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

Perhaps science will eventually stumble on some unexpected method or framework for dealing with qualia empirically and rationally, but such advances could easily be as remote from our present-day grasp as molecular genetics was to those living in the Middle Ages. Unless there is a potential Einstein of neurology lurking around somewhere.

I suggested that qualia and self are different. Yet you can’t solve the former without the latter. The notion of qualia without a self experiencing/introspecting on them is an oxymoron. In similar vein Freud had argued that we cannot equate the self with consciousness. Our mental life, he said, is governed by the unconscious, a roiling cauldron of memories, associations, reflexes, motives, and drives. Your “conscious life” is an elaborate after-the-fact rationalization of things you really do for other reasons. Because technology had not yet advanced sufficiently to allow observation of the brain, Freud lacked the tools to take his ideas beyond the couch, and so his theories were caught in the doldrums between true science and untethered rhetoric.³

Might Freud have been right? Could most of what constitutes our “self” be unconscious, uncontrollable, and unknowable?⁴ Despite Freud’s current unpopularity (to put it mildly), modern neuroscience has in fact revealed that he was right in arguing that only a limited part of the brain is conscious. The conscious self is not some sort of “kernel” or concentrated essence that inhabits a special throne at the center the neural labyrinth, but neither is it a property of the whole brain. Instead, the self seems to emerge from a relatively small cluster of brain areas that are linked into an amazingly powerful network. Identifying these regions is important since it helps narrow the search. We know, after all, that the liver and the spleen are not conscious; only the brain is. We are simply taking a step further and saying that only some parts of the brain are conscious. Knowing which parts are and what they are doing is the first step toward understanding consciousness.

The phenomenon of blindsight is a particularly clear indicator that there may be a grain of truth in Freud’s theory of the unconscious. Recall from Chapter 2 that someone with blindsight has damage to the V1 area in the visual cortex, and as a result cannot see anything. She is blind. She experiences none of the qualia associated with vision. If you project a spot of light on the wall in front of her, she will tell you categorically that she does not see anything. Yet if asked to reach out to touch the spot, she can do so with uncanny accuracy even though to her it feels like a wild guess. She is able to do this, as we saw earlier, because the old pathway between her retina and her parietal lobe is intact. So even though she can’t see the spot, she can still reach out and touch it. Indeed, a blindsight patient can often even guess the color and orientation of a line (vertical or horizontal) using this pathway even though she cannot perceive it consciously.

This is astonishing. It implies that only the information streaming through your visual cortex is associated with consciousness and linked to your sense of self. The other parallel pathway can go about its business performing the complex computations required for hand guidance (or even correctly guessing color) without consciousness ever coming into the picture. Why? These two paths for visual information are made up of identical-looking neurons, after all, and they seem to be performing equally complex computations, yet only the new pathway casts the light of consciousness on visual information. What’s so special about these circuits that they “require” or “generate” consciousness? In other words, why aren’t all aspects of vision and vision-guided behavior similar to blindsight, chugging along with competence and accuracy but without conscious awareness and qualia? Might the answer to this question give clues to solving the riddle of consciousness?

The example of blindsight is suggestive not only because it supports the idea of the unconscious mind (or several unconscious minds). It also demonstrates how neuroscience can marshal evidence about the innermost workings of the brain in order to make its way through the cold-case file, so to speak, addressing some of the unanswered questions about the self that have plagued philosophers and scientists for millennia. By studying patients who have disturbances in self-representation and observing how specific brain areas malfunction, we can better understand how a sense of self arises in the normal human brain. Each disorder becomes a window on a specific aspect of the self.

First, let’s define these aspects of the self, or at the very least, our intuitions about them.

1. Unity: Despite the teeming diversity of sensory experiences that you are deluged with moment to moment, you feel like one person. Moreover, all of your various (and sometimes contradictory) goals, memories, emotions, actions, beliefs, and present awareness seem to cohere to form a single individual.

2. Continuity: Despite the enormous number of distinct events punctuating your life, you feel a sense of continuity of identity through time—moment to moment, decade to decade. And as Endel Tulving has noted, you can engage in mental “time travel,” starting from early childhood and projecting yourself into the future, sliding to and fro effortlessly. This Proustian virtuosity is unique to humans.

3. Embodiment: You feel anchored and at home in your body. It never occurs to you that the hand you just used to pick up your car keys might not belong to you. Nor would you think you’re in any danger of believing the arm of a waiter or a cashier is in fact your own arm. However, scratch the surface and it turns out your sense of embodiment is surprisingly fallible and flexible. Believe it or not, you can be optically tricked into temporarily leaving your body and experiencing yourself in another location. (This happens to some extent when you view a live, real-time video of yourself or stand in a carnival hall of mirrors.) By wearing heavy makeup to disguise yourself and looking at your own video image (which doesn’t have to do a left-right reversal like a mirror), you can get an inkling of an out-of-body experience, especially if you move various body parts and change your expression. Furthermore, as we saw in Chapter 1, your body image is highly malleable; it can be altered in position and size using mirrors. And as we will see later in this chapter, it can be profoundly disturbed in disease.

4. Privacy: Your qualia and mental life are your own, unobservable by others. You can empathize with your neighbor’s pain thanks to mirror neurons, but you can’t literally experience his pain. Yet, as we noted in Chapter 4, there are circumstances under which your brain generates touch sensations that precisely simulate the sensations being experienced by another individual. For instance, if I anesthetize your arm and have you watch me touch my own arm, you begin to feel my touch sensations. So much for the privacy of self.

5. Social embedding: The self maintains an arrogant sense of privacy and autonomy that belies how closely it is linked to other brains. Can it be coincidental that almost all of our emotions make sense only in relation to other people? Pride, arrogance, vanity, ambition, love, fear, mercy, jealousy, anger, hubris, humility, pity, even self-pity—none of these would have any meaning in a social vacuum. It makes perfect evolutionary sense to feel grudges, gratitude, or bonhomie, for example, toward other people based on your shared interpersonal histories. You take intent into account and attribute the faculty of choice, or free will, to fellow social beings and apply your rich palette of social emotions to their actions on that basis. But we are so deeply hardwired for imputing things such as motive, intent, and culpability to the actions of others that we often overextend our social emotions to nonhuman, nonsocial objects, or situations. You can get “angry” with the tree branch that fell on you, or even with the freeways or the stock market. It is worth noting that this is one of the major roots of religion: We tend to imbue nature itself with human-like motives, desire, and will, and hence we feel compelled to supplicate, pray to, bargain with, and look for reasons why God or karma or what have you has seen fit to punish us (individually or collectively) with natural disasters or other hardships. This persistent drive reveals just how much the self needs to feel part of a social environment that it can interact with and understand on its own terms.

6. Free will: You have a sense of being able to consciously choose between alternative courses of action with the full knowledge that you could have chosen otherwise. You normally don’t feel like an automaton or as though your mind is a passive thing buffeted by chance and circumstance—although in some “diseases” such as romantic love, you come close. We don’t yet know how free will works, but, as we shall see later in the chapter, at least two brain regions are crucially involved. The first is the supramarginal gyrus on the left side of the brain, which allows you to conjure up and envisage different potential courses of action. The second is the anterior cingulate, which makes you desire (and helps you choose) one action based on a hierarchy of values dictated by the prefrontal cortex.

7. Self-awareness: This aspect of the self is almost axiomatic; a self that is not aware of itself is an oxymoron. Later in this chapter I will argue that your self-awareness might partly depend on your brain using mirror neurons recursively, allowing you to see yourself from another person’s (allocentric) viewpoint. Hence the use of terms like “self-conscious” (embarrassed), when what you really mean is being conscious of someone else being conscious of you.

These seven aspects, like the legs of a table, work together to hold up what we call the self. However, as you can already see, they are vulnerable to illusions, delusions, and disorders. The table of the self can continue to stand without one of these legs, but if too many are lost then its stability becomes severely compromised.

How did these multiple attributes of self emerge in evolution? What parts of the brain are involved, and what are the underlying neural mechanisms? There are no simple answers to these questions—certainly nothing to rival the simplicity of a statement like “because that is how God made us”—but just because the answers are complicated and counterintuitive is no reason to give up the quest. By exploring several syndromes that straddle the boundary between psychiatry and neurology, I believe we can glean invaluable clues to how the self is created and sustained in normal brains. In this regard my approach is similar to that used elsewhere in the book: considering odd cases to illuminate normal function.⁵ I do not claim to have “solved” the problem of self (I wish!), but I believe these cases provide very promising ways it can be approached. Overall, I think this is not a bad start for tackling a problem that is not even considered legitimate by many scientists.

Several points are worth noting before we examine particular cases. One is that despite the bizarreness of symptoms, each patient is relatively normal in other respects. A second is that each patient is completely sincere and confident in his belief and this belief is immune from intellectual correction (just like persistent superstitions in otherwise rational people). A patient with panic attacks might agree with you intellectually that his forebodings of doom are not “real,” but during the attack itself, nothing will convince him that he isn’t dying.

One last caveat: We need to be careful when drawing insights from psychiatric syndromes because some of them (none, I hope, that I am examining here) are bogus. Take for example de Clérambault syndrome, which is defined as a young woman developing an obsessive delusion that a much older and famous man is madly in love with her but he is in denial about it. Google it if you don’t believe me. (Ironically there’s no name for the very real and common delusion in which an older gentleman believes that a young hottie is in love with him but doesn’t know it! One reason for this might be that the psychiatrists who “discover” and name syndromes have historically been men.)

Then there is Koro, the alleged disorder said to afflict Asian gentlemen who claim that their penis is shrinking and will eventually wither away. (Again the converse does exist in some elderly Caucasian men—the delusion that the penis is expanding—when it actually isn’t. This was pointed out to me by my colleague Stuart Anstis.) Koro is likely to have been fabricated by Western psychiatrists, though it is not inconceivable that it might arise from a reduced representation of the penis in the body-image center, the right superior parietal lobule.

And let’s not forget another notable invention, “oppositional defiant disorder.” This diagnosis is sometimes given to smart, spirited youngsters who dare to question the authority of older establishment figures, such as psychiatrists. (Believe it or not, this is a diagnosis for which a psychologist can actually bill the patient’s insurance company.) The person who concocted this syndrome, whoever he or she is, is brilliant, for any attempt by the patient to challenge or protest the diagnosis can itself be construed as evidence for its validity! Irrefutability is built into its very definition. Another pseudomalady, again officially recognized, is “chronic under-achievement syndrome”—what used to be called stupidity.

With these caveats in mind let us try to tackle the syndromes themselves and explore their relevance to the self and to human uniqueness.

Embodiment

We will begin with three disorders that allow us to examine the mechanisms involved in creating a sense of embodiment. These conditions reveal that the brain has an innate body image, and when that body image doesn’t match up with the sensory input from the body—whether visual or somatic—the ensuing disharmony can disrupt the self’s sense of unity as well.

APOTEMNOPHILIA: DOCTOR, REMOVE MY ARM PLEASE

Vital to the human sense of self is a person’s feeling of inhabiting his own body and owning his body parts. Although a cat has an implicit body image of sorts (it doesn’t try to squeeze into a rat hole), it can’t go on a diet seeing that it is obese or contemplate its paw and wish it weren’t there. Yet the latter is precisely what happens in some patients who develop apotemnophilia, a curious disorder in which a completely normal individual has an intense and ever-present desire to amputate an arm or a leg. (“Apotemnophila” derives from the Greek: apo, “away from” temnein, “to cut” and philia, “emotional attachment to.”) He may describe his body as being “overcomplete” or his arm as being “intrusive.” You get the feeling that the subject is trying to convey something ineffable. For instance he might say, “It’s not as if I feel it doesn’t belong to me, Doctor. On the contrary, it feels like it’s too present.” More than half the patients go on to actually have the limb removed.

Apotemnophilia is often viewed as being “psychological.” It has even been suggested that it arises from a Freudian wish-fulfillment fantasy, the stump resembling a large penis. Others have regarded the condition as attention-seeking behavior, although why the desire for attention should take this strange form and why so many of these people keep their desires secret for much of their lives is never explained.

Frankly, I find these psychological explanations unconvincing. The condition usually begins early in life, and it is unlikely that a ten-year-old would desire a giant penis (although an orthodox Freudian wouldn’t rule it out). Moreover, the subject can point to the specific line—say, two centimeters above the elbow—along which she desires amputation. It isn’t simply a vague desire to eliminate a limb, as one would expect from a psychodynamic account. Nor can it be a desire to attract attention, for if that were the case, why be so particular about where the cut should be made? Finally, the subject usually has no other psychological issues of any consequence.

There are also two other observations I made of these patients that strongly suggest a neurological origin for the condition. First, in more than two-thirds of cases the left limb is involved. This disproportionate involvement of the left arm reminds me of the decidedly neurological disorder of somatoparaphrenia (described later), in which the patient, who has a right-hemisphere stroke, not only denies the paralysis of his left arm but also insists that the arm doesn’t belong to him. This is rarely seen in those with left-hemisphere strokes. Second, my students Paul McGeoch and David Brang and I have found that touching the limb below the line of the desired amputation produces a big jolt in the patient’s GSR (galvanic skin response), but touching above the line or touching the other limb does not. The patient’s alarm bells really and truly go off when the affected limb is touched below the line. Since it’s hard to fake a GSR, we can be fairly sure of a neurological basis for the disorder.

How does one explain this strange disorder in terms of the known anatomy? As we saw in Chapter 1, nerves for touch, muscle, tendon, and joint sensation project to your primary (S1) and secondary (S2) somatosensory cortices in and just behind the postcentral gyrus. Each of these areas of the cortex contains a systematic, topographically organized map of bodily sensations. From there, somatosensory information gets sent to your superior parietal lobule (SPL), where it gets combined with balance information from your inner ear and visual feedback about the limbs’ positions. Together these inputs construct your body image: a unified, real-time representation of your physical self. This representation of the body in the SPL (and probably its connections with the posterior insula) is partly innate. We know this because some patients with arms missing from birth experience vivid phantom arms, implying the existence of scaffolding that is hardwired by genes.⁶ It doesn’t require a leap of faith to suggest that this multisensory body image is organized topographically in the SPL the same way it is in S1 and S2.

If a particular body part such as an arm or a leg failed to be represented in this hardwired scaffolding of your body image, the result could conceivably be a sense of strangeness or possibly revulsion toward it. But why? Why is the patient not merely indifferent to the limb? After all, patients with nerve damage to the arm resulting in a complete loss of sensation don’t say they want their arm removed.

The answer to this question lies in the key concept of mismatch aversion, which as you will see plays a crucial role in many forms of mental illness. The general idea is that lack of coherence, or mismatch, between the outputs of brain modules can create alienation, discomfort, delusion, or paranoia. The brain abhors internal anomalies—such as the mismatch between emotion and identification in Capgras syndrome—and will often go to absurd lengths to deny them or explain them away. (I emphasize “internal” because generally speaking, the brain is more tolerant of anomalies in the external world. It may even enjoy them: Some people love the thrill of solving baffling mysteries.) It isn’t clear where the internal mismatch is detected to create unpleasantness. I suggest it’s done by the insula (especially the insula in the right hemisphere), a small patch of tissue which receives signals from S2 and sends outputs to the amygdala, which in turn sends sympathetic arousal signals down to the rest of the body.

In the case of nerve damage, the input to S1 and S2 itself is lost, so there is no mismatch or discrepancy between S2 and the multisensory body image in the SPL. In apotemnophilia, by contrast, there is normal sensory input from the limb to the body maps in S1 and S2, but there is no “place” for the limb signals to output to in the SPL body image maintained by the SPL.⁷ The brain does not tolerate this mismatch well, and so this discrepancy is crucial for creating the feelings of “overpresence” and mild aversiveness of the limb, and the accompanying desire for amputation. This explanation of apotemnophilia would account for the heightened GSR and also the essentially ineffable and paradoxical nature of the experience: part of the body and not part of the body at the same time.

Consistent with this overall framework I have noticed that merely having the patient look at his affected limb through a minifying lens to optically shrink it makes the limb feel far less unpleasant, presumably by reducing the mismatch. Placebo-controlled experiments are needed to confirm this.

Finally, my lab conducted a brain-scanning study on four patients with apotemnophilia and compared the results with four normal control subjects. In the controls, touching any part of the body activated right SPL. In all four patients, touching the part of the limb each one wanted removed evoked no activity in the SPL—the brain’s map of the body didn’t light up, so to speak, on the scans. But touching the unaffected limb did. If we can replicate this finding with a larger number of patients, our theory will be well supported.

One curious aspect of apotemnophilia that is unexplained by our model is the associated sexual inclinations in some subjects: desire for intimacy with another amputee. These sexual overtones are probably what misled people to propose a Freudian view of the disorder.

Let me suggest something different. Perhaps one’s sexual “aesthetic preference” for certain body morphology is dictated in part by the shape of the body image as represented—and hardwired—in the right SPL and possibly insular cortex. This would explain why ostriches prefer ostriches as mates (presumably even when smell cues are eliminated) and why pigs prefer porcine shapes over humans.

Expanding on this, I suggest that there is a genetically specified mechanism that allows a template of one’s body image (in the SPL) to become transcribed into limbic circuitry, thereby determining aesthetic visual preference. If this idea is right, then someone whose body image was congenitally armless or legless would be attracted to people missing the same limb. Consistent with this view, people who wish to have their leg amputated are almost always attracted to leg amputees, not arm amputees.

SOMATOPARAPHRENIA: DOCTOR, THIS IS MY MOTHER’S ARM

Distortion of body-part ownership also occurs in one of the strangest syndromes in neurology, which has the tongue-twisting name “somatoparaphrenia.” Patients with a left-hemisphere stroke have damage to the band of fibers issuing from the cortex down into the spinal cord. Because the left side of the brain controls the right side of the body (and vice versa), this leaves the right side of their bodies paralyzed. They complain about their paralysis, asking the doctor whether the arm will ever recover, and not surprisingly they are often depressed.

When the stroke is in the right hemisphere, the paralysis is on the left. The majority of such patients are troubled by the paralysis as expected, but a small minority deny the paralysis (anosognosia), and an even smaller subset actually deny ownership of the left arm, ascribing it to the examining physician or to a spouse, sibling, or parent. (Why a particular person is chosen isn’t clear, but it reminds me of the manner in which the Capgras delusion often also involves a specific individual.)

In this subset of patients there is usually damage to the body maps in S1 and S2. In addition to this, the stroke has destroyed the corresponding body-image representation in the right SPL, which would ordinarily receive input from S1 and S2. Sometimes there is also additional damage to the right insula—which receives input the directly from S2 and also contributes to the construction of the person’s body image. The net result of this combination of lesions—S1, S2, SPL, and insula—is a complete sense of disownership of the arm. The ensuing tendency to ascribe it to someone else may be a desperate, unconscious attempt to explain the alienation of the arm (shades of Freudian “projection” here).

