any simple phrenological model of synesthesia is bound to be incomplete, although it is not a bad place to start.
In doing science one is often forced to choose between providing precise answers to boring (or trivial) questions such as, How many cones are there in the human eye? or vague answers to big questions such as, What is consciousness? or, What is a metaphor? Fortunately, every now and then we get a precise answer to a big question and hit the jackpot (like DNA being the answer to the riddle of heredity). So far, synesthesia seems to lie halfway between those two extremes.
10. For up-to-date information, see the entry “Synesthesia,” by David Brang and me, at Scholarpedia (www.scholarpedia.org/article/Synesthesia). Scholarpedia is an open-access online encyclopedia written and peer-reviewed by scholars from around the world.
CHAPTER 4 THE NEURONS THAT SHAPED CIVILIZATION
1. A young orangutan in the London zoo once watched Darwin play a harmonica, grabbed it from him, and started to mime him; Darwin had already been thinking of the imitative capacities of apes in the nineteenth century.
2. Since their original discovery, the concept of mirror neurons has been confirmed repeatedly in experiments and has had tremendous heuristic value in our understanding the interface between structure and function in the brain. But it has also been challenged on various grounds. I will list the objections and reply to each.
(a) “Mirroritis”: There is a great deal of media hype surrounding the mirror-neuron system (MNS), with anything and everything being attributed to them. This is true, but the existence of hype doesn’t by itself negate the value of a discovery.
(b) The evidence for their existence in humans is unconvincing. This criticism seems odd to me given that we are closely related to monkeys; the default assumption should be that human mirror neurons do exist. Furthermore, Marco Iacoboni has shown their presence by directly recording from nerve cells in human patients (Iacoboni & Dapretto, 2006).
(c) If such a system exists, why isn’t there a neurological syndrome in which damage to a small region leads to difficulty in BOTH performing and miming skilled or semiskilled actions (such as combing your hair or hammering a nail) AND recognizing the same action performed by someone else? Answer: Such a syndrome does exist, although most psychologists are unaware of it. It is called ideational apraxia and it’s seen after damage to the left supramarginal gyrus. Mirror neurons have been shown to exist in this region.
(d) The antireductionist stance: “Mirror neurons” is just a sexy phrase synonymous with what psychologists have long called “theory of mind.” There’s nothing new about them. This argument confounds metaphor with mechanism: It’s like saying that, since we know what the phrase “passage of time” means, there is no need to understand how clocks work. Or that, since we already knew Mendel’s laws of heredity during the first half of the twentieth century, understanding DNA structure and function would have been superfluous. Analogously, the idea of mirror neurons doesn’t negate the concept of theory of mind. On the contrary, the two concepts complement each other and allow us to home in on the underlying neural circuitry.
This power of having a mechanism to work with can be illustrated with many examples; here are three: In the 1960s, John Pettigrew, Peter Bishop, Colin Blakemore, Horace Barlow, David Hubel, and Torsten Wiesel discovered disparity-detecting neurons in the visual cortex; this finding alone provides an explanation for stereoscopic vision. Second, the discovery that the hippocampus is involved in memory allowed Eric Kandel to discover long-term potentiation (LTP), one of the key mechanisms of memory storage. And finally, one could argue that more was learned about memory in five years of research by Brenda Milner on the single patient “HM,” who had hippocampal damage, than in the previous hundred years of purely psychological approaches to memory. The falsely constructed antithesis between reductionist and holistic views of brain function is detrimental to science, something I discuss at length in Note 16 of Chapter 9.
(e) The MNS is not a dedicated set of hardwired neural circuits; it may be constructed through associative learning. For instance, every time you move your hand, there is activation of motor-command neurons, with simultaneous activation of visual neurons by the appearance of the moving hand. By Hebb’s rule, such repeated coactivations will eventually result in the visual appearance itself triggering these motor neurons, so that they become mirror neurons.
I have two response to this criticism: First, even if the MNS is set up partially through learning, that wouldn’t diminish its importance. The question of how the system works is logically orthogonal to how it is set up (as already mentioned under point d above). Second, if this criticism were true, why wouldn’t all the motor-command neurons become mirror neurons through associative learning? Why only 20 percent? One way to settle this would be to see if there are touch mirror neurons for the back of your head that you have never seen. Since you don’t often touch the back of your head or see the back of it being touched, you aren’t likely to construct an internal mental model of the back of your head in order to deduce that it’s being touched. So you should have far fewer mirror neurons, if any, on this part of your body.
3. The basic idea of the coevolution between genes and culture isn’t new. Yet my claim that a sophisticated mirror- neuron system—conferring an ability to imitate complex actions—was a turning point in the emergence of civilization might be construed as an overstatement. So let’s see how the events may have played out.
Assume that a large population of early hominins (such as Homo erectus or early H. sapiens) had some degree of genetic variation in innate creative talent. If one rare individual through his or her special intellectual gifts had invented something useful, then without the concomitant emergence of sophisticated imitative ability among peers (which requires adopting the other’s point of view and “reading” that person’s intentions), the invention would have died with the inventor. But as soon as the ability to imitate emerged, such one-of-a-kind innovations (including “accidental” ones) would have spread rapidly through the population, both horizontally through kin and vertically through offspring. Then, if any new “innovative ability” mutation later appeared in another individual, she could instantly capitalize on the preexisting inventions in novel ways, leading to the selection and stabilization of the “innovatability” gene. The process would have spread exponentially, setting up an avalanche of innovations that transforms evolutionary change from Darwinian to Lamarckian, culminating in modern civilized humans. Thus the great leap forward was indeed propelled by genetically selected circuits, but ironically the circuits were specialized for learnability—that is, for liberating us from genes! Indeed, cultural diversity is so vast in modern humans that there is probably a greater difference in mental quality and behavior between a university professor and (say) a Texan cowboy (or president) than between the latter and early H. sapiens. Not only is the human brain phylogenetically unique as a whole, but the “brain” of each different culture is unique (through “nurture”)—much more so than in any other animal.
CHAPTER 5 WHERE IS STEVEN? THE RIDDLE OF AUTISM
1. Another way of testing the mirror-neuron hypothesis would be to see if autistic children do not show unconscious subvocalization when listening to others talking. (Laura Case and I are testing this.)
2. Many studies have confirmed my original observation (made with Lindsay Oberman, Eric Altschuler, and Jaime Pineda) of a dysfunctional mirror-neuron system (MNS) in autism (which we accomplished by using mu-wave suppression and fMRI). There is an fMRI study, however, claiming that in one specific brain region (the ventral premotor area, or Broca’s area), autistic children have normal mirror-neuron-like activity. Even if we accept this observation at face value (despite the inherent limitations of fMRI), my theoretical reasons for postulating such a
