“I gotta come out of this again,” he’d say.
Henry spent the night in the hospital. The following day, August 25, somebody on the nursing staff shaved his head, then brought him to the operating room.
—
Just as he had done so many times before in the asylums, my grandfather injected a local anesthetic into his patient’s scalp, sliced an arc across the top of his head, and rolled the skin of his forehead down like a carpet. He then used his trephine drill to remove two silver-dollar-size plugs of bone, a scalpel to cut through the meninges that protected the cerebrum, and a flat brain spatula to lever up the frontal lobes, exposing the deeper structures beyond. He scanned the region visually, his eyes picking out the glistening pink outlines of the hippocampus, the amygdala, the uncus, the entorhinal cortex, trying to identify any obvious defects, any coarse or atrophied tissue, any scars or tumors or other defects that might be the source of Henry’s epilepsy. He saw nothing. Before proceeding further, he did something he didn’t normally do in the asylums: Under the direction of the electroencephalographer W. T. Liberson, he used a slender, forcepslike instrument to reach into the holes and apply tiny wire-trailing electrodes to a number of spots along the surface of Henry’s medial temporal lobes. He and the rest of his surgical team then waited while Liberson monitored the EEG readouts, making one last attempt to find a discrete epileptic focus. Liberson peered at the wavy lines on the scroll, looking for a telltale pattern, one that could point my grandfather toward a specific target in a specific hemisphere. He told my grandfather that once again he’d come up empty and had failed to find a focus.
Though the anesthetic ensured that Henry felt no pain, he was conscious, and throughout all the slicing and peeling and drilling, a symphony of unsettling and unfamiliar sensations had trickled through his blunted nervous system. When my grandfather leaned over to extract the electrodes, Henry had a direct view of his upside-down face, or at least the parts of his face that weren’t covered by his surgical mask and surgical bonnet and surgical loupes. Henry’s pupils contracted against the blinding light of the headlamp.
Maybe, at that moment, Henry told himself that this whole experience would all be worth it, that the frightening things that were happening to him would finally free him of epilepsy’s burden, would allow him at last to be fully present, fully alive, able to achieve his potential. Whatever Henry was thinking, though, it didn’t really matter at that point. He had said yes, had agreed to be operated upon, and whatever happened next was out of his control.
The same could not be said about my grandfather, who now had an important decision to make.
—
There was no focus.
This meant, of course, that there was no target, no specific place in Henry’s medial temporal lobes to attack, not even a hint of which hemisphere Henry’s seizures originated in.
If another neurosurgeon had been in my grandfather’s shoes that day, things might have turned out differently. Wilder Penfield, for example, would have conceded defeat. Penfield had clear rules of engagement in the operating room: If he couldn’t determine a focus either visually or through EEG, he wouldn’t make any lesions. In fact, even if the EEG hinted at the presence of an epileptic focus, but visual inspection of the brain revealed no abnormalities, Penfield made it a point to do nothing rather than make an excision that might do more harm than good. “The neurosurgeon,” Penfield once wrote, “must balance the chance of freeing his patients from seizures against the risks and functional losses that may be associated with ablation.” In that balancing act, Penfield always erred on the side of caution, and in Henry’s case, with no target, he would have decided not to proceed with the operation. He would have stitched Henry up, kept him a few days for observation, and sent him home with an apology and a refill of his prescriptions. He would have told him that there didn’t appear to be anything he could do for him surgically, at least not then, and not with the information they had.
My grandfather was not Wilder Penfield.
Standing there in his operating room, looking down at the wet expanse of Henry’s skull, glimpsing his exposed brain through the two trephine holes, my grandfather could have admitted defeat, could have ended the operation. This would have been the safest move. There was no chance Henry would be improved by following that course of inaction, but there was also no chance he would be hurt by it.
Alternately, he could have chosen to take one, and only one, of the paths ahead. He could have operated on Henry’s left hemisphere, or Henry’s right hemisphere, then withdrawn, patched him up, and seen what happened. He had no target, no specific evidence of an epileptic focus in either hemisphere, but maybe he would get lucky. This would be the surgical equivalent of a coin toss: If one hemisphere of Henry’s medial temporal lobes was the hidden source of his epilepsy, then that approach would have a 50 percent chance of eliminating it. It would be much riskier, of course, than doing nothing, but that might be viewed as a reasonable risk considering the severity of Henry’s condition. Also, by leaving the structures in one hemisphere intact, he would minimize the chance of destroying whatever the unknown functions of those structures were.
My grandfather chose a third option. He picked up his suction catheter, inserted it carefully into one of the trephine holes, and proceeded to suction out that hemisphere of Henry’s medial temporal lobes. His amygdala, his uncus, his entorhinal cortex. His hippocampus. A good portion of all of those mysterious structures disappeared into the vacuum. Then he pulled the tool out of the first hole, cleaned it off, and inserted it into the second. Lacking a specific target in a specific hemisphere of Henry’s medial temporal lobes, my grandfather had decided to destroy both.
This decision was the riskiest possible one for Henry. Whatever the functions of the medial temporal lobe structures were—and, again, nobody at the time had any idea what they did—my grