| Summary: | This thesis investigated the role of the amygdala in social cognition by examining variability in social-perceptual abilities within the normal population and via experiments with individuals who have Asperger's syndrome (AS). I found that a significant proportion of men from the general population had a fear recognition deficit akin to that seen in patients with bilateral amygdala lesion and that poor fear recognition was associated with poor theory of mind ability and with reduced activation of the amygdala and associated areas of the 'social brain'. Further experiments suggested a mechanism for these impairments - reduced fixation of the eye region of the face - similar to that exhibited by patient SM, who has suffered bilateral amygdala damage. Overall, I found that AS subjects also had a fear recognition deficit when compared with matched controls. However, there was great variability in responses, with scores ranging from normal to severely impaired. Again, an eyetracking experiment showed that low fear recognition was related to a reduced amount of time spent fixating the eyes. Informed by recent neurodevelopmental models of amygdala involvement in autistic- spectrum disorders, I conducted psychological, neurophysiological and neuroanatomical experiments in order to examine the cause of this failure to attend to the eyes in some AS subjects. As a whole, the findings support a 'hyper-active amygdala model', in which social stimuli induce an aversive level of arousal and so are avoided. I suggest that inattention to social stimuli, which could have a number of possible aetiologies, might be at the heart of a general route to social cognitive impairment, which could be shared by several distinct populations.
|
|---|
