The Mind and the Brain (13 page)

Mental force needs the brain to express itself. But it is more than brain, and not reducible to brainstuff. In the fractions of a second when the brain might activate either the pathological circuit underlying a dash to the sink to wash or the healthy circuit underlying a stroll to the garden to prune, mental force amplifies activity in the healthy circuit. You can generate a mental force that activates one circuit rather than another. In a more innocent age, we called that will. But the very idea that the brain can change at all, much less that it can change in response to mind, first had to overcome a century-old dogma.

Martha Curtis was, if not a musical prodigy, then certainly musically gifted. She was playing the piano at age five and at nine took up the violin, eventually coaxing from the instrument passionate and even heartbreaking concertos. But something else made Martha stand out: she had begun suffering convulsions at age three and a half. Her doctors diagnosed her condition as epilepsy and started her on the standard medication prescribed to control the seizures. But the seizures only continued, and by the time she was eleven, they were sometimes leaving the little girl unconscious on the floor, terrifying her parents. Martha soldiered on, however, and won a place in the junior orchestra at Michigan’s Interlochen Arts Camp, from whose academy she graduated as her class’s salutatorian. But by the time she entered the Eastman School of Music in the mid-1970s, she was seizing on stage. As a twenty-something, while performing with various orchestras, Martha had seizures that punched through the pharmaceutical overlay of the drugs frequently and relentlessly.

In April 1990, she suffered four grand mal seizures, three while performing. Knowing that no orchestra would let her back on stage if she kept seizing, she sought help at the Cleveland Clinic. There,
the neurologist Hans Luders took Martha off drugs and admitted her to an inpatient epilepsy unit, where electrodes could monitor her temporal lobes twenty-four hours a day. The electroencephalogram showed a constant storm of abnormal electrical activity emanating from Martha’s right temporal lobe and spreading over her entire brain like a fast-moving squall—the hallmark of epilepsy. Surgery to remove the spawning ground of the storms, Luders told his patient, was the only option: the quantity of carbamazepine (Tegretol) needed to quiet the pathological electrical activity, Luders said, was already toxic. There was one problem, however. The right temporal lobe seems to be where the brain stores musical memories. Removing it might well eliminate Martha’s epilepsy; it might also leave her unable to play the violin ever again. That was something she could hardly face. It was only because she had music in her life than she had been able to bear her illness. “I am alive today,” she said in 2000, “because I had a violin.”

Martha had surgery in January 1991. As soon as she left intensive care, she took up her violin and, fearing the worst, tried to play a Bach composition. She chose it because, before her surgery, she had found it one of the hardest pieces to play from memory. She nailed it. But although her musical ability seemed intact, her brain seemed to have been left too intact: the surgery had apparently not removed enough of her right temporal lobe (specifically, it had left behind too much of the hippocampus) : Martha’s seizures persisted. She returned to Cleveland for a second operation. This surgery removed all the hippocampus and much of the amygdala, but the seizures continued, for they were originating from a specific tiny spot in the amygdala. But still Martha could play. When she asked for a third surgery, her doctors warned that taking away so much of her right temporal lobe could prove catastrophic, leaving her paralyzed or even dead. But Martha had decided that she simply could not go on living with the unpredictable and debilitating seizures.

By the time she emerged from the third surgery, close to 50 percent of her right temporal lobe, including the entire hippocampus,
was gone. So were her seizures. Her musical memory, however, was very much intact, allowing her to memorize complex pieces even better than before her surgeries, when the anticonvulsants left her in a mental fog. Her brain, doctors concluded, must have been damaged when she was still a toddler, probably by the measles she contracted at age three. Because Martha had begun learning music at such a young age, her brain, it seems, adapted to the damage, with the result that regions other than the abnormal right temporal lobe were drafted during childhood to support musical memory. Because the real estate that the brain usually zones for musical memory was essentially unusable, the brain—exploiting its youthful plasticity—picked up and moved its musical operations across the neural road.

