The Tell-Tale Brain: A Neuroscientist's Quest for What Makes Us Human

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 physiological signal from a subject’s body or brain is tracked by a machine and represented back to the subject through some sort of external display. The goal is for the subject to concentrate on nudging that signal up or down and thereby gain some measure of conscious control over it. For example, a biofeedback system can show a person his heart rate, represented as a bouncing, beeping dot on a display screen; most people, with practice, can use this feedback to learn how to slow their hearts at will. Brain waves can also be used for biofeedback. For example, Stanford University professor Sean Mackey put chronic pain patients in a brain-imaging scanner and showed them a computer-animated image of a flame. The size of the flame at any given moment was a representation of the neural activity in each patient’s anterior cingulate (a cortical region involved in pain perception), and was thus proportional to the subjective amount of pain he or she was in. By concentrating on the flame, most of the patients were able to gain some control over its size and to keep it small, and ipso facto to reduce the amount of pain they were experiencing. By the same token, one could monitor mu waves on an autistic child’s scalp and display them on a screen in front of her, perhaps in the guise of a simple thought-controlled video game, to see if she can somehow learn to suppress them. Assuming her mirror-neuron function is weak or dormant rather than absent, this kind of exercise might boost her ability to see through to the intentionality of others, and bring her a step closer to joining the social world that swirls invisibly around her. As this book went to press, this approach was being pursued by our colleague Jaime Pineda at UC San Diego.

A third possibility—one that I suggested in an article for Scientific American that I coauthored with my graduate student Lindsay Oberman—would be to try certain drugs. There is a great deal of anecdotal evidence that MDMA (the party drug ecstasy) enhances empathy, which it may do by increasing the abundance of neurotransmitters called empathogens, which naturally occur in the brains of highly social creatures such as primates. Could a deficiency in such transmitters contribute to the symptoms of autism? If so, could MDMA (with its molecule suitably modified) ameliorate some of the most troubling symptoms of the disorder? It is also known that prolactin and oxytocin—so-called affiliation hormones—promote social bonding. Perhaps this connection, too, could be exploited therapeutically. If administered sufficiently early, cocktails of such drugs might help tide over some early symptom manifestations enough to minimize the subsequent cascade of events that lead to the full spectrum of autistic symptoms.

Speaking of prolactin and oxytocin, we recently encountered an autistic child whose brain MRI showed a substantial reduction in the size of the olfactory bulb, which receives smell signals from the nose. Given that smell is a major factor in the regulation of social behavior in most mammals, we wondered, Is it conceivable that olfactory-bulb malfunction plays a major role in the genesis of autism? Reduced olfactory-bulb activity would diminish oxytocin and prolactin, which in turn might reduce empathy and compassion. Needless to say, this is all pure speculation on my part, but in science, fancy is often the mother of fact—at least often enough that premature censorship of speculation is never a good idea.

One final option for reviving dormant mirror neurons in autism would be to take advantage of the great delight that all humans—including autistics—take in dancing to a rhythm. Although such dance therapy using rhythmic music has been tried with autistic children, no attempt has been made to directly tap into the known properties of the mirror-neuron system. One way to do this might be, for example, to have several model dancers moving simultaneously to rhythm and having the child mime the same dance in synchrony. Immersing all of them in a hall of multiply reflecting mirrors might also help by multiplying the impact on the mirror-neuron system. It seems like a far-fetched possibility, but then so was the idea of using vaccines to prevent rabies or diphtheria.³