Quieting the OCD Circuit ,
As discussed in the two preceding chapters, scientists were piling up examples
of how sensory input—signals carried into the brain from the outside world—
can alter the structure of the adult human brain. Thanks to neuroplasticity, the fingering digits to expand, and the extra sensory input a stroke patient
experiences in constraint-induced movement therapy causes the brain’s
representation of the injured arm and hand to move to healthy tissue. Thanks to
neuroplasticity, depriving the visual cortex of visual signals causes it to seek
other employment opportunities, such as handling sounds or touch or even
language. All of these changes arose from the world outside the brain.
Neuropsychiatrist Jeffrey Schwartz of the University of California–Los Angeles
suspected that signals capable of changing the brain could arrive not only from
the outside world through the senses. They could come from the mind itself.
Schwartz and colleague Lewis Baxter had launched a behavior-therapy group
to study and treat obsessive-compulsive disorder. In this neuropsychiatric
disease, patients are barraged by upsetting, intrusive, unwanted thoughts
(obsessions) that trigger intense urges to perform ritualistic behaviors
(compulsions). Depending on the patient, the compulsion can be to wash hands,
to check door locks or stove burners, to count stop signs or windows or
blackbirds or anything else on which he or she has fixated. Together, the
obsessions and compulsions can become all-consuming, making leaving the
house, holding a job, or forming meaningful relationships just about impossible.
Oddly, however, in all but the most severe cases, the intrusive thoughts and
fixations feel as if they are arising from a part of the mind that is not the real
you. Sufferers describe feeling as if a hijacker has taken over their brain’s
controls. As a result, OCD patients who feel compelled to wash their hands
know full well that their hands are not dirty; those who feel compelled to dash
home to check that the front door is locked know that it is securely bolted. OCD
has a lifetime prevalence of 2 to 3 percent. In round numbers, it affects an
estimated 1 person in 40, or more than 67 million Americans, typically striking
in adolescence or early adulthood and showing no marked preference for males
or females.
According to brain-imaging studies, OCD is characterized by hyperactivity in
two regions: the orbital frontal cortex and the striatum. The main job of the
orbital frontal cortex, which is tucked into the underside of the front of the brain, seems to be to notice when something is amiss. It is the brain’s error detector, its
neurological spell-checker. When overactive, as in OCD patients, it fires
repeatedly, bombarding the rest of the brain with the crushing feeling that
something is wrong. The second overactive structure, the striatum, is nestled
deep in the core of the brain just forward of the ears. It receives inputs from
other regions, including the orbital frontal cortex and the amygdalae, twin
structures that are the seat of fear and dread. Together, the circuit linking the
orbital frontal cortex and striatum has been dubbed “the worry circuit” or “the
OCD circuit.”
Until the mid-1960s, psychiatrists thought of OCD as “treatment intractable.”
They tried all sorts of therapies, from electroshock and brain surgery to drugs
and lie-on-the-couch talk therapy. In the late 1960s and early 1970s, however,
psychiatrists noticed that when OCD patients who were also suffering from
depression took the tricyclic antidepressant clomipramine, some experienced
relief from one or more of their OCD symptoms. Newer antidepressants,
including Prozac, Paxil, and Zoloft, also help some patients: about 60 percent
respond at least a little, and among these responders, there is a 30 to 40 percent
reduction in symptoms, measured by how often the patient feels an urge to carry
out a compulsion. But with some 40 percent of patients not helped at all, and
with those who are helped left with 60 percent of their symptoms, there is clearly
room for improvement.
At about the same time that researchers found that antidepressants helped
some OCD patients, a British psychologist working in a London psychiatric
ward began to develop what would become the first effective behavioral therapy
for the disease. In what he called “exposure and response prevention,” or ERP,
Victor Meyer had patients face their fears. He first exposed them to the “trigger”
of their obsessive thoughts. For instance, he would have a patient who was
convinced the world is covered with germs touch all the doorknobs in a public
building but would not let her wash her hands afterward (the “prevention” part
of ERP can be anything from gentle coercion to physical restraint). Although
Meyer reported improvement in his patients, a number of them—estimates run
from 10 percent to 30 percent—are so distressed by the treatment they never
complete it and never improve.
By the late 1980s, UCLA’s Schwartz had another objection to ERP: its cruelty.
