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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Available from: Edward T Bullmore
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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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    ABSTRACT: Autism is marked by impairments in social reciprocity and communication, along with restricted, repetitive and stereotyped behaviors. Prior studies have separately investigated social processing and executive function in autism, but little is known about the brain mechanisms of cognitive control for both emotional and nonemotional stimuli. We used functional magnetic resonance imaging to identify differences in neurocircuitry between individuals with high functioning autism (HFA) and neurotypical controls during two versions of a go/no-go task: emotional (fear and happy faces) and nonemotional (English letters). During the letter task, HFA participants showed hypoactivation in ventral prefrontal cortex. During the emotion task, happy faces elicited activation in ventral striatum, nucleus accumbens and anterior amygdala in neurotypical, but not HFA, participants. Response inhibition for fear faces compared with happy faces recruited occipitotemporal regions in HFA, but not neurotypical, participants. In a direct contrast of emotional no-go and letter no-go blocks, HFA participants showed hyperactivation in extrastriate cortex and fusiform gyrus. Accuracy for emotional no-go trials was negatively correlated with activation in fusiform gyrus in the HFA group. These results indicate that autism is associated with abnormal processing in socioemotional brain networks, and support the theory that autism is marked by a social motivational deficit. Copyright © 2015. Published by Elsevier Inc.
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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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    ABSTRACT: Impaired social interaction is one of the hallmarks of Autism Spectrum Disorder (ASD). Emotional faces are arguably the most critical visual social stimuli and the ability to perceive, recognize, and interpret emotions is central to social interaction and communication, and subsequently healthy social development. However, our understanding of the neural and cognitive mechanisms underlying emotional face processing in adolescents with ASD is limited. We recruited 48 adolescents, 24 with high functioning ASD and 24 typically developing controls. Participants completed an implicit emotional face processing task in the MEG. We examined spatiotemporal differences in neural activation between the groups during implicit angry and happy face processing. While there were no differences in response latencies between groups across emotions, adolescents with ASD had lower accuracy on the implicit emotional face processing task when the trials included angry faces. MEG data showed atypical neural activity in adolescents with ASD during angry and happy face processing, which included atypical activity in the insula, anterior and posterior cingulate and temporal and orbitofrontal regions. Our findings demonstrate differences in neural activity during happy and angry face processing between adolescents with and without ASD. These differences in activation in social cognitive regions may index the difficulties in face processing and in comprehension of social reward and punishment in the ASD group. Thus, our results suggest that atypical neural activation contributes to impaired affect processing, and thus social cognition, in adolescents with ASD.
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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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