As you read these lines, you are inducing neuroplasticity in your brain. In fact, when you experience anything new (and no two moments are ever quite the same), it triggers changes in the organization of neural networks in your brain. If the new experience is slight, these changes may be subtle; learning a new skill, which changes behavior, can effect far more dramatic neuroplastic changes. Where brain damage is involved, the neuroplastic changes can be breathtaking. In The Mind and the Brain: Neuroplasticity and the Power of Mental Force, neuropsychiatrist Jeffrey Schwartz, M.D., and veteran science journalist Sharon Begley argue that behavioral changes can induce a degree of neuroplasticity that may actually aid in the treatment of a condition like obsessive-compulsive disorder (OCD). Their case is embedded in a wonderful review of advances in understanding brain plasticity, a tour with side trips to the worlds of physics and philosophy.
Scientists have recently made much progress in mapping the functions of the human brain, speciﬁcally in ascertaining the knowledge, representations, and processes stored in neural networks in certain brain regions. Much remains to be done to create a detailed atlas of functions in the human cerebral cortex and subcortical structures, but there is consensus on some assumptions about how information is stored in the brain. The brain appears to be composed of modular neural networks, within which a deﬁned unit of knowledge is stored. Such a unit may be, for example, the edge detectors used in visual processing, which we now know are stored in the occipital cortex. Another unit may be high-level plan representations used to guide behavior; these are stored in the prefrontal cortex. Carrying out a task requires activating a set of these modules. Neuroplasticity is the capacity of these local neuronal networks and neural systems to change their topography and local architecture in response to new information (learning) or to brain damage or dysfunction.
After they review the relationship of mind to brain in a discussion of philosophy ranging from seventeenth-century French philosopher René Descartes to current philosophical musings by philosophers such as Patricia Churchland, Schwartz and Begley introduce the reader to the disease that Dr. Schwartz specializes in treating in his clinical practice: obsessive-compulsive disorder (OCD). The authors portray this disorder in vignettes of patients compelled to repeat behaviors such as hand washing or collecting items until their rooms are ﬁlled to the top. They also describe the standard treatment for OCD, review the dysfunctional neuroanatomy that scientists now think underlies it, and discuss some of the normal functions of brain systems implicated in OCD. Schwartz explains how he used this knowledge to shape a new behavioral therapy approach, which he calls the Four Step Method, to reduce the frequency and severity of OCD’s symptoms. By helping his patients relabel their obsessions and compulsions as false signals, reattribute them to pathological brain circuits, refocus on new ideas, and revalue their obsessions as having no inherent power, Schwartz has enabled patients to control their previously abnormal behaviors.
This convinced Schwartz that the brain can change fundamentally in response to new learning, and he plunged into the new science of brain plasticity.
What is fascinating is that these essentially mental strategies induce changes in behavior and in brain chemistry that can be seen using Positron Emission Tomography (PET). Those changes in turn lead to more normal brain functions. This convinced Schwartz that the brain can change fundamentally in response to new learning, and he plunged into the new science of brain plasticity.
DISTINGUISHING VARIETIES OF NEUROPLASTIC CHANGE
Scientists suggest that there are at least four types of neuroplastic change that operate at the level of modules in the brain. They label these homologous area adaptation, cross-modal reassignment, map change, and compensatory masquerade.
Homologous area adaptation appears to be most active during an early critical stage of human development if a particular brain region and its cognitive operation are damaged. To compensate, that operation (or set of operations) shifts to brain areas that do not include the affected module. Often, the brain shifts the function to a module in the matching, or homologous, region of the opposite brain hemisphere. Scientists hypothesize that the brain area accepting a new cognitive operation then becomes more crowded with cognitive representations. The crowding increases the likelihood of interference when two tasks must be performed that simultaneously involve the activation of adjacent modules in the cortex—one of them shifted from its former, natural location in the brain.
My colleagues and I recently examined an adolescent who as a child had sustained a severe right parietal lobe brain injury. Despite the severity and location of the injury, this boy had developed relatively normal visuospatial skills, but his arithmetic skills were impaired. We inferred that when he was injured, the left parietal lobe took over responsibility for some of the functions normally stored in the right. As a result, spatial processes had claimed the left parietal region before he began to learn arithmetic in school. This made it much more difﬁcult for him to learn the arithmetic because, in essence, little room for this knowledge remained in his crowded left parietal lobe. Functional magnetic resonance imaging (fMRI) of his brain while he was processing arithmetic showed that he did indeed activate parts of the left parietal lobe (among other regions), suggesting that part of the brain was still genetically programmed to store arithmetic facts, despite the fact that it was even more committed to spatial processing. The lesson of this complex readjustment is that plasticity may come at a cost to functions usually stored in a brain region that is forced to make room for new functions.
