The Tale of the Dueling Neurosurgeons: The History of the Human Brain as Revealed by True Stories of Trauma, Madness, and Recovery

by Sam Kean

  Synesthesia probably has a genetic component, since it runs in families and pops up in most cultures. Importantly, too, neurologists have ruled out the idea that synesthetes are just talking metaphorical jive, the way the rest of us speak of “loud shirts” and “sharp cheddar.” These people’s brains actually work differently, as tests reveal. One experiment involved filling a piece of paper with a bunch of alarm-clock fives (5), but also scattering a few blocky twos (2) in there. Normal people find it nearly impossible to pick out the 2s without hunting one by one. To synesthetes, each 2 pops out in Technicolor, instantly. (It’s similar to the way numbers pop out automatically on color-blind tests.) As another trick, if you show a synesthete, say, a giant numeral 4 made up of rows and rows of tiny 8s, the figure’s color will flip depending on whether she focuses on the whole (the 4) or the pixels (the 8s). Other tests make synesthetes squirm. Normal people have no trouble reading text of basically any color. For synesthetes, numbers or letters that are the “wrong” color can disorient or repel them, since the colors on the page do battle with the colors in their minds.

  Neuroscientists know in a general way how synesthesia must work: the neuron circuits that process one sense must be accidentally strumming the circuits that process another sense, causing both sets to hum simultaneously. Determining exactly why that happens, though, has proved tricky. Two possible explanations have emerged, one anatomical, one functional. The anatomical theory blames poor pruning of neurons during childhood. All babies have far more neurons than they need; their neurons also have an excessive number of axon and dendrite branches. (As a result, young children probably experience synesthesia all the time.) As children develop, certain neurons begin firing together and wiring together, and those active neurons remain healthy. Meanwhile, unused neurons starve and die off. Excess branches get pruned back as well, like a maple near a power line. This destruction sounds brutal—neural Darwinism—but it leads to tighter, stronger, more efficient circuits among survivors. Perhaps the brains of synesthetes don’t prune well. Perhaps their brains leave extra connections in place that link different sensory regions.

  The functional theory suggests that neurons get pruned just fine, but that some neurons can’t inhibit their neighbors very well. Again, our highly connected neurons have to discourage signals from shooting down stray paths to the wrong parts of the brain; they do so by skunking certain neighbors with inhibitory chemicals. But even if those stray paths lie dormant, they still exist—and could, in theory, open up and become active. Perhaps, then, the brains of synesthetes fail to inhibit these underground channels, and information leaks from one brain region to another.

  The first clue for deciding between the functional and anatomical theories came from a Swiss chemist. In 1938 Albert Hofmann’s drug company was searching for new stimulants, and he began investigating some chemicals derived from a fungus. He soon drifted to other compounds but had a nagging feeling that the fungi had more to teach him. So on a Friday afternoon in April 1943, he whipped up a fresh batch of one chemical, called lysergic acid diethylamide (in German, Lyserg-Säure-Diäthylamid). During the synthesis he suddenly felt woozy and saw streaks of color. He later guessed he’d gotten some powder on his finger, then rubbed his eyes. But he wasn’t sure, so he tested his guess on Monday, April 19—forevermore known as Bicycle Day. He dissolved a tiny amount of powder, a quarter of a milligram, in a quarter shot of water. It had no taste, and down the hatch it went. This happened at 4:20 p.m., and although Hofmann tried to record his sensations in his lab journal, by five o’clock his handwriting had deteriorated into a scrawl. His last words were “desire to laugh.” Feeling unsettled, he asked his assistant to escort him home on his bicycle. It was quite a trip.

