The Broken Brain: The Biological Revolution in Psychiatry
Brain, Mind, and Behavior
In 1895 Freud wrote his last work on the physiology of the nervous system. For the rest of his life he paid little attention to developments in neurobiology, a neglect characteristic of most modern therapists and psychologists. But recent work in the neurosciences has begun to challenge the separation of psychology from neurobiology. Mentally crippling diseases such as depression and schizophrenia (the latter considered by Freud beyond the reach of psychoanalysis) can now, in varying degrees, be relieved or controlled. Their physiological mechanisms, as well as those of other diseases, are beginning to be discerned. And the neuroanatomy and chemistry of moods and emotions are no longer complete mysteries. The observations of psychology and psychoanalysis are becoming part of a larger body of knowledge whose central questions concern the mechanisms and functions of the human brain.
But how “revolutionary” are the new discoveries in the neurosciences? Nancy Andreasen’s new book The Broken Brain gives an enthusiastic report on what she calls “the biological revolution in psychiatry.” The PBS television series The Brain and the books written to accompany it, Brain, Mind, and Behavior (an undergraduate textbook) and The Brain, more cautiously suggest that the remarkable findings of the past two decades may unravel the mysteries of the brain. Ornstein and Thompson, in The Amazing Brain, give a clear account of recent research without making undue claims about its consequences.
These works revise in some detail the popularizations of ten years ago. They retain the late-nineteenth-century view that the brain can be understood through studies of the local functioning of its separate parts and combine it with recent discoveries of the details of brain chemistry. Our ways of understanding the brain, however, have changed dramatically in the past decade and much of the excitement of that change has been missed by the authors and scriptwriters of these books and television programs.
Localization of function was the principal issue at the Seventh International Medical Congress, meeting in London in 1881. At that meeting, Frederick Goltz, a forty-seven-year-old professor of physiology at the University of Strasbourg, opened a suitcase and removed the damaged head of a dog. The dog, he explained, had survived four major operations on its brain before it had been killed, and its mental and physical functions had been badly impaired. But not a muscle of its body was paralyzed, not a spot on its hide was robbed of sensation. It was neither blind, nor had it lost the sense of smell.
Goltz’s purpose in demonstrating this damaged dog was to prove that brain function was not localized. Dogs might become imbeciles if they lost most of their brains, but they could still run, jump, hear, and smell.
David Ferrier, then a thirty-eight-year-old London physician who had been born near Aberdeen, had performed a series of experiments on monkeys at the West Riding Lunatic Asylum in 1873 and had come to a very different conclusion. At the same congress of 1881, Ferrier showed two monkeys from which he had carefully removed specific parts of the brain. One monkey had a paralysis of the right arm and leg. Ferrier’s other monkey was deaf, but otherwise quite “normal.” Ferrier concluded that different anatomical areas of the brain were associated with different functions.
A committee of experts then examined the brains of Ferrier’s monkeys and Goltz’s dog. The experts supported Ferrier’s claim, noting that the brain of Goltz’s dog showed considerably less damage than Goltz had stated. Localization of brain function had won the day at the Seventh International Medical Congress, and, except for a few dissenters, remained the guiding principle of brain research for more than fifty years.
At the same time scientists were trying to understand the workings of the nerve cells that made up all the brain’s functional units. Our understanding of brain chemistry began when they recognized that there were tiny spaces between nerve cells, gaps that the English neurophysiologist Charles Scott Sherrington in 1897 called synapses. Anatomists had long since identified pathways through which sensations pass back and forth between the nerve cells in the body and those in the brain. But how information passed from one nerve cell to another through synapses remained unknown until the 1920s when Otto Loewi discovered that when nerve cells are stimulated they release a chemical into the synaptic gap. Although some electrical transmission also takes place, chemical transmission seems far more important.