Some investigators suspect a relationship between the proportion of a functional region that is damaged and the amount of adaptation that can occur in the homologous region. They argue as follows. Neighboring or homologous cortical regions have both primary and secondary functions.
Usually, the secondary function is inhibited by connections from the neighboring or homologous region—whose secondary functional assignment, in turn, is to inhibit the primary function. The relationship sounds complex, but the upshot is that the homologous or neighboring region is able to give a primary role to an ordinarily secondary function only when the inhibitory input is removed. Given this logic, it would be more useful to have complete rather than incomplete damage to a region where a primary function was represented: a superior transfer of function to the secondary area could then occur.
. . . new neuronal development in adulthood may be possible. Schwartz and Begley leap on that ﬁnding to claim that the adult brain can change its neural representations in signiﬁcant ways.
Previous thinking was that the major reorganization of cortical networks to accompany learning was limited to childhood; new neurons were no longer added to the neural networks in adulthood. Recent work by Elizabeth Gould and her colleagues, however, suggests that new neuronal development in adulthood may be possible. Schwartz and Begley leap on that ﬁnding to claim that the adult brain can change its neural representations in signiﬁcant ways.
In chapters 4 and 5, they chronicle the odyssey of Ed Taub, a brain scientist famous for two reasons. First, his monkey studies led directly to the development of constraint therapy, a method to immobilize the good hand of a semi-paralyzed stroke patient in order to force the use of the semi-paralyzed hand, thereby facilitating brain plasticity in a way that improved the functions of the impaired hand. This therapeutic approach succeeded with stroke patients. Taub’s second claim to fame is as a victim of People for the Ethical Treatment of Animals (PETA), one of whose agents slipped into his lab in Silver Spring, Maryland, and ﬁlmed some of the constrained monkeys there, claiming that they were being tortured for no obvious scientiﬁc beneﬁt. I will not recount the details of Taub’s battle over the next two decades, but the book’s description of his experiments and his heroic battle for his good name is the best I have read on this topic. These two chapters alone make reading the book worthwhile.
CHANGING MODES, CHANGING MAPS
The second kind of neuroplasticity that Schwartz and Begley discuss, cross-modal reassignment, entails the introduction of new inputs into a brain region deprived of its main inputs. For example, PET studies of tactile discrimination ability show that subjects who became blind early in childhood, and are now being tested as adults, have input from touch (somatosensory input) that has been redirected into area V1 of the occipital cortex, the visual cortex. Sighted people show no evidence of any V1 activation during the same task. Scientists speculate that in a blind person the input from touch activates the representations stored in the visual cortex because those representations are in an abstract format. That is, the cognitive operations of the so-called visual cortex may be independent of which sense brought in the stimulus.
For example, discrimination of meaningful geometric forms (such as braille letters) could occur in what had been primary visual areas if the new modality of input (touch) required the same kind of geometric form discrimination ordinarily handled by the visual system. In this particular study, only tactile discrimination of raised braille dots that revealed geometric form (not simply passing the hand across a raised but formless ﬁeld of tactile stimuli) or language activated V1 in the blind. When sighted subjects were exposed to the same stimuli and tasks, not only was V1 not activated, but there was evidence of decreased activation—suggesting that attention devoted to brain regions processing the tactile features of stimuli ordinarily inhibit competitive brain systems such as the visual system. This inhibitory activity also suggests that even in normal adults there may be a pathway (usually used for inhibition) that has the potential to be transformed to help process information presented in a different mode, such as touch.
Schwartz and Begley point out, for example, that adults blind from birth use the visual cortex to “read” braille. These changes are not simply a matter of brain areas compensating for the lack of vision; they are actual changes in the functional assignment of a local brain region. Such dramatic changes in the primary sensory cortices were deemed impossible a few decades ago. The authors emphasize that the early work of scientists like Donald Hebb and Eric Kandel has led to dramatic breakthroughs in our understanding of cellular and neural network learning using connectivity patterns, pruning of neurons and their connections, and the identiﬁcation of molecular compounds that assist learning. Probably there are limits to this form of neuroplasticity. For example, color-processing cells in the occipital cortex are so specialized for visual input that they would be unlikely to accept input from other modalities.
Map change, the third major type of neuroplasticity, exempliﬁes the ﬂexibility of local brain regions, which are typically devoted to storing a particular kind of knowledge or cognitive operation. Research shows that the cortical maps devoted to a particular information-processing function may enlarge or shrink with frequent exposure to a stimulus—for example, skilled practice at playing the violin.
Using the groundbreaking brain research of Michael Merzenich (University of California, San Francisco), Jon Kaas (Vanderbilt University), and Randy Nudo (University of Kansas), Schwartz and Begley lay out the principles of map change and how neurophysiological and anatomical observations eventually led Merzenich and a colleague, Paula Tallal, at the State University of New Jersey, Rutgers, to propose a new therapy for training dyslexic children to read. While initial results from this training have been very positive, it is not clear whether it generalizes to all forms of dyslexia or can be replicated by other investigators using similar materials.
In two studies using different techniques, my colleagues and I demonstrated that implicit, or nonconscious, learning of a visuomotor sequence causes a sensorimotor-region map to expand in the early stages of learning. We repeatedly showed subjects a very long sequence of spatially distributed asterisks on a computer screen and directed them to press a key below the spot where each asterisk had appeared. For some time, subjects did not explicitly realize that they were being shown a repeated sequence. Even without that realization, however, their key presses became faster each time as a result of implicit learning. When learning becomes explicit, the size of the cortical map shrinks to baseline. The initial map enlargement, seen over the ﬁrst few minutes of practice or exposure, can persist in individuals who develop, or are trained, in a particular skill that they use regularly.
. . . how can we understand the observation that as a skill is practiced, some brain regions show increased activation but others may show decreasing activation?
The behavior correlates of map change are still unclear, but two implications are possible. One is that, with use, a cortical region devoted to a particular function or kind of memory can expand into other regions usually dedicated to another function or kind of memory—in essence, new neurons are drafted into the network. But then, how can we understand the observation that as a skill is practiced, some brain regions show increased activation but others may show decreasing activation? Another implication of map change follows from this. The area of the brain that processes a speciﬁc type of incoming information is called the memory unit of representation. When the type of information a person is experiencing is still undetermined, the entire regional brain network containing that memory and similar memories needs to be active. But once the exact memory unit of representation has been selected, the brain network can relax and expend less energy, resulting in observed decrease in overall activation.
WAYS TO COMPENSATE FOR IMPAIRMENT
Compensatory masquerade is the fourth and ﬁnal major form of neuroplasticity. This occurs when an established, intact cognitive process is used to perform a task that used to depend on a different cognitive process, now impaired. Compensatory masquerade can be an insidious process, which we can tease out only through careful study. For example, there may be many ways to navigate a route from your home to your ofﬁce. One way may depend most upon a sense of spatial coordinates, which are relatively implicit and processed rapidly. Another way may depend on verbal labeling of landmarks; this process is relatively explicit and is performed more slowly. A severe brain injury may affect both spatial and verbal processes but, typically, one will be much more affected than the other. The patient may then be able, over a short period, to learn to use the spared strategy.
Note that unless our neuropsychological study had evaluated both processes in some detail, we could have been misled into thinking that a more fundamental form of neuroplasticity had occurred—for example, homologous area adaptation.
A severe brain injury may affect both spatial and verbal processes but, typically, one will be much more affected than the other. The patient may then be able, over a short period, to learn to use the spared strategy.
Schwartz says that he used his understanding of map change and skill learning to fashion his Four Step plan to change the behavior of his OCD patients. But it may be that he also depended on his knowledge of compensatory masquerade.
TOWARD A GRAND THEORY OF BRAIN AND BEHAVIOR
Schwartz and Begley are sidetracked a bit when, in chapter 8, they ask how, in light of certain principles of physics, the mind is able to affect brain matter and function. They failed to convince me, at least, that the physics they introduced illuminated the relationship of mind and brain. Chapter 9 is also a diversion. Here the authors report on Schwartz’s interactions with various scientists as he prepared a paper for a special edition of a journal. The focus is on Benjamin Libet’s research on the “timing of a desire to move” and the observation that with the help of computer chips implanted in the brain, stroke patients can learn to “will” a cursor to move. The pertinent research ﬁndings in this and the following chapter could have been integrated into earlier chapters.
In the ﬁnal chapter, the authors emphasize the role of attention (from the narrow viewpoint of neuroplasticity) in enabling OCD patients to focus on new ways of learning that lead to a change in their behavior. An ancillary discussion of physics distracts the reader from their main points, which are nicely distilled in a set of cartoons that illustrate how Schwartz’s Four Step therapy works.
