UNTIL ABOUT 35 years ago scientists believed there was only a single visual-processing area, called the visual cortex, situated at the back of the brain. We now know more than 30 areas in the brains of primates—including humans—are involved in handling aspects of vision such as the perception of motion, color and depth. Vision, it turns out, is a much more complex and sophisticated affair than anyone had imagined. It makes sense that responsibility for processing is divided into various areas that have different computational objectives.
We take our sight for granted because it usually seems so effortless. It is only when parts of these different visual areas are damaged, causing selective yet often profound disturbances in perception, that we begin to appreciate the range and subtlety of normal human vision. This approach parallels our study of “normal” illusions—by understanding misperceptions, whether for intact or damaged systems, we gain insight into brain processes involved in perception.
Consider the case of a man known as GY. Damage to his visual cortex resulted in complete blindness in one half of the visual field. He could not consciously see anything, not even a spot of light, shown to him in that region. Yet when asked to reach out and touch the spot, he could do so accurately; he could touch a spot he couldn’t see! It seems downright spooky, but, as you will soon learn, we can explain—at least partially—his condition, known as blindsight, in terms of the multiple specialized anatomical pathways devoted to vision that we mentioned earlier. [For more on blindsight, see “Subconscious Sight,” by Susana Martinez-Conde; Scientific American Mind, April/May 2008.]
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Or consider the strange case of John, elegantly studied in 1987 by M. Jane Riddoch and Glyn W. Humphreys, both now at the University of Birmingham in England. John had served as an air force pilot. Soon after his retirement he suffered a stroke that partially damaged visual regions of both hemispheres of his brain. He could observe things around him; he was not blind in the usual sense. But when he saw his wife—or anyone else for that matter—he could not recognize her. He knew her by her voice; his brain areas for hearing were unaffected, as were his memories. Indeed, he could not visually distinguish among umbrellas, chairs or other common objects, even though he claimed to be able to see them perfectly clearly. “They are out of focus in my mind, doctor,” he would say, “not in my eye.”
The doctors confirmed this assertion by asking him to copy a drawing of, for example, St. Paul’s Cathedral that was hanging on the wall. John could produce a faithful rendering, almost a carbon copy, of the picture but had no idea what it was. He might as well have been copying a meaningless jumble of lines.
John had a condition known as visual agnosia, a phrase coined by Sigmund Freud meaning “lack of visual knowledge.” Unlike some of Freud’s more outlandish ideas such as “penis envy” or the “Oedipus complex,” this one has survived the test of time.
What must it feel like to have such a condition, seeing yet not knowing? You can get an inkling by looking at the famous old woman/young lady illustration (a). The first time you look at this illusion, you probably see the girl. But after a while, you can mentally flip the image to see an old face. The young woman’s chin becomes the hag’s nose, and the young ear becomes the old eye. Now, when you were perceiving the face as a young woman, you were also simultaneously seeing the lines and curves constituting the old hag. Yet you were not perceiving (or “knowing”) the old woman. In effect, you suffer from a temporary form of agnosia for her. Intriguingly, some people, including our colleague Stuart M. Anstis, a psychologist at the University of California, San Diego, are permanently “stuck” on the young lady and cannot see the hag. Psychologist Richard L. Gregory of the University of Bristol in England refers to this inability as visual hagnosia.
Another compelling example is the rat/man illustration (b) (image here?). When you perceive the rat, you are, effectively, agnosic for the man, and vice versa. For normal people, it is a bistable figure; but for John, perception of neither rat nor man would ever occur, despite his normal visual acuity.
You can also get a feel for agnosia by thinking of what happens when you listen to a foreign tongue. You hear all the sounds, syllables, intonations and rhythms of the speech, but none of it makes any sense to you (c) (image?). You simply cannot create a meaningful perception from these sensations.
Problems in the Pathways
To understand GY’s and John’s predicaments, we will need to take a brief tour through the anatomy of the visual pathways. Those more than 30 visual-processing areas have staggeringly complex connections among them. Fortunately, despite this complexity, we can discern a simple overall pattern.
Messages from the retina of the eye get transmitted along the optic nerve before diverging into two parallel anatomical pathways, which we shall call “old” and “new” pathways to indicate their evolutionary sequence(d). The old pathway, also called the where pathway, goes to a structure called the superior colliculus, which forms a bump on the roof of the brain stem, the stalk that emerges from below the brain and continues as the spinal cord. The colliculus helps to determine the location of an object. When a novel or salient event occurs in your environment (for example, when there is an object looming over your left shoulder), you reflexively orient and swivel your eyeballs toward it without knowing what it is. That is, you orient to it or locate it before you proceed to identify it.
