by Oliver Sacks
But color vision, in real life, is part and parcel of our total experience, is linked with our own categorizations and values, becomes for each of us a part of our life-world, of us. V4 may be an ultimate generator of color, but it signals to, it converses with, a hundred other systems in the mind-brain; and perhaps it can also be modulated by these. It is at higher levels that integration occurs, that color fuses with memories, expectations, associations, and desires to make a world with resonance and meaning for each of us. 21
21. The power of expectation and mental set in the perception of color is clearly shown in those with partial red-green colorblindness. Such people may not, for example, be able to spot scarlet holly berries against the dark green foliage, or the delicate salmon-pink of dawn—until these are pointed out to them. “Our poor impoverished cone cells”, says a dyschromatope of my acquaintance, “need the amplification of intellect, knowledge, expectation, and attention in order to ‘see’ the colors that we are normally ‘blind’ to.”
Mr. I. not only presented a rather “pure” case of cerebral achromatopsia (virtually uncontaminated by additional defects in the perception of form, motion, or depth), but was a highly intelligent and expert witness as well, one who was skilled at drawing and reporting what he saw. Indeed, when we first met, and he described how objects and surfaces “fluctuated” in different lights, he was, so to speak, describing the world in wavelengths, not in colors. The experience was so unlike anything he had ever experienced, so strange, so anomalous, that he could find no parallels, no metaphors, no paints or words to depict it.
When I phoned Professor Zeki to tell him of this exceptional patient, he was greatly intrigued and wondered, in particular, how Mr. I. might do with Mondrian testing, such as he and Land had used with normally sighted people and with animals. He at once arranged to come to New York to join us—Bob Wasserman, my ophthalmologist colleague; Ralph Siegel, a neurophysiologist; and myself—in a comprehensive testing of Jonathan I. No patient with achromatopsia had ever been examined in this way before.
We used a Mondrian of great complexity and brilliance, illuminated either by white light or by light filtered through narrow-band filters allowing only long wavelengths (red), intermediate wavelengths (green), or short wavelengths (blue) to pass. The intensity of the illuminating beam, in every case, was the same.
Mr. I. could distinguish most of the geometric shapes, though only as consisting of differing shades of grey, and he instantly ranked them on a one-to-four grey scale, although he could not distinguish some color boundaries (for example, between red and green, which both appeared to him, in white light, as black). With rapid, random switching of the filters, the grey-scale value of all the shapes dramatically changed—some shades previously indistinguishable now became very different, and all shades (except actual black) changed, either grossly or subtly, with the wavelength of the illuminating beam. (Thus a green area would be seen by him as white in medium-wavelength light, but as black in white or long-wavelength light.)
All Mr. I.’s responses were consistent and immediate. (It would have been very difficult, if not impossible, for a normally sighted person to make these instant and invariably “correct” estimations, even with a perfect memory and a profound knowledge of the latest color theory.) Mr. I., it was clear, could discriminate wavelengths, but he could not go on from this to translate the discriminated wavelengths into color; he could not generate the cerebral or mental construct of color.
This finding not only clarified the nature of the problem, but also served to pinpoint the location of the trouble. Mr. I.’s primary visual cortex was essentially intact, and it was the secondary cortex (specifically the V4 areas, or their connections) that bore virtually the whole brunt of the damage. These areas are very small, even in man; yet all our perception of color, all our ability to imagine or remember it, all our sense of living in a world of color, depend crucially on their integrity. A mischance had devastated these bean-sized areas of Mr. I.’s brain—and with this, his whole life, his life-world, had been changed.
The Mondrian testing had demonstrated damage in these areas; we wondered now if we could see this, using brain scans. But CAT and MRI scans were entirely normal. This could have been because the scanning techniques of the time had a resolution inadequate to visualize what may have been only a patchy damage to V4; it could have been that the damage sustained was metabolic only, not structura; or it could have been that the main damage was not in V4 itself, but in the structures (the so-called “blobs” in Vi or the “stripes” in V2) leading up to it. 22
22. Malfunction in V4 can be shown by a newer technique, PET scanning (which pictures the metabolic activity of different brain areas), even if no anatomical lesion is visible on CAT or MRI scans. Unfortunately, this was not available to us at the time.