Why is somatoparaphrenia only seen when the right parietal is damaged but not when the left one is? To understand this we have to invoke the idea of division of labor between the two hemispheres (hemispheric specialization), a topic I will consider in some detail later in this chapter. Rudiments of such specialization probably exist even in the great apes, but in humans it is much more pronounced and may be yet another factor contributing to our uniqueness.

TRANSSEXUALITY: DOCTOR, I’M TRAPPED IN THE WRONG KIND OF BODY!

The self also has a sex: You think of yourself as male or female and expect others to treat you as such. It is such an ingrained aspect of your self-identity that you hardly ever pause to think about it—until things go awry, at least by the standards of a conservative, conformist society. The result is the “disorder” called transsexuality.

As with somatoparaphrenia, distortions or mismatches in the SPL can also explain the symptoms of transsexuals. Many male-to-female transsexuals report feeling that their penis seems to be redundant or, again, overpresent and intrusive. Many female-to-male transsexuals report feeling like a man in a woman’s body, and a majority of them have had a phantom penis since early childhood. Many of these women also report having phantom erections.⁸ In both kinds of transsexuals the discrepancy between internally specified sexual body image—which, surprisingly, includes details of sexual anatomy—and external anatomy leads to an intense discomfort and, again, a yearning to reduce the mismatch.

Scientists have shown that during fetal development, different aspects of sexuality are set in motion in parallel: sexual morphology (external anatomy), sexual identity (what you see yourself as), sexual orientation (what sex you are attracted to), and sexual body image (your brain’s internal representation of your body parts). Normally these harmonize during physical and social development to culminate in normal sexuality, but they can become uncoupled, leading to deviations that shift the individual toward one or the other end of the spectrum of normal distribution.

I am using the words “normal” and “deviation” here only in the statistical sense relative to the overall human population. I do not mean to imply that these ways of being are undesirable or perverse. Many transsexuals have told me that they would rather have surgery than be “cured” of their desire. If this seems strange, think of intense but unrequited romantic love. Would you request that your desire be removed? There is no simple answer.

Privacy

In Chapter 4, I explained the role of the mirror-neuron system in viewing the world from another person’s point of view, both spatially and (perhaps) metaphorically. In humans this system may have turned inward, enabling a representation of one’s own mind. With the mirror-neuron system thus “bent back” on itself full-circle, self-awareness was born. There is a subsidiary evolutionary question of which came first—other-awareness or self-awareness—but that’s tangential. My point is that the two coevolved, enriching each other enormously and culminating in the kind of reciprocity between self-awareness and other-awareness seen only in humans.

Although mirror neurons allow you to tentatively adopt another person’s vantage point, they don’t result in an out-of-body experience. You don’t literally float out to where that other vantage point is, nor do you lose your identity as a person. Similarly, when you watch another person being touched, your “touch” neurons fire, but even though you empathize, you don’t actually feel the touch. It turns out that in both cases, your frontal lobes inhibit the activated mirror neurons at least enough to stop all this from happening so you remain anchored in your own body. Additionally, “touch” neurons in your skin send a null signal to your mirror neurons, saying, “Hey, you are not being touched” to ensure that you don’t literally feel the other guy being touched. Thus in the normal brain a dynamic interplay of three sets of signals (mirror neurons, frontal lobes, and sensory receptors) is responsible for preserving both the individuality of your own mind and body, and your mind’s reciprocity with others—a paradoxical state of affairs unique to humans. Disturbances in this system, we shall see, would lead to a dissolution of interpersonal boundaries, personal identity, and body image—allowing us to explain a wide spectrum of seemingly incomprehensible symptoms seen in psychiatry. For example, derangements in frontal inhibition of mirror-neuron system may lead to a disturbing out-of-body experience—as though you were really watching yourself from above. Such syndromes reveal how blurred the boundary between reality and illusion can become under certain circumstances.

MIRROR NEURONS AND “EXOTIC” SYNDROMES

Mirror-neuron activity can go awry in many ways, sometimes in full-blown neurological disorders but also, I suspect, in numerous, more subtle ways as well. For instance, I wonder whether a dissolution of interpersonal boundaries may also explain more exotic syndromes such as folie à deux, in which two people, such as Bush and Cheney, share each other’s madness. Romantic love is a minor form of folie à deux, a mutual delusional fantasy that often afflicts otherwise normal people. Another example is Munchausen syndrome by proxy, in which hypochondriasis (where every trifling symptom is experienced as a harbinger of fatal illness) is unconsciously projected onto another (the “proxy”)—often by a parent onto his or her child—instead of onto oneself.

Much more bizarre is the Couvade syndrome, in which men in Lamaze classes start developing pseudocyesis, or false signs of pregnancy. (Perhaps mirror-neuron activity results in the release of empathy hormones such as prolactin, which act on the brain and body to generate a phantom pregnancy.)

Even Freudian phenomena such as projection begin to make sense: You wish to deny your unpleasant emotions, but they are too salient to deny completely so you ascribe them to others; it’s the I-you confusion again. As we will see, this is not unlike a patient with somatoparaphrenia “projecting” her paralyzed arm to her mother. Lastly, there is Freudian countertransference, in which the psychoanalyst’s self starts fusing with the patient’s, which can sometimes land the psychoanalist in legal trouble if the patient is of the opposite sex.

Obviously, I am not claiming to have “explained” these syndromes; I am merely pointing out how they might fit into our overall scheme and how they may give us hints about the manner in which the normal brain constructs a sense of self.

AUTISM

In Chapter 5, I presented evidence that a paucity of mirror neurons, or the circuits they project to, may underlie autism. If mirror neurons do indeed play a role in self-representation, then one would predict that an autistic person, even a high-functioning one, could probably not introspect, could never feel self-esteem or self-deprecation—let alone experience self-pity or self-aggrandizement—or even know what these words mean. Nor could the child experience the embarrassment—and the blush—that accompanies the state of being self-conscious. Casual observations of autistic people suggest that all this might be true, but there have been no systematic experiments to determine the limits of their introspective abilities. For example, if I were to ask you what’s the difference between need and desire (you need toothpaste; you desire a woman or man), or between pride and arrogance, hubris and humility, or sadness and sorrow, you would typically think for a bit before being able to spell out the distinction. An autistic child may be incapable of these distinctions while still being capable of other abstract distinctions (such as “What’s the difference between a Democrat and a Republican, other than IQ?”).

Another subtle test might be to see whether a high-functioning autistic child (or adult) can understand a conspiratorial wink, which usually involves a three-way social interaction between you, the person you are winking at, and a third person—real or imaginary—in the vicinity. This requires representing one’s own as well as the other two people’s minds. If I give you a sly wink when telling a lie to someone else (who can’t see the wink), then I have an implied social contract with you: “I am letting you in on this—see how I am tricking that person?” A wink is also used when flirting with someone, unbeknownst to others in the vicinity, although I don’t know if this is universal to all cultures. (And, lastly, you wink to someone to whom you are saying something in jest as if to say, “You realize I am only are joking, right?”) I once asked the famous high-functioning autist and writer Temple Grandin whether she knew what winking meant. She told me that she understands winking intellectually but doesn’t ever do it and has no intuitive feel for it.

More directly relevant to the framework of the present chapter is the observation made by Leo Kanner (who first described autism) that autistic children often confuse the pronouns “me” and “you” in conversation. This shows a poor differentiation of ego boundaries and a failure of the self-other distinction which, as we have seen, depends partially on mirror neurons and associated frontal inhibitory circuitry.

THE FRONTAL LOBES AND THE INSULA

Earlier in this chapter, I suggested that apotemnophilia results from a mismatch between somatosensory cortices S1 and S2, on the one hand, and on the other the superior (and inferior) parietal lobules, the region where you normally construct a dynamic image of your body in space. But where exactly is the mismatch detected? Probably in the insula, which is buried in the temporal lobes. The posterior (back) half of this structure combines multiple sensory inputs—including pain—from internal organs, muscles, joints, and vestibular (sense of balance) organs in the ear to generate an unconscious sense of embodiment. Discrepancies between different inputs here produce vaguely articulated discomfort, as when your vestibular and visual senses are put in conflict on a ship and you feel queasy.

The posterior insula then relays to the front (anterior) part of the insula. The eminent neuroanatomist, Arthur D. (Bud) Craig, from the Barrow Neurological Institute in Phoenix, has suggested that the posterior insula registers only rudimentary unconscious sensations, which need to be “re-represented” in more sophisticated form in the anterior insula before your body image can be consciously experienced.

Craig’s “re-representations” are loosely similar to what I called “metarepresentations” in Phantoms in the Brain. But in my scheme, further back-and-forth interactions with the anterior cingulate and other frontal structures are required for constructing your full sense of being a person reflecting on your sensations and making choices. Without these interactions it makes little sense to speak of a conscious self, whether embodied or not.

So far in this book, I have said very little about the frontal lobes, which became especially well developed in hominins and must play an important role in our uniqueness. Technically the frontal lobes are comprised of the motor cortex as well as the bulk of the cortex in front of it—the prefrontal cortex. Each prefrontal lobe has three subdivisions: the ventromedial prefrontal (VMF), or bottom inner part; the dorsolateral (DLF), or upper outer part; and the dorsomedial (DMF), or upper inner part (see Figure Int.2, in the Introduction). (Because the colloquial term “frontal lobes” includes the prefrontal cortex as well, I use “F” in these abbreviations, not “P.”) Let’s consider some of the functions of these three prefrontal regions.

I invoked the VMF in Chapter 8 when discussing pleasurable aesthetic responses to beauty. The VMF also receives signals from the anterior insula to generate your conscious sense of being embodied. In conjunction with parts of the anterior cingulate cortex (ACC), it motivates “desire” to take action. For instance, the discrepancy in body image in apotemnophilia, picked up in the right anterior insula, would be relayed to the VMF and the anterior cingulate to motivate a conscious plan of action: “Go to Mexico and get the arm removed!” In parallel, the insula projects directly to the amygdala, which activates the autonomic fight-or-flight response via the hypothalamus. That would explain the heightened skin sweating (galvanic skin response, or GSR) that we saw in our patients with apotemnophilia.

Of course, all this is pure speculation; at this point we don’t even know whether my explanation of apotemnophilia is correct. Nonetheless, my hypothesis illustrates the style of reasoning needed to explain many brain disorders. Just brushing such disorders aside as being “mental” or “psychological” problems serves no purpose; such labeling neither illuminates normal function nor helps the patient.

Given their extensive connections with limbic structures, it is hardly surprising that the medial frontal lobes—the VMF and possibly the DMF—are also involved in setting up the hierarchy of values that govern your ethics and morality, traits that are especially well developed in humans. Unless you are a sociopath (who has disturbances in these circuits, as shown by Antonio Damasio), you don’t usually lie or cheat, even when 100 percent sure you could get away with it if you tried. Indeed, your sense of morality and your concern for what others think of you are so powerful that you even act to extend them beyond your death. Imagine you have been diagnosed with terminal cancer and have old letters in your drawers that could be dredged up after your death, incriminating you in a sex scandal. If you are like most people, you will promptly destroy the evidence, even though logically, why should your posthumous reputation matter to you once you are gone?

I have already hinted at the role of mirror neurons in empathy. Apes almost certainly have empathy of sorts, but humans have both empathy and “free will,” the two necessary ingredients for moral choice. This trait requires a more sophisticated deployment of mirror neurons—acting in conjunction with the anterior cingulate—than any ape before us has achieved.

Let’s turn now to the dorsomedial prefrontal area (DMF). The DMF has been found in brain-imaging studies to be involved in conceptual aspects of the self. If you are asked to describe your own attributes and personality traits (rather than someone else’s), this area lights up in brain-imaging studies. On the other hand, if you were to describe the raw feel of your embodiment, one would expect your VMF to light up, but this hasn’t been tested yet.

Lastly, there is the dorsolateral prefrontal area. The DLF is required for holding things in your current, ongoing mental landscape, so you can use your ACC to direct attention to different aspects of the information and act according to your desires. (The technical name for this function is working memory.) The DLF is also required for logical reasoning, which involves paying attention to different facets of a problem and juggling abstractions—such as words and numbers—synthesized in the inferior parietal lobules (see Chapter 4). How and where the precise rules for this juggling arise is anybody’s guess.

The DLF also interacts with the parietal lobe. The two act jointly to construct a consciously experienced, animated body moving in space and time (which complements the insula-VMF pathway’s creation of a more viscerally felt anchoring of your self in your body). The subjective boundary between these two types of body image is somewhat blurred, reminding us of the sheer complexity of connections needed for even something as “simple” as your body image. This point will be driven home later; we will encounter a patient with a phantom twin next to him. Vestibular stimulation caused the twin to shrink and move. This implies powerful interactions between (a) vestibular input to the insula, which produces a visceral anchoring of the body, and (b) vestibular input to the right parietal lobe, which—along with muscle, joint sense, and vision—constructs a vivid sense of a consciously experienced, moving body.

Unity

What if the self is produced not by a single entity but by the push and pull of multiple forces of which we are largely unconscious? Now I’ll use the lenses of anosognosia and out-of-body experiences to examine the unity—and disunity—of the self.

HEMISPHERIC SPECIALIZATION: DOCTOR, I AM IN TWO MINDS

A great deal of pop psychology deals with the question of how the two hemispheres might be specialized for different roles. For example, the right hemisphere is thought to be more intuitive, creative, and emotional than the left, which is said to be more linear, rational, and Spock-like in its mentality. Many a New Age guru has used the idea to promote ways of unleashing the hidden potential of the right hemisphere.

As with most pop ideas, there is a kernel of truth to all this. In Phantoms in the Brain, I postulated that the two hemispheres have different, but complementary, coping styles in dealing with the world. Here I will consider the relevance of this to understanding anosognosia, the denial of paralysis seen in some stroke patients. Speaking more generally, it can help us understand why even most normal people—including you and me—engage in minor denials and rationalizations to cope with the stresses of our daily lives. What is the evolutionary function of these hemispheric differences, if any?

Information arriving through the senses is ordinarily merged with preexisting memories to create a belief system about yourself and the world. This internally consistent belief system, I suggest, is constructed mainly by the left hemisphere. If there is a small piece of anomalous information that doesn’t fit your “big picture” belief system, the left hemisphere tries to smooth over the discrepancies and anomalies in order to preserve the coherence of self and the stability of behavior. In a process called confabulation, the left hemisphere sometimes even fabricates information to preserve its harmony and overall view of itself. A Freudian might say that the left hemisphere does this to avoid shattering the ego, or to reduce what psychologists refer to as cognitive dissonance, a disharmony between different internal aspects of self. Such disconnects give rise to the confabulations, denials, and delusions that one sees in psychiatry. In other words, Freudian defenses originate mainly in the left hemisphere. In my account, however, unlike in orthodox Freudianism, they evolved not to “protect the ego” but to stabilize behavior and impose a sense of coherence and narrative to your life.

But there has to be a limit. If left unchecked, the left hemisphere would likely render a person delusional or manic. It is one thing to play down some of your weaknesses to yourself (an unrealistic “optimism” may be useful temporarily for forging ahead), but another thing to delude yourself into thinking you are rich enough to buy a Ferrari (or that your arm is not paralyzed) when neither is true. So it seems reasonable to postulate a “devil’s advocate” in the right hemisphere that allows “you” to adopt a detached, objective (allocentric) view of yourself.⁹ This right-brain system would often be able to detect major discrepancies that your egocentric left hemisphere has ignored or suppressed but shouldn’t have. You are then alerted to this, and the left hemisphere is jolted into revising its narrative.

The notion that many aspects of the human psyche might arise from a push-pull antagonism between complementary regions of the two hemispheres might seem like a gross oversimplification; indeed, the theory itself might be the result of “dichotomania,” the brain’s tendency to simplify the world by dividing things into polarized opposites (night and day, yin and yang, male and female, and so on). But it makes perfect sense from a systems engineering point of view. Control mechanisms that stabilize a system and help avoid oscillations are the rule rather than the exception in biology.

I will now explain how the difference between coping styles of the two hemispheres accounts for anosognosia—the denial of disability, in this case paralysis. As we saw earlier, when either hemisphere is damaged by stroke the result is hemiplegia, a complete paralysis of one side of the body. If the stroke is in the left hemisphere, then the right side of the body is paralyzed, and as expected the patient will complain about the paralysis and request treatment. The same is true for a majority of right-hemisphere strokes, but a significant minority of patients remain indifferent. They play down the extent of the paralysis and stubbornly deny that they cannot move—or even deny ownership of a paralyzed limb! Such denial usually happens as a result of additional damage to the postulated “devil’s advocate” in the right hemisphere’s frontoparietal regions, which allows the left hemisphere to go into an “open loop,” taking its denials to absurd limits.

I recently examined an intelligent, sixty-year-old patient named Nora, who had an especially striking version of this syndrome.

“Nora, how are you today?” I asked.

“Fine, Sir, except the hospital food. It’s terrible.”

“Well, let’s take a look at you. Can you walk?”

“Yes.” (Actually, she hadn’t taken a single step in the last week.)

“Nora, can you use your hands, can you move them?”

“Yes.”

“Both hands?”

“Yes.” (Nora had not used a fork in a week.)

“Can you move your left hand?”

“Yes, of course.”

“Touch my nose with your left hand.”

Nora’s hand remains motionless.

“Are you touching my nose?”

“Yes.”

“Can you see your hand touching my nose?”

“Yes, it’s now almost touching your nose.”

A few minutes later I grabbed Nora’s lifeless left arm, raised it toward her face, and asked, “Whose hand is this, Nora?”

“That’s my mother’s hand, Doctor.”

“Where is your mother?”

At this point Nora looked puzzled and glanced around for her mother. “She is hiding under the table.”

“Nora, you said you can move your left hand?”

“Yes.”

“Show me. Touch your own nose with your left hand.”

Without the slightest hesitation Nora moved her right hand toward her flaccid left hand, grabbed it and used it like a tool to touch her nose. The amazing implication is that even though she was denying that her left arm was paralyzed, she must have known at some level that it was, for if not, why would she spontaneously reach out to grab it? And why does she use “her mother’s” left hand as a tool to touch her own nose? It would appear that there are many Noras within Nora.

Nora’s case is an extreme manifestation of anosognosia. More commonly the patient tries to play down the paralysis, rather than engaging in outright denial or confabulation. “No problem, Doc. It’s getting better every day!” Over the years I have seen many such patients and been struck by the fact that many of their comments bear a striking resemblance to the kinds of everyday denials and rationalizations that we all engage in to tide over the discrepancies in our daily lives. Sigmund (and more especially his daughter Anna) Freud referred to these as “defense mechanisms,” suggesting that their function is to “protect the ego”—whatever that means. Examples of such Freudian defenses would include denial, rationalization, confabulation, reaction formation, projection, intellectualization, and repression. These curious phenomena have only a tangential relevance to the problem of Consciousness (with a big C), but—as Freud urged—they represent the dynamic interplay of between the conscious and unconscious, so studying them may indirectly illuminate our understanding of consciousness and other related aspects of human nature. So I’ll list them.