  On the ride, the streaks of color reappeared before his eyes, and everything became elongated and distorted, as if reflected in a curved mirror. Time slowed down as well: Hofmann thought the trip took ages, but the assistant remembered furious pedaling. In his drawing room at home, Hofmann struggled to form coherent sentences, but finally made it clear that (for some reason) he thought milk would cure him. A neighbor woman patiently hauled bottle after bottle to him, and he chugged two liters that night, to no avail. Worse, Hofmann began having supernatural visions. His mind transmogrified the neighbor into a witch, and he felt a demon rise up inside him and clutch his soul. Even his furniture seemed possessed, trembling with menace. He felt certain he’d die right there on his couch.

  Only hours later did he calm down, and he actually enjoyed the last hour. His eyes became veritable kaleidoscopes, with Fantasia-like fountains of color “exploding [and] rearranging and hybridizing themselves in constant flux.” It also pleased him, he later reported, that “every acoustic perception, such as the sound of a door handle or a passing automobile, became transformed into optical perceptions. Every sound generated a vividly changing image, with its own consistent form and color.” In other words, the drug produced synesthesia, something he’d never experienced.

  Hofmann’s Lyserg-Säure-Diäthylamid eventually became known as LSD, and since then thousands of Phish and Grateful Dead fans have had similar experiences. Tripping on LSD obviously can’t change the brain’s hardwired circuits. LSD can interfere with neurotransmitters, however, and warp the information flowing through those circuits for a few hours. It’s like flipping your television from a Ken Burns documentary to a David Lynch nightmare sequence—the same circuitry is providing the picture, but the content is much wilder. This provides strong support for the functional theory of synesthesia. There’s some evidence that natural synesthetes still might have brains that are wired a little differently. But the experience of Hofmann and others suggests that we all might have a talent for synesthesia latent inside us, if only we could tap it.

  Hofmann’s drug-induced synesthesia showed that certain experiences can alter the flow of information through our neuronal wires, at least temporarily. But can any experiences actually rewire brain circuits in a permanent way?

  Children’s brains can remodel themselves quite easily and form all sorts of new connections: that’s how they sponge up language and so much else. For most of the past century, though, neuroscientists considered remodeling in the adult brain impossible, thanks in part to Santiago Ramón y Cajal. Cajal spent a decade injuring the nerves and neurons of animals to test how well those tissues recovered. He found that peripheral nerves could often regenerate themselves (which explains why surgeons can reattach severed hands, feet, and penises, and get them working again). But neurons in the adult brain never grew back. This led Cajal to make the bleak declaration that “in the adult brain, nervous pathways are fixed and immutable. Everything may die, nothing may be regenerated.”

  Other observations supported Cajal’s pessimism. Compared to children, adults have a much tougher time learning new skills like languages, a sign of neural sclerosis. And if adults suffer strokes or other brain damage, they might lose certain skills permanently, since neurons never grow back. Moreover, the lack of adult plasticity made sense from an evolutionary perspective. If the adult brain changed too easily, the thinking went, circuits controlling important behaviors and memories would unravel, and skills would evaporate from our minds. As one scientist observed, a fully plastic brain “learns everything and remembers nothing.”

  All that’s true. But neuroscientists were a little hasty in declaring that the soft, pliable clay of the infant brain always gives way to sturdy but brittle ceramic. Even if the adult brain cannot grow new neurons

  * or repair damaged ones, that doesn’t mean that all neuron pathways are fixed and immutable. With the right training, neurons can indeed change how they behave and transmit data. Old brain wires can learn astounding new tricks.

  In the late 1960s, a degenerative eye disease claimed both retinas of a sixteen-year-old Wisconsinite named Roger Behm, rendering him blind. Forty years later he took a flier on a “vision substitution” device that a local scientist had built. The device consisted of a black-a
nd-white video camera mounted on Behm’s forehead, with a ribbon of wires leading down into his mouth. The wires ended in a rectangular green electrode, not much bigger than a postage stamp, that rested on Behm’s tongue. The camera fed its images to this electrode, which transformed each pixel into a buzz of electricity reminiscent of seltzer bubbles: white pixels tingled his tongue a lot; black pixels gave no tingle; gray were intermediate. Behm was supposed to use the tongue “image” to interact with the world around him.

