The Mind and the Brain (30 page)

So they did. The following summer, they held Camp Rutgers II. For twenty days, twenty-two SLI kids aged five to nine played CD-ROM games structured to coax the brain into building those absent phonological representations. One game, for instance, asked the child to “point to rake” when pictures of a lake as well as a rake were presented, or to click a mouse when a series of spoken
g
’s was interrupted by a
k
. At first, the computer voice stretched out the target sounds:
rrrrrake
. The usual 0.03-second (30-millisecond) difference between
day
and
bay
, for instance, lasted several times that long. The modified speech seemed to be recruiting neurons to make progressively faster and more accurate distinctions between sounds. When a child mastered the difference between
ba
and
pa
when the initial phoneme was stretched to 300 milliseconds, the software shortened the transition to, say, 280 milliseconds. The goal was to push the auditory cortex to process faster and faster phonemes. The kids also took home books like
The Cat in the Hat
on tape, recorded in processed speech. Again the results were striking: a few months after receiving twenty to forty hours of training, all the children tested at normal or above in their ability to distinguish phonemes. Their language ability rose by two years. Although the research did not include brain scans, it seemed for all the world that Fast ForWord (as the program was now called) was doing something a bit more revolutionary than your run-of-the-mill educational CD: it was rewiring brains.

In January 1996, the Rutgers and UCSF teams reported their results in the journal
Science
. Modified speech, they concluded, had altered the children’s brains in such a way that they could now distinguish phonemes and map them correctly onto written words. Just as Greg Recanzone showed that when monkeys pay attention to a frequency-discrimination task their auditory cortex changes and their ability to hear tiny differences in tone improves, so SLI children who had received intensive training in discriminating acoustically modified phonemes seemed to have undergone cortical reorganization in the region of the brain that carries out auditory processing. “You create your brain from the input you get,” says Paula Tallal.

“We realized we had a tiger by the tail,” says Jenkins. Merzenich fretted that once the results were out, everyone with a language-impaired child would want it. He was right. The work was covered in newspapers and magazines, and in just ten days some 17,000 people had jammed the Rutgers switchboard, blowing out the e-mail and phone systems, in an effort to get hold of the miraculous CD-ROM that seemed to conquer dyslexia. Desperate parents awakened Merzenich at 2
A.M.
(his phone number was listed), imploring him to help their children. Representatives from the venture capital firm E. M. Warburg, Pincus & Co. descended on Tallal’s lab to figure out whether she had the basis for a profit-making business. Fellow scientists were appalled. Some even suspected that the Rutgers/UCSF team had manufactured all the media interest, as if in a replay of the cold fusion claims of the 1980s.

A Rutgers regent offered advice on how they might license the CD-ROM, but Merzenich, who had been on the team that developed the cochlear implant for hearing loss, was convinced that if you license a scientific discovery, “you lose all control over it.” He and Bill Jenkins discussed the dilemma endlessly. “We were afraid that if we just licensed the software to Broderbund or the Learning Company or something they wouldn’t understand the scientific
complexity of it, and wouldn’t implement it right,” says Jenkins. “And if that happened, the opportunity would be lost. We wanted to make sure the science got properly translated.” So the month after the
Science
publication, Merzenich, Paula Tallal, Bill Jenkins, Steve Miller, and recruits from the business world raised enough private financing to form Scientific Learning Corp., the first company dedicated to making money from neuroplasticity.

Merzenich told colleagues that forming a business was the only way to get the benefits of neuroplasticity out of the lab and into the hands—or brains, actually—of the people it could help. When Ed Taub once expressed frustration about how slow the rehabilitation community was to embrace constraint-induced movement therapy for stroke, Merzenich responded that only the profit motive was strong enough to overcome entrenched professional interests and the prejudice that the brain has lost plasticity after infancy. By October 1996 Merzenich and his partners had secured venture capital funding from E.M. Warburg, and the next month Scientific Learning conducted its first public demonstration of Fast ForWord, at the annual meeting of the American Speech-Language-Hearing Association. “No one would be using Fast ForWord if there were not a commercial force driving it into the world,” Merzenich said four years later. “The nonprofit motive is simply too slow.”

