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

by V.S. Ramachandran

A Brief Tour of Your Brain

Neurons “talk” to each other through threadlike fibers that alternately resemble dense, twiggy thickets (dendrites) and long, sinuous transmission cables (axons). Each neuron makes from one thousand to ten thousand contacts with other neurons. These points of contact, called synapses, are where information gets shared between neurons.

And the smallest muscle in the body, which is used to abduct the little toe, is the abductor ossis metatarsi digiti quinti minimi. I think it sounds like a poem. (With the first wave of the Harry Potter generation now coming up through medical school, perhaps soon we’ll finally start hearing these terms pronounced with more of the relish they deserve.)

(In contrast, the cortex of most other mammals is smooth and flat for the most part, with few if any folds in the surface.) The cortex is essentially the seat of higher thought, the tabula (far from) rasa where all of our highest mental functions are carried out. Not surprisingly, it is especially well developed in two groups of mammals: dolphins and primates.

This thickening is called the brainstem, and it is divided into three lobes: medulla, pons, and midbrain. The medulla and nuclei (neural clusters) on the floor of the pons control important vital functions like breathing, blood pressure, and body temperature. A hemorrhage from even a tiny artery supplying this region can spell instant death. (Paradoxically, the higher areas of the brain can sustain comparatively massive damage and leave the patient alive and even fit. For example, a large tumor in the frontal lobe might produce barely detectable neurological symptoms.)

Surrounding the top portion of the brainstem are the thalamus and the basal ganglia. The thalamus receives its major inputs from the sense organs and relays them to the sensory cortex for more sophisticated processing. Why we need a relay station is far from clear.

Broadly speaking, the occipital lobes are mainly concerned with visual processing. In fact, they are subdivided into as many as thirty distinct processing regions, each partially specialized for a different aspect of vision such as color, motion, and form. The temporal lobes are specialized for higher perceptual functions, such as recognizing faces and other objects and linking them to appropriate emotions.

In addition to all this, the upper part of the left temporal lobe contains a patch of cortex known as Wernicke’s area. In humans this area has ballooned to seven times the size of the same area in chimpanzees; it is one of the few brain areas that can be safely declared unique to our species. Its job is nothing less than the comprehension of meaning and the semantic aspects of language—functions

Even more remarkable is somatoparaphrenia, the patient’s vehement denial of ownership of her own left arm and insistence that it belongs to someone else.

The parietal lobes have expanded greatly in human evolution, but no part of them has grown more than the inferior parietal lobules (IPL; see Figure Int.2). So great was this expansion that at some point in our past a large portion of it split into two new processing regions called the angular gyrus and the supramarginal gyrus.

The frontal lobes also perform several distinct and vital functions. Part of this region the motor cortex—the vertical strip of cortex running just in front of the big furrow in the middle of the brain (Figure Int.2)—is involved in issuing simple motor commands. Other parts are involved in planning actions and keeping goals in mind long enough to follow through on them.

But when you move to the more anterior part of the frontal lobes you enter the most inscrutable terra incognita of the brain: the prefrontal cortex (parts of which are identified in Figure Int.2). Oddly enough, a person can sustain massive damage to this area and come out of it showing no obvious signs of any neurological or cognitive deficits. The patient may seem perfectly normal if you casually interact with her for a few minutes. Yet if you talk to her relatives, they will tell you that her personality has changed beyond recognition.

It is difficult to overstate the importance of understanding mirror neurons and their function. They may well be central to social learning, imitation, and the cultural transmission of skills and attitudes—perhaps even of the pressed-together sound clusters we call “words.” By hyper-developing the mirror-neuron system, evolution in effect turned culture into the new genome. Armed with culture, humans could adapt to hostile new environments and figure out how to exploit formerly inaccessible or poisonous food sources in just one or two generations—instead of the hundreds or thousands of generations such adaptations would have taken to accomplish through genetic evolution.

Victor said he had never discovered this virtual hand on his face before, but as soon as he knew about it he found a way to put it to good use: Whenever his phantom palm itches—a frequent occurrence that used to drive him crazy—he says he can now relieve it by scratching the corresponding location on his face. Why does all this happen? The answer, I realized, lies in the brain’s anatomy. The entire skin surface of the left side of the body is mapped onto a strip of cortex called the postcentral gyrus (see Figure Int.2 in the Introduction) running down the right side of the brain.