1. Outright denial—“My arm isn’t paralyzed.”

2. Rationalization—The tendency we all have to ascribe some unpleasant fact about ourselves to an external cause: For example, we might say, “The exam was too hard” rather than “I didn’t study hard enough,” or “The professor is sadistic” rather than “I am not smart.” This tendency is amplified in patients.

For example, when I asked a patient, Mr. Dobbs, “Why are you not moving your left hand like I asked you to?” his replies varied:

“I am an army officer, Doctor. I don’t take orders.”

“The medical students have been testing me all day. I am tired.”

“I have severe arthritis in my arm; it’s too painful to move.”

3. Confabulation—The tendency to make things up to protect your self image: This is done unconsciously; there is no deliberate intention to deceive. “I can see my hand moving, Doctor. It’s an inch from your nose.”

4. Reaction formation—The tendency to assert the opposite of what you unconsciously know to be true about yourself, or, to paraphrase Hamlet, the tendency to protest too much. An example of this is closeted homosexuals engaging in vehement disapproval of same-sex marriages.

Another example: I remember pointing to a heavy table in a stroke clinic and asking a patient whose left arm was paralyzed, “Can you lift that table with your right hand?”

“Yes.”

“How high can you lift it?”

“By about an inch.”

“Can you lift the table with your left hand?”

“Yes, by two inches.”

Clearly “someone” in there knew she was paralyzed for, if not, why would she exaggerate the arm’s ability?

5. Projection—Ascribing your own deficiencies to another person. In the clinic: “The [paralyzed] arm belongs to my mother.” In ordinary life: “He is a racist.”

6. Intellectualization—Transforming an emotionally threatening fact into an intellectual problem, thereby deflecting attention from and blunting its emotional impact. Many a person with a terminally ill spouse or family member, unable to face the potential loss, starts treating the illness as a purely intellectual challenge. This could be regarded as a combination of denial and intellectualization, though the terminology is unimportant.

7. Repression—The tendency to block the retrieval of painful memories, which if dredged up would be “painful to the ego.” Although the word has made it into pop psychology, memory researchers have long been suspicious of repression. I lean toward thinking that the phenomenon is real, for I have seen many clear instances of it in my patients, providing what mathematicians call an “existence proof.”

For example, most patients recover from anosognosia after having been in denial for a few days. I had been seeing one such patient who insisted for nine days in a row that his paralyzed arm was “working fine,” even with repeated questioning. Then on the tenth day he recovered completely from his denial.

When I questioned him about his condition, he immediately stated, “My left arm is paralyzed.”

“How long has it been paralyzed?” I asked, surprised.

He replied, “Why, for the last several days that you have been seeing me.”

“What did you tell me when I asked about your arm yesterday?”

“I told you it was paralyzed, of course.”

Clearly he was “repressing” his denials!

Anosognosia is a striking illustration of what I have repeatedly stressed in this book—that “belief” is not a single thing. It has many layers that can be peeled away one at a time until the “true” self becomes nothing more than an airy abstraction. As the philosopher Daniel Dennett once said, the self is more akin conceptually to the “center of gravity” of a complicated object, its many vectors intersecting at a single imaginary point.

Thus anosognosia, far from being just another odd syndrome, gives us fresh insights into the human mind. Each time I see a patient with this disorder, I feel like I am looking at human nature through a magnifying glass. I can’t help thinking that if Freud had known about anosognosia, he would have taken great delight in studying it. He might ask, for example, what determines which particular defense you use; why use rationalization in some cases and outright denial for others? Does it depend entirely on the particular circumstances or on the patient’s personality? Would Charlie always use rationalization and Joe use denial?

Apart from explaining Freudian psychology in evolutionary terms, my model may also be relevant to bipolar disorder (manic-depressive illness). There is an analogy between the coping styles of the left and right hemispheres—manic or delusional for the left, anxious devil’s advocate for the right—and the mood swings of bipolar illness. If so, is it possible that such mood swings may actually result from alternation between the hemispheres? As my former teachers Dr. K. C. Nambiar and Jack Pettigrew have shown, even in normal individuals there may be some spontaneous “flipping” between the hemispheres and their corresponding cognitive styles. An extreme exaggeration of this oscillation may be regarded as “dysfunctional” or “bipolar illness” by psychiatrists even though I have known some patients who are willing to tolerate the bouts of depression in order to (for example) continue their brief euphoric communions with God.

OUT OF BODY EXPERIENCE: DOCTOR, I LEFT MY BODY BEHIND

As we saw earlier, one job of the right hemispheres is to take a detached, big-picture view of yourself and your situation. This job also extends to allowing you to “see” yourself from an outsider’s point of view. For example, when you are rehearsing a lecture, you may imagine watching yourself from the audience pacing up and down the podium.

This idea can also account for out-of-body experiences. Again, we only need to invoke disruption to the inhibitory circuits that ordinarily keep mirror-neuron activity in check. Damage to the right frontoparietal regions or anesthesia using the drug ketamine (which may influence the same circuits) removes this inhibition. As a result, you start leaving your body, even to the extent of not feeling your own pain; you see your pain “objectively” as if someone else were experiencing it. Sometimes you get the feeling that you have actually left your body and are hovering over it, watching yourself from outside. Note that if these “embodying” circuits are especially vulnerable to lack of oxygen to the brain, this could also explain why such out-of-body sensations are common in near-death experiences.

Odder still than most out-of-body sensations are the symptoms experienced by a patient named Patrick, a software engineer from Utah who had been diagnosed with a malignant brain tumor in his frontoparietal region. The tumor was on the right side of his brain, which was fortunate because he was less worried about it than he would have been had it been on the left. Patrick had been told he had less than two years to live even after the tumor had been removed, but he tended to play it down. What really intrigued him was much stranger than either he or anyone else could have imagined.

He noticed that he had an invisible but vividly felt “phantom twin” attached to the left side of his body. This was different from the more common sort of out-of-body experience in which a patient feels he is looking down on his own body from above. Patrick’s twin mimicked his every action in near-perfect synchrony. Patients like him have been studied extensively by Peter Brugger of the University Hospital Zürich. They remind us that even the congruence between different aspects of your mind such as subjective “ego” and body image can be deranged in brain disease. There must be a specific brain mechanism (or dovetailing suite of mechanisms) that ordinarily preserves such congruence; if there weren’t, it could not have been affected selectively in Patrick while leaving other aspects of his mind intact—for indeed, he was emotionally normal, introspective, intelligent, and amiable.¹⁰

Out of curiosity I irrigated his left ear canal with ice water. This procedure is known to activate the vestibular system and can provide a certain jolt to the body image; it can, for example, fleetingly restore awareness of the paralysis of the body to a patient with anosognosia due to a parietal stroke. When I did this for Patrick, he was astonished to notice the twin shrinking in size, moving, and changing posture. Ah, how little we know about the brain!

Out-of-body experiences are seen often in neurology, but they blend imperceptibly into what we call dissociative states, which are usually seen by psychiatrists. The phrase refers to a condition in which the person mentally detaches herself from whatever is going on in her body during a highly traumatic experience. (Defense lawyers often use the dissociative state diagnosis: that the accused was in a such a state, and that she was watching her body “acting out” the murder without personal involvement.)

The dissociative state involves the deployment of some of the same neural structures already discussed, but in addition two other structures: the hypothalamus and the anterior cingulate.¹¹ Ordinarily, when confronted with a threat, two outputs flow out from the hypothalamus: a behavioral output, such as running away or fighting; and an emotional output, such as fear or aggression. (We already mentioned the third output: autonomic arousal leading to sweating GSR, blood pressure, and heart-rate elevation.) The anterior cingulate is simultaneously active; it allows you to remain aroused and ever vigilant for new threats and new opportunities for fleeing. But the degree of threat determines the degree to which each of these three subsystems is engaged. When one is confronted with an extreme threat, it is sometimes best to lie still and do nothing at all. This could be regarded as a form of “playing possum,” shutting down both the behavioral and emotional output. The possum becomes completely still when a predator is so close that escape is no longer an option, and in fact any attempt would only activate the carnivore’s instinct to chase down fleeing prey. Nonetheless, the anterior cingulate remains powerfully engaged the whole time to preserve vigilance, just in case the predator isn’t fooled or a quick escape route becomes available.

A vestige of this “possum reflex,” or an exaptation of it, may manifest itself as dissociative states in humans in extreme emergencies. You shut down overt behavior as well as emotions and view yourself with objective detachment from your own pain or panic. This sometimes happens in rape, for example, where the woman gets into a paradoxical state: “I was viewing myself being raped as a detached external observer might—feeling the pain but not the agony. And there was no panic.” The same thing must have occurred when the explorer David Livingstone was mauled by a lion chewing his arm off; he felt no pain or fear.

The ratio of activation among these circuits and interactions between them can also give rise to less extreme forms of dissociation in which action is not inhibited but emotions are. We have dubbed this the “James Bond reflex”: his nerves of steel allow him to remain unperturbed by distracting emotions as he pursues and tackles the villain (or has sex with a woman without paying the “penalty” of love).

Social Embedding

The self defines itself in relation to its social environment. When that environment becomes incomprehensible—for example, when familiar people suddenly seem unfamiliar or vice versa—the self can experience extreme distress or even feel that it is under threat.

THE MISIDENTIFICATION SYNDROMES:

DOCTOR, THAT’S NOT MY MOTHER

A person’s brain creates a unified, internally consistent picture of his social world—a stage occupied by different selves like you and me. Seems like a banal statement, but when the self is deranged you begin to realize there are specific brain mechanisms at work to clothe the self with a body and an identity.

In Chapter 2, I offered an explanation for the Capgras syndrome in terms of visual pathways 2 and 3 as they diverge from the fusiform gyrus (Figures 9.1 and 9.2). If pathway 3 (the “so what” stream, which evokes emotions) is compromised while pathway 2 (the “what” stream, which enables identification) remains intact, the patient can recall facts and memories about his nearest and dearest—in a word, he can recognize them—but, jarringly, distressingly, he does not get the warm fuzzy feelings that he “should.” The mismatch is either too painful or too bewildering to accept, so he embraces the delusion of an identical imposter. Going further down the path of delusion, he may say things like “my other mother,” or even assert that there are several mother-like beings. This is called duplication, or reduplication.

Now think about what happens when the Capgras scenario is reversed: intact pathway 3, compromised pathway 2. The patient loses her ability to recognize faces. She becomes face blind, a condition called prosopagnosia. And yet her pure unconscious discrimination of people’s faces continues to be carried out by her intact fusiform gyrus, which can still send signals down her intact “so what” stream (pathway 3) to her amygdala. As a result, she still responds emotionally to familiar faces—she gives a nice big GSR signal when seeing her mother, for example—even though she has no idea who she is looking at. Strangely, her brain—and skin—“knows” something that her mind is unaware of consciously. (This was shown in an elegant series of experiments by Antonio Damasio.) So you can think of the Capgras and prosopagnosia disorders as mirror images of each other, both structurally and in terms of clinical symptoms.¹²

To most of us with our undamaged brains, it seems counterintuitive that identity (facts known about a person) should be segregated from familiarity (emotional reactions to a person). How can you recognize someone yet not recognize her at the same time? You might get an inkling of what this is like if you think back to an occasion when you ran into an acquaintance somewhere completely out of context, such as an airport in a foreign country, and could not for the life of you remember who he was. You experienced familiarity with lack of identity. The fact that such dissociation can occur at all is proof that separate mechanisms are involved, and in such “airport” moments you experience a miniature, fleeting “syndrome” that is the converse of Capgras. The reason you don’t experience this cognitive discrepancy as unpleasant (except briefly as you buy time with small talk while racking your brain) is because such episodes do not last long. If this acquaintance continued to look strange all the time, irrespective of context and no matter how much or how often you spoke with him, he might start looking sinister and you might indeed develop a strong aversion or paranoia.

FIGURE 9.1 A highly schematic diagram of the visual pathways and other areas invoked to explain symptoms of mental illness: The superior temporal sulcus (STS) and supramarginal gyrus (SM) are probably rich in mirror neurons. Pathways 1 (“how”) and 2 (“what”) are identified anatomical pathways. The split of the “what” pathway into two streams—“what” (pathway 2) and “so what” (pathway 3)—is based mainly on functional considerations and neurology. The superior parietal lobule (SPL) is involved in the construction of body image and visual space. The inferior parietal lobule (IPL) is also concerned with body image, but also with prehension in monkeys and (probably) apes. The supramarginal gyrus (SM) is unique to humans. During hominin development, it split off from the IPL and became specialized for skilled and semiskilled movements such as tool use. Selection pressure for its split and specialization came from the need to use hands for making tools, wielding weapons, hurling missiles, as well as fine hand and finger manipulation. Another gyrus (AG) is probably unique to us. It split off from IPL and originally subserved cross-modal abstraction capacities, such as tree climbing, and matching visual size and orientation with muscle and joint feedback. The AG became exapted for more complex forms of abstraction in humans: reading, writing, lexicon, and arithmetic. Wernicke’s area (W) deals with language (semantics). The STS also has connections with the insula (not shown). The amygdaloid complex (A, including the amygdala) deals with emotions. The lateral geniculate nucleus (LGN) of the thalamus relays information from the retina to area 17 (also known as V1, the primary visual cortex). The superior colliculus (SC) receives and processes signals from the retina that are to be sent via the old pathway to the SPL (after a relay via the pulvinar, not shown). The fusiform gyrus (F) is involved in face and object recognition.

FIGURE 9.2 An abbreviated version of Figure 9.1, showing the distinction between emotions and semantics (meaning).

SELF DUPLICATION: DOCTOR, WHERE IS THE OTHER DAVID?

Astonishingly, we have found that the reduplication seen in Capgras syndrome can even involve the patient’s own self. As previously noted, the recursive activity of mirror neurons may result in a representation not only of others’ minds but of one’s own mind as well.¹³ Some mix-up of this mechanism could explain why our patient David pointed to a profile-view photo of himself and said, “That’s another David.” On other occasions he referred to “the other David” in casual conversation, even asking, poignantly, “Doctor, if the other David comes back, will my real parents disown me?” Of course, we all indulge in role playing from time to time but not to the point where the metaphorical (“I am in two minds,” “I’m not the young man that I once was”) becomes literal. Again, bear in mind that despite these specific dreamlike misreadings of reality, David was perfectly normal in other respects.

I might add that the Queen of England also refers to herself in the third person, but would hesitate to ascribe this to pathology.

FREGOLI SYNDROME: DOCTOR, EVERYONE LOOKS LIKE AUNT CINDY

In Fregoli syndrome, the patient claims that all people seem to resemble a prototype person he knows. For example, I once met a man who said everyone looked like his aunt Cindy. Perhaps this arises because the emotional pathway 3 (as well as links from pathway 2 to amygdala) has been strengthened by disease. This could happen because of repeated volleys of signals accidentally activating pathway 3, as in epilepsy; it is sometimes called kindling. The outcome is that everyone looks strangely familiar rather than unfamiliar. Why the patient should latch onto a single prototype is unclear, but it may arise from the fact that “diffuse familiarity” makes no sense. By analogy, the diffuse anxiety of the hypochondriac seldom floats free for long, but latches onto a specific organ or disease.

Self-Awareness

Earlier in this chapter I wrote that a self that is not aware of itself is an oxymoron. There are nevertheless certain disorders that can seriously distort one’s self-awareness, whether by causing patients to believe that they are dead or by inspiring the delusion that they have become one with God.

COTARD SYNDROME: DOCTOR, I DON’T EXIST

If you do a survey and ask people—whether neuroscientists or Eastern mystics—what the most important puzzling aspect of the self is, the most common answer would be the fact that the self is aware of itself; it can contemplate its own existence and (alas!) its mortality. No nonhuman creature can do this.

I often visit Chennai, India, during the summer to give lectures and see patients at the Institute of Neurology on Mount Road. A colleague of mine, Dr. A. V. Santhanam, often invites me to lecture there and draws my attention to interesting cases. On one particular evening after giving a lecture, I found Dr. Santhanam waiting for me in my office with a patient, a disheveled, unshaven young man of thirty named Yusof Ali. Ali had suffered from epilepsy starting in his late teens. He had periodic bouts of depression, but it was hard to know whether this was related to his seizures or to reading too much Sartre and Heidegger, as many intelligent teenagers do. Ali told me of his deep interest in philosophy.

The fact that Ali was acting strangely was obvious to nearly everyone who knew him long before his epilepsy was diagnosed. His mother had noticed that a couple of times a week there were brief periods when he would become somewhat detached from the world, appear to experience a clouding of consciousness and engage in incessant lip smacking and postural contortions. This clinical history, together with his EEG (electroencephalograph, a record of his brain waves), led us to diagnose Ali’s miniseizures as a form of epilepsy called complex partial seizures. Such seizures are different from the dramatic grand-mal (whole-body) seizures most people associate with epilepsy; these miniseizures, in contrast, mainly affect the temporal lobes and produce emotional changes. During his long seizure-free intervals Ali was perfectly lucid and intelligent.

“What brings you to our hospital?” I asked.

Ali remained silent, looking a me intently for nearly a minute. He then whispered slowly, “Not much can be done: I am a corpse.”

“Ali, where are you?”

“At the Madras Medical College, I think. I used to be a patient at the Kilpauk.” (Kilpauk was the only mental hospital in Chennai.)

“Are you saying you are dead?”

“Yes. I don’t exist. You could say I am an empty shell. Sometimes I feel like a ghost that exists in an another world.”

“Mr. Ali, you are obviously an intelligent man. You are not mentally insane. You have abnormal electrical discharges in certain parts of your brain that can affect the way you think. That’s why they moved you here from the mental hospital. There are certain drugs that are very effective for controlling seizures.”

“I don’t know what you’re saying. You know the world is illusory as the Hindus say. Its all maya [the Sanskrit word for “illusion”]. And if the world doesn’t exist, then in what sense do I exist? We take all that for granted, but it simply isn’t true.”

“Ali, what are you saying? Are you saying you may not exist? How do you explain that you are here talking to me right now?”

Ali appeared confused and a tear started forming in his eye. “Well, I am dead and immortal at the same time.”

In Ali’s mind—as in the minds of many otherwise “normal” mystics—there is no essential contradiction in his statement. I sometimes wonder whether such patients who have temporal lobe epilepsy have access to another dimension of reality, a wormhole of sorts into a parallel universe. But I usually don’t say this to my colleagues, lest they doubt my sanity.

Ali had one of the strangest disorders in neuropsychiatry: Cotard syndrome. It would be all too easy to jump to the conclusion that Ali’s delusion was the result of extreme depression. Depression very often accompanies Cotard syndrome. However, depression alone cannot be the cause of it. On the one hand, less extreme forms of depersonalization—in which the patient feels like an “empty shell” but, unlike a Cotard patient, retains insight into his illness—can occur in the complete absence of depression. Conversely, most patients who are severely depressed don’t go around claiming they are dead. So something else must be going on in Cotard syndrome.

Dr. Santhanam started Ali on a regimen of the anticonvulsant drug lamotrigine.

“This should help you get better,” he said. “We are going to start you on a small dose because in a few rare cases patients develop a very severe allergic skin rash. If you develop such a rash, stop the medicine immediately and come and see us.”

