The proposed deficits in reading other people’s feelings and thoughts and the lack in empathizing with other people have been commonly used to explain the impairments in social interactions and communication as well as inappropriate responses in social encounters even in high-functioning forms of autism such as in an Asperger. It was suggested that these deficits are mediated by a not sufficiently activated amygdala. These and other data, such as post-mortem examinations of amygdaloid morphology , amygdala lesion studies in non-human primates , as well as comparison between amygdala- lesioned patients and autistics have led to the Amygdala Theory of autism . In its current version it implies that the amygdala is hypo-functioning, thus the autistic person does not “feel” enough or does not process socio-emotional cues sufficiently .
On the other hand there is evidence that the amygdala may be overly activated in autism. First, structurally the amygdala is enlarged in autism as early as 18 months of age and this enlargement persists throughout childhood until about 12 years of age. In adolescence the enlargement disappears and by early adulthood the amygdala may even end up smaller than in control subjects . These changes may reflect an over-activation of the amygdala in early childhood. Second, functional hyper-reactivity was demonstrated when autistic subjects are confronted with socially relevant stimuli, such as faces and eyes . For example, Kleinhans et al. (2009) showed that compared to controls the amygdala of autistic subjects exhibits attenuated habitation to facial stimuli and that increased amygdala- arousal in autistics was associated with increased social impairment. Monk et al. (2010) recently showed that right amygdala activation is enhanced in autistic subjects during face processing when controlling for attention, that is when the autistic subjects pay attention to the stimuli. Dalton et al. (2005) revealed that high-functioning autistics showed greater activation in the right amygdala when viewing familiar and unfamiliar faces and greater activation in the left amygdala and also in the left orbito-frontal cortex when viewing emotional faces. Both areas form part of the emotion circuit of the brain and increased reactivity to faces in these areas means a heightened emotional response to these stimuli.
Moreover, in autistics, but not in controls, the amount of eye gaze fixation was strongly correlated with amygdala activation when viewing both, inexpressive or emotional faces (Dalton et al., 2005). This suggests that that eye gaze fixation is associated with emotional and possibly negative arousal in autistics and this could explain why autistics have “trouble looking other people in the eye.” Eye contact and watching the facial expressions are one of the first signs of cognitively healthy infants, are natural to people, and serve to build the basis for successful navigation through a social environment. For an autistic person however, these stimuli may be just too intense or even aversive to cope with and hence they are avoided. The Intense World Theory proposes that amygdaloid hyper-reactivity and hyper-plasticity may in particular provoke a dis-proportional level of negative emotions and affect in autism, such as elevated stress responses and anxiety as well as enhanced fear memory formation. Enhanced phobias and anxiety levels were first noted by Kanner himself in his original case studies and later confirmed by population studies on children with autism. However, contrary to the deficit-oriented or disconnected Amygdala Theory and Theory of Mind of autism, we propose that the amygdala may be overtly active in autism, and hence autistic individuals may in principle be very well able to attend to social cues, feel emotions and even empathize with others or read their minds, but they avoid doing so, because it is emotionally too overwhelming, anxiety-inducing, and stressful.
We can't really know, so I'm don't bother with it. Certainly some people had AS before it was recognized as a diagnosis, but it's futile trying to diagnose them in retrospect.