correctly touched the spot. Gy insisted that he had been guessing, and was surprised when he was told that he had pointed correctly. But repeated trials proved that it had not been a lucky stab in the dark; Gy’s finger homed in on target after target, even though he had no conscious visual experience of where they were or what they looked like. Weizkrantz dubbed the syndrome blindsight to emphasize its paradoxical nature. Short of ESP, how can we explain this? How can a person locate something he cannot see? The answer lies in the anatomical division between the old and new pathways in the brain. Gy’s new pathway, running through V1, was damaged, but his old pathway was perfectly intact. Information about the spot’s location traveled up smoothly to his parietal lobes, which in turn directed the hand to move to the correct location.
This explanation of blindsight is elegant and widely accepted, but it raises an even more intriguing question: Doesn’t this imply that only the new pathway has visual consciousness? When the new pathway is blocked, as in Gy’s case, visual awareness winks out. The old pathway, on the other hand, is apparently performing equally complex computations to guide the hand, but without a wisp of consciousness creeping in. This is one reason why I likened this pathway to a robot or a zombie. Why should this be so? After all, they are just two parallel pathways made up of identical-looking neurons, so why is only one of them linked to conscious awareness?
Why indeed. While I have raised it here as a teaser, the question of conscious awareness is a big one that we will leave for the final chapter.
Now let’s have look at pathway 2, the “what” stream. This stream is concerned mainly with recognizing what an object is and what it means to you. This pathway projects from V1 to the fusiform gyrus (see Figure 3.6), and from there to other parts of the temporal lobes. Note that the fusiform area itself mainly performs a dry classification of objects: It discriminates Ps from Qs, hawks from handsaws, and Joe from Jane, but it does not assign significance to any of them. Its role is analogous to that of a shell collector (conchologist) or a butterfly collector (lepidopterist), who classifies and labels hundreds of specimens into discrete nonoverlapping conceptual bins without necessarily knowing (or caring) anything else about them. (This is approximately true but not completely; some aspects of meaning are probably fed back from higher centers to the fusiform.)
But as pathway 2 proceeds past the fusiform to other parts of the temporal lobes, it evokes not only the name of a thing but a penumbra of associated memories and facts about it—broadly speaking the semantics, or meaning, of an object. You not only recognize Joe’s face as being “Joe,” but you remember all sorts of things about him: He is married to Jane, has a warped sense of humor, is allergic to cats, and is on your bowling team. This semantic retrieval process involves widespread activation of the temporal lobes, but it seems to center on a handful of “bottlenecks” that include Wernicke’s language area and the inferior parietal lobule (IPL), which is involved in quintessentially human abilities as such as naming, reading, writing, and arithmetic. Once meaning is extracted in these bottleneck regions, the messages are relayed to the amygdala, which lies embedded in the front tip of the temporal lobes, to evoke feelings about what (or whom) you are seeing.
In addition to pathways 1 and 24 there seems to be an alternate, somewhat more reflexive pathway for emotional response to objects that I call pathway 3. If the first two were the “how” and “what” streams, this one could be thought of as the “so what” stream. In this pathway, biologically salient stimuli such as eyes, food, facial expressions, and animate motion (such as someone’s gait and gesturing) pass from the fusiform gyrus through an area in the temporal lobe called the superior temporal sulcus (STS) and then straight to the amygdala.5 In other words, pathway 3 bypasses high-level object perception—and the whole rich penumbra of associations evoked through pathway 2—and shunts quickly to the amygdala, the gateway to the emotional core of the brain, the limbic system. This shortcut probably evolved to promote fast reaction to high-value situations, whether innate or learned.
The amygdala works in conjunction with past stored memories and other structures in the limbic system to gauge the emotional significance of whatever you are looking at: Is it friend, foe, mate? Food, water, danger? Or is it just something mundane? If it’s insignificant—just a log, a piece of lint, the trees rustling in the wind—you feel nothing toward it and most likely will ignore it. But if it’s important, you instantly feel something. If it is an intense feeling, the signals from the amygdala also cascade into your hypothalamus (see Figure Int.3), which not only orchestrates the release of hormones but also activates the autonomic nervous system to prepare you to take appropriate action, whether it’s feeding, fighting, fleeing, or wooing. (Medical students use the mnemonic of the “four Fs” to remember these.) These autonomic responses include all the physiological signs of strong emotion such as increased heart rate, rapid shallow breathing, and sweating. The human amygdala is also connected with the frontal lobes, which add subtle flavors to this “four F” cocktail of primal emotions, so that you have not just anger, lust, and fear, but also arrogance, pride, caution, admiration, magnanimity, and the like.
LET US NOW return to John, our stroke patient from earlier in the chapter. Can we explain at least some of his symptoms based on the broad-brushstrokes layout of the visual system I have just painted? John was definitely not blind. Remember, he could almost perfectly copy an engraving of St. Paul’s Cathedral even though he did not recognize what he was drawing. The earlier stages of visual processing were intact, so John’s brain could extract lines and shapes and even discern relationships between them. But the crucial next link in the “what” stream—the fusiform gyrus—from which visual information could trigger recognition, memory, and feelings—had been cut off. This disorder is called agnosia, a term coined by Sigmund Freud meaning that the patient sees but doesn’t know. (It would have been interesting to see if John had the right emotional response to a lion even while being unable to distinguish it consciously from a goat, but the researchers didn’t try that. It would have implied a selective sparing of pathway 3.)
John could still “see” objects, could reach out and grab them, and walk around the room dodging obstacles because his “how” stream was largely intact. Indeed, anyone watching him walk around wouldn’t even suspect that his perception had been profoundly deranged. Remember, when he returned home from the hospital, he could trim hedges with shears or pull out a plant from the soil. And yet he could not tell weeds from flowers, or for that matter recognize faces or cars or tell salad dressing from cream. Thus symptoms that would otherwise seem bizarre and incomprehensible begin to make sense in terms of the anatomical scheme with it’s the multiple visual pathways that I’ve just outlined.
This is not to say that his spatial sense was completely intact. Recall that he could grab an isolated coffee cup easily enough but was befuddled by a cluttered buffet table. This suggests that he was also experiencing some disruption of a process vision researchers call segmentation: knowing which fragments of a visual scene belong together to constitute a single object. Segmentation is a critical prelude to object recognition in the “what” stream. For instance, if you see the head and hindquarters of a cow protruding from opposite sides of a tree trunk, you automatically perceive the entire animal—your mind’s eye fills it in without question. We really have no idea how neurons in the early stages of visual processing accomplish this linking so effortlessly. Aspects of this process of segmentation were probably also damaged in John.
Additionally, John’s lack of color vision suggests that there was damage to his color area, V4, which not surprisingly lies in the same brain region—the fusiform gyrus—as the face recognition area. John’s main symptoms can be partially explained in terms of damage to specific aspects of visual function, but some of them cannot be. One of his most intriguing symptoms became manifest when he was asked to draw flowers from memory. Figure 2.11 shows the drawings he produced, which he confidently labeled rose, tulip, and iris. Notice that the flowers are drawn well but they don’t look like any real flowers that we know! It’s as though he had a generic concept of a flower and, lacking access to memories of real flowers, produces what might be called Martian flowers that really don’t exist.
