Overall I am happy with the way our research has proceeded since then. We have come up with partial answers to all four questions. More important, we have galvanized an unprecedented interest in this phenomenon; there is now virtually a synesthesia industry, with over a dozen books published on the topic.
WE DON’T KNOW when synesthesia was first recognized as a human trait, but there are hints that Isaac Newton could have experienced it. Aware that the pitch of a sound depends on its wavelength, Newton invented a toy—a musical keyboard—that flashed up different colors on a screen for different notes. Thus every song was accompanied by a kaleidoscopic display of colors. One wonders if sound-color synesthesia inspired his invention. Could a mixing of senses in his brain have provided the original impetus for his wavelength theory of color? (Newton proved that white light is composed of a mixture of colors which can be separated by a prism, with each color corresponding to a particular wavelength of light.)
Francis Galton, a cousin of Charles Darwin and one of the most colorful and eccentric scientists of the Victorian era, conducted the first systematic study of synesthesia in the 1890s. Galton made many valuable contributions to psychology, especially the measurement of intelligence. Unfortunately, he was also an extreme racist; he helped usher in the pseudoscience of eugenics, whose goal was to “improve” mankind by selective breeding of the kind practiced with domesticated livestock. Galton was convinced that the poor were poor because of inferior genes, and that they must be forbidden from breeding too much, lest they overwhelm and contaminate the gene pool of the landed gentry and rich folk like him. It isn’t clear why an otherwise intelligent man should hold such views, but my hunch is that he had an unconscious need to attribute his own fame and success to innate genius rather than acknowledging the role of opportunity and circumstance. (Ironically, he himself was childless.)
Galton’s ideas about eugenics seem almost comical in hindsight, yet there is no denying his genius. In 1892 Galton published a short article on synesthesia in the journal Nature. This was one of his lesser-known papers, but about a century later it piqued my interest. Although Galton wasn’t the first to notice the phenomenon, he was the first to document it systematically and encourage people to explore it further. His paper focused on the two most common types of synesthesia: the kind in which sounds evoke colors (auditory-visual synesthesia) and the kind in which printed numbers always seem tinged with inherent color (grapheme-color synesthesia). He pointed out that even though a specific number always produces the same color for any given synesthete, the number-color associations are different for different synesthetes. In other words, it’s not as though all synesthetes see a 5 as red or a 6 as green. To Mary, 5 always looks blue, 6 is magenta, and 7 is chartreuse. To Susan, 5 is vermillion, 6 is light green, and 4 is yellow.
How to explain these people’s experiences? Are they crazy? Do they simply have vivid associations from childhood memories? Are they just speaking poetically? When scientists encounter anomalous oddities such as synesthetes, their initial reaction is usually to brush them under the carpet and ignore them. This attitude—which many of my colleagues are very vulnerable to—is not as silly as it seems. Because a majority of anomalies—spoon bending, alien abduction, Elvis sightings—turn out to be false alarms, it’s not a bad idea for a scientist to play it safe and ignore them. Whole careers, even lifetimes, have been wasted on the pursuit of oddities, such as polywater (a hypothetical form of water based on crackpot science), telepathy, or cold fusion. So I wasn’t surprised that even though we had known about synesthesia for over a century, it has generally been sidelined as a curiosity because it didn’t make “sense.”
Even now, the phenomenon is often dismissed as bogus. When I bring it up in casual conversation, I often hear it shot down on the spot. I’ve heard, “So you study acid junkies?” and “Whoa! Cuckoo!” and a dozen other dismissals. Unfortunately even physicians are not immune—and ignorance in a physician can be quite hazardous to people’s health. I know of at least one case in which a synesthete was misdiagnosed as having schizophrenia and was prescribed antipsychotic medication to rid her of hallucinations. Fortunately her parents took it upon themselves to get informed, and in the course of their reading came across an article on synesthesia. They drew this to the doctor’s attention, and their daughter was quickly taken off the drugs.
Synesthesia as a real phenomenon did have a few supporters, including the neurologist Dr. Richard Cytowic, who wrote two books about it: Synesthesia: A Union of the Senses (1989) and The Man Who Tasted Shapes (1993/2003). Cytowic was a pioneer, but he was a prophet preaching in the wilderness and was largely ignored by the establishment. It didn’t help matters that the theories he put forward to explain synesthesia were a bit vague. He suggested that the phenomenon was a kind of evolutionary throwback to a more primitive brain state in which the senses hadn’t quite separated and were being mingled in the emotional core of the brain.
This idea of an undifferentiated primitive brain didn’t make sense to me. If the synesthete’s brain was reverting to an earlier state, then how would you explain the distinctive and specific nature of the synesthete’s experiences? Why, for example, does Esmeralda “see” C-sharp as being invariably blue? If Cytowic was correct, you would expect the senses to just blend into each other to create a blurry mess.
A second explanation that is sometimes posed is that synesthetes are just remembering childhood memories and associations. Maybe they played with refrigerator magnets, and the 5 was red and the 6 was green. Maybe they remember this association vividly, just as you might recall the smell of a rose, the taste of Marmite or curry, or the trill of a robin in the spring. Of course, this theory doesn’t explain why only some people remain stuck with such vivid sensory memories. I certainly don’t see colors when looking at numbers or listening to tones, and I doubt whether you do either. While I might think of cold when I look at a picture of an ice cube, I certainly don’t feel it, no matter how many childhood experiences I may have had with ice and snow. I might say that I feel warm and fuzzy when stroking a cat, but I would never say touching metal makes me feel jealous.
A third hypothesis is that synesthetes are using vague tangential speech or metaphors when they speak of C-major being red or chicken tasting pointy, just as you and I speak of a “loud” shirt or “sharp” cheddar cheese. Cheese is, after all, soft to touch, so what do you mean when you say it is sharp? Sharp and dull are tactile adjectives, so why do you apply them without hesitation to the taste of cheese? Our ordinary language is replete with synesthetic metaphors—hot babe, flat taste, tastefully dressed—so maybe synesthetes are just especially gifted in this regard. But there is a serious problem with this explanation. We don’t have the foggiest idea of how metaphors work or how they are represented in the brain. The notion that synesthesia is just metaphor illustrates one of the classic pitfalls in science—trying to explain one mystery (synesthesia) in terms of another (metaphor).
What I propose, instead, is to turn the problem on its head and suggest the very opposite. I suggest that synesthesia is a concrete sensory process whose neural basis we can uncover, and that the explanation might in turn provide clues for solving the deeper question of how metaphors are represented in the brain and how we evolved the capacity to entertain them in the first place. This doesn’t imply that metaphor is just a form of synesthesia; only that understanding the neural basis of the latter can help illuminate the former. So when I resolved to do my own investigation of synesthesia, my first goal was to establish whether it was a genuine sensory experience.
IN 1997 A doctoral student in my lab, Ed Hubbard, and I set out to find some synesthetes to begin our investigations. But how? According to most published surveys, the incidence was anywhere from one in a thousand to one in ten thousand. That fall I was lecturing to an undergraduate class of three hundred students. Maybe we’d get lucky. So we made an announcement:
“Certain otherwise normal people claim they see sounds, or that certain numbers always evoke certain colors,” we told the class. “If any one of you experiences this, please raise your hands.”
To our disappointment, not a single hand went up. But later that day, as I was chatting with Ed in my office, two students knocked on the door. One of them, Susan, had striking blue eyes, streaks of red dye in her blonde ringlets, a silver ring in her belly button and an enormous skateboard. She said to us, “I’m one of those people you talked about in class, Dr. Ramachandran. I didn’t raise my hand because I didn’t want people to think I was weird or something. I didn’t even know that there were others like me or that the condition had a name.”
Ed and I looked at each other, pleasantly surprised. We asked the other student to come back later, and waved Susan into a chair. She leaned the skateboard against the wall and sat down.
“How long have you experienced this?” I asked.
“Oh, from early childhood. But I didn’t really pay much attention to it at that time, I suppose. But then it gradually dawned on me that it was really odd, and I didn’t discuss it with anyone…I didn’t want people thinking I was crazy or something. Until you mentioned it in class, I didn’t know that it had a name. What did you call it, syn…es…something that rhymes with anesthesia?”
“It’s called synesthesia,” I said. “Susan, I want you to describe your experiences to me in detail. Our lab has a special interest in it. What exactly do you experience?”
“When I see certain numbers, I always see specific colors. The number 5 is always a specific shade of dull red, 3 is blue, 7 is bright blood red, 8 is yellow, and 9 is chartreuse.”
I grabbed a felt pen and pad that were on the table and drew a big 7.
“What do you see?”
“Well, it’s not a very clean 7. But it looks red…I told you that.”
“Now I want you to think carefully before you answer this question. Do you actually see the red? Or does it just make you think of red or make you visualize red…like a memory image. For example, when I hear the word ‘Cinderella,’ I think of a young girl or of pumpkins or coaches. Is it like that? Or do you literally see the color?”
“That’s a tough one. It’s something I have often asked myself. I guess I do really see it. That number you drew looks distinctly red to me. But I can also see that it’s really black—or I should say, I know it’s black. So in some sense it is a memory image of sorts…I must be seeing it in my mind’s eye or something. But it certainly doesn’t feel like that. It feels like I am actually seeing it. It’s very hard to describe, Doctor.”
“You are doing very well, Susan. You are a good observer and that makes everything you say valuable.”
“Well, one thing I can tell you for sure is that it isn’t like imagining a pumpkin when looking at a picture of Cinderella or listening to the word ‘Cinderella.’ I do actually see the color.”
One of the first things we teach medical students is to listen to the patient by taking a careful history. Ninety percent of the time you can arrive at an uncannily accurate diagnosis by paying close attention, using physical examination and sophisticated lab tests to confirm your hunch (and to increase the bill to the insurance company). I started to wonder whether this dictum might be true not just for patients but for synesthetes as well.
I decided to give Susan some simple tests and questions. For example, was it the actual visual appearance of the numeral that evoked the color? Or was it the numerical concept—the idea of sequence, or even of quantity? If the latter, then would Roman numerals do the trick or only Arabic ones? (I should call them Indian numerals really; they were invented in India in the first millennium B.C.E. and exported to Europe via Arabs.)
I drew a big VII on the pad and showed it to her.
“What do you see?”
“I see it’s a seven, but it looks black—no trace of red. I have always known that. Roman numerals don’t work. Hey, Doctor, doesn’t that prove it can’t be a memory thing? Because I do know it’s a seven but it still doesn’t generate the red!”
Ed and I realized that we were dealing with a very bright student. It was starting to look like synesthesia was indeed a genuine sensory phenomenon, brought on by the actual visual appearance of the numeral—not by the numerical concept. But this was still well short of proof. Could we be absolutely sure that this wasn’t happening because early in kindergarten she had repeatedly seen a red seven on her refrigerator door? I wondered what would happen if I showed her black-and-white halftone photos of fruits and vegetables which (for most of us) have strong memory-color associations. I drew pictures of a carrot, a tomato, a pumpkin, and a banana, and showed them to her.
“What do you see?”
“Well, I don’t see any colors, if that’s what you’re asking. I know the carrot is orange and can imagine it to be so, or visualize it to be orange. But I don’t actually see the orange color the way I see red when you show me the 7. It’s hard to explain, Doctor, but it’s like this: When I see the black-and-white carrot, I kinda know it’s orange, but I can visualize it as being any bizarre color I want, like a blue carrot. It’s very hard for me to do that with 7; it keeps screaming red at me! Is all of this making any sense to you guys?”
“Okay,” I told her, “now I want you to close your eyes and show me your hands.”
She seemed slightly startled by my request but followed my instructions. I then drew the numeral 7 on the palm of her hand.
“What did I draw? Here, let me do it again.”
“It’s a 7!”
“Is it colored?”
“No, absolutely not. Well, let me rephrase that; I don’t initially see red even though I ‘feel’ it’s 7. But then I start visualizing the 7, and it’s sort of tinged red.”
“Okay, Susan, what if I say ‘seven’? Here, let’s try it: Seven, seven, seven.”
“It wasn’t red initially, but then I started to experience red…Once I start visualizing the appearance of the shape of 7, then I see the red—but not before that.”
On a whim I said, “Seven, five, three, two, eight. What did you see then, Susan?”
“My God…that’s very interesting. I see a rainbow!”
“What do you mean?”
“Well, I see the corresponding colors spread out in front of me as in a rainbow, with the colors matching the number sequence you read aloud. It’s a very pretty rainbow.”
“One more question, Susan. Here is that drawing of 7 again. Do you see the color directly on the number, or does it spread around it?”
“I see it directly on the number.”
“What about a white number on black paper? Here is one. What do you see?”
“It’s even more clearly red than the black one. Dunno why.”
“What about double-digit numbers?” I drew a bold 75 on the pad and showed it to her. Would her brain start blending the colors? Or see a totally new color?
“I see each number with its appropriate color. But I have often noticed this myself. Unless the numbers are too close.”
“Okay, let’s try that. Here, the 7 and 5 are much closer together. What do you see?”
“I still see them in the correct colors, but they seem to ‘fight’ or cancel each other; they seem dimmer.”
“And what if I draw the number seven in the wrong-color ink?”
I drew a green 7 on the pad and showed it to her.
“Ugh! It looks hideous. It jars, like there is something wrong with it. I certainly don’t mix the real color with the mental color. I see both colors simultaneously, but it looks hideous.”
Susan’s remark reminded me of what I had read in the older papers on synesthesia, that the experience of color was often emotionally tinged for them and that incorrect colors could produce a strong aversion. Of course, we all experience emotions with certain colors. Blue seems calming, and red is passionate. Could it be that the same process is, for some odd reason, exaggerated in synesthetes? What can synesthesia tell us about the link between color and emotion that artists like Van Gogh and Monet have long been fascinated by?
There was a hesitant knock on the door. We hadn’t noticed that almost an hour had passed and that the other student, a girl named Becky, was still outside my office. Fortunately, she was cheerful despite having waited so long. We asked Susan to come back the following week and invited Becky in. It turned out that she too was a synesthete. We repeated the same questions and conducted the same tests on her as we had on Susan. Her answers were uncannily similar with a few minor differences.
Becky saw colored numbers, but hers were not the same as Susan’s. For Becky, 7 was blue and 5 was green. Unlike Susan, she saw letters of the alphabet in vivid colors. Roman numerals and numbers drawn on her hand were ineffective, which suggested that, as in Susan, the colors were driven by the visual appearance of the number and not by the numerical concept. And lastly, she saw the same rainbow-like effect that Susan saw when we recited a string of random numbers.
I realized then and there that we were hot on the trail of a genuine phenomenon. All my doubts were dispelled. Susan and Becky had never met each other before, and the high level of similarity between their reports couldn’t possibly be a coincidence. (We later learned that there’s a lot of variation among synesthetes, so we were very lucky to have stumbled on two very similar cases.) But even though I was convinced, we still had a lot of work to do to produce evidence strong enough to publish. People’s verbal commentaries and introspective reports are notoriously unreliable. Subjects in a laboratory setting are often highly suggestible and may unconsciously pick up what you want to hear and oblige by telling you that. Furthermore, they sometimes speak ambiguously or vaguely. What was I to make of Susan’s perplexing remark? “I really do see red, but I also know it’s not—so I guess I must be seeing it in my mind’s eye or something.”
SENSATION IS INHERENTLY subjective and ineffable: You know what it “feels” like to experience the vibrant redness of a ladybug’s shell, for instance, but you could never describe that redness to a blind person, or even to a color-blind person who cannot distinguish red from green. And for that matter, you can never truly know whether other people’s inner mental experience of redness is the same as yours. This makes it somewhat tricky (to put it mildly) to study the perception of other people. Science traffics in objective evidence, so any “observations” we make about people’s subjective sensory experience are necessarily indirect or secondhand. I would point out though that subjective impressions and single-subject case studies can often provide strong clues toward designing more formal experiments. Indeed, most of the great discoveries in neurology were initially based on simple clinical testing of single cases (and their subjective reports) before being confirmed in other patients.
One of the first “patients” with whom we launched a systematic study in search of hard proof of the reality of synesthesia was Francesca, a mild-mannered woman in her midforties who had been seeing a psychiatrist because she had been experiencing a mild low-grade depression. He prescribed lorazepam and Prozac, but not knowing what to make of her synesthetic experiences, referred her to my lab. She was the same woman I mentioned earlier who claimed that right from very early childhood she experienced vivid emotions when she touched different textures. But how could we test the truth of her claim? Perhaps she was just a highly emotional person and simply enjoyed speaking about the emotions that various objects triggered in her. Perhaps she was “mentally disturbed” and just wanted attention or to feel special.
