The Mind and the Brain (2 page)

My deep doubts that human actions can be explained away through materialist determinism simmered just below the surface throughout my years of medical school. But by the time I completed my psychiatric residency at Cedars-Sinai Medical Center in 1984, my research interests had converged on the question of the role of the brain in mental life. After two years conducting brain research under the mentorship of Floyd Bloom at the Salk Institute in La Jolla from 1980 to 1982—investigating a possible role for the endogenous opiate beta-endorphin in manic depression, as well as doing basic research on the functional neuroanatomy of changes in mood states—I was growing ever more curious about the mysterious connection between mental events and the activity of discrete brain structures. The timing was perfect: even then, that area of neuroscience, broadly known as functional neuroanatomy, was achieving gains few even dreamed of. Brain imaging techniques such as PET (and, later, functional magnetic resonance imaging, or fMRI) were, for the first time, allowing neuroscientists to observe the living, working human brain in action. Ordering a forefinger to lift, reading silently, matching verbs to nouns, cogitating on faces,
conjuring up a mental image of a childhood event, mentally manipulating blocks to solve the game Tetris—scans were mapping the parts of the brain responsible for each of these activities, and for many more.

But even as Congress declared the 1990s the Decade of the Brain, a nagging doubt plagued some neuroscientists. Although learning which regions of the brain become metabolically active during various tasks is crucial to any understanding of brain function, this mental cartography seemed ultimately unsatisfying. Being able to trace brain activity on an imaging scan is all well and good. But what does it
mean
to see that the front of the brain is underactive in people with schizophrenia? Or that there is a quieting of the frontal “executive attention network” when experienced practitioners of the ancient technique of
yoga nidra
attain meditative relaxation? Or even that a particular spot in the visual cortex becomes active when we see green? In other words, what kind of internal experience is generated by the neuronal activity captured on a brain scan? Even more important, how can we use scientific discoveries linking inner experience with brain function to effect constructive changes in everyday life? Soon after I joined the UCLA faculty in 1985, I realized that obsessive-compulsive disorder might offer a model for these very questions of mind and brain.

At the same time, I was regaining an interest in Buddhist philosophy that I had developed a decade earlier, when a poet friend (who later perished on that ill-fated KAL flight that ran into the wrong end of the cold war) became deeply involved in Buddhist meditation. As a premed philosophy major I always had a healthy dose of skepticism about what my poet friends were into, but I was nevertheless intrigued. The first Noble Truth, Dukkha—or, as it is generally translated, “Suffering”—had an immense intuitive sensibility to me. Life, I already felt, was not an easy undertaking. In addition, Buddhist philosophy’s emphasis on the critical importance of observing the Basic Characteristic of Anicca, or Impermanence, appealed to me. As an aspiring psychiatrist in self-directed training,
I was drawn to the practical aspect of Buddhist philosophy: the systematic development and application of a clear-minded observational power, known in the Buddhist lexicon as Mindfulness.

I had first pursued this new direction in earnest during my first year of medical school. I added two self-taught extracurricular courses to my required studies: introductory training in Yoga as expounded in the classic text
Light on Yoga
, by B. K. S. Iyengar, and regular reading of the
Archives of General Psychiatry
, which, of all the leading journals, seemed most focused on the newly developing field of neuropsychiatry (I had already decided that I would specialize in the brain-related aspects of psychiatry). During that first year I arranged to continue these pursuits by setting up a summer clerkship in neuropsychiatry research and enrolling, at the end of the summer, in an intensive retreat in the practice of Buddhist mindfulness meditation. When the second year of medical school began in September 1975, I knew I was setting off on what would become a lifelong quest, to develop and integrate these two fields.