  As you might expect, this flummoxed him at first. He nevertheless learned how to detect motion versus stillness rather quickly. He started picking out triangles, circles, and other Euclidians not long afterward. He graduated to common objects like cups, chairs, and telephones. Soon he could pick out logos on football helmets and sort playing cards by their suits, even navigate a simple obstacle course. Nor was Behm unique or special in picking up these skills. Other blind people learned how to use mirrors, pick out overlapping objects, or follow the writhing dance of a candle flame.

  The man behind the device, Paul Bach-y-Rita, became a neuroscientist in a roundabout way. (Although a Bronx native, Bach-y-Rita had a compound Catalan surname, like Santiago Ramón y Cajal.) Bach-y-Rita attended medical school in Mexico City on a dare, then dropped out to work, among other itinerant jobs, as a masseur and a fisherman in Florida. He also taught anatomy to blind people who were studying to become masseurs, which helped him understand how they interacted with the world. (The blind, with their heightened sense of touch, make fine masseurs and masseuses.) Eventually he returned to medical school and started working with blind patients. But Bach-y-Rita really found his purpose in life after his father, Pedro, suffered a massive stroke in 1959 and was left half paralyzed and speechless.

  Pedro entered a rehabilitation clinic, but when his progress plateaued, his doctors declared him doomed and suggested a nursing home, since his fixed and immutable brain would never recover. This fatalism—so common in rehab facilities then—angered Bach-y-Rita’s brother, a doctor named George. So George designed his own rehab regimen. It sounded harsh: George made Pedro crawl like an infant at first, learning how to move each limb again, before gradually working him up to his feet. He then made Pedro do household chores such as sweeping the porch and scrubbing pots and pans. Pedro struggled mightily and appeared to make little progress, but the repetitive motions eventually retrained his brain: he not only regained the ability to talk and walk, he resumed his teaching job, remarried, and started hiking again. Pedro in fact died (seven years later, of a heart attack) while hiking in the mountains of Colombia, at age seventy-three. His autopsy revealed extensive lingering damage, especially to white matter cables that connect certain patches of gray matter to each other. Importantly, though, the gray matter itself still worked. And his brain proved plastic enough to reroute the cues for walking and talking around the ravaged tissue. That is, instead of routing signals from A to B, it now routed them from A to C and then C to B—not the most efficient path, but one that improved over time as the mental ruts grew deeper.

  Inspired, Paul Bach-y-Rita did additional residencies in neurology and rehab medicine, and decided to investigate brain plasticity himself, especially how blind people might regain a vestige of sight. His first “brain port” used a hand-cranked video camera; it projected an image onto the viewer’s back via vibrating Teflon studs implanted in a dentist’s chair. With just four hundred pixels, the images looked like a black-and-white television with poor focus. Nevertheless, with practice people could pick out individuals based on their hairstyles and faces, including 1960s supermodel Twiggy. (The patients shrugged when shown Playboy centerfolds, however—touch still beats sight in some areas.)

  When microprocessors got small enough, Bach-y-Rita built devices to stimulate the tongue, one of the body’s most sensitive tactile areas. (Saliva also makes the mouth more conductive than bare skin, lowering the necessary voltage.) And the devices really gained legitimacy when scientists started scanning the brains of patients while they used them. The scans revealed that, even though the video information came streaming in through the tongue, the brain’s vision centers crackled with activity. Neurologically, this input was indistinguishable from “sight.” Psychologically, too, the patient experienced the tactile tongue data as vision. Blind people using the devices perceived objects as being “out there” in space in front of them, not on their tongues. They flinched from balls flung at them, and could sense when objects moved closer or farther away because they grew larger or smaller. They even fell prey to certain optical illusions, like the “waterfall effect.” If you stare at something in motion (like a waterfall) for several seconds and then look away, whatever you focus on next seems to move of its own accord. Bach-y-Rita’s device induces this same vertiginous feeling in blind people, further proof of a latent neurological ability to see.