Francesca came into the lab one day, having seen an ad in the San Diego Reader. After tea and the usual pleasantries my student David Brang and I hooked her up to our ohmmeter to measure her GSR. As we saw in the Chapter 2, this device measures the moment-to-moment microsweating produced by fluctuating levels of emotional arousal. Unlike a person, who can verbally dissemble or even be subconsciously deluded about how something makes her feel, GSR is instantaneous and automatic. When we measured GSR in normal subjects who touched various mundane textures such as corduroy or linoleum, it was clear they experienced no emotions. But Francesca was different. For the textures that she reported gave her strong emotional reactions, such as fear or anxiety or disgust, her body produced a strong GSR signal. But when she touched textures that she said gave her warm, relaxed feelings, there was no change in the electrical resistance of her skin. Since you cannot fake GSR responses, this provided strong evidence that Francesca was telling us the truth.
But to be absolutely sure that Francesca was experiencing specific emotions, we used an added procedure. Again we took her into a room and hooked her up to the ohmmeter. We asked her to follow instructions on a computer screen that would tell her which of several objects that were laid out on the table in front of her she was to touch and for how long. We said she would be alone in the room since noises from our presence might interfere with the GSR monitoring. Unbeknownst to her, we had a hidden video camera behind the monitor to record all her facial expressions. The reason we did this secretively was to ensure that her expressions were genuine and spontaneous. After the experiment, we had independent student evaluators rate the magnitude and quality of the expressions on her face, such as fear or calm. Of course we made sure that the evaluators didn’t know the purpose of the experiment and didn’t know what object Francesca had been touching on any given trial. Once again we found that there was clear correlation between Francesca’s subjective ratings of various textures and her spontaneous facial expressions. It seemed quite clear, therefore, that the emotions she claimed to experience were authentic.
MIRABELLE, AN EBULLIENT, dark-haired young lady, had been eavesdropping on a conversation I had been having with Ed Hubbard at the Espresso Roma Cafe on campus, a stone’s throw away from my office. She arched her eyebrows—whether from amusement or skepticism, I couldn’t tell.
She came to our lab shortly thereafter to volunteer as a subject. Like Susan and Becky, every number appeared to Mirabelle to be tinged with a particular color. Susan and Becky had convinced us informally that they were reporting their experience accurately and truthfully, but with Mirabelle we wanted to see if we could scare up some hard proof that she was really seeing color (as when you see an apple) rather than just experiencing a vague mental picture of color (as when you imagine an apple). This boundary between seeing and imagining has always proved elusive in neurology. Perhaps synesthesia would help resolve the distinction between them.
I waved her toward a chair in my office, but she was reluctant to sit. Her eyes darted all around the room looking at the various antique scientific instruments and fossils lying on the table and on the floor. She was like the proverbial kid in a candy store as she crawled all around the floor looking at a collection of fossil fishes from Brazil. Her jeans were sliding down her hips, and I tried not to gaze directly at the tattoo on her waist. Mirabelle’s eyes lit up when she saw a long, polished fossilized bone which looked a bit like a humerus (upper arm bone). I asked her to guess what it was. She tried rib, shin bone, and thigh bone. In fact, it was the baculum (penis bone) of an extinct Pleistocene walrus. This particular one had obviously been fractured in the middle and had rehealed at an angle while the animal was alive, as evidenced by a callus formation. There was also a healed, callused tooth mark on the fracture line, suggesting the fracture had been caused by a sexual or predatory bite. There is a detective aspect to paleontology just as there is in neurology, and we could have gone on with all this for another two hours. But we were running out of time. We needed to get back to her synesthesia.
We began with a simple experiment. We showed Mirabelle a white number 5 on a black computer screen. As expected, she saw it in color—in her case, bright red. We had her fix her gaze on a small white dot in the middle of the screen. (This is called a fixation spot; it keeps the eyes from wandering). We then gradually moved the number farther and farther away from the central spot to see if this did anything to the color that was evoked. Mirabelle pointed out that the red color became progressively less vivid as the number was moved away, eventually becoming a pale desaturated pink. This in itself may not seem very surprising; a number seen off-axis prompts a weaker color. But it was nonetheless telling us something important. Even seen off to the side the number itself was still perfectly identifiable, yet the color was much weaker. In one stroke this result showed that synesthesia can’t be just a childhood memory or a metaphorical association.1 If the number were merely evoking the memory or the idea of a color, why should it matter where it was placed in the visual field, so long as it is still clearly recognizable?
We then used a second, more direct test called popout, which psychologists employ to determine whether an effect is truly perceptual (or only conceptual). If you look at Figure 3.1 you will see a set of tilted lines scattered amid a forest of vertical lines. The tilted lines stick out like a sore thumb—they “pop out.” Indeed, you can not only pick them out of the crowd almost instantly but can also group them mentally to form a separate plane or cluster. If you do this, you can easily see that the cluster of tilted lines forms the global shape of an X. Similarly in Figure 3.2, red dots scattered among green dots (pictured here as black dots among gray dots) pop out vividly and form the global shape of a triangle.
In contrast, look at Figure 3.3. You see a set of Ts scattered amid the Ls, but unlike the tilted lines and colored dots of the previous two figures, the Ts don’t give you the same vivid, automatic “here I am!” popout effect, in spite of the fact that Ls and Ts are as different from each other as vertical and tilted lines. You also cannot group the Ts nearly as easily, and must instead engage in an item-by-item inspection. We may conclude from this that only certain “primitive,” or elementary, perceptual features such as color and line orientation can provide a basis for grouping and popout. More complex perceptual tokens such as graphemes (letters and numbers) cannot do so, however different they might be from each other.
FIGURE 3.1 Tilted lines embedded in a matrix of vertical lines can be readily detected, grouped, and segregated from the straight lines by your visual system. This type of segregation can occur only with features extracted early in visual processing. (Recall from Chapter 2 that three-dimensional shape from shading can also lead to grouping.)
To take an extreme example, if I showed you a sheet of paper with the word love typed all over it and a few hates scattered about, you could not find the hates very easily. You would have to search for them in a more or less serial fashion. And even as you found them, one by one, they still wouldn’t segregate from the background the way the tilted lines or colors do. Again, this is because linguistic concepts like love and hate cannot serve as a basis for grouping, however dissimilar they might be conceptually.
FIGURE 3.2 Dots of similar colors or shading can also be grouped effortlessly. Color is a feature detected early in visual processing.
Your ability to group and segregate similar features probably evolved mainly to defeat camouflage and discover hidden objects in the world. For instance, if a lion hides behind a mottling of green foliage, the raw image that enters your eye and hits your retina is nothing but a bunch of yellowish fragments broken up by intervals of green. However, this is not what you see. Your brain knits together the fragments of tawny fur to discern the global shape, and activates your visual category for lion. (And from there, it’s straight on to the amygdala!) Your brain treats the probability that all those yellow patches could be truly isolated and independent from each other as essentially zero. (This is why a painting or a photograph of a lion hiding behind foliage, in which the patches of color actually are independent and unrelated, still makes you “see” the lion.) Your brain automatically tries to group low-level perceptual features together to see if they add up to something important. Like lions.
FIGURE 3.3 Ts scattered among Ls are not easy to detect or group, perhaps because both are made up of the same low-level features: vertical and horizontal lines. Only the arrangement of the lines is different (producing corners versus T-junctions), and this is not extracted early in visual processing.
Perceptual psychologists routinely exploit these effects to determine whether a particular visual feature is elementary. If the feature gives you popout and grouping, the brain must be extracting it early in sensory processing. If popout and grouping are muted or absent, higher-order sensory or even conceptual processing must be involved in representing the objects in question. L and T share the same elementary features in common (one short short horizontal and one short vertical line touching at right angles); the main things that distinguish them in our minds are linguistic and conceptual factors.
So let’s get back to Mirabelle. We know that real colors can lead to grouping and popout. Would her “private” colors be able to elicit the same effects?
To answer this question I devised patterns similar to the one shown in Figure 3.4: a forest of blocky 5s with a few blocky 2s scattered among them. Since the 5s are just mirror images of the 2s, they are composed of identical features: two vertical lines and three horizontal ones. When you look at this image, you manifestly do not get popout; you can only spot the 2s through item-by-item inspection. And you can’t easily discern the global shape—the big triangle—by mentally grouping the 2s; they simply don’t segregate from the background. Although you can eventually deduce logically that the 2s form a triangle, you don’t see a big triangle the way you see the one in Figure 3.5, where the 2s have been rendered in black and the 5s in gray. Now, what if you were to show Figure 3.4 to a synesthete who claims to experience 2s as red and 5s as green? If she were merely thinking of red (and green) then, just like you and me, she wouldn’t instantly see the triangle. On the other hand if synesthesia were a genuinely low-level sensory effect, she might literally see the triangle the way you and I do in Figure 3.5.
For this experiment we first showed images much like Figure 3.4 to twenty normal students and told them to look for a global shape (made of little 2s) among the clutter. Some of the figures contained a triangle, others showed a circle. We flashed these figures in a random sequence on a computer monitor for about half a second each, too short a time for detailed visual inspection. After seeing each figure the subjects had to press one of two buttons to indicate whether they had just been shown a circle or a triangle. Not surprisingly, the students’ hit rate was about 50 percent; in other words, they were just guessing, since they couldn’t spontaneously discern the shape. But if we colored all the 5s green and all the 2s red (in Figure 3.5 this is simulated with gray and black), their performance went up to 80 or 90 percent. They could now see the shape instantly without a pause or a thought.
The surprise came when we showed the black-and-white displays to Mirabelle. Unlike the nonsynesthetes, she was able to identify the shape correctly on 80 to 90 percent of trials—just as if the numbers were actually colored differently! The synesthetically induced colors were just as effective as real colors in allowing her to discover and report the global shape.2 This experiment provides unassailable proof that Mirabelle’s induced colors are genuinely sensory. There is simply no way she could fake it, and no way it could be the result of childhood memories or any of the other alternative explanations that have been proposed.
FIGURE 3.4 A cluster of 2s scattered among 5s. It is difficult for normal subjects to detect the shape formed by the 2s, but lower synesthetes as a group perform much better. The effect has been confirmed by Jamie Ward and his colleagues.
FIGURE 3.5 The same display as Figure 3.4 except that the numbers are shaded differently, allowing normal people to see the triangle instantly. Lower synesthetes (“projectors”) presumably see something like this.
Ed and I realized that, for the first time since Francis Galton, we had clear, unambiguous proof from our experiments (grouping and popout) that synesthesia was indeed a real sensory phenomenon—proof that had eluded researchers for over a century. Indeed, our displays could not only be used to distinguish fakes from genuine synesthetes, but also to ferret out closet synesthetes, people who might have the ability but not realize it or not be willing to admit it.
ED AND I sat back in the café discussing our findings. Between our experiments with Francesca and Mirabelle, we had established that synesthesia exists. The next question was, why does it exist? Could a glitch in brain wiring explain it? What did we know that could help us figure this out? First, we knew that the most common type of synesthesia is apparently number-color. Second, we knew that one of the main color centers in the brain is an area called V4 in the fusiform gyrus of the temporal lobes. (V4 was discovered by Semir Zeki, professor of neuroesthetics at University College of London, and a world authority on the organization of the primate visual system.) Third, we knew that there may be areas in roughly the same part of the brain that are specialized for numbers. (We know this because small lesions to this part of the brain cause patients to lose arithmetic skills.) I thought, wouldn’t it be wonderful if number-color synesthesia were simply caused by some accidental “cross-wiring” between the number and color centers in the brain? This seemed almost too obvious to be true—but why not? I suggested we look at some brain atlases to see exactly how close these two areas really are in relation to each other.
“Hey, maybe we can ask Tim,” Ed responded. He was referring to Tim Rickard, a colleague of ours at the center. Tim had used sophisticated brain-imaging techniques like fMRI to map out the brain area where visual number recognition occurs. Later that afternoon, Ed and I compared the exact location of V4 and the number area in an atlas of the human brain. To our amazement, we saw that the number area and V4 were right next to each other in the fusiform gyrus (Figure 3.6). This was strong support for the cross-wiring hypothesis. Can it really be a coincidence that the most common type of synesthesia is the number-color type, and the number and color areas are immediate neighbors in the brain?
FIGURE 3.6 The left side of the brain showing the approximate location of the fusiform area: black, a number area; white, a color area (shown schematically on the surface).
This was starting to look too much like nineteenth-century phrenology, but maybe it was true! Since the nineteenth century a debate has raged between phrenology—the notion that different functions are sharply localized in different brain areas—versus holism, which holds that functions are emergent properties of the entire brain whose parts are in constant interaction. It turns out this is an artificial polarization to some degree, because the answer depends on the particular function one is talking about. It would be ludicrous to say that gambling or cooking are localized (although there may be aspects of them that are) but it would be equally silly to say that the cough reflex or the pupils’ reflex to light is not localized. What’s surprising, though, is that even some nonstereotyped functions, such as seeing colors or numbers (as shapes or even as numerical ideas), are in fact mediated by specialized brain regions. Even high-level perceptions such as tools or vegetables or fruits—which border on being concepts rather than mere perceptions—can be lost selectively depending on the particular small region of the brain that is damaged by stroke or accident.
So what do we know about brain localization? How many specialized regions are there, and how are they arranged? Just as the CEO of a corporation delegates different tasks to different people occupying different offices, your brain parcels out different jobs to different regions. The process begins when neural signals from your retina travel to an area in the back of your brain where the image gets categorized into different simple attributes such as color, motion, form, and depth. After that, information about separate features gets divvied up and distributed to several far-flung regions in your temporal and parietal lobes. For example, information about the direction of moving targets goes to V5 in your parietal lobes. Color information gets sent mainly to V4 in your temporal lobes.
The reason for this division of labor is not hard to divine. The kinds of computation you need for extracting information about wavelength (color) is very different from the computations required for extracting information about motion. It may be simpler to accomplish this if you have separate areas for each task, keeping the neural machinery distinct for economy of wiring and ease of computation.
It also makes sense to organize specialized regions into hierarchies. In a hierarchical system, each “higher” level carries out more sophisticated tasks but, just like in a corporation, there is an enormous amount of feedback and crosstalk. For example, color information processed in V4 gets relayed to higher color areas that lie farther up in the temporal lobes, near the angular gyrus. These higher areas may be concerned with more complex aspects of color processing. The eucalyptus leaves I see all over campus appear to be the same shade of green at dusk as they do midday, even though the wavelength composition of light reflected is very different in the two cases. (Light at dusk is red, but you don’t suddenly see leaves as reddish green; they still look green because your higher color areas compensate.)
Numerical computation, too, seems to occur in stages: an early stage in the fusiform gyrus where the actual shapes of numbers are represented, and a later stage in the angular gyrus concerned with numerical concepts such as ordinality (sequence) and cardinality (quantity). When the angular gyrus is damaged by a stroke or a tumor, a patient may still be able to identify numbers but can no longer divide or subtract. (Multiplication often survives because it is learned by rote.) It was this aspect of brain anatomy—the close proximity of colors and numbers in the brain in both the fusiform gyrus and near the angular gyrus—that made me suspect that number-color synesthesia was caused by crosstalk between these specialized brain areas.
But if such neural cross-wiring is the correct explanation, why does it occur at all? Galton observed that synesthesia runs in families, a finding that has been repeatedly confirmed by other researchers. Thus it is fair to ask whether there is a genetic basis for synesthesia. Perhaps synesthetes harbor a mutation that causes some abnormal connections to exist between adjacent brain areas that are normally well segregated from each other. If this mutation is useless or deleterious, why hasn’t it been weeded out by natural selection?
Furthermore, if the mutation were to be expressed in a patchy manner, it might explain why some synesthetes “cross-wire” colors and numbers whereas others, like a synesthete I once saw named Esmerelda, see colors in response to musical notes. Consistent with Esmerelda’s case, hearing centers in the temporal lobes are close to the brain areas that receive color signals from V4 and higher color centers. I felt the pieces were starting to fall into place.
The fact that we see various types of synesthesia provides additional evidence for cross-wiring. Perhaps the mutant gene expresses itself to a greater degree, in more brain regions, in some synesthetes than in others. But how exactly does the mutation cause cross-wiring? We know that the normal brain does not come ready-made with neatly packaged areas that are clearly delineated from each other. In the fetus there is an initial dense overproliferation of connections that get pruned back as development proceeds. One reason for this extensive pruning process is presumably to avoid leakage (signal spread) between adjacent areas, just as Michelangelo whittled away excess marble to produce David. This pruning is largely under genetic control. It’s possible that the synesthesia mutation leads to incomplete pruning between some areas that lie close to each other. The net result would be the same: cross-wiring.
