Ashwin C, Baron-Cohen S, Wheelwright S, O’Riordan M, Bullmore ET. Differential activation of the amygdala and the ‘social brain’ during fearful face-processing in Asperger Syndrome. Neuropsychologia 45: 2-14

Autism Research Centre, University of Cambridge, Department of Psychiatry, Douglas House, 18b Trumpington Rd, Cambridge CB2 2AH, UK.
Neuropsychologia (Impact Factor: 3.3). 02/2007; 45(1):2-14. DOI: 10.1016/j.neuropsychologia.2006.04.014
Source: PubMed


Impaired social cognition is a core feature of autism. There is much evidence showing people with autism use a different cognitive style than controls for face-processing. We tested if people with autism would show differential activation of social brain areas during a face-processing task. Thirteen adults with high-functioning autism or Asperger Syndrome (HFA/AS) and 13 matched controls. We used fMRI to investigate 'social brain' activity during perception of fearful faces. We employed stimuli known to reliably activate the amygdala and other social brain areas, and ROI analyses to investigate brain areas responding to facial threat as well as those showing a linear response to varying threat intensities. We predicted: (1) the HFA/AS group would show differential activation (as opposed to merely deficits) of the social brain compared to controls and (2) that social brain areas would respond to varied intensity of fear in the control group, but not the HFA/AS group. Both predictions were confirmed. The controls showed greater activation in the left amygdala and left orbito-frontal cortex, while the HFA/AS group showed greater activation in the anterior cingulate gyrus and superior temporal cortex. The control group also showed varying responses in social brain areas to varying intensities of fearful expression, including differential activations in the left and right amygdala. This response in the social brain was absent in the HFA/AS group. HFA/AS are associated with different patterns of activation of social brain areas during fearful emotion processing, and the absence in the HFA/AS brain of a response to varying emotional intensity.

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    • "Interestingly, we also observed increased activation in the anterior amygdala for happy faces relative to fear faces in control, but not HFA, participants. Based on prior evidence, we had expected to find this group difference in the contrast of fear faces relative to happy faces (Ashwin et al., 2007; Monk et al., 2010). In partial agreement with our third hypothesis, we found that response inhibition for happy faces relative to response inhibition for fear faces recruited the pregenual ACC in the HFA group, but not the control group. "
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    • "Given that individuals with ASD are often poor at recognizing others3 mental states or social norms, they have likely encountered displays of anger without understanding the implications (Bal et al., 2010; Baron-Cohen et al., 1999; Begeer et al., 2006). Past studies have specifically noted atypical angry facial processing in individuals with ASD (Ashwin et al., 2006; Kuusikko et al., 2009; Rieff et al., 2007; Rump et al., 2009). Age-effects in anger processing have also been noted, as older children and adolescents are able to correctly identify angry faces more often than younger children, regardless of diagnosis (Lindner & Rosén, 2006). "
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    • "Nonetheless, contextual effects on social cognition performance in AS are not well-understood. Individuals with AS exhibit deficits in emotion recognition from faces (Philip et al., 2010), particularly those conveying negative emotions (Ashwin et al., 2007; Falkmer et al., 2011; Doi et al., 2013). Also, studies using the Faux Pas Test (FPT) have revealed ToM impairments, especially in understanding the intentions (cognitive ToM) and the emotional impact of others' actions (affective ToM) (Zalla et al., 2009; Gonzalez-Gadea et al., 2013). "
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