  Meanwhile, Bach-y-Rita’s team developed other sensory substitution devices. A leper who’d lost the sense of touch in his hands (leprosy destroys nerves) donned a special glove that piped tactile information to his forehead instead; within minutes he could feel the cracks on a table and distinguish between rough logs, smooth aluminum tubes, and soft rolls of toilet paper. Bach-y-Rita also worked on “electric condoms.” Many paralyzed men can still get erections, even if they can’t feel them, and Bach-y-Rita’s device, if ever completed, would pipe electric orgasms into their brains.

  Most dramatically, Bach-y-Rita’s team has restored people’s sense of balance. This work started with a thirty-nine-year-old Wisconsin woman named Cheryl Schiltz, who’d taken an antibiotic called gentamicin after a hysterectomy in 1997. Gentamicin fights infections well but has a nasty habit of destroying the tiny hairs in the inner ear that keep us balanced and upright. Although these hairs are located in different tubes than the hairs that help us hear, they work the same basic way. A gel inside the tubes sloshes back and forth like jiggled Jell-O as our heads tip this way and that. This causes the hairs embedded in the gel to bend to and fro and thereby trigger certain neurons. From this data the brain determines whether we’re standing upright and then corrects for deviations. With those hairs destroyed, the balance center in Schiltz’s brain (the vestibular nuclei) went on the fritz and started shooting out signals at random to her muscles, forcing her to sway side to side, with little jerks. Worse, she always felt on the verge of toppling over, even while she was lying down, like a permanent case of the drunken spinnies. Schiltz and other gentamicin victims call themselves Wobblers. Most can barely navigate their own homes much less brave the outside world, where a simple zigzag on a carpet can send them reeling. Not a few Wobblers commit suicide.

  Although skeptical, Schiltz let Bach-y-Rita’s team rig her up in a green construction helmet with a tiny balance and some electronics mounted inside. Like Behm’s device, wires snaked down from the headpiece to an electrode in Schiltz’s mouth. When standing tall and true, she felt a kazoo buzz on the center of her tongue. When her head drooped or swayed, she felt the buzz slide forward, backward, or sideways. Her goal was to shift her posture to keep the buzz in the center at all times. The buzz felt bizarre to her, but she got the hang of it quickly. After sessions of just five minutes, she found she could stand on her own for a few precious seconds. One day she drilled for twenty straight minutes and found she could walk without staggering. Further practice improved her balance still more, and eventually Schiltz dispensed with the helmet altogether. She even learned to jump rope and ride a bike again.

  More poignantly, she began training others on how to use the device, including Bach-y-Rita himself. After being diagnosed with cancer in 2004, Bach-y-Rita took a chemotherapy drug that damaged his own inner ear hairs and wiped out his sense of balance. So Schiltz walked him through how to use the green helmet—returning the favor to him, and ensuring that he would walk on his own right up until his death in 2006.

  Scientists are still debating exactly how sensory substitution devices changed the brains of people like Behm and Schi
ltz. One good guess is that these devices, in rerouting information from the tongue to the vision and balance centers, take advantage of pathways and feedback loops that already exist. When eating an apple, for instance, your brain naturally combines information about its taste, crunch, and shiny red finish to give you a more comprehensive understanding. So we already mix some sensory input, and maybe the tongue data getting transformed into visual data is just an extreme example. In addition, as LSD synesthesia shows, there are plenty of dormant, underground, pseudo-synesthesic channels inside the brain to exploit as well.

  It seems that our brains, being partly plastic, can swap one sense for another no matter how it gets piped in. This has profound implications for how we understand the senses in general. From this point of view, all the ears, eyes, and nostrils really do is tickle certain nerves. As a result, all sensory input looks pretty much the same after it leaves the sense organ and enters the nervous system: it’s nothing but chemical and electrical blips. It’s really our neuron circuits, not our sensory equipment, that decipher incoming signals and conjure up perceptions.