I Can Hear You Whisper Page 13
We brought home videotapes prepared by the three cochlear implant manufacturers. Of course, they showcased the success stories. But what stories they were. In the “before” videos, the children were Alex’s age, laboring with speech therapists to pronounce a few words. In the “after” videos, they were school-age, in mainstream classrooms, all of them speaking, some of them virtually indistinguishable from their hearing classmates. One particularly captivating profoundly deaf girl had used sign language until she was three, when she got her implant. By the movie’s end, she was nine, a busy, happy fourth-grader, singing in her mainstream school’s choir. As the credits on the video ran, Mark and I looked at each other.
“That’s what I want,” he said.
“Me too,” I agreed.
We emerged with a case of emotional whiplash: We went from desperately wanting to hang on to every decibel of Alex’s hearing to desperately hoping his hearing was bad enough to qualify him as a candidate.
White-haired and soft-spoken, Dr. Parisier had a gentle, matter-of-fact manner, but he didn’t mince words when he delivered his opinion. He clipped several CT scan images of Alex’s head up on the light board and tapped a file containing the reports of Alex’s latest hearing tests and speech/language evaluations. “He is not getting what he needs from the hearing aids. There’s no high-frequency access. His language is not developing the way we’d like,” he said. Then he turned and looked directly at us. “We should implant him before he turns three.”
A deadline? So there was now a countdown clock to spoken language ticking away in Alex’s head? What would happen when it reached zero? Alex’s third birthday was only a few months away.
As Parisier explained that the age of three marked a critical juncture in the development of language, I began to truly understand that we were not just talking about Alex’s ears. We were talking about his brain.
• • •
Even more than his hearing, Alex’s brain was mysterious. It required faith. I couldn’t touch it or caress it, as I did his ears, running my fingertips along their small curving lobes. Of course, I knew his brain was there. When he breathed or blinked or blew me a kiss, it was sending proof of its existence, like postcards from a far-off land I can point to on the globe but never visit. Still, I struggled to imagine the reality of it. Even the vocabulary of the brain is hard to fathom with its map of place names that sound simultaneously alien and ancient—superior temporal gyrus and perisylvian cortex, amgydala and hippocampus.
In among the models and diagrams of the ear in every doctor’s office we had visited, there was not one map of the brain on the wall. Perhaps there should have been. I wanted to know more than that the cochlear implant would deliver sound to Alex’s auditory nerve, which would convey it to the brain. I needed to know what would happen to that sound once it arrived. I needed to know what the brain would do with that sound while Alex was two that it might not be able to do once he turned three.
The answers lay in the burgeoning science of brain plasticity—the study of the capacity of the brain to change with experience. Helped by advances in technology, neuroscientists have built up atlases of normal brain development. That is the starting point for understanding what happens in brains that are atypical.
The differences between a brain at birth and that same brain at twenty-one years of age are considerable and driven both by genetics, which is “merely an opening gambit on nature’s part,” as science writer Sharon Begley put it, and by environment. The baby’s brain arrives in the world primed for learning. It is now thought to contain seventy to eighty billion neurons, or nerve cells, down from previous estimates of one hundred billion, but still most of the neurons a person will need as an adult. What is lacking is communication from neuron to neuron. The process of generating the remaining necessary neurons and creating connections between neurons is what the learning of childhood is all about.
Neurons are often compared to trees, with roots and branches, but to me they look more like spindly sea creatures or insects with long skinny bodies and arms like tendrils waving away at each end. Information comes in through those tendrils, the dendrites, and travels along the axon to the other end of the cell. At the base of each axon there’s a gap before the next neuron. The electrical signal is carried over that gap, or synapse, by chemical neurotransmitters, like a written message wrapped around the shaft of an arrow and fired over a moat.