We now know a considerable amount about the chemical transmitters and the mechanisms by which they are released. When a nerve impulse reaches a synapse, tiny packets containing about a thousand neurotransmitter molecules release their contents into the synaptic gap. The molecules diffuse across to the connecting cell where they lock into molecules on the cell’s surface known as receptors. (See illustration on facing page.) In some cases, this results in the opening of channels into the nerve cell that permit the passage of electrically charged atoms (ions) that are constantly present in the fluid in and around the nerve cells. If enough neurotransmitters are released and if enough channels are opened, the recipient cell will in turn become stimulated, or inhibited. Until the 1950s only three neurotransmitters were known1 and nobody suspected that there were others yet to be discovered.
Then in 1949 Henri Laborit, a Paris surgeon, began looking for a chemical that would prevent surgical shock, the sudden and often fatal lowering of blood pressure during operations. Laborit hit on the idea of trying chemicals, called antihistamines, that are commonly used against allergic reactions. He not only succeeded in preventing shock, but he also noticed that the drugs had a dramatic calming effect on his patients both before and after the surgery. He suggested that they be tested for more general psychiatric use. His idea proved justified: for the first time in history a humane, relatively effective treatment had been found for the devastating mental disease of schizophrenia. By the late 1950s chlorpromazine and several other antipsychotic drugs were widely used throughout Europe and America. Schizophrenics, formerly put in straitjackets and confined to padded cells in mental institutions, were able to carry on relatively normal lives. Psychiatry had undergone a small revolution.
Treatment of psychiatric patients with antischizophrenic drugs frequently caused symptoms similar to those of Parkinson’s disease: tremors, a shuffling gait, difficulty in starting and stopping movements. During the late 1950s neurologists showed that Parkinson’s disease itself occurred in patients whose brains had low levels of a newly discovered neurotransmitter, dopamine. The neurologists subsequently suggested that schizophrenia was caused in part by an excess of dopamine or of dopamine receptors; and in fact the antischizophrenic drugs were eventually shown to be blocking the dopamine receptors in the brain. During the 1960s, L-dopa, a drug that is converted to dopamine in the brain, was found to relieve the symptoms of Parkinson’s disease, and it is still the most effective treatment. As with the antischizophrenic drugs, however, it remains a partial treatment. Observing a Parkinson’s patient in a recent TV program by Jonathan Miller, a critic wrote, “L-dopa…smooths away with sinister ease the fearsome combination of rigidity and tremor. What replaces it, though, is a constant snaking movement throughout the body, which the patient cannot control. Which would you prefer: partly controllable tremor or uncontrollable sinuosity?”2
Depression is also connected with neurotransmitter imbalances, and therapies aimed at restoring the balances of neurotransmitters such as norepinephrine and serotonin have proved effective in relieving depressive symptoms. But once again, they often provide only a partial cure. This is not surprising since our knowledge of the underlying chemical imbalances in depression is incomplete, and today’s therapies can correct only some of those that are known.
That schizophrenia and other forms of mental illness result from chemical imbalances in the brain is clearly suggested, if not openly stated, in most recent writing about these diseases. Drug companies now spend enormous sums of money on research on drugs that can affect behavior. Of the works under review, Andreasen’s book makes the strongest claim for this position: “A large amount of evidence has been amassed suggesting that mental illness is caused by biochemical abnormalities, neuroendocrine abnormalities, structural brain abnormalities, and genetic abnormalities.”3
As neuroscientists concentrated their attention on the neurotransmitters, in the hope of unraveling the mysteries of the mind, they found more neurotransmitters than had ever been suspected. The original list of the 1950s has now grown to more than fifty, among them an important new group of chemicals called neuropeptides (peptides are strings of amino acids). Some of these were already known, but as hormones, released by nerve and other cells directly into the bloodstream, with specific effects on cells in organs such as the heart, the intestine, or the uterus. Research during the 1970s showed that neuropeptides also serve as neurotransmitters in the brain. While it was once claimed that each nerve cell releases only one kind of neurotransmitter, it is now known that this is not true. Many nerve cells apparently release neuropeptides as well as the “classical” transmitters. There may still be dozens if not hundreds of neuropeptides yet to be discovered and their function in the brain is far from certain. However, there is good evidence that some are associated, in some way, with a variety of emotional states and the perceptions of pleasure and pain.