Over the next few months Ali’s seizures disappeared, and as an added bonus his mood swings diminished and he became less depressed. Yet even three years later he continued to maintain that he was dead.¹⁴

What would be causing this Kafkaesque disorder? As I noted earlier, pathways 1 (including parts of the inferior parietal lobule) and 3 are both rich in mirror neurons. The former is involved in inferring intentions and the latter, in concert with the insula, is involved in emotional empathy. You have also seen how mirror neurons might not only be involved in modeling other people’s behavior—the conventional view—but may also turn “inward” to inspect your own mental states. This could enrich introspection and self-awareness.

The explanation I propose is to think of Cotard syndrome as an extreme and more general form of Capgras syndrome. People with Cotard syndrome often lose interest in viewing art and listening to music, presumably because such stimuli also fail to evoke emotions. This is what we might expect if all or most sensory pathways to the amygdala are totally severed (as opposed to Capgras syndrome, in which just the “face” area in the fusiform gyrus is disconnected from the amygdala). Thus for a Cotard patient, the entire sensory world, not just Mum and Dad, would seem derealized—unreal, as in a dream. If you added to this cocktail a derangement of reciprocal connections between the mirror neurons and the frontal lobe system, you would lose your sense of self as well. Lose yourself and lose the world—that’s as close to death in life as you can get. No wonder severe depression frequently, though not always, accompanies Cotard syndrome.

Note that in this framework it is easy to see how a less extreme form of Cotard syndrome could underlie the peculiar states of derealization (“The world looks unreal as in a dream”) and depersonalization (“I don’t feel real”) that are frequently seen in clinical depression. If depressed patients have selective damage to the circuits that mediate empathy and the salience of external objects, but intact circuitry for self-representation, the result could be derealization and a feeling of alienation from the world. Conversely, if self-representation is mainly affected, with normal reactions to the outside world and people, the sense of internal hollowness or emptiness that characterizes depersonalization would be the result. In short, the feeling of unreality is attributed to either oneself or the world depending on differential damage to these closely linked functions.

The extreme sensory-emotional disconnection and diminishment of self I am proposing as an explanation for Cotard syndrome would also explain such patients’ curious indifference to pain. They feel pain as a sensation but, like Mikhey (whom we met in Chapter 1), there is no agony. As a desperate attempt to restore the ability to feel something—anything!—such patients may try to inflict pain on themselves in order to feel more “anchored” in their bodies.

It would also explain the paradoxical finding (not proven, but suggestive) that some severely depressed patients commit suicide when first put on antidepressant drugs such as Prozac. It is arguable that in extreme Cotard cases suicide would be redundant, since the self is already “dead” there is no one there who can or should be put out of her suffering. On the other hand, an antidepressant drug may restore just enough self-awareness for the patient to recognize that her life and world are meaningless; now that it matters that the world is meaningless, suicide may seem the only escape. In this scheme, Cotard syndrome is apotemnophilia for one’s entire self, rather than just one arm or leg, and suicide is its successful amputation.¹⁵

DOCTOR, IAMONE WITH GOD

Now consider what would happen if the extreme opposite were to occur—if there were a tremendously overactivation of pathway 3 caused by the kind of kindling one sees in temporal lobe epilepsy (TLE). The result would be an extreme heightening of empathy for others, for the self, and even for the inanimate world. The universe and everything in it become deeply significant. It would feel like union with God. This, too, is frequently reported in TLE.

Now, as in Cotard syndrome, imagine adding into this cocktail some damage to the system in the frontal lobes that inhibits mirror-neuron activity. Ordinarily this system preserves empathy while preventing “overempathy,” thus preserving your sense of identity. The result of damaging this system would be a second, even deeper sense of merging with everything.

This sense of transcending your body and achieving union with some immortal, timeless essence is also unique to humans. To their credit, apes are not preoccupied with theology and religion.

DOCTOR, I’M ABOUT TO DIE

Incorrect “attribution” of our internal mental states to the wrong trigger in the external world is very much a part of the complex web of interactions that lead to mental illness in general. Cotard syndrome and “merging with God” are extreme forms of this.¹⁶ A far more common form is the syndrome of panic attacks.

A certain proportion of otherwise normal people are seized for forty to sixty seconds by a sudden feeling of impending doom—a sort of transient Cotard syndrome (combined with a strong emotional component). The heart starts beating faster (felt as palpitations, an intensification of heartbeats), palms sweat, and there is an extreme sense of helplessness. Such attacks can occur several times a week.

One possible source of panic attacks might be brief miniseizures affecting pathway 3, especially the amygdala and its emotional and autonomic arousal outflow through the hypothalamus. In such a case, a powerful fight-or-flight reaction would be triggered, but since there is nothing external you can ascribe the changes to, you internalize it and start to feel as if you’re dying. It’s the brain’s aversion to discrepancy again—this time between the neutral external input and the far-from-neutral internal physiological feelings. The only way your brain can account for this combination is to ascribe the changes to some indecipherable and terrifying internal source. The brain finds free-floating (inexplicable) anxiety less tolerable than anxiety which can be clearly attributed to a source.

If this is correct, one wonders if it might be possible to “cure” panic attacks by taking advantage of the fact that the patient often knows a few seconds ahead of time that an attack is about to occur. If you are the patient, then as soon as you sense the attack coming on, you could quickly start watching a horror movie on your iPhone, for example. This might abort the attack by allowing your brain to ascribe the physiological arousal to the external horror, rather than to some terrifying but intangible inner cause. The fact that you “know” that it’s only a movie at some higher intellectual level doesn’t necessarily rule out this treatment; after all, you do feel fear when watching a horror movie even while recognizing that it’s “only a movie.” Belief is not monolithic; it exists in many layers whose interactions one can manipulate clinically using the right trick.

Continuity

Implicit in the idea of the self is the notion of sequentially organized memories accumulated over a lifetime. There are syndromes that can profoundly affect different aspects of memory formation and retrieval. Psychologists classify memory (the word is used loosely synonymous with learning) into three distinct types that might have separate neural substrates. The first of these, called procedural memory, allows you to acquire new skills, such as riding a bicycle or brushing your teeth. Such memories are summoned up instantly when the occasion demands; no conscious recollection is involved. This type of memory is universal to all vertebrates and some invertebrates; it certainly isn’t unique to humans. Second, there are memories that comprise your semantic memory, your factual knowledge of objects and events in the world. For example, you know that winter is cold and bananas are yellow. This form of memory, too, is not unique to humans. The third category, first recognized by Endel Tulving, is called episodic memory, memories for specific events, such as your prom night, or the day you broke your ankle playing basketball, or as the psycholinguist Steve Pinker puts it, “When and where who did what to whom.” Semantic memories are like a dictionary whereas episodic ones are like a diary. Psychologists also refer to them as “knowing” versus “remembering” only humans are capable of the latter.

Harvard psychologist Dan Schacter has made the ingenious suggestion that episodic memories may be intimately linked to your sense of self: you need a self to which you attach the memories, and the memories in turn enrich your self. In addition to this we tend to organize episodic memories in approximately the correct sequence and can engage in a sort of mental time travel, conjuring them up in order to “visit” or “relive” episodes in our lives in vivid nostalgic detail. These abilities are almost certainly unique to humans. More paradoxical is our ability to engage in more open-ended forward time travel to anticipate and plan the future. This ability is probably also unique to us (and may require well-developed frontal lobes). Without such planning, our ancestors couldn’t have made stone tools in advance of a hunt or sown seeds for the next harvest. Chimpanzees and orangutans engage in opportunistic tool making and tool use (stripping leaves from twigs in order to fish termites from their mounds) but they cannot make tools with the intent to store them for future use.

DOCTOR, WHEN AND WHERE DID MY MOTHER DIE?

All of this makes intuitive sense but there is also evidence from brain disorders—some common, others rare—in which the different components of memory are selectively compromised. These syndromes vividly illustrate the different subsystems of memory, including ones that have evolved only in humans. Almost everyone has heard of amnesia following head trauma: The patient has difficulty recollecting specific incidents that took place during the weeks or months preceding the injury, even though he is smart, recognizes people and is able to acquire new episodic memories. This syndrome—retrograde amnesia—is quite common, seen as often in real life as in Hollywood.

Far rarer is a syndrome described by Endel Tulving, whose patient Jake had damage to parts of both his frontal and temporal lobes. As a result Jake had no episodic memories of any kind, whether from childhood or from the recent past. Nor could he form new episodic memories. However, his semantic memories about the world remained intact; he knew about cabbages, kings, love, hate, and infinity. It is very hard for us to imagine Jake’s inner mental world. Yet despite what you would expect from Schacter’s theory, there was no denying that he had a sense of self. The various attributes of self, it would seem, are like arrows pointing toward an imaginary point: the mental “center of gravity” of the self that I mentioned earlier. Losing any one arrow might impoverish the self but does not destroy it; the self valiantly defies the slings and arrows of outrageous fortune. Even so, I would agree with Schacter that the autobiography we each carry around in our minds based on a lifetime of episodic memories is intimately linked to our sense of self.

Tucked away in the lower, inner portion of the temporal lobes is the hippocampus, a structure required for the acquisition of new episodes. When it is damaged on both sides of the brain, the result is a striking memory disorder called anterograde amnesia. Such patients are mentally alert, talkative, and intelligent but cannot acquire any new episodic memories. If you were introduced to such a patient for the first time, walked out, and returned after five minutes, there would be no glimmer of recognition on her part; it’s as if she had never seen you before. She could read the same detective novel again and again and never get bored. Yet, unlike Tulving’s patient, her old memories, acquired prior to the damage, are for the most part intact: she remembers the boy she was dating in the year of her accident, her fortieth birthday party, and so on. So you need your hippocampus to create new memories, but not to retrieve old memories. This suggests that memories are not actually stored in the hippocampus. Furthermore, the patient’s semantic memories are unaffected. She still knows facts about people, history, word meanings and so forth. A great deal of pioneering work has been done on these disorders by my colleagues Larry Squire and John Wixted at UC San Diego and by Brenda Milner at McGill University, Montreal.

What would happen if someone were to lose both his semantic and episodic memories, so that he had neither factual knowledge of the world nor episodic memories of a lifetime? No such patient exists, and even if you were to stumble on one who had the right combination of brain lesions, what would you expect him to say about his sense of self? In fact, if he really had neither factual nor episodic memories, it is unlikely that he could even talk to you or understand your question, let alone understand the meaning of “I.” However, his motor skills would be unaffected; he might surprise you by cycling home.

Free Will

One attribute of the self is your sense of “being in charge” of your actions and, as a corollary, of your belief that you could have acted otherwise if you had chosen to. This may seem like an abstract philosophical issue but it plays an important role in the criminal justice system. You can deem someone guilty only if he (1) could fully envisage alternate courses of action available to him; (2) he was fully aware of the potential consequences of his actions, both short-and long-term; (3) he could have chosen to withhold the action; and (4) he wanted the result that ensued.

The upper gyrus branching from the left inferior parietal lobule, which I earlier referred to as the supramarginal gyrus, is very much involved in this ability to create a dynamic internal image of anticipated actions. This structure is highly evolved in humans; damage to it results in a curious disorder called apraxia, defined as an inability to carry out skilled actions. For example, if you ask an apraxic patient to wave goodbye, she will simply stare at her hand and start wiggling her fingers. But if you ask her, “What does ‘goodbye’ mean?” she will reply, “Well, you wave your hand when parting company.” Furthermore, her hand and arm muscles are fine; she can untie a knot. Her thinking and language are unaffected and so is her motor coordination, but she cannot translate thought into action. I have often wondered whether this gyrus, which exists only in humans, evolved initially for the manufacture and deployment of multicomponent tools, such as hafting an axe head on a suitably carved handle.

All of this is only part of the story. We usually think of free will as the drive to perform that is linked to your sense of being a purposeful agent with multiple choice options. We have only a few clues as to where this sense of agency—your desire to act, and belief in your ability—emerges from. Strong hints come from studying patients with damage to the anterior cingulate in the frontal lobes, which in turn gets a major input from the parietal lobes, including supramarginal gyrus. Damage here can result in the akinetic mutism, or vigilant coma, we saw in Jason at the beginning of this chapter. A few patients recover after some weeks and say things like, “I was fully conscious and aware of what was going on, Doctor. I understood all your questions but I simply didn’t want to reply or do anything.” Wanting, it turns out, is crucially dependent on the anterior cingulate.

Another consequence of damage to the anterior cingulate is the alien-hand syndrome, in which the person’s hand does something he doesn’t “will” it to do. I saw a woman with this disorder in Oxford (together with Peter Halligan). The patient’s left hand would reach out and grab objects without her intending to, and she had to use her right hand to pry loose her fingers to let go of the object. (Some of the male graduate students in my lab have dubbed this the “third-date syndrome.”) Alien-hand syndrome underscores the important role of the anterior cingulate in free will, transforming a philosophical problem into a neurological one.

Philosophy has set up a way of looking at the consciousness problem by considering abstract questions such as qualia and their relationship to the self. Psychoanalysis, while able to frame the problem in terms of conscious and unconscious brain processes, hasn’t formulated clearly testable theories nor do they have the tools to test them. My goal in this chapter has been to demonstrate that neuroscience and neurology provide us with a new and unique opportunity to understand the structure and function of the self, not only from the outside by observing behavior, but also from studying the inner workings of the brain.¹⁷ By studying patients such as those in this chapter, who have deficits and disturbances in the unity of self, we can gain deeper insight into what it means to be human.¹⁸

If we succeed in this, it will be the first time in evolution that a species has looked back on itself and not only understood its own origins but also figured out what or who is the conscious agent doing the understanding. We don’t know what the ultimate outcome of such a journey will be, but surely it is the greatest adventure humankind has ever embarked on.

EPILOGUE

…gives to airy nothing a local habitation and a name…

—WILLIAM SHAKESPEARE

ONE OF THE MAJOR THEMES IN THE BOOK—WHETHER TALKING about body image, mirror neurons, language evolution, or autism—has been the question of how your inner self interacts with the world (including the social world) while at the same time maintaining its privacy. The curious reciprocity between self and others is especially well developed in humans and probably exists only in rudimentary form in the great apes. I have suggested that many types of mental illness may result from derangements in this equilibrium. Understanding such disorders may pave the way not only for solving the abstract (or should I say philosophical) problem of the self at a theoretical level, but also for treating mental illness.

My goal has been to come up with a new framework to explain the self and its maladies. The ideas and observations I have presented will hopefully inspire new experiments and set the stage for a more coherent theory in the future. Like it or not, this is the way science often works in its early stage: Discover the lay of the land first before attempting all-encompassing theories. Ironically it’s also the stage when science is most fun; every little experiment you do, you feel like Darwin unearthing a new fossil or Richard Burton turning another bend of the Nile to discover its source. You may not share their lofty stature, but in trying to emulate their style you feel their presence as guardian angels.

To use an analogy from another discipline, we are now at the same stage that chemistry was in the nineteenth century: discovering the basic elements, grouping them into categories, and studying their interactions. We are still grouping our way toward the equivalent of the periodic table but are not anywhere near atomic theory. Chemistry had many false leads—such as the postulation of a mysterious substance, phlogiston, which seemed to explain some chemical interactions until it was discovered that to do so phlogiston had to have a negative weight! Chemists also came up with spurious correlations. For example, John Newlands’s law of octaves, which claimed that elements came in clusters of eight like the eight notes in one octave of the familiar do-re-mi-fa-so-la-ti-do scale of Western music. (Though wrong, this idea paved the way for the periodic table.) One hopes the self isn’t like phlogiston!

I started by outlining an evolutionary and anatomical framework for understanding many strange neuropsychiatric syndromes. I suggested that these disorders could be regarded as disturbances of consciousness and self-awareness, which are quintessentially human attributes. (It’s hard to imagine an ape suffering from Cotard syndrome or God delusions.) Some of the disorders arise from the brain’s attempts to deal with intolerable discrepancies among the outputs of different brain modules (as in Capgras syndrome and apotemnophilia) or inconsistencies between internal emotional states and a cognitive appraisal of the external circumstances (as in panic attacks). Other disorders arise from derangement of the normally harmonious interplay of self-awareness and other-awareness that partly involves mirror neurons and their regulation by the frontal lobes.

I began this book with Disraeli’s rhetorical question, “Is man an ape or angel?” I discussed the clash between two Victorian scientists, Huxley and Owen, who argued over this issue for three decades. The former emphasized continuity between the brains of apes and humans, and the latter emphasized human uniqueness. With our increasing knowledge of the brain, we need not take sides on this issue anymore. In a sense they were both right, depending on how you ask the question. Aesthetics exists in birds, bees, and butterflies, but the word “art” (with all its cultural connotations) is best applied to humans—even though, as we have seen, art taps into much of the same circuitry in us as in other animals. Humor is exclusively human but laughter isn’t. No one would ascribe humor to a hyena or even to an ape that “laughs” when tickled. Rudimentary imitation (such as opening a lock) can be also accomplished by orangutans, but imitation of more demanding skills such as spearing an antelope or hafting a hand axe—and in the wake of such imitation the rapid assimilation and spread of sophisticated culture—is seen only in humans. The kind of imitation humans do may have required, among other things, a more complexly evolved mirror-neuron system than what exists in lower primates. A monkey can learn new things, of course, and retain memory. But a monkey cannot engage in conscious recollection of specific events from its past in order to construct an autobiography, imparting a sense of narrative and meaning to its life.

Morality—and its necessary antecedent “free will,” in the sense of envisioning consequences and choosing among them—requires frontal lobe structures that embody values on the basis of which choices are made via the anterior cingulate. This trait is seen only in humans, although simpler forms of empathy are surely present in the great apes.

Complex language, symbol juggling, abstract thought, metaphor, and self-awareness are all almost certainly unique to humans. I have offered some speculation on their evolutionary origins, and suggested also that these functions are mediated partly by specialized structures, such as the angular gyrus and Wernicke’s area. The manufacture and deployment of multicomponent tools intended for future use probably requires yet another uniquely human brain structure, the supramarginal gyrus, which branched off from its ancestor (the inferior parietal lobule) in apes. Self-awareness (and the interchangeably used word “consciousnesses”) has proved to be an especially elusive quarry, but we have seen how it can be approached through studying the inner mental life of neurological and psychiatric patients. Self-awareness is a trait that not only makes us human but also paradoxically makes us want to be more than merely human. As I said in my BBC Reith Lectures, “Science tells us we are merely beasts, but we don’t feel like that. We feel like angels trapped inside the bodies of beasts, forever craving transcendence.” That’s the essential human predicament in a nutshell.

We have seen that the self consists of many strands, each of which can be unraveled and studied by doing experiments. The stage is now set for understanding how these strands harmonize in our normal day-to-day consciousness. Moreover, treating at least some forms of mental illness as disorders of self might enrich our understanding of them and help us devise new therapies to complement traditional ones.

