate that this finding cannot be attributed to differences in the perceived arousal of the stimuli, or to a global impairment affecting any type of modulation of perceptual encoding. Because a functioning amygdala is critical for emotional modulation of the attentional blink, the findings support a role for the amygdala in the pathophysiology of AS. More specifically, they suggest there is a fundamental failure of the amygdala to modulate processing in cortex, a concept at the heart of some recent theories of amygdala involvement in the aetiology of autistic-spectrum disorders.