Hallucinations

9 Bisected: Hallucinations in the Half-Field

One does not see with the eyes; one sees with the brain, which has dozens of different systems for analyzing the input from the eyes. In the primary visual cortex, located in the occipital lobes, at the back of the brain, there are point-to-point mappings of the retina onto the cortex, and it is here that light, shape, orientation, and location in the visual field are represented. Impulses from the eyes take a circuitous route to the cerebral cortex, some of them crossing to the opposite side of the brain as they do so, so that the left half of the visual field of each eye goes to the right occipital cortex, and vice versa. If, therefore, one occipital lobe is damaged (as by a stroke, for example), there will be blindness or impaired vision in the opposite half of the visual field — a hemianopia.

Besides the impairment or loss of vision to one side, there may be positive symptoms, too — hallucinations in the blind or purblind area. About 10 percent of patients with sudden hemianopia get such hallucinations — and immediately recognize them to be hallucinations.

In contrast to the relatively brief and stereotyped hallucinations of migraine or epilepsy, the hallucinations of hemianopia may continue for days or weeks on end; and, far from being fixed or uniform in format, they tend to be ever changing. Here, one might envisage not a small knot of irritable cells discharging paroxysmally, as in an attack of migraine or epilepsy, but a large area of the brain — whole fields of neurons — in a state of chronic hyperactivity, out of control and misbehaving because of the lessening of forces that normally control or organize them. The mechanism here thus resembles that of Charles Bonnet syndrome.

While such notions were implicit in Hughlings Jackson’s vision of the nervous system as having hierarchically ordered levels (the higher levels controlling the lower ones, and lower ones starting to behave independently, even anarchically, if released from control by damage at the higher levels), the idea of “release” hallucinations was made explicit by L. Jolyon West in his 1962 book Hallucinations. A decade later, David G. Cogan, an ophthalmologist, published an influential paper that included short, vivid histories of fifteen patients. Some of them had damage to their eyes, some had damage to their optic nerves or tracts, some had occipital lobe lesions, some had temporal lobe lesions, and some had lesions in the thalamus or the midbrain. Lesions in any of these different places, it seemed, could break the normal network of controls and lead to a release of complex visual hallucinations.

Ellen O. was a young woman who came to see me in 2006, about a year after surgery for a vascular malformation in her right occipital lobe. The procedure was a fairly simple one, sealing off the swollen vessels of the malformation. As her doctors had warned her, she had some visual problems following the procedure: a blurring of vision to the left side, as well as some agnosia and alexia — difficulties recognizing people and printed words (English words looked like “Dutch,” she said). These difficulties prevented her from driving for six weeks and interfered with her reading and enjoyment of television, but they were transient. She also had visual seizures in the first weeks after surgery. These took the form of simple visual hallucinations, flashes of light and color to the left that lasted a few seconds. The seizures came several times a day at first but had practically ceased by the time she returned to work. She was not too concerned about them, for her doctors had warned her that she might experience such aftereffects.

What they had not warned her about was that she might develop complex hallucinations later. The first of these, about six weeks after her surgery, was of a huge flower, occupying most of the left half of her vision. This had been stimulated, she thought, by seeing an actual flower in bright, dazzling sunlight; it seemed to burn itself into her brain, and the vision of it persisted in the left half of her visual field, “like an afterimage” — but an afterimage that lasted not for a few seconds but for an entire week. The following weekend, after her brother visited, she saw his face — or, rather, part of his profile, just one eye and cheek — for several days.[51]

Then she moved from abnormalities of perception — seeing things that were actually there, with perseveration or distortion — to hallucinations, seeing things that were not there. Visions of people’s faces (including, at times, her own) became a frequent sort of hallucination. But the faces Ellen saw were “abnormal, grotesque, exaggerated,” often just a profile with the teeth or perhaps one eye hugely magnified, completely out of scale with the rest of the features. At other times she saw figures with “simplified” faces, expressions, or postures — “like sketches or cartoons.” Then Ellen started to hallucinate Kermit the Frog, the Sesame Street puppet, many times a day. “Why Kermit?” she asked. “He means nothing to me.”

Most of Ellen’s hallucinations were flat and still, like photographs or caricatures, though sometimes an expression would change. Kermit the Frog sometimes looked sad, sometimes happy, occasionally angry, though she could not connect his expressions with any of her own moods. Silent, motionless, ever changing, these hallucinations were almost continuous throughout her waking hours (“They are 24/7,” she said). They did not occlude her vision but were superimposed like transparencies over the left half of her visual field. “They have been getting smaller lately,” she told me. “Kermit the Frog is tiny now. He used to occupy most of the left half, and now he’s down to a little fraction of it.” Ellen wondered whether she would have these hallucinations for the rest of her life. I said that I thought their diminution a very good sign; perhaps one day Kermit would be too small to see at all.

