The Man Who Wasn't There: Investigations into the Strange New Science of the Self (6 page)

Scoville drilled two holes just above Henry’s eye sockets, into which he inserted flat brain spatulas—a neurosurgeon’s version of the tongue depressor—parting the frontal and temporal lobes in the two brain hemispheres. This gave him access to brain structures of the medial temporal lobe, such as the amygdala and hippocampus. He then sucked out a chunk of normal brain tissue, including much of the amygdala and hippocampus. The effect this surgery had on Henry, his name now anonymized to H. M. in the academic literature, is neuroscience lore.

H. M. continued to take anticonvulsant medication, and his grand mal seizures dropped dramatically in intensity and frequency (from once a week to once a year). But something far more intriguing happened to his memory. He “
could no longer recognize the hospital staff nor find his way to the bathroom, and he seemed to recall nothing of the day-to-day events of his hospital life.” In a paper published in 1957, Scoville and a psychologist at the Montreal Neurological Institute, Brenda Milner, wrote about H. M.’s psychological examination: “
This was performed on April 26, 1955. The memory defect was immediately apparent. The patient gave the date as March, 1953, and his age
as 27. Just before coming into the examining room he had been talking to Dr. Karl Pribram, yet he had no recollection of this at all and denied that anyone had spoken to him. In conversation, he reverted constantly to boyhood events and seemed scarcely to realize that he had had an operation.”

H. M. continued to live a life lacking in new memories (a condition called anterograde amnesia), and there was also a limit to what he could recollect about his past. Milner continued to study H. M., a baton she would pass on to her student Suzanne Corkin. In 1984, Corkin wrote:

A striking feature of H.M. is the stability of his symptoms during the 31 postoperative years. He still exhibits a profound anterograde amnesia, and does not know where he lives, who cares for him, or what he ate at his last meal. His guesses as to the current year may be off by as much as 43 years, and, when he does not stop to calculate it, he estimates his age to be 10 to 26 years less than it is. In 1982, he did not recognize a picture of himself that had been taken on his 40th birthday in 1966. Nevertheless, he has islands of remembering, such as knowing that an astronaut is someone who travels in outer space, that a public figure named Kennedy was assassinated, and that rock music is “that new kind of music we have.”

H. M.’s condition highlighted the different kinds of memory we possess, some of which were intact in him, while others had been obliterated. For starters, his short-term working memory was fine; he could retain a handful of numbers for tens of seconds. But surgery had scarred some forms of H. M.’s long-term memory.

His semantic memory—the ability to remember facts and concepts—was largely intact, but only for things that he had experienced before his surgery. Meanwhile, his episodic memory, which is the memory of an episode of experience and is linked to place and time, was ruined even for his pre-surgery days. Semantic and episodic memories are forms of long-term memory called declarative or explicit memory, which requires us to consciously access information. H. M.’s anterograde amnesia was so complete that he had no declarative memory for anything that happened after his surgery (though he did manage to remember the floor plan of the house he moved into after his surgery, and lived in from 1958 to 1974; gradual accumulation of knowledge over the years, aided no doubt by the fact that he physically inhabited and moved about in the same space for years, had somehow helped H. M. form a memory of where he lived—tantalizing evidence for the body’s place in forming the self in concert with the brain).

The other broad category of long-term memory is called implicit, nondeclarative, or procedural memory. This is memory that does not require conscious access. Think about knowing how to ride a bicycle. It’s memory that we access unconsciously. It was Milner’s classic study of H. M., published in 1962, that showed us that distinct brain structures are involved in these various types of memory. In this study, H. M. was shown two star-shaped patterns, one inside the other. He was asked to replicate the pattern by drawing between the lines of the outer and inner patterns. To complicate things further, H. M. had to draw while looking at the reflection of his hand, the pencil, and the patterns in a mirror. Amazingly, H. M. got better and better at the task over three days—while retaining absolutely no memory of having done the task. It was clear that the surgery had not messed up his procedural memory. The question was: what exactly were the brain
structures that had been removed by the surgery? The papers written by Scoville after he performed H. M.’s surgery in 1953 were extremely illustrative for their time, but weren’t the definitive word. In the 1990s and 2000s, H. M. underwent several brain scans, but they were, like all scans, noninvasive and hence somewhat limited in what they could precisely reveal about the excised brain regions. But more was revealed upon his death.