However, it is important to note that anatomical cross-wiring between brain areas cannot be the complete explanation for synesthesia. If it were, how could you account for the commonly reported emergence of synesthesia during the use of hallucinogenic drugs such as LSD? A drug can’t suddenly induce sprouting of new axon connections, and such connections would not magically vanish after the drug wore off. Thus it must be enhancing the activity of preexisting connections in some way—which is not inconsistent with the possibility that synesthetes have more of these connections than the rest of us. David Brang and I also encountered two synesthetes who temporarily lost their synesthesia when they started taking antidepressant drugs called selective serotonin reuptake inhibitors (SSRIS), a drug family that famously includes Prozac. While subjective reports cannot entirely be relied on, they do provide valuable clues for future studies. One person was able to switch her synesthesia on or off by starting or stopping her drug regimen. She detested the antidepressant Wellbutrin because it deprived her of the sensory magic that synesthesia provided; the world looked drab without it.
I have been using the word “cross-wiring” somewhat loosely, but until we know exactly what’s going on at the cellular level, the more neutral term “cross-activation” might be better. We know, for instance, that adjacent brain regions often inhibit each other’s activity. This inhibition serves to minimize crosstalk and keeps areas insulated from one other. What if there were a chemical imbalance of some kind that reduces this inhibition—say, the blocking of an inhibitory neurotransmitter, or a failure to produce it? In this scenario there would not be any extra “wires” in the brain, but the synesthete’s wires would not be properly insulated. The result would be the same: synesthesia. We know that, even in a normal brain, extensive neural connections exist between regions that lie far apart. The normal function of these is unknown (as with most brain connections!), but a mere strengthening of these connections or a loss of inhibition might lead to the kind of cross-activation I suggest.
In light of the cross-activation hypothesis we can now also start to guess why Francesca had such powerful emotional reactions to mundane textures. All of us have a primary touch map in the brain called the primary somatosensory cortex, or S1. When I touch you on the shoulder, touch receptors in your skin detect the pressure and send a message to your S1. You feel the touch. Similarly when you touch different textures, a neighboring touch map, S2, is activated. You feel the textures: the dry grain of a wooden deck, the slippery wetness of a bar of soap. Such tactile sensations are fundamentally external, originating from the world outside your body.
Another brain region, the insula, maps internal feelings from your body. Your insula receives continuous streams of sensation from receptor cells in your heart, lungs, liver, viscera, bones, joints, ligaments, fascia, and muscles, as well as from specialized receptors in your skin that sense heat, cold, pain, sensual touch, and perhaps tickle and itch as well. Your insula uses this information to represent how you feel in relation to the outside world and your immediate environment. Such sensations are fundamentally internal, and comprise the primary ingredients of your emotional state. As a central player in your emotional life, your insula sends signals to and receives signals from other emotional centers in your brain including the amygdala, the autonomic nervous system (powered by the hypothalamus), and the orbitofrontal cortex, which is involved in nuanced emotional judgments. In normal people these circuits are activated when they touch certain emotionally charged objects. Caressing, say, a lover, could generate complex feelings of ardor, intimacy, and pleasure. Squeezing a lump of feces, in contrast, likely leads to strong feelings of disgust and revulsion. Now think of what would happen if there were an extreme exaggeration of these very connections linking S2, the insula, the amygdala, and the orbitofrontal cortex. You would expect to see precisely the sort of touch-triggered complex emotions that Francesca experiences when she touches denim, silver, silk, or paper—things that would leave most of us unmoved.
Incidentally, Francesca’s mother also has synesthesia. But in addition to emotions, she reports taste sensations in response to touch. For example, caressing a wrought-iron fence evokes an intense salty flavor in her mouth. This too makes sense: The insula receives strong taste input from the tongue.
WITH THE IDEA of cross-activation we seemed to be homing in on a neurological explanation for number-color and textural synesthesia.3 But as other synesthetes showed up in my office, we realized there are many more forms of the condition. In some people, days of the week or months of the year produced colors: Monday might be green, Wednesday pink, and December yellow. No wonder many scientists thought they were crazy! But, as I said earlier, I’ve learned over the years to listen to what people say. In this particular case, I realized that the only thing days of the week, months, and numbers have in common is the concept of numerical sequence or ordinality. So in these individuals, unlike Becky and Susan, perhaps it is the abstract concept of numerical sequence that evokes the color, rather than the visual appearance of the number. Why the difference between the two types of synesthetes? To answer this, we have to return to brain anatomy.
After the shape of a number is recognized in your fusiform, the message is relayed further on to your angular gyrus, a region in your parietal lobes involved, among other things, in higher color processing. The idea that some types of synesthesia might involve the angular gyrus is consistent with an old clinical observation that this structure is involved in cross-sensory synthesis. In other words, it is thought that this is a grand junction where information about touch, hearing, and vision flow together to enable the construction of high-level percepts. For example, a cat purrs and is fluffy (touch), it purrs and meows (hearing), and it has a certain appearance (vision) and fishy breath (smell)—all of which are evoked by the memory of a cat or the sound of the word “cat.” No wonder patients with damage here lose the ability to name things (anomia) even though they can recognize them. They have difficulty with arithmetic, which, if you think about it, also involves cross-sensory integration: in kindergarten you learn to count with your fingers, after all. (Indeed, if you touch the patient’s finger and ask her which one it is, she often can’t tell you.) All of these bits of clinical evidence strongly suggest that the angular gyrus is a great center in the brain for sensory convergence and integration. So perhaps it’s not so outlandish, after all, that a flaw in the circuitry could lead to colors being quite literally evoked by certain sounds.
According to clinical neurologists, the left angular gyrus in particular may be involved in juggling numerical quantity, sequences, and arithmetic. When this region is damaged by stroke, the patient can recognize numbers and can still think reasonably clearly, but he has difficulty with even the simplest arithmetic. He can’t subtract 7 from 12. I have seen patients who cannot tell you which of two numbers—3 or 5—is larger.
Here we have the perfect arrangement for another type of cross-wiring. The angular gyrus is involved in color processing and numerical sequences. Could it be that, in some synesthetes, the crosstalk occurs between these two higher areas near the angular gyrus rather than lower down in the fusiform? If so, that would explain why, in them, even abstract number representations or the idea of a number prompted by days of the week or months will strongly manifest color. In other words, depending on which part of the brain the abnormal synesthesia gene is expressed, you get different types of synesthetes: “higher” synesthetes driven by numerical concept, and “lower” synesthetes driven by visual appearance alone. Given the multiple back-and-forth connections between brain areas, it is also possible that numerical ideas about sequentiality are sent back down to the fusiform gyrus to evoke colors.
In 2003 I began a collaboration with Ed Hubbard and Geoff Boynton from the Salk Institute for Biological Studies to test these ideas with brain imaging. The experiment took four years, but we were finally able to show that, in grapheme-color synesthetes, the color area V4 lights up even when you present colorless numbers. This cross-activation could never happen in you or me. In recent experiments carried out in Holland, researchers Romke Rouw and Steven Scholte found that there were substantially more axons (“wires”) linking V4 and the grapheme area in lower synesthetes compared to the general population. And even more remarkably, in higher synesthetes, they found a greater number of fibers in the general vicinity of the angular gyrus. This all is precisely what we had proposed. The fit between prediction and subsequent confirmation rarely proceeds so smoothly in science.
The observations we had made so far broadly support the cross-activation theory and provide an elegant explanation of the different perceptions of “higher” and “lower” synesthetes.4 But there are many other tantalizing questions we can ask about the condition. What if a letter synesthete were bilingual and knew two languages with different alphabets, such as Russian and English? The English P and the Cyrillic 
represent more or less the same phoneme (sound) but look completely dissimilar. Would they evoke the same or different colors? Is the grapheme alone critical, or is it the phoneme? Maybe in lower synesthetes it’s the visual appearance that drives it whereas in higher synesthetes it’s the sound. And what about uppercase versus lowercase letters? Or letters depicted in cursive writing? Do the colors of two adjacent graphemes run or flow into each other, or do they cancel each other out? To my knowledge none of these questions have been adequately answered yet—which means we have many exciting years of synesthesia research ahead of us. Fortunately, many new researchers have joined us in the enterprise including Jamie Ward, Julia Simner, and Jason Mattingley. There is now a whole thriving industry on the subject.
Let me tell you about one last patient. In Chapter 2 we noted that the fusiform gyrus represents not only shapes like letters of the alphabet but faces as well. Thus, shouldn’t we expect there to be cases in which a synesthete sees different faces as possessing intrinsic colors? We recently came across a student, Robert, who reported experiencing exactly that. He usually saw the color as a halo around the face, but when he was inebriated the color would become much more intense and spread into the face itself.5 To find out if Robert was being truthful we did a simple experiment. I asked him to stare at the nose of a photograph of another college student and asked Robert what color he saw around the face. Robert said the student’s halo was red. I then briefly flashed either red or green dots on different locations in the halo. Robert’s gaze immediately darted toward a green spot but only rarely toward a red one; in fact, he claimed not to have seen the red spots at all. This provides compelling evidence that Robert really was seeing halos: On a red background, green would be conspicuous while red would be almost imperceptible.
To add to the mystery, Robert also had Asperger syndrome, a high-functioning form of autism. This made it difficult for him to understand and “read” people’s emotions. He could do so through intellectual deduction from the context, but not with the intuitive ease most of us enjoy. Yet for Robert, every emotion also evoked a specific color. For example, anger was blue and pride was red. So his parents taught him very early in life to use his colors to develop a taxonomy of emotions to compensate for his deficit. Interestingly, when we showed him an arrogant face, he said it was “purple and therefore arrogant.” (It later dawned on all three of us that purple is a blend or red and blue, evoked by pride and aggression, and the latter two, if combined, would yield arrogance. Robert hadn’t made this connection before.) Could it be that Robert’s whole subjective color spectrum was being mapped in some systematic manner onto his “spectrum” of social emotions? If so, could we potentially use him as a subject to understand how emotions—and complex blends of them—are represented in the brain? For example, are pride and arrogance differentiated solely on the basis of the surrounding social context, or are they inherently distinct subjective qualities? Is a deep-seated insecurity also an ingredient of arrogance? Are the whole spectrum of subtle emotions based on various combinations, in different ratios, of a small number of basic emotions?
Recall from Chapter 2 that color vision in primates has an intrinsically rewarding aspect that most other components of visual experience do not elicit. As we saw, the evolutionary rationale for neurally linking color with emotion was probably initially to attract us to ripe fruits and/or tender new shoots and leaves, and later to attract males to swollen female rumps. I suspect that these effects arise through interactions between the insula and higher brain regions devoted to color. If the same connections are abnormally strengthened—and perhaps slightly scrambled—in Robert, this would explain why he saw many colors as strongly tinged with arbitrary emotional associations.
BY NOW I was intrigued by another question. What’s the connection—if any—between synesthesia and creativity? The only thing they seem to have in common is that both are equally mysterious. Is there truth to the folklore that synesthesia is more common in artists, poets, and novelists, and perhaps in creative people in general? Could synesthesia explain creativity? Wassily Kandinsky and Jackson Pollock were synesthetes, and so was Vladimir Nabokov. Perhaps the higher incidence of synesthesia in artists is rooted deep in the architecture of their brains.
Nabokov was very curious about his synesthesia and wrote about it in some of his books. For example:
…In the green group, there are alder-leaf f, the unripe apple of p, and pistachio t. Dull green, combined somehow with violet, is the best I can do for w. The yellows comprise various e’s and i’s, creamy d, bright-golden y, and u, whose alphabetical value I can express only by “brassy with an olive sheen.” In the brown group, there are the rich rubbery tone of soft g, paler j, and the drab shoelace of h. Finally, among the reds, b has the tone called burnt sienna by painters, m is a fold of pink flannel, and today I have at last perfectly matched v with “Rose Quartz” in Maerz and Paul’s Dictionary of Color. (From Speak, Memory: An Autobiography Revisited, 1966)
He also pointed out that both his parents were synesthetes and seemed intrigued that his father saw K as yellow, his mother saw it as red, and he saw it as orange—a blend of the two! It isn’t clear from his writings whether he regarded this blending as a coincidence (which it almost certainly is) or thought of it as a genuine hybridization of synesthesia.
Poets and musicians also seem to enjoy a higher incidence of synesthesia. On his website the psychologist Sean Day provides his translation of a passage from an 1895 German article that quotes the great musician Franz Liszt:
When Liszt first began as Kapellmeister in Weimar (1842), it astonished the orchestra that he said: “O please, gentlemen, a little bluer, if you please! This tone type requires it!” Or: “That is a deep violet, please, depend on it! Not so rose!” First the orchestra believed Liszt just joked;…later they got accustomed to the fact that the great musician seemed to see colors there, where there were only tones.
The French poet and synesthete Arthur Rimbaud wrote the poem, “Vowels,” which begins:
A black, E white, I red, U green, O blue: vowels,
I shall tell, one day, of your mysterious origins:
A, black velvety jacket of brilliant flies
which buzz around cruel smells,…
According to one recent survey, as many as a third of all poets, novelists, and artists claim to have had synesthetic experiences of one sort or another, though a more conservative estimate would be one in six. But is this simply because artists have vivid imaginations and are more apt to express themselves in metaphorical language? Or maybe they are just less inhibited about admitting having had such experiences? Or are they simply claiming to be synesthetes because it is “sexy” for an artist to be a synesthete? If the incidence is genuinely higher, why?
One thing that poets and novelists have in common is that they are especially good at using metaphor. (“It is the East, and Juliet is the sun!”) It’s as if their brains are better set up than the rest of ours to forge links between seemingly unrelated domains—like the sun and a beautiful young woman. When you hear “Juliet is the sun,” you don’t say, “Oh, does that mean she is an enormous, glowing ball of fire?” If asked to explain the metaphor, you instead say things like, “She is warm like the sun, nurturing like the sun, radiant like the sun, dispels darkness like the sun.” Your brain instantly finds the right links highlighting the most salient and beautiful aspects of Juliet. In other words, just as synesthesia involves making arbitrary links between seemingly unrelated perceptual entities like colors and numbers, metaphor involves making nonarbitrary links between seemingly unrelated conceptual realms. Perhaps this isn’t just a coincidence.
The key to this puzzle is the observation that at least some high-level concepts are anchored, as we have seen, in specific brain regions. If you think about it, there is nothing more abstract than a number. Warren McCulloch, a founder of the cybernetics movement in the mid-twentieth century, once asked the rhetorical question, “What is a number that Man may know it? And what is Man that he may know number?” Yet there it is, number, neatly packaged in the small, tidy confines of the angular gyrus. When it is damaged, the patient can no longer do simple arithmetic.
Brain damage can make a person lose the ability to name tools but not fruits and vegetables, or only fruits and not tools, or only fruits but not vegetables. All of these concepts are stored close to one other in the upper parts of the temporal lobes, but clearly they are sufficiently separated so that a small stroke can knock out one but leave the others intact. You might be tempted to think of fruits and tools as perceptions rather than concepts, but in fact two tools—say, a hammer and saw—can be visually as dissimilar from each other as they are from a banana; what unites them is a semantic understanding about their purpose and use.
If ideas and concepts exist in the form of brain maps, perhaps we have the answer to our question about metaphor and creativity. If a mutation were to cause excess connections (or alternatively, to permit excess cross-leakage) between different brain areas, then depending on where and how widely in the brain the trait was expressed, it could lead to both synesthesia and a heightened facility for linking seemingly unrelated concepts, words, images, or ideas. Gifted writers and poets may have excess connections between word and language areas. Gifted painters and graphic artists may have excess connections between high-level visual areas. Even a single word like “Juliet” or “sun” can be thought of as the center of a semantic whirlpool, or of a rich swirl of associations. In the brain of a gifted wordsmith, excess connections would mean larger whirlpools and therefore larger regions of overlap and a concomitantly higher propensity toward metaphor. This could explain the higher incidence of synesthesia in creative people in general. These ideas take us back full circle. Instead of saying “Synesthesia is more common among artists because they are being metaphorical,” we should say, “They are better at metaphors because they are synesthetes.”
If you listen to your own conversations, you will be amazed to see how frequently metaphors pop up in ordinary speech. (“Pop up”—see?) Indeed, far from being mere decoration, the use of metaphor and our ability to uncover hidden analogies is the basis of all creative thought. Yet we know almost nothing about why metaphors are so evocative and how they are represented in the brain. Why is “Juliet is the sun” more effective than “Juliet is a warm, radiantly beautiful woman”? Is it simply economy of expression, or is it because the mention of the sun automatically evokes a visceral feeling of warmth and light, making the description more vivid and in some sense real? Maybe metaphors allow you to carry out a sort of virtual reality in the brain. (Bear in mind also that even “warm” and “radiant” are metaphors! Only “beautiful” isn’t.)
There is no simple answer to this question, but we do know that some very specific brain mechanisms—even specific brain regions—might be critical, because the ability to use metaphors can be selectively lost in certain neurological and psychiatric disorders. For instance, in addition to experiencing difficulty using words and numbers, there are hints that people with damage to the left inferior parietal lobule (IPL) often also lose the ability to interpret metaphors and become extremely literal minded. This hasn’t been “nailed down” yet, but the evidence is compelling.