It has been stressed—by both Zeki and Francis Crick—that these small structures, the blobs and stripes, are intensely active metabolically and may be unusually vulnerable to even temporary reductions of oxygen. Crick, in particular (with whom I discussed the case in great detail), wondered whether Mr. I. could have suffered from carbon monoxide poisoning, which is known to cause changes in color vision through its effects on the oxygenation of the blood to the color areas. Mr. I. might have been exposed to carbon monoxide through a leaky exhaust in his car, Crick speculated—perhaps due to the accident, conceivably even causing it. 23
23. Mr. I., fond of spending time in sports clubs and bars, did some research here himself and told us that he had spoken to a number of boxers who had had transient, and sometimes persistent, losses of color vision following blows to the head. Partial or total achromatopsia (“greying-out”), also temporary, is characteristic of fainting or shock, in which there is a reduction of blood supply to the posterior, and especially the visual parts, of the brain. Greying-out also occurs in transient ischemic attacks, due to arterial insufficiency—Zeki speculates that this affects the wavelength-selective cells in the blobs of V1 and the thin stripes of V2. Transient alterations of color vision—including bizarre instabilities or transformations of color (dyschromatopsia)—may also occur in visual migraines and epilepsies and are well known to users of mescaline and other drugs. They can be a disquieting side effect of ibuprofen.
But all this was in a sense academic. Mr. I.’s achromatopsia, after three months, remained absolute, and he had persisting impairments of contrast vision, too. 24
24. It was never quite clear from Mr. I.’s descriptions of daily life whether or not he had some slight impairment of form vision. But, interestingly, when he was being tested on the Mondrians, boundaries between rectangles tended to disappear with prolonged fixation, though they would be rapidly restored if the stimulus was moved. There are two other systems besides the blob system in early visual processing: the M system, which deals with movement and depth perception particularly, but not color; and a P-interblob system, which probably deals with high-resolution form perception. Zeki thought that the dissolution of boundaries with prolonged fixation suggested a defect in the P system, and their rapid restoration with movement “a healthy and active M system.”
Whether these would clear eventually we could not say—some cases of acquired cerebral achromatopsia improve with time, but others do not. We still did not know what had caused the damage to Mr. I.’s brain, whether it was a toxin such as carbon monoxide, or the impact of the car accident, or the result of an impairment of blood flow to the visual areas of the brain. It was possible that if it had been caused by a stroke, there might be more such strokes. The prognosis had to remain uncertain, although his situation by now seemed to be stable.
We were, however, able to offer a little practical help. Mr. I. had consistently seen the boundaries of the Mondrian patches most clearly when these were illuminated by medium-wavelength light, and Dr. Zeki therefore suggested we give him a pair of green sunglasses, transmitting only this waveband in which he saw most clearly. A pair of glasses was specially made, and Mr. I. took t
o wearing them, especially in bright sunlight. The new glasses delighted him, for although they did nothing to restore his lost color vision, they did seem noticeably to enhance his contrast vision and his perception of form and boundaries. He could even enjoy color TV with his wife again. (The dark-green glasses, in effect, rendered the color set monochromatic—though he continued to prefer his old black-and-white set when alone.)
