Permanent Present Tense

by Suzanne Corkin

  In the test phase, we gave Henry and the control participants a new sheet of paper showing the six dot patterns, and asked them to draw any figure they wished, as long as they connected the five dots in each pattern with straight lines. We wanted to see whether participants drew the target figures they had copied earlier; if they did, it was proof they had been primed. The number of target figures Henry and the controls drew in the primed (post-copying) condition far exceeded the number of target figures they had produced by chance in the baseline condition. In short, after participants copied a target figure onto a dot pattern, they were more likely to draw that target figure when asked to draw whatever they wanted. Henry showed a normal magnitude of priming on three different test forms administered on three separate occasions.25

  This demonstration of priming with novel stimuli suggested that the learning was tied, not to Henry’s preoperatively established memory representations, but instead to newly acquired representations of the specific target figures. This discovery was the first report of intact nonverbal priming in a memory-impaired individual, providing strong evidence that the priming spared in amnesia is not limited to language-based stimuli.26

  How do we account for pattern priming? It seemed unlikely that the normal participants or Henry had preexisting memory representations of the target figures, so it is difficult to describe pattern priming as the activation of long-term memory representations. What, then, is the alternative explanation? In the course of copying the target figures onto the dot patterns, Henry and the controls formed new associations between them. The new associations influenced perceptual processing that assigned a specific structure to the dot pattern and guided the primed drawings. Henry’s severe amnesia eliminated the possibility that his intact pattern priming reflected the operation of recall and recognition mechanisms, underscoring the conclusion that new associations supporting perceptual priming may be established nondeclaratively, despite severe deficits in episodic memory.27

  Notably, on a pattern-recognition task, when declarative memory was required, Henry’s performance was significantly weaker than the controls’. We administered another test in which we instructed Henry and the controls to copy a new set of target figures onto dot patterns, and after a three-minute break, to select from four figures the one they had just copied. Henry, consistent with his poor declarative memory, had trouble recognizing the target figures he had just copied, whereas the control participants did not.28

  Henry’s capacity for pattern priming demonstrated that this kind of memory did not rely on the medial temporal-lobe structures that supported recall and recognition memory. Instead, the perceptual associations that mediate pattern priming are likely established in the early stages of visual processing, located in the back of the cortex. These associations are relatively inaccessible to conscious awareness. This observation gave rise to further experiments—a broad quest for the specific cortical circuits that support the various kinds of priming. We conducted a series of studies that uncovered the functional architecture of repetition priming. Henry played a major role in this research, but we also needed participants whose brains had damage in other areas. We, therefore, recruited patients with Alzheimer disease and others with lesions in discrete brain areas. In addition, we tested a control group of healthy adults who were comparable to each patient group in terms of age, sex, and education.

  Our first breakthrough came in 1991 when we demonstrated that priming is a multipart concept: priming represents a family of learning processes. By studying patients with Alzheimer disease, we were able to show that separate circuits in the cortex mediate two different kinds of priming. Like Henry, Alzheimer patients have damage to medial temporal-lobe structures and are impaired on measures of declarative memory, such as recall and recognition. They also have cell loss in certain cortical areas but not others. Our experiment revealed that Alzheimer patients had normal priming when we asked them in the test phase to visually identify words—perceptual identification priming—but not when we asked them to generate words based on their meaning—conceptual priming. This finding indicated a clear distinction between these two types of priming, suggesting that priming based on simple visual memory depends on a different brain network from priming based on more complex thinking. Henry showed normal priming on both measures because they did not require the participation of medial temporal-lobe circuits.29