The real drive to understand the self, though, comes not from the need to develop treatments, but from a more deep-seated urge that we all share: the desire to understand ourselves. Once self-awareness emerged through evolution, it was inevitable that an organism would ask, “Who am I?” Across vast stretches of inhospitable space and immeasurable time, there suddenly emerged a person called Me or I. Where does this person come from? Why here? Why now? You, who are made of star-dust, are now standing on a cliff, gazing at the starlit sky pondering your own origins and your place in the cosmos. Perhaps another human stood in that very same spot fifty thousand years ago, asking the very same question. As the mystically inclined, Nobel Prize–winning physicist Erwin Schrödinger once asked, Was he really another person? We wander—to our peril—into metaphysics, but as human beings we cannot avoid doing so.

When informed that their conscious self emerges “simply” from the mindless agitations of atoms and molecules in their brains, people often feel let down, but they shouldn’t. Many of the greatest physicists of this century—Werner Heisenberg, Erwin Schrödinger, Wolfgang Pauli, Arthur Eddington, and James Jeans—have pointed out that the basic constituents of matter, such as quanta, are themselves deeply mysterious if not downright spooky, with properties bordering on the metaphysical. So we need not fear that the self might be any less wonderful or awe inspiring for being made of atoms. You can call this sense of awe and perpetual astonishment God, if you like.

Charles Darwin himself was at times ambivalent about these issues:

I feel most deeply that this whole question of Creation is too profound for human intellect. A dog might as well speculate on the mind of Newton! Let each man hope and believe what he can.

And elsewhere:

I own that I cannot see as plainly as others do, and as I should wish to do, evidence of design and beneficence on all sides of us. There seems to me too much misery in the world. I cannot persuade myself that a beneficent and omnipotent God would have designedly created the Ichneumonidae [a family of parasitic wasps] with the express intention of their feeding within the living bodies of caterpillars or that a cat should play with mice…On the other hand, I cannot anyhow be contented to view this wonderful universe, and especially the nature of man, and to conclude that everything is the result of brute force.

These statements¹ are pointedly directed against creationists, but Darwin’s qualifying remarks are hardly the kind you would expect from the hard-core atheist he is often portrayed to be.

As a scientist, I am one with Darwin, Gould, Pinker, and Dawkins. I have no patience with those who champion intelligent design, at least not in the sense that most people would use that phrase. No one who has watched a woman in labor or a dying child in a leukemia ward could possibly believe that the world was custom crafted for our benefit. Yet as human beings we have to accept—with humility—that the question of ultimate origins will always remain with us, no matter how deeply we understand the brain and the cosmos that it creates.

GLOSSARY

Words and terms in italics have their own entries.

AGNOSIA A rare disorder characterized by an inability to recognize and identify objects and people even though the specific sensory modality (such as vision or hearing) is not defective nor is there any significant loss of memory or intellect.

ALIEN-HAND SYNDROME The feeling that one’s hand is possessed by an uncontrollable outside force resulting in its actual movement. The syndrome usually stems from an injury to the corpus collosum or anterior cingulate.

AMES ROOM ILLUSION A distorted room used to create the optical illusion that a person standing in one corner appears to be a giant while a person standing in another corner appears to be a dwarf.

AMNESIA A condition in which memory is impaired or lost. Two of the most common forms are anterograde amnesia (the inability to acquire new memories) and retrograde amnesia (the loss of preexisting memories).

AMYGDALA A structure in the front end of the temporal lobes that is an important component of the limbic system. It receives several parallel inputs including two projections arriving from the fusiform gyrus. The amygdala helps activate the sympathetic nervous system (fight-or-flight responses). The amygdala sends outputs via the hypothalamus to trigger appropriate reactions to objects—namely, feeding, fleeing, fighting, and sex. Its affective component (the subjective emotions) partly involves connections with the frontal lobes.

ANGULAR GYRUS A brain area situated in the lower part of the parietal lobe near its junction with the occipital and temporal lobes. It is involved in high-level abstraction and abilities such as reading, writing, arithmetic, left-right discrimination, word representation, the representation of fingers, and possibly also comprehension of metaphor and proverbs. The angular gyrus is possibly unique to humans. It is also probably rich in mirror neurons that allow you to see the world from another’s point of view spatially and (perhaps) metaphorically—a key ingredient in morality.

ANOSOGNOSIA A syndrome in which a person who suffers a disability seems unaware of, or denies the existence of, the disability. (Anosognosia is Greek for “denial of illness.”)

ANTERIOR CINGULATE A C-shaped ring of cortical tissue abutting and partially encircling the front part of the large bundle of nerve fibers, called the corpus callosum, that link the left and right hemispheres of the brain. The anterior cingulate “lights up” in many—almost too many—brain-imaging studies. This structure is thought to be involved in free will, vigilance, and attention.

APHASIA A disturbance in language comprehension or production, often as a result of a stroke. There are three main kinds of aphasia: anomia (difficulty finding words), Broca’s aphasia (difficulty with grammar, more specifically the deep structure of language), and Wernicke’s aphasia (difficulty with comprehension and expression of meaning).

APOTEMNOPHILIA A neurological disorder in which an otherwise mentally competent person desires to have a healthy limb amputated in order to “feel whole.” The old Freudian explanation was that the patient wants a large amputation stump resembling a penis. Also called body integrity identity disorder.

APRAXIA A neurological condition characterized by an inability to carry out learned purposeful movements despite knowing what is expected and having the physical ability and desire to do so.

ASPERGER SYNDROME A type of autism in which people have normal language skills and cognitive development but have significant problems with social interaction.

ASSOCIATIVE LEARNING A form of learning in which the mere exposure to two phenomena that always occur together (such as Cinderella and her carriage) leads subsequently to one of the two things spontaneously evoking the memory of the other. Often invoked, incorrectly, as an explanation of synesthesia.

AUTISM One of a group of serious developmental problems called autism spectrum disorders that appear early in life, usually before age three. While symptoms and severity vary, autistic children have problems communicating and interacting with others. The disorder may be related to defects in the mirror-neuron system or the circuits it projects to, although this has yet to be clearly established.

AUTONOMIC NERVOUS SYSTEM A part of the peripheral nervous system responsible for regulating the activity of internal organs. It includes the sympathetic and parasympathetic nervous systems. These originate in the hypothalamus; the sympathetic component also involves the insula.

AXON The fiber-like extension of a neuron by which the cell sends information to target cells.

BASAL GANGLIA Clusters of neurons that include the caudate nucleus, the putamen, the globus pallidus, and the substantia nigra. Located deep in the brain, the basal ganglia play an important role in movement, especially control of posture and equilibrium and unconscious adjustments of certain muscles for execution of more voluntary movements regulated by the motor cortex (see frontal lobe). The finger and wrist movements for screwing a bolt are mediated by the motor cortex, but adjusting the elbow and shoulder to carry this out requires the basal ganglia. Cell death in the substantia nigra contributes to signs of Parkinson’s disease, including a stiff gait and the absence of postural adjustments.

BIPOLAR DISORDER A psychiatric disorder characterized by wild mood swings. Individuals experience manic periods of high energy and creativity and depressed periods of low energy and sadness. Also called manic depressive disorder.

BLACK BOX Before the advent of modern imaging technologies in the 1980s and 1990s, there was no way to peer inside the brain, hence it was likened to a black box. (The phrase is borrowed from electrical engineering.) The black-box approach is also one favored by cognitive psychologists and perceptual psychologists, who draw flow diagrams, or charts that indicate purported stages of information processing in the brain without being burdened by knowledge of brain anatomy.

BLINDSIGHT A condition in some patients who are effectively blind because of damage to the visual cortex but can carry out tasks which would ordinarily appear to be impossible unless they can see the objects. For instance they can point out an object and accurately describe whether a stick is vertical or horizontal, even though they can’t consciously perceive the object. The explanation appears to be that visual information travels along two pathways in the brain: the old pathway and the new pathway. If only the new pathway is damaged, a patient may lose the ability to see an object but still be aware of its location and orientation.

BRAINSTEM The major route by which the cerebral hemispheres send information to and receive information from the spinal cord and peripheral nerves. It also gives rise directly to cranial nerves that go out to muscles of facial expression (frowning, winking, smiling, biting, kissing, pouting, and so forth) and facilitates swallowing and shouting. The brainstem also controls, among other things, respiration and the regulation of heart rhythms.

BROCA’S AREA The region that is located in the left frontal lobe and is responsible for the production of speech that has syntactic structure.

CAPGRAS SYNDROME A rare syndrome in which the person is convinced that close relatives—usually parents, spouse, children or siblings—are imposters. It may be caused by damage to connections between areas of the brain dealing with face recognition and those handling emotional responses. Someone with Capgras syndrome might recognize the faces of loved ones but not feel the emotional reaction normally associated with that person. Also called Capgras delusion.

CEREBELLUM An ancient region of the brain that plays an important role in motor control and in some aspects of cognitive functioning. The cerebellum (Latin for “little brain”) contributes to the coordination, precision, and accurate timing of movements.

CEREBRAL CORTEX The outermost layer of the cerebral hemispheres of the brain. It is responsible for all forms of high(er)-level functions, including perception, nuanced emotions, abstract thinking, and planning. It is especially well developed in humans and to a lesser extent in dolphins and elephants.

CEREBRAL HEMISPHERES The two halves of the brain partially specialized for different things—the left hemisphere for speech, writing, language, and calculation; the right hemisphere for spatial abilities, face recognition in vision, and some aspects of music perception (scales rather than rhythm or beat). A speculative conjecture holds that the left hemisphere is the “conformist,” trying to make everything fit in order to forge ahead, whereas the right hemisphere is your devil’s advocate, or reality check. Freudian defense mechanisms probably evolved in the left hemisphere to confer coherence and stability on behavior.

CLASSICAL CONDITIONING Learning in which a stimulus that naturally produces a specific response (an unconditioned stimulus) is repeatedly paired with a neutral stimulus (a conditioned stimulus). As a result, the conditioned stimulus starts evoking a response similar to that of the unconditioned stimulus. Related to associative learning.

COGNITION The process or processes by which an organism gains knowledge of, or becomes aware of, events or objects in its environment and uses that knowledge for comprehension and problem solving.

COGNITIVE PSYCHOLOGY The scientific study of information processing in the brain. Cognitive psychologists often do experiments to isolate the stages of information processing. Each stage can be described as a black box within which certain specialized computations are performed before the output goes to the next box, so the researcher can construct a flow diagram. The British psychologist Stuart Sutherland defined cognitive psychology as the “ostentatious display of flow diagrams as a substitute for thought.”

COGNITIVE NEUROSCIENCE The discipline that attempts to provide neurological explanations of cognition and perception. The emphasis is on basic science, although there may be clinical spin-offs.

CONE A primary receptor cell for vision located in the retina. Cones are sensitive to color and used primarily for daytime vision.

COTARD SYNDROME A disorder in which a patient asserts that he or she is dead, even claiming to smell rotting flesh or worms crawling over the skin (or some other equally absurd delusion). It may be an exaggerated form of the Capgras syndrome, in which not just one sensory area (such as face recognition) but all sensory areas are cut off from the limbic system, leading to a complete lack of emotional contact with the world and with oneself.

CROSS-MODAL Describes interactions across different sensory systems, such as touch, hearing, and vision. If I showed you an unnameable, irregularly shaped object, then blindfolded you and asked you to pick out the object with your hands from a collection of similar objects, you would use cross-modal interactions to do so. These interactions occur especially in the inferior parietal lobule (especially the angular gyrus) and in certain other structures such as the claustrum (a sheet of cells buried in the sides of the brain that receives inputs from many brain regions) and the insula.

DEFENSE MECHANISMS Term coined by Sigmund and Anna Freud. Information that is potentially threatening to the integrity of one’s “ego” is deflected unconsciously by various psychological mechanisms. Examples include repression of unpleasant memories, denial, rationalization, projection, and reaction formation.

DENDRITE A treelike extension of the neuron cell body. Along with the cell body, it receives information from other neurons.

ELECTROENCEPHALOGRAPHY (EEG) A measure of the brain’s electrical activity in response to sensory stimuli. This is obtained by placing electrodes on the surface of the scalp (or, more rarely, inside the head), repeatedly administering a stimulus, and then using a computer to average the results. The result is an electroencephalogram (also abbreviated EEG).

EPISODIC MEMORY Memory for specific events from your personal experience.

EXAPTATION A structure evolved through natural selection for a particular function that becomes subsequently used—and refined through further natural selection—for a completely novel unrelated function. For example, bones of the ear that evolved for amplifying sound were exapted from reptilian jaw bones used for chewing. Computer scientists and evolutionary psychologists find the idea irritating.

EXCITATION A change in the electrical state of a neuron that is associated with an enhanced probability of action potentials (a train of electrical spikes that occurs when a neuron sends information down an axon).

FRONTAL LOBE One of the four divisions of each cerebral hemisphere. (The other three divisions are the parietal, temporal, and occipital lobes.) The frontal lobes include the motor cortex, which sends commands to muscles on the opposite side of the body; the premotor cortex, which orchestrates these commands; and the prefrontal cortex, which is the seat of morality, judgment, ethics, ambition, personality, character, and other uniquely human attributes.

FUNCTIONAL MAGNETIC RESONANCE IMAGINING (FMRI) A technique—in which the baseline activity of the brain (with the person doing nothing) is subtracted from the activity during task performance—that determines which anatomical regions of the brain are active when a person engages in a specific motor, perceptual, or cognitive task. For example, subtracting a German brain’s activity from that of an Englishman might reveal the “humor center” of the brain.

FUSIFORM GYRUS A gyrus near the bottom inner part of the temporal lobe that has subdivisions specialized for recognizing color, faces, and other objects.

GALVANIC SKIN RESPONSE (GSR) When you see or hear something exciting or significant (such as a snake, a mate, prey, or a burglar), your hypothalamus is activated; this causes you to sweat, which changes your skin’s electrical resistance. Measuring this resistance provides an objective measure of emotional arousal. Also called skin conductance response (SCR).

HEMISPHERES See Cerebral hemispheres.

HIPPOCAMPUS A seahorse-shaped structure located within the temporal lobes. It functions in memory, especially the acquisition of new memories.

HOMININS Members of the Hominini tribe, a taxonomic group recently reclassified to include chimpanzees (Pan), human and extinct protohuman species (Homo), and some ancestral species with a mix of human and apelike features (such as Australopithecus). The hominins are thought to have diverged from the gorillas (Gorillini tribe).

HORMONES Chemical messengers secreted by endocrine glands to regulate the activity of target cells. They play a role in sexual development, calcium and bone metabolism, growth, and many other activities.

“HOW” STREAM The pathway from the visual cortex to the parietal lobe that guides muscle twitch sequences that determine how you move your arm or leg in relation to your body and environment. You need this pathway to accurately reach for an object, and for grasping, pulling, pushing, and other types of object manipulation. To be distinguished from the “what” stream in the temporal lobes. Both “what” and “how” streams diverge from the new pathway, whereas the old pathway starts from the superior colliculus and projects onto the parietal lobe, converging on it with the “how” stream. Also called pathway 1.

HYPOTHALAMUS A complex brain structure composed of many cell clusters with various functions. These include emotions, regulating the activities of internal organs, monitoring information from the autonomic nervous system, and controlling the pituitary gland.

INFERIOR PARIETAL LOBULE (IPL) A cortical region in the middle part of the parietal lobe, just below the superior parietal lobule. It became several times bigger in humans compared with apes, especially on the left. In humans the IPL split into two entirely new structures: the supramarginal gyrus (on top), which is involved in skilled actions such as tool use; and the angular gyrus, involved in arithmetic, reading, naming, writing, and possibly also in metaphorical thinking.

INHIBITION In reference to neurons, a synaptic message that prevents the recipient cell from firing.

INSULA An island of cortex buried in the folds on the side of the brain, divided into anterior, middle, and posterior sections, each of which has many subdivisions. The insula receives sensory input from the viscera (internal organs) as well as taste, smell, and pain inputs. It also gets inputs from the somatosensory cortex (touch, muscle and joint, and position sense) and the vestibular system (organs of balance in the ear). Through these interactions, the insula helps construct a person’s “gut level,” but not fully articulated, sense of a rudimentary “body image.” In addition, the insula has mirror neurons that both detect disgusting facial expressions and express disgust toward unpleasant food and smells. The insula is connected via the parabrachial nucleus to the amygdala and the anterior cingulate.

KORO A disorder that purportedly afflicts young Asian men who develop the delusion that their penises are shrinking and may eventually drop off. The converse of this syndrome—aging Caucasian men who develop the delusion that their penises are expanding—is much more common (as noted by our colleague Stuart Anstis). But it has not been officially given a name.

LIMBIC SYSTEM A group of brain structures—including the amygdala, anterior cingulate, fornix, hypothalamus, hippocampus, and septum—that work to help regulate emotion.

MIRROR NEURONS Neurons that were originally identified in the frontal lobes of monkeys (in a region homologous to the Broca’s language area in humans). The neurons fire when the monkey reaches for an object or merely watches another monkey start to do the same thing, thereby simulating the other monkey’s intentions, or reading its mind. Mirror neurons have also been found for touch; that is, sensory touch mirror neurons fire in a person when she is touched and also when she watches another person being stroked. Mirror neurons also exist for making and recognizing facial expressions (in the insula) and for pain “empathy” (in the anterior cingulate).

MOTOR NEURON A neuron that carries information from the central nervous system to a muscle. Also loosely used to include motor-command neurons, which program a sequence of muscle contractions for actions.

MU WAVES Some specific brain waves that are affected in autism. Mu waves may or may not be an index of mirror-neuron function, but they get suppressed both during action performance and action observation, suggesting a close link with the mirror-neuron system.

NATURAL SELECTION Sexual reproduction results in shuffling genes into novel combinations. Nonlethal mutations arise spontaneously. Those mutations or gene combinations that make some species better adapted to their current environment are the ones that survive more often because the parents survive and reproduce more often. The term is used in opposition to creationism (which holds that all species were created at once) and in contrast to artificial selection by humans to improve livestock and plants. Natural selection is not synonymous with evolution; it is a mechanism that drives evolutionary change.

NEURON Nerve cell. It is specialized for the reception and transmission of information, and is characterized by long fibrous projections called axons and shorter, branchlike projections called dendrites.

NEUROTRANSMITTER A chemical released by neurons at a synapse for the purpose of relaying information via receptors.

NEW PATHWAY Passes information from visual areas to the temporal lobes, via the fusiform gyrus, to help with the recognition of objects as well as with their meaning and emotional significance. The new pathway diverges into the “what” stream and the “how” stream.

OCCIPITAL LOBE One of the four subdivisions (the others being frontal, temporal, and parietal lobes) of each cerebral hemisphere. The occipital lobes play a role in vision.

OLD PATHWAY The older of two main pathways in the brain for visual processing. This pathway goes from the superior colliculus (a primitive brain structure in the brain stem) via the thalamus to the parietal lobes. The old pathway converges on the “how” stream to help move eyes and hands toward objects even when the person does not consciously recognize them. The old pathway is involved in mediating blindsight, when the new pathway alone is damaged.

