The Tell-Tale Brain

(Unfortunately, many brain regions are tucked away in the brain’s deep folds, but plenty of other regions, including the motor cortex, are conveniently located directly beneath the skull where TMS can “zap” them easily.) The researchers used TMS to stimulate the motor cortex, then recorded electromuscular activation while the subjects watched other people performing actions. When a normal subject watches another person performing an action— say, squeezing a tennis ball with the right hand—the muscles in the subject’s own right hand will register a tiny uptick in their electrical “chatter.” Even though the subject doesn’t perform a squeezing action herself, the mere act of watching the action leads to a tiny but measurable increase in the action-readiness of the muscles that would contract if she were performing it. The subject’s own motor system automatically simulates the perceived action, but at the same time it automatically suppresses the spinal motor signal to prevent it from being carried out—and yet a tiny trickle of the suppressed motor command still manages to leak through and down to reach the muscles. That’s what happens in normal subjects. But the autistic subjects showed no sign of increased muscle potentials while watching actions being performed. Their mirror neurons were missing in action. These results, taken together with our own, provide conclusive evidence that the hypothesis is correct.

THE MIRROR-NEURON HYPOTHESIS can explain several of the more quirky manifestations of autism. For instance, it has been known for some time that autistic children often have problems interpreting proverbs and metaphors. When asked to “get a grip on yourself,” the autistic child may literally start grabbing his own body. When asked to explain the meaning of “all that glitters is not gold,” we have noticed that some high-functioning autistics provide literal answers: “It means it’s just some yellow metal—doesn’t have to be gold.” Although seen in only a subset of autistic children, this difficulty with metaphor cries out for an explanation.

There is a branch of cognitive science known as embodied cognition, which holds that human thought is deeply shaped by its interconnection with the body and by the inherent nature of human sensory and motor processes. This view stands in contrast to what we might call the classical view, which dominated cognitive science from the mid- through late twentieth century, and held that the brain was essentially the same thing as a general-purpose “universal computer” that just happened to be connected to a body. While it is possible to overstate the view of embodied cognition, it now has a lot of support; whole books have been written on the subject, Let me just give you one specific example of an experiment I did in collaboration with Lindsay Oberman and Piotr Winkielman. We showed that if you bite into a pencil (as if it were a bridle bit) to stretch your mouth into a wide, fake smile, you will have difficulty detecting another person’s smile (but not a frown). This is because biting the pencil activates many of the same muscles as a smile, and this floods your brain’s mirror-neuron system, creating a confusion between action and perception. (Certain mirror neurons fire when you make a facial expression and when you observe the same expression on another person’s face.) The experiment shows that action and perception are much more closely intertwined in the brain than is usually assumed.

So what has this got to do with autism and metaphor? We recently noticed that patients with lesions in the left supramarginal gyrus who have apraxia—an inability to mime skilled voluntary actions, such as stirring a cup of tea or hammering a nail—also have difficulty interpreting action-based metaphors such as “reach for the stars.” Since the supramarginal gyrus also has mirror neurons, our evidence suggests that the mirror-neuron system in humans is involved not only in interpreting skilled actions but in understanding action metaphors and, indeed, in other aspects of embodied cognition. Monkeys also have mirror neurons, but for their mirror neurons to play a role in metaphor monkeys may have to reach a higher level of sophistication—of the kind seen only in humans.

The mirror-neuron hypothesis also lends insight into autistic language difficulties. Mirror neurons are almost certainly involved when an infant first repeats a sound or word that she hears. It may require internal translation: the mapping of sound patterns onto corresponding motor patterns and vice versa. There are two ways such a system could be set up. First, as soon as the word is heard, a memory trace of the phonemes (speech sounds) is set up in the auditory cortex. The baby then tries various random utterances and, using error feedback from the memory trace, progressively refines the output to match memory. (We all do this when we internally hum a recently heard tune and then sing it out loud, progressively refining the output to match the internal humming.) Second, the networks for translating heard sounds into spoken words may have been innately specified through natural selection. In either case the net result would be a system of neurons with properties of the kind we ascribe to mirror neurons. If the child could, without delay and opportunity for feedback from rehearsal, repeat a phoneme cluster it has just heard for the first time, that would argue for a hardwired translational mechanism. Thus there is a variety of ways this unique mechanism could be set up. But whatever the mechanism, our results suggest that a flaw in its initial setup might cause the fundamental deficit in autism. Our empirical results with mu-wave suppression support this and also allow us to provide a unitary explanation for an array of seemingly unrelated symptoms.

Finally, although the mirror-neuron system evolved initially to create an internal model of other people’s actions and intentions, in humans it may have evolved further—turning inward to represent (or re-rep-resent) one’s own mind to itself. A theory of mind is not only useful for intuiting what is happening in the minds of friends, strangers, and enemies; but in the unique case of Homo sapiens, it may also have dramatically increased the insight we have into our own minds’ workings. This probably happened during the mental phase transition we underwent just a couple hundred millennia ago, and would have been the dawn of full-fledged self awareness. If the mirror-neuron system underlies theory of mind and if theory of mind in normal humans is super- charged by being applied inward, toward the self, this would explain why autistic individuals find social interaction and strong self-identification so difficult, and why so many autistic children have a hard time correctly using the pronouns “I” and “you” in conversation: They may lack a mature-enough mental self-representation to understand the distinction. This hypothesis would predict that even otherwise high-functioning autistics who can talk normally (highly verbal autistics are said to have Asperger syndrome, a subtype among autistic spectrum disorders) would have difficulty with such conceptual distinctions between words such as “self-esteem,” “pity,” “mercy,” “forgiveness,” and “embarrassment,” not to mention “self-pity,” which would make little sense without a full-fledged sense of self. Such predictions have never been tested on a systematic basis, but my student Laura Case is doing so. And we will return to these questions about self-representation and self-awareness, and derangements of these elusive faculties, in the last chapter.

This may be a good place to add three qualifying remarks. First, small groups of cells with mirror-neuron-like properties are found in many parts of the brain, and should really be thought of as parts of a large, interconnected circuit—a “mirror network,” if you will. Second, as I noted earlier, we must be careful not to attribute all puzzling aspects about the brain to mirror neurons. They don’t do everything! Nonetheless, they seem to have been key players in our transcendence of apehood, and they keep turning up in study after study of various mental functions that go far beyond our original “monkey see, monkey do” conception of them. Third, ascribing certain cognitive capacities to certain neurons (in this case, mirror neurons) or brain regions is only a beginning; we still need to understand how the neurons carry out their computations. However, understanding the anatomy can substantially guide the way and help reduce the complexity of the problem. In particular anatomical data can constrain our theoretical speculations and help eliminate many initially promising hypotheses. On the other hand, saying that “mental capacities emerge in a homogeneous network” gets you nowhere and flies in the face of empirical evidence of the exquisite anatomical specialization in the brain. Diffuse networks capable of learning exist in pigs and apes as well, but only humans are capable of language and self-reflection.

AUTISM IS STILL very difficult to treat, but the discovery of mirror-neuron dysfunction opens up some novel therapeutic approaches. For example, the lack of mu-wave suppression could become an invaluable diagnostic tool for screening for the disorder in early infancy, so that currently available behavioral therapies can be instituted long before other, more “florid” symptoms appear. Unfortunately, in most cases it is the unfolding of the florid symptoms, during the second or third year of life, that tips parents and doctors off. The earlier autism is caught, the better.

A second, more intriguing possibility would be to use biofeedback to treat the disorder. In biofeedback, a