by Paul Pietsch
To the holist, mind depends on the brain as a whole; the mental cosmos cannot be mapped like the surface of the earth or broken into subunits, this bit going here, that bit over there. Historically, holists have based their beliefs on the survival of cognition and the retention of memory after massive injury to the brain. Structuralists conceded that the brain's programs are not easily found; but holists consistently failed to link their theories to physical reality. To me, structuralist that I was, holism looked at best like metaphysics, and at worst like magic.
***
Let me say a few words about the genesis of my former faith in structuralism, and about anatomy as it is practiced in the latter half of the 20th Century. Anatomy of course includes what rests on the dissecting table, but the scope of the science goes far beyond this. Anatomy is an attempt to explain living events by observing, analyzing, and, if necessary, conceptualizing the body's components, whether the object of study happens to be a genital organ or the genes within its cells, whether the search calls for a sophisticated Japanese electron microscope or the stout crucible steel blade of a Swedish butcher knife. Anatomy rests upon a belief shared by many in our culture, in and out of science. Robert Traver's Anatomy of a Murder and Ashley Montagu's Anatomy of Swearing express metaphorically what many in our day embrace epistemologically: in order to find out how something really works, take it apart. What could seem reasonable than that?
As a student entering science in the 1950s, during some of the most exciting moments in intellectual history, I could see no basic philosophical difference between what anatomists were seeking to discover and what other scientists, with different titles, were actually finding out about the cell and the molecular side of life. In the 1950s and 1960s, scientists in large numbers and from diverse fields had begun accepting the anatomist's already ancient credo: physiological functions explicitly and specifically reduce to the interplay between discrete structural entities. Structure was suddenly being used to account for events that only a generation before seemed beyond reason: how genes maintain a molecular record of heredity; how muscles contract, cells divide, the sperm penetrates the egg; how a cell's membrane actively picks and chooses from the body's milieu what shall and shall not pass across its boundary; how an irritated nerve cell generates and propagates a neural signal and then transmits the message to the next cell in the network; how cells fuel and refuel their insatiable demands for energy. Those investigators who abided by the structural faith were coming up with answers any child of our thing-bound culture could easily comprehend--and they were winning the Nobel Prizes in the process. The intellectual environment in which I grew up vindicated every fundamentalism of my chosen field, virtually everywhere anyone chose to look. Everywhere except the brain.
***
Judging from artifacts, club-wielding cave men seemed to know that something essential to behavior existed inside the skull of a foe or quarry. Physicians of ancient Egypt correlated malfunctioning minds with diseased brains. Gladiators wore helmets, and those who lost them sometimes contributed personally to the early anecdotal wisdom about the brain's biology. Phrenologists, seeking to map the facets of the human personality over the surface of the cerebrum, laid the very foundations for modern neuroanatomy. High-velocity rifle bullets, which could inflict discrete wounds, afforded mid-nineteenth century battlefield surgeons with insights into the brain that they and others pursued at the laboratory bench. And the study of the nervous system in our own times can be traced directly to the science and surgery of Victorian and Edwardian Europe.
Today there are entire libraries, whole university departments, and specialized learned societies devoted exclusively to storing, disseminating, and promoting the wisdom of the "neurosciences." So vast is knowledge about the nervous system that the study of human neuroanatomy alone requires a completely separate course. Facts abound on the brain's chemical composition, anatomical organization, and electrophysiological activities. The main routes for incoming sensory messages, for example, have been plotted and replotted--the signals enabling us to see a sunrise, hear a sparrow, smell a rose, taste a drop of honey, feel the sting of a wasp, appreciate the texture of another human hand. The images of these words, for instance, land on the retinas of the reader's eyes and trigger well-worked-out photochemical reactions, which, in turn, detonate electrical signals within the receptor cells--the rods and cones. The retina itself begins sorting, integrating, and encoding the signals into messages, which it transmits through highly specific routes via the optic nerves and optic tracts to relays in the core of the brain. From the relays, the message moves to specific cells in what are called the occipital lobes of the cerebrum, and there establishes point-for-point communication between loci out in the visual fields, and particular input stations in the brain.
Much is known, too, of outflow pathways used in carrying direct orders to the effectors of our overt behavior--the muscles and glands that let us walk, talk, laugh, blush, cry, sweat, or give milk. In spite of admittedly vast gaps among the facts, enough is known today to fill in many of the blanks with plausible hypotheses about circuits used in language, emotions, arousal, and sleep--hypotheses for many of our actions and even a few of our feelings and thoughts. Damage to a known pathway yields reasonably predictable changes or deficits in behavior, perception, or cognition. Neurological diagnoses would be impossible, otherwise. For example, a person with partial blindness involving the upper, outer sector of the visual field, with accompanying hallucinations about odors and with a history of sudden outbursts of violence, quite likely has a diseased temporal lobe of the cerebrum --- the forward part of the temporal lobe on the side opposite the blindness, in fact. Or a person who suffers a stroke, cannot speak but understands language, and is paralyzed on the right side of the body almost assuredly has suffered damage at the rear of the cerebrum's frontal lobe--the of the left frontal lobe, to be precise.
