The Mind and the Brain (31 page)

Suspecting that Tourette’s might be amenable to a mindfulness-based approach like the one that was succeeding with OCD, I began (in a nice way) jawboning researchers who might be sympathetic. In 1989, at the annual meeting of the American College of Neuropsychopharmacology (ACNP), I struck up a conversation with Jim Leckman. Jim is arguably the country’s leading expert on the cause of Tourette’s. On top of that, he is trained as a psychoana
lyst and so is keenly interested in the mind-brain interface. After 1989 we became good friends, but it was not until the mid-1990s, at another ACNP meeting, that I began telling Jim about the broader implications of the PET data we had collected on OCD patients—implications about the power of the mind to shape the brain. Although he kept an open mind, he was decidedly skeptical. Because Jim is perhaps the most polite member of the baby boom generation, it took me almost a decade to realize just how much he had been graciously humoring me. Eventually, he became convinced that there might be clinical advantages to giving patients an active role in therapy—in the case of Tourette’s, by using mindfulness to modulate the physical expression of the tics. Only then did he start to believe that my arguments were more than a lot of hot air.

Even after Jim started to come around, his boss at the Yale Child Study Center remained less than a true believer in this idea. When I visited Jim’s lab in July 1998, he and his department chair, Donald Cohen, arranged for me to meet with an adolescent boy with OCD in what’s called an observed interview. As Jim, Cohen, and a group of the clinical staff looked on, I did a brief, interactive, and animated overview of the Four Steps with this bright kid. Afterward, as we reviewed the clinical interaction, Cohen looked at me with an amused expression and said, “So, it seems like you managed to sell that young man on your shtick.” “Well, it’s not really a shtick…” I began. “It sounds like a shtick to me,” he shot back. I tried to point out that it’s not a gimmick to teach patients suffering with OCD that their intrusive thoughts and urges are caused by brain imbalances, and that we now know they can physically alter those imbalances through mindfulness and self-directed behavioral therapy techniques. Although to psychiatry professors the Four Steps of Relabel, Reattribute, Refocus, Revalue may initially seem like a shtick, we had strong scientific evidence that this approach can bring about changes in brain function. (Of course Cohen already knew all this, or I wouldn’t have been at Yale in the first place.)

This seemed to calm matters down a bit. In any event, we all went out for a nice dinner. And besides, the Yale Child Study group had already done a major brain imaging study relevant to this point. Just three months before, in April 1998, in a study based on reasoning quite similar to the Four Steps approach to changing the brain circuits underlying OCD, Brad Peterson, Jim Leckman, and their Yale colleagues published important data on what happens when Tourette’s patients use willful effort to suppress tic expression. The Yale group had patients undergo fMRIs while they alternated forty seconds of letting their tics be expressed with forty seconds of volitionally suppressing them. Hearing the word
now
told the volunteers when to switch—particularly, when to call up whatever reserves of will they could muster to prevent the tics from causing bodily movements. The investigators noted how brain activity changed during tic suppression compared to when tics are given free rein. The most relevant regions seemed to house the circuit involving our old friends the prefrontal cortex, anterior cingulate gyrus, basal ganglia, and thalamus. Activity in this circuit—the very one involved in OCD and in the formation of habits—was noticeably altered (activity in the caudate increased and activity in the putamen decreased) when patients willfully prevented themselves from moving in response to the intrusive bothersome urges of Tourette’s. The study also found that the worse the tics, the less the basal ganglia and thalamus activity change when the tics are suppressed.

This finding is quite consistent with the notion of a “brain lock” in Tourette’s, which may be similar to that in OCD patients. You’ll remember from Chapter 2 that prior to cognitive-behavioral treatment the brain structures of the OCD circuit—the orbital frontal cortex, anterior cingulate gyrus, caudate, and thalamus—showed such high correlations in their activity they seemed to be functioning in lockstep. This same circuit also seems to be “locked up” in patients with Tourette’s. As the Yale researchers put it, “A failure to inhibit tics may result from an impaired ability to alter subcorti
cal neuronal activity.” Thus in Tourette’s, as in OCD, the gearshift of the basal ganglia seems to be locked. As it happened, my UCLA colleague John Piacentini was in the middle of a study designed to gauge whether mindful awareness and directed mental force could help unfreeze this jammed transmission.

