Is autism caused by a defect in the mirror neuron system?

The cause of autism is still under discussion. Some experts believe that the cause is a defect in the mirror neuron system. But is that really true?

This FactCheck is a collaboration with the editors of the popular scientific magazine EOS and is also published on the platform FactCheck.vlaanderen.

In 1992 the Italian neurobiologist Giacomo Rizzolatti did an experiment in which electrodes were implanted in the brain of a test monkey. He wanted to register which brain cells were activated when the animal took a peanut and ate it. The researchers, who also occasionally ate the peanuts from the laboratory pot, noticed that the same brain cells in the monkey's brains got reactivated. Mirror neurons - the brain cells that enable us to empathize with the other - not only fire signals at our own movements but also at the movements of others. Mirror neurons were bombed into 'the foundation of civilization' and could suddenly explain a whole bunch of human skills. For example, autism would be caused by a defect in that mirror neuron system. Over time, the 'mirror neuron hype' became more and more criticised.

Imitation hormone Mirror neurons occur in the premotor cortex, the brain area involved in the planning of movements. It is connected to the motor cortex, that controls nerves and activates our muscles. Mirror neurons become active not only when someone performs a certain action, but also when another person performs the same action. And it goes even further. Even when we think of a movement or when we 'hear' a movement, mirror neurons are activated. If you would read somewhere: 'Raise your arm', then the parts of your brain involved in raising your arm are activated. Furthermore, mirror neurons cause you to imitate facial expressions and postures. This strengthens the social bond and allows us to better understand the other person. Two researchers examined various studies that linked a defective mirror neuron system to autism. At the time, Lindsay Oberman was working as a postdoctoral researcher at Harvard Medical School. Vilayanur Ramachandran leads the Center for Brain and Cognition at the University of California, San Diego, where he is a professor of psychology and neuroscience.

'When you read "Raise your arm", the parts of your brain involved in raising your arm are activated.'

In the studies they examined, different methods were used such as EEG, a system that measures electrical signals in the brain, and fMRI, which maps the active brain areas. The studies had similar conclusions: people with autism appeared to have fewer active mirror neurons than people without autism. Mirror neurons enable us to be empathic and provide for our empathy. People with autism have trouble empathizing with others. Thus, the studies studied showed that people with autism have less active mirror neurons. Oberman and Vilayanur related this to each other and came to the hypothesis that the lower number of mirror neurons would be the cause of autism. They called their discovery the broken mirror hypothesis.

And even Rizzolatti, the original discoverer of mirror neurons, joins the researchers who criticize the broken mirror hypothesis. The proposition that autism is caused by a defect in the mirror neuron system is also incorrect according to Antonia Hamilton. The British professor and leader of the group of Social Neurosciences at University College London studied 25 studies that used neuroscientific methods to determine whether the hypothesis was correct or not.

'The problem often lies in causality: a link does not necessarily point to a cause.'

She concluded that there is little evidence to confirm the hypothesis. 'Ten years ago, the idea that autism could be caused by a defect in the mirror neuron system was one of the plausible hypotheses. But after several tests, I don't think anyone believes in that idea anymore.'

Jean Steyaert, child and adolescent psychiatrist and coordinator of the Autism Expertise Centre (ECA) of the UPC KU Leuven, confirms that a lot of empirical research has been done on the issue, in different centres. A 'defect' of the mirror neurons has never been demonstrated. According to him, the theorem is incorrect and outdated to the letter. At the same time, he adds that the complete answer is much more nuanced than that. Harold Bekkering, professor of social-cognitive neuroscience at the Donders Institute for Brain, Cognition and Behaviour at Radboud University in Nijmegen, did research in the 1990s together with Rizzolatti on the role of mirror neurons in imitation. 'In several studies, a connection was found between the degree of autism and the activity of mirror neurons. The more severe the form of autism spectrum disorder, the less active the mirror neurons are'. 'The problem often lies in causality: if a connection is found between two things, it does not mean that one also causes the other. You cannot conclude that autism is caused by a lower activity of the mirror neurons. The opposite is also possible: people with autism never look at others because they are not interested in people and therefore have fewer mirror neurons.' Conclusion For a while, the broken mirror hypothesis was much appreciated and followed. Later research questioned it, and nowadays the hypothesis is seen as outdated. There are indications of a link between a decreased functioning of the mirror neuron system and autism, but there is too little conclusive evidence. Moreover, a connection does not immediately mean that a defect in the mirror neurons is also the cause of autism. The claim that autism is caused by a defective mirror neuron system is therefore untrue.