At Johns Hopkins University Medical Center, surgeons challenged the adaptability of a child’s brain even more. In 2000 a three-and-a-half-year-old girl named Alexandria Moody had arrived at the Baltimore hospital from her home in Indiana with her mother and stepfather, suffering from chronic seizures. Her physicians back home suspected the little girl was suffering from a brain aneurysm, but an MRI revealed something completely unexpected: the entire left hemisphere of Alex’s brain had suffered severe developmental abnormalities. The seizures seemed to be emanating from there, concluded John Freeman, a specialist in pediatric epilepsy. He recommended a complete hemispherectomy—removal of the entire left side of the brain. The operation sounds radical, and it is. But starting in the mid-1980s it became the treatment of choice for children suffering from uncontrollable and often life-threatening seizures due to developmental abnormalities, stroke, or Rasmussen syndrome that do not respond to drugs. Although the brain’s deep structures (the brainstem, thalamus, and basal ganglia) are left intact, patients almost always suffer some paralysis on the side of the body opposite the lost hemisphere. But the reward is generally worth the risk: in June 2001, Hopkins surgeons performed their one hundredth hemispherectomy.

The pediatric neurosurgeon Ben Carson performed the operation on Alexandria. Having done more than eighty hemispherectomies since 1985, he was optimistic. “If you see the patients who have had hemispherectomies, you’re always amazed,” he said. “Here they are, running, jumping, talking, doing well in school. They’re able to live a normal life”—despite losing half their brain. What saves these children is their youth. “You can take out the right half of the brain or the left half,” Carson said. “Plasticity works in both directions. The reason it works so well in very young patients is that their neurons haven’t decided what they want to do when they grow up. They’re not committed. So they can be recruited to do other things. Whereas if I had a hemispherectomy it would be devastating.” The worst a child suffers from losing half her brain, however, is some impairment of the peripheral vision and fine motor skills on one side of the body.

The brain of a child is almost miraculously resilient, or plastic: surgeons can remove the entire left hemisphere, and thus (supposedly) all of the brain’s language regions, and the child still learns to talk, read, and write as long as the surgery is performed before age four or five. Although in most people the left cerebral hemisphere supports language, the brain, it seems, can roll with the punches (or the surgery) well enough to reassign language function to the right cerebral hemisphere, all the way over on the other side of the head. Therefore, if the brain suffers damage before age two, and loses the areas originally designated as language regions, it usually reorganizes itself to reassign those language functions to another area. By age four to six, a brain injury that wipes out the original language areas usually leaves the child with a profound learning deficit, although she will typically retain the language she had learned up to then. After six or seven, however, the brain is already becoming set in its ways, and loss of its language regions can leave a severe and lasting language deficit. If an adult suffers damage to the left perisylvian, the site of language areas in the brain, the result is typically (though as recent stroke research shows, not always) perma
nent
aphasia
, the inability to use or understand words. A preschooler can recover from the loss of half her brain, but a little lesion in the same hemisphere leaves an elderly stroke patient mute. So although the brain of a young child retains impressive plasticity, that malleability yields, within a few short years, to something like neural obstinacy: the brain balks at rearranging itself in the face of changed circumstances.

As far as scientists can tell, then, a young brain can usually compensate for injury to a particular region by shifting the function of the damaged region to an unaffected region. But this comes at a cost. The area to which an otherwise-lost function is shifted becomes neurologically crowded, says Jordan Grafman of the National Institute of Neurological Disorders and Stroke, part of the National Institutes of Health. As a result, when the brain tries to execute two tasks in adjacent regions it can cause a sort of traffic jam. Grafman offers the example of an adolescent boy whose brain had been injured years before in a freak childhood accident. His right parietal lobe, a structure that supports visual and spatial skills, suffered a lesion. Yet despite the injury, the boy developed normal visual and spatial skills. Oddly, however, he had great difficulty with math, which is normally a function of the left parietal lobe. Through brain imaging, researchers learned that functions ordinarily controlled by the (injured) right side of the brain had moved over to the left hemisphere. Spatial skills typically develop before math skills do. As a result, when it came time for the child to learn math, the region of his brain that would ordinarily be responsible for that function had already been taken, and there was little neural real estate left to support mathematical reasoning.