If asked, “What does ‘a stitch in time saves nine’ mean?” a patient with an IPL stroke might say, “It’s good to stitch up a hole in your shirt before it gets too large.” He will completely miss the metaphorical meaning of the proverb even when told explicitly that it is a proverb. This leads me to wonder whether the angular gyrus may have originally evolved for mediating cross-sensory associations and abstractions but then, in humans, was coopted for making all kinds of associations, including metaphorical ones. Metaphors seem paradoxical: On the one hand, a metaphor isn’t literally true, and yet on the other hand a well-turned metaphor seems to strike like lightning, revealing the truth more deeply or directly than a drab, literal statement.
I get chills whenever I hear Macbeth’s immortal soliloquy from Act 5, Scene 5:
Out, out, brief candle!
Life’s but a walking shadow, a poor player
That struts and frets his hour upon the stage,
And then is heard no more. It is a tale
Told by an idiot, full of sound and fury,
Signifying nothing.
Nothing he says is literal. He is not actually talking about candles or stagecraft or idiots. If taken literally, these lines really would be the ravings of an idiot. And yet these words are one of the most profound and deeply moving remarks about life that anyone has ever made!
Puns, on the other hand, are based on superficial associations. Schizophrenics, who have miswired brains, are terrible at interpreting metaphors and proverbs. Yet according to clinical folklore, they are very good at puns. This seems paradoxical because, after all, both metaphors and puns involve linking seemingly unrelated concepts. So why should schizophrenics be bad at the former but good with the latter? The answer is that even though the two appear similar, puns are actually the opposite of metaphor. A metaphor exploits a surface-level similarity to reveal a deep hidden connection. A pun is a surface-level similarity that masquerades as a deep one—hence its comic appeal. (“What fun do monks have on Christmas?” Answer: “Nun.”) Perhaps a preoccupation with “easy” surface similarities erases or deflects attention from deeper connections. When I asked a schizophrenic what an elephant had in common with a man, he answered “They both carry a trunk” alluding maybe to the man’s penis (or maybe to an actual trunk used for storage).
Leaving puns aside, if my ideas about the link between synesthesia and metaphor are correct, then why isn’t every synesthete highly gifted or every great artist or poet a synesthete? The reason may be that synesthesia might merely predispose you to be creative, but this does not mean other factors (both genetic and environmental) aren’t involved in the full flowering of creativity. Even so, I would suggest that similar—though not identical—brain mechanisms might be involved in both phenomena, and so understanding one might help us understand the other.
An analogy might be helpful. A rare blood disorder called sickle cell anemia is caused by a defective recessive gene that causes red blood cells to assume an abnormal “sickle” shape, making them unable to transport oxygen. This can be fatal. If you happen to inherit two copies of this gene (in the unlikely event that both your parents had either the trait or the disease itself), then you develop the full-blown disease. However, if you inherit just one copy of this gene, you do not come down with the disease, though you can still pass it on to your children. Now it turns out that, although sickle-cell anemia is extremely rare in most parts of the world, where natural selection has effectively weeded it out, its incidence is ten times higher in certain parts of Africa. Why should this be? The surprising answer is that the sickle-cell trait actually seems to protect the affected individual from malaria, a disease caused by a mosquito-borne parasite that infects and destroys blood cells. This protection conferred on the population as a whole from malaria outweighs the reproductive disadvantage caused by the occasional rare appearance of an individual with double copies of the sickle-cell gene. Thus the apparently maladaptive gene has actually been selected for by evolution, but only in geographic locations where malaria is endemic.
A similar argument has been proposed for the relatively high incidence of schizophrenia and bipolar disorder in humans. The reason these disorders have not been weeded out may be because having some of the genes that lead to the full-blown disorder are advantageous—perhaps boosting creativity, intelligence, or subtle social-emotional faculties. Thus humanity as a whole benefits from keeping these genes in its gene pool, but the unfortunate side effect is a sizable minority who get bad combinations of them.
Carrying this logic forward, the same could well be true for synesthesia. We have seen how, by dint of anatomy, genes that lead to enhanced cross-activation between brain areas could have been highly advantageous by making us creative as a species. Certain uncommon variants or combinations of these genes might have the benign side effect of producing synesthesia. I hasten to emphasize the part about benign: Synesthesia is not deleterious like sickle-cell disease and mental illness, and in fact most synesthetes seem to really enjoy their abilities and would not opt to have them “cured” even if they could. This is only to say that the general mechanism might be the same. This idea is important because it makes clear that synesthesia and metaphor are not synonymous, and yet they share a deep connection that might give us deep insights into our marvelous uniqueness.6
Thus synesthesia is best thought of as an example of subpathological cross-modal interactions that could be a signature or marker for creativity. (A modality is a sensory faculty, such as smell, touch, or hearing. “Cross-modal” refers to sharing information between senses, as when your vision and hearing together tell you that you’re watching a badly dubbed foreign film.) But as often happens in science, it got me thinking about the fact that even in those of us who are nonsynesthetes a great deal of what goes on in our mind depends on entirely normal cross-modal interactions that are not arbitrary. So there is a sense in which at some level we are all “synesthetes.” For example, look at the two shapes in Figure 3.7. The one on the left looks like a paint splat. The one on the right resembles a jagged piece of shattered glass. Now let me ask you, if you had to guess, which of these is a “bouba” and which is a “kiki”? There is no right answer, but odds are you picked the splat as “bouba” and the glass as “kiki.” I tried this in a large classroom recently, and 98 percent of the students made this choice. Now you might think this has something to do with the blob resembling the physical form of the letter B (for “bouba”) and the jagged thing resembling a K (as in “kiki”). But if you try the experiment on non-English-speaking people in India or China, where the writing systems are completely different, you find exactly the same thing.
Why does this happen? The reason is that the gentle curves and undulations of contour on the amoeba-like figure metaphorically (one might say) mimic the gentle undulations of the sound bouba, as represented in the hearing centers in the brain and in the smooth rounding and relaxing of the lips for producing the curved booo-baaa sound. On the other hand, the sharp wave forms of the sound kee-kee and the sharp inflection of the tongue on the palate mimic the sudden changes in the jagged visual shape. We will return to this demonstration in Chapter 6 and see how it might hold the key to understanding many of the most mysterious aspects of our minds, such as the evolution of metaphor, language, and abstract thought.7
FIGURE 3.7 Which of these shapes is “bouba” and which is “kiki”? Such stimuli were originally used by Heinz Werner to explore interactions between hearing and vision.
I HAVE ARGUED so far that synesthesia, and in particular the existence of “higher” forms of synesthesia (involving abstract concepts rather than concrete sensory qualities) can provide clues to understanding some of the high-level thought processes that humans alone are capable of.8 Can we apply these ideas to what is arguably the loftiest of our mental traits, mathematics? Mathematicians often speak of seeing numbers laid out in space, roaming this abstract realm to discover hidden relationships that others might have missed, such as Fermat’s Last Theorem or Goldbach’s conjecture. Numbers and space? Are they being metaphorical?
One day in 1997, after I had consumed a glass of sherry, I had a flash of insight—or at least thought I had. (Most of the “insights” I have when inebriated turn out to be false alarms.) In his original Nature paper, Galton described a second type of synesthesia that is even more intriguing than the number-color condition. He called it “number forms.” Other researchers use the phrase “number line.” If I asked you to visualize the numbers 1 to 10 in your mind’s eye, you will probably report a vague tendency to see them mapped in space sequentially, left to right, as you were taught in grade school. But number-line synesthetes are different. They able to visualize numbers vividly and do not see the numbers arranged sequentially from left to right, but on a snaking, twisting line that can even double back on itself, so that 36 might be closer to 23, say, than it is to 38 (Figure 3.8). One could think of this as “number-space” synesthesia, in which every number is always in a particular location in space. The number line for any individual remains constant even if tested on intervals separated by months.
FIGURE 3.8 Galton’s number line. Notice that 12 is a tiny bit closer to 1 than it is to 6.
As with all experiments in psychology, we needed a method to prove Galton’s observation experimentally. I called upon my students Ed Hubbard and Shai Azoulai to help set up the procedures. We first decided to look at the well-known “number distance” effect seen in normal people. (Cognitive psychologists have examined every conceivable variation of the effect on hapless student volunteers, but its relevance to number-space synesthesia was missed until we came along.) Ask anyone which of two numbers is larger, 5 or 7? 12 or 50? Anyone who has been through grade school will get it right every time. The interesting part comes when you clock how long it takes people to spit out each of their answers. This latency between showing them a number pair and their verbal response is their reaction time (RT). It turns out that the greater the distance between two numbers the shorter the RT, and contrariwise, the closer two numbers are, the longer it takes to form an answer. This suggests that your brain represents numbers in some sort of an actual mental number line which you consult “visually” to determine which is greater. Numbers that are far apart can be easily eyeballed, while numbers that are close together need closer inspection, which takes a few extra milliseconds.
We realized we could exploit this paradigm to see if the convoluted number-line phenomenon really existed or not. We could ask a number-space synesthete to compare number pairs and see if her RTs corresponded to the real conceptual distance between numbers or would reflect the idiosyncratic geometry of her own personal number line. In 2001 we managed to recruit an Austrian student named Petra who was a number-space synesthete. Her highly convoluted number line doubled back on itself so that, for example, 21 was spatially closer to 36 than it was to 18. Ed and I were very excited. As of that time there had not been any study on the number-space phenomenon since the time when Galton discovered it in 1867. No attempt had been made to establish its authenticity or to suggest what causes it. So any new information, we realized, would be valuable. At least we could set the ball rolling.
We hooked Petra up to a machine that measured her RT to questions such as “Which is bigger, 36 or 38?” or (on a different trial) “36 or 23?” As often happens in science, the result wasn’t entirely clear one way or the other. Petra’s RT seemed to depend partially on the numerical distance and partially on spatial distance. This wasn’t the conclusive result we had hoped for, but it did suggest that her number-line representation wasn’t entirely left-to-right and linear as it is in normal brains. Some aspects of number representation in her brain were clearly messed up.
We published our finding in 2003 in a volume devoted to synesthesia, and it inspired much subsequent research. The results have been mixed, but at the very least we revived interest in an old problem that had been largely ignored by the pundits, and we suggested ways of testing it objectively.
Shai Azoulai and I followed up with a second experiment on two new number-space synesthetes that was designed to prove the same point. This time we used a memory test. We asked each synesthete to remember sets of nine numbers (for example, 13, 6, 8, 18, 22, 10, 15, 2, 24) displayed randomly on various spatial locations on the screen. The experiment contained two conditions. In condition A, nine random numbers were scattered randomly about the two-dimensional screen. In condition B, each number was placed where it “should” be on each synesthete’s personal convoluted line as if it had been projected, or “flattened,” onto the screen. (We had initially interviewed each subject to find out the geometry of his or her personal number line and determined which numbers the subject placed close to each other within that idiosyncratic coordinate system.) In each condition the subjects were asked to view the display for 30 seconds in order to memorize the numbers. After a few minutes they were simply asked to report all the numbers they could recall having seen. The result was striking: The most accurate recall was for the numbers they had seen in condition B. Again we had shown that these people’s personal number lines were real. If they weren’t, or if their shapes varied across time, why should it matter where the numbers had been placed? Putting the numbers where they “should” be in each synesthete’s personal number line apparently facilitated that person’s memory for the numbers—something you wouldn’t see in a normal person.
One more observation deserves special mention. Some of our number-space synesthetes told us spontaneously that the shape of their personal number lines strongly influenced their ability to do arithmetic. In particular, subtraction or division (but not multiplication, which, again, is memorized by rote) was much more difficult across sudden sharp kinks in their lines than it was along relatively straight portions of it. On the other hand, some creative mathematicians have told me that their twisted number lines enable them to see hidden relationships between numbers that elude us lesser mortals. This observation convinced me that both mathematical savants and creative mathematicians are not being merely metaphorical when they speak of wandering a spatial landscape of numbers. They are seeing relationships that are not obvious to us less-gifted mortals.
As for how these convoluted number lines come to exist in the first place, that is still hard to explain. A number represents many things—eleven apples, eleven minutes, the eleventh day of Christmas—but what they have in common are the semiseparate notions of order and quantity. These are very abstract qualities, and our apish brains surely were not under selective pressure to handle mathematics per se. Studies of hunter-gatherer societies suggest that our prehistoric ancestors probably had names for a few small numbers—perhaps up to ten, the number of our fingers—but more advanced and flexible counting systems are cultural inventions of historical times; there simply wouldn’t have been enough for the brain to evolve a “lookup table” or number module starting from scratch. On the other hand (no pun intended), the brain’s representation of space is almost as ancient as mental faculties come. Given the opportunistic nature of evolution, it is possible that the most convenient way to represent abstract numerical ideas, including sequentiality, is to map them onto a preexisting map of visual space. Given that the parietal lobe originally evolved to represent space, is it a surprise that numerical calculations are also computed there, especially in the angular gyrus? This is a prime example of what might have been a unique step in human evolution.
In the spirit of taking a speculative leap, I would like to argue that further specialization might have occurred in our space-mapping parietal lobes. The left angular gyrus might be involved in representing ordinality. The right angular gyrus might be specialized for quantity. The simplest way to spatially map out a numerical sequence in the brain would be a straight line from left to right. This in turn might be mapped onto notions of quantity represented in the right hemisphere. But now let’s assume that the gene that allows such remapping of sequence on visual space is mutated. The result might be a convoluted number line of the kind you see in number-space synesthetes. If I were to guess, I’d say other types of sequence—such as months or weeks—are also housed in the left angular gyrus. If this is correct, we should expect that a patient with a stroke in this area might have difficulty in quickly telling you whether, for example, Wednesday comes after or before Tuesday. Someday I hope to meet such a patient.
ABOUT THREE MONTHS after I had embarked on synesthesia research, I encountered a strange twist. I received an email from one of my undergraduate students, Spike Jahan. I opened it expecting to find the usual “please reconsider my grade” request, but it turned out that he’s a number-color synesthete who had read about our work and wanted to be tested. Nothing strange so far, but then he dropped a bombshell: He’s color-blind. A color-blind synesthete! My mind began to reel. If he experiences colors, are they anything like the colors you or I experience? Could synesthesia shed light on that ultimate human mystery, conscious awareness?
Color vision is a remarkable thing. Even though most of us can experience millions of subtly different hues, it turns out our eyes use only three kinds of color photoreceptors, called cones, to represent all of them. As we saw in Chapter 2, each cone contains a pigment that responds optimally to just one color: red, green, or blue. Although each type of cone responds optimally only to one specific wavelength, it will also respond to a lesser extent to other wavelengths that are close to the optimum. For example, red cones respond vigorously to red light, fairly well to orange, weakly to yellow, and hardly at all to green or blue. Green cones respond best to green, less well to yellowish green, and even less to yellow. Thus every specific wavelength of (visible) light stimulates your red, green, and blue cones by a specific amount. There are literally millions of possible three-way combinations, and your brain knows to interpret each one as a separate color.
Color blindness is a congenital condition in which one or more of these pigments is deficient or absent. A color-blind person’s vision works perfectly normally in nearly every respect, but she can see only a limited range of hues. Depending on which cone pigment is lost and on the extent of loss, she may be red-green color-blind or blue-yellow color-blind. In rare cases two pigments are deficient, and the person sees purely in black and white.
Spike had the red-green variety. He experienced far fewer colors in the world than most of us do. What was truly bizarre, though, was that he often saw numbers tinged with colors that he had never seen in the real world. He referred to them, quite charmingly and appropriately, as “Martian colors” that were “weird” and seemed quite “unreal.” He could only see these when looking at numbers.
Ordinarily one would be tempted to ignore such remarks as being crazy, but in this case the explanation was staring me in the face. I realized that my theory about cross-activation of brain maps provides a neat explanation for this bizarre phenomenon. Remember, Spike’s cone receptors are deficient, but the problem is entirely in his eyes. His retinas are unable to send the full normal range of color signals up to the brain, but in all likelihood his cortical color-processing areas, such as V4 in the fusiform, are perfectly normal. At the same time, he is a number-color synesthete. Thus number shapes are processed normally all the way up to his fusiform and then, due to cross-wiring, produce cross-activation of cells in his V4 color area. Since Spike has never experienced his missing colors in the real world and can do so only by looking at numbers, he finds them incredibly strange. Incidentally, this observation also demolishes the idea that synesthesia arises from early-childhood memory associations such as having played with colored magnets. For how can someone “remember” a color he has never seen? After all, there are no magnets painted with Martian colors!
It is worth pointing out that non-color-blind synesthetes may also see “Martian” colors. Some describe letters of the alphabet as being composed of multiple colors simultaneously “layered on top of each other” making them not quite fit the standard taxonomy of colors. This phenomenon probably arises from mechanisms similar to those observed in Spike; the colors look weird because the connections in his visual pathways are weird and thus uninterpretable.
