The Mind and the Brain (17 page)

The key role that experience plays in wiring the human brain shows up most clearly when sensory stimuli are completely absent. In a human version of the kitten’s sewn-shut eyelids, babies are sometimes born with a cataract—an opaque lens—in one eye or both. This congenital defect strikes about 1 baby in 10,000 in the United States. If both eyes suffer cataracts, the brain never develops the ability to see normally. If only one eye has a cataract, vision in the affected eye never develops, as a result of active suppression by the normal eye, explains Ruxandra Sireteanu of the Max-Planck Institute for Brain Research in Frankfurt: “The two eyes compete for a glimpse of the outer world. If left untreated, vision in the affected eye, and the ability to use both eyes for binocular vision, will be permanently lost. It is not actually the eye that suffers, but the brain.” In this case acuity, the size of the field of vision, and the ability (or, rather, inability) to see stereoscopically remain stuck at the level of a newborn. Without normal visual input, the developing brain fails to establish the amazing network of connections that allow it to receive, process, and interpret electrical signals triggered by the fall of light on the retina.

Nowadays, doctors realize that removing the affected lens and replacing it with a clear, artificial one (the same sort of cataract surgery performed on elderly people) allows the brain to receive clear, sharp signals. What had remained unknown until recently, however, was how much visual input was required for the repaired eye to begin seeing. Was it hundreds of hours? Or mere seconds? In a 1999 study, researchers at the Hospital for Sick Children in Toronto went a long way toward finding an answer. They studied twenty-eight babies who had been born with dense cataracts: sixteen of the babies suffered cataracts in one eye, twelve had them in both. Between one week and nine months of age the babies underwent surgery to remove the cataracts; they had therefore been deprived
of normal visual input for that length of time. Within days or weeks of surgery, the babies were fitted with contact lenses so that, for the first time in their lives, “visual input was focused on the retina.” To test the babies’ eyesight, the researchers showed them black-and-white vertical stripes on a gray background. By varying the spacing between the stripes, and using infants’ well-established propensity to pay attention to novel objects, the researchers were able to measure the babies’ visual resolution. Although the initial acuity of the treated eye or eyes was significantly worse than that of babies born with normal vision, it improved after as little as a single hour of this exposure. “It appears that lack of visual exposure maintains the visual cortex of infants at the newborn level,” says Sireteanu. “But even a one-hour exposure to the visual world sets the stage for rapid visual improvements.”

Other sensory systems are similarly dependent on environmental input to finish the neuronal wiring that remains to be done once genetic instructions are exhausted. Auditory neurons first appear at three weeks after conception, and auditory centers in the brainstem emerge by thirteen weeks. In experiments with lab animals, removing the cochlea of one ear soon after birth reduces the number as well as the size of auditory neurons in the brainstem. Since these neurons receive no input, they essentially fold their tents and go out of business. But that kind of brain change can apparently be reversed, again through sensory input. In congenitally deaf children given cochlear implants, which bypass the damaged sensory hair cells of the inner ear and carry acoustical signals directly to the cortex, the sudden onset of sound after weeks or months of silence leads to nearly (depending on the age at which the implants are given) perfect speaking and hearing, as well as normal language development.

A 1999 experiment with kittens revealed the neurological basis for the rapid improvement. Researchers led by Rainer Klinke at the Physiologisches Institut of Frankfurt, Germany, tested the effects
of the cochlear implants on a group of three- to four-month-old kittens that were deaf at birth. Brain imaging had already shown that the unstimulated auditory nervous system in the deaf kittens was not developing as it does in normal cats. But after the implants, the cats began to respond to sounds in the same way as cats born with normal hearing. Their auditory cortex changed, too: within a short time the size of the region of auditory cortex that responded to sound increased, the amplitude of the electrical signals in the auditory cortex soared, and measures of information processing within the cortex (called
long-latency neural responses
) increased. The experiment offers some explanation for the fact that cochlear implants in children born deaf prove quite successful. “It is quite likely that a similar ‘awakening’ of the visual cortex takes place in congenitally blind infants newly exposed to visual information after cataract removal and the fitting of an artificial lens,” says Sireteanu.