In August 2000 Jim Leckman was in Los Angeles attending to family matters, so he, John Piacentini, and I got together. Piacentini had just put together the data from his ongoing study using a cognitive-behavioral approach incorporating mindfulness to treat children with Tourette’s. This new approach had been designed with an eye toward combining classical behavioral techniques for treating tics with the mindfulness component of the Four Steps. The key was to make patients understand that tics are an expression of a biological brain malfunction, much as the Four Steps makes OCD patients aware that their obsessions and compulsions originate in an overactive brain circuit. This new treatment aims to teach the patient that the behavioral response to the tic urge can be modified so that both the functional impairments (social and otherwise) and the physical damage to joints and muscles are reduced. After all, tics can be painful.

As Piacentini explained it to Jim Leckman and me, he asks each child to describe his or her tic occurrences in detail and reenact them in front of a mirror. Piacentini points out a tic if one occurs during a session. He also teaches the patient to identify the situations when a tic is most likely to recur, to recognize the very first glimmerings of the urge to tic, and to enhance that awareness by labeling it with the verbal or mental note
t:
as soon as the child feels a tic coming on, he says
t
to himself.

But the distinctive ingredient is training patients to develop what are called
competing responses
. Then, every time the urge to tic arises, that urge is paired with a behavior designed to modify the expression of the urge in order to control it better. If it is a verbal tic, John teaches the patient to breathe through the nose, slowly; that makes it physically impossible to bark out a curse. If it is a
motor tic, John coaches him to hold his arm close to his body, tense the neck muscles, or slowly open and close his eyes—activities that preclude wild arm swings, head jerks, or fast blinking, respectively. In the really creative part of the therapy John teaches the patient attenuated behavior, such as moving the arm slowly and wiping his brow to make the movement more volitional and controlled. The strategy has a good deal in common with directing OCD patients to Refocus attention away from a pathological compulsion and onto a healthy behavior. “What you want to do is substitute voluntary, controlled movement for the involuntary tic,” says Piacentini. “You need to be able to recognize the onset of the urge to tic, pay attention, and be motivated. It’s similar to the Four Steps approach to OCD. Patients are trained to recognize and label tic urges consciously and then either try to resist these urges, or else respond in a controlled and attenuated way. Most youngsters are eventually able to significantly diminish and/or eliminate targeted tics.”

When Leckman, Piacentini, and I sat down to look at John’s preliminary data, it was clear he had something. Twenty-four Tourette’s children, aged seven to seventeen, had enrolled in the study. Piacentini had divided the kids into two groups. In one, the children practiced recognizing when an urge to tic arose. In this stage, analogous to the Relabel and Reattribute parts of the Four Steps, they would realize that the urge to tic had arisen and give it that label
t
. “This is the urge to tic.” This is called
awareness training
. In the other group, Piacentini combined awareness training with habit modulation, in which the child is taught to respond to the urge to tic in a safe way by, for instance, executing a less intense movement. This is analogous to the Refocus step. Seventeen of the children completed the eight-week program. The assessors, gauging the children’s tic severity, were blind to which treatment group each child had been assigned to.

The results were striking. Patients receiving awareness training alone had an approximately 10 percent improvement in tic severity. But those also receiving habit modulation training had a 30 percent
reduction in tic severity and a 56 percent improvement in tic-related impairment. “Now it is being accepted that you can use behavioral intervention to treat a biologically-mediated disease,” Piacentini says. Although John has not yet done before-and-after brain scans to ascertain whether the children’s clinical improvement is accompanied by brain changes of the kind we detected in OCD patients, it is quite likely that brain changes analogous to those we found in OCD were occuring.

Innumerable studies have now shown that the mind can affect the body: mere thoughts can set hearts racing and hormones surging. Although mind-body medicine is usually understood as the mind’s effect on the body from the neck down, the power of the Four Steps to remodel neuronal connections—strengthening those underlying healthy habits and inhibiting those between the frontal cortex and basal ganglia (the OCD circuit) underlying pathological ones—strongly suggests that the mind can also affect the brain. In 1997, colleagues who knew of my interest in mindfulness told me about the work of John Teasdale at the Medical Research Council Cognition and Brain Sciences Unit in Cambridge, England. They said that Teasdale, working with Mark Williams and Zindel Segal, seemed to be harnessing exactly this power of the mind, but to treat depression: he proposed that patients would lower their risk of falling back into clinical depression if they learned to experience their depressive thoughts “simply as events in the mind.” That, of course, is a hallmark of the Impartial Spectator and mindful awareness. Teasdale and colleagues suspected that this perspective would diminish the power of so-called triggering cues to tip someone into a depressive episode. Just as my OCD patients learned to recognize intrusive thoughts as the manifestation of their brain’s misbehavior, so Teasdale’s depressives, the researchers thought, could learn to prevent a relapse by processing emotional material in a new way. By 1995, they were was boldly using
mindfulness
in the titles of
their research papers, and in 2000 Teasdale named his approach
mindfulness-based cognitive therapy
.