What was going on in her brain? she asked me. Why, above all, was she getting these odd and sometimes nightmarish hallucinations of grotesque faces? From what depths did they come? Surely it was not normal to imagine such things. Was she becoming psychotic, going mad?

I told her that the impairment of vision on one side following her surgery had probably led to heightened activity in parts of the brain higher up in the visual pathway, in the temporal lobes, where figures and faces are recognized, and perhaps in the parietal lobes, too; and that this heightened, at times uncontrolled, activity was causing her complex hallucinations and also the extraordinary persistence of vision, the palinopsia, she was experiencing. The particular hallucinations which so horrified her — of deformed and dismembered faces or faces with exaggerated, monstrous eyes or teeth — were, in fact, typical of abnormal activity in an area of the temporal lobes called the superior temporal sulcus. They were neurological faces, not psychotic ones.

Ellen wrote to me periodically with updates, and six years after our initial visit, she wrote: “I would not say that I am entirely recovered from my visual problems; more that I am living more harmoniously with them. My hallucinations are much smaller, but they are still there. Mostly I see the colorful orb all the time, but it no longer distracts me as much.”

She still has some difficulty with reading, especially when she is tired. When she read a book recently, she said,

But Ellen’s blind spot has not prevented her from pursuing graduate courses and even marathon running, as she reported with characteristic good humor:

While Ellen’s complex hallucinations started several weeks after her operation, similar “release” hallucinations may appear almost immediately with sudden damage to the occipital cortex. This was the case with Marlene H., a woman in her fifties who came to see me in 1989. She told me that she had awoken one Friday morning in December 1988 with a headache and visual symptoms. She had had migraines for years, and at first she took this as just another visual migraine. But the visual symptoms were different this time: she saw “flashing lights all over … shimmering lights … arcs of lightning … like a Frankenstein thing,” and these did not go away in a few minutes, like her usual migraine zigzags, but continued all through the weekend. Then, on Sunday evening, the visual disturbances took on a more complex character. In the upper part of the visual field, to the right, she saw a writhing form “like a Monarch caterpillar, black and yellow, its cilia glistening,” along with “incandescent yellow lights, like a Broadway show, going up and down, on and off, nonstop.” Though her doctor had reassured her that this was just “an atypical migraine,” things went from bad to worse. On Wednesday, “the bathtub seemed to be crawling with ants … there were cobwebs covering the walls and ceiling … people seemed to have lattices on their faces.” Two days later she started to experience gross perceptual disturbances: “My husband’s legs looked really short, distorted, like someone in a trick mirror. It was funny.” But it was less funny, and rather frightening, in the market that afternoon: “Everyone looked ugly, parts of their faces were gone, and eyes — there seemed a blackness in their eyes — everyone looked grotesque.” Cars seemed to appear suddenly to the right. Testing her visual fields, waggling her fingers to either side, Marlene found that she could not see them on the right until they crossed the mid-line; she had lost all vision to the right side.

It was only at this point, days after her initial symptoms, that she was finally investigated medically. A CAT scan of her brain revealed a large hemorrhage in the left occipital lobe. There was little to be done therapeutically at this stage; one could only hope that there would be some resolution of her symptoms, some healing or adaptation with time.

After some weeks, the hallucinations and perceptual distortions, which had been largely confined to the right side, did start to die down, but Marlene was left with a variety of visual deficits. She could see, at least to one side, but was bewildered by what she saw: “I would have preferred to be blind,” she told me, “instead of not being able to make sense of what I saw.… I had to go slowly, deliberately, to put things together. I would see my sofa, a chair — but I couldn’t put it together. It did not add up, at first, to a ‘scene.’ … I was a very fast reader before. Now I was slow. The letters looked different.”

“When she looks at her watch,” her husband interpolated, “at first she can’t process it.”

Besides these problems of visual agnosia and visual alexia, Marlene was experiencing a sort of runaway visual imagery, outside her control. At one point, she saw a woman wearing a red dress on the street. Then, she said, “I closed my eyes. This woman, almost puppetlike, was moving around, took on a life of her own.… I realize that I had been ‘taken over’ by the image.”

