The Mind and the Brain (32 page)

Teasdale then began to construct a therapy to achieve this. Through mindfulness-based cognitive therapy, he wanted to make patients more aware of their thoughts. In particular, he wanted them to recognize that sadness can (through a brain-based biological mechanism) escalate into depression. To prevent it from doing so, they would learn to meet the onset of dysphoria with such responses as “Thoughts are not facts” and “I am not my thoughts.” Or as Teasdale puts it, they would learn to prevent what he calls
depressive interlock
(again, reminiscent of my “brain lock”) : the strong, physical connection between unhappy thoughts and the memories, associations, and modes of thought that inflate sadness into depression. To do that, the therapist needs to help patients encode in memory alternative thought patterns that can be activated by the very same cues that otherwise tap into the despairing ones.

When I read this, in 1999, I was thrilled. Finally, I thought, I’ve found a kindred spirit in this profession. This guy is actually using mindfulness to help patients to see the passing, ephemeral nature of their depressive thoughts. Teasdale’s proposed treatment also gave me a sense of déjà vu. Healthy emotional processing prevents the dysphoria from triggering global thoughts of hopelessness and self-worthlessness. It instead activates alternative memories and associations, so that the next time the patient encounters something that makes her sad she reacts not with despair but by calling up other, healthier associations. To me, this was reminiscent of OCD patients learning to respond to the compulsive urge to wash by deciding instead to crochet or garden—that is, by Refocusing. As Teasdale put it, “The new schematic models rather than the old will be
accessed and these new models will determine emotional response.” Much as I had, he was proposing that patients could learn to weaken the physical connections to the old, pathological schema—habitual way of thinking—and strengthen those to a new, healthier one. And as with the Four Steps approach, mindfulness was to be the key.

How, then, to apply mindfulness to depression? Teasdale identified three ways that depressives can process emotion-laden thoughts. They can mindlessly emote, or allow themselves to be engulfed by their feelings with little self-awareness or reflection. Patients who respond this way typically have poor outcomes to psychotherapy. Alternatively, patients can engage in “conceptualizing/doing.” By this, Teasdale means having impersonal, even detached thoughts about the self, about depression, and about its causes and consequences. Conceptualizing/doing lacks the introspection inherent in mindfulness. Depressed patients who think this way also tend not to do well in therapy.

The third option is what Teasdale named “mindful experiencing/being.” In this way of thinking about your emotions, you sense feelings, sensations, and thoughts from the perspective of the Impartial Spectator. You regard your thoughts and feelings as passing, ephemeral “mental events” rather than as accurate reflections of reality. Instead of reacting to negative thoughts and feelings as “these are me,” you come to regard them as “events in the mind that can be considered and examined.” You recognize that thoughts are not facts (just as my OCD patients learned that their obsessions are only their brain’s causing their mind to misbehave) but are instead “events that come and go through the mind,” as Teasdale explains it. Mindfulness gives patients the attentional skills that allow them to disengage from, and focus instead on alternatives to, the dysfunctional ways of thinking that trigger a relapse of their depression. Teasdale had independently constructed, and taken the first steps toward proving, a model of depression much like my model of OCD.
In a landmark paper in August 2000, Teasdale and his colleagues reported the results of his yearlong study on using mindfulness to prevent the relapse of depression, offering strong support for the findings in OCD patients that mindfulness can alter brain circuits. Using an approach pioneered by the American psychologist Jon Kabat-Zinn, Teasdale had his patients participate in two-hour group sessions once a week for eight weeks, receiving mindfulness training through tape-recorded instructions that taught them to direct their attention to specific regions of the body in succession. The goal was to become acutely aware of whatever sensations an arm, a cheek, a knee was experiencing at the moment. The patients then learned to focus on their breathing. If the mind wandered, patients acknowledged the distractions with “friendly awareness”—that is, not with frustration or anger—and learned to return calmly to a focus on the breath. Repeating this process over and over, patients learned to use their inhalations and exhalations as an anchor to pull them back to a mindful awareness of the present moment. The patients also had homework, including exercises designed to increase their moment-by-moment awareness of feelings, thoughts, and sensations and to allow them to view thoughts and feelings (particularly negative ones) as merely passing events in the mind and brain.