By unleashing the force of commercialism, Merzenich is convinced, Fast ForWord reached more children than it would have if he and Tallal had simply sung its praises from the offices of their ivy-walled universities. In October 1997 19 schools in nine districts across the country participated in a pilot program using Fast ForWord, enrolling more than 450 students with specific language impairment. Within four years some 500 school systems had learning specialists trained to use Fast ForWord (soon renamed Fast ForWord Language), and by the year 2000 25,000 SLI children had practiced on it for at least 100 minutes a day, five days a week. Once the children master recognition of the stretched-out phonemes, the
program speeds them up until eventually the children are hearing ordinary speech. After about four weeks, the kids can process phonemes pronounced at normal speed. After six to eight weeks, “90 percent of the kids who complete the program have made 1.5 to two years of progress in reading skills,” says Tallal. Scientific Learning itself graduated, too, financially speaking: in July 1999 it announced its initial public offering. Anyone who believed in neuroplasticity, and its power to turn a profit, could now ante up.

Scientific Learning has hardly won universal acceptance. Critics say it is too expensive for most schools. Some also say the system is being rushed to market before its stunning claims have been proved in independent tests. The claim that Fast ForWord reshapes the brain has been the target of the most vituperation. In one representative comment, Dr. Michael Studdert-Kennedy, past president of the Haskins Laboratories, a center for the study of speech and language at Yale University, told the
New York Times
in 1999 that inducing neuroplasticity was “an absurd stunt” that would not help anyone learn to read.

Yet only a year later, researchers reported compelling evidence that Fast ForWord changes the brain no less than Taub’s constraint-induced movement therapy or Merzenich’s monkey training does. Merzenich, Tallal, and colleagues had teamed up with John Gabrieli of Stanford University to perform brain imaging on dyslexic and normal adults. For the first time, brain scans would be used to look for changes that accompanied the use of their learning program. Using functional magnetic resonance imaging (fMRI), the researchers first ascertained that their eight adult dyslexics and ten matched controls differed in their processing of rapid acoustic stimuli. When they heard rapid, computer-generated nonsense syllables (designed to mimic the consonant-vowel-consonant pattern of English, but without being real words), the brains of nine of ten normal readers showed greater activation (compared to that triggered by slower sounds) in the left prefrontal
region of what are called Brodmann’s areas 46/10/9. Only two of eight dyslexics showed such left prefrontal activity when they heard rapid acoustic signals. The highly significant difference between the groups strongly suggests that the response in that region had been disrupted in the dyslexics. Since this area is thought to be responsible for the processing of staccato sounds, its lack of activity could explain dyslexics’ inability to hear those sounds.

The researchers next performed fMRIs on the three dyslexics who had undergone Fast ForWord training for 100 minutes a day, five days a week, for about thirty-three sessions. Two of the three showed significantly greater activation in this left prefrontal region. These were also the subjects who showed the greatest improvements, after Fast ForWord, in their processing of rapid auditory signals and language comprehension. (The dyslexic whose brain showed no such change also did not improve on auditory processing.) Training in rapid acoustic discrimination can apparently induce the left prefrontal cortex, which is normally attuned to fast-changing acoustic stimuli but is disrupted in dyslexics, to do its job. The region, even in adults, remains “plastic enough…to develop such differential sensitivity after intensive training,” the scientists concluded.

The discovery that modified speech can drive neuroplasticity in the mature brain is just the most dramatic example (so far) of how sensory stimuli can rewire neuronal circuits. In fact, soon after Merzenich and Tallal published their results, other scientists began collecting data showing that, as in my own studies of OCD patients, brain changes do not require changes in either the quantity or the quality of sensory input. To the contrary: the brain could change even if all patients did was use mindfulness to respond to their thoughts differently. Applied mindfulness could change neuronal circuitry.