“I just couldn’t see myself hauling patients to a public restroom, forcing them to
wipe their hands all over the toilet seats, and then preventing them from
washing,” he recalls. As he cast about for alternatives that were both more
humane and more effective, Schwartz, a practicing Buddhist, became intrigued
with the therapeutic potential of mindfulness meditation. Mindfulness, or
mindful awareness, is the practice of observing one’s inner experiences in a way
that is fully aware but nonjudgmental. You stand outside your own mind,
observing the spontaneous thoughts and feelings that the brain throws up,
observing all this as if it were happening to someone else. In The Heart of
Buddhist Meditation, the German-born Buddhist monk Nyanaponika Thera
described it as “the clear and single-minded awareness of what actually happens
to us and in us, at the successive moments of perception. It … attends just to the
bare facts of a perception as presented either through the five physical senses or
through the mind … without reacting to them by deed, speech or by mental
comment which may be one of self-reference (like, dislike, etc.), judgment or
reflection.”
Schwartz decided to see if mindfulness could help his OCD patients. He had
two goals for them: to experience an OCD symptom without reacting
emotionally and to realize that the feeling that something is amiss is just the
manifestation of a wiring defect in the brain—overactivity in the OCD circuit.
Mindfulness practice, he thought, might make OCD patients aware of the true
nature of their obsessions and therefore better able to focus their attention away
from them. “It seemed worth investigating whether learning to observe your
sensations and thoughts with the calm clarity of an external witness could
strengthen the capacity to resist the insistent thoughts of OCD,” says Schwartz.
“I felt that if I could get patients to experience the OCD symptom without
reacting emotionally to the discomfort it caused, realizing instead that even the
most visceral OCD urge is actually no more than the manifestation of a brain
wiring defect that has no reality in itself, it might be tremendously therapeutic.”
If so, then mindfulness-based cognitive therapy, in which patients learn to think
about their thoughts differently, might succeed where drugs, plain-vanilla
cognitive therapy, and exposure and response prevention had failed.
The mental note-taking central to mindfulness would go something like this.
When an obsessive thought popped up, the patient would think, “My brain is
generating another obsessive thought. Don’t I know it is not real but just some
garbage thrown up by a faulty circuit?” He would think, that’s not really an urge
to wash; that’s a brain-wiring problem.
In 1987, Schwartz launched a group-therapy session in conjunction with an
ongoing study of OCD’s underlying brain abnormalities. Patients came in for
therapy, and scientists tracked their progress using the brain-imaging technique
positron-emission tomography (PET). Schwartz began showing patients their
PET scans, to emphasize that their symptoms arose from a faulty neurological circuit. One patient got it right away: “It’s not me, it’s my OCD!” she exclaimed
one day. Soon other patients, too, saw that their obsessions and compulsions
were not really “them” but were instead the electronic detritus of brain circuitry.
Schwartz wondered, could getting patients to respond in a new way to the
obsessive thoughts characteristic of their OCD actually change their brains? He
therefore taught patients to use mindfulness to sharpen awareness of the fact that
they do not truly believe that they left the stove on or that their hands need
washing. Instead, he said, tell yourself you are just experiencing the arrival of an
obsessive thought. Start saying to yourself, this thing that feels like an urge to
check is in reality just a brain-wiring problem.That hunch was based on the fact that cognitive therapy is, in essence, a form
of mental training. It teaches patients a different way of approaching their
thoughts. In the case of depression, those thoughts are, all too often, sad, glum,
bleak, or otherwise “dysphoric.” Everyone gets those thoughts now and then, of
course. What’s different in patients with depression is that the thought tips them
over the emotional edge into an abyss of negative, hopeless thinking powerful
and sustained enough to trigger a full-blown episode of (typically) months-long
depression. A setback at work or a romantic rejection escalates to “Nothing will
ever go right for me; life is hopeless, and I will always be a complete loser.” As
described above, cognitive therapy teaches patients to think about these
triggering thoughts and feelings so they do not bring on a cascade of depression-triggering thoughts and major depression itself but instead become “short-lived
and self-limiting,” as John Teasdale of the University of Cambridge, England,
suggested.
So he made people sad. By then head of the Cognitive behavior Therapy clinic at the Center for Addiction and Mental Health in Toronto, he recruited
thirty-four people who had been successfully treated for depression within the
previous twenty-four months. To induce sadness, he had two surefire methods:
asking the volunteers to think about a time when they felt sad and having them
listen to Prokofiev’s Russia under the Mongolian Yoke. Played at half-speed,
Segal says, it induces five to ten minutes of deep sadness as reliably as Beth’s
death scene in Little Women.
Once the volunteers were feeling blue, Segal asked them to indicate how
much they agreed or disagreed with statements such as “If I fail at my work, then
I am a failure as a person,” “If someone disagrees with me, it probably indicates
he does not like me,” “If I don’t set the highest standards for myself, I am likely
to end up as a second-rate person”—all known to reveal whether someone holds
attitudes that make him vulnerable to depressive relapse.
