An Investigation Into the Role of the Mirror Neuron System in Facial Emotion Processing in High Functioning Autism Utilizing Transcranial Magnetic Stimulation

Thursday, May 17, 2012
Sheraton Hall (Sheraton Centre Toronto)
9:00 AM
K. Young1, T. J. Perkins2, D. Kidgell3, J. A. McGillivray2 and M. A. Stokes4, (1)School of Psychology, Deakin University, Melbourne, Australia, (2)Psychology, Deakin University, Burwood, Australia, (3)School of Exercise and Nutrition Science, Faculty of Health, Deakin University, Burwood, Australia, (4)School of Psychology, Deakin University, Burwood, Australia
Background:  

Theoretical accounts suggest that the mirror neuron system (MNS) (neurons which respond to executed and observed actions) plays an important role in social cognition and thus a deficit in this system may be linked to social difficulties in autism spectrum disorders (ASD). However an important element of social cognition that has not been well examined in the context of the MNS is facial emotion processing. As facial emotion processing involves the ability to identify emotion through the observation of facial expression, this ability may be attributable to the MNS. Automatic processing by MNs may allow for an internal representation of another’s facial expression, thus facilitating the understanding of the observed internal state of another (Enticott et al., 2008). Research has established that viewing emotional faces often elicits spontaneous mimicry in typically developing individuals, thus providing further support for this account. This suggests that difficulties with facial emotion processing in ASDs may in part be due to a dysfunctional MNS, and contribute to difficulties in higher order abilities such as tehory of mind and empathy.

Objectives:  

The present study examined whether mirror neuron activation was associated with facial emotion processing in typically developing individuals and in individuals with HFA. Transcranial magnetic stimulation (TMS) was used as it is a non-invasive means of stimulating nerve cells in the motor cortex via the administration of a brief magnetic pulse to the scalp. This pulse produces a motor evoked potential (MEP) in the specific muscle stimulated that can be measured via electromyography. When TMS is delivered during the observation of action within the stimulated muscle, premotor MN activity increases excitability in the motor cortex resulting in enhanced MEP amplitude. 

Methods:  

Subjects with a diagnosis of HFA were compared to TD individuals (N=10 males in each group). Participants were shown a number of emotional facial expressions in the experimental conditions and a number of neutral expressions in the control conditions. During this time, the motor cortex was stimulated using TMS. The effects of the motor cortex stimulation was assessed by recording responses produced in facial muscles specific to the expression presented via electromyography.  It was hypothesized that TD individuals would actively engage in facial emotional processing as demonstrated by increased MEP amplitude in emotional conditions compared to neutral conditions. Further, it was also hypothesized that individuals with HFA would demonstrate a lack of facial emotional processing as demonstrated by no difference in MEP amplitude between conditions.

Results:  

Although data analysis is only preliminary at present as more HFA data needs to be collected; the results indicate that TD individuals are demonstrating higher MEP amplitude in emotional conditions compared to neutral conditions. In contrast, individuals with HFA are demonstrating no difference in MEP amplitude between conditions.

Conclusions:  

On the basis of preliminary analyses this research appears to support the notion that the MNS plays an important role in social cognition and that a dysfunction in this system may provide a neural basis for a number of social cognitive deficits exhibited in individuals with HFA.

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