  The perceptual and conceptual priming tasks consisted of a study condition and a test condition. The study condition was the same for both measures—patients and control participants saw a series of words one at a time on a computer screen and read each word aloud. The test conditions differed. For perceptual identification priming, the experimenter told participants that they would perform another task unrelated to the one just completed. She then presented a series of words briefly on the screen and instructed participants to read each word. Half the words had been in the study list, and half were new words. Priming was present if the time—measured in milliseconds—needed to identify the studied words was less than the time needed to identify the unstudied words. We discovered that the priming effect in the Alzheimer group did not differ from that in the matched control group, so mild-to-severe dementia did not interfere with priming in perceptual identification. This finding indicated that the circuits in the Alzheimer brains that supported this kind of priming were undamaged.30

  In the test for conceptual priming, participants saw three-letter stems on the computer screen and completed each one with the first word that came to mind. Half were words they had seen before in the study list, and half were new words. This time, when the Alzheimer group had to make each stem into a word, they completed no more of the stems to the studied words than they would have by chance. Their magnitude of conceptual priming was significantly depressed.31

  From autopsies of Alzheimer patients, we knew that the disease does not damage the cortex in uniform ways. The cortical areas that receive basic information through vision, hearing, and touch, as well as the cortical areas that issue motor commands, are relatively spared, but the high-order areas in the frontal, temporal, and parietal lobes that support complex cognitive processes are compromised. Our priming study implied that a memory network within visual areas in the occipital cortex—intact in Alzheimer disease—supported perceptual priming effects, whereas a different network in the temporal and parietal cortices—damaged in Alzheimer disease—supported conceptual priming effects. All of these areas were intact in Henry’s brain, which is why he had no problem with both kinds of priming.32

  In 1995, our investigation of a patient with damage to the visual areas in his brain buttressed the argument that perceptual and conceptual priming processes are separate. This man’s MRI scans showed multiple areas of abnormality, particularly in his visual areas, and he had marked deficits on tests of visual perception. He did not have amnesia, however, and his medial temporal-lobe structures were spared. We gave him the same tests the Alzheimer patients had performed, and the results showed the reverse pattern. He had no capacity for perceptual priming, identifying briefly presented words and pseudowords, but he did show normal conceptual priming, completing words based on meaning, and could still explicitly recognize words he had seen before. The dramatic contrast between this man’s normal performance on the conceptual priming task and his lack of priming on perceptual priming tasks was a vital addition to our thinking. When considered beside the opposite distinction observed in the Alzheimer patients, the results provided convincing proof of the existence of two priming processes that depend on separate neural circuits.33

  Our studies of repetition priming with Henry and other patients helped reveal in increasingly finer detail how our experiences influence us without our explicit knowledge. Because we included measures of declarative memory in our priming experiments, the results highlighted the distinction between priming—nondeclarative memory—and explicit retrieval—declarative memory. This dissociation that we teased apart so meticulously in the la
b is also blatantly apparent in daily life. When we forget appointments or friends’ birthdays, our memory has failed us; but if we lose a tennis game, we do not blame our memory and say, “I couldn’t retrieve the correct motor sequence for my serve.” By using the term memory in the first case but not the second, we acknowledge that declarative and procedural memories are different.

  But anecdotes from daily life do not prove that such a distinction exists in the functional organization of the brain. We needed Henry and other patients to make that dissociation stick scientifically. Henry had already shown us that the hippocampus and neighboring tissue were critical for declarative memory—the ability to intentionally remember experiences and information. His normal performance in our priming experiments supports the view that conceptual and perceptual priming are localized to memory circuits embedded in high-order association cortex in the frontal, temporal, and parietal lobes—areas known to support complex cognitive functions. These circuits work independently from the medial temporal-lobe memory circuits.

  Henry was important to our understanding of the various kinds of memory that operate outside of conscious awareness. Our studies of classical eyeblink conditioning, perceptual learning, and repetition priming further uncovered his capacity to acquire new nondeclarative knowledge. Despite massive damage to his hippocampus and surrounding structures, on both sides of his brain, resulting in profound amnesia, he could learn, without using explicit retrieval processes and without consciously recollecting the learning episodes. He acquired conditioned responses during delay and trace conditioning and retained these learned responses months later; he mentally completed picture fragments, showing the benefit of prior exposure to those pictures; and he primed with both verbal and pictorial test items. These accomplishments testify to Henry’s residual cognitive abilities and the neural circuits that support them.