This book’s chapters on neuroplasticity and its sections on OCD are its highlights —and a great read. Later chapters are less compelling. That said, I want to emphasize that anyone seeking to learn about the amazing neuroplasticity of the human brain should read The Mind and the Brain. Readers interested in current conceptions of OCD and how it is treated will beneﬁt, too, from the book’s intimate discussion of that topic.
The authors give readers hope that scientists may be starting to learn enough about the ﬂexible brain to make theory-driven therapies around the corner.
In their epilogue, Schwartz and Begley urge closer integration of research and clinical practice, so that additional novel theories of the brain, plasticity, and volition can be developed and tested. In their view, only this will give us a grand theory of brain and behavior. The authors give readers hope that scientists may be starting to learn enough about the ﬂexible brain to make theory-driven therapies around the corner. The future certainly looks promising as we probe the limits of the brain’s plasticity and, as we do, shed new light on the ever-changing maps of the human cortex caught in the act of experiencing the world.
From The Mind and the Brain: Neuroplasticity and the Power of Mental Force, by Jeffrey Schwartz, M.D., and Sharon Begley. © 2002 Jeffrey Schwartz, M.D., and Sharon Begley. Reprinted with permission of Regan Books.
The discovery of links between structure and function gave rise to a view that became axiomatic, namely, that different parts of the brain are hard-wired for certain functions. Nowhere was this clearer than in every medical illustrator's favorite brain structure, the somatosensory cortex. A band that runs from about halfway along the top of the brain to just above each ear, the somatosensory cortex processes feelings picked up by peripheral nerves. Every surface of the body has a corresponding spot on this strip of cortical tissue, called a representation zone, as the Canadian Neurosurgeon Wilder Penfield found in his experiments in the 1940s and 1950s...
But it was an odd map. True, the part of the somatosensory cortex that registers sensation from the lips lies between the regions that register sensation from the forehead and the chin. So far, so good. The cortical representation of one finger is positioned relative to those of the other fingers, reflecting the arrangement of the finger on the hand. Also good. But beyond these basics, the cortical representations of different regions of the body are arranged in a way that makes you suspect nature has a bizarre sense of humor. The somatosensory representation of the hand, for instance, sits beside the face. The representation of the genitals lies below the feet. The reason for this arrangement remains lost in the mists of evolution. One intriguing hypothesis, however, is that it reflects the experience of the curled-up fetus: in utero, our arms are often bent so that our hands touch our cheeks, our legs curled up so that our feet touch our genitals. Perhaps months of simultaneous activation of these body parts, with the corresponding synchronous firing of cortical neurons, results in those cortical neurons “being fooled” into thinking that those body parts are contiguous. It would be another example of coincident input’s producing coherent structures during prenatal development.
The other oddity of the somatosensory cortex is easier to explain. The amount of cortical territory assigned to a given part of the body reflects not the size of that body part but its sensitivity. As a consequence, the somatosensory representation of the lips dwarfs the representation of the trunk or calves. The result is a hommunculus with dinner-plate lips. Our little man also has monstrous hands and fingers: the touch sensitive neurons on the tip of your index finger are fifteen times as dense as those on, for instance, your shin, so that hommunculus’s index finger receives more cortical real estate than a whole leg. The density of touch receptors on the tongue is also more than fifteen times as great as that of those on the back of your hand. Place the tip of your tongue under your front teeth and you'll feel the little ridges; but place the back of your hand against the teeth and all you’re likely to feel is a dull edge.
The motor cortex, which controls the voluntary actions of muscles moving every part of the body, is also laid out like a hommunculus... Despite a contradictory experiment here and an iconoclast there, for decades it had been axiomatic that there was no plasticity in the somatosensory or motor cortex of the adult brain...
This dogma had profound real-world consequences. It held that if the brain sustained injury through stroke or trauma to, say, a region responsible for moving the left arm, then other regions could not step up to the plate and pinch-hit. The function of the injured region would be lost forever. Observations that challenged this paradigm were conveniently explained away. Faced with the fact that stroke-related brain injury, for instance, is not always permanent—someone who suffers an infarct in the region of the right motor cortex responsible for moving the left leg might nevertheless regain some control of the left leg—the antiplasticity camp didn’t budge. No; it isn’t possible that another region of the motor cortex assumes control of the left leg in such cases, they argued. At best, lower and more primitive regions such as the basal ganglia, which encode grosser patterns of movement, might take over some of the functions of the injured regions. But recovery from brain injury, held this camp, in no way undermined the paradigm that neural circuitry in the adult is fixed (except for memory and learning through Hebbian processes). The possibility that the adult brain might have the power to adapt or change as the result of experience was dismissed.