This began to become clear during the early 1970s, when much excitement was produced by the discovery that the drug morphine, which is derived from opium, locks into specific receptors on nerve cells in particular areas of the brain. Scientists therefore suspected that morphine imitates the action of an as yet unknown neurotransmitter. By 1975 the brain’s “natural opiates”—the enkephalins (meaning “in the head”) and the endorphins (a morphine-like chemical in the brain)—were discovered. These are peptides that serve as neurotransmitters and that modulate painful stimuli. Since they are more powerful painkillers than morphine (and more addictive), their release within the brain may be the mechanism underlying the effectiveness of acupuncture and other unconventional treatments for chronic pain. Recently, it has been found that the endorphins and enkephalins also modulate our emotional reactions. As the authors of Brain, Mind, and Behavior note, people who suffer from claustrophobia, and therefore develop severe anxiety in elevators and other enclosed spaces, probably have some kind of endorphin malfunction. The same book summarizes some fascinating studies suggesting that in order for us to experience an emotion, both a physiological disturbance, such as a rapidly palpitating heart, and a psychological evaluation of that disturbance, such as fear, are necessary.
Endorphins may link these two mechanisms. People with spinal injuries (which may affect the release of endorphins in the brain), and who consequently have little sensation from their bodies, have claimed that their ability to “feel” emotions such as joy or grief diminished since their injuries. The release of endorphins within the brain may also provide the key to understanding “the ‘high’ experienced by most serious joggers,” we are told in The Amazing Brain.
These and related findings have suggested to many, including the authors of the works under review, that our moods, emotions, and other psychological states will ultimately have neurophysiological explanations. Such explanations may one day be possible, but these books and TV programs unwittingly also show how much there is to be done if the relations between human psychology and neurobiology are to be clarified.
According to The Amazing Brain, “The chemical molecules are indeed the messengers, but they are not the messages. The immensely complex and highly structured circuitry of the brain is the ultimate repository of the mind.” But the book then ignores, as do the other works under review, the ways that recent attempts to analyze the workings of this circuitry—the study of information processing and artificial intelligence—can provide important links between neurochemistry and psychology. Computers, of course, are not biological systems, but they do give us important clues about how the brain may sort out and use information, including the information that is conveyed within the nervous system.
For example, the process by which our brains transform visual stimuli so that we see in three dimensions follows relatively fixed procedures—a kind of information processing—which have been identified through the work of David Marr, among others. The two-dimensional images that we register on our retinas, which resemble a collection of dots of various levels of grayness on a television screen, are initially transformed into an unconscious “image” that marks the variations in light intensity in the retina, which is called a primal sketch. The primal sketch undergoes a series of further unconscious transformations until we become aware of the three-dimensional image. At each stage of the processing an intermediary “image,” or symbol, is created by the activity of the neurotransmitters and this internal image is further transformed into the scene of which we become conscious. The new understanding of vision suggests how a series of discrete functions is performed as part of an interconnected process. 4
We can find the distant antecedents of this approach in the nineteenth-century studies of Paul Broca and Karl Wernicke on the localization of language function. In 1861 Broca announced to the Société d’Anthropologie in Paris his findings that aphasia, or difficulty in speaking, reading, and writing, resulted from damage in a well-defined area in the left hemisphere of the brain. Broca’s work led to an intense interest in aphasia throughout Europe and it became widely accepted that he had discovered “the” language center in the brain. In 1874 Karl Wernicke published his discovery of another area in the left hemisphere that also controlled speech. Wernicke noted that patients with damage in the area discovered by Broca had a peculiar telegraphic speech pattern (“I New York come”) but had no difficulty understanding those who addressed them. Patients with damage to the part of the brain discovered by Wernicke, however, had grammatically correct, but “roundabout,” speech (“Before I was here I was there, and then they came and I was here”).
Unlike Broca’s patients, Wernicke’s patients had much difficulty in comprehending speech. Wernicke correctly suggested that the areas he discovered are connected by a bundle of nerve fibers and that each one controls a different aspect of language function. During the following years such studies connecting parts of the brain with specific functions became very popular in Europe. Scientists tried to determine which areas of the brain controlled particular movements or sensations, and seemed content to think that this would “explain” brain function. They ignored Wernicke’s point that studies of localization are not so simple: they provide important clues to how a given function, such as language, is broken into various subtasks.