  Members of my lab and I eagerly communicated the results of our experiments on nondeclarative learning and memory to the medical and scientific communities in the form of articles in scientific journals and book chapters. Recognition of Henry’s contributions is evident in the hundreds of citations of our work by other researchers.

  Ten

  Henry’s Universe

  Henry’s mother continued to take care of him for several years after his father’s death, but eventually the responsibility became too much for her. In 1974, when Henry was forty-eight, he and his mother moved in with Lillian Herrick, whose first husband was related to Henry on his mother’s side of the family. Mrs. Herrick was a registered nurse who before retiring had been employed at the Institute of Living, an expensive psychiatric treatment facility in Hartford, Connecticut. In her sixties, she sometimes took in older people who needed help in their daily lives.

  Mrs. Herrick and her husband lived in an established residential neighborhood on New Britain Avenue in Hartford, near Trinity College. Their large three-story white wooden house had a front porch and was surrounded by tall trees. Mrs. Herrick’s son, Mr. M., described her as “prim, proper, and very English.” She had a good sense of humor and laughed a lot. At home, she wore old-fashioned housedresses but also enjoyed dressing up to go out. Her son never saw her in a pair of pants.

  Even though Mrs. Herrick’s first husband had died, she maintained her connection to the Molaisons, taking pity on Henry and keeping in touch with him and his mother for years. This bond was fortunate for Mrs. Molaison, who was aging and becoming infirm. On one visit, Mrs. Herrick was shocked to find that Mrs. Molaison had a large, terribly inflamed ulcer on her right leg. Mrs. Herrick immediately drove her to the ER at Hartford Hospital, and for the next two days she was in danger of losing her leg. Fortunately, her leg healed, and after that incident Mrs. Herrick checked in on Henry and his mother every two or three weeks.

  In December 1974, Mrs. Herrick received a telephone call from Molaison family friends who lived in the neighborhood, reporting that when they took a Christmas package over to her house, Mrs. Molaison did not recognize them. Mrs. Herrick was scheduled to go on duty at the Institute of Living but called in to say that she was unable to work that day, and instead drove to the Molaison home. She described Mrs. Molaison as “on the floor and completely out of it.” It is unclear what happened to her, but Henry seemed unaware that anything was amiss; he thought that his mother was just resting or sleeping. An ambulance transported Mrs. Molaison, in a very bad state, to the ER. The doctors wanted to send her directly into a nursing home, but in January 1975, kindhearted Mrs. Herrick accepted Mrs. Molaison and Henry into her own home.

  Mrs. Herrick immediately noticed that their personal hygiene was deplorable, including soiled underwear and excessive body odor. She improved their personal care and, in her words, got Mrs. Molaison “back to where she was very good for a long time.” At Mrs. Herrick’s house, Henry’s relationship with his mother was initially stormy. They may have had conflicts in the past, but no one had had a chance to observe them up close. According to Mrs. Herrick, Mrs. Molaison nagged her son constantly, and he would become “really, really angry” with her, kicking her in the shin or hitting her on the forehead with his glasses. Mrs. Herrick soon intervened and relegated Mrs. Molaison to the upstairs of her house and Henry to the downstairs. If they were together, Mrs. Herrick stayed in the room with them to keep the peace. This strategy worked, and Henry settled down considerably.

  Mrs. Herrick introduced a routine into Henry’s life. Every morning, he would have his breakfast, take his medicine, shave, and go to the bathroom. She would remind him to get clean underwear and socks from his drawer and get dressed. On weekdays, at quarter to nine, Mr. or Mrs. Herrick drove him to a “school” for people with intellectual disabilities—HARC, the Hartford Association for Retarded Citizens. Henry and a few others sat around a table doing piecework submitted by Hartford businesses, such as placing key chains on a cardboard display. In return, they received a small check every other week.