What is it like to experience colors that don’t appear anywhere in the rainbow, colors from another dimension? Imagine how frustrating it must be to sense something you cannot describe. Could you explain what it feels like to see blue to a person who has been blind from birth? Or the smell of Marmite to an Indian, or saffron to an Englishman? It raises the old philosophical conundrum of whether we can ever really know what someone else is experiencing. Many a student has asked the seemingly naïve question, “How do I know that your red isn’t my blue?” Synesthesia reminds us that this question may not be that naïve after all. As you may recall from earlier, the term for referring to the ineffable subjective quality of conscious experience is “qualia.” These questions about whether other people’s qualia are similar to our own, or different, or possibly absent, may seem as pointless as asking how many angels can dance on the head of a pin—but I remain hopeful. Philosophers have struggled with these questions for centuries, but here at last, with our blooming knowledge about synesthesia, a tiny crack in the door of this mystery may be opening. This is the way science works: Begin with simple, clearly formulated, tractable questions that can pave the way for eventually answering the Big Questions, such as “What are qualia,” “What is the self,” and even “What is consciousness?”
Synesthesia might be able to give us some clues to these abiding mysteries9,10 because it provides a way of selectively activating some visual areas while skipping or bypassing others. It is not ordinarily possible to do this. So instead of asking the somewhat nebulous questions “What is consciousness?” and “What is the self?” we can refine our approach to the problem by focusing on just one aspect of consciousness—our awareness of visual sensations—and ask ourselves, Does conscious awareness of redness require activation of all or most of the thirty areas in the visual cortex? Or only a small subset of them? What about the whole cascade of activity from the retina to the thalamus to the primary visual cortex before the messages get relayed to the thirty higher visual areas? Is their activity also required for conscious experience, or can you skip them and directly activate V4 and experience an equally vivid red? If you look at a red apple, you would ordinarily activate the visual area for both color (red) and form (apple-like). But what if you could artificially stimulate the color area without stimulating cells concerned with form? Would you experience disembodied red color floating out there in front of you like a mass of amorphous ectoplasm or other spooky stuff? And lastly, we also know that there are many more neural projections going backward from each level in the hierarchy of visual processing to earlier areas than there are going forward. The function of these back-projections is completely unknown. Is their activity required for conscious awareness of red? What if you could selectively silence them with a chemical while you looked at a red apple—would you lose awareness? These questions come perilously close to being the kind of impossible-to-do armchair thought experiments that philosophers revel in. The key difference is that such experiments really can be done—maybe within our lifetimes.
And then we may finally understand why apes care about nothing beyond ripe fruit and red rumps, while we are drawn to the stars.
CHAPTER 4
The Neurons That Shaped Civilization
Even when we are alone, how often do we think with pain and pleasure of what others think of us, or their imagined approbation or disapprobation; and this all follows from sympathy, a fundamental element of the social instincts.
—CHARLES DARWIN
A FISH KNOWS HOW TO SWIM THE INSTANT IT HATCHES, AND OFF it darts to fend for itself. When a duckling hatches, it can follow its mother over land and across the water within moments. Foals, still dripping with amniotic fluid, spend a few minutes bucking around to get the feel of their legs, then join the herd. Not so with humans. We come out limp and squalling and utterly dependent on round-the-clock care and supervision. We mature glacially, and do not approach anything resembling adult competence for many, many years. Obviously we must gain some very large advantage from this costly, not to mention risky up-front investment, and we do: It’s called culture.
In this chapter I explore how a specific class of brain cells, called mirror neurons, may have played a pivotal role in our becoming the one and only species that veritably lives and breathes culture. Culture consists of massive collections of complex skills and knowledge which are transferred from person to person through two core mediums, language and imitation. We would be nothing without our savant-like ability to imitate others. Accurate imitation, in turn, may depend on the uniquely human ability to “adopt another’s point of view”—both visually and metaphorically—and may have required a more sophisticated deployment of these neurons compared with how they are organized in the brains of monkeys. The ability to see the world from another person’s vantage point is also essential for constructing a mental model of another person’s complex thoughts and intentions in order to predict and manipulate his behavior. (“Sam thinks I don’t realize that Martha hurt him.”) This capacity, called theory of mind, is unique to humans. Finally, certain aspects of language itself—that vital medium of cultural transmission—was probably built at least partly on our facility for imitation.
Darwin’s theory of evolution is one of the most important scientific discoveries of all time. Unfortunately, however, the theory makes no provision for an afterlife. Consequently it has provoked more acrimonious debate than any other topic in science—so much so that some school districts in the United States have insisted on giving the “theory” of intelligent design (which is really just a fig leaf for creationism) equal status in textbooks. As has been pointed out repeatedly by the British scientist and social critic Richard Dawkins, this is little different from giving equal status to the idea that the sun goes around Earth. At the time evolutionary theory was proposed—long before the discovery of DNA and the molecular machinery of life, back when paleontology had just barely begun to piece together the fossil record—the gaps in our knowledge were sufficiently large to leave room for honest doubt. That point is long past, but that doesn’t mean we have solved the entire puzzle. It would be arrogant for a scientist to deny that there are still many important questions about the evolution of the human mind and brain that remain unanswered. At the top of my list would be the following:
1. The hominin brain reached nearly its present size, and perhaps even its present intellectual capacity, about 300,000 years ago. Yet many of the attributes we regard as uniquely human—such as toolmaking, fire building, art, music, and perhaps even full-blown language—appeared only much later, around 75,000 years ago. Why? What was the brain doing during that long incubation period? Why did it take so long for all this latent potential to blossom, and then why did it blossom so suddenly? Given that natural selection can only select expressed abilities, not latent ones, how did all this latent potential get built up in the first place? I shall call this “Wallace’s problem” after the Victorian naturalist Alfred Russel Wallace, who first proposed it when discussing the origins of language:
The lowest savages with the least copious vocabularies [have] the capacity of uttering a variety of distinct articulate sounds and of applying them to an almost infinite amount of modulation and inflection [which] is not in any way inferior to that of the higher [European] races. An instrument has been developed in advance of the needs of its possessor.
2. Crude Oldowan tools—made by just a few blows to a core stone to create an irregular edge—emerged 2.4 million years ago and were probably made by Homo habilis, whose brain size was halfway between that of chimps and modern humans. After another million years of evolutionary stasis, aesthetically pleasing symmetrical tools began to appear which reflected a standardization of production technique. These required switching from a hard hammer to a soft, perhaps wooden, hammer while the tool was being made, so as to ensure a smooth rather than a jagged, irregular edge. And lastly, the invention of stereotyped assembly-line tools—sophisticated symmetrical bifacial tools that were hafted to a handle—took place only two hundred thousand years ago. Why was the evolution of the human mind punctuated by these relatively sudden upheavals of technological change? What was the role of tool use in shaping human cognition?
3. Why was there a sudden explosion—what Jared Diamond, in his book Guns, Germs, and Steel, calls the “great leap”—in mental sophistication around sixty thousand years ago? This is when widespread cave art, clothing, and constructed dwellings appeared. Why did these advances come along only then, even though the brain had achieved its modern size almost a million years earlier? It’s the Wallace problem again.
4. Humans are often called the “Machiavellian primate,” referring to our ability to predict other people’s behavior and out-smart them. Why are we humans so good at reading one another’s intentions? Do we have a specialized brain module, or circuit, for generating a theory of other minds, as proposed by the British cognitive neuroscientists Nicholas Humphrey, Uta Frith, Marc Hauser, and Simon Baron-Cohen? Where is this circuit and when did it evolve? Is it present in some rudimentary form in monkeys and apes, and if so, what makes ours so much more sophisticated than theirs?
5. How did language evolve? Unlike many other human traits such as humor, art, dancing, and music, the survival value of language is obvious: It lets us communicate our thoughts and intentions. But the question of how such an extraordinary ability actually came into being has puzzled biologists, psychologists, and philosophers since at least Darwin’s time. One problem is that the human vocal apparatus is vastly more sophisticated than that of any other ape, but without the correspondingly sophisticated language areas in the human brain, such exquisite articulatory equipment alone would be useless. So how did these two mechanisms with so many elegant interlocking parts evolve in tandem? Following Darwin’s lead, I suggest that our vocal equipment and our remarkable ability to modulate our voice evolved mainly for producing emotional calls and musical sounds during courtship in early primates, including our hominin ancestors. Once that evolved, the brain—especially the left hemisphere—could start using it for language.
But an even bigger puzzle remains. Is language mediated by a sophisticated and highly specialized mental “language organ” that is unique to humans and that emerged completely out of the blue, as suggested by the famous MIT linguist Noam Chomsky? Or was there a more primitive gestural communication system already in place that provided scaffolding for the emergence of vocal language? A major piece of the solution to this riddle comes from the discovery of mirror neurons.
I HAVE ALREADY alluded to mirror neurons in earlier chapters and will return to them again in Chapter 6, but here in the context of evolution let’s take a closer look. In the frontal lobes of a monkey’s brain, there are certain cells that fire when the monkey performs a very specific action. For instance, one cell fires during the pulling of a lever, a second for grabbing a peanut, a third for putting a peanut in the mouth, and yet a fourth for pushing something. (Bear in mind, these neurons are part of a small circuit performing a highly specific task; a single neuron by itself doesn’t move a hand, but its response allows you to eavesdrop on the circuit.) Nothing new so far. Such motor-command neurons were discovered by the renowned Johns Hopkins University neuroscientist Vernon Mountcastle several decades ago.
While studying these motor-command neurons in the late 1990s, another neuroscientist, Giacomo Rizzolatti, and his colleagues Giuseppe Di Pellegrino, Luciano Fadiga, and Vittorio Gallese, from the University of Parma in Italy, noticed something very peculiar. Some of the neurons fired not only when the monkey performed an action, but also when it watched another monkey performing the same action! When I heard Rizzolatti deliver this news during a lecture one day, I nearly jumped off my seat. These were not mere motor-command neurons; they were adopting the other animal’s point of view (Figure 4.1). These neurons (again, actually the neural circuit to which they belong; from now on I’ll use the word “neuron” for “the circuit”) were for all intents and purposes reading the other monkey’s mind, figuring out what it was up to. This is an indispensable trait for intensely social creatures like primates.
It isn’t clear how exactly the mirror neuron is wired up to allow this predictive power. It is as if higher brain regions are reading the output from it and saying (in effect), “The same neuron is now firing in my brain as would be firing if I were reaching out for a banana; so the other monkey must be intending to reach for that banana now.” It is as if mirror neurons are nature’s own virtual-reality simulations of the intentions of other beings.
In monkeys these mirror neurons enable the prediction of simple goal-directed actions of other monkeys. But in humans, and in humans alone, they have become sophisticated enough to interpret even complex intentions. How this increase in complexity took place will be hotly debated for some time to come. As we will see later, mirror neurons also enable you to imitate the movements of others, thereby setting the stage for the cultural “inheritance” of skills developed and honed by others. They may have also propelled a self-amplifying feedback loop that kicked in at one point to accelerate brain evolution in our species.
FIGURE 4.1 Mirror neurons: Recordings of nerve impulses (shown on the right) from the brain of a rhesus monkey (a) watching another being reach for a peanut, and (b) reaching out for the peanut. Thus each mirror neuron (there are six) fires both when the monkey observes the action and when the monkey executes the action itself.
As Rizzolatti noted, mirror neurons may also enable you to mime the lip and tongue movements of others, which in turn could provide the evolutionary basis for verbal utterances. Once these two abilities are in place—the ability to read someone’s intentions and the ability to mimic their vocalizations—you have set in motion two of the many foundational events that shaped the evolution of language. You need no longer speak of a unique “language organ,” and the problem doesn’t seem quite so mysterious anymore. These arguments do not in any way negate the idea that there are specialized brain areas for language in humans. We are dealing here with the question of how such areas may have evolved, not whether they exist or not. An important piece of the puzzle is Rizzolatti’s observation that one of the chief areas where mirror neurons abound, the ventral premotor area in monkeys, may be the precursor of our celebrated Broca’s area, a brain center associated with the expressive aspects of human language.
Language is not confined to any single brain area, but the left inferior parietal lobe is certainly one of the areas that are crucially involved, especially in the representation of word meaning. Not coincidentally, this area is also rich in mirror neurons in the monkey. But how do we actually know that mirror neurons exist in the human brain? It is one thing to saw open the skull of a monkey and spend days or weeks probing around with a microelectrode, but 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 else moving his hand, but not if he watches a similar movement by an inanimate object, such as a ball bouncing up and down. We suggested at the Society for Neuroscience meeting in 1998 that this suppression was caused by Rizzolatti’s mirror-neuron system.
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 sensory mirror neurons for touch and pain, why doesn’t their firing automatically make us feel everything we witness? It occurred to me that perhaps the null signal (“I am not being touched”) from skin and joint receptors in your own hand block the signals from your mirror neurons from reaching conscious awareness. The overlapping presence of the null signals and the mirror-neuron activity is interpreted by higher brain centers to mean, “Empathize, by all means, but don’t literally feel that other guy’s sensations.” Speaking in more general terms, it is the dynamic interplay of signals from frontal inhibitory circuits, mirror neurons (both frontal and parietal), and null signals from receptors that allow you to enjoy reciprocity with others while simultaneously preserving your individuality.
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 together,” as the old mnemonic goes, eventually even the mere sight of a moving hand (its own or another monkey’s) triggers a response from the command neurons. But if this is the correct explanation, why do only a subset of the command neurons fire? Why aren’t all the command neurons for this action mirror neurons? Furthermore, the visual appearance of another person reaching toward a peanut is very different from your view of your own hand. So how does the mirror neuron apply the appropriate correction for vantage point? No simple straightforward associationist model can account for this. And finally, so what if learning plays a role in constructing mirror neurons? Even if it does, that doesn’t make them any less interesting or important for understanding brain function. The question of what mirror neurons are doing and how they work is quite independent of the question of whether they are wired up by genes or by the environment.
Highly relevant to this discussion is an important discovery made by Andrew Meltzoff, a cognitive psychologist at the University of Washington’s Institute for Learning and Brain Sciences in Seattle. He found that a newborn infant will often protrude its tongue when watching its mother do it. And when I say newborn I mean it—just a few hours old. The neural circuitry involved must be hardwired and not based on associative learning. The child’s smile echoing the mother’s smile appears a little later, but again it can’t be based on learning since the baby can’t see its own face. It has to be innate.
It has not been proven whether mirror neurons are responsible for these earliest imitative behaviors, but it’s a fair bet. The ability would depend on mapping the visual appearance of the mother’s protruding tongue or smile onto the child’s own motor maps, controlling a finely adjusted sequence of facial muscle twitches. As I noted in my BBC Radio Reith Lectures in 2003, entitled “The Emerging Mind,” this sort of translation between maps is precisely what mirror neurons are thought to do, and if this ability is innate, it is truly astonishing. I’ll call it the “sexy” version of the mirror-neuron function.
Some people argue that the complex computational ability for true imitation—based on mirror neurons—emerges only later in development, whereas the tongue protrusion and first smile are merely hardwired reflexes in response to simple “triggers” from mom, the same way a cat’s claws come out when it sees a dog. The only way to distinguish the sexy from the mundane explanation would be to see whether a baby can imitate a nonstereotyped movement it is unlikely to ever encounter in nature, such as an asymmetrical smile, a wink, or a curious distortion of the mouth. This couldn’t be done by a simple hardwired reflex. The experiment would settle the issue once and for all.
INDEPENDENT OF THE question of whether mirror neurons are innate or acquired, let us now take a closer look at what they actually do. Many functions were proposed when they were first reported, and I’d like to build on these earlier speculations.2 Let’s make a list of things they might be doing. Bear in mind they may have originally evolved for purposes other than the ones listed here. These secondary functions may simply be a bonus, but that doesn’t make them any less useful.
First, and most obvious, they allow you to figure out someone else’s intentions. When you see your friend Josh’s hand moves toward the ball, your own ball-reaching neurons start firing. By running this virtual simulation of being Josh, you get the immediate impression that he is intending to reach for the ball. This ability to entertain a theory of mind may exist in the great apes in rudimentary form, but we humans are exceptionally good at it.
Second, in addition to allowing us to see the world from another person’s visual vantage point, mirror neurons may have evolved further, enabling us to adopt the other person’s conceptual vantage point. It may not be entirely coincidental that we use metaphors like “I see what you mean” or “Try to see it from my point of view.” How this magic step from literal to conceptual viewpoint occurred in evolution—if indeed it occurred—is of fundamental importance. But it is not an easy proposition to test experimentally.
As a corollary to adopting the other’s point of view, you can also see yourself as others see you—an essential ingredient of self-awareness. This is seen in common language: When we speak of someone being “self-conscious,” what we really mean is that she is conscious of someone else being conscious of her. Much the same can be said for a word like “self-pity.” I will return to this idea in the concluding chapter on consciousness and mental illness. There I will argue that other-awareness and self-awareness coevolved in tandem, leading to the I-you reciprocity that characterizes humans.
A less obvious function of mirror neurons is abstraction—again, something humans are especially good at. This is well illuminated by the bouba-kiki experiment discussed discussed in Chapter 3 in the context of synesthesia. To reiterate, over 95 percent of people identify the jagged form as the “kiki” and the curvy one as “bouba.” The explanation I gave is that the sharp inflections of the jagged shape mimic the inflection of the sound ki-ki, not to mention the sudden deflection of the tongue from the palate. The gentle curves of bulbous shape, on the other hand, mimic the boooooo-baaaaaa contour of the sound and the tongue’s undulation on the palate. Similarly, the sound shhhhhhhh (as in “shall”) is linked to a blurred, smudged line, whereas rrrrrrrrrrrrrrrrr is linked to a sawtooth-shaped line, and an sssssssssss (as in “sip”) to a fine silk thread—which shows that it’s not the mere similarity of the jagged shape to the letter K that produces the effect, but genuine cross-sensory abstraction. The link between the bouba-kiki effect and mirror neurons may not be immediately evident, but there is a fundamental similarity. The main computation done by mirror neurons is to transform a map in one dimension, such as the visual appearance of someone else’s movement, into another dimension, such as the motor maps in the observer’s brain, which contain programs for muscle movements (including tongue and lip movements).
This is exactly what’s going on in the bouba-kiki effect: Your brain is performing an impressive feat of abstraction in linking your visual and auditory maps. The two inputs are entirely dissimilar in every way except one—the abstract properties of jaggedness or curviness—and your brain homes in on this common denominator very swiftly when you are asked to pair them up. I call this process “cross-modal abstraction.” This ability to compute similarities despite surface differences may have paved the way for more complex types of abstraction that our species takes great delight in. Mirror neurons may be the evolutionary conduit that allowed this to happen.
Why did a seemingly esoteric ability like cross-modal abstraction evolve in the first place? As I suggested in a previous chapter, it may have emerged in ancestral arboreal primates to allow them to negotiate and grasp tree branches. The vertical visual inputs of tree limbs and branches reaching the eye had to be matched with totally dissimilar inputs from joints and muscles and the body’s felt sense of where it is in space—an ability that would have favored the development of both canonical neurons and mirror neurons. The readjustments that were required in order to establish a congruence between sensory and motor maps may have initially been based on feedback, both at the genetic level of the species and at the experiential level of the individual. But once the rules of congruence were in place, the cross-modal abstraction could occur for novel inputs. For instance, picking up a shape that is visually perceived to be tiny would result in a spontaneous movement of almost-opposed thumb and forefingers, and if this were mimicked by the lips to produce a correspondingly diminutive orifice (through which you blow air), you would produce sounds (words) that sound small (such as “teeny weeny,” “diminutive,” or in French “un peu,” and so on). These small “sounds” would in turn feed back via the ears to be linked to tiny shapes. (This, as we shall see in Chapter 6, may have been how the first words evolved in our ancestral hominins.) The resulting three-way resonance between vision, touch, and hearing may have progressively amplified itself as in an echo chamber, culminating in the full-fledged sophistication of cross-sensory and other more complex types of abstraction.
If this formulation is correct, some aspects of mirror-neuron function may indeed be acquired through learning, building on a genetically specified scaffolding unique to humans. Of course, many monkeys and even lower vertebrates may have mirror neurons, but the neurons may need to develop a certain minimum sophistication and number of connections with other brain areas before they can engage in the kinds of abstractions that humans are good at.
What parts of the brain are involved in such abstractions? I already hinted (about language) that the inferior parietal lobule (IPL) may have played a pivotal role, but let’s take a closer look. In lower mammals the IPL isn’t very large, but it becomes more conspicuous in primates. Even within primates it is disproportionately large in the great apes, reaching a climax in humans. Finally, only in humans do we see a major portion of this lobule splitting further into two, the angular gyrus and the supramarginal gyrus, suggesting that something important was going on in this region of the brain during human evolution. Lying at the crossroads between vision (occipital lobes), touch (parietal lobes), and hearing (temporal lobes), the IPL is strategically located to receive information from all sensory modalities. At a fundamental level, cross-modal abstraction involves the dissolution of barriers to create modality-free representations (as exemplified by the bouba-kiki effect). The evidence for this is that when we tested three patients who had damage to the left angular gyrus, they performed poorly on the bouba-kiki task. As I already noted, this ability to map one dimension onto another is one of the things that mirror neurons are thought to be doing, and not coincidentally such neurons are plentiful in the general vicinity of the IPL. The fact that this region in the human brain is disproportionately large and differentiated suggests an evolutionary leap.
The upper part of the IPL, the supramarginal gyrus, is another structure unique to humans. Damage here leads to a disorder called ideomotor apraxia: a failure to perform skilled actions in response to the doctor’s commands. Asked to pretend he is combing his hair, an apraxic will raise his arm, look at it, and flail it around his head. Asked to mime hammering a nail, he will make a fist and bang it on the table. This happens even though his hand isn’t paralyzed (he will spontaneously scratch an itch) and he knows what “combing” means (“It means I am using a comb to tidy up my hair, Doctor”). What he lacks is the ability to conjure up a mental picture of the required action—in this case combing—which must precede and orchestrate the actual execution of the action. These are functions one would normally associate with mirror neurons, and indeed the supramarginal gyrus has mirror neurons. If our speculations are on the right track, then one would expect patients with apraxia to be terrible at understanding and imitating other people’s movements. Although we have seen some hints of this, the matter requires careful investigation.
One also wonders about the evolutionary origin of metaphors. Once the cross-modal abstraction mechanism was set up between vision and touch in the IPL (originally for grasping branches), this mechanism could have paved the way for cross-sensory metaphors (“stinging rebuke,” “loud shirt”) and eventually for metaphors in general. This is supported by our recent observations that patients with angular gyrus lesions not only have difficulty with bouba-kiki, but also with understanding simple proverbs, interpreting them literally rather than metaphorically. Obviously these observations need to be confirmed on a larger sample of patients. It is easy to imagine how cross-modal abstraction might work for bouba-kiki, but how do you explain metaphors that combine very abstract concepts like “it is the east, and Juliet is the sun” given the seemingly infinite number of such concepts in the brain? The surprising answer to this question is that the number of concepts is not infinite, nor is the number of words that represent them. For all practical purposes, most English speakers have a vocabulary of about ten thousand words (although you can get by with far fewer if you are a surfer). There may be only some mappings that make sense. As the eminent cognitive scientist and polymath Jaron Lanier pointed out to me, Juliet can be the sun, but it makes little sense to say she is a stone or an orange juice carton. Bear in mind that the metaphors that get repeated and become immortal are the apt ones, the resonant ones. In doggerel, comically bad metaphors abound.
Mirror neurons play another important role in the uniqueness of the human condition: They allow us to imitate. You already know about tongue protrusion mimicry in infants, but once we reach a certain age, we can mime very complex motor skills, such as your mom’s baseball swing or a thumbs-up gesture. No ape can match our imitative talents. However, I will note as an interesting aside here, the ape that comes closest to us in this regard is not our nearest cousin, the chimpanzee, but the orangutan. Orangutans can even open locks or use an oar to row, once they have seen someone else do it. They are also the most arboreal and prehensile of the great apes, so their brains may be jam-packed with mirror neurons for allowing their babies to watch mom in order to learn how to negotiate trees without the penalties of trial and error. If by some miracle an isolated pocket of orangs in Borneo survives the environmental holocaust that Homo sapiens seems hell-bent on bringing about, these meek apes may well inherit the earth.
Miming may not seem like an important skill—after all, “aping” someone is a derogatory term, which is ironic given that most apes are actually not very good at imitation. But as I have previously argued, miming may have been the key step in hominin evolution, resulting in our ability to transmit knowledge through example. When this step was taken, our species suddenly made the transition from gene-based Darwinian evolution through natural selection—which can take millions of years—to cultural evolution. A complex skill initially acquired through trial and error (or by accident, as when some ancestral hominid first saw a shrub catching fire from lava) could be transmitted rapidly to every member of a tribe, both young and old. Other researchers including Merlin Donald have made the same point, although not in relation to mirror neurons.3
THIS LIBERATION FROM the constraints of a strictly gene-based Darwinian evolution was a giant step in human evolution. One of the big puzzles in human evolution is what we earlier referred to as the “great leap forward,” the relatively sudden emergence between sixty thousand and a hundred thousand years ago of a number of traits we regard as uniquely human: fire, art, constructed shelters, body adornment, multicomponent tools, and more complex use of language. Anthropologists often assume this explosive development of cultural sophistication must have resulted from a set of new mutations affecting the brain in equally complex ways, but that doesn’t explain why all of these marvelous abilities should have emerged at roughly the same time.
One possible explanation is that the so-called great leap is just a statistical illusion. The arrival of these traits may in fact have been smeared out over a much longer period of time than the physical evidence depicts. But surely the traits don’t have to emerge at exactly the same time for the question to still be valid. Even spread out, thirty thousand years is just a blip compared to the millions of years of small, gradual behavioral changes that took place prior to that. A second possibility is that the new brain mutations simply increased our general intelligence, the capacity for abstract reasoning as measured by IQ tests. This idea is on the right track, but it doesn’t tell us much—even leaving aside the very legitimate criticism that intelligence is a complex, multifaceted ability which can’t be meaningfully averaged into a single general ability.
That leaves a third possibility, one that brings us back full circle to mirror neurons. I suggest that there was indeed a genetic change in the brain, but ironically the change freed us from genetics by enhancing our ability to learn from one another. This unique ability liberated our brain from its Darwinian shackles, allowing the rapid spread of unique inventions—such as making cowry-shell necklaces, using fire, constructing tools and shelter, or indeed even inventing new words. After 6 billion years of evolution, culture finally took off, and with culture the seeds of civilization were sown. The advantage of this argument is that you don’t need to postulate separate mutations arriving nearly simultaneously to account for the coemergence of our many and various unique mental abilities. Instead, increased sophistication of a single mechanism—such as imitation and intention reading—could explain the huge behavioral gap between us and apes.
I’ll illustrate with an analogy. Imagine a Martian naturalist watching human evolution over the last five hundred thousand years. She would of course be puzzled by the great leap forward that occurred fifty thousand years ago, but would be even more puzzled by a second great leap which occurred between 500 B.C.E. and the present. Thanks to certain innovations such as those in mathematics—in particular, the zero, place value, and numerical symbols (in India in the first millennium B.C.E.), and geometry (in Greece during the same period)—and, more recently, in experimental science (by Galileo)—the behavior of a modern civilized person is vastly more complex than that of humans ten thousand to fifty thousand years ago.
This second leap forward in culture was even more dramatic than the first. There is a greater behavioral gap between pre–and post–500 B.C.E. humans than between, say, Homo erectus and early Homo sapiens. Our Martian scientist might conclude that a new set of mutations made this possible. Yet given the time scale, that’s just not possible. The revolution stemmed from a set of purely environmental factors which happened fortuitously at the same time. (Let’s not forget the invention of the printing press, which allowed the extraordinary spread and near universal availability of knowledge that usually remained confined to the elite.) But if we admit this, then why doesn’t the same argument apply to the first great leap? Maybe there was a lucky set of environmental circumstances and a few accidental inventions by a gifted few which could tap into a preexisting ability to learn and propagate information quickly—the basis of culture. And in case you haven’t guessed by now, that ability might hinge on a sophisticated mirror-neuron system.
A caveat is in order. I am not arguing that mirror neurons are sufficient for the great leap or for culture in general. I’m only saying that they played a crucial role. Someone has to discover or invent something—like noticing the spark when two rocks are struck together—before the discovery can spread. My argument is that even if such accidental innovations were hit upon by chance by individual early hominins, they would have fizzled out were it not for a sophisticated mirror-neuron system. After all, even monkeys have mirror neurons, but they are not bearers of a proud culture. Their mirror-neuron system is either not advanced enough or is not adequately connected to other brain structures to allow the rapid propagation of culture. Furthermore, once the propagation mechanism was in place, it would have exerted selective pressure to make some outliers in the population more innovative. This is because innovations would only be valuable if they spread rapidly. In this respect, we could say mirror neurons served the same role in early hominin evolution as the Internet, Wikipedia, and blogging do today. Once the cascade was set in motion, there was no turning back from the path to humanity.
CHAPTER 5
Where Is Steven? The Riddle of Autism
You must always be puzzled by mental illness. The thing I would dread most, if I became mentally ill, would be your adopting a common sense attitude; that you could take it for granted that I was deluded.
—LUDWIG WITTGENSTEIN
“I KNOW STEVEN IS TRAPPED IN THERE SOMEWHERE, DR. RAMACHANDRAN. If only you could find a way to tell our son how dearly we love him, perhaps you could bring him out.”
How often have physicians heard that heartbreaking lament from parents of children with autism? This devastating developmental disorder was discovered independently by two physicians, Leo Kanner in Baltimore and Hans Asperger in Vienna, in the 1940s. Neither doctor had any knowledge of the other, and yet by an uncanny coincidence they gave the syndrome the same name: autism. The word comes from the Greek autos meaning “self,” a perfect description because the most striking feature of autism is a complete withdrawal from the social world and a marked reluctance or inability to interact with people.
Take Steven, for instance. He is six years old, with freckled cheeks and sandy-brown hair. He is sitting at a play table drawing pictures, his brow lightly furrowed in concentration. He is producing some beautiful drawings of animals. There’s one of a galloping horse that is so wonderfully animated that it seems to leap out of the paper. You might be tempted to walk over and praise him for his talent. The possibility that he might be profoundly incapacitated would never cross your mind. But the moment you try to talk to him, you realize that there’s a sense in which Steven the person simply isn’t there. He is incapable of anything remotely resembling the two-way exchange of normal conversation. He refuses to make eye contact. Your attempts to engage him make him extremely anxious. He fidgets and rocks his body to and fro. All attempts to communicate with him meaningfully have been, and will be, in vain.
Since the time of Kanner and Asperger, there have been hundreds of case studies in the medical literature documenting, in detail, the various seemingly unrelated symptoms that characterize autism. These fall into two major groups: social-cognitive and sensorimotor. In the first group we have the single most important diagnostic symptom: mental aloneness and a lack of contact with the world, particularly the social world, as well as a profound inability to engage in normal conversation. Going hand in hand with this is an absence of emotional empathy for others. Even more surprising, autistic children express no outward sense of play, and they do not engage in the untrammeled make-believe with which normal children fill their waking hours. Humans, it has been pointed out, are the only animals that carry our sense of whimsy and playfulness into adulthood. How sad it must for parents to see their autistic sons and daughters impervious to the enchantment of childhood. Yet despite this social withdrawal, autistic children have a heightened interest in their inanimate surroundings, often to the point of being obsessive. This can lead to the emergence of odd, narrow preoccupations and a fascinations with things that seem utterly trivial to most of us, like memorizing all the phone numbers in a directory.
Let us turn now to the second cluster of symptoms: sensorimotor. On the sensory side, autistic children may find specific sensory stimuli highly distressing. Certain sounds, for example, can set off a violent temper tantrum. There is also a fear of novelty and change, and an obsessive insistence on sameness, routine, and monotony. The motor symptoms include a to-and-fro rocking of the body (such as we saw with Steven), repetitive hand movements including flapping motions and self-slapping, and sometimes elaborate, repetitive rituals. These sensorimotor symptoms are not quite as definitive or as devastating as the social-emotional ones, but they co-occur so frequently that they must be connected somehow. Our picture of what causes autism would be incomplete if we failed to account for them.
There is one more motor symptom to mention, one that I think holds the key to unraveling the mystery: Many autistic children have difficulty with miming and imitating other people’s actions. This simple observation suggested to me a deficiency in the mirror-neuron system. Much of the remainder of this chapter chronicles my pursuit of this hypothesis and the fruit it has borne so far.
Not surprisingly, there have been dozens of theories of what causes autism. These can be broadly divided into psychological explanations and physiological explanations—the latter emphasizing innate abnormalities in brain wiring or neurochemistry. One ingenious psychological explanation, put forward by Uta Frith of University College of London and Simon Baron-Cohen of Cambridge University, is the notion that children with autism have a deficient theory of other minds. Less credible is the psychodynamic view that blames bad parenting, an idea that is so absurd that I won’t consider it further.
We encountered the term “theory of mind” in passing in the previous chapter in relation to apes. Now let me explain it more fully. It is a technical term that is widely used in the cognitive sciences, from philosophy to primatology to clinical psychology. It refers to your ability to attribute intelligent mental beingness to other people: to understand that your fellow humans behave the way they do because (you assume) they have thoughts, emotions, ideas, and motivations of more or less the same kind as you yourself possess. In other words, even though you cannot actually feel what it is like to be another individual, you use your theory of mind to automatically project intentions, perceptions, and beliefs into the minds of others. In so doing you are able to infer their feelings and intentions and to predict and influence their behavior. Calling it a theory can be a little misleading, since the word “theory” is normally used to refer to an intellectual system of statements and predictions, rather than in this sense, where it refers to an innate, intuitive mental faculty. But that is the term my field uses, so that is the term I will use here. Most people do not appreciate just how complex and, frankly, miraculous it is that they possess a theory of mind. It seems as natural, as immediate, and as simple as looking and seeing. But as we saw in Chapter 2, the ability to see is actually a very complicated process that engages a widespread network of brain regions. Our species’ highly sophisticated theory of mind is one of the most unique and powerful faculties of the human brain.
Our theory-of-mind ability apparently does not rely on our general intelligence—the rational intelligence you use to reason, to draw inferences, to combine facts, and so forth—but on a specialized set of brain mechanisms that evolved to endow us with our equally important degree of social intelligence. The idea that there might be specialized circuitry for social cognition was first suggested by psychologist Nick Humphrey and primatologist David Premack in the 1970s, and it now has a great deal of empirical support. So Frith’s hunch about autism and theory of mind was compelling: Perhaps autistic children’s profound deficits in social interactions stem from their theory-of-mind circuitry being somehow compromised. This idea is undoubtedly on the right track, but if you think about it, saying that autistic children cannot interact socially because they have a deficient theory of mind doesn’t go very far beyond restating the observed symptoms. It’s a good starting point, but what is really needed is to identify brain systems whose known functions match those that are deranged in autism.
Many brain-imaging studies have been conducted on children with autism, some pioneered by Eric Courchesne. It has been noted, for example, that children with autism have larger brains with enlarged ventricles (cavities in the brain). The same group of researchers has also noted striking changes in the cerebellum. These are intriguing observations that will surely have to be accounted for when we have a clearer understanding of autism. But they do not explain the symptoms that characterize the disorder. In children with damage to the cerebellum due to other organic diseases, one sees very characteristic symptoms, such as intention tremor (when the patient attempts to touch his nose, the hand begins to oscillate wildly), nystagmus (jerky eye movements), and ataxia (swaggering gait). None of these symptoms are typical of autism. Conversely, symptoms typical of autism (such as lack of empathy and social skills) are never seen in cerebellar disease. One reason for this might be that the cerebellar changes observed in autistic children may be the unrelated side effects of abnormal genes whose other effects are the true causes of autism. If so, what might these other effects be? What’s needed, if we wish to explain autism, is candidate neural structures in the brain whose specific functions precisely match the particular symptoms that are unique to autism.
The clue comes from mirror neurons. In the late 1990s it occurred to my colleagues and me that these neurons provided precisely the candidate neural mechanism we were looking for. You can refer back to the previous chapter if you want a refresher, but suffice it to say, the discovery of mirror neurons was significant because they are essentially a network of mind-reading cells within the brain. They provided the missing physiological basis for certain high-level abilities that had long been challenging for neuroscientists to explain. We were struck by the fact that it is precisely these presumed functions of mirror neurons—such as empathy, intention-reading, mimicry, pretend play, and language learning—that are dysfunctional in autism.1 (All of these activities require adopting the other’s point of view—even if the other is imaginary—as in pretend play or enjoying action figures.) You can make two columns side by side, one for the known characteristics of mirror neurons and one for the clinical symptoms of autism, and there is an almost precise match. It seemed reasonable, therefore, to suggest that the main cause of autism is a dysfunctional mirror-neuron system. The hypothesis has the advantage of explaining many seemingly unrelated symptoms in terms of a single cause.
It might seem quixotic to suppose that there could be a single cause behind such a complex disorder, but we have to bear in mind that multiple effects do not necessarily imply multiple causes. Consider diabetes. Its manifestations are numerous and varied: polyuria (excessive urination), polydypsia (incessant thirst), polyphagia (increased appetite), weight loss, kidney disorders, ocular changes, nerve damage, gangrene, plus quite a few others. But underlying this miscellany is something relatively simple: either insulin deficiency or fewer insulin receptors on cell surfaces. Of course the disease is not simple at all. There are a lot of complex ins and outs; there are numerous environmental, genetic, and behavioral effects in play. But in the big picture, it comes down to insulin or insulin receptors. Analogously, our suggestion was that in the big picture the main cause of autism is a disturbed mirror-neuron system.
ANDREW WHITTEN’S GROUP in Scotland made this proposal at about the same time ours did, but the first experimental evidence for it came from our lab working in collaboration with researchers Eric Altschuler and Jaime Pineda here at UC San Diego. We needed a way to eavesdrop on mirror-neuron activity noninvasively, without opening the children’s skulls and inserting electrodes. Fortunately, we found there was an easy way to do this using EEG (electroencephalography), which uses a grid of electrodes placed on the scalp to pick up brain waves. Long before CT scans and MRIs, EEG was the very first brain-imaging technology invented by humans. It was pioneered in the early twentieth century, and has been in clinical use since the 1940s. As the brain hums along in various states—awake, asleep, alert, drowsy, daydreaming, focused, and so on—it generates tell-tale patterns of electrical brain waves at different frequencies. It had been known for over half a century that, as mentioned in Chapter 4, one particular brain wave, the mu wave, is suppressed anytime a person makes a volitional movement, even a simple movement like opening and closing the fingers. It was subsequently discovered that mu-wave suppression also occurs when a person watches another person performing the same movement. We therefore suggested that mu-wave suppression might provide a simple, inexpensive, and noninvasive probe for monitoring mirror-neuron activity.
We ran a pilot experiment with a medium-functioning autistic child, Justin, to see if it would work. (Very young low-functioning children did not participate in this pilot study as we wanted to confirm that any difference between normal and autistic mirror-neuron activity that we found was not due to problems in attention, understanding instructions, or a general effect of mental retardation.) Justin had been referred to us by a local support group created to promote the welfare of local children with autism. Like Steven, he displayed many of the characteristic symptoms of autism but was able to follow simple instructions such as “look at the screen” and was not reluctant to have electrodes placed on his scalp.
As in normal children, Justin exhibited robust a mu wave while he sat around idly, and the mu wave was suppressed whenever we asked him to make simple voluntary movements. But remarkably, when he watched someone else perform the action, the suppression did not occur as it ought to. This observation provided a striking vindication of our hypothesis. We concluded that the child’s motor-command system was intact—he could, after all, open doors, eat potato chips, draw pictures, climb stairs, and so on—but his mirror-neuron system was deficient. We presented this single-subject case study at the 2000 annual meeting of the Society for Neuroscience, and we followed it up with ten additional children in 2004. Our results were identical. This observation has since received extensive confirmation over the years from many different groups, using a variety of techniques.2
For example, a group of researchers led by Riitta Hari at the Aalto University of Science and Technology corroborated our conjecture using MEG (magnetoencephalography), which is to EEG what jets are to biplanes. More recently, Michele Villalobos and her colleagues at San Diego State University used fMRI to show a reduction in functional connectivity between the visual cortex and the prefrontal mirror-neuron region in autistic patients.
Other researchers have tested our hypothesis using TMS (transcranial magnetic stimulation). TMS is, in one sense, the opposite of EEG: Rather than passively eavesdropping on the electrical signals emanating from the brain, TMS creates electrical currents in the brain using a powerful magnet held over the scalp. Thus with TMS you can induce neural activity artificially in any brain region that happens to be near the scalp. (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 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
THE MIRROR-NEURON HYPOTHESIS does a good job of accounting for the defining features of autism: lack of empathy, pretend play, imitation, and a theory of mind.4 However, it is not a complete account, because there are some other common (though not defining) symptoms of autism that mirror neurons do not have any apparent bearing on. For example, some autistics display a rocking to-and-fro movement, avoid eye contact, show hypersensitivity and aversion to certain sounds, and often engage in tactile self-stimulation—sometimes even beating themselves—which seems intended to dampen this hypersensitivity. These symptoms are common enough that they too need to be explained in any full account of autism. Perhaps beating themselves is a way of enhancing the salience of the body, thereby helping anchor the self and reaffirming its existence. But can we put this idea in the context of the rest of what we have said so far about autism?
In the early 1990s our group (in collaboration with Bill Hirstein, my postdoctoral colleague; and Portia Iversen, cofounder of Cure Autism Now, an organization devoted to autism) thought a lot about how to account for these other symptoms of autism. We came up with what we called the “salience landscape theory”: When a person looks at the world, she is confronted with a potentially bewildering sensory overload. As we saw in Chapter 2 when we considered the two branches of the “what” stream in the visual cortex, information about the world is first discriminated in the brain’s sensory areas and then relayed to the amygdala. As the gateway to the emotional core of your brain, the amygdala performs an emotional surveillance of the world you inhabit, gauges the emotional significance of everything you see, and decides whether it is trivial and humdrum or something worth getting emotional over. If the latter, the amygdala tells the hypothalamus to activate the autonomic nervous system in proportion to the arousal worthiness of the triggering sight—it could be anything from mildly interesting to downright terrifying. Thus the amygdala is able to create a “salience landscape” of your world, with hills and valleys corresponding to high and low salience.
It is sometimes possible for this circuit to go haywire. Your autonomic response to something arousing manifests as increased sweating, heart rate, muscular readiness, and so on, to prepare your body for action. In extreme cases this surge of physiological arousal can feed back into your brain and prompt your amygdala to say, in effect, “Wow, it’s even more dangerous than I thought. We’ll need more arousal to get out of this!” The result is an autonomic blitzkrieg. Many adults are prone to such panic attacks, but most of us, most of the time, are not in danger of getting swept away by such autonomic maelstroms.
With all this in mind, our group explored the possibility that children with autism have a distorted salience landscape. This may be partially due to indiscriminately enhanced (or reduced) connections between sensory cortices and the amygdala, and possibly between limbic structures and the frontal lobes. As a result of these abnormal connections, every trivial event or object sets off an uncontrollable autonomic storm, which would explain autistics’ preference for sameness and routine. If the emotional arousal is less florid, on the other hand, the child might attach abnormally high significance to certain unusual stimuli, which could account for their strange preoccupations, including their sometimes savant-like skills. Conversely, if some of the connections from the sensory cortex to the amygdala are partially effaced by the distortions in salience landscape, the child might ignore things, like eyes, that most normal children find highly attention grabbing.
To test the salience landscape hypothesis we measured galvanic skin response (GSR) in a group of 37 autistic and 25 normal children. The normal children showed arousal for certain categories of stimuli as expected but not for others. For example, they had GSR responses to photos of parents but not of pencils. The children with autism, on the other hand, showed a more generally heightened autonomic arousal that was further amplified by the most trivial objects and events, whereas some highly salient stimuli such as eyes were completely ineffective.
If salience landscape theory is on the right track, one would expect to find abnormalities in visual pathway 3 of autistic brains. Pathway 3 not only projects to the amygdala, but it routes through the superior temporal sulcus, which—along with its neighboring region, the insula—is rich in mirror neurons. In the insula, mirror neurons have been shown to be involved in perceiving as well as expressing certain emotions—like disgust, including social and moral disgust—in an empathetic manner. Thus damage to these areas, or perhaps a deficiency of mirror neurons within them, might not only distort the salience landscape, but also diminish empathy, social interaction, imitation, and pretend play.
As an added bonus, salience landscape theory may also explain two other quirky aspects of autism that have always been puzzling. First, some parents report that their child’s autistic symptoms are temporarily relieved by a bout of high fever. Fever is ordinarily caused by certain bacterial toxins that act on temperature-regulating mechanisms in the hypothalamus in the base of your brain. Again, this is part of pathway 3. I realized that it may not be coincidental that certain dysfunctional behaviors such as tantrums originate in networks that neighbor the hypothalamus. Thus the fever might have a “spillover” effect that happens to dampen activity at one of the bottlenecks of the feedback loop that generates those autonomic-arousal storms and their associated tantrums. This is a highly speculative explanation but it’s better than none at all, and if it pans out it could provide another basis for intervention. For example, there might be some way to safely dampen the feedback loop artificially. A damped circuit might be better than a malfunctioning one, especially if it could get a kid like Steven to engage even just a little bit more with his mother. For example, one could give him high fever harmlessly by injecting denatured malarial parasites; repeated injections of such pyrogens (fever-inducing substances) might help “reset” the circuit and alleviate symptoms permanently.
Second, children with autism often repeatedly bang and beat themselves. This behavior is called somatic self-stimulation. In terms of our theory, we would suggest that this leads to a damping of the autonomic-arousal storms that the child suffers from. Indeed, our research team has found that such self-stimulation not only has a calming effect but leads to a measurable reduction in GSR. This suggests a possible symptomatic therapy for autism: One could have a portable device for monitoring GSR that then feeds back to a body stimulation device which the child wears under his clothing. Whether such a device would prove practical in a day-to-day setting remains to be seen; it is being tested by my postdoctoral colleague Bill Hirstein.
The to-and-fro rocking behavior of some autistic children may serve a similar purpose. We know it likely stimulates the vestibular system (sense of balance), and we know that balance-related information splits at some point to travel down pathway 3, especially to the insula. Thus repetitive rocking might provide the same kind of damping that self-beating does. More speculatively, it might help anchor the self in the body, providing coherence to an otherwise chaotic world, as I’ll describe in a moment.
Aside from possible mirror-neuron deficiency, what other factors might account for the distorted salience landscapes through which many autistic people seem to view the world? It is well documented that there are genetic predispositions to autism. But less well known is the fact that nearly a third of children with autism have had temporal lobe epilepsy (TLE) in infancy. (The proportion could be much higher if we include clinically undetected complex partial seizures.) In adults TLE manifests as florid emotional disturbances, but because their brains are fully mature, it does not appear to lead to deep-seated cognitive distortions. But less is known about what TLE does to a developing brain. TLE seizures are caused by repeated random volleys of nerve impulses coursing through the limbic system. If they occur frequently in a very young brain, they might lead, through a process of synapse enhancement called kindling, to selective but widespread, indiscriminate enhancement (or sometimes effacement) of the connections between the amygdala and the high-level visual, auditory, and somatosensory cortices. This could account both for the frequent false alarms set off by trivial or mundane sights and otherwise neutral sounds, and conversely for the failure to react to socially salient information, which are so characteristic of autism.
In more general terms, our sense of being an integrated, embodied self seems to depend crucially on back-and-forth, echo-like “reverberation” between the brain and the rest of the body—and indeed, thanks to empathy, between the self and others. Indiscriminate scramblings of the connections between high-level sensory areas and the amygdala, and the resulting distortions to one’s salience landscape, could as part of the same process cause a disturbing loss of this sense of embodiment—of being a distinct, autonomous self anchored in a body and embedded in a society. Perhaps somatic self-stimulation is some children’s attempt to regain their embodiment by reviving and enhancing body-brain interactions while at the same time damping spuriously amplified autonomic signals. A subtle balance of such interactions may be crucial for the normal development of an integrated self, something we ordinarily take for granted as the axiomatic foundation of being a person. No wonder, then, that this very sense of being a person is profoundly disturbed in autism.
We have so far considered two candidate theories for explaining the bizarre symptoms of autism: the mirror-neuron dysfunction hypothesis and the idea of a distorted salience landscape. The rationale for proposing these theories is to provide unitary mechanisms for the bewildering array of seemingly unrelated symptoms that characterize the disorder. Of course, the two hypotheses are not necessarily mutually exclusive. Indeed, there are known connections between the mirror-neuron system and the limbic system. It is possible that distortions in limbic-sensory connections are what lead ultimately to a deranged mirror-neuron system. Clearly, we need more experiments to resolve these issues. Whatever the underlying mechanisms turn out to be, our results strongly suggest that children with autism have a dysfunctional mirror-neuron system that may help explain many features of the syndrome. Whether this dysfunction is caused by genes concerned with brain development or by genes that predispose to certain viruses (that in turn might predispose to seizures), or is due to something else entirely remains to be seen. Meanwhile, it might provide a useful jumping off point for future research into autism, so that someday we may find a way to “bring Steven back.”
Autism reminds us that the uniquely human sense of self is not an “airy nothing” without “habitation and a name.” Despite its vehement tendency to assert its privacy and independence, the self actually emerges from a reciprocity of interactions with others and with the body it is embedded in. When it withdraws from society and retreats from its own body it barely exists; at least not in the sense of a mature self that defines our existence as human beings. Indeed, autism could be regarded fundamentally as a disorder of self-consciousness, and if so, research on this disorder may help us understand the nature of consciousness itself.