PARASYMPATHETIC NERVOUS SYSTEM A branch of the autonomic nervous system concerned with the conservation of the body’s energy and resources during relaxed states. This system causes pupils to constrict, blood to be diverted to the gut for leisurely digestion, and heart rate and blood pressure to fall in order to diminish the load on the heart.

PARIETAL LOBE One of the four subdivisions (the others being frontal, temporal, and occipital lobes) of each cerebral hemisphere. A portion of the parietal lobe in the right hemisphere plays a role in sensory attention and body image, while the left parietal is involved in skilled movements and in aspects of language (object naming, reading, and writing). Ordinarily the parietal lobes have no role in the comprehension of language, which happens in the temporal lobes.

PERIPHERAL NERVOUS SYSTEM A division of the nervous system consisting of all nerves not part of the central nervous system (in other words, not part of the brain or spinal cord).

PHANTOM LIMB The perceived existence of a limb lost through accident or amputation.

PONS A part of the stalk on which the brain sits. Together with other brain structures, it controls respiration and regulates heart rhythms. The pons is a major route by which the cerebral hemispheres send information to and receive information from the spinal cord and the peripheral nervous system.

POPOUT TEST A test visual psychologists use to determine whether or not a particular visual feature is extracted early in visual processing. For example, a single vertical line will “pop out” in a matrix of horizontal lines. A single blue dot will “pop out” against a collection of green dots. There are cells tuned to orientation and color in low-level (early) visual processing. On the other hand, a female face will not pop out from a matrix of male faces, because cells responding to the sex of a face occur at a much higher level (later) in visual processing.

PREFRONTAL CORTEX See Frontal lobe.

PROCEDURAL MEMORY Memory for skills (such as learning to ride a bicycle), as opposed to declarative memory, which is storage of specific information that can be consciously retrieved (such as Paris being the capital of France).

PROTOLANGUAGE Presumed early stages of language evolution that may have been present in our ancestors. It can convey meaning by stringing together words in the right order (for example, “Tarzan kill ape”) but has no syntax. The word was introduced by Derek Bickerton of the University of Hawaii.

QUALIA Subjective sensations. (Singular: quale.)

RECEPTOR CELL Specialized sensory cells designed to pick up and transmit sensory information.

RECEPTOR MOLECULE A specific molecule on the surface or inside of a cell with a characteristic chemical and physical structure. Many neurotransmitters and hormones exert their effects by binding to receptors on cells. For example, insulin released by islet cells in the pancreas acts on receptors on target cells to facilitate glucose intake by the cells.

REDUCTIONISM One of the most successful methods used by scientists to understand the world. It only makes the innocuous claim that the whole can be explained in terms of lawful interactions between (not simply the sum of) the component parts. For example, heredity was “reduced” to the genetic code and complementarity of DNA strands. Reducing a complex phenomenon to its component parts does not negate the existence of the complex phenomenon. For ease of human comprehension, complex phenomena can also be described in terms of lawful interactions between causes and effects that are at the “same level” of description as the phenomenon (such as when your doctor tells you, “Your illness is caused by a reduction in vitality”), but this rarely gets us very far. Many psychologists and even some biologists resent reductionism, claiming, for example, that you cannot explain sperm if you know only its molecular constituents but not about sex. Conversely, many neuroscientists are mesmerized by reductionism for its own sake, quite independent of whether it helps explain higher-level phenomena.

REUPTAKE A process by which released neurotransmitters are absorbed at the synapse for subsequent reuse.

SEIZURES A brief paroxysmal discharge of a small group of hyperexcitable brain cells that results in a loss of consciousness (grand mal seizure) or disturbances in consciousness, emotions, and behavior without loss of consciousness (temporal lobe epilepsy). Petit mal seizures are seen in children as a brief “absence.” Such seizures are completely benign and the child almost always outgrows them. Grand mal is often familial and begins in the late teens.

SELF-OTHER DISTINCTION The ability to experience yourself as a self-conscious being whose inner world is separate from the inner worlds of others. Such separateness does not imply selfishness or lack of empathy for others, although it may confer a propensity in that direction. Disturbances of self-other distinctions, as we have argued in Chapter 9, may underlie many strange types of neuropsychiatric illness.

SEMANTIC MEMORY Memory for the meaning of an object, event, or concept. Semantic memory for a pig’s appearance would include a cluster of associations: ham, bacon, oink oink, mud, obesity, Porky the Pig cartoons, and so on. The cluster is bound together by the name “pig.” But our research on patients with anomia and Wernicke’s aphasia suggests that the name is not merely another association; it is a key that opens a treasury of meanings and a handle that can be used for juggling the object or concept around in accordance with certain rules, such as those required for thinking. I have noticed that if an intelligent person with anomia or Wernicke’s aphasia, who can recognize objects but names them incorrectly, initially misnames an object (such as calling a paintbrush a comb), she often proceeds to use it as a comb. She is forced to head up the wrong semantic path by the mere act of mislabeling the object. Language, visual recognition, and thought are more closely interlinked than we realize.

SEROTONIN A monoamine neurotransmitter believed to play many roles including, but not limited to, temperature regulation, sensory perception, and inducing the onset of sleep. Neurons using serotonin as a transmitter are found in the brain and in the gut. A number of antidepressant drugs are used to target serotonin systems in the brain.

“SO WHAT” STREAM Not well defined or anatomically delineated, this pathway involves parts of the temporal lobes concerned with the biological significance of what you are looking at. Includes connections with the superior temporal sulcus, the amygdala, and the insula. Also called pathway 3.

STIMULUS A highly specific environmental event capable of being detected by sensory receptors.

STROKE An impeded blood supply to the brain, caused by a blood clot forming in a blood vessel, the rupture of a blood vessel wall, or an obstruction of flow caused by a clot or fat globule released from injury elsewhere. Deprived of oxygen (which is carried by the blood), nerve cells in the affected area cannot function and thus die, leaving the part of the body controlled by these cells also unable to function. A major cause of death in the West, stroke can result in loss of consciousness and brain function, and in death. During the last decade, studies have shown that feedback from a mirror can accelerate recovery of sensory and motor function in the arm in some stroke patients.

SUPERIOR PARIETAL LOBULE (SPL) A brain region that lies near the top of the parietal lobe. The right SPL is partially concerned with creating one’s body image using inputs from vision and area S2 (joint and muscle sense). The inferior parietal lobule is also involved in this function.

SUPERIOR TEMPORAL SULCUS (STS) The topmost of two horizontal furrows, or sulci, in the temporal lobes. The STS has cells that respond to changing facial expressions, biological movements such as gait, and other biologically salient inputs. The STS sends its output to the amygdala.

SUPRAMARGINAL GYRUS An evolutionarily recent gyrus that split off from the inferior parietal lobule. The supramarginal gyrus is involved in the contemplation and execution of skilled or semiskilled movements. It is unique to humans, and damage to it leads to apraxia.

SYMPATHETIC NERVOUS SYSTEM A branch of the autonomic nervous system, responsible for mobilizing the body’s energy and resources during times of stress and arousal. It does this by regulating temperature as well as increasing blood pressure, heart rate, and sweating in anticipation of exertion.

SYNAPSE A gap between two neurons that functions as the site of information transfer from one neuron to another.

SYNESTHESIA A condition in which a person literally perceives something in a sense besides the sense being stimulated, such as tasting shapes or seeing colors in sounds or numbers. Synesthesia is not just a way of describing experiences as a writer might use metaphors; some synesthetes actually experience the sensations.

SYNTAX Word order that enables compact representation of complex meaning for communicative intent; loosely synonymous with grammar. In the sentence “The man who hit John went to the car,” we recognize instantly that “the man” went to the car, not John. Without syntax we could not arrive at this conclusion.

TEMPORAL LOBE One of the four major subdivisions (the others being frontal, parietal, and occipital lobes) of each cerebral hemisphere. The temporal lobe functions in perception of sounds, comprehension of language, visual perception of faces and objects, acquisition of new memories, and emotional feelings and behavior.

TEMPORAL LOBE EPILEPSY (TLE) Seizures confined mainly to the temporal lobes and sometimes the anterior cingulate. TLE may produce a heightened sense of self and has been linked to religious or spiritual experiences. The person may undergo striking personality changes and/or become obsessed with abstract thoughts. People with TLE have a tendency to ascribe deep significance to everything around them, including themselves. One explanation is that repeated seizures may strengthen the connections between two areas of the brain: the temporal cortex and the amygdala. Interestingly, people with TLE tend to be humorless, a characteristic also seen in seizure-free religious people.

THALAMUS A structure consisting of two egg-shaped masses of nerve tissue, each about the size of a walnut, deep within the brain. The thalamus is the key “relay station” for sensory information, transmitting and amplifying only information of particular importance from the mass of signals entering the brain.

THEORY OF MIND The idea that humans and some higher primates can construct a model in their brains of the thoughts and intentions of other people. The more accurate the model, the more accurately and rapidly the person can predict the other person’s thoughts, beliefs, and actions. The idea is that there are specialized brain circuits in human (and some apes’) brains that allow for theory of mind. Uta Frith and Simon Baron-Cohen have suggested that autistic children may have a deficient theory of mind, which complements our view that a dysfunction of mirror neurons or their targets may underlie autism.

WERNICKE’S AREA A brain region responsible for the comprehension of language and the production of meaningful speech and writing.

“WHAT” STREAM The temporal lobe pathway concerned with recognizing objects and their meaning and significance. Also called pathway 2. See also new pathway and “how” stream.

NOTES

PREFACE

1. I have since learned that this observation has resurfaced from time to time, but for obscure reasons isn’t part of mainstream oncology research. See, for example, Havas (1990), Kolmel et al. (1991), or Tang et al. (1991).

INTRODUCTION: NO MERE APE

1. This basic method for studying the brain is how the whole field of behavioral neurology got started back in the nineteenth century. The major difference between then and now is that in those days there was no brain imaging. The doctor had to wait around for a decade or three for the patient to die, then dissect his brain.

2. In contrast to the hobbits, African pigmies, who are also extraordinarily short, are modern humans in every way, from their DNA right on up through their brains, which are the same size as those of all other human groups.

CHAPTER 2 SEEING AND KNOWING

1. Strictly speaking, the fact that octopuses and humans both have complex eyes is probably not an example of true convergent evolution (unlike the wings of birds, bats, and pterosaurs). The same master control genes are at work in “primitive” eyes as in our own. Evolution sometimes reuses genes that have been stored away in the attic.

2. John was originally studied by Glyn Humphreys and Jane Riddoch, who wrote a beautiful monograph about him: To See but Not to See: A Case Study of Visual Agnosia (Humphreys & Riddoch, 1998). What follows is not a literal transcript but for the most part preserves the patient’s original comments. John suffered from an embolus following appendectomy as indicated, but the circumstances leading up to the appendectomy are a reenactment of the way things might have occurred during a routine diagnosis of appendicitis. (As mentioned in the Preface, to preserve patient confidentiality, throughout the book I often use fictitious names for patients and alter circumstances of hospital admission that are not relevant to the neurological symptoms.)

3. Can you see the Dalmatian dog in Figure 2.7?

4. The distinction between the “how” and “what” pathways is based on the pioneering work of Leslie Ungerleider and Mortimer Mishkin working at the National Institutes of Health. Pathways 1 and 2 (“how” and “what”) are clearly defined anatomically. Pathway 3 (dubbed “so what,” or the emotional pathway) is currently considered a functional pathway, as inferred from physiological and brain lesion studies (such as studies on the double dissociation between the Capgras delusion and prosopagnosia; see Chapter 9).

5. Joe LeDoux has discovered there is also a small, ultra-shortcut pathway from the thalamus (and possibly the fusiform gyrus) directly to the amygdala in rats, and quite possibly in primates. But we won’t concern ourselves with that here. The details of neuroanatomy are unfortunately far messier than we would like, but that shouldn’t stop us from looking for overall patterns of functional connectedness, as we’ve been doing.

6. This idea about the Capgras syndrome was proposed independently of us by Hadyn Ellis and Andrew Young. However, they postulate a preserved “how” stream (pathway 1) and combined damage to the two components of the “what” stream (pathways 2 plus 3), whereas we postulate a selective damage to the emotional stream (pathway 3) alone with sparing of pathway 2.

CHAPTER 3 LOUD COLORS AND HOT BABES: SYNESTHESIA

1. Several experiments point to the same conclusion. In our very first paper on synesthesia, published in 2001 in the Proceedings of the Royal Society of London, Ed Hubbard and I noted that in some synesthetes the strength of color induced seemed to depend not just on the number but on where in the visual field it was presented (Ramachandran & Hubbard, 2001a). When the subject looked straight, then numbers or letters presented off to one side (but made larger to be equally visible) seemed less vividly colored than ones presented in central vision. This, in spite of the fact that they were equally identifiable as particular numbers and in spite of the fact that real colors are just as vividly visible in off-axis (peripheral) vision. Again, these results exclude high-level memory associations as the source of synesthesia. Visual memories are spatially invariant. By that I mean that when you learn something in one region of your visual field—recognizing a particular face, for instance—you can recognize the face presented in a completely new visual location. The fact that the evoked colors are different in different regions argues strongly against memory associations. (I should add that even for the same eccentricity the color is sometimes different for left and right halves of the visual field; possibly because the cross-activation is more pronounced in one hemisphere than the other.)

2. This basic result—that the 2s are more quickly segregated from the 5s in synesthetes than in nonsynesthetes—has been confirmed by other scientists, especially Randolph Blake and Jamie Ward. In a meticulously controlled experiment, Ward and his colleagues found that synesthetes as a group are significantly better than control subjects at seeing the embedded shape made of 2s. Intriguingly, some of them perceived the shape even before any color was evoked! This lends credibility to our early cross-activation model; it’s possible that during brief presentations the colors are evoked sufficiently strongly to permit segregation to occur but not strongly enough to evoke consciously perceived colors.

3. In lower, “projection,” synesthetes there are several lines of evidence (in addition to segregation) supporting the low-level perceptual cross-activation model as opposed to the notion that synesthesia is based entirely on high-level associative learning and memories:

(a) In some synesthetes, different parts of a single number or letter are seen as colored differently. (For example, the V part of an M might be colored red, whereas the vertical lines might be green.)

Soon after the popout/segregation experiment had been done, I noticed something strange in one of the many synesthetes we had been recruiting. He saw numbers as being colored—nothing unusual so far—but what surprised me was his claim that some of the numbers (for example, 8) had different portions colored differently. To make sure he wasn’t making this up, we showed him the same numbers a few months later—without letting him know ahead of time that he would be retested. The new drawing he produced was virtually identical to the first, making it unlikely that he was fibbing.

This observation provides further evidence that, at least in some synesthetes, the colors should be seen as emerging from (to use a computer metaphor) a glitch in neural hardware rather than from an exaggeration of memories or metaphors (a software glitch) Associative learning cannot explain this observation; for example, we don’t play with multicolored magnets. On the other hand, there may be “form primitives” such as line orientation, angles, and curves that get linked to color neurons that execute an earlier stage of form processing within the fusiform than the one at which full-fledged graphemes are assembled.

(b) As previously noted, in some synesthetes the evoked color becomes less vivid when the number is viewed off-axis (in peripheral vision). This probably reflects the greater emphasis on color in central vision (Ramachandran & Hubbard, 2001a; Brang & Ramachandran, 2010). In some of these synesthetes the color is also more saturated in one visual field (left or right) relative to the other. Neither of these observations supports the high-level associative learning model for synesthesia.

(c) An actual increase in anatomical connectivity within the fusiform area of lower synesthetes has been observed by Rouw and Scholte (2007) using diffusion tensor imaging.

(d) The synesthetically evoked color can provide an input to apparent motion perception (Ramachandran & Hubbard, 2002; Kim, Blake, Palmeri, 2006; Ramachandran & Azoulai, 2006).

(e) If you have one type of synesthesia, then you are more likely to have a second unrelated one as well. This supports my “increased cross activation model” of synesthesia; with the mutated gene being more prominently expressed in certain brain regions (in addition to making some synesthetes more creative).

(f) The existence of color-blind (strictly speaking, color anomalous) synesthetes who can see colors in numbers that they can’t see in the real world. The subject couldn’t have learned such associations.

(g) Ed Hubbard and I showed in 2004 that letters that are similar in shape (e.g., curvy rather than angular) tend to evoke similar colors in “lower” synesthetes. This shows that certain figural primitives that define the letters cross-activate colors even before they are fully processed. We suggested that the technique might be used to map an abstract color-space in a systematic manner onto form-space. More recently David Brang and I confirmed this using brain imaging (MEG or magnetoencephalography) in collaboration with Ming Xiong Huang, Roland Lee, and Tao Song.

Taken collectively these observations strongly support the sensory cross-activation model. This is not to deny that learned associations and high-level rules of cross-domain mapping are not also involved (see Notes 8 and 9 for this chapter). Indeed, synesthesia may help us discover such rules.

4. The model of cross-activation—either through disinhibition (a loss or lessening of inhibition) of back projections, or through sprouting—can also explain many forms of “acquired” synesthesia that we have discovered. One blind patient with retinitis pigmentosa whom we studied (Armel and Ramachandran, 1999) vividly experienced visual phosphenes (including visual graphemes) when his fingers were touched with a pencil or when he was reading Braille. (We ruled out confabulation by measuring thresholds and demonstrating their stability across several weeks; there is no way he could have memorized the thresholds.) A second blind patient, whom I tested with my student Shai Azoulai, could quite literally see his hand when he waved it in front of his eyes, even in complete darkness. We suggest that this is caused either by hyperactive back projections or by disinhibition caused by visual loss, so that the moving hand is not merely felt but is also seen. Cells with multimodal receptive fields in the parietal lobes may also be involved in mediating this phenomenon (Ramachandran and Azoulai, 2004).

5. Although synesthesia often involves adjacent brain areas (an example is grapheme-color synesthesia in the fusiform), it doesn’t have to. Even far-flung brain regions, after all, may have preexisting connections that could be amplified (through disinhibition, say). Statistically speaking, however, adjacent brain areas tend to be more “cross-wired” to begin with, so synesthesia is likely to involve those more often.

6. The link between synesthesia and metaphor has already been alluded to. The nature of the link remains elusive given that synesthesia involves arbitrarily connecting two unrelated things (such as color and number), whereas in metaphor there is a nonarbitrary conceptual connection between two things (for example, Juliet and the sun).

One potential solution to this problem emerged from a conversation I had with the eminent polymath Jaron Lanier: We realized that any given word has only a finite set of strong, first-order associations (sun = warm, nurturing, radiant, bright) surrounded by a penumbra of weaker, second-order associations (sun = yellow, flowers, beach) and third-and fourth-order associations that fade way like an echo. It is the overlapping region between two halos of associations that forms the basis of metaphor. (In our example of Juliet and the sun, this overlap derives from observations that both are radiant, warm, and nurturing). Such overlap in halos of associations exists in all of us, but the overlaps are larger and stronger in synesthetes because their the cross-activation gene produces larger penumbras of associations.