The warmth of a baby blanket, the smell of a father’s aftershave, the sight of a mother’s loving gaze, the soothing melody of a lullaby: Together, these perceptions contribute to a baby’s sense of security, but each is also altering the configuration of the baby’s brain. Each is a piece of sensory information that travels through the nervous system to the appropriate area of the brain. The image of a mother’s face, for example, enters the retina of the eyes and passes along a pathway to the visual cortex in the occipital lobe at the back of the brain. Every time the baby sees his mother’s face, the same chain of nerve cells fires. As neuroscientists say, neurons that fire together wire together. Pretty soon, a circuit has been created and the baby recognizes his mother instantly. There are similarly specialized areas for touch, sound, and smell.
In this manner, information travels through the brain leaping from neuron to neuron, creating circuits that receive and then process and act on information. Zip, zip, zip. The more often a specific signal is sent down a particular path, the more defined and efficient that path becomes, like a hiking trail that is well maintained versus one that’s overgrown. Paths that are traveled less often or not at all—connections that aren’t made, in other words—eventually disappear. The brain assumes they are unnecessary and prunes them away. Snip, snip, snip. As neuroscientist Helen Neville puts it, “experience is like a sculptor who begins with more clay than he needs.” This idea is somewhat counterintuitive—that a child’s brain is simultaneously strengthening and eliminating brain circuits. But that is the beauty of the system. It is as if the landscape of the brain is under the control of a master gardener who creates paths where they are wanted, plants new seeds as necessary, directs the flowerings and branchings, and cuts back to concentrate growth where it is most desirable.
Today, scientists can watch the brain maturation process unfold. In a prospective study published in 2004, a group of researchers based at the National Institutes of Health and UCLA followed thirteen healthy children for close to ten years. The children, who ranged in age throughout the study from four to twenty-one, underwent functional magnetic resonance imaging (fMRI) every two years. The images were color-coded to indicate relative levels of gray matter density in the children’s brains, with red and yellow indicating more gray matter and blue and purple less. As neural connections explode early in childhood, gray matter density increases. As those connections are pruned back and insulated with myelin, that gray matter volume decreases and white matter increases. So more white matter indicates a more mature brain.
In the time-lapse movie of the results, large swathes of yellow and red are slowly washed with blue as the exuberant bursts of neuron growth in early childhood become cooler and more efficient, mature neural pathways. The sequences showed that the brain’s most basic functions, those concerning vision and touch, developed first, followed by centers for language in late childhood and early adolescence and then, toward early adulthood, by the areas that control reasoning, self-reflection, and planning. (Interestingly, in Alzheimer’s patients the sequence is reversed. Their brain matter loss progresses from front to back, beginning with the higher-order functioning and finally enveloping more basic functions of the brain.)
Most of the growth in neurons takes place between birth and the age of five, which is why the UCLA movies, whose youngest subjects were four, begin with brains full of gray matter (i.e., uninsulated neurons). The pruning begins in earnest around five, and children will lose 35 percent of the nerve cells they have at five before adulthood. For many years, the assumption was that after early childhood
our brains did not continue to generate new nerve cells, but within the past ten years, researchers discovered a second, smaller wave of neuron creation in puberty. And we now know that it is possible to keep learning—and even generating new neurons—into adulthood, though it takes far more effort to see results.
According to the brain’s basic division of labor, sensory areas receive all the incoming information from our eyes, ears, nostrils, tongue, and fingertips. The back of the brain, the occipital lobe, handles vision. Hearing is processed in the temporal lobe on the side of the head just above the ear. A strip across the top of the head collects information about everything we touch, whether with our toes, palms, shoulder, cheek, or any other part of the body. Motor areas control our movements. The limbic system is involved with emotion. “Cortex” is the collective name for the exterior surface of the brain, the wavy, lumpy gray matter familiar from anatomy books. It’s here, particularly in the section right behind the forehead known as the prefrontal cortex, that the higher-order processing occurs that marks us as distinctly human and controls our ability to plan, to reason, to remember, to reflect.
