No, autistic people do not have a "broken" mirror neuron system – new evidence

Scientists are still struggling to understand the causes of autism. A difficulty bonding with others represents one of the core symptoms and has been the focus of several theories that try and explain exactly why these deficits come about.

One of the more prominent examples, the "broken mirror hypothesis", suggests that an impaired development of the mirror neuron system (MNS) is to blame. First observed in monkeys, mirror neurons are more active when you perform a certain action and when you see someone else engage in the same behavior – for example, when you smile or when you see someone else smile.

This "mirroring" has been hypothesised to help us understand what others are feeling by sharing their emotional states, although this is disputed. Another behaviour that is thought to depend on an intact mirror neuron system is facial mimicry – the way that people spontaneously and unconsciously mimic the emotional facial expressions of others.

Interestingly, studies have shown that people with autism do not spontaneously mimic others' facial expressions, which could explain why they often struggle to "read" people's emotions or have trouble interacting socially. Some experts have claimed these findings lend support to "broken" mirroring in autism, but this has remained controversial. Now a study in Autism Research has used a new way to measure facial mimicry and the results cast fresh doubt on the idea that autism is somehow caused by a broken mirror neuron system.

Martin Schulte-Rüther and his colleagues made use of a well-studied psychological phenomenon: that performing certain movements (e.g. lifting the right finger) is more difficult when we see another person perform a similar (but not the same) movement (e.g. lifting the middle finger). This could be explained by us automatically mirroring the movements of the other person, which then interferes with our own action. Something similar happens with facial expressions, too: Seeing someone smile makes frowning more difficult for us. Because this relies on an intact mirror neuron system, the authors hypothesised that, if this system is perturbed in autism, then people on the spectrum will not experience interference by others' facial expressions.

The researchers asked 18 boys/teenagers with autism (average age 16 years) and 18 neurotypical age-matched male controls to smile or frown depending on the color of a dot that appeared superimposed on the picture of a smiling, frowning or neutral face. Participants were instructed to focus on the dot color rather than the faces, but actually part of the idea of this design was that the location of the dots meant the faces were impossible to ignore – this was to counteract the possibility that participants with autism would simply be less inclined than normal to look at facial or social stimuli.

To check if any observed deficits were specific to emotional stimuli, the participants also completed a similar task with dots superimposed on non-facial stimuli devoid of emotion, such as a diamond. For all stimuli types, the researchers assessed whether and how fast participants performed the appropriate emotional expressions by recording their facial muscle activity with a technique called electromyography.

Across both tasks, control participants and those with autism performed faster and with fewer errors where the required action was congruent with the emotional expression of the superimposed face – in other words, automatic facial mimicry was intact in autism. Interestingly, controls with higher self-rated empathy showed faster smiling in congruent conditions whereas individuals with autism showed no correlation between automatic facial mimicry and empathy.

What does this mean for understanding autistic spectrum conditions?

These results do not support the broken mirror hypothesis because they show that involuntary, spontaneous facial mimicry – which supposedly depends on the mirror neuron system – is intact in individuals with autism. This is an exciting result because it contrasts with previous investigations and indicates that while people with autism struggle to understand others this is not attributable to "broken mirrors".

In line with a functional mirror neuron system, autism-related deficits in social interactions/bonding might instead be the consequence of reduced social motivation. For example, perhaps individuals with autism mimic the facial expression of others less not because they lack the capacity to do so, but because they are less motivated to bond socially or because social stimuli are not as salient or rewarding to them. On a positive note, since the mirror neuron system seems to be intact in autism, future studies could zoom in on how to make use of this fact for developing possible therapies.

About the author

Post written by Helge Hasselmann for the BPS Research Digest. Helge studied psychology and clinical neurosciences. Since 2014, he is a PhD student in medical neurosciences at Charité University Hospital in Berlin, Germany, with a focus on understanding the role of the immune system in major depression.

Further reading

Schulte-Rüther, M., Otte, E., Adigüzel, K., Firk, C., Herpertz-Dahlmann, B., Koch, I., & Konrad, K. (2016). Intact mirror mechanisms for automatic facial emotions in children and adolescents with autism spectrum disorder Autism Research DOI: 10.1002/aur.1654