Abstract
The mirror neuron system has been argued to be a key brain system responsible for action understanding and imitation. Subsequently, mirror neuron system dysfunction has therefore been proposed to explain the social deficits manifested within autism spectrum condition, an approach referred to as the broken mirror hypothesis. Despite excitement surrounding this hypothesis, extensive research has produced insufficient evidence to support the broken mirror hypothesis in its pure form, and instead two alternative models have been formulated: EP-M model and the social top-down response modulation (STORM) model. All models suggest some dysfunction regarding the mirror neuron system in autism spectrum condition, be that within the mirror neuron system itself or systems that regulate the mirror neuron system. This literature review compares these three models in regard to recent neuroscientific investigations. This review concludes that there is insufficient support for the broken mirror hypothesis, but converging evidence supports an integrated EP-M and STORM model.Lay abstractThe mirror neuron system has been argued to be a key brain system responsible for understanding the actions of others and for imitation. It has therefore been proposed that problems within this system could explain the social difficulties experienced by people with autism spectrum condition. This idea is referred to as the broken mirror hypothesis. However, research has produced insufficient evidence to support the broken mirror hypothesis in its original form. Therefore, two other models have been suggested: EP-M model and the social top-down response modulation (STORM) model. All models suggest something is different regarding the mirror neuron system in autism spectrum condition: either within the mirror neuron system itself or within the systems that control the activity of the mirror neuron system. This literature review compares these three models in regard to recent neuroscientific investigations. This review concludes that there is insufficient support for both the broken mirror hypothesis, but converging evidence supports an integrated EP-M and STORM model.
Highlights
Papers were selected based on the following criteria: (1) they must refer to both ASC and the mirror neuron system (MNS); (2) they must focus on the MNS rather than the whole action imitation network; (3) they must not have been incorporated in Hamilton’s 2008 or 2013 review; (4) they must not be a systematic review and (5) they must use quantitative neurological measures rather than behavioural or qualitative measures
If autistic participants have a dysfunctional MNS, as proposed by the broken mirror hypothesis (BMH), ASC participants should show a lack of mu suppression or reduced mu suppression compared to controls during action observation
Since all models would predict some form of neuronal difference within this area, affecting either the top-down pathways to the MNS (STORM model) or the efficiency of the M-pathway or entire MNS (EP-M model and BMH respectfully), such limited investigation cannot differentiate between the models in question
Summary
Given continued neuroscientific research into the MNS in ASC, a review and comparison of these two models is timely. Behavioural evidence (i.e. imitation deficits in autism) has been reviewed elsewhere, demonstrating robust deficits in imitation in autistic individuals (Edwards, 2014) This deficit was argued to be specific to tasks which required participants to reproduce the precise movements of the action to achieve a goal, and ASC participants showed no difference to NT participants when they could use their own method of execution to imitate the goal of a task (emulation). Tasks in which stimuli have an end goal, and utilise the EP pathway, should produce no significant differences between ASC and NT participants on measures of mirror neuron activity In contrast to both of the preceding models, the STORM model would predict that differences between NT and ASC groups are not due to deficits within the MNS itself but within its connections to and regulation by frontal regions of the brain.
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