The sense of loss following his accident was overwhelming to Jonathan I., as it must be to anyone who loses color, a sense that interweaves itself in all our visual experiences and is so central in our imagination and memory, our knowledge of the world, our culture and art. This sense of loss, in relation to the natural world, has been remarked upon in every case. For the nineteenth-century physician thrown from his horse, flowers had “lost more than half their beauty”, and entering his garden, abruptly bereft of color, was not short of shocking. This sense of loss and of shock was doubled and redoubled for Mr. I., for he had not only lost the beauty of the natural world, and the world of people, and of the innumerable objects whose colors are part of daily life, but he had also lost the world of art, he felt—the world that, for fifty years or more, had absorbed his profoundly visual and chromatic talents and sensibilities. The first weeks of his achromatopsia were thus weeks of an almost suicidal depression. 25
25. This sense of loss is not, of course, experienced by those born totally colorblind. This is brought out in another letter I received recently from a charming and intelligent woman, Frances Futterman, born totally colorblind. She contrasted her own situation with that of Jonathan I.:
I was struck by how different that kind of experience must be, compared to my own experience of never having seen color before, thus never having lost it—and also never having been depressed about my colorless world—The way I see in and of itself is not depressing. In fact, I am frequently overwhelmed by the beauty of the natural world—People say I must see in shades of gray or in “black and white”, but I don’t think so. The word gray has no more meaning for me than the word pink or blue—in fact, even less meaning, because I have developed inner concepts of color words like pink and blue; but, for the life of me, I can’t conceive of gray.
Though Mrs. Futterman’s experience is certainly different from Mr. I.’s, both remark on the meaninglessness of the word “grey, ” a word that can no more convey anything to the achromatopic than can “darkness” to the blind, or “silence” to the deaf. Mrs. Futterman remarks, as Mr. I. came to, on the beauty of her world. “I would also be willing to bet”, she says, “that if we were tested along with normals in low lighting levels, we would be able to detect far more shades of gray. Black and white photos look far too stark to me. The world I see has so much more richness and variety than black-and-white photos or TV shows—My vision is a lot richer than normals can imagine.”
In addition to his sense of loss, Jonathan I. found his changed visual world, at first, abhorrent and abnormal. This, too, is the experience of most people in his position: the concussed physician thrown from his horse found his vision “perverted”, one of Damasio’s patients found her grey world “dirty.” Why, one must wonder, do all subjects with a cerebral achromatopsia express themselves in such terms—why should their experience seem so abnormal? Mr. I. was seeing with his cones, seeing with the wavelength-sensitive cells of V1, but unable to use the higher-order, color-generating mechanism of V4. For us, the output of V1 is unimaginable, because it is never experienced as such and is immediately shunted on to a higher level, where it is further processed to yield the perception of color. Thus the raw output of V1 never appears in awareness for us. But for Mr. I. it did—his brain damage had made him privy to, indeed trapped him within, a strange in-between state—the uncanny world of V1—a world of anomalous and, so to speak, prechromatic sensation, which could not be categorized as either colored or colorless. 26
26. We may experience something like this, Zeki has recently shown, by using an inhibitory magnetic stimulation to V4, which produces a temporary achromatopsia.
Mr. I., with his heightened visual and aesthetic sensibilities, found these changes particularly intolerable. We know too little about what determines emotion and aesthetic appeal in relation to color, and indeed in relation to seeing generally—and this is a matter of individual experience and taste. 27
27. We also know too little about the interactions of the three major systems in early vision—the M, interblob, and blob systems. But Crick wonders whether some of the unpleasantness and abnormality, at least—the “leaden” vision of which Mr. I. complained—might not in part be due to the unmoderated action of the preserved M system, which, he emphasizes, “sees few shades of grey, [so that] its white would correspond to what was (in normal people) a dirty white.” This notion gains support from the fact that people with congenital achromatopsia, who have not sustained any damage to their higher visual systems, do not have any such perceptual abnormalities. Thus Knut Nordby writes: “I have never experienced ‘dirty,’ ‘impure,’ ‘stained,’ or ‘washed-out’ colors, as reported by the artist Jonathan I.”