CHAPTER 6
The Power of Babble: The Evolution of Language
…Thoughtful men, once escaped from the blinding influences of traditional prejudice, will find in the lowly stock whence Man has sprung, the best evidence of the splendor of his capacities; and will discern in his long progress through the past, a reasonable ground of faith in his attainment of a nobler future.
—THOMAS HENRY HUXLEY
ON THE LONG FOURTH OF JULY WEEKEND OF 1999, I RECEIVED A phone call from John Hamdi, who had been a colleague of mine at Trinity College, Cambridge, nearly fifteen years earlier. We hadn’t been in contact and it was a pleasant surprise to hear his voice after such a long time. As we exchanged greetings, I smiled to myself, reminded of the many adventures we had shared during our student days. He was now a professor of orthopedic surgery in Bristol, he said. He had noticed a book I’d recently published.
“I know you are mainly involved in research these days,” he said, “but my father, who lives in La Jolla, has had a head injury from a skiing accident followed by a stroke. His right side is paralyzed, and I’d be grateful if you could take a look at him. I want to make sure he’s getting the best treatment available. I heard there’s a new rehab procedure which employs mirrors to help patients recover the use of a paralyzed arm. Do you know anything about this?”
A week later John’s father, Dr. Hamdi, was brought to my office by his wife. He had been a world-renowned professor of chemistry here at UC San Diego until his retirement three years earlier. About six months prior to my seeing him he sustained a skull fracture. In the emergency room at Scripps Clinic he was informed that a stroke, caused by a blood clot in his middle cerebral artery, had cut off the blood supply to the left hemisphere of his brain. Since the left hemisphere controls the right side of the body, Dr. Hamdi’s right arm and leg were paralyzed. Much more alarming than the paralysis, though, was the fact that he could no longer speak fluently. Even simple requests such as “I want water” required great effort, and we had to pay careful attention to understand what he was saying.
Assisting me in examining Dr. Hamdi was Jason Alexander, a medical student on a six-month rotation in our lab. Jason and I looked at Dr. Hamdi’s charts and also obtained a medical history from Mrs. Hamdi. We then conducted a routine neurological workup, testing in sequence his motor functions, sensory functions, reflexes, cranial nerves, and his higher mental functions such as memory, language, and intelligence. I took the handle of my knee hammer and, while Dr. Hamdi was lying in bed, stroked the outer border of his right foot and then the left foot, running the tip of the hammer handle from the pinky to sole. Nothing much happened in the normal foot, but when I repeated the procedure on the paralyzed right foot, the big toe instantly curled upward and all the other toes fanned out. This is Babinski’s sign, arguably the most famous sign in neurology. It reliably indicates damage to the pyramidal tracts, the great motor pathway that descends from the motor cortex down into the spinal cord conveying commands for volitional movements.
“Why does the toe go up?” asked Jason.
“We don’t know,” I said, “but one possibility is that it’s a throwback to an early stage in evolutionary history. The reflexive withdrawal tendency for the toes to fan out and curl up is seen in lower mammals. But the pyramidal tracts in primates become especially pronounced, and they inhibit this primitive reflex. Primates have a more sophisticated grasp reflex, with a tendency for the toes to curl inward as if to clutch a branch. It may be a reflex to avoid falling out of trees.”
“Sounds far-fetched,” said Jason skeptically.
“But when the pyramidal tracts are damaged,” I said, ignoring his remark, “the grasp reflex goes away and the more primitive withdrawal reflex emerges because it’s no longer inhibited. That’s why you also see it in infants; their pyramidal tracts haven’t fully developed yet.”
FIGURE 6.1 The two main language areas in the brain are Broca’s area (in the frontal lobes) and Wernicke’s area (in the temporal lobes). The two are connected by a band of fibers called the arcuate fasciculus. Another language area, the angular gyrus (not labeled in this figure), lies near the bottom of the parietal lobe, at the intersection of temporal, occipital, and parietal lobes.
The paralysis was bad enough, but Dr. Hamdi was more troubled by his speech impediment. He had developed a language deficit called Broca’s aphasia, named after the French neurologist Paul Broca, who first described the syndrome in 1865. The damage is usually in the left frontal lobe in a region (Figure 6.1) that lies just in front of the large fissure, or vertical furrow, that separates the parietal and frontal lobes.
Like most patients with this disorder, Dr. Hamdi could convey the general sense of what he was trying to say, but his speech was slow and effortful, conveyed in a flat monotone, filled with pauses, and almost completely devoid of syntax (loosely speaking, grammatical structure). His utterances were also deficient in (though not devoid of) so-called function words such as “and,” “but,” and “if,” which don’t refer to anything in the world but specify relationships between different parts of a sentence.
“Dr. Hamdi, tell me about your skiing accident,” I said.
“Ummmmm…Jackson, Wyoming,” he began. “And skied down and ummmmm…tumbled, all right, gloves, mittens, uhhhh…poles, uhhhh…the uhhhh…but the blood drained three days pass hospital and ummmmm…coma…ten days…switch to Sharpe [memorial hospital]…mmmmm…four months and back…ummmmmmm…it’s ummmmm slow process and a bit of medicine ummmmm…six medicines. One tried eight or nine months.”
“Okay continue.”
“And seizures.”
“Oh? Where was the blood hemorrhage from?”
Dr. Hamdi pointed to the side of his neck.
“The carotid?”
“Yeah. Yeah. But…uhhhh, uhhh, uhhh, this, this and this, this…” he said, using his left hand to point to multiple places on his right leg and arm.
“Go on,” I said, “Tell us more.”
“It’s ummmmm…it’s difficult [referring to his paralysis], ummm, left side perfectly okay.”
“Are you right-handed or left-handed?”
“Right-handed.”
“Can you write with the left now?”
“Yeah.”
“Okay. Good. What about word processing?”
“Processing ummmm write.”
“But when you write, is it slow?”
“Yeah.”
“Just like your speech?”
“Right.”
“When people talk fast you have no problem understanding them?”
“Yeah, yeah.”
“You can understand.”
“Right.”
“Very good.”
“Uhhhhhh…but uhhhh…the speech, uhhhhh, ummmmm slowed down.”
“Okay, do you think your speech is slowed down, or your thought is slowed down?”
“Okay. But ummmm [points to head] uhhh…words are beautiful. Ummmmm speech…”
He then made twisting motions with his mouth. Presumably he meant that his flow of thought felt intact, but the words were not coming out fluently.
“Supposing I ask you a question,” I said. “Mary and Joe together have eighteen apples.”
“All right.”
“Joe has twice as many apples as Mary.”
“Okay.”
“So how many does Mary have? How many does Joe have?”
“Ummmmm…lemme think. Oh God.”
“Mary and Joe together have eighteen apples…”
“Six, ahhhh twelve!” he blurted.
“Excellent!”
So Dr. Hamdi had basic conceptual algebra, was able to do simple arithmetic, and had good comprehension of language even for relatively complex sentences. I was told he had been a superb mathematician before his accident. Yet later, when Jason and I tested Dr. Hamdi on more complex algebra using symbols, he kept trying hard but failing. I was intrigued by the possibility that the Broca’s area might be specialized not just for the syntax, or syntactic structure, of natural language, but also for other, more arbitrary languages that have formal rules, such as algebra or computer programming. Even though the area might have evolved for natural language, it may have the latent capacity for other functions that bear a certain resemblance to the rules of syntax.
What do I mean by “syntax”? To understand Dr. Hamdi’s main problem, consider a routine sentence such as “I lent the book you gave me to Mary.” Here an entire noun phrase—“the book you gave me”—is embedded in a larger sentence. That embedding process, called recursion, is facilitated by function words and is made possible by a number of unconscious rules—rules that all languages follow, no matter how different they may seem on the surface. Recursion can be repeated any number of times to make a sentence as complex as it needs to be in order to convey its ideas. With each recursion, the sentence adds a new branch to its phrase structure. Our example sentence can be expanded, for instance, to “I lent the book you gave me while I was in the hospital to Mary,” and from there to “I lent the book you gave me while I was in the hospital to a nice woman I met there named Mary,” and so on. Syntax allows us to create sentences as complex as our short-term memory can handle. Of course, if we go on too long, it can get silly or start to feel like a game, as in the old English nursery rhyme:
This is the man all tattered and torn
That kissed the maiden all forlorn
That milked the cow with the crumpled horn
That tossed the dog that worried the cat
That killed the rat that ate the malt
That lay in the house that Jack built.
Now, before we go on discussing language, we need to ask how we can be sure Dr. Hamdi’s problem was really a disorder of language at this abstract level and not something more mundane. You might think, reasonably, that the stroke had damaged the parts of his cortex that control his lips, tongue, palate, and other small muscles required for the execution of speech. Because talking required such effort, he was economizing on words. The telegraphic nature of his speech may have been to save effort. But I did some simple tests to show Jason that this couldn’t be the reason.
“Dr. Hamdi, can you write down on this pad the reason why you went to the hospital? What happened?”
Dr. Hamdi understood our request and proceeded to write, using his left hand, a long paragraph about the circumstances that brought him to our hospital. Although the handwriting wasn’t good, the paragraph made sense. We could understand what he had written. Yet remarkably, his writing also had poor grammatical structure. Too few “ands,” “ifs,” and “buts.” If his problem were related to speech muscles, why did his writing also have the same abnormal form as his speech? After all, there was nothing wrong with his left hand.
I then asked Dr. Hamdi to sing “Happy Birthday.” He sang it effortlessly. Not only could he carry the tune well, but all the words were there and correctly pronounced. This was in stark contrast to his speech, which, in addition to missing important connecting words and lacking phrase structure, also contained mispronounced words and lacked the intonation, rhythm, and the melodious flow of normal speech. If his problem were poor control of his vocal apparatus, he shouldn’t have been able to sing, either. To this day we don’t know why Broca’s patients can sing. One possibility is that language function is based mainly in the left hemisphere, which is damaged in these patients, whereas singing is done by the right hemisphere.
We had already learned a great deal after just a few minutes of testing. Dr. Hamdi’s problems with expressing himself were not caused by a partial paralysis or weakness of his mouth and tongue. He had a disorder of language, not of speech, and the two are radically different. A parrot can talk—it has speech, you might say—but it doesn’t have language.
HUMAN LANGUAGE SEEMS so complex, multidimensional, and richly evocative that one is tempted to think that almost the entire brain, or large chunks of it at least, must be involved. After all, even the utterance of a single word like “rose” evokes a whole host of associations and emotions: the first rose you ever got, the fragrance, rose gardens you were promised, rosy lips and cheeks, thorns, rose-colored glasses, and so on. Doesn’t this imply that many far-flung regions of the brain must cooperate to generate the concept of a rose? Surely the word is just the handle, or focus, around which swirls a halo of associations, meanings, and memories.
There’s probably some truth to this, but the evidence from aphasics such as Dr. Hamdi suggests the very opposite—that the brain has neural circuits specialized for language. Indeed, it may even be that separate components or stages of language processing are dealt with by different parts of the brain, although we should really think of them as parts of one large interconnected system. We are accustomed to thinking of language as a single function, but this is an illusion. Vision feels like a unitary faculty to us as well, yet as noted in Chapter 2, seeing relies on numerous quasi-independent areas. Language is similar. A sentence, loosely speaking, has three distinct components, which are normally so closely interwoven that they don’t feel separate. First, there are the building blocks we call words (lexicon) that denote objects, actions, and events. Second, there is the actual meaning (semantics) conveyed by the sentence. And third, there is syntactic structure (loosely speaking, grammar), which involves the use of function words and recursion. The rules of syntax generate the complex hierarchical phrase structure of human language, which at its core allows the unambiguous communication of fine nuances of meaning and intention.
Human beings are the only creatures to have true language. Even chimps, who can be trained to sign simple sentences like “Give me fruit,” can’t come close to complex sentences such as “It’s true that Joe is the big alpha male, but he’s starting to get old and lazy, so don’t worry about what he might do unless he seems to be in an especially nasty mood.” The seemingly infinite flexibility and open-endedness of our language is one of the hallmarks of the human species. In ordinary speech, meaning and syntactic structure are so closely intertwined that it’s hard to believe that they are really distinct. But you can have a perfectly grammatical sentence that is meaningless gibberish, as in the linguist Noam Chomsky’s famous example, “Colorless green ideas sleep furiously.” Conversely, a meaningful idea can be conveyed adequately by a nongrammatical sentence, as Dr. Hamdi has shown us. (“It’s difficult, ummm, left side perfectly okay.”)
It turns out that different parts of the brain are specialized for these three different aspects of language: lexicon, semantics, and syntax. But the agreement among researchers ends there. The degree of specialization is hotly debated. Language, more than any other topic, tends to polarize academics. I don’t quite know why, but fortunately it isn’t my field. In any case, by most accounts Broca’s area seems mainly concerned with syntactic structure. So Dr. Hamdi had no better chance than a chimp of generating long sentences full of hypotheticals and subordinate clauses. Yet he had no difficulty in communicating his ideas by just stringing words together in approximately the right order, like Tarzan. (Or surfer dudes in California.)
One reason for thinking that Broca’s area is specialized exclusively for syntactic structure is the observation that it seems to have a life of its own, quite independent of the meaning conveyed. It’s almost as though this patch of cortex has an autonomous set of grammatical rules that are intrinsic to its networks. Some of them seem quite arbitrary and apparently nonfunctional, which is the main reason linguists assert its independence from semantics and meaning and dislike thinking of it as having evolved from anything else in the brain. The extreme view is exemplified by Chomsky, who believes that it didn’t even evolve through natural selection!
The brain region concerned with semantics is located in the left temporal lobe near the back of the great horizontal cleft in the middle of the brain (see Figure 6.1). This region, called Wernicke’s area, appears to be specialized for the representation of meaning. Dr. Hamdi’s Wernicke’s area was obviously intact. He could still comprehend what was said to him and could convey some semblance of meaning in his conversations. Conversely, Wernicke’s aphasia—what you get if your Wernicke’s area is damaged but your Broca’s area remains intact—is in a sense the mirror image of Broca’s aphasia: The patient can fluently generate elaborate, smoothly articulated, grammatically flawless sentences, but it’s all meaningless gibberish. At least that’s the official party line, but later I’ll provide evidence that this isn’t entirely true.
THESE BASIC FACTS about the major language-related brain areas have been known for more than a century. But many questions remain. How complete is the specialization? How does the neural circuitry within each area actually do its job? How autonomous are these areas, and how do they interact to generate smoothly articulated, meaningful sentences? How does language interact with thought? Does language enable us to think, or does thinking enable us to talk? Can we think in a sophisticated manner without silent internal speech? And lastly, how did this extraordinarily complex, multicomponent system originally come into existence in our hominin ancestors?
This last question is the most vexing. Our journey into full-blown humanity began with nothing but the primitive growls, grunts, and groans available to our primate cousins. By 75,000 to 150,000 years ago, the human brain was brimming with complex thoughts and linguistic skills. How did this happen? Clearly, there must have been a transitional phase, yet it’s hard to imagine how linguistic brain structures of intermediate complexity might have worked, or what functions they might have served along the way. The transitional phase must have been at least partially functional; otherwise it couldn’t have been selected for, nor served as an evolutionary bridge for the eventual emergence of more sophisticated language functions.
To understand what this bridge might have been is the main purpose of this chapter. I should point out that by “language” I don’t mean just “communication.” We often use the two words interchangeably, but in fact they are very different. Consider the vervet monkey. Vervets have three alarm calls to alert each other about predators. The call for leopard prompts the troupe to bolt for the nearest trees. The call for serpent causes the monkeys to stand up on two legs and peer down into the grass. And when vervets hear the eagle call, they look up into the air and seek shelter in the underbrush. It’s tempting to conclude that these calls are like words, or at least the precursors to words, and that the monkey does have a primitive vocabulary of sorts. But do the monkeys really know there’s a leopard, or do they just rush for the nearest tree reflexively when an alarm call is sounded? Or perhaps the call really just means “climb” or “there’s danger on the ground,” rather than the much richer concept of leopard that a human brain harbors. This example tells us that mere communication isn’t language. Like an air-raid siren or a fire alarm, vervets’ cries are generalized alerts that refer to specific situations; they are almost nothing like words.
In fact, we can list a set of five characteristics that make human language unique and radically different from other types of communication we see in vervets or dolphins:
1. Our vocabulary (lexicon) is enormous. By the time a child is eight years old, she has almost six hundred words at her disposal—a figure that vastly exceeds the nearest runner-up, the vervet monkey, by two orders of magnitude. One could argue, though, that this is really a matter of degree than a qualitative jump; maybe we just have much better memories.
2. More important than the sheer size of our lexicon is the fact that only humans have function words that exist exclusively in the context of language. While words like “dog,” “night,” or “naughty” refer to actual things or events, function words have no existence independent of their linguistic function. So even though a sentence such as “If gulmpuk is buga, then gadul will be too” is meaningless, we do understand the conditional nature of the statement because of the conventional usage of “if” and “then.”
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