A child need not suffer a congenital defect to demonstrate the power of sensory experience to wire the brain. Consider the somatosensory cortex. As mentioned, during fetal development it forms a rudimentary “map” of the body, so that the area receiving signals from the right hand abuts the area that receives signals from the right arm, which in turn abuts the area that receives signals from the right shoulder—you get the idea. But even at birth the somatosensory cortex has a long way to go. It is only through the experience of sensation that the map becomes precise. What seems to happen is that a baby is touched on, say, the back of her right hand. The neurons that run from that spot into the brain therefore fire together. But a neuron from the right wrist that took a wrong turn and wound up in the hand area of the somatosensory cortex is out of step. It does not fire in synchrony with the others (since touching the back of a hand does not stimulate the wrist). The tentative synapse it formed in the somatosensory cortex therefore weakens and eventually disappears. The region of the somatosensory cortex that receives inputs from the back of the right hand
now receives inputs only from the back of the right hand. As similar mismappings are corrected through experience and the application of the “neurons that fire together wire together” rule, a once-ambiguous map becomes sharp and precise.

That the newborn brain needs stimulation in order to form the correct wiring pattern is uncontested. A bitter and somewhat politicized dispute has arisen, however, over the meaning of
stimulation
. To many neuroscientists, it means nothing more than what a baby with functioning senses would receive from being alive and awake in the everyday world: sights, sounds, tastes, touches, and smells. Numerous observations have documented that babies who are severely neglected, and who do little but lie in their crib for the first year or more of life, develop abnormally: few can walk by the age of three, and some cannot sit up at twenty-one months. Whether more stimulation, especially cognitive stimulation, would produce even better wiring is hotly contested. Selling desperate parents video tapes that promise to turn their not-yet-crawling baby into a junior Einstein, persuading them to fill the house with the strains of Mozart, admonishing them that a family meal without a math lesson using forks and spoons is a missed opportunity—such gambits have given “stimulation” a bad name. It is clear that some amount of stimulation is crucial to the development of the human brain. But in all likelihood, it’s enough for the baby to explore the environment actively and interact with parents, to play peekaboo and hide-and-seek, to listen to and participate in conversations.

The great wave of synaptic sprouting and pruning was supposed to wash over the brain in infancy and toddlerhood, finishing in the first few years of life. But in the late 1990s scientists at several institutions, including here at UCLA, rocked the world of neuroscience with the discovery that a second wave of synaptic sprouting occurs just before puberty. In 1999, neuroscientists led by Elizabeth Sowell of UCLA’s Lab of Neuro Imaging MRI compared the brains of twelve- to sixteen-year-olds to those of twenty-somethings. They found that the frontal lobes, responsible for such “executive” func
tions as self-control, judgment, emotional regulation, organization, and planning, undergo noticeable change during late adolescence: they start growing at ten to twelve years (with girls’ growth spurt generally occuring a little earlier than boys’), much as they did during fetal development. And in another surprising echo of infancy, the frontal lobes then shrink in people’s twenties as extraneous branchings are pruned back into efficient, well-organized circuitry. No sooner have teens made their peace (sort of) with the changes that puberty inflicts on the body than their brain changes on them, too, reprising a dance of the neurons very much like the one that restructured the brain during infancy. Contrary to the notion that the brain has fully matured by the age of eight or twelve, with the truly crucial wiring complete as early as three, it turns out that the brain is an ongoing construction site. “Maturation does not stop at age 10, but continues into the teen years and even the 20s,” says Jay Giedd of the National Institute of Mental Health, whose MRI scans of 145 healthy four- to twenty-one-year-olds also found that the gray matter in the frontal lobes increased through age eleven or twelve. “What is most surprising is that you get a second wave of overproduction of gray matter, something that was thought to happen only in the first 18 months of life. Then there is a noticeable decline. It looks like there is a second wave of creation of gray matter at puberty, probably related to new connections and branches, followed by pruning.”

