“Through a Computer Darkly: Group Selection and Higher Brain Function” 36, No. 1 (October 1982)
“Neural Darwinism: Population Thinking and Higher Brain Function”
“Group Selection and Phasic Reentrant Signaling: A Theory of Higher Brain Function”
“Group Selection as the Basis for Higher Brain Function” ed.
“Neuronal Group Selection in the Cerebral Cortex”
“Cell Adhesion Molecules”
“Expression of Cell Adhesion Molecules During Embryogenesis and Regeneration”
“Interaction of Synaptic Modification Rules Within Populations of Neurons” (February 1985)
“Selective Networks and Recognition Automata”
In 1895, Sigmund Freud made his last attempt to explain the neurophysiological basis of the way the brain functions. His essay on the subject, “Project for a Scientific Psychology,” was never published during his lifetime. We have learned much about the brain since 1895, yet no equally ambitious attempt has since been made to examine the broad implications of neuroscientific research for the functioning of the brain and for psychology. Recently, Gerald M. Edelman, director of The Neurosciences Institute at The Rockefeller University, has proposed a new theory, one that gives us powerful reasons to revise our ideas about how we think, act, and remember. Although this theory is not directly based on Freud’s work, it confronts several of the problems with which Freud wrestled throughout his creative life.
Central to Freud’s work was the connection between memory and the psychology of everyday life. He considered memory to be a permanent record of past events, a record that was anatomically separate from the brain mechanisms that are responsible for our ability to make sense of the world around us. As he wrote in the final chapter of The Interpretation of Dreams,
[T]here are obvious difficulties involved in supposing that one and the same system can accurately retain modifications of its elements and yet remain perpetually open to the reception of fresh occasions for modificationsâ€Ś. [Therefore] we shall distribute these two functions on to different systems.
On December 6, 1896, Freud wrote to his close friend Wilhelm Fliess,
As you know, I am working on the assumption that our psychical mechanism has come into being by a process of stratification: the material present in the form of memory-traces being subjected from time to time to a re-arrangement in accordance with fresh circumstancesâ€”to a re-transcription. Thus what is essentially new about my theory is the thesis that memory is present not once but several times over, that it is laid down in various species of indications.
In the same letter he writes, “If I could give a complete account of the psychological characteristics of perception and of the [registrations of memory], I should have described a new psychology.”
Freud was acutely aware that recollections are often imperfect and fragmentary, and that they can and do alter perceptions. His theory attempted to explain how what he took to be perfect stores of memory were so transformed, arguing that memories cannot be released in their permanent form because the satisfactions and pleasures once associated with youthful impressions can no longer be experienced directly. Hence they reappear in dreams, but disguised and reworked. Ideas, Freud argued, become separated from associated emotions (affects) and disappear from consciousness. The emotions become attached to apparently unrelated ideas, disguising their real meaning. And we often appear to forget the memories themselves. Repression, screen memories, latent dream content, the return of the repressedâ€”all were mechanisms elaborated in Freud’s theory to account for the ways in which fixed memories, however distorted and incomplete, can manifest themselves and affect our present view of the world. Freudian theory attempts to account for an apparent paradox: if we believe that memories are, by their very nature, permanently stored in the brain, why are they rarely recalled in their original form? It is the inaccuracy of recollection that Freudian psychology evokes so well. The reasons for this apparent inaccuracy may, however, be quite different from those that Freud suggested. In fact, the assumption that memories are in any sense part of a fixed record may be wrong.
If memory is a fixed record, neurophysiologists still cannot say precisely where and how memories are stored. The hypothesis of a fixed record may have been formulated prematurely, without sufficient attention to the means by which we recognize objects and events. We are probably much better at recognition than we are at recollection. We recognize people despite changes wrought by aging, and we recognize photographs of places we have visited and personal items we have misplaced. We can recognize paintings by Picasso and adept imitations of Picasso. When we recognize a painting that we have never seen as by Picasso or as an imitation, we are doing something more than recalling earlier impressions. We are categorizing: Picassos and fakes. Our recognition of paintings or of people is the recognition of a category, not a specific item. People are never exactly what they were moments before and objects are never seen in exactly the same way.
One possible explanation for this is that our capacity to remember is not for specific recall of an image stored somewhere in our brain. Rather it is an ability to organize the world around us into categories, some general, some specific. When we speak of a stored mental image of a friend, which image or images are we referring to? The friend doing what, when, and where? One reason why the search for memory molecules and specific information storage zones in the brain has so far been fruitless may be that they are just not there. Unless we can understand how we categorize people and things and how we generalize, we may never understand how we remember. Yet we do remember names, telephone numbers, words and their definitions. Are these not examples of items that must be stored in some kind of memory? Notice, however, that we generally recall names and telephone numbers in a particular context; each of our recollections is different, just as we use the same word in different sentences. These are categorical, not just specific recollections.