In 1891 Freud made a similar argument in his book on aphasia; he thought that anatomy, by itself, failed to explain the varieties of functional breakdowns that are observed in patients with speech difficulties (particularly in the ability to express emotion in language). Freud’s stress on function as opposed to anatomy brought Wernicke’s argument close to the contemporary view of the brain as a complicated network of information-processing circuits. The works under review describe the shift from anatomy to neurochemistry, but fail to see how information processing can provide a deeper perspective for understanding the tasks that the neurotransmitters perform.5
Much of our limited knowledge of these tasks derives, as in the past, from research that connects the breakdown of mental function to anatomy. During the late 1940s the Norwegian neurologist Monrad-Krohn observed a woman who had been wounded by shrapnel and had suffered damage to Broca’s area, in the left hemisphere. Though she fully recovered from her wounds her speech was marred by what sounded like a German accent when she spoke her native Norwegian, causing considerable suspicion among her countrymen during the war.6
This and much other subsequent work have given us important clues about how the brain processes language. We can see that it divides the task of speaking a language into various subunits—in this case a damaged subunit can affect accent while other subunits function as before. Knowing what these individual subtasks are may tell us not only about the nature of the brain damage in a particular disease, but how and why we manifest the normal psychological characteristics that we do. In fact, many psychological observations can now be explained in part by neurophysiological mechanisms. The phenomenon of repression of ideas, memories, and emotions provides a striking example. Freud argued that the history of one’s relations with one’s family and intimate friends determined what was and what was not repressed. Inappropriate emotional reactions, or the failure to manifest any emotional reaction at all, were to be explained by psychological mechanisms.
Yet, whatever the truth of Freud’s theory, physiological mechanisms can also help to explain some cases of repression and the release of repressed ideas and emotions. The neurologist Oliver Sacks, for example, recently described to me the case of a man who committed a murder after taking the drug PCP (“angel dust”) and had no memory of his actions. Following a traffic accident that caused frontal lobe damage, the patient “had an overwhelming resurgence, or ‘de-repression,’ of the memory,” suggesting that frontal lobe integrity is necessary for repression.
Some cases of brain damage appear to mimic repression. A schoolteacher with right hemisphere brain damage complained of her inability to control her classes because “I cannot put the emotion into my voice or actions, and the pupils do not know that I mean business.” She is perfectly aware of her incapacity and has every apparent desire to express feelings that she fully understands. In this case the patient’s awareness and understanding of her feelings suggest that she is prevented from expressing them by a mechanism that may be very different from that of Sacks’s patient.
Just as different aspects of language seem to be processed in different parts of the brain, then, emotions are also broken into various subunits. What might appear to be gradations of the same emotion may, from the point of view of brain processing, be very different emotions. Patients unable to express moderate sadness because of damage to the right hemisphere have no difficulty in letting loose a torrent of tears, since extreme emotional displays are under the control of an area in the brain called the limbic system.
Such findings make it difficult—more difficult than most exclusively psychological or physiological approaches would suggest—to decide when the root cause is physiological and when it can be analyzed as psychological, or, indeed, when there might be a combination of causes. But if we understand the purposes of the physiological mechanisms and the subtasks they perform (which, of course, requires more than a descriptive analysis of those mechanisms), we might begin to understand better both normal and abnormal patterns of behavior.
Take, for example, the problem of schizophrenia, which dominates one of the programs in the PBS series The Brain and provides the basis for the discussion of the disease in Restak’s The Brain and in Brain, Mind, and Behavior. The PBS program and the two books derived from it all present the following dialogue.
Doctor: How are you doing?
Gerry: I’m not doing so hot. I think and feel as though people have called me here to electrocute me, judge me, put me in jail…or kill me because of some sins I’ve been in.
Doctor: It must be very frightening for you, if it feels like you’re about to be killed?
Gerry: …It’s so scary, I could tell you that picture’s got a headache….
Doctor: Schizophrenia. What does that mean? Different people use the word different ways.
Gerry: Schizophrenia is when you…hear voices inside your head.
