A disembodied mind : the role of dysfunctional simulation systems in the social and cognitive deficits of autism spectrum disorders
- Author(s): Oberman, Lindsay Meredith
- et al.
Disorders on the autism spectrum are characterized by deficits in social and communicative skills as well as the presence of restricted, repetitive, and stereotyped patterns of behaviors, interests and activities. The recent discovery of mirror neurons in macaque monkeys by Rizzolatti and colleagues may provide a basis for explaining some of the behavioral deficits seen in individuals with autism spectrum disorders (ASD). Mirror neurons are primarily thought to be involved in perception and comprehension of motor actions, but may also play a critical role in higher order cognitive processes such as imitation, empathy, and language. Studies have suggested that the MNS is dysfunctional in individuals with ASD. The following dissertation includes our original discovery of this dysfunction as well as follow-up studies aimed at further characterizing the extent of the dysfunction in this population and factors that may modulate it. Study 1 investigated the response of the MNS to the observation and performance of actions in individuals with ASD. Results suggest a dysfunction in this system in ASD. Study 2 followed up on this finding exploring the extent of this dysfunction and if it could be ameliorated by the presentation of socially relevant stimuli. Results of this study replicated and extended the original finding in a different sample, finding no significant mu suppression to the observation of an unfamiliar person in the ASD group. However, if the person in the video was either a member of the participant's family or the participant himself performing the action, the ASD group showed a "normal" degree of suppression. Study 3 investigated the role of a mirror-like system in another domain, facial mimicry. Results suggest a delay in the appropriate spontaneous mimicry response to observed facial expressions in the ASD group. Despite showing a "normal" amplitude of response and overall activity level, the latency of a response was approximately 150 milliseconds delayed as compared to the control group. Together, these results provide a candidate functional mechanism underlying some of the behavioral deficits that characterize ASD and provide hope for the development of therapeutic interventions aimed at improving the functioning of the MNS