It seemed to me that if the mindfulness-based Four Steps had
any chance of finding applicability beyond obsessive-compulsive disorder, its best hope lay in Tourette’s syndrome. Recent evidence indicates that this disease strikes about 5 people per 1,000. Although its precise cause remains to be worked out, Tourette’s has a strong genetic component. Drs. James Leckman and David Pauls of Yale University had shown in 1986 that there is a biological link between OCD and Tourette’s, such that the presence of Tourette’s in a family puts relatives at risk of OCD. But I was interested in a different common characteristic of the two diseases. The defining symptoms of Tourette’s are sudden stereotypical outbursts, called tics. They include vocalizations such as grunting or barking or spouting profanities, as well as muscle movements such as twitches and jerks of the face, head, or shoulders. These echo the compulsions of OCD, but there is more: the motor and vocal tics that characterize Tourette’s usually have a harbinger, a vague discomfort that patients often describe as an irresistible urge to perform the head jerk, to utter the profanity. The more the patient suppresses the tic, the more insistent the urge becomes, until the inevitable surrender brings immediate (albeit temporary) relief. The similarities to OCD are obvious: Tourette’s patients suffer a bothersome urge to twitch their face, blink their eyes, purse their lips, sniffle, grunt, or clear their throat in much the same way as OCD patients feel compelled to count, organize, wash, or check.

The two diseases also seem to share a neural component. The symptoms of Tourette’s apparently arise from impaired inhibition in the circuit linking the cortex and the basal ganglia—a circuit that is also impaired in OCD. The basal ganglia, you’ll recall from Chapter 2, play a central role in switching from one behavior to another. Impairment there could account for the perseveration of obsessions and compulsions, as well as the tics characteristic of Tourette’s.

The first case study of this disease appeared in 1825, with a description of one Marquise de Dampierre. “In the midst of a con
versation that interests her extremely, all of a sudden, without being able to prevent it, she interrupts what she is saying or what she is listening to with bizarre shouts and with words that are more extraordinary and which make a deplorable contrast with her intellect and her distinguished manners,” reads the translation of the account in
Archives Générales de Médecine
. “The words are for the most part gross swear words and obscene epithets and, something that is no less embarrassing for her than for the listeners, an extremely crude expression of a judgment or of an unfavorable opinion of someone in the group.” Sixty years later, Georges Gilles de la Tourette took up “the case of the cursing marquise,” identifying it as the prototypical example of what he called
maladie des tics
. The disease was given its current name in 1968 by the psychiatrist Arthur Shapiro and his wife, the psychologist Elaine Shapiro. In the search for a cause, physicians suspected patients’ families of inflicting early psychological trauma, and patients themselves were blamed for a failure of will.

The disease’s mysterious cause inspired a wide range of treatments, from leeches to hypnosis and even lobotomies. More recently, physicians, suspecting that dopamine transmission in the basal ganglia circuit causes the disease, have tried to treat Tourette’s with haloperidol and pimozide, drugs that block the neurotransmitter dopamine. (Uncertainty remains, however, over whether an excess of dopamine, sensitivity of dopamine receptors, basal ganglia malfunction, or some combination of these is at fault. In any case, it is likely that the genetic basis of the disease manifests itself somewhere in the dopamine system.) Drugs typically reduce tic symptoms 50 to 60 percent in the 80 percent of patients who respond at all. But dopamine blockers do not work for every patient. Worse, the drugs have big drawbacks, often producing serious side effects, even leaving some patients in a zombielike state. In fact, side effects lead up to 90 percent of patients to discontinue the drugs. Of those who stick with the regimen, inconsistent compliance is common. Many parents, concerned about the lack of
information on the long-term effects of the medications on children, are understandably reluctant to keep their kids drugged. No wonder drugs have fallen from their perch as the treatment of choice.

That leaves behavioral treatment. But behavioral approaches have been hampered by—and there is no way to put this politely—lousy science. Over several decades, almost a hundred studies have investigated half a dozen behavioral therapies. They looked into
massed practice
, in which the patient performs his worst tic for perhaps five minutes at a time, with a minute of rest, before repeating the process for a total of about thirty minutes. Other studies investigated
operant conditioning
, in which parents and others are taught to praise and encourage a child when he is not performing a tic, and punish the performance of a tic. Others tried
anxiety management
(since tics seem to get worse with stress) and
relaxation training
, with deep breathing and imagery; although many patients managed to control tics during the therapy session, the improvement seldom carried over into the real world. Some studies explored awareness training, using videotapes and mirrors to make the patient realize how bad his tics were. But few of the studies included more than nine subjects, few included children, most failed to use standard measures of tics, and many piled so many behavioral interventions on top of one another that it was impossible to tease out which therapy was responsible for any observed effects. Follow-up was poor (a real problem since tics wax and wane naturally). In other words, the scientific underpinnings of this generation of behavioral therapies were so seriously flawed as to compromise their credibility.