Williams Justin H G
Department of Child Health, University of Aberdeen Medical School, Royal Aberdeen Children's Hospital, Aberdeen, UK.
Autism Res. 2008 Apr;1(2):73-90. doi: 10.1002/aur.15.
Mirror neuron system dysfunction may underlie a self-other matching impairment, which has previously been suggested to account for autism. Embodied Cognition Theory, which proposes that action provides a foundation for cognition has lent further credence to these ideas. The hypotheses of a self-other matching deficit and impaired mirror neuron function in autism have now been well supported by studies employing a range of methodologies. However, underlying mechanisms require further exploration to explain how mirror neurons may be involved in attentional and mentalizing processes. Impairments in self-other matching and mirror neuron function are not necessarily inextricably linked and it seems possible that different sub-populations of mirror neurons, located in several regions, contribute differentially to social cognitive functions. It is hypothesized that mirror neuron coding for action-direction may be required for developing attentional sensitivity to self-directed actions, and consequently for person-oriented, stimulus-driven attention. Mirror neuron networks may vary for different types of social learning such as "automatic" imitation and imitation learning. Imitation learning may be more reliant on self-other comparison processes (based on mirror neurons) that identify differences as well as similarities between actions. Differential connectivity with the amygdala-orbitofrontal system may also be important. This could have implications for developing "theory of mind," with intentional self-other comparison being relevant to meta-representational abilities, and "automatic" imitation being more relevant to empathy. While it seems clear that autism is associated with impaired development of embodied aspects of cognition, the ways that mirror neurons contribute to these brain-behavior links are likely to be complex.
镜像神经元系统功能障碍可能是自我与他人匹配受损的潜在原因，此前有人认为这种受损可解释自闭症。具身认知理论提出，行动为认知提供了基础，这进一步支持了这些观点。自闭症中自我与他人匹配缺陷及镜像神经元功能受损的假说，现已得到一系列方法研究的有力支持。然而，潜在机制仍需进一步探索，以解释镜像神经元如何参与注意力和心理化过程。自我与他人匹配及镜像神经元功能的损害不一定紧密相连，位于多个区域的不同亚群镜像神经元，似乎有可能对社会认知功能有不同贡献。据推测，为发展对自我导向行动的注意力敏感性，进而发展以人为主、刺激驱动的注意力，可能需要对行动方向进行镜像神经元编码。对于不同类型的社会学习，如“自动”模仿和模仿学习，镜像神经元网络可能有所不同。模仿学习可能更依赖自我与他人的比较过程（基于镜像神经元），该过程能识别行动之间的差异和相似之处。与杏仁核 - 眶额系统的不同连接也可能很重要。这可能对“心理理论”的发展有影响，有意的自我与他人比较与元表征能力相关，而“自动”模仿与同理心更相关。虽然自闭症显然与具身认知方面的发展受损有关，但镜像神经元对这些脑 - 行为联系的贡献方式可能很复杂。
