Unbroken mirror neurons in autism spectrum disorders
The ‘broken mirror’ theory of autism, which proposes that a dysfunction of the human mirror neuron system (MNS) is responsible for the core social and cognitive deficits in individuals with autism spectrum disorders (ASD), has received considerable attention despite weak empirical evidence. Methods:
In this electroencephalographic study, we examined mu suppression, as an indicator of sensorimotor resonance, concurrent with oculomotor performance while individuals (n = 20) with ASD and control participants (n = 20) either executed hand actions or observed hand actions or a moving dot. No difference in visual attention between groups was found as indicated by fixation duration and normalized fixation number on the presented stimuli. Results:
The mu suppression over the sensorimotor cortex was significantly affected by experimental conditions, but not by group membership, nor by the interaction between groups and conditions. Individuals with ASD, similar to the controls, exhibited stronger mu suppression when watching hand actions relative to a moving dot. Notably, participants with ASD failed to imitate the observed actions while their mu suppression indicating the MNS activity was intact. In addition, the mu suppression during the observation of hand actions was positively associated with the communication competence of individuals with ASD. Conclusion:
Our study clearly challenges the broken mirror theory of autism. The functioning of the mirror neuron system might be preserved in individuals with ASD to a certain degree. Less mu suppression to action observation coupled with more communicational severity can reflect the symptom heterogeneity of ASD. Additional research needs to be done, and more caution should be used when reaching out to the media.
Document Type: Research Article
Affiliations: 1: Institute of Neuroscience, National Yang-Ming University, Taipei, Taiwan 2: Departments of Psychology and Psychiatry, and Center for Cognitive and Social Neuroscience, The University of Chicago, Illinois, USA 3: Institute of Biomedical Engineering, Ming-Chuan University, Taoyuan, Taiwan
Publication date: September 1, 2010