Self-other relations in social development and autism: multiple roles for mirror neurons and other brain bases.
Mirror-neuron hiccups can guide social lesson design, but basic mimicry may still work fine.
01Research in Context
What this study did
Laties (2008) looked at years of brain studies and argued that broken mirror-neuron cells make it hard for people with autism to match self and other.
The paper says this glitch shows up in poor eye gaze, weak imitation, and trouble telling who did what.
It is a story paper, not an experiment, so no kids were tested here.
What they found
The review claims mirror-neuron trouble sits under many social problems in autism.
It lists attention, copying, and "mentalizing" as linked holes in the same net.
How this fits with other research
Reddy et al. (2010) watched preschoolers play in front of a mirror and saw fewer coy smiles and reflecting moves in autism, giving real behavior to the theory.
Hsieh et al. (2014) then built a teaching game with joint-attention mirror play and kids liked it and learned self-awareness, showing you can act on the idea.
Schulte-Rüther et al. (2017) seem to push back: they found automatic facial mimicry was intact in autistic youth once you held their attention, but they only tested quick muscle copy, not higher self-other mapping, so the fight is only skin-deep.
Wang et al. (2023) updates the whole map, adding newer circuits beyond mirror neurons, making the 2008 story part of a bigger picture.
Why it matters
Keep mirror-neuron ideas in your pocket when you write social-cognitive lessons. Use simple mirror games to boost eye contact and self-recognition, but break complex social scenes into one cue at a time since attention links may still be weak.
Want CEUs on This Topic?
The ABA Clubhouse has 60+ free CEUs — live every Wednesday. Ethics, supervision & clinical topics.
Join Free →Start session with a 30-second mirror imitation game to warm up eye contact and self-focus.
02At a glance
03Original abstract
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.
Autism research : official journal of the International Society for Autism Research, 2008 · doi:10.1002/aur.15