Abstract
Background Impaired imitation has been found to be an important factor contributing to social communication deficits in individuals with autism spectrum disorder (ASD). It has been hypothesized that the neural correlates of imitation, the mirror neuron system (MNS), are dysfunctional in ASD, resulting in imitation impairment as one of the key behavioral manifestations in ASD. Previous MNS studies produced inconsistent results, leaving the debate of whether mirror neurons are “broken” in ASD unresolved.Methods This meta-analysis aimed to explore the differences in MNS activation patterns between typically developing (TD) and ASD individuals when they observe/imitate biological motions with/without emotional components. Effect-size signed differential mapping (ES-SDM) was adopted to synthesize the available fMRI data. Results The MNS is dysfunctional in ASD; not only the brain regions containing mirror neurons were affected, the brain regions supporting MNS functioning were also impaired. Second, MNS dysfunction in ASD is modulated by task complexity; differential activation patterns during the presentation of “cold” and “hot” stimuli might be a result of atypical functional connectivity in ASD. Third, MNS dysfunction in ASD individuals is modulated by age. MNS regions were found to show delayed maturation; abnormal lateralization development in some of the brain regions also contributed to the atypical development of the MNS in ASD. Limitations We have attempted to include a comprehensive set of original data for this analysis. However, whole brain analysis data were not obtainable from some of the published papers, these studies could not be included as a result. Moreover, the results indicating the age effect on MNS in ASD could only be generalized to individuals aged 11-37, as MNS activation remains unstudied for populations beyond this age range. Also, the ES-SDM linear regression modelling might not be ideal to illustrate the associations between age and MNS activation; the meta-regression results should be treated with caution. Conclusion There is a “global” rather than a “local” network dysfunction, which may underlie the imitation impairments in individuals with ASD. Task complexity and age modulate the functioning of the MNS, which may explain the previous peculiar results contributing to the unresolved “broken mirror neuron” debate.