How could one test such an outlandish theory? I hit on the idea of constructing a mirror box (Figure 1.4). I placed an upright mirror in the center of a cardboard box whose top and front had been removed. If you stood in front of the box, held your hands on either side of the mirror and looked down at them from an angle, you would see the reflection of one hand precisely superimposed on the felt location of your other hand. In other words, you would get the vivid but false impression that you were looking at both of your hands; in fact, you would only be looking at one actual hand and one reflection of a hand.

How does this explain Mikhey’s laughter? I didn’t know this at that time, but many years later I saw another patient named Dorothy with a similar “laughter from pain” syndrome. A CT (computed tomography) scan revealed that one of the pain pathways in her brain was damaged. Even though we think of pain as a single sensation, there are in fact several layers to it. The sensation of pain is initially processed in a small structure called the insula (“island”), which is folded deep beneath the temporal lobe on each side of the brain (see Figure Int.2, in the Introduction). From the insula the pain information is then relayed to the anterior cingulate in the frontal lobes. It is here you feel the actual unpleasantness—the agony and the awfulness of the pain—along with an expectation of danger. If this pathway is cut, as it was in Dorothy and presumably in Mikhey, the insula continues to provide the basic sensation of pain but it doesn’t lead to the expected awfulness and agony: The anterior cingulate doesn’t get the message. It says, in effect, “all’s okay.” So here we have the two key ingredients for laughter: A palpable and imminent indication that alarm is warranted (from the insula) followed by a “no big whoop” follow-up (from the silence of the anterior cingulate). So the patient laughs uncontrollably. And the same holds for tickling.

Lastly, consider that universal greeting gesture in humans: the smile. When an ape is approached by another ape, the default assumption is that it is being approached by a potentially dangerous stranger, so it signals its readiness to fight by protruding its canines in a grimace. This evolved further and became ritualized into a mock threat expression, an aggressive gesture warning the intruder of potential retaliation. But if the approaching ape is recognized as a friend, the threat expression (baring canines) is aborted halfway, and this halfway grimace (partly hiding the canines) becomes an expression of appeasement and friendliness. Once again a potential threat (attack) is abruptly aborted—the key ingredients for laughter.

For example, look at the two shapes in Figure 3.7. The one on the left looks like a paint splat. The one on the right resembles a jagged piece of shattered glass. Now let me ask you, if you had to guess, which of these is a “bouba” and which is a “kiki”? There is no right answer, but odds are you picked the splat as “bouba” and the glass as “kiki.” I tried this in a large classroom recently, and 98 percent of the students made this choice. Now you might think this has something to do with the blob resembling the physical form of the letter B (for “bouba”) and the jagged thing resembling a K (as in “kiki”). But if you try the experiment on non-English-speaking people in India or China, where the writing systems are completely different, you find exactly the same thing.

What parts of the brain are involved in such abstractions? I already hinted (about language) that the inferior parietal lobule (IPL) may have played a pivotal role, but let’s take a closer look. In lower mammals the IPL isn’t very large, but it becomes more conspicuous in primates. Even within primates it is disproportionately large in the great apes, reaching a climax in humans. Finally, only in humans do we see a major portion of this lobule splitting further into two, the angular gyrus and the supramarginal gyrus, suggesting that something important was going on in this region of the brain during human evolution. Lying at the crossroads between vision (occipital lobes), touch (parietal lobes), and hearing (temporal lobes), the IPL is strategically located to receive information from all sensory modalities.

The answer has to do with how the accident affected the visual and auditory pathways in Jason’s brain. To a surprising extent, the activity of each pathway—vision and hearing—must be segregated all the way up to the critically important anterior cingulate. This collar of tissue, as we shall see, is where your sense of free will partly originates. If the anterior cingulate is extensively damaged, the result is the full picture of akinetic mutism; unlike Jason, the patient is in a permanent twilight state, not interacting with anyone under any circumstances. But what if the damage to the anterior cingulate is more subtle—say, the visual pathway to the anterior cingulate is damaged selectively at some stage, but the auditory pathway is fine. The result is telephone syndrome: Jason springs to action (speaking metaphorically!) when chatting on the phone but lapses into akinetic mutism when his father walks into the room.