The Broken Mirrors theory is a controversial principle put forward to explain the symptoms of Autism Spectrum Disorders (or ASD); a group of neurodevelopmental disorders characterised by restricted, repetitive behaviours and difficulties with social interactions and communication. The cause of ASD is unknown, but there is a consensus that complex genetic interactions have a major role.
The broken ‘mirror’ refers to a group of brain cells known as mirror neurons. These were first discovered by Rizzolatti and his lab in Italy in the 1990’s. Rizzolatti observed a group of neurons in macaque monkeys which fired not only when the monkeys performed an action, but when they watched another monkey perform the same action. It was as if these neurons were taking the perspective of the monkey they were observing. Later research indicated the existence of mirror neurons in humans, and some work, though controversial, suggested that mirror neurons may have a role in understanding others’ intentions, or even in empathy.
Given this possible link between mirror neurons and social information processing, Ramachandran and colleagues then used EEG to investigate whether the mirror neuron system appeared to be working differently in individuals with ASD. An EEG activity pattern known as the Mu wave is blocked when a person performs a voluntary action. It is also blocked when observing someone else perform an action, so a blocking of the mu wave was considered an indicator of mirror neuron activity, although EEG cannot record from areas as specific as the mirror neuron system. Ramachandran observed that, although the Mu wave was blocked when children with ASD performed an action, no blocking occurred when they observed others performing the action. This effect was more pronounced amongst the children with more severe ASD symptoms. Ramachandran concluded that the mirror neuron system is dysfunctional in ASD, and that this explains the core features of ASD. This is the essence of the Broken Mirrors theory.
The theory is certainly controversial, and has rightly received criticism. For one thing, it is thought that the main role of the mirror neuron system is to allow imitation. However, it is unclear whether problems with imitation are reliably found in individuals with ASD. A 2007 study found that children with ASD imitated actions in the same way as typical children, but, unlike typical children, they struggled with Theory of Mind tasks, which require an appreciation of different character’s knowledge and intentions in social situations. What’s more, when typical children and children with ASD were put in an MRI scanner, they showed the same pattern of mirror neuron activity when viewing and executing hand movements. Another research team found that children with ASD showed reduced activation in a region believed to contain mirror neurons, there was no impairment in imitation. Ergo, it would seem that children with ASD have mirror neuron systems which are reasonably capable of representing observed actions and do not hinder imitation.
Whilst it is possible that only some functions of mirror neurons are impaired, the case for the role of mirror neurons in ASD is also weak. The theory makes some very sweeping statements about what Autism is, but it is a very diverse condition, with many features, not all of which are present in every individual with ASD. It is unlikely that this theory explains the cause of ASD as a whole, assuming that a single cause exists. The theory may account for some of the social difficulties often noted in ASD, and perhaps difficulties in language development, due to the importance of interactions with caregivers. But whether it is the most fitting theory is not evident, and it is hard to see how the theory would easily account for the often literal interpretation of language, the greater focus on details at the expense of the bigger picture, or over- or under-sensitivity of the senses. At best, mirror neurons may have a role in the social symptoms only, and is perhaps compatible with another theory that individuals have difficulties reasoning about others’ knowledge, intentions and motives – the Theory of Mind account.
Additionally, there is no conclusive evidence suggesting that understanding others’ intentions is exclusively the responsibility of the mirror neuron system. The idea that mirror neurons account for our empathy skills all on their own, without interacting at all with other groups of cells, is highly unlikely – and this is not a claim made by the theory. It is possible that other processes, before or after the involvement of the mirror neuron system, are altered in ASD, accounting for any differences. The cause of the observed association between ASD and a lack of mirror neuron activity is also unclear – it is just as plausible that atypical activation of the mirror neuron system is a consequence of ASD, or particular ASD symptoms – in which case, the cause of the disorder remains at large.
The broken mirrors theory may be intuitively appealing, but its shortfalls and inconsistencies make it far from compelling. Mirror neurons are controversial, and ASD is incredibly complex – and uncertainty at both ends of a theory is far from ideal.