I visited Vilayanur S. Ramachandran's lab 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.