Brain Lock: Free Yourself From Obsessive-Compulsive Behavior by Jeffrey M. Schwartz, Beverly Beyette

as they’ve been taught. We have found it extremely helpful to show patients these pictures as a graphic way of helping them understand “It’s not me—it’s my brain.” The knowledge of what’s causing their urges motivates them to work to change from pathological to healthful behavior and, in so doing, to actually change their brain chemistry.
    These positron emission tomography (PET) scans clearly demonstrate that the orbital cortex, the underside of the front of the brain, is hypermetabolic, or overheated, in people with OCD (see Figure 1 on Introduction). The colors represent different rates of brain glucose metabolism, or energy use, with red as the hottest and blue as the coolest. One thing these PET scan pictures can tell us is that the more automatic a behavior, the less energy the cortex may require to perform it. For now, keep in mind one key finding: The caudatenucleus, deep in the core of the brain, which appears to be the source of the primary problem in those with OCD, “cools down” in response to drug therapy, to drug therapy in combination with behavior therapy, and to behavior therapy alone. This is particularly true on the right side of the brain. We can now say we have scientifically demonstrated that by changing your behavior, you can change your brain. If you change your behavioral responses to OCD’s false messages, you will change the brain circuits that cause OCD, which will lead to an improvement in your symptoms.
    During the ten years of research that led to this truly ground-breaking finding, my colleagues and I at UCLA undertook a number of experiments that greatly enhanced our understanding of mind-brain interaction.
    Dr. John Mazziotta, who heads the Brain Mapping Division of the UCLA Neuropsychiatric Institute, designed an experiment in which the subjects were required to learn to make simple finger-to-thumb rotational movements of the hand, movements that mimicked those used in handwriting. But, because they’d been instructed to make these movements precisely and in a given order, the subjects actually had to think about doing so. What happened—as expected—was that the part of the cortex that controls hand and finger movements became very metabolically activated. In other words, its energy use increased, and it heated up. Next, the subjects were asked to sign their names repeatedly. Now, you know if you’ve ever signed forty traveler’s checks that you don’t think about it a lot after the fourth or fifth check. What we learned was that when the motor task is extremely familiar, the striatum seems to take over. The cortex expends only marginal energy, but the energy use in the striatum increases noticeably. It’s that smooth, automatic transmission in the striatum at work again.
    Think of concert pianists: When they first learn to play, they have to think about moving their fingers, which takes considerable energy in the finger-moving part of the cortex. But once they’ve achieved concert-hall status, they move their fingers automatically. Then, they think about the shades and tones of the music. The cortex doesn’t have to expend much energy thinking about moving fingers; the striatum does that. Thus, the advanced parts of the cortexare freed up to think about the fine points of the music. The experiment with our handwriting subjects gave us insights into this entire process.
    When Dr. Mazziotta repeated the signature-signing experiment with a group of subjects with Huntington’s disease, a genetically inherited disease that manifests itself at midlife with the loss of motor control, the results were different. The area of the brain that normally is stimulated by doing an unfamiliar task that requires thinking was stimulated by doing the familiar signature-signing task. Through the degenerative effects of their disease, these subjects’ caudate nucleus and putamen had become mal-functional, and parts of them were dead or dying. The subjects had to use a lot of energy