The results were impressive. Of the 145 patients from ages eighteen to sixty-five, who had suffered at least two episodes of major depression within the last five years, about half were randomly assigned to receive the standard treatment and half to receive the mindfulness training, too. All had been off antidepressants for at least the previous twelve weeks, long enough to clear the drugs from their system. Over the sixty-week study period (eight weeks of treatment then fifty-two weeks of follow-up), among patients who had suffered at least three episodes of major depression there was a 44 percent reduction in the rate of relapse among those who received mindfulness therapy compared to those receiving standard therapy. Adding mindfulness, then, cut the rate
of relapse by almost half. This was the first demonstration that a mindfulness-based psychological intervention can reduce the rate of relapse in depression.

The will, it was becoming clear, has the power to change the brain—in OCD, in stroke, in Tourette’s, and now in depression—by activating adaptive circuitry. That a mental process alters circuits involved in these disorders offers dramatic examples of how the ways someone thinks about thoughts can effect plastic changes in the brain. Jordan Grafman, chief of cognitive neuroscience at the National Institute of Neurological Disorders and Stroke, calls this top-down plasticity, because it originates in the brain’s higher-order functions. “Bottom-up” plasticity, in contrast, is induced by changes in sensory stimuli such as the loss of input after amputation. Merzenich’s and Tallal’s work shows the power of this bottom-up plasticity to resculpt the brain. The OCD work hints at the power of top-down plasticity, the power of the mind to alter brain circuitry. I suspect that when the requisite brain imaging is done with Teasdale’s depressives, that research will also show the power of mind to change the brain. In fact, recent studies using a somewhat different form of psychotherapy called interpersonal therapy already have.

Sitting somewhere between purely mental events and purely sensory ones is this vast sea of life called experience. Research into how experience affects the brain is only in its infancy, but one of my favorite examples suggests where we may be heading.

One wag called the study “taxicology.” When researchers at University College London decided to study how navigation expertise might change the brain, they didn’t have to look far for subjects. London cabbies are renowned for their detailed knowledge of the capital’s streets: to get their license, they have to pass a stringent police test assessing how well they know the fastest way from point A to point B and what streets are where. Drivers call it “being on The Knowledge,” and it takes them an average of two years to learn it.

Earlier studies in small mammals, monkeys, birds, and humans had established that the right half of an unassuming little structure near the center of the brain called the hippocampus is involved in the formation of directional memories; in fact, the back of the right hippocampus seems to store a mental map of the environment. Eleanor Maguire and her colleagues at the university therefore decided to examine the hippocampi of London taxi drivers, using magnetic resonance imaging, and compare them to the hippocampi of Londoners who hadn’t the faintest notion of the best way to get from Fleet and Chancery to Gresham and Noble.

Maguire scanned the brains of sixteen cabbies, aged thirty-two to sixty-two, and fifty ordinary right-handed men of the same age. Everyone’s brain structures looked about the same, in both size and shape—except the hippocampus. In the taxi drivers, the back was significantly larger than it was in the other men, and the front was smaller. That might simply reflect the fact that if you’re born with a big rear hippocampus, you are a navigational ace, and hence are more likely to take up hacking than if you can’t tell east even at sunrise. So to see if the brain differences reflected experience, Maguire plotted the differences in the volume of the hippocampus against how experienced a driver was. There it was: the more years a man had been a taxi driver, the smaller the front of his hippocampus and the larger the posterior. “Length of time spent as a taxi driver correlated positively with volume in…the right posterior hippocampus,” found the scientists. Acquiring navigational skills causes a “redistribution of gray matter in the hippocampus” as a driver’s mental map of London grows larger and more detailed with experience.