Such auditory hallucinations and paranoia, characteristic of some forms of schizophrenia, can be relatively well controlled by antischizophrenic drugs. As we have seen, and as all the books under review emphasize, these drugs block the receptors for the neurotransmitter dopamine. Do such symptoms suggest any specific mechanism in the brain in which dopamine might be important? And could this explain how chemical changes in the brain can have profound psychological consequences?
Recent research, mentioned only in Brain, Mind, and Behavior, suggests that it might. In 1980 the English psychiatrist T.J. Crow distinguished between what he called Type I and Type II schizophrenia. Type I symptoms include auditory hallucinations and paranoia. Type II schizophrenia is characterized by a general intellectual deterioration and cannot so far be treated with drugs. (CAT scans show brain atrophy in Type II but not in Type I.)
Type I schizophrenics, Crow notes, are confused about the sources of information. They believe that the voices they hear are other people ordering them about. If I curse myself for not having told my boss to go to hell, my outward behavior will not be much altered by this private fantasy. I may, from time to time, appear preoccupied. But if I hear a voice that sounds as if it is coming from an invisible person standing nearby, that voice will carry an authority and conviction that my private fantasy lacks. Paranoia and auditory hallucinations can be interpreted as confusions about the sources of information. What seems to have broken down here is a sorting mechanism that tells the brain where information is coming from.
Misjudging the source of information does not necessarily depend on content or meaning. The post office sorts mail according to its zip code, disregarding the contents of the envelope. The brain’s mechanisms for sorting information are unknown, but to some extent they too must be independent of meaning. That these mechanisms can break down because of a chemical imbalance is therefore not very surprising. Antischizophrenic drugs may be correcting the balance of neurotransmitters in a way that allows the source of information to be accurately determined. Yet if sorting helps to explain one aspect of Type I schizophrenia, it probably will not explain the content of the auditory hallucinations any more than postal sorting classifies the contents of letters.
In the case of depression, the psychology of the disease may also give us important clues to its chemistry. In his 1914 essay “Mourning and Melancholia,” Freud suggested that there were many similarities between the grief we feel when a loved one dies and cases of melancholic depression. The parallel is interesting, I think, because it suggests that loss (of someone) may be central to the psychology of depression. This may not sound very surprising. What is important is how one reacts to loss. A curious clue comes from patterns found in the animal world. Konrad Lorenz noticed a long time ago that among ducks and geese the death of one member of a pair leads to a search (with abnormal behavioral manifestations) for the missing partner that can go on for several days. Some of the symptoms of depression may derive from search procedures within the brain. Such procedures are well known to computer scientists, and the brain performs analogous operations.
Failure to solve problems—for example a crossword puzzle—can lead to a state of trivial misery that we may call a “minidepression.” The solution found, the “minidepression” disappears. Depression during a time of loss (of a job, friends, prestige, etc.) may be a period during which the brain is looking (searching) for a solution to problems that cannot be solved, at least in a relatively brief period of time. Eventually, we may find a way of accepting a substitute for the person we have lost, but this may require a considerable reevaluation of what we may desire in our personal relations with others. Whether by conscious effort or unconscious mechanisms, the information stored in our brains may have to be reorganized. We may eventually piece together a solution to our being unemployed or our friends’ misrepresentation of our worth. A loss of self-esteem, for example, may motivate us to “outdo” a former friend and to change our mental image of him.
The resolution of such problems may require a reorganization of our patterns of thought and even, perhaps, values. The period of rearrangement—which may involve trial and error—is one in which we may have the hopeless feeling associated with depression. The search procedures may be arbitrary. There may be a great many different paths to a solution, and no one solution may necessarily be “right.”