In this formulation, synesthesia is not synonymous with metaphor, but the gene that produces synesthesia confers a propensity toward metaphor. A side effect of this may be that associations that are only vaguely felt in all of us (for example, masculine or feminine letters, or good and bad shapes produced by subliminal associations) become more explicitly manifest in synesthetes, a prediction that can be tested experimentally. For instance, most people consider certain female names (Julie, Cindy, Vanessa, Jennifer, Felicia, and so on) to be “sexier” than others (such as Martha and Ingrid). Even though we may not be consciously aware of it, this may be because saying the former involves pouting and other tongue and lip movements with unconscious sexual overtones. The same argument would explain why the French language is often thought of as being more sexy than German. (Compare Busten-halten with brassière.) It might be interesting to see if these spontaneously emerging tendencies and classifications are more pronounced in synesthetes.

Finally, my student David Brang and I showed that completely new associations between arbitrary new shapes and colors are also learned more readily by synesthetes.

Taken collectively, these results show that the different forms of synesthesia span the whole spectrum from sensation to cognition, and indeed this is precisely why synesthesia is so interesting to study.

Another familiar yet intriguing kind of visual metaphor, where meaning resonates with form, is the use (in advertising, for example) of type that mirrors the meaning of the word; for example, using tilted letters to print “tilt,” and wiggly lines to print “fear,” “cold,” or “shiver.” This form of metaphor hasn’t yet been studied experimentally.

7. Effects similar to this were originally studied by Heinz Werner, although he didn’t put it in the broader context of language evolution.

8. We have observed that chains of associations, which would normally evoke only memories in normal individuals, would sometimes seem to evoke qualia-laden sense impressions in some higher synesthetes. So the merely metaphorical can become quite literal. For example, R is red and red is hot so R is hot, and so forth. One wonders whether the hyperconnectivity (either the sprouting or disinhibition) has affected back projections between different areas in the neural hierarchy in these subjects. This would also explain an observation David Brang and I made—that eidetic imagery (photographic memory) is more common in synesthetes. (Back projections are thought to be involved in visual imagery.)

9. The introspections of some higher synesthetes are truly bewildering in their complexity; as they go completely “open loop.” Here is a quotation from one of them: “Most men are shades of blue. Women are more colorful. Because people and names both have color associations, the two don’t necessarily match.” Such remarks imply that any simple phrenological model of synesthesia is bound to be incomplete, although it is not a bad place to start.

In doing science one is often forced to choose between providing precise answers to boring (or trivial) questions such as, How many cones are there in the human eye? or vague answers to big questions such as, What is consciousness? or, What is a metaphor? Fortunately, every now and then we get a precise answer to a big question and hit the jackpot (like DNA being the answer to the riddle of heredity). So far, synesthesia seems to lie halfway between those two extremes.

10. For up-to-date information, see the entry “Synesthesia,” by David Brang and me, at Scholarpedia (www.scholarpedia.org/article/Synesthesia). Scholarpedia is an open-access online encyclopedia written and peer-reviewed by scholars from around the world.

CHAPTER 4 THE NEURONS THAT SHAPED CIVILIZATION

1. A young orangutan in the London zoo once watched Darwin play a harmonica, grabbed it from him, and started to mime him; Darwin had already been thinking of the imitative capacities of apes in the nineteenth century.

2. Since their original discovery, the concept of mirror neurons has been confirmed repeatedly in experiments and has had tremendous heuristic value in our understanding the interface between structure and function in the brain. But it has also been challenged on various grounds. I will list the objections and reply to each.

(a) “Mirroritis”: There is a great deal of media hype surrounding the mirror-neuron system (MNS), with anything and everything being attributed to them. This is true, but the existence of hype doesn’t by itself negate the value of a discovery.

(b) The evidence for their existence in humans is unconvincing. This criticism seems odd to me given that we are closely related to monkeys; the default assumption should be that human mirror neurons do exist. Furthermore, Marco Iacoboni has shown their presence by directly recording from nerve cells in human patients (Iacoboni & Dapretto, 2006).

(c) If such a system exists, why isn’t there a neurological syndrome in which damage to a small region leads to difficulty in BOTH performing and miming skilled or semiskilled actions (such as combing your hair or hammering a nail) AND recognizing the same action performed by someone else? Answer: Such a syndrome does exist, although most psychologists are unaware of it. It is called ideational apraxia and it’s seen after damage to the left supramarginal gyrus. Mirror neurons have been shown to exist in this region.

(d) The antireductionist stance: “Mirror neurons” is just a sexy phrase synonymous with what psychologists have long called “theory of mind.” There’s nothing new about them. This argument confounds metaphor with mechanism: It’s like saying that, since we know what the phrase “passage of time” means, there is no need to understand how clocks work. Or that, since we already knew Mendel’s laws of heredity during the first half of the twentieth century, understanding DNA structure and function would have been superfluous. Analogously, the idea of mirror neurons doesn’t negate the concept of theory of mind. On the contrary, the two concepts complement each other and allow us to home in on the underlying neural circuitry.

This power of having a mechanism to work with can be illustrated with many examples; here are three: In the 1960s, John Pettigrew, Peter Bishop, Colin Blakemore, Horace Barlow, David Hubel, and Torsten Wiesel discovered disparity-detecting neurons in the visual cortex; this finding alone provides an explanation for stereoscopic vision. Second, the discovery that the hippocampus is involved in memory allowed Eric Kandel to discover long-term potentiation (LTP), one of the key mechanisms of memory storage. And finally, one could argue that more was learned about memory in five years of research by Brenda Milner on the single patient “HM,” who had hippocampal damage, than in the previous hundred years of purely psychological approaches to memory. The falsely constructed antithesis between reductionist and holistic views of brain function is detrimental to science, something I discuss at length in Note 16 of Chapter 9.

(e) The MNS is not a dedicated set of hardwired neural circuits; it may be constructed through associative learning. For instance, every time you move your hand, there is activation of motor-command neurons, with simultaneous activation of visual neurons by the appearance of the moving hand. By Hebb’s rule, such repeated coactivations will eventually result in the visual appearance itself triggering these motor neurons, so that they become mirror neurons.

I have two response to this criticism: First, even if the MNS is set up partially through learning, that wouldn’t diminish its importance. The question of how the system works is logically orthogonal to how it is set up (as already mentioned under point d above). Second, if this criticism were true, why wouldn’t all the motor-command neurons become mirror neurons through associative learning? Why only 20 percent? One way to settle this would be to see if there are touch mirror neurons for the back of your head that you have never seen. Since you don’t often touch the back of your head or see the back of it being touched, you aren’t likely to construct an internal mental model of the back of your head in order to deduce that it’s being touched. So you should have far fewer mirror neurons, if any, on this part of your body.

3. The basic idea of the coevolution between genes and culture isn’t new. Yet my claim that a sophisticated mirror-neuron system—conferring an ability to imitate complex actions—was a turning point in the emergence of civilization might be construed as an overstatement. So let’s see how the events may have played out.

Assume that a large population of early hominins (such as Homo erectus or early H. sapiens) had some degree of genetic variation in innate creative talent. If one rare individual through his or her special intellectual gifts had invented something useful, then without the concomitant emergence of sophisticated imitative ability among peers (which requires adopting the other’s point of view and “reading” that person’s intentions), the invention would have died with the inventor. But as soon as the ability to imitate emerged, such one-of-a-kind innovations (including “accidental” ones) would have spread rapidly through the population, both horizontally through kin and vertically through offspring. Then, if any new “innovative ability” mutation later appeared in another individual, she could instantly capitalize on the preexisting inventions in novel ways, leading to the selection and stabilization of the “innovatability” gene. The process would have spread exponentially, setting up an avalanche of innovations that transforms evolutionary change from Darwinian to Lamarckian, culminating in modern civilized humans. Thus the great leap forward was indeed propelled by genetically selected circuits, but ironically the circuits were specialized for learnability—that is, for liberating us from genes! Indeed, cultural diversity is so vast in modern humans that there is probably a greater difference in mental quality and behavior between a university professor and (say) a Texan cowboy (or president) than between the latter and early H. sapiens. Not only is the human brain phylogenetically unique as a whole, but the “brain” of each different culture is unique (through “nurture”)—much more so than in any other animal.

CHAPTER 5 WHERE IS STEVEN? THE RIDDLE OF AUTISM

1. Another way of testing the mirror-neuron hypothesis would be to see if autistic children do not show unconscious subvocalization when listening to others talking. (Laura Case and I are testing this.)

2. Many studies have confirmed my original observation (made with Lindsay Oberman, Eric Altschuler, and Jaime Pineda) of a dysfunctional mirror-neuron system (MNS) in autism (which we accomplished by using mu-wave suppression and fMRI). There is an fMRI study, however, claiming that in one specific brain region (the ventral premotor area, or Broca’s area), autistic children have normal mirror-neuron-like activity. Even if we accept this observation at face value (despite the inherent limitations of fMRI), my theoretical reasons for postulating such a dysfunction will still stand. More important, such observations highlight the fact that the MNS is composed of many far-flung subsystems in the brain that are interconnected for a common function: action and observation. (As an analogy, consider the lymphatic system of the body, which is distributed throughout the body but is functionally a distinct system.)

It is also possible that this part of the MNS itself is normal but its projections or recipient zones in the brain are abnormal. The net result would be the same kind of dysfunction that I originally suggested. In another analogy, consider the fact that diabetes is fundamentally a disturbance of carbohydrate metabolism; no one disputes that. While it is sometimes caused by damage to the pancreatic islet cells, causing a reduction of insulin and an elevation of blood glucose, it can also be caused by a reduction of insulin receptors on cell surfaces throughout the body. This would produce the same syndrome as diabetes without damage to the islets (for islets in the pancreas, think “mirror neurons in the brain’s premotor area called F5”), but the logic of the original argument is unaffected.

Having said all this, let me emphasize that the evidence for MNS dysfunction in autism is, at this point, compelling but not conclusive.

3. The treatments I have proposed for autism in this chapter were inspired in part by the mirror-neuron hypothesis. But their plausibility does not in itself depend on the hypothesis; they would be interesting to try anyway.

4. To further test the mirror-neuron hypothesis of autism, it would be interesting to monitor the activity of the mylohyoid muscle and vocal cords to determine whether autistic children do not show unconscious subvocalization when listening to others talking (unlike normal children, who do). This might provide an early diagnostic tool.

CHAPTER 6 THE POWER OF BABBLE: THE EVOLUTION OF LANGUAGE

1. This approach was pioneered by Brent Berlin. For cross-cultural studies similar to Berlin’s, see Nuckolls (1999).

2. The gestural theory of language origins is also supported by several other ingenious arguments. See Corballis (2009).

3. Even though Wernicke’s area was discovered more than a century ago, we know very little about how it works. One of our main questions in this chapter has been, What aspects of thought require Wernicke’s language area? In collaboration with Laura Case, Shai Azoulai, and Elizabeth Seckel, I examined two patients (LC and KC) on whom I did several experiments (in addition to the ones described in the chapter); here is a brief description of these and other casual observations that are revealing:

(a) LC was shown two boxes: one with a cookie, one without. A student volunteer entered the room and looked at each box expectantly, hoping to open the one with the cookie. I had previously winked to the patient, gesturing him to “lie.” Without hesitation LC pointed out the empty box to the student. (KC responded to this situation the same way.) This experiment shows you don’t need language for a theory-of-mind task.

(b) KC had a sense of humor, laughing at nonverbal Gary Larson cartoons and playing a practical joke on me.

(c) Both KC and LC could play a reasonable game of chess and tic-tac-toe, implying that they have at least a tacit knowledge of if-then conditionals.

(d) Both could understand visual analogy (for example, airplane is to bird as submarine is to fish) when probed nonverbally using pictorial multiple choice.

(e) Both could be trained to use symbols designating the abstract idea “similar but not identical” (wolf and dog, for example).

(f) Both were blissfully unaware of their profound language problem, even though they were producing gibberish. When I spoke to them in Tamil (a south Indian language), one of them said, “Spanish,” while the other nodded as if in understanding and replied in gibberish. When we played a DVD recording of LC’s own utterances back to him, LC nodded and said, “It’s okay.”

(g) LC had profound dyscalculia (for example, reporting 14 minus 5 as 3). Yet he could do nonverbal subtraction. We showed him two opaque cups A and B, and dropped three cookies in A and four in B while he watched. When we removed two cookies from B (as he watched), LC subsequently went straight for A. (KC was not tested.)

(h) LC had a profound inability to understand even simple gestures such as “okay,” “hitchhike,” or “salute,” Nor could he comprehend iconic signs like the restroom sign. He couldn’t match a dollar with four quarters. And preliminary tests showed he was poor at transitivity.

A paradox arises: Given that LC was okay at learning paired associations (for example, pig = nagi) after extensive training, why can’t he relearn his own language? Perhaps the very attempt to engage his preexisting language introduces a software “bug” that forces the malfunctioning language system to go on autopilot. If so, then teaching the patient a completely new language may, paradoxically, be easier than retraining the patient to the original.

Could he learn pidgin, which requires only that words be strung together in the right order (given that his concept formation is unimpaired)? And if he could be taught something as complex as “similar but not same,” why can’t he be taught to attach arbitrary Sassurian symbols (that is, words) to other concepts such as “big,” small,” “on,” “if,” “and,” and “give”? Would this not enable him to understand a new language (such as French or American Sign Language), which would allow him to at least converse with French people or signers? Or if the problem is in linking heard sounds with objects and ideas, why not use a language based on visual tokens (as was done with Kanzi, the bonobo)?

The oddest aspects of Wernicke’s aphasia are the patients’ complete lack of insight into their own profound inability to comprehend or produce language, whether written or spoken, and their total lack of any frustration. We once gave LC a book to read and walked out of the room. Even though he couldn’t understand a single word, he kept scanning the print and turning the pages for fifteen minutes. He even bookmarked some pages! (He was unaware of the fact that the video camera filming him had been left on during our absence.)

CHAPTER 7 BEAUTY AND THE BRAIN: THE EMERGENCE OF AESTHETICS

1. One has to be careful to not overdo this type of reductionist thinking about art and the brain. I recently heard an evolutionary psychologist give a lecture about why we like kinetic art, which includes pieces like Calder mobiles made up of moving cutout shapes dangling from the ceiling. With a perfectly straight face he proclaimed that we like such art because an area in our brain called the MT (middle temporal) area possesses cells that are specialized for detecting the direction of motion. This claim is nonsense. Kinetic art obviously excites such cells, but so would a snowstorm. So would a copy of the Mona Lisa set spinning on a peg. Neural circuitry for motion detection is certainly necessary for kinetic art but it’s not sufficient: It doesn’t explain the appeal of kinetic art by any stretch of logic. This chap’s explanation is like saying that the existence of face-sensitive cells in the fusiform gyrus of your brain explains why you like Rembrandt. Surely to explain Rembrandt you need to show how he enhanced his images and why such embellishments elicit responses from the neural circuits in your brain more powerfully than a realistic photograph does. Until you do that, you have explained nothing.

2. Note that peak shift should also be applicable in animation. For example, you can create a striking perceptual illusion by mounting tiny LEDs (light-emitting diodes) on a person’s joints and having her walk around in a dark room. You might expect to see just a bunch of LEDs moving around randomly, but instead you get a vivid sense of seeing a whole person walking, even though all her other features—face, skin, hair, outline, and so forth—are invisible. If she stops moving, you suddenly cease to see the person. This implies that the information about her body is conveyed entirely by the motion trajectories of the light spots. It’s as though your visual areas are exquisitely sensitive to the parameters that distinguish this type of biological motion from random motion. It’s even possible to tell if the person is a man or woman by looking at the gait, and a couple dancing provides an especially amusing display.

Can we exploit our laws to heighten this effect? Two psychologists, Bennett Bertenthal of Indiana University and James Cutting of Cornell University, mathematically analyzed the constraints underlying biological motion (which depend on permissible joint motions) and wrote a computer program that incorporates the constraints. The program generates a perfectly convincing display of a walking person. While these images are well known, their aesthetic appeal has rarely been commented on. In theory it should be possible to amplify the constraints so that the program could produce an especially elegant feminine gait caused by a large pelvis, swaying hips and high heels as well as an especially masculine gait caused by erect posture, stiff stride, and tight buttocks. You’d create a peak shift with a computer program.

We know the superior temporal sulcus (STS) has dedicated circuitry for extracting biological motion, so a computer manipulation of human gait might hyperactivate those circuits by exploiting two aesthetic laws in parallel: isolation (isolating the biological motion cues from other static cues) and peak shift (amplifying the biological characteristics of the motion). The result might end up being an evocative work of kinetic art that surpasses any Calder mobile. I predict that STS cells for biological motion could react even more strongly to “peak-shifted” point-light walkers.

CHAPTER 8 THE ARTFUL BRAIN: UNIVERSAL LAWS

1. Indeed, peekaboo in children may be enjoyable for precisely the same reason. In early primate evolution while still primarily inhabiting the treetops, most juveniles often became temporarily occluded completely by foliage. Evolution saw fit to make peekaboo visually reinforcing for offspring and mother, as they periodically glimpsed each other, thereby ensuring that the child was kept safe and within a reasonable distance. Additionally, the smile and laugh of parent and offspring would have mutually reinforced each other. One wonders whether apes enjoy peekaboo.

The laughter seen after peekaboo is also explained by my ideas on humor (see Chapter 1), that it results from; a buildup of expectation followed by a surprising deflation. Peakaboo could be regarded as a cognitive tickle.

2. See also Note 6 of Chapter 3, where the effect of altering type to match the meaning of the words was discussed—there from the standpoint of synesthesia rather than humor and aesthetics.

3. To these nine laws of aesthetics we may add a tenth law that overarches the others. Let’s call it “resonance” because it involves the clever use of multiple laws enhancing each other in a single image. For example, in many Indian sculptures, a sexy nymph is portrayed languorously standing beneath the arched branch of a tree which has ripe fruits dangling from it. There are the peak shifts in posture and form (for example, large breasts) that make her exquisitely feminine and voluptuous. Additionally, the fruits are a visual echo of her breasts, but they also conceptually symbolize the fecundity and fertility of nature just as the nymph’s breasts do; so the perceptual and conceptual elements resonate. The sculptor will also often add baroque ornate jewelry on her otherwise naked torso to enhance, by contrast, the smoothness and suppleness of her youthful estrogen-charged skin. (I mean contrast of texture rather than of luminance here.) A more familiar example would be a Monet in which peekaboo, peak shift, and isolation are all combined in a single painting.

CHAPTER 9 AN APE WITH A SOUL: HOW INTROSPECTION EVOLVED

1. Two questions may legitimately be raised about metarepresentations. First, isn’t this just a matter of degree? Perhaps a dog has a metarepresentation of sorts that’s richer than what a rat has but not quite as rich as a human’s (the “When to you start calling a man bald” issue). This question was raised and answered in the Introduction, where we noted that nonlinearities are common in nature—especially in evolution. A fortuitous coemergence of attributes can produce a relatively sudden, qualitative jump, resulting in a novel ability. A metarepresentation doesn’t merely imply richer associations; it also requires the ability to intentionally summon up these associations, attend to them at will, and manipulate them mentally. These abilities require frontal lobe structures, including the anterior cingulate, to direct attention to different aspects of the internal image (although concepts such as “attention” and “internal image” conceal vast depths of ignorance). An idea similar to this was originally proposed by Marvin Minsky.