Young brains are also relatively nimble at a form of neuroplasticity called
cross-modal reassignment
. This occurs when a brain region that ordinarily handles one form of sensory input does not receive the expected input. Rather than sit around unused, it seems, that region becomes more receptive to receiving a different input, as a satellite dish receiving no signal when pointed in one direction
shifts to catch signals from another direction. Such reassignment within the brain seems to explain the changes that occur in children who become blind at a very young age. The visual cortex no longer receives sensory input from the retina through the optic nerve, and as a result the somatosensory cortex, which receives tactile input, invades areas normally dedicated to processing visual input. People who have been blind from birth often have an exquisitely sensitive sense of touch, particularly if they learn to read Braille when still young. The feel of the raised dots is processed in the visual cortex.

Similarly, in children who are congenitally deaf, the brain seems to reassign its auditory cortex (which is receiving no auditory information) to process visual information instead. In one clear demonstration of this, scientists exposed subjects who had been deaf since birth to a flash of light in their peripheral vision: the auditory cortex experienced a wave of electrical activity, showing that it had been rewired for sight rather than sound. What seems to have happened is that, during gestation, a visual neuron from the retina took a wrong turn and found itself in the auditory cortex. Under normal circumstances, the connections that neuron formed with other neurons would wither away; retinal neurons just don’t make connections in the auditory cortex. But in a deaf child auditory neurons are silent and so offer no competition for the wayward retinal neuron. Synapses made by the wayward neuron survive and actually come in handy: congenitally deaf people typically perform better on tests of peripheral vision than people with normal hearing, probably thanks to these extra visual synapses. And the deaf often use their auditory cortex to register sign language; people with normal hearing typically use the visual cortex.

Since the early 1990s, MIT researchers led by Mriganka Sur had been probing the limits of neuroplasticity in somewhat unheralded lab animals: newborn ferrets. In these animals as well as in humans, the optic and auditory nerves grow from the eye and the ear, respectively, through the brainstem and thalamus before reaching the visual or auditory cortex. In humans, as we’ll discuss later,
this basic wiring plan is present at birth; in ferrets, however, these connections reach the thalamic way station to the cortex only after birth. In their breakthrough experiment, the MIT scientists took advantage of this delay. They lesioned the normal inputs to the auditory thalamus on one side of the brain. With the competition out of the way, as it were, projections from the retina, arriving at the thalamus, grew into the auditory cortex. Now the auditory cortex on that side was receiving signals from the retina and only the retina.

The result: When the ferrets were shown flashes of light on the rewired side of their brain, they responded not as if they saw the light but as if they heard it. The retinal nerve had carried the signal to the auditory cortex. This part of the brain, normally dedicated to sensing sounds, had been rewired to respond to sight.

Whatever the zoning law that originally destined this patch of cortex to bloom into primary auditory cortex, on receiving input from the retina it was transformed into the animal’s primary visual cortex. The result: when the ferrets were shown a flash of light, they saw it with their auditory cortex. And there was more. Just as in the visual cortex of normal ferrets, the “auditory” cortex of rewired ferrets contained neurons that specialized in inputs of different spatial orientations—vertical, horizontal, and everything in between. The ferrets consistently responded to a light stimulus presented to the rewired auditory cortex as if it were indeed a light signal, even though the retinal neurons carrying the input fed in to what is normally the turf of “auditory” cortex. This bears emphasizing. Whether the nerves run from the retina or from the cochlea, they carry signals in the same way, through electrical impulses that I’ll discuss later. There is nothing inherently “sightlike” or “soundlike” in the signals. It was once considered a fundamental principle of brain organization that the way signals are perceived depends on which part of the brain processes them. In the rewired ferrets, retinal nerves carry signals to what had been auditory cortex. Yet the rewiring had given the auditory cortex a new identity, turning it
into a de facto visual cortex. As Michael Merzenich of the University of California, San Francisco, commented, “The animals ‘see’ with what was their auditory cortex…. [I]n these rewired animals, the experience of sight appears to arise from visual inputs to the auditory cortex area.” The findings reminded Merzenich of a comment William James once made: if we could tinker with the nerves so that exciting the ear activated the brain center concerned with vision, and vice versa, then we would “hear the lightning and see the thunder.”