4.7 Article

Mirror Neuron Activity Associated with Social Impairments but not Age in Autism Spectrum Disorder

期刊

BIOLOGICAL PSYCHIATRY
卷 71, 期 5, 页码 427-433

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.biopsych.2011.09.001

关键词

Asperger's disorder; autism; electromyography; mirror neuron system; primary motor cortex; transcranial magnetic stimulation

资金

  1. National Health and Medical Research Council (NHMRC, Australia) [545811]
  2. Canadian Institutes of Health Research
  3. Constance and Stephen Lieber through a National Alliance
  4. NHMRC
  5. Neuronetics, Inc.
  6. Aspect Medical, Inc.

向作者/读者索取更多资源

Background: The neurobiology of autism spectrum disorder (ASD) is not particularly well understood, and biomedical treatment approaches are therefore extremely limited. A prominent explanatory model suggests that social-relating symptoms may arise from dysfunction within the mirror neuron system, while a recent neuroimaging study suggests that these impairments in ASD might reduce with age. Methods: Participants with autism spectrum disorder (i.e., DSM-IV autistic disorder or Asperger's disorder) (n = 34) and matched control subjects (n = 36) completed a transcranial magnetic stimulation study in which corticospinal excitability was assessed during the observation of hand gestures. Results: Regression analyses revealed that the ASD group presented with significantly reduced corticospinal excitability during the observation of a transitive hand gesture (relative to observation of a static hand) (p < .05), which indicates reduced putative mirror neuron system activity within ventral premotor cortex/inferior frontal gyrus. Among the ASD group, there was also a negative association between putative mirror neuron activity and self-reported social-relating impairments, but there was no indication that mirror neuron impairments in ASD decrease with age. Conclusions: These data provide general support for the mirror neuron hypothesis of autism; researchers now must clarify the precise functional significance of mirror neurons to truly understand their role in the neuropathophysiology of ASD and to determine whether they should be used as targets for the treatment of ASD.

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