One of the less discussed aspects of the chemistry of depression lends considerable weight, I believe, to such a view of depression as related to the mechanisms for searching out and sorting information. The amount of the neurotransmitter acetylcholine released in the brain becomes elevated during states of depression. The same transmitter is also believed to be important during normal memory searches. (Indeed, it is thought that acetylcholine can help us improve our memories.) High levels of this neurotransmitter apparently cause the abnormally early onset of dreams when we sleep—one of the characteristic features of depression and a cause of insomnia, since the normal sleep-dream cycle is disrupted. (In fact, the association between dreaming and acetylcholine suggests that dreaming too involves some kind of memory search procedure.) The “pain” of depression may come, in part, from the slowness of the search procedures and their apparent futility.7
One legitimate complaint against the chemical view of the mind is that we often “know” the cause is psychological, not chemical. In the model I have outlined the psychological “causes” remain. They set off search procedures that, when they go on too long, or are unresolved for other reasons, give rise to the disease.
Jonathan Miller’s fascinating TV show on Parkinson’s disease for the BBC provided some clues suggesting that search procedures are important for understanding Parkinson’s disease as well. When he is not using L-dopa, the patient, Ivan, has great difficulty initiating any movements, or stopping them once they have begun. But if he performs certain ritualistic acts (such as swinging a golf club), or concentrates on an object (such as a car key) he can then often perform the desired act. Ivan himself notes that he can never do more than one thing at a time.
This suggests that access to those parts of his memory that control or initiate the desired movements is blocked when he tries to retrieve the information directly. Concentration on objects that are not connected with the desired action apparently allows indirect access to the information required to carry out these movements. This is not an uncommon phenomenon—we are often unable to recall something no matter how much we concentrate on it, yet it suddenly springs to mind when making an unrelated observation. Part of the breakdown in Parkinson’s disease may be in the brain’s system for retrieving the memory of motor acts in the brain. Studies of the disease may give us important hints of how that system works.8
If understanding such subtasks, or subunits, of brain function can help us to understand symptoms in a given disease, we still know little about how the neurotransmitters actually perform these tasks. Here analogies with the recent discovery of the function of DNA can be illuminating. Scientists looked for the genetic code in DNA because they had already established that genetic information had to be translated into proteins, which are strings of amino acids and serve important structural, metabolic, and hormonal functions in living things. They knew the functional role of DNA was one of coding. If they had believed that the shape of the DNA molecule determined the shape of the embryo (similar to the preformationist beliefs in the eighteenth century) they would not have looked for any codes. Biotechnology would still be unknown. The real breakthrough in brain research will come when we have learned how connections are established within the brain, what kinds of information the neurotransmitters represent at the synaptic junctions, and how that information is processed. This may occur in ways that are quite different from the coding patterns of DNA.
Only when we understand all this will we understand why variations in the levels of neurotransmitters produce different behavioral consequences. Both the information being processed and the tasks being performed, however, will often be unintelligible if psychological observations are not taken into account. If we ignore the insights psychology can provide into brain functions, we will never understand what brain chemistry is all about.
Unfortunately, the works under review are a compendium of the confusions that result when this fundamental requirement is ignored. Brain, Mind, and Behavior, for example, makes little apology for ignoring psychology:
The view taken in this book is that the biological science of the brain can give us a better and deeper understanding of the nature and causes of mental illness than any other approach available now. Everything the brain does is becoming explainable in terms of specific nerve cells, their neurotransmitters, and their neurotransmitters, and their responsive cells. Given this bias, we cannot examine abnormal psychology or psychiatry comprehensively…. Instead, we shall look at these biological discoveries that might explain disorders of thinking and behaving.
One problem with this approach is that identical brain states may correspond to very different states of mind and body in the same person. As Restak notes, for example, actors show no change in basic brain patterns (revealed in measurements of the brain’s electrical activity) when they play different roles. (Patients with a “multiple personality,” by contrast, show marked changes as they go from one “personality” to another.) Andreasen, for her part, makes the quite misleading claim that
we need not look to theoretical constructs of the “mind” or to influences from the external environment in order to understand how people feel, why they behave as they do, or what becomes disturbed when people develop mental illness. Instead, we can look directly to the brain and try to understand both normal behavior and mental illness in terms of how the brain works and how the brain breaks down.
To the extent that mental disease concerns what other people and the world outside mean to the patient, however, analysis of neurochemistry and circuits may miss the most important clues to the disease. And the effectiveness of any drug therapy will be limited as well. Just as we cannot know the role an actor is playing by studying basic electrical patterns in his brain, no analysis of the circuits of a computer can tell us whether the computer is playing chess or predicting the whether. In one case a particular state of the machine might mean “queen takes knight,” whereas in a second case it could mean “cold front moves over New York.”