I kept in touch with Marlene at intervals and saw her most recently in 2008, twenty years after her stroke. She no longer had hallucinations, perceptual distortions, or runaway visual imagery. She was still hemianopic, but her remaining vision was good enough for her to travel independently and to work (which involved reading and writing, albeit at her own slow pace).

While Marlene experienced protracted perceptual changes as well as hallucinations after a massive occipital lobe hemorrhage, even a “little” occipital lobe stroke can evoke striking, though transient, visual hallucinations. Such was the case with a bright, deeply religious old lady whose hallucinations appeared, “evolved,” then disappeared, all within the space of a few days in July of 2008. I got a call from one of the nurses in a nursing home where I work — we had worked together for many years, and she knew that I was especially interested in visual problems. She asked whether she could bring her great-aunt Dot to see me, and between them, they reconstructed the story. Aunt Dot told me that her vision had seemed “blurry” on July 21, and the following day, “it was like looking through a kaleidoscope … all this rotating color going through,” with sudden “lightning streaks” to the left. She went to her doctor, who, finding that she had a hemianopia to the left, sent her to an emergency room. There it was found that she had atrial fibrillation, and a CAT scan and MRI showed a small area of damage in the right occipital lobe, probably the result of a blood clot dislodged by the fibrillation.

The following day, Aunt Dot saw “octagons with red centers … moving past me like a film strip, and the moving octagons changed into hexagonal snowflakes.” On July 24, she saw “an American flag, outstretched, as if flying.”

On July 26, she saw green dots, like little balls, floating to the left, and these turned into “elongated silvery leaves.” When her niece remarked that an early autumn was on the way in Canada and the leaves were already changing color, the hallucinated silvery leaves immediately turned reddish brown. These ushered in a day full of complex visual hallucinations, including “daffodils in bouquets” and “fields of goldenrod.” They were followed by a very particular image, which was multiplied. When her niece visited that day, Aunt Dot said, “I’m seeing sailor boys … one on top of the other, like a film strip.” They were colored, but flat and motionless and small, “like stickers.” She did not recognize their origin until her niece reminded her that she (the niece) often used a sailor-boy sticker when she sent her aunt a letter — so here, the sailor boy was not a complete invention, but a reproduction of the stickers Aunt Dot had once seen, now multiplied.

The sailor boys were replaced by “fields of mushrooms” and then by a golden Star of David. A neurologist in the hospital had been wearing such a star prominently when he visited her, and she continued to “see” this for hours, though not multiplied like the sailor boys. The Star of David was superseded by “traffic lights, red and green, turning on and off,” then by scores of tiny golden Christmas bells. The Christmas bells were replaced by a hallucination of praying hands. Then she saw “gulls, sand, waves, a beach scene,” with the gulls flapping their wings. (Up to this point, apparently, there had not been movement within an image; she had seen only static images passing in front of her.) The flying gulls were replaced by “a Greek runner wearing a toga … he looked like an Olympic athlete.” His legs were moving, as the gulls’ wings had been. The next day she saw stacked and serried coat hangers — this was the last of her complex hallucinations. The day after that, she saw only lightning streaks to the left, as she had seen six days before. And this was the end of what she called her “visual odyssey.”

Aunt Dot was not a nurse, like her great-niece, but she had worked for many years as a volunteer in the nursing home. She knew that she had had a small stroke on one side in the visual part of her brain. She realized that the hallucinations were caused by this and were probably transient; she did not fear that she was losing her mind. She did not for a moment think that her hallucinations were “real,” although she observed that they were quite unlike her normal visual imagery — much more detailed, more brightly colored, and, for the most part, independent of her thoughts or feelings. She was curious and intrigued, and so she made a careful note of the hallucinations as they occurred and tried to draw them. Both she and her niece wondered why particular images popped up in her hallucinations, to what extent they reflected her life experiences, and how much they might have been prompted by her immediate environment.

She was struck by the sequence of her hallucinations — that they had gone from simple and unformed to more complex, and then back to simple before disappearing. “It’s like they moved up the brain, then down again,” she said. She was struck by how things she had seen could change into similar forms: octagons turning into snowflakes, blobs into leaves, and perhaps gulls into Olympic athletes. She observed that, in two instances, she had hallucinated something she had seen shortly before: the neurologist’s Star of David and the sailor-boy stickers. She noted a tendency to “multiplication” — bunches of daffodils, fields of flowers, octagons galore, snowflakes, leaves, gulls, scores of Christmas bells, and multiple copies of the sailor-boy stickers. She wondered whether the fact that she was a deeply religious Catholic who prayed several times a day had played a part in her seeing a hallucination of praying hands. She was struck by the way in which the silvery leaves she was seeing instantly turned reddish brown when her niece said, “The leaves are changing.” She thought the Olympic runner might have been provoked by the fact that the 2008 Olympic Games were coming up, with constant previews on television. I found it impressive and moving that this old lady, curious and intelligent, though not intellectual, would observe her own hallucinations so calmly and thoughtfully and, without being prompted, raise virtually all the questions a neurologist might ask about them.