Color perception had been an essential part not only of Mr. I.’s visual sense, but his aesthetic sense, his sensibility, his creative identity, an essential part of the way he constructed his world—and now color was gone, not only in perception, but in imagination and memory as well. The resonances of this were very deep. At first he was intensely, furiously conscious of what he had lost (though “conscious”, so to speak, in the manner of an amnesiac). He would glare at an orange in a state of rage, trying to force it to resume its true color. He would sit for hours before his (to him) dark grey lawn, trying to see it, to imagine it, to remember it, as green. He found himself now not only in an impoverished world, but in an alien, incoherent, and almost nightmarish one. He expressed this soon after his injury, better than he could in words, in some of his early, desperate paintings.
But then, with the “apocalyptic” sunrise, and his painting of this, came the first hint of a change, an impulse to construct the world anew, to construct his own sensibility and identity anew. Some of this was conscious and deliberate: retraining his eyes (and hands) to operate, as he had in his first days as an artist. But much occurred below this level, at a level of neural processing not directly accessible to consciousness or control. In this sense, he started to be redefined by what had happened to him—redefined physiologically, psychologically, aesthetically—and with this there came a transformation of values, so that the total otherness, the alienness of his V1 world, which at first had such a quality of horror and nightmare, came to take on, for him, a strange fascination and beauty.
Immediately after his accident, and for a year or more thereafter, Jonathan I. insisted that he still “knew” colors, knew what was right, what was appropriate, what was beautiful, even if he could no longer visualize them in his mind. But, thereafter, he became somewhat less sure, as if now, unsupported by actual experience or image, his color associations had started to give way. Perhaps such a forgetting—a forgetting at once physiological and psychological, at once strategic and structural—may have to occur, to some extent, sooner or later, in anyone who is no longer able to experience or imagine, or in any way to generate, a particular mode of perception. (Nor is it necessary that the primary damage be cortical; it may occur, after months or years, even in those who are peripherally or retinally blind.) 28
28. J.D. Mollon et al. describe the case of a young police cadet who, following a severe febrile illness (probably cerebral herpes) was left with achromatopsia, hemianopia, and some agnosia and amnesia. Testing him five years after the illness, Mollon reports that “he was able to name (presumably by means of verbal memory) the colours of e.g., grass, traffic lights, and the union jack, but made errors on other common objects (e.g., banana, pillarbox).” Thus here, after five years of total colorblindness, the colors of even the most familiar objects were often forgotten. Such effects have been recorded in ordinary retinal blindness, t
oo, where after some years there may be a widespread loss of all visual memories, including those of color.
There was a lessening concern with what he had lost, and indeed with the whole subject of color, which at first had so obsessed him. Indeed, he now spoke of being “divorced” from color. He could still speak fluently about it, but there seemed to be a certain hollowness to his words, as if he were drawing only from past knowledge and no longer understood it.
Nordby writes:
Although I have acquired a thorough theoretical knowledge of the physics of colours and the physiology of the colour receptor mechanisms, nothing of this can help me to understand the true nature of colours.
What was true for Nordby was now true for Jonathan I., too. He had in some ways started to resemble a person born colorblind, even though he had lived in a color world for the first sixty-five years of his life. At once forgetting and turning away from color, turning away from the chromatic orientation and habits and strategies of his previous life, Mr. I., in the second year after his injury, found that he saw best in subdued light or twilight, and not in the full glare of day. Very bright light tended to dazzle and temporarily blind him—another sign of damage to his visual systems—but he found the night and nightlife peculiarly congenial, for they seemed to be “designed”, as he once said, “in terms of black and white.”
He started becoming a “night person”, in his own words, and took to exploring other cities, other places, but only at night. He would drive, at random, to Boston or Baltimore, or to small towns and villages, arriving at dusk, and then wandering about the streets for half the night, occasionally talking to a fellow walker, occasionally going into little diners: “Everything in diners is different at night, at least if it has windows. The darkness comes into the place, and no amount of light can change it. They are transformed into night places. I love the nighttime”, Mr. I. said. “Gradually I am becoming a night person. It’s a different world: there’s a lot of space—you’re not hemmed in by streets, by people—It’s a whole new world.”