Again as during fetal development, synapses that underlie cognitive and other abilities stick around if they’re used but wither if they’re not. The systematic elimination of unused synapses, and thus unused circuits, presumably results in greater efficiency for the neural networks that are stimulated—the networks that support, in other words, behaviors in which the adolescent is actively engaged. Just as early childhood seems to be a time of exquisite sensitivity to the environment (remember the babies who dedicate auditory circuits only to the sounds of their native language, eliminating those for phonemes that they do not hear), so may adolescence. The teen
years are, then, a second chance to consolidate circuits that are used and prune back those that are not—to hard-wire an ability to hit a curve ball, juggle numbers mentally, or turn musical notation into finger movements almost unconsciously. Says Giedd, “Teens have the power to determine their own brain development, to determine which connections survive and which don’t, [by] whether they do art, or music, or sports, or videogames.”

This second wave of synaptogenesis is not confined to the frontal lobes. When the UCLA team scanned the brains of nineteen normal children and adolescents, ages seven and sixteen, they found that the parietal lobes (which integrate information from far-flung neighborhoods of the brain, such as auditory, tactile, and visual signals) are still maturing through the midteens. The long nerve fibers called white matter are probably still being sheathed in myelin, the fatty substance that lets nerves transmit signals faster and more efficiently. As a result, circuits that make sense of disparate information are works in progress through age sixteen or so. The parietal lobes reach their gray matter peak at age ten (in girls) or twelve (in boys) and are then pruned. But the temporal lobes, seats of language as well as emotional control, do not reach their gray matter maximum until age sixteen, Giedd finds. Only then do they undergo pruning. The teen brain, it seems, reprises one of the most momentous acts of infancy, the overproduction and then pruning of neuronal branches. “The brain,” says Sowell, “undergoes dynamic changes much later than we originally thought.”

The wiring up of the brain during gestation, infancy, and childhood—and, we now know, adolescence—is almost as wondrous as the formation of a living, breathing, sensing, moving, behaving organism from a single fertilized ovum. The plasticity of the young brain is based on the overabundance of synapses, which allows only those that are used to become part of enduring circuits that underlie thinking, feeling, responding, and behaving. But does the dance of the neurons eventually end?

The great Spanish neuroanatomist Santiago Ramon y Cajal concluded his 1913 treatise “Degeneration and Regeneration of the Nervous System” with this declaration: “In adult centres the nerve paths are something fixed, ended, immutable. Everything may die, nothing may be regenerated.” Cajal based his pessimistic conclusion on his meticulous studies of brain anatomy after injury, and his gloomy sentiment remained neuroscience dogma for almost a century. “We are still taught that the fully mature brain lacks the intrinsic mechanisms needed to replenish neurons and reestablish neuronal networks after acute injury or in response to the insidious loss of neurons seen in neurodegenerative diseases,” noted the neurologists Daniel Lowenstein and Jack Parent in 1999.

This doctrine of the adult hard-wired brain, of the loss of neuroplasticity with the end of childhood, had profound ramifications. It implied that rehabilitation for adults who had suffered brain damage was useless. It suggested that cognitive rehab in psychiatry was a misbegotten dream. But the doctrine, as was becoming apparent even as Lowenstein and Parent wrote, was wrong. Years after birth, even well into adolescence, the human brain is still forming the circuits that will determine how we react to stress, how we think, even how we see and hear. The fact that (even) adults are able to learn and that learning reflects changes in synapses tells us that the brain retains some of its early dynamism and malleability throughout life. The adult has the ability not only to repair damaged regions but also to grow new neurons. Even the adult brain is surprisingly plastic. Thus the power of willful activity to shape the brain remains the working principle not only of early brain development, but also of brain function as an ongoing, living process.

Even as I recorded changes in the brains of my OCD patients after mindfulness-based cognitive-behavioral therapy, a decades-long dogma was beginning to fall. Contrary to Cajal and virtually every neuroscientist since, the adult brain can change. It can grow
new cells. It can change the function of old ones. It can rezone an area that originally executed one function and assign it another. It can, in short, change the circuitry that weaves neurons into the networks that allow us to see and hear, into the networks that remember, feel, suffer, think, imagine, and dream.