The other pathway, the newer one, as we shall see, is required for identifying an item, even though it is incapable of locating it or orienting to it. The new pathway projects to the visual cortex (V1 for short) in the back of the brain, where the features of the object are analyzed (for color, orientation of edges, movement, and so on). Information from V1 splits again into two pathways farther along the visual-processing course: the how pathway projecting into the parietal lobes (“How” do I use or interact with this object?) and the what pathway (“What” exactly is this object? What does it mean for me?) into the temporal lobes (d). The 30 visual areas we spoke of are shared between these pathways. Bear in mind that we have described a grossly oversimplified caricature: many fibers go back and forth between the areas; they are heavily interconnected and not entirely autonomous. But in science it is not a bad idea to start with a simple picture.
Now let us return to GY, who has blindsight. GY has complete damage to V1. No information reaches either the what or how pathway, rendering him blind in the sense that he cannot consciously see objects. But because his where pathway (going through the superior colliculus and bypassing the damaged V1 en route to higher cortical centers) is intact, he can guide his hand unerringly toward the light spot that he cannot consciously see. It is as if there is an unconscious zombie trapped in him that can point accurately even though the conscious person is oblivious. The paradox of blindsight is resolved.
A curious philosophical implication of all this is that only the new pathway is “conscious”; the old pathway can go about its business without consciousness creeping into it. Both pathways are composed of neural circuits, but only one of them (as far as we can tell) is conscious. Scientists have no idea why, although being linked to tasks such as language and meaning might be important. Activity in the what pathway eventually evokes a verbal label or name (“mother”) and nuances of emotions however pronounced (“terror”) or subtle (“warmth”).
Now imagine your V1 is normal, but an evil genius removes your temporal lobes (the what pathway) under anesthesia. What would the world look like when you woke up? Without the what pathway, you wouldn’t be able to recognize, name or appreciate the meanings of things around you. Yet because the how pathway is intact, you would still “see” in the sense of being able to reach out for objects, to dodge missiles hurled at you or to avoid obstacles. It is hard to imagine this scenario, but it would be roughly equivalent to being transported to the Red Planet (without your knowledge) and waking up in a gallery of Martian abstract art. You could not recognize anything or understand it but could still find your way around, copy the shapes of things and step over fallen objects. Everything around you—chairs, tables, people, cars—would look like meaningless abstract art. You would have profound visual agnosia.
This kind of complete damage is rare, but even with partial damage a condition called Klüver-Bucy may develop. In this variant of agnosia the patient has some difficulty identifying common objects but more profound agnosia for food and appropriate “sex objects.” Patients cannot discriminate food from inedible objects, so they may put pebbles in their mouth. Such people may make sexual overtures to the patient in the adjacent bed, to the doctor or even to animals, though they are mentally normal in other respects.
Seeing without Naming
John’s predicament is somewhat similar. In some ways, it is more severe because he has great difficulty identifying any object. Yet he doesn’t take this to the absurd lengths of trying to eat inedible objects or engaging in indiscriminate sexual behavior. In Klüver-Bucy patients there is probably relatively greater damage to regions in the temporal lobes concerned with sex, food and other primal urges, whereas in John the damage mainly affects regions involved in recognizing more neutral and commonplace objects such as chairs, goats and carrots.
Recall, especially, that he could copy pictures accurately, although he was unable to identify or name them. This is because his how pathway is undamaged, and it can guide the hand around to draw a faithful rendering. Without the what (temporal lobe) pathway, he does not know what it is. Amazingly, he could even use shears to trim the hedge in his garden (which only requires how) but could not weed the garden because he had lost the ability to discriminate weeds from flowers. But his problems were not quite as extreme as seen in Klüver-Bucy; he could often recognize the general category that an object belonged to (“it’s an animal”) albeit not the specific exemplar (he might say “dog” instead of the correct “goat”). Or he would identify a carrot as a paintbrush (“because it’s long and has a tuft at its end”).
And thus we can begin to explain the unusual perceptions of GY and John, by examining their particular deficits in terms of our detailed knowledge of the visual areas and their connections and evolutionary origins. In doing so, we have not only explained these bizarre symptoms but also gained new insights into how normal vision works. Contrary to naive intuition, vision is not a single process. Instead it involves multiple specialized areas working in parallel. How the outputs of these areas are combined to create a seamless unity of conscious perception, however, is as yet an unsolved mystery.
Note: This story was originally published with the title, "I See, But I Don't Know".
