Schulte-Rüther et al. (2010)

Dysfunctions in brain networks supporting empathy: An fMRI study in adults with autism spectrum disorders.

Background information: Most previous studies of autistic spectrum disorders focused solely on the ability to infer other people’s thoughts and intentions although the representation of both other and self may be altered in autism. Little is known about the neural bases of atypical self-reference and empathy in individuals with autism. Previous research used tasks requiring the imitation and observation of emotional faces, which lacked the demand of explicit self-reference and empathizing. Therefore, important behavioural and brain function aspects of self-related emotional processing and its possible disturbance in people with autism may have been overlooked.

Aim: To identify dysfunctions in brain networks that may underlie disturbed empathic behaviour in autism spectrum disorders.

Method: Eighteen male adults with a diagnosis of ASD and 18 male control subjects without a history of neurological or psychiatric disease and matched for age and IQ took part in this study. 14 participants in each group were included in the final fMRI data analysis.

They were asked to empathize with facial expressions of emotions and indicate either the emotional state observed in each face (other-task) or their own emotional reaction to the emotional facial expressions (self-task), while undergoing an fMRI scan. Happy and sad facial expressions were chosen as stimuli in order to focus on the emergence of contagious emotional responses as one possible outcome of empathic processing.

Results: Participants with autism spectrum disorder performed equally to the control group during the other-task, but showed less emotionally congruent responses in the self-task.

Activations of the medial prefrontal cortex were located in dorsal sub-regions in autistic subjects and in ventral areas in control subjects. During the self-task, autistic subjects activated an additional network of frontal and inferior temporal areas. Frontal areas previously associated with the human mirror neuron system were activated in both tasks in control subjects, while autistic participants recruited these areas during the self-task only. Activations in the ventral medial prefrontal cortex may provide the basis for one’s “emotional bond” with other persons’ emotions. Such atypical patterns of activation may underlie disturbed empathy in individuals with autism.

Conclusion: Subjects with autism spectrum disorder may use an atypical cognitive strategy to gain access to their own emotional state in response to other people’s emotions.

Evaluation:

Strengths of the study: Strong experimental design: the reactions and neuronal activity of the participants with autism were compared to a control group, on a control task, on other-face mood recognition and on self-mood recognition.

Limitations of the study: The choice of computerized faces gave standardisation of facial expressions but more natural stimuli (e.g., videoclips of emotional faces in a naturalistic context) may perhaps trigger stronger empathic reactions.

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