Segal found that when people had been made melancholic by remembering a
sad episode in their lives or listening to the brooding Slavic melody, they were
much more likely to hold these attitudes. “The experience of depression can
establish strong links in the mind between sad moods and ideas of hopelessness
and inadequacy,” he says. “Through repeated use, this becomes the default
option for the mind: it’s like mental kindling. Even among recovered depressed
patients, the degree to which sad moods ‘switch on’ these attitudes is a
significant predictor of whether the patient will relapse eighteen months later.”
In some people, sad thoughts unleash beliefs that put them at risk for depression..
What these patients needed, he realized, was a different way to relate to the
inevitable sadness everyone experiences at one time or another, a way that would
not let a passing sense of unhappiness (from schmaltzy music, no less) send
them tumbling down the rabbit hole of depression. And for that, they needed to
forge new neuronal connections.
Mindfulness and Depression,
In 1992, Segal met with Cambridge’s John Teasdale and Mark Williams to turn
his theory of depressive relapse—that people who hold despairing attitudes are
more vulnerable to falling back into depression as a result of minor setbacks—
into a treatment. Teasdale, who had been practicing mindfulness meditation for a
number of years, had been learning about a mindfulness program developed by
Jon Kabat-Zinn of the University of Massachusetts, a longtime participant in the
Mind and Life Institute’s meetings with the Dalai Lama. Although Kabat-Zinn
used it mostly for stress reduction, Teasdale saw other possibilities: to harness
the power of the mind to treat depression. He suspected that patients might
escape repeated descents into clinical depression if they learned to regard
depressive thoughts “simply as events in the mind,” as he put it. The key would
be to help patients become aware of their thoughts and relate to them as merely
brain events rather than as absolute truths. Instead of letting a bleak experience
or thought kindle another episode of depression as predictably as a spark ignites
a fire in bone-dry kindling, instead of allowing their feeling to drag them down
into the pit of depression, patients would learn to respond with “Thoughts are not
facts” or “I can watch this thought come and go without having to respond to it.”
That, Teasdale suspected, might break the connection the brain made between
momentary unhappy thoughts and the memories, associations, and patterns of
thinking that inflate sadness into depression. It would be like putting a wall of
asbestos between the spark and the kindling. It would be, literally, rewiring the
brain.
The program the scientists developed, called mindfulness-based cognitive
therapy, consisted of eight weekly individual sessions, each lasting two hours.
Using the mindfulness training pioneered by Kabat-Zinn, the patients steered
their attention to one region of the body after another, trying to focus intently on
the sensations their hand, knee, foot was feeling at that moment. They then
learned to focus on their breathing. If their mind wandered, they were to
acknowledge it with “friendly awareness”—not frustration or anger—and focus
once again on the breath, which served as a magnet pulling them back to mindful
awareness of the moment. The patients also practiced at home, trying to notice
their thoughts impartially rather than reacting to them, and regarding their
feelings and thoughts (especially the bleak, despairing ones) as merely transient
mental events that happen to “come and go through the mind” and that are no
more significant than a butterfly floating into your field of vision. Most crucially,
they kept telling themselves that the thoughts did not reflect reality.
n 2004, Teasdale and his colleague Helen Ma replicated the findings,
showing again that mindfulness-based cognitive therapy reduced relapse. This
time, in a study of fifty-five patients, they found that for patients with three or
more episodes of major depression, the rate of relapse fell from 78 percent in the
treatment-as-usual group to 36 percent in the mindfulness-based cognitive
therapy group. “Mindfulness-based cognitive therapy,” they concluded, “is an
effective and efficient way to prevent relapse/recurrence in recovered depressed
patients with three or more previous episodes.” Or as Segal put it, “There are
modes of thinking which are more easily triggered the more they’re accessed.
Mindfulness works to keep you from triggering the depression network.” By
monitoring their own thoughts, patients who practice mindfulness are able to
keep the dysfunctional products of their mind from cascading into full-blown
depression.
You don’t have to believe in any spooky power of mind over brain to guess
what might be happening in these patients. Somehow, mental training was
altering brain circuits, in what we might call top-down plasticity, since it
originates in the brain’s cognitive processes. (“Bottom-up” plasticity is the kind
that arises when plain old sensory inputs resculpt the brain, as they do when
dyslexic children hear specially crafted sounds or lab monkeys carry out a
repetitive finger motion.) Brain-imaging technology would show precisely how mindfulness meditation was training the mind to alter brain circuitry.