Second, doesn’t postulating a metarepresentation make us fall into the homunculus trap? (See Chapter 2, where the homunculus fallacy was discussed.) Doesn’t it imply a little man in the brain watching the metarepresentation and creating a meta-metarepresentation in his brain? The answer is no. A metarepresentation is not a picture-like replica of sensory representation; it results from further processing of early sensory representations and packaging them into more manageable chunks for linking to language and symbol juggling.

The telephone syndrome, which Jason had, has been studied by Axel Klee and Orrin Devinsky.

2. I recall a lecture given at the Salk Institute by Francis Crick, who with James Watson codiscovered the structure of DNA and deciphered the genetic code, thereby unraveling the physical basis of life. Crick’s lecture was on consciousness, but before he could begin, a philosopher in the audience (from Oxford, I believe) raised his hand and protested, “But Professor Crick, you say you are going to talk about the neural mechanisms of consciousness, but you haven’t even bothered to define the word properly.” Crick’s response: “My dear chap, there was never a time in the history of biology when a group of us sat around the table saying let’s define life first. We just went out there and found out what it was—a double helix. We leave matters of semantic distinctions and definitions to you philosophers.”

3. Almost everyone knows of Freud as the father of psychoanalysis, but few realize that he began his career as a neurologist. Even as a student he published a paper on the nervous system of a primitive fishlike creature called a lamprey, convinced that the surest way to understand the mind was to approach it through neuroanatomy. But he soon became bored with lampreys and began to feel that his attempts to bridge neurology and psychiatry were premature. So he switched to “pure” psychology, inventing all the ideas we now associate with his name: id, ego, superego, Oedipus complex, penis envy, thanatos, and the like.

In 1896 he became disillusioned once again and wrote his now famous “Manifesto for a Scientific Psychology” urging a neuroscientific approach to the human mind. Unfortunately he was way ahead of his time.

4. Although we intuitively understand what Freud meant, one could argue that the phrase “unconscious self” is an oxymoron since self-awareness (as we shall see) is one of the defining characteristics of the self. Perhaps the phrase “unconscious mind(s)” would be better, but the exact terminology isn’t important at this stage. (See also Note 2 for this chapter.)

5. Since Freud’s era there have been three major approaches to mental illness. First, there is “psychological,” or talk therapy, which would include psychodynamic (Freudian) as well as more recent “cognitive” accounts. Second, there are the anatomical approaches, which simply point out correlations between certain mental disorders and physical abnormalities in specific structures. For example, there is a presumed link between the caudate nucleus and obsessive-compulsive disorder, or between right frontal lobe hypometabolism and schizophrenia. Third there are neuropharmacological interpretations: think Prozac, Ritalin, Xanax. Of these three, the last approach has paid rich dividends (at least to the pharmaceutical industry) in terms of treating psychiatric disease; for better or worse, it has revolutionized the field.

What is missing, though, and what I have attempted to broach in this book, is what might be called “functional anatomy”—to explain the cluster of symptoms that are unique to a given disorder in terms of functions that are equally unique to certain specialized circuits in the brain. (Here one must distinguish between a vague correlation and an actual explanation.) Given the inherent complexity of the human brain, it is unlikely that there will be a single climactic solution like DNA (although I don’t rule it out). But there may well be many instances where such a synthesis is possible on a smaller scale, leading to testable predictions and novel therapies. These examples may even pave the way for a grand unified theory of the mind—of the kind physicists have been dreaming about for the material universe.

6. The idea of a hardwired genetic scaffolding for one’s body image was also brought home to me vividly when Paul McGeoch and I recently saw a fifty-five-year-old woman with a phantom hand. She had been born with a birth defect called phocomelia; most of her right arm had been missing since birth except for a hand dangling from her shoulder with only two fingers and a tiny thumb. When she was twenty-one, she was in a car crash that entailed amputation of the crushed hand, but much to her surprise she experienced a phantom hand with four fingers instead of two! It was as if her entire hand was hardwired and lying dormant in her brain, being suppressed and refashioned by the abnormal proprioception (joint and muscle sense) and visual image of her deformed hand. Until the age of twenty-one, when removal of the deformed hand allowed her dormant hardwired hand to reemerge into consciousness as a phantom. The thumb did not come back initially, but when she used the mirror box (at age fifty-five) her thumb was resurrected as well.

In 1998, in a paper published in Brain, I reported that by using visual feedback with mirrors positioned in the right manner, one could make the phantom hand adopt anatomically impossible positions (such as fingers bending backward)—despite the fact that the brain had never previously computed or experienced that before. The observation has since then been confirmed by others.

Findings such as these emphasize the complexity of interactions between nature and nurture in constructing body image.

7. We don’t know where the discrepancy between S2 and the SPL is picked up, but my intuition is that the right insula is involved, given the GSR increase. (The insula is partly involved in generating the GSR signal.) Consistent with this, the insula is also involved in nausea and vomiting due to discrepancies between the vestibular and visual senses (which familiarly produces seasickness, for example).

8. Intriguingly, even some otherwise normal men report having mainly phantom erections rather than real ones, as my colleague Stuart Anstis pointed out to me.

9. This “adopting an objective view” toward oneself is also an essential requirement for discovering and correcting one’s own Freudian defenses, which is partially achieved through psychoanalysis. The defenses are ordinarily unconscious; the concept of “conscious defenses” is an oxymoron. The therapist’s goal, then, is to bring the defenses to the surface of your consciousness so you can deal with them (just as an obese person needs to analyze the source of his obesity to take corrective measures). One wonders whether adopting a conceptual allocentric stance (in plain English: encouraging the patient to adopt a realistic detached view of herself and her follies) for psychoanalysis could be aided by encouraging the patient to adopt a perceptual allocentric stance (such as pretending she is someone else watching her own lecture). This in turn could, in theory, be facilitated by ketamine anesthesia. Ketamine generates out-of-body experiences, making you see yourself from outside.

Or perhaps we could mimic the effects of ketamine by using mirrors and video cameras, which can also produce out-of-body experiences. It seems ludicrous to suggest the use of optical tricks for psychoanalysis, but believe me, I have seen stranger things in my career in neurology. (For example, Elizabeth Seckel and I used a combination of multiple reflections, delayed video feedback, and makeup to create a temporary out-of-body experience in a patient with fibromyalgia, a mysterious chronic pain disorder that affects the entire body. The patient reported a substantial reduction in pain during the experience. As for all pain disorders, this requires placebo-controlled evaluation.)

Returning to psychoanalysis: surely, removing psychological defenses raises a dilemma for the analyst; it’s a double-edged sword. If defenses are normally an adaptive response by the organism (mainly by the left hemisphere) to avoid destabilization of behavior, wouldn’t laying bare these defenses be maladaptive, disturbing one’s sense of an internally consistent self along with your inner peace? The way out of this dilemma is to realize that mental illness and neuroses arise from a misapplication of defenses—no biological system is perfect. Such a misapplication would, if anything, lead to additional chaos rather than restoring coherence.

And there are two reasons for this. First, chaos may result from “leakage” of improperly suppressed emotions from the right hemisphere, leading to anxiety—a poorly articulated internal feeling of lacking harmony in one’s life. Second, there may be instances in which defenses might be maladaptive for the person in his real life; a little overconfidence is adaptive but too much isn’t; it leads to hubris and to unrealistic delusions about one’s abilities; you start buying Ferraris you can’t afford. There is a fine line between what’s maladaptive and what’s not, but an experienced therapist knows how to correct only the former (by bringing them out) while preserving the latter, so that she avoids causing what Freudians call a catastrophic reaction (a euphemism for “The patient breaks down and starts crying”).

10. Our sense of coherence and unity as a single person may—or may not—require a single brain region, but if it does, reasonable candidates would include the insula and the inferior parietal lobule—each of which receives a convergence of multiple sensory inputs. I mentioned this idea to my colleague Francis Crick just before his death. With a sly conspiratorial wink he told me that a mysterious structure called the claustrum—a sheet of cells buried in the sides of the brain—also receives inputs from many brain regions, and may therefore mediate the unity of conscious experience. (Perhaps we are both right!) He added that he and his colleague Christof Koch had just finished writing a paper on this very topic.

11. This speculation is based on a model proposed by German Berrios and Mauricio Sierra of Cambridge University.

12. The distinction between the “how” and “what” pathways was first made by Leslie Ungerleider and Mortimer Mishkin of the National Institutes of Health; it is based on meticulous anatomy and physiology. The further subdivision of the “what” pathway into pathways 2 (semantics and meaning) and 3 (emotions) is more speculative and based on functional criteria; a combination of neurology and physiology. (For example, cells in the STS respond to changing facial expressions and biological motion, and the STS has connections with the amygdala and the insula—both involved in emotions.) Postulating a functional distinction between pathways 2 and 3 also helps explain Capgras syndrome and prosopagnosia, which are mirror images of each other, in terms of both symptoms and GSR responses. This cannot occur if messages were processed entirely in a sequence from meaning to emotion and there was no parallel output from the fusiform area to the amygdala (either directly or via the STS).

13. Here and elsewhere, although I invoke the mirror-neuron system as a candidate neural system, the logic of the argument doesn’t depend critically on that system. The crux of the argument is that there must be specialized brain circuitry for recursive self-representation and for maintaining a distinction—and reciprocity—between the self and the other in the brain. A dysfunction of this system would contribute to many of the seemingly bizarre syndromes described in this chapter.

14. To complicate matters further, Ali started developing other delusions as well. A psychiatrist diagnosed him as having schizophrenia or “schizoid traits” (in addition to his epilepsy) and prescribed him antipsychotic medication. The last time I saw Ali, in 2009, he was claiming that in addition to being dead he had grown to enormous size, reaching out into the cosmos to touch the moon, becoming one with the Universe—as if nonexistence and union with the cosmos were synonymous. I began to wonder if his seizure activity had spread into his right parietal lobe, where body image is constructed, which might explain why he had lost his sense of scale, but I have not yet had a chance to investigate this hunch.

15. One might expect, therefore, that in Cotard syndrome there would initially be no GSR whatsoever, but it should be partially restored with SSRIs (selective serotonin reuptake inhibitors). This can be tested experimentally.

16. When I make remarks of this nature about God (or use the word “delusion”), I do not wish to imply that God doesn’t exist; the fact that some patients develop such delusions doesn’t disprove God—certainly not the abstract God of Spinoza or Shankara. Science has to remain silent on such maters. I would argue, like Erwin Schrödinger and Stephen Jay Gould, that science and religion (in the nondoctrinaire philosophical sense) belong to different realms of discourse and one cannot negate the other. My own view, for what it is worth, is best exemplified by the poetry of the bronze Nataraja (The Dancing Shiva), which I described in Chapter 8.

17. There has long been a tension in biology between those who advocate a purely functional, or black-box approach, and those who champion reductionism, or understanding how component parts interact to generate complex functions. The two groups are often contemptuous of each other.

Psychologists often promote black-box functionalism and attack reductionist neuroscience—a syndrome I have dubbed “neuron envy.” The syndrome is partly a legitimate reaction to the fact that most funding from grant-giving agencies tends to be siphoned off, unfairly, by neuroreductionists. Neuroscience also garners the lion’s share of attention from the popular press, partly because people (including scientists) like looking at the results of brain imaging; all those pretty colored dots on pictures of brains. At a recent meeting of the Society for Neuroscience, a colleague approached me to describe an elaborate-brain imaging experiment he had done which used a complex cognitive-perceptual task to explore brain mechanisms. “You will never guess which area of the brain lit up, Dr. Ramachandran,” he said, brimming with enthusiasm. I responded with a sly wink saying, “Was it the anterior cingulate?” The man was astonished, failing to realize that the anterior cingulate lights up on so many of these tasks that the odds were already stacked in my favor, even though I was just guessing.

But by itself, pure psychology or “black boxology” (which Stuart Sutherland once defined as “the ostentatious display of flow diagrams as a substitute for thought”) is unlikely to generate revolutionary advances in biology, where mapping function onto structure has been the most effective strategy. (And I would consider psychology to be a branch of biology.) I will drive home this point using an analogy from the history of genetics and molecular biology.

Mendel’s laws of heredity, which established the particulate nature of genes, was an example of the black-box approach. These laws were established by simply studying the patterns of inheritance that resulted from mating different types of pea plants. Mendel derived his laws by simply looking at the surface appearance of hybrids and deducing the existence of genes. But he didn’t know what or where genes were. That became known when Thomas Hunt Morgan zapped the chromosomes of fruit flies with X-rays and found that the heritable changes in appearance that occurred in the flies (mutations) correlated with changes in banding patterns of chromosomes. (This would be analogous to lesion studies in neurology.) This discovery allowed biologists to home in on chromosomes—and the DNA within them—as the carriers of heredity. Which in turn paved the way for decoding DNA’s double helical structure and the genetic code of life. But once the molecular machinery of life was decoded, it not only explained heredity but a great many other previously mysterious biological phenomena as well.

The key idea came when Crick and Watson saw the analogy between the complementarity of the two strands of DNA and the complementarity between parent and offspring, and recognized that the structural logic of DNA dictates the functional logic of heredity: a high-level phenomenon. That flash of insight gave birth to modern biology. I believe that the same strategy of mapping function onto structure is the key to understanding brain function.

More relevant to this book is the discovery that damage to the hippocampus leads to anterograde amnesia. This allowed biologists to focus on synapses in the hippocampus, leading to the discovery of LTP (long-term potentiation), the physical basis of memory. Such changes were originally discovered by Eric Kandel in a mollusk named Aplysia.

In general, the problem with the pure black-box approach (psychology) is that sooner or later you get multiple competing models to explain a small set of phenomena, and the only way to find out which is right is through reductionism—opening the box(es). A second problem is that they very often have an ad hoc “surface level” quality, in that they may partially “explain” a given “high level” or macroscopic phenomenon but don’t explain other macroscopic phenomena and their predictive power is limited. Reductionism, on the other hand, often explains not just the phenomenon in question at a deeper level but often also ends up explaining a number of other phenomena as well.

Unfortunately, for many physiologists reductionism becomes an end in itself, a fetish almost. An analogy to illustrate this comes from Horace Barlow. Imagine that an asexual (parthenogenetic) Martian biologist lands on Earth. He has no idea what sex is since he reproduces by dividing into two, like an ameba. He (it) examines a human and finds two round objects (which we call testes) dangling between the legs. Being a reductionist Martian, he dissects them and, looking through microscope, finds them swarming with sperms; but he wouldn’t know what they were for. Barlow’s point is that no matter how meticulous the Martian is at dissection and how detailed an analysis he performs on them he will never truly understand the function of the testes unless he knew about the “macroscopic” phenomenon of sex; he may even think the sperm are wriggling parasites. Many (fortunately not all!) of our physiologists recording from brain cells are in the same position as the asexual Martian.

The second, related point is that one must have the intuition to focus on the appropriate level of reductionism for explaining a given higher-level function (such as sex). If Watson and Crick had focused on the subatomic level or atomic level of chromosomes instead of the macromolecular level (DNA), or if they had focused on the wrong molecules (the histones in the chromosomes instead of DNA) they would have made no headway in discovering the mechanism of heredity.

18. Even simple experiments on normal subjects can be instructive in this regard. I will mention an experiment I did (with my student Laura Case) inspired by the “rubber hand illusion” discovered by Botvinick and Cohen (1998) and by the dummy-head illusion (Ramachandran and Hirstein, 1998). You, the reader, stand about a foot behind a bald-headed manikin looking at its head. I stand on the right side of you both and randomly tap and stroke the back of your head (especially ears) with my left hand (so you can’t see my hand) while simultaneously doing the same thing on the plastic head with my right hand, in perfect synchrony. In about two minutes you will experience that the stroking and tapping on your head is emerging from the dummy you are looking at. Some people develop the illusion of a twin or phantom head in front of them, especially if they get it going by “imagining” their head displaced forward. The brain regards it as highly improbable that the plastic head is seen to be tapped in the same precise sequence as you feel on own head by chance and so is willing to temporarily to project your head on the manikin’s shoulder. This has powerful implications since, contrary to recent proposals, it rules out simple associative learning as the basis of the rubber hand illusion. (Every time you saw your hand touched you felt it touched as well.) After all, you have never seen the back of your head being touched. It is one thing to regard your hand sensations as being slightly out of register with your real hand but quite another to project them to the back of a dummy head!

The experiment proves that your brain has constructed an internal model of your head—even unseen parts—and used Bayesian inference to experience (incorrectly) your sensations as arising from the dummy’s head even though it is logically absurd. Would doing something like this help alleviate your migraine symptoms (“the dummy is experiencing migraine; not me”)? I wonder.

Olaf Blanke and Henrik Ehrsson of the Karolinska Institute in Sweden have shown that out-of-body experiences can also be induced by having subjects watch video images of themselves moving or being touched. Laura Case, Elizabeth Seckel, and I found that such illusions are enhanced if you wear a Halloween mask and introduce a tiny time delay together with a left-right reversal in the image. You suddenly start inhabiting and controlling the “alien” in the video image. Remarkably, if you wear a smiling mask you actually feel happy because “you, out there” look happy! I wonder if you could use it to “cure” depression.

EPILOGUE

1. These two Darwin quotes come from the London Illustrated News, April 21, 1862 (“I feel most deeply…”), and Darwin’s letter to Asa Gray, May 22, 1860 (“I own that I cannot see…”).

BIBLIOGRAPHY

Entries marked with an asterisk are suggestions for further reading.

Aglioti, S., Bonazzi, A., & Cortese, F. (1994). Phantom lower limb as a perceptual marker of neural plasticity in the mature human brain. Proceedings of the Royal Society of London, Series B: Biological Sciences, 255, 273–278.

Aglioti, S., Smania, N., Atzei, A., & Berlucchi, G. (1997). Spatio-temporal properties of the pattern of evoked phantom sensations in a left index amputee patient. Behavioral Neuroscience, 111, 867–872.

Altschuler, E. L., & Hu, J. (2008). Mirror therapy in a patient with a fractured wrist and no active wrist extension. Scandinavian Journal of Plastic and Reconstructive Surgery and Hand Surgery, 42(2), 110–111.

Altschuler, E. L., Vankov, A., Hubbard, E. M., Roberts, E., Ramachandran, V. S., & Pineda, J. A. (2000, November). Mu wave blocking by observer of movement and its possible use as a tool to study theory of other minds. Poster session presented at the 30th annual meeting of the Society for Neuroscience, New Orleans, LA.

Altschuler, E. L., Vankov, A., Wang, V., Ramachandran, V. S., & Pineda, J. A. (1997). Person see, person do: Human cortical electrophysiological correlates of monkey see monkey do cells. Poster session presented at the 27th Annual Meeting of the Society for Neuroscience, New Orleans, LA.