The central auditory system begins where the inner ear passes a signal to the auditory nerve. A part of the eighth cranial nerve, the auditory nerve is not just one nerve but a bundle of nerve fibers—a coaxial cable of sorts—connecting the cochlea to the brain stem. Within the brain stem, where the auditory nerve ends at two collections of neurons called the cochlear nuclei, things start to get complicated. That is as it should be. Very literally, brain processing gets more sophisticated as it ascends, the way a good curriculum builds on itself and asks more of students as they move through school.
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KEY:
SO: Superior olive; IC: Inferior colliculus; MGB: Medial geniculate body
The cochlear nuclei sort the incoming auditory signal along two different tracks, and the various types of cells of the cochlear nuclei each specialize in just one kind of signal. The organization by tone of the basilar membrane, for instance, is repeated in the brain stem, so that some cells respond to high-frequency sounds and others to low-frequency sounds. It is thought that features such as your ability to tell where a sound came from or the fact that you jump at loud noises can be traced to specific cells in the dorsal and ventral pathways respectively. From the cochlear nuclei, sound signals follow these two parallel pathways—along the back and the belly of the brain—in an intricate and complex route passing through regions such as the superior olive (really) and the medial geniculate until they reach the auditory cortex in the temporal lobe, just above the ear where the sound started. Here, too, there are specialized cells to extract features of the sound and make sense of it. With practice, the auditory cortex gets better and better at sophisticated listening, which is why a trained technician, for example, can tune a piano by ear.
If we wanted Alex to be able to listen and talk, he needed first to hear sounds (to recognize simply that someone is speaking) and then to make sense of those sounds (to someday follow a teacher’s explanation of how to do long division). The former would require a jet assist from technology. The latter would require practice and time.
• • •
Information about plasticity first really reached parents in the mid-1990s, just when I was thinking about having my first child. It was easy to freak out about the responsibilities now incumbent on parents to oversee the creation of perfect brains. The possibilities for learning seemed to be pushed to younger and younger ages. Now it wasn’t enough to nurture and care for your child; a parent had to be always considering how to maximize learning potential. Toy manufacturers take advantage of this worry by selling us as many “enriching” and “brain-boosting” products as possible.
Frankly, most middle-class, educated, professional parents like me have the luxury of thinking in terms of enrichment. Our children have the good luck to be born into families where basic needs are easily met; in their early years, these kids are carefully nurtured, fed nutritious meals, talked to, read to, played with. All of that is essential to building strong brain architecture in a way that Baby Mozart tapes and foreign language playgroups are not.
In brain plasticity terms, the flip side of enrichment is deprivation. That’s what neurologists call it when a brain lacks stimulation. “If a system can be influenced by the environment and enhanced, that same system is vulnerable because if the right input isn’t available then it won’t develop optimally,” says the University of Oregon’s Helen Neville, one of the pioneers in the study of plasticity. You can see this plainly in studies that compare certain brain functions in children from different socioeconomic groups. A study published in 2009 asked both low-and middle-income nine-and ten-year-olds to watch images flashing on a computer. The children were instructed to press a button when a tilted triangle appeared. This is a skill that reflects activity in the prefrontal cortex, which controls planning and executive function. The poorer children were far less able to detect the tilted triangles and block out distractions—so much so that one of the researchers likened the results to what he sees in stroke victims who have lesions in the prefrontal cortex.
I had generally considered all the hype about enrichment just that: hype. Even so, I was susceptible to worry and guilt. I might have forgotten what a cause-and-effect toy was, but like so many of my friends, I had signed my boys up for baby music classes, read to them daily, owned educational puzzles, and so on.
Suddenly, in Alex’s case, I was staring deprivation straight in the face. Alex wasn’t talking because not enough sound was traveling the pathways that led to the parts of his brain that deal with hearing.
11
WHAT IF THE BLIND COULD SEE?