  In June 1977, Henry’s vocational progress report noted that he “has adjusted well to the workshop.” His instructor wrote this description of Henry’s “work assets”:

  Henry does not retain instructions well. Periodically, must be reinstructed. Is willing to adapt to job changes but gets confused. Perseveres at his work task. Henry’s work must be checked occasionally. Henry’s work does not improve with repetition. The quality of his work decreases as the number of steps to the task increases. Has difficulty with multi-step assembly tasks. Can follow verbal instructions.

  The instructor specifically noted that Henry could not handle a project that had more than three steps to it.

  After his work breaks, Henry often went to the office to ask what he was supposed to do, but as soon as he was shown his desk, he knew exactly what his task was. The context helped him remember the procedures that comprised his work, skills he had stored away in his nondeclarative memory circuits, which could be activated in response to the appropriate environmental cues.

  Back at Mrs. Herrick’s house after school, Henry’s routine included washing his hands and having a snack. He liked to sit on the patio with his rifle magazines and crosswords, and if others were outside, he would talk with them. He was much more sociable in that setting than he had been when living alone with his mother. Henry wanted to be useful at home; he would take out the trash cans and help Mr. Herrick with yard work. In the evening, he sat in an overstuffed armchair, watching television or doing crossword puzzles. Mrs. Herrick posted a sign on the television set saying that it was to be shut off at nine-thirty, and Henry always obeyed; he willingly went to bed at nine-thirty or ten. Having been raised Roman Catholic, Henry watched one or more masses on TV on Sunday morning, and afterward Mrs. Herrick would often take him out for a drive and dinner. He loved to go out to dinner. These afternoon outings lasted several hours. Henry was not fussy about their destination, just delighted to go anyplace she took him. “He goes as long as the car will go,” she said.

  Henry did not get lost in Mrs. Herrick’s house. H
e knew where his room was and was conscientious about turning off his lights. He was cognizant of safety around the house. On one occasion, Mrs. Herrick had something cooking on the stove, and Henry, thinking she had gone off and left it, turned off the gas. One night, she went upstairs to set her hair and told Henry to leave the light on in the kitchen because she would be down later. After she left, however, Henry had trouble remembering with certainty what her instructions had been, so instead of going to bed he waited downstairs forty-five minutes until Mrs. Herrick returned.

  My conversations and correspondence with Mrs. Herrick assured me that she was taking excellent care of Henry and creating a warm but disciplined environment for him. When he moved into her house he was a heavy smoker with a daily pack-and-a-half habit; Mrs. Herrick gradually cut him down to about ten cigarettes a day, and eventually to five. At some point during the six years Henry lived with Mrs. Herrick, his chest X-ray during a physical exam showed emphysema, so she cut him off completely. After he stopped smoking, his complaints of stomach pains subsided, but I suspect that the urge to smoke lingered. Around this time, while I was testing him, he automatically reached into his chest pocket; when I asked him what he was looking for, he replied, “My smokes.” His old habit was tenacious. Henry’s nondeclarative memory was intact—he could remember the gesture of reaching for his cigarettes, which he had learned before his surgery. His declarative memory, however, was gone—he could not recall why his pocket was empty.

  To ensure proper hygiene, Mrs. Herrick left notes around the house reminding Henry to do things such as wash his hands and raise the toilet seat. He seemed to be in better health, more alert, and eating a more varied diet than when he had lived alone with his mother. Henry stuck to his routine; he missed schooldays only when he had a major seizure and was lethargic afterward. These grand mal seizures were infrequent, but he still had quite a few petit mal episodes—temporary absences. According to Mrs. Herrick, he would be watching television and suddenly “just go blank,” returning to his usual self within seconds. She looked after his medical care and coordinated his visits to our lab, graciously driving him to MIT for testing whenever we wanted to see him.