people do not seem interested in volunteering for such procedures.
One unexpected hint comes from patients with a strange disorder called anosognosia, a condition in which people seem unaware of or deny their disability. Most patients with a right-hemisphere stroke have complete paralysis of the left side of their body and, as you might expect, complain about it. But about one in twenty of them will vehemently deny their paralysis even though they are mentally otherwise lucid and intelligent. For example, President Woodrow Wilson, whose left side was paralyzed by a stroke in 1919, insisted that he was perfectly fine. Despite the clouding of his thought processes and against all advice, he remained in office, making elaborate travel plans and major decisions pertaining to American involvement in the League of Nations.
In 1996 some colleagues and I made our own little investigation of anosognosia and noticed something new and amazing: Some of these patients not only denied their own paralysis, but also denied the paralysis of another patient—and let me assure you, the second patient’s inability to move was as clear as day. Denying one’s own paralysis is odd enough, but why deny another patient’s paralysis? We suggest that this bizarre observation is best understood in terms of damage to Rizzolatti’s mirror neurons. It’s as if anytime you want to make a judgment about someone else’s movements, you have to run a virtual-reality simulation of the corresponding movements in your own brain. And without mirror neurons you cannot do this.
The second piece of evidence for mirror neurons in humans comes from studying certain brain waves in humans. When people perform volitional actions with their hands, the so-called mu wave disappears completely. My colleagues Eric Altschuler, Jaime Pineda, and I found that mu-wave suppression also occurs when a person watches someone
Since Rizzolatti’s discovery, other types of mirror neurons have been found. Researchers at the University of Toronto were recording from cells in the anterior cingulate in conscious patients who were undergoing neurosurgery. Neurons in this area have long been known to respond to physical pain. On the assumption that such neurons respond to pain receptors in the skin, they are often called sensory pain neurons. Imagine the head surgeon’s astonishment when he found that the sensory pain neuron he was monitoring responded equally vigorously when the patient watched another patient being poked! It was as though the neuron was empathizing with someone else. Neuroimaging experiments on human volunteers conducted by Tania Singer also supported this conclusion. I like calling these cells “Gandhi neurons” because they blur the boundary between self and others—not just metaphorically, but quite literally, since the neuron can’t tell the difference. Similar neurons for touch have since been discovered in the parietal lobe by a group headed by Christian Keysers using brain-imaging techniques.
Think of what this means. Anytime you watch someone doing something, the neurons that your brain would use to do the same thing become active—as if you yourself were doing it. If you see a person being poked with a needle, your pain neurons fire away as though you were being poked. It is utterly fascinating, and it raises some interesting questions. What prevents you from blindly imitating every action you see? Or from literally feeling someone else’s pain?
In the case of motor mirror neurons, one answer is that there may be frontal inhibitory circuits that suppress the automatic mimicry when it is inappropriate. In a delicious paradox, this need to inhibit unwanted or impulsive actions may have been a major reason for the evolution of free will. Your left inferior parietal lobe constantly conjures up vivid images of multiple options for action that are available in any given context, and your frontal cortex suppresses all but one of them. Thus it has been suggested that “free won’t” may be a better term than free will. When these frontal inhibitory circuits are damaged, as in frontal lobe syndrome, the patient sometimes mimics gestures uncontrollably, a symptom called echopraxia. I would predict, too, that some of these patients might literally experience pain if you poke someone else, but to my knowledge this has never been looked for. Some degree of leakage from the mirror-neuron system can occur even in normal individuals. Charles Darwin pointed out that, even as adults, we feel ourselves unconsciously flexing our knee when watching an athlete getting ready to throw a javelin, and clench and unclench our jaws when we watch someone using a pair of scissors.1
Turning now to the
At first this explanation was an idle speculation on my part, but then I met a patient named Humphrey. Humphrey had lost his hand in the first Gulf War and now had a phantom hand. As is true in other patients, whenever he was touched on his face, he felt sensations in his missing hand. No surprises so far. But with ideas about mirror neurons brewing in my mind, I decided to try a new experiment. I simply had him watch another person—my student Julie—while I stroked and tapped her hand. Imagine our amazement when he exclaimed with considerable surprise that he could not merely see but actually feel the things being done to Julie’s hand on his phantom. I suggest this happens because his mirror neurons were being activated in the normal fashion but there was no longer a null signal from the hand to veto them. Humphrey’s mirror neuron activity was emerging fully into conscious experience. Imagine: The only thing separating your consciousnesses from another’s might be your skin! After seeing this phenomenon in Humphrey we tested three other patients and found the same effect, which we dubbed “acquired hyperempathy.” Amazingly, it turns out that some of these patients get relief from phantom limb pain by merely watching another person being massaged. This might prove useful clinically because, obviously, you can’t directly massage a phantom.
These surprising results raise another fascinating question. Instead of amputation, what if a patient’s brachial plexus (the nerves connecting the arm to the spinal cord) were to be anesthetized? Would the patient then experience touch sensations in his anesthetized hand when merely watching an accomplice being touched? The surprising answer is yes. This result has radical implications, for it suggests that no major structural reorganization in the brain is required for the hyperempathy effect; merely numbing the arm is adequate. (I did this experiment with my student Laura Case.) Once again, the picture that emerges is a much more dynamic view of brain connections than what you would be led to believe from the static picture implied by textbook diagrams. Sure enough, brains are made up of modules, but the modules are not fixed entities; they are constantly being updated through powerful interactions with each other, with the body, the environment, and indeed with other brains.
MANY NEW QUESTIONS have emerged since mirror neurons were discovered. First, are mirror-neuron functions present innately, or learned, or perhaps a little of both? Second, how are mirror neurons wired up, and how do they perform their functions? Third, why did they evolve (if they did)? Fourth, do they serve any purpose beyond the obvious one for which they were named? (I will argue that they do.)
I have already hinted at possible answers but let me expand. One skeptical view of mirror neurons is that they are just a result of associative learning, as when a dog salivates in anticipation of dinner when she hears her master’s key in the front door lock each evening. The argument is that every time a monkey moves his hand toward the peanut, not only does the “peanut grabbing” command neuron fire, but so does the visual neuron that is activated by the appearance of his own hand reaching for a peanut. Since neurons that “fire together wire