At the core of Buddhist philosophy lies this concept of mindfulness, or mindful awareness: the capacity to observe one’s inner experience in what the ancient texts call a “fully aware and non-clinging” way. Perhaps the most lucid modern description of the process comes from the German monk Nyanaponika Thera (his name means “inclined toward knowledge,” and
thera
is a title roughly analogous to “teacher”). A major figure of twentieth-century Buddhist scholarship, he coined the term
Bare Attention
to explain to Westerners the type of mental activity required to attain mindful awareness. In his landmark book
The Heart of Buddhist Meditation
, Nyanaponika wrote, “Bare Attention is the clear and single-minded awareness of what actually happens
to
us and
in
us at the successive moments of perception. It is called ‘Bare’ because 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.” One Buddhist scholar captured the difference between mindfulness and the usual mode of mind this way: “You’re
walking in the woods and your attention is drawn to a beautiful tree or a flower. The usual human reaction is to set the mind working, ‘What a beautiful tree, I wonder how long it’s been here, I wonder how often people notice it, I should really write a poem.’…The way of mindfulness would be just to see the tree…as you gaze at the tree there is nothing between you and it.” There is full awareness without running commentary. You are just watching, observing all facts, both inner and outer, very closely.

The most noteworthy result of mindfulness, which requires directed willful effort, is the ability it affords those practicing it to observe their sensations and thoughts with the calm clarity of an external witness: through mindful awareness, you can stand outside your own mind as if you are watching what is happening to another rather than experiencing it yourself. In Buddhist philosophy, the ability to sustain Bare Attention over time is the heart of meditation. The meditator views his thoughts, feelings, and expectations much as a scientist views experimental data—that is, as natural phenomena to be noted, investigated, reflected on, and learned from. Viewing one’s own inner experience as data allows the meditator to become, in essence, his own experimental subject. (This kind of directed mental activity, as it happens, was critical to the psychological and philosophical work of William James, though as far as we know he had no more than a passing acquaintance with Buddhist meditation.)

Through the centuries, the idea of mindfulness has appeared, under various names, in other branches of philosophy. Adam Smith, one of the leading philosophers of the eighteenth-century Scottish Enlightenment, developed the idea of “the impartial and well-informed spectator.” This is “the man within,” Smith wrote in 1759 in
The Theory of Moral Sentiments
, an observing power we all have access to, which allows us to observe our internal feelings as if from without. This distancing allows us to witness our actions, thoughts, and emotions not as an involved participant but as a disinterested observer. In Smith’s words:

It was in this way, Smith concluded, that “we suppose ourselves the spectators of our own behaviour.” The change of perspective accomplished by the impartial spectator is far from easy, however: Smith clearly recognized the “fatiguing exertions” it required.

For years I had wondered what psychiatric ailment might best lend itself to a study of the effects of mindfulness on brain function. So within a few days of beginning to study the literature on obsessive-compulsive disorder at UCLA, I suspected that the disease might offer an entrée into some of the most profound questions of mind and brain, and an ideal model in which to examine the interface between the two. And soon after I began working intensively with people who had the condition and looked at the PET data being collected on them, I realized I’d stumbled onto a neuropsychiatrist’s gold mine.

The obsessions that besiege the patient seemed quite clearly to be caused by pathological, mechanical brain processes—mechanical in the sense that we can, with reasonable confidence, trace their origins and the brain pathways involved in their transmission. OCD’s clear and discrete presentation of symptoms, and reasonably well-understood pathophysiology, suggested that the brain side of the equation could, with enough effort, be nailed down.

As for the mind side, although the cardinal symptom of obsessive-compulsive disorder is the persistent, exhausting intru
sion of an unwanted thought and an unwanted urge to act on that thought, the disease is also marked by something else: what is known as an ego-dystonic character. When someone with the disease experiences a typical OCD thought, some part of his mind knows quite clearly that his hands are not really dirty, for instance, or that the door is not really unlocked (especially since he has gone back and checked it four times already). Some part of his mind (even if, in serious cases, it is only a small part) is standing outside and apart from the OCD symptoms, observing and reflecting insightfully on their sheer bizarreness. The disease’s intrinsic pathology is, in effect, replicating an aspect of meditation, affording the patient an impartial, detached perspective on his own thoughts. As far as I knew, the impartial spectator in the mind of an OCD patient—overwhelmed by the biochemical imbalances in the brain that the disease causes—remained only that, a mere spectator and not an actor, noting the symptoms that were laying siege to the patient’s mind but powerless to intercede. The insistent thoughts and images of OCD, after all, are experienced passively: the patient’s volition plays no role in their appearance.