H. M. died on December 2, 2008. His body was transported to Mass General Hospital in Charlestown, Massachusetts, where neuroscientists spent nine hours imaging his brain. Later, a neuropathologist skillfully removed H. M.’s brain from his skull. All this led to a high-resolution 3-D model of H. M.’s brain, based on numerous fine-grained MRI scans. It was possible, finally, to dissect H. M.’s brain inside the computer. The new images confirmed what the earlier MRI scans had revealed:
the back half of H. M.’s hippocampus in both hemispheres—which Scoville thought he had fully removed—was intact. But Scoville had removed something else in its entirety: the entorhinal cortex—the interface between the hippocampus and the neocortex (the part of the cortex that’s unique to mammals). Alzheimer’s disease begins in the entorhinal cortex and spreads. According to the literature, “
It is the most heavily damaged of all cortical areas in Alzheimer’s disease.”

As for H. M., the “
unforgettable amnesiac,” he might have left no survivors, but he left behind an indelible mark on science. His profound amnesia sparked a debate over the question of whether he had a sense of self after his surgery. A similar question haunts those who are confronted with Alzheimer’s disease today.

When most of us think of the sense of self, we are thinking of the stories in our heads about who we are. If you had to tell a story about yourself to someone else (or even to yourself) you may have to delve into your album of episodic memories that defines you. Call it the narrative self (aspects of this selfhood would not just be cognitive, but embodied, as Pia Kontos emphasizes). A narrative, by definition, is a sequence of episodes strung together. In some sense, that’s what we are—a seemingly seamless narrative. As humans, we also have the ability to project this story into the future. Our narrative self, then, is not merely a remembered past but also an imagined future. Over the past decade, numerous studies have shown that
the same brain networks that are responsible for remembering past events are also recruited when constructing future scenarios. For example, if you are a good sailor, as Clare’s father was, you will use the same brain networks to remember last year’s sailing trip as for imagining navigating the seas a few years hence. Key brain regions that form these networks include structures in the medial temporal lobe (the parts closer to the midline), including the hippocampus and the entorhinal cortex. It’s these regions that are often first affected by Alzheimer’s disease; it’s here that the disease gains a foothold for its destructive march, eventually erasing a person’s ability to construct a coherent narrative self.

In some Alzheimer’s patients, this disruption of the narrative self manifests initially as anosognosia—not recognizing that you in fact have Alzheimer’s. Joseph Babinski coined the term “anosognosia” in 1914 (in Greek,
agnosia
means lack of knowledge and
nosos
means disease) to describe an extremely odd behavior in some of his patients whose entire left sides were paralyzed. In his influential paper he wrote, “
I want to draw attention to a mental disorder that I had the
opportunity to observe . . . which consists in the fact that patients seem unaware of or ignore the existence of their paralysis.” Babinski’s patients not only denied or were unaware of their paralysis, they also came up with rationalizations for their lack of knowledge. Babinski wrote about one patient, “
If she was asked to move her right arm, she immediately executed the command. If she was asked to move the left one, she stayed still, silent, and behaved as if the question had been put to somebody else.” A particularly severe form of anosognosia is seen in Anton’s syndrome (named after neuroscientist Gabriel Anton, 1858–1933), in which patients who have become blind because of damage to both sides of their occipital lobes insist that they can see.