What exactly did deprivation do to the brain? For a long time, no one really knew and this was mostly a philosophical question, famously encapsulated by Irish scientist and politician William Molyneux, who wrote to John Locke in 1688, What if a blind person who has learned to distinguish a cube from a globe by touch, was suddenly able to see? Would he then be able to recognize these objects by sight? Molyneux and Locke both suspected the answer was no. The question was passed down and contemplated anew through the years like a philosophical folktale. Some philosophers argued yes; others echoed Molyneux and Locke and said no.
As for neuroscientists, once such a job title existed, they thought about such problems in anatomical and physiological terms. What parts of the brain were involved in perception and learning, and how did they work? Well into the twentieth century, it was believed that the brain was unchangeable beyond early childhood. (The few researchers who produced evidence suggesting otherwise were mostly ignored.) Furthermore, it was thought that structure determined function, that each region of the brain could perform only its assigned task. In 1913, Santiago Ramón y Cajal, whom many consider the father of modern neuroscience, wrote that the adult brain’s pathways are “fixed, ended, immutable.” Even though it was understood that the brains of children were works in progress, the details of how that developmental work got done were mysterious.
A series of experiments with cats in the 1950s and 1960s forced a radical reassessment of accepted ideas about how experience might affect the brain. David Hubel was born and raised in Canada and Torsten Wiesel in Sweden. They met at Johns Hopkins University, where both were conducting research in physiology, and teamed up, ostensibly for a few months; their partnership lasted twenty-five years, most of them spent at Harvard.
Hubel and Wiesel concentrated on vision, beginning with the question: What is it to see? Compared to the machines that let researchers see inside the brain today, they used spectacularly low-tech equipment. Hubel fashioned a lathe himself to make the electrodes they would use to probe the brain cells of cats and monkeys. When they needed a screen on the ceiling on which to project images, they hung white sheets. And they plotted the data they received from their recordings of the electrical activity of individual cells using pencils and paper tacked to the wall.
Their first few years of work, much of it described in a 1962 paper Hubel called their “magnum opus,” laid the groundwork for what we know today about how visual information comes into the brain and what happens to it there—cell by cell. But they didn’t stop there. Their curiosity had been piqued by the fact that, in children, cataracts led to blindness, whereas in adults, they did not. They were also struck by experiments in which animals raised in darkness were left with impaired vision even though there was nothing wrong with their eyes. So after establishing the physiology of normal vision in adult animals, Hubel and Wiesel asked what happens as vision develops in younger animals and, critically, what happens if there’s a problem.
They thought the first logical step was to suture shut one eye of young kittens, so that they could compare the information from each eye. In these kittens, they expected vision to develop relatively normally in the non-deprived eye. When the sutures had been removed and they covered up the good eye, the cats were effectively blind in the eye that had been deprived of vision, even though there was technically nothing wrong with the eye. The damage was obvious. The first cat they experimented with fell off the table when released. “That is something,” wrote Hubel, “that no self-respecting cat would do.” When they sacrificed the animals and looked at their brains, though, they were surprised to find that the cells in the visual cortex looked radically different from those in cats with normal vision. The good eye had co-opted much of the neurological territory of the deprived eye like a vine that spreads into the neighbor’s yard. Was it from a failure to develop or a withering from disuse of connections that were already formed? They weren’t sure, but proposed the latter. Hubel and Wiesel also discovered that some of the visual connections wired up in spite of disuse, which meant that some of the neurological functioning had to be innate.
The next round of experiments involved suturing both eyes of kittens. (Science can undoubtedly be cruel.) After about three months, they reopened the cats’ eyes. Again, the cats were effectively blind, even though there was nothing wrong with their eyes. The problem lay in their brains, which had no experience processing visual information and were no longer capable of the task. Finally, Hubel and Wiesel wanted to know how variations in the length of deprivation or the moment of its onset made a difference. Cats hardly use their eyes in the first three weeks after birth, but their visual systems are fairly mature by three months of age. It turned out that if kittens were deprived of sight at any point during the fourth through the eighth week of development, the damage was considerable. After three months of age, however, a cat could have its eyes sutured for months with no appreciable consequences.