For a quick pictorial neuroanatomy lesson, go here.
Up to a point, in other words, the brain fits neatly and simply into the anatomical scheme of things. But throughout history, the battle-ax, shrapnel, tumors, infections, even the deliberate stroke of the surgeon's knife, have paralyzed, blinded, deafened, muted, and numbed human beings, via the brain, without necessarily destroying cognition, erasing memory, or fractionating the mind. It wasn't that anatomists couldn't link specific functions to particular parts of the brain. Far from it. But when we reached for the dénouement, for an explanation of the most pivotal features of the brain, the structural argument teetered under the weight of contradictory evidence.
***
Consider a paradox about vision known as macular sparing. No part of the human brain has been worked on more exhaustively and extensively than the visual system. Nor, seemingly, could any structural realist ask for a more explicit relationship between form and function than one finds there. Every locus in our fields of view corresponds virtually point-for-point with microscopic routes through our visual pathways. As you can demonstrate to yourself with gentle pressure on an eyelid, you form an image of right and left fields in both retinas. (The nose blocks the periphery of the eye's inner half and the right eye's outer half; vice versa for the right field). For optical reasons however, the images of the field do a 180-degree rotation in projecting onto the two retinas. Thus the left field registers on the left eye's inner half and the right eye's outer half; vice versa for the right field. The fibers from the retina, which form the optic nerve strictly obey the following rule: those from the inner half of the retina cross to the opposite side of the brain; those from the outer half do not. Thus all information about the visual fields splits precisely down the middle and flashes to the opposite side of the brain. Corresponding fibers from the two eyes join each other in the centers of our heads (at a structure known as the optic chiasm) and form what are called optic tracts--the right tract carrying messages about left field exclusively, and the left tract carrying information about right field. If an optic tract is totally destroyed, we become blin
d to the entire opposite visual field.
Optic tracts end where they make connections with a highly organized collection of cells known as the LGB (lateral geniculate body). The LGB has the job of communicating visual signals to the visual cortex of the occipital lobe. Now there is every anatomical reason to predict that destruction of one occipital lobe will split a visual field map into seen and blank halves, as sometimes occurs.
Usually, though, a person with a lesion beyond the LGB will lose the peripheral parts of the opposite field but retain a whole, un-split view of the central field. The macula, a yellowish spot on the center of the retina, receives the projection from the central field. Thus the term macular sparing means that an otherwise split visual field remains un-split on both sides of the central zone, which is precisely as it should
not
be.
If the visual pathways were haphazardly arranged, with fibers coursing everywhere, macular sparing would be understandable. But clinical records, autopsy reports, the results of direct stimulation of conscious human brains during surgery, and probings into ape and monkey brains with minute electrodes--all means of gathering evidence--consistently show that the visual system is minutely precise in organization. For a while, some authors explained away macular sparing by assuming that central retinal fibers violate the crossing rule. But in 1934, a famous ophthalmologist, Stephen Polyak, studied the chimpanzee's visual pathways and found that central fibers
do
obey crossing rules, just like fibers of the rest of the retina: nasals cross, temporals don't! And repeated searches of human pathways has led to an identical conclusion-- namely that crossing doesn't explain macular sparing.
[2 ]
Until 1940, one could assume either or both of two additional hypotheses to explain macular sparing: that of partial survival of the visual pathways, and/or that of sloppy examination of the visual fields. But in that year, Ward Halstead and his colleagues published data in the Archives of Ophthalmology that eliminated these simple hypotheses as well.
Halstead's group reported the case history of a twenty-five year old filing clerk who arrived at a clinic in Chicago in the autumn of 1937 with a massive tumor in her left occipital lobe. Summarizing what the surgeons had to cut out to save the woman's life, Halstead et al. wrote, "The ablation had removed completely the left striate [visual] cortex and areas 18 and 19 of the occipital lobe posterior to the parieto-occipital fissure." Translated, this means that the young woman lost her entire left optic lobe--the entire half of her brain onto which the right visual field projects and in which information is processed into higher-order percepts. Visual field maps showed that the operation caused blindness in the young woman's right visual field (homonymous hemianopsia, as it is called), but with macular sparing.
***
If macular sparing always occurred after occipital-lobe damage, one might explain the phenomenon by assuming that the macular-projection area of one LGB somehow sends fibers to both occipital lobes. But the Halstead article nullified this explanation, too, with an almost identical case history of a twenty-two year old stenographer. A patient in the same hospital, she also had a massive tumor, but in her right occipital lobe. After surgery, visual field mapping showed that she was totally blind to the left field of view--without macular sparing!
In other words, not only did Halstead's group document macular sparing as a genuine anatomical paradox; they even showed that one cannot apply simple, linear cause-and-effect reasoning to it: in the case of the two young women, the same antecedents had produced decidedly different consequences.
In no way does macular sparing detract from the orderliness of the visual system. Indeed, this was part of the mystery. Specific places on the retina excite particular cells in both the LGB and the visual cortex. When stimulated, the macular zone on the retina does excite specific cells of the occipital cortex--in the rear tip of the lobe, to be exact--on the side opposite the half visual field. But the phenomenon of macular sparing (and thousands of people have exhibited the sign) shows that there is not an exclusive center in the brain for seeing the central field of view. If the message can make it into the LGB, it may make it to the mind.