That the discovery of the neurotransmitters has increased control of some of the more devastating symptoms of mental diseases is a major advance, but of a limited kind. It provides no reasons to confuse therapy with understanding, or to exaggerate its benefits, as Andreasen often tends to do. Giving pills may be better than tying people up in tranquilizing chairs, but we should have no illusions that we really know what we are doing when we use many of the therapies administered today. Andreasen complains that electroshock therapy has had a bad press because of the way it is dramatized in One Flew Over the Cuckoo’s Nest, and she endorses its use. She seems unaware that we are still uncertain about what permanent damage it may cause.9 Electroshock therapy is a good example of a desperate measure whose success we cannot even begin to explain. The nearly total ignorance on the part of psychiatrists of how this therapy works is hardly reassuring, and this is probably the reason it is widely distrusted.10
One day a better understanding of the relationship between psychology and the brain may be possible; but just how radically our views may have to change is hinted at in the recent research of Fernando Nottebohm at Rockefeller University. This work appears to challenge a long-held belief that no new nerve cells are formed after birth in the brains of higher animals, including human beings. Our brains, according to the commonly held view, lose nerve cells at the rate of some ten thousand a day after puberty, and we have no way of replacing them.
Nottebohm’s work suggests this may not be so. During the past twenty years, he and his coworkers have studied the relation between brain structure and the production of songs in canaries. They found that the part of the brain that controls song production undergoes seasonal variations in size, and that these variations were induced by varying levels of sex hormones. Canaries apparently relearn their songs from year to year. Parts of their brains disappear and are rebuilt. Nor was this peculiar to the part of the brain that produces songs.11 Recently Nottebohm found new neurons appearing in other regions of the canaries’ brains as well. And he speculates that this might be true of humans too—a conclusion that is “so contrary to anything we anticipated that we are not yet prepared to sound intelligent when we talk about it.”12
Ornstein and Thompson’s The Amazing Brain is an excellent introductory book. It avoids clichés and it gives a careful and often fascinating descriptive account of recent research. For example, the authors discuss recent experiments, principally by Richard Wurtman atMIT, suggesting that some food, when digested, contains large amounts of amino acids that normally serve as neurotransmitters. As their levels increase in the blood, they pass directly into the brain where they can affect our mood and the food we will crave for our next meal. (Perhaps more curious, simply seeing food can apparently cause weight increase, although the mechanism of this remains unclear.) Jon Levine at the University of California was able to show that when dental patients are given placebos as painkillers, endorphins (the brain’s “natural opiates”) are released. Indeed, recent research is beginning to suggest that the brain may have profound effects on the body’s immune system and that consequently our “thoughts” may somehow play a central role in our susceptibility to disease.
Brain, Mind, and Behavior gives a more detailed account of the brain, and, like Restak’s book, covers many findings of contemporary neuroscience. Unfortunately, the discussion of the visual system in both books is inadequate and misleading, a serious fault since we know more about the working of the visual system than we do about most other functions of the brain. But both books contain interesting discussions of the role of the brain in regulating sleep, body temperature, menstruation, etc., and they give a clear summary of our present limited understanding of learning and memory. Restak’s book presents many interesting findings, but his philosophical comments are unhelpful. In describing the effects of PCP on monkey brains he typically writes: “That such extensive changes in personality could be brought about by a chemical provides confirmation of what neuroscientists are telling us: We are our brain.”
These works are certainly superior to the PBS series The Brain that they are meant to accompany. The individual programs lacked thematic unity, and the series as a whole gave the impression that the neurosciences consist of many unrelated fields of research. Unlike an earlier BBC series (some of whose material is used in these programs), the programs made no attempt to understand the deeper philosophical issues that would have given a clearer idea of what neurobiology is about. Unfortunately, all these books and television programs are limited by the conceptual premises of old-fashioned neuroscience. By failing to connect physiological findings with our increasing knowledge of the ways information is stored, sorted, and processed, they reveal a gap in understanding that needs to be filled.13
Electroconvulsive Therapy: An Exchange May 30, 1985
They were acetylcholine, norepinephrine, and epinephrine, although most scientists probably thought acetylcholine the only important transmitter in the brain. (See the article by Solomon H. Snyder in Science, August 1980, pp. 976–983: “Until the 1960s the amines acetylcholine, norepinephrine, and serotonin were the only well-recognized transmitters.” See also J. Glowinsky et al., “The mesocortico-prefrontal dopaminergic neurons” in Trends in Neuro-Sciences, November 1984, pp. 415–418. ↩
See Julian Barnes’s review of the BBC 2 Horizon program “Ivan” (The Observer, December 9, 1984). His description, of course, would not apply to many other patients using L-dopa. My thanks to the BBC for making available a tape of this film, which I hope will be shown in the US. ↩
Restak wants to take a broader view: ↩
See my article on Marr’s work (The New York Review of Books, October 11, 1984). Of the books under review, only Restak’s deals with Marr’s findings, but he fails to see their larger implications for understanding the brain. Brain, Mind, and Behavior argues, “The fact that human beings can design a computer that arranges manipulable information and arrives at conclusions the way a human being does says nothing at all about how the human brain achieves the same operation.” This is not true. Marr’s work has shown that, at least for vision, computer procedures give us important clues about how the brain achieves its goals. ↩
Andreasen seems to think that empirical research is done in the absence of “theory” and that the contemporary neurosciences are still carrying out the nineteenth-century program of localizing brain functions: ↩
Monrad-Krohn’s vivid description of the Norwegian woman appeared in Brain, vol. 70 (1947), pp. 405–415. For a discussion of this and the following cases see Elliott D. Ross, “Right hemisphere’s role in language, affective behavior and emotion,” Trends in NeuroSciences, September 1984, vol. 7, no. 9, p. 342. Restak discusses Ross’s work. ↩
In his recent book Brain and Psyche (Doubleday/Anchor 1985), Jonathan Winson describes a mechanism that provides a kind of traffic control, or “gating,” of the movement of information in the hippocampus, a part of the brain that is important for long-term memory. Norepinephrine, low levels of which are found in the brain in some forms of depression, apparently has deep effects on the gating mechanism. This again suggests the possible importance of memory search procedures in depression. ↩
The role in memory of the area affected in Parkinson’s disease—the basal ganglia—is suggested in some recent studies. See, for example, E. V. Evarts et al. in Trends in NeuroSciences, November 1984. See also related articles by Glowinski et al. and Wise et al. in the same issue of Trends in NeuroSciences. In Awakenings, Oliver Sacks makes the interesting comment that even Parkinson’s patients who had successfully been taught “elaborate programs or procedures for movement” at times became so “frozen” they could not even think of them, or “remember” them, let alone act on them. (Awakenings, Dutton, 1983, p. 292.) ↩
See Behavioral and Brain Sciences (1984) 7; 1–53. For example, “The results of numerous studies of memory performance after ECT (electroconvulsive therapy) still have not provided a definitive answer to the question of whether and if so, to what degree ECT is associated with persistent memory loss” (p. 15). And, “The nature, incidence, and severity of possible persistent memory deficits with ECT must be more carefully studied” (p. 22). ↩
Andreasen’s cultural history is as objectionable as her medical science. She claims, for example, that “In Europe and the developing nations, psychiatry is predominantly biological and medical.” And, “In every country except the United States, Kraepelin, not Freud, is regarded as the founding father of modern psychiatry.” I will not discuss her exaggerated view of Kraepelin, but she should at least have been aware that Jacques Lacan’s work in France stimulated one of Europe’s most powerful antibiological movements in psychiatry in recent decades. ↩
Ornstein and Thompson discuss this work, but their book must have gone to press before Nottebohm revealed that more general neuronal turnover takes place in canary brains. ↩
Science, June 22, 1984, p. 1327. ↩
I would like to thank Sydney Brenner, Oliver Sacks, and Ronald B. de Sousa for their invaluable help, although of course they should not be held responsible for the views in this article. ↩