If one loses half the visual field from a stroke or other injury, one may or may not be aware of the loss. Monroe Cole, a neurologist, became aware of his own field loss only by doing a neurological exam on himself after his coronary bypass surgery. He was so surprised by his lack of awareness of this deficit that he published a paper about it. “Even intelligent patients,” he wrote, “often are surprised when a hemianopia is demonstrated, despite the fact that it has been demonstrated on numerous examinations.”

The day after his surgery, Cole began to have hallucinations, in the blind half of his visual field, of people (most of whom he recognized), dogs, and horses. These apparitions did not frighten him; they “moved, danced and swirled, but their purpose was unclear.” Often he hallucinated “a pony with his head cradled in my right arm”; he recognized this as his granddaughter’s pony, but as with many of his hallucinations, “the colour was wrong.” He always realized that these visions were unreal.

In a 1976 paper, the neurologist James Lance provided rich descriptions of thirteen hemianopic patients, and he emphasized that their hallucinations were always recognized as such, if only by their absurdity or irrelevance: giraffes and hippopotamuses sitting on one side of a pillow, visions of spacemen or Roman soldiers to one side, and so on. Other physicians have made similar reports; none of their patients ever confuses such hallucinations with reality.

I was therefore surprised and intrigued to receive the following letter from a physician in England, about his eighty-six-year-old father, Gordon H., who had long-standing glaucoma and macular degeneration. He had never had hallucinations before, but recently he had had a small stroke affecting his right occipital lobe. He was “quite sane and largely intellectually undiminished,” his son wrote, but

Gordon H.’s normal visual perception to the right side, one might think, by its normalcy and detail, would immediately show up the relative poverty of the mental construct, the hallucination, on the left. But, his son asserts, he cannot tell one from the other — there is no sense of a boundary; the two halves seem continuous. Mr. H.’s case is unique, to my knowledge.[52] He has none of the outlandish, obviously out-of-context hallucinations commonly reported in hemianopia. His hallucinations blend perfectly well with his environment and seem to “complete” his missing perception.

In 1899, Gabriel Anton described a singular syndrome in which patients totally blind from cortical damage (usually from a stroke affecting the occipital lobes on both sides) seemed to be unaware of it. Such patients may be sane and intact in all other ways, but they will insist that they can see perfectly well. They will even behave as if sighted, boldly walking in unfamiliar places. If, in so doing, they collide with a piece of furniture, they will insist that the furniture has been moved, that the room is poorly lit, and so on. A patient with Anton’s syndrome, if asked, will describe a stranger in the room by providing a fluent and confident, though entirely incorrect, description. No argument, no evidence, no appeal to reason or common sense is of the slightest use.

It is not clear why Anton’s syndrome should produce such erroneous but unshakable beliefs. There are similar irrefutable beliefs in patients who lose the perception of their left side and the left side of space but maintain that there is nothing missing, even though we can demonstrate convincingly that they live in a hemi-universe. Such syndromes — so-called anosognosias — occur only with damage to the right half of the brain, which seems to be especially concerned with the sense of bodily identity.

An even stranger twist was given to the matter in 1984, with the publication of a paper by Barbara E. Swartz and John C. M. Brust. Their patient was an intelligent man who had lost the sight in both eyes from retinal injuries. Normally, he recognized that he was blind and behaved as if blind. But he was also an alcoholic, and twice, while on a drinking binge, he believed that his sight had returned. Swartz and Brust wrote:

Returning to Gordon H., I would hazard a guess that damage to the right occipital lobe has produced a unilateral Anton’s syndrome (though I do not know if such a syndrome has ever been described). His hallucinations (unlike those of Lance’s patients) are informed and shaped by what he perceives in the intact part of his visual field, and mesh seamlessly with his intact perception to the right.

Mr. H. has only to turn his head to discover that he has been deceived, but this does not shake his conviction that he can see equally to both sides. He may, if pressed, accept the term “hallucination,” but if he does so he must feel that, for him, hallucination is veridical, that he is hallucinating reality.