***
But what about the mind after the loss of a visual lobe of the brain? Halstead's group had something to say about this, too. The twenty-two year old secretary had scored 133 points on an IQ test before surgery. A month after the operation, she again scored 133. And five weeks after the operation, she left the hospital and returned to her job--as a secretary, no less! About the filing clerk, whose IQ also remained unchanged, Halstead et al. wrote, "Immediately on awakening from the anesthetic, the patient talked coherently and read without hesitation. At no time was there any evidence of aphasia [speech loss] or alexia [reading deficits].
Thus, in spite of the loss of half the visual areas of their cerebrums, despite a halved, or nearly halved, view of the external world, both young women retained whole visual memories. They are far from unique. Three floors below where I sit, there is an eye clinic whose filing cabinets contain thousands of visual-field maps and case upon case documenting the survival of a complete human mind on the receiving end of severely damaged human visual pathways.
The structuralists attempted to dodge Halstead's evidence by insisting that visual cognition and memory must lie outside the occipital lobe--somewhere! Others just plain ignored it (and still do.)
***
Nor is vision the sole brain function whose story begins true to an anatomist's expectations only to end in uncertainty. Take language. Certain speech and reading deficits correlate with damage to particular areas of the brain (and provide important diagnostic signs). Broca's motor speech aphasia most often results from blockage or hemorrhage of the arteries supplying the rear of the frontal lobe, and occurs on the left cerebral hemisphere about 80 to 85 percent of the time. In Broca's aphasia, a person understands language, communicates nonverbally, and writes, if not also paralyzed, but cannot articulate or speak fluently. (A sudden drop in fluency may, in fact, signal an impending stroke). In contrast, another speech aphasia is associated with damage to the temporal lobe. Known as Wernicke's aphasia, this malady is characterized not by apparent loss of fluency but by absence of meaning in what the person says. The words don't add up to informative sentences; or the person may have problems naming familiar objects, and call a cup an ashtray, for instance, or be unable to name a loved one.
Broca's and Wernicke's speech areas intercommunicate via a thick arching bundle (called the arcuate bundle). When damage to this pathway disconnects the two speech areas, language fluency and comprehension are not affected; however, the sufferer cannot repeat newly presented phrases.
Alexia, the inability to read, and its partial form, dyslexia, may suggest a tumor or arteriosclerosis in an area directly in front of the occipital lobe. Or, if a person begins to have problems writing down what he or she hears, a lesion may be developing in a span of brain between the occipital lobe and Wernicke's area.
In other words, anatomy functions in language as it does in vision. And those who tend to our health ought to be well informed about what a particular malfunction may portend. But aphasias do not supply evidence for a theory of mind. Damage to a specific cerebral area does not always produce the anticipated deficit. Individuals vary. Many malfunctions correlate with no detectable anatomical lesion (this is often true in dyslexia). And, whereas, massive cerebral damage (for instance, surgical removal of an entire cerebral hemisphere) may have only marginal effects on one person, a pin prick in the same area may destroy another's personality. Scientific law, qua law, cannot be founded on maybes and excuses. Yet in every bona fide case the structuralist has been able to make for the anatomy of memory, the holist has managed to find maybes-- and excuses. One of the best illustrations of this occurs in what is called "split-brain" research.
***
The two cerebral hemispheres intercommunicate via a massive formation of nerve fibers
called the corpus callosum. A splitting headache marks roughly where the corpus callosum crosses the midline (although pain signals travel along nerves in blood vessels and connective tissue wrappings of the brain). A feature of mammals, the corpus callosum develops in our embryonic brain as we start acquiring mammalian form. On occasion, however, a person is born without a corpus callosum.
In spite of its relatively large mass--four inches long, two inches wide, and as thick as the sole of a shoe--the corpus callosum received surprisingly little attention until the 1950s. But in the 1960s, it made the newspapers. When surgeons split the corpus callosum, they produced two independent mentalities within one human body.
Surgeons had cut into the corpus callosum many years earlier, in an attempt to treat epilepsy. In fact, brain surgery developed in the 1880s after Sir Victor Horsley found that cutting into the brains of laboratory animals could terminate seizures. Until the drug dilantin came along in the 1930's, surgery, when it worked at all, was the only effective therapy for epilepsy. In epilepsy, convulsions occur when electrical discharges sweep the surface of the brain. A diseased locus may initiate the discharges, and removal of the zone may reduce or even eliminate seizures. Often, just an incision works, possibly by setting up countercurrents and short-circuiting the discharge. At any rate, splitting the entire corpus callosum seemed too drastic a measure. What would two half-minds be like?
In the 1950s, Ronald Meyers, a student of Roger Sperry's at California Institute of Technology, showed that cats can lead a fairly normal life even after total disconnection of their cerebral hemispheres. Sperry and his associates soon extended their investigations to include the monkey. The ensuing success prompted two California neurosurgeons, Joseph Bogen and P. J. Vogel, to try the split-brain operation on human beings.