Clinical neurologists have long been aware that brain disease may lead to severe alterations in memory, but they have yet to analyze deeply the nature of categorization. In a rare abnormality resulting from brain damage and known as prosopagnosia, patients lose the ability to identify the faces of friends and well-known public personalities. But they can recognize faces as faces. And while they cannot identify their own car or their own coat, they do recognize cars and clothing as such. They apparently can recall general categories but cannot identify specific items. Something similar may occur in some forms of amnesia as well. Antonio Damasio and his colleagues at the University of Iowa Medical School described a patient with amnesia sitting in a room with the curtains drawn and unable to recall the season. When the patient looked out the window, he noted the color of the trees and the dress of a passerby, and exclaimed, “By golly, it must be July or August.” He could not recall the month of the year, but he could deduce it given appropriate evidence.
These studies appear to suggest that our ability to recognize general categories as opposed to the recognition of specific items such as Mary’s face or Alison’s hat depends on two different brain functions. But the ability to recognize Alison’s hat is, in part at least, based on temporal associations. We may have seen Alison wearing that hat last Sunday. The loss of the ability to categorize events in time can cause a nearly total loss of specific references. It is not the specific items that are no longer recalled, but their temporal order or their arrangement in succession that has not been formed or has been lost. When Damasio and his colleagues examined the man with amnesia about the calendar year, they found he had brain damage which made him unable to establish “temporal and spatial relationships between separate sensory information items.”1
Individual needs and desires, then, determine how we classify the people, places, and events that fill our daily lives. Moreover, the categories we use seem to depend on cross-correlations, or context. Yet many influential theories of mental function posit fixed entities that have an independent existence of their own. Freud, for example, described many ordinary objects as fitting into categories based on their resemblance to male or female sexual organs (phallic symbols, for example) and tended to view such categories as representing deeper drives that are universal within the human species. Many clinical neurologists and psychologists disagree with Freud’s notion of universal sexual drives; they nevertheless hold that information is organized into permanent categories in one or more memory systems within the brain, and that it can systematically be brought to consciousness in ways analogous to memory searches used in computers. The processes that are responsible for our recognition of categories, however, do not seem to depend on such fixed mechanisms.
There are good biological reasons to question the idea of fixed universal categories. In a broad sense, they run counter to the principles of the Darwinian theory of evolution. Darwin stressed that populations are collections of unique individuals. In the biological world there is no typical animal and no typical plant. When we say a salt molecule has a specific size we are giving a measurement which, allowing for error, is true for all salt molecules. But there is no set of measurements that will universally describe more than the one example of a plant or animal we are measuring. Qualities we associate with human beings and other animals are abstractions invented by us that miss the nature of the biological variation. The central conception in Darwinian thought is that variations in populations occur from which selection may take place. It is the variation that is real, not the mean. It was Darwin’s recognition of this profound difference between the biological and physical worlds that led to the rise of modern biology. The mechanisms of inheritance through genes create diversity within populations; selection from these populations allows certain organisms to survive in unpredictable environments.
Darwinian ideas have had a variable influence on psychological thinking, which has sometimes strayed away from biological explanation. Modern ethology, which studies the relation of animal and human behavior, has recaptured much of the Darwinian flavor that unfortunately left psychology when early learning theorists such as Pavlov seemed to be successful in explaining behavior without paying heed to the differences between animal species. But as important as their insights are, ethologists have not applied Darwinian thinking to the workings of the brain in each individual of a species.
Does evolutionary thought have anything to do with the explanation of the psychology of individual human beings? The theory of the brain Gerald Edelman proposed in 1978 sought to explain neurophysiological function as a Darwinian system involving variation and selection. Although his theory is confined to neurobiology, implicit in this work is a bold attempt to unify the biological and psychological sciences, one that strongly depends on the ideas of evolution and the facts of developmental biology.
Edelman had earlier studied the immune system. For years, scientists had wondered how the body produced antibodies against viruses or bacteria it had never encountered. Linus Pauling had suggested in 1940 that there was one basic kind of antibody molecule in the body. When the body was invaded by a bacterium, he had argued, the antibody molecule would mold itself around the intruder, thus acquiring a definite shape. Copies of the mold were made and released into the bloodstream where they would bind to the invading bacteria. The system learned, or was instructed by, the shape of a bacterium only after being exposed to it.
A.R. Damasio, P.J. Eslinger, H. Damasio, G.W. Van Hoesen, and S. Cornell, "Multi-Modal Amnesic Syndrome Following Bilateral Temporal and Basal Forebrain Damage," Archives of Neurology, Vol. 42 (March 1985), pp. 252–259. Damasio et al.'s interpretation is quite different from the one I have suggested.↩
A.R. Damasio, P.J. Eslinger, H. Damasio, G.W. Van Hoesen, and S. Cornell, “Multi-Modal Amnesic Syndrome Following Bilateral Temporal and Basal Forebrain Damage,” Archives of Neurology, Vol. 42 (March 1985), pp. 252–259. Damasio et al.’s interpretation is quite different from the one I have suggested.↩