I visited Vilayanur S. Ramachandran at the University of California, San Diego recently, and interviewed him and several members of his lab about their work. Rama and I talked, among other things, about the controversial broken mirror hypothesis, which he and others independently proposed in the early 1990s as an explanation for autism. I’ve written a short article about it for the Simons Foundation Autism Research Initiative (SFARI), and the transcript of that part of the interview is below. I also wrote an article summarizing the latest findings about the molecular genetics of autism, which were presented in a symposium held at the Society for Neuroscience annual meeting last November.
MC: Autism is an umbrella term referring to numerous conditions. Can the broken mirror hypothesis account for all of them?
Ramachandran: Autism is characterized by a specific subset of symptoms. There may be three or four that are lumped together, but by and large it is one syndrome, as good a syndrome as any in neurology. It’s not like dyslexia, where there are half a dozen or a dozen types. With autism, people are debating whether high functioning and low functioning autistics should be lumped together or not. There’s a tendency to group them together rather than saying they’re distinct.
We have suggested that the mirror neuron system is deficient in autism, and there’s mixed evidence of that, but most groups support our view. [Marco] Iaconobi‘s group at UCLA did a brain imaging study showing that the mirror neuron system is deficient, but others claim that it’s normal. That may partly be based on the heterogeneity of autism. The mirror neuron system itself could be normal but its projections, or the regions it’s projecting to, could be abnormal. It’s still up in the air.
One of the things I say in my book [The Tell-Tale Brain] is that the mirror neuron system allows you to take an allocentric view of other peoples’ actions, to view the intentions to their actions. It may even be turning inwards and looking at one’s self from an allocentric perspective, so it may be partly contributing to self-awareness. In addition to an allocentric perceptual view, the same system then evolved into adopting an allocentric conceptual, or metaphorical, view – “I see your point of view”. This could have been an evolutionary step from perception to conception, but we don’t know exactly when than magic line was crossed.
MC: There’s another hypothesis, which states that theory of mind is defective in autism. What are the similarities and differences between this and the broken mirror hypothesis? It seems to me that the two aren’t necessarily mutually exclusive, because mirror neurons are likely to be involved in theory of mind.
Ramachandran: The broken mirror hypothesis and defective theory of mind are complementary. It’s like saying genetics excludes DNA, or something. They complement each other. The broken mirror theory is the one we proposed. We also proposed in the same paper that the salience landscape is defective, due to a derangement of connections between the amygdala and other limbic structures. Normally you assign zero salience to that [points to coffee] – well, it’s tasty, so I assign some salience to it – but not much salience to that [taps the table]. The brain is constructing a salience landscape, and in autism that gets messed up, for some reason. You get trivial things provoking a fight or flight response, so you get the autonomic storms that characterize autism.
MC: You did an early experiment showing mu wave suppression in one person with autism. Have you obtained any more evidence for the phenomenon since then?
Ramachandran: We repeated it on 25 or 30 autistic kids and got the same result, and others have found evidence supporting the idea. Mu wave suppression occurs when they perform an action, but not when they watch somebody else performing it. There are people, like Iacoboni, who used functional neuroimaging to show mu wave suppression. The salience landscape idea was proposed with Bill Hirstein, and we published that in Proceedings of the Royal Society about 10 years ago. It’s also described in our broken mirror article in Scientific American.
MC: One recent study failed to find any evidence for the existence of mirror neurons in the human brain, and some say there’s a lack of evidence that the human brain actually contains mirror neurons.
Ramachandran: That’s nonsense. First of all, there’s functional brain imaging data. Secondly, why would the monkeys and anthropoid apes have mirror neurons, only to suddenly disappear in humans? It doesn’t make intuitive sense and empirically it’s flawed.
On the other hand, what people have said is that there’s a lot of media hype about the magical properties that have been attributed to mirror neurons. But just because there’s hype, doesn’t mean it’s wrong. That’s a stupid argument.
The third argument is that some of the properties attributed to mirror neurons are acquired through learning. Every time a monkey reaches and grabs a peanut, a motor neuron fires when it sees its hand reach out, creating a Hebbian link, and the same neuron fires when it watches a peanut being grabbed. The counter-argument there is, why is it that only 30% of the neurons are mirror neurons? If it’s just Hebbian association, what happens to the other neurons? Why don’t they learn? So there are some hardware constraints. Secondly, even if it is learnt, what’s the big deal? If we’re interested in knowing what the mechanism is, the question of nature versus nurture is orthogonal. The existence of stereoscopic neurons and their circuitry is what you want to understand. How the behaviour is learned, or acquired or can be modified is a separate issue.
There’s also a strong anti-reductionist streak, with psychologists saying it’s the same as theory of mind. That’s an idiotic argument, it’s like saying that if you know Mendellian genetics you don’t need to understand DNA. Mirror neurons provide a mechanism for the theory of mind, not a substitute for the idea. They complement each other very nicely. So that criticism goes down the tube.