But perhaps, I thought, the impartial spectator needn’t remain a bystander. Perhaps it would be possible to use mindfulness training to empower the impartial spectator to become more than merely an effete observer. Maybe, just maybe, patients could learn a practical, self-directed approach to treatment that would give them the power to strengthen and utilize the healthy parts of their brain in order to resist their compulsions and quiet the anxieties and fears caused by their obsessions. And then, despite the painful intrusions into consciousness caused by the faulty brain mechanisms, the patient could exercise the power to make a choice about whether the next idea the brain attends to will be “I am going to work in the garden now,” rather than “I am going to wash my hands again.” Although the passive stream of the contents of consciousness may well be determined by brain mechanism, the mental and emotional
response to that stream may not be. The OCD patient, in other words, may have the capacity to focus attention in a way that is not fixed or predestined by the (pathological) brain state.

To my way of thinking, the Buddhist concept of mindfulness offered a guide to what would be a radically new approach to OCD treatment. In what came to be called the Four Steps regimen of cognitive-behavioral therapy for OCD, patients gain insight into the true nature and origin of the bothersome OCD thoughts and urges. They
Relabel
their obsessions and compulsions as false signals, symptoms of a disease. They
Reattribute
those thoughts and urges to pathological brain circuitry (“This thought reflects a malfunction of my brain, not a real need to wash my hands yet again”). They
Refocus
, turning their attention away from the pathological thoughts and urges onto a constructive behavior. And, finally, they
Revalue
the OCD obsessions and compulsions, realizing that they have no intrinsic value, and no inherent power. If patients could systematically learn to reassess the significance of their OCD feelings and respond differently to them through sustained mindful awareness, I reasoned, they might, over time, substantially change the activity of the brain regions that underlie OCD. Their mind, that is, might change their brain.

At first, whenever I tried to discuss these ideas with colleagues, the reaction ranged from mere amusement to frank annoyance. Like all of modern science, the field of psychiatry, especially in its current biological incarnation, has become smitten with
materialist reductionism
, the idea that all phenomena can be explained by the interaction and movements of material particles. As a result, to suggest that anything other than brain mechanisms in and of themselves constitute the causal dynamics of a mental phenomenon is to risk being dismissed out of hand. But there was another problem. For decades, a key tenet of neuroscience held that although the organization and wiring of the infant brain are molded by its environment, the functional organization and structure of the adult brain are immutable. Experiments in rats, monkeys, ferrets, and
people showing that the adult brain can indeed change, and change in profound ways, still lay in the future. Since I was arguing that the mind can change the brain, persuading the scientific community that I was right required that scientists accept an even more basic fact: that the adult brain can change at all.

The chapters that follow explore the new vistas in neuroscience opened by the original UCLA work on obsessive-compulsive disorder. We’ll survey both historical and current approaches to the mind-brain enigma surrounding how mental phenomena emerge from three pounds of grayish, gelatinous tissue encased in the human skull. We’ll also explore the OCD research in further detail. My discovery that mental action can alter the brain chemistry of an OCD patient occurred when neuroscientists were reopening a question that most had thought long settled: can the adult brain change in ways that are significant for its function? Does it, in other words, display an attribute that researchers had thought lost with the final years of childhood—neuroplasticity?
Neuroplasticity
refers to the ability of neurons to forge new connections, to blaze new paths through the cortex, even to assume new roles. In shorthand, neuroplasticity means rewiring of the brain. After chronicling the ongoing discoveries of neuroplasticity in the brain of the developing child—from the first tentative neuronal synapses as they form in fetal life to the wiring of the visual, auditory, and somatosensory systems and higher cortical functions such as cognition and emotions—we will review the notorious tale of the Silver Spring monkeys. The mistreatment of these seventeen macaques at a behavioral psychology institute in the 1970s led to their seizure by federal agents, conviction of the lead researcher on six counts of animal cruelty, and, more than any other single event, the rise of the animal rights movement in the United States. But experiments on the Silver Spring monkeys also demonstrated, for the first time, the massive plasticity of the adult primate brain.