What cabbies might be sacrificing in the front part of their hippocampus for an enlarged posterior part remains unknown, as does the mechanism for the volume changes. Although neurogenesis might explain the enlargement of the rear of the hippocampus, the London scientists have their money on an overall reorganization of the hippocampus’s circuitry “in response to a need to store an
increasingly detailed spatial representation.” One thing, however, is clear: a key brain structure can change in response to your experience as an adult. Published in 2000, this was the first demonstration that the basic anatomy of the adult brain, not just the details of its wiring, can be altered by the demands its owner places on it.

The study of neuroplasticity began with scientists’ cataloguing the changes in sensory input that induce cortical remapping and rewiring. Now, even as they add to the list of examples of neuroplasticity, researchers are also exploring the cellular and molecular mechanisms that underlie it. We know that the formation of new synapses, as a result of the growth of existing axons or dendrites, is involved in both the remodeling of circuits and cortical remapping. A change in the quantity of available neurotransmitters, or the enzymes that regulate them, can also foster plasticity. But now researchers are examining a mechanism that had long been dismissed as an avenue to plasticity: the actual creation of new neurons. Although a slew of animal experiments had demonstrated that new synapses can form when the animal is exposed to an “enriched” environment, that was one step short of showing that new neurons, as opposed to new connections between neurons, were being born.

That changed in 1997. Fred Gage and colleagues at the Salk Institute in La Jolla, California, placed adult mice in an “enriched” environment (one that resembles the complex surroundings of the wild more than the near-empty cages of the rats in the “nonen-riched” environment do). By the end of the experiment, the formation and survival of new neurons had increased 15 percent in a part of the hippocampus called the dentate gyrus. These animals also learned to navigate a maze better. In 1999 Elizabeth Gould of Princeton University used similar techniques in adult rats to demonstrate that the creation of new neurons, called neurogenesis, was not a talent lost in infancy: the increased neurogenesis, she found, is directly related to learning tasks that involve the hip
pocampus. Also in 1999, Gage showed again that new neurons grow in the hippocampus of adult mice as a result of exercising on a wheel, and in 2001 Gould and colleagues demonstrated that newly generated neurons are “associated with the ability to acquire…memories.”

“Neurogenesis was a hard thing for scientists to come to grips with,” said Gage. But by the new millennium it was clear that new neurons arise from stem cells, immature cells capable of differentiating into virtually any type of cell. There is now abundant evidence that neural stem cells persist in the adult brain and support ongoing neurogenesis. And the evidence is no longer confined to mice. In 1998, Peter Eriksson of Goteborg, Sweden, working with Gage, demonstrated that neurogenesis occurs in the adult human hippocampus. Thus Gage’s and Gould’s discoveries suggest that the possibilities for neuroplasticity are greater than even diehard believers thought: the brain may not be limited to working with existing neurons, fitting them together in new networks. It may, in addition, add fresh neurons to the mix. The neural electrician is not restricted to working with existing wiring, we now know: he can run whole new cables through the brain.

Neuroplasticity has come a long way since Nobel laureates ridiculed Mike Merzenich for his audacity in claiming to have shown that the mature central nervous system has the capacity to change. Even in the early 1990s neuroplasticity was viewed as, at best, an interesting little field. By the middle of the decade, however, it had become one of the hottest topics in neuroscience, and as the decade ended, hundreds of researchers had made it the focus of their studies. “If you had taken a poll of neuroscientists in the early 1990s, I bet only 10 to 15 percent would have said that neuroplasticity exists in the adult,” Merzenich says. “Even by the middle of the decade the split would have been 50–50. What changed that was the human experiments” like Taub’s. Now there is no question that the brain remodels itself throughout life, and that it retains the capacity to change itself as the result not only of passively experi
enced factors such as enriched environments, but also of changes in the ways we behave (taking up the violin) and the ways we think (“That’s just my OCD acting up”). Nor is there any question that every treatment that exploits the power of the mind to change the brain involves an arduous effort—by patients afflicted by stroke or depression, by Tourette or OCD—to improve both their functional capacity and their brain function.