Depression is often a chronic disorder, characterized by frequent relapses. Over a lifetime, a patient has an 80 percent chance of suffering a recurrence and, on average, experiences four major depressive episodes lasting twenty weeks each. Antidepressants are the most widely used treatment. But in the 1990s, studies had begun to suggest that cognitive therapy, too, had the power to prevent relapses. In one study of 158 patients who had been treated with only partial success by antidepressants, some received cognitive therapy as well as drugs for their remaining symptoms. The rest received only the medication. The difference in relapse rates over the sixty-eight-week period of the study was significant: patients undergoing cognitive therapy experienced a 40 percent reduction in their rate of relapse compared to the drugs-only group.

Clearly, cognitive therapy helps prevent depressive relapse, and Teasdale thought he knew why. Other studies were showing that people are at greatest risk for becoming depressed when a sad, dysphoric, or “blue” mood produces patterns of negative, hopeless thinking. What distinguishes people who get depressed from those who don’t, Teasdale suspected, may be this: in the first group, dysphoria, that down-in-the-dumps feeling that most of us experience at least once in a while, triggers “patterns of depressogenic thinking” powerful enough to trigger full-blown depression. In these patients, dysphoria that may make a healthy person feel kind of blue plunges depression-prone patients into a well of despair. They ruminate on their perceived deficiencies and on the hopelessness of life. Although in a healthy person a bad day at work or a disastrous date may induce some passing sadness, in someone susceptible to depression it can readily escalate to “I’m completely incompetent and life is pointless.” In these vulnerable people, a dysphoric thought or experience seems to trigger the onslaught of depression much as a burning ember kindles a brushfire: the sad thought
ignites a conviction that one is pathetic and worthless, or that one’s current problems are irreparable and eternal. In relapsing depressives, this connection becomes so habitual and automatic that they “keep the system ‘stuck’ in repetitively generating [depressogenic thoughts].” It follows, then, that the risk of relapse can depend on how easily sadness tips someone into the self-perpetuating biological imbalances that characterize major depression.

To Teasdale, the corollary to this hypothesis was clear. To prevent the recurrence of depression, it may be sufficient for a patient to process her emotions in a new way, a way that does not trigger the thoughts and mood states characteristic of a depressive episode. That is, it may be enough to find a way to disrupt the automatic segue from sadness to sickness—and the pathological brain states associated with it. With the right therapy, thoughts and feelings that once tipped the person into full-blown depression would instead become “short-lived and self-limiting,” Teasdale suggested. His proposed therapy would change the very way patients think about their thoughts.

If Teasdale’s hunch seems reminiscent of my work with OCD patients—in which the urge to perform some compulsive act still intrudes but is thwarted when patients think about their thoughts and feelings differently—well, so it seemed to me, too. Studies at a handful of labs were already demonstrating the power of cognitive therapy over depression. When patients were presented with a scenario such as “You go out with someone and it goes badly” and were then asked how much they agreed or disagreed with such statements as “My value as a person depends greatly on what others think of me,” patients receiving only drugs were more likely to sink into dysfunctional thinking than those who also received cognitive-behavioral therapy. (The extent to which dysfunctional thinking follows dysphoria predicts the likelihood that a patient will suffer a relapse of depression.) That patients receiving cognitive-behavioral therapy are better able to resist being plunged into despair by sad thoughts suggests that this therapy changes
emotional processing—the way people think about their feelings—in ways that prevent dysphoria from triggering full-blown depression. Such research, Teasdale concludes, “suggests that emotional processing should focus primarily on changing emotional responses to internal affective events and thoughts, so that these responses are short-lived and self-limiting, rather than the first stages of an escalating process.”