Anosognosia in Alzheimer’s can range from mild unawareness to outright denial. Neuroscientist William Jagust, an expert on Alzheimer’s disease at the Lawrence Berkeley National Laboratory, has encountered the entire gamut of reactions during his years of clinical practice. “The spouse brings the patient to the doctor, and the patient says, ‘Nothing’s wrong with me, you are crazy,’ and they have fights and all that. . . . But more often, it’s that the patient doesn’t really notice [the disease], is unaware, rather than [in denial],” Jagust told me. Often, after intense meetings in which Jagust would tell the patient and the family about the diagnosis, the patient would soon forget the diagnosis. It’s in the nature of the disease. “After you tell them they have Alzheimer’s disease, they have to stop driving, they will want to drive. The family will say, ‘The doctor said you have Alzheimer’s disease’ and they say, ‘He didn’t say that!’”

Allan, too, didn’t want to give up driving. Before his formal diagnosis, he began having panic attacks while driving on freeways. So he stuck to local city driving, which still worried Michaele. She’d find unexplained dents on his car, even signs of being sideswiped by
another vehicle (Allan claimed the other driver was to blame, but Michaele suspected it was Allan’s fault). Allan once tried to cover up an accident by spray-painting a scraped fender. A social worker at Allan’s clinic warned Michaele that Allan could be sued if he got into an accident (by now he had been formally diagnosed). Allan’s doctor alerted the Department of Motor Vehicles, and the DMV sent Allan a letter, asking him to come in and redo his written and road tests. “Damn it if he didn’t pass the test,” said Michaele. “I couldn’t believe it.” Eventually, to her relief, Allan’s car was stolen and trashed by thieves. For Allan, it was a body blow. “He was very sad. He wrote a whole lament to his Honda on yellow paper, on just how much it meant to him, how the loss of his autonomy was a tragedy, that he wasn’t a whole person anymore,” Michaele told me. “It’s like his sense of self was eroding.”

Allan’s anosognosia was perhaps mild in comparison to the level of denial of those with paralysis. Nevertheless, Alzheimer’s is allowing us to understand the neural mechanisms behind anosognosia and its relationship to the sense of self. It’s these mechanisms that Giovanna Zamboni, a neurologist at Oxford University, is studying. In one of her studies, she found that Alzheimer’s patients with anosognosia were far better at judging traits of a close friend, caregiver, or relative than they were at judging themselves. The tasks, which were done inside an fMRI scanner, revealed that
the medial prefrontal cortex (MPFC) and the left anterior temporal lobe in Alzheimer’s patients were less active during self-appraisal than during tasks that required the appraisal of others (normal controls and those with mild cognitive impairment showed no such difference).

The tests reveal that anosognosia in Alzheimer’s is not just a problem of memory—it’s also a problem of self. “It reflects a very selective
inability of updating the information regarding you, but not regarding others,” Zamboni told me.

Robin Morris, a neuropsychologist at the Institute of Psychiatry at King’s College London, would agree. Morris thinks anosognosia in Alzheimer’s stems from a bigger problem than merely not remembering you have been diagnosed with the disease. We have, Morris argues, a special form of semantic memory that has to do with knowledge about ourselves—a self-representation system. This “personal database” is different from semantic knowledge about objects and facts about the world and other external things. “There is something particularly special about self-representation,” Morris said when we met at his office in London. He hypothesized that in Alzheimer’s, “people are not integrating new information into their self-representations.”

According to Morris, this self-representation is essentially episodic memory that has somehow been turned into semantic memory about oneself—it’s been semanticized, so to speak. Patient H. M. lends support to the idea that the essential meaning of our episodic memories is captured and stored in a semanticized form, separate from other episodic memories. When Suzanne Corkin asked H. M., “
What is your favorite memory that you have of your mother?” he replied, “Well I, that she’s just my mother.” As Corkin found out, even though H. M. had memories of his childhood, “H.M. was unable to supply an episodic memory of his mother or his father—he could not narrate even one event that occurred at a specific time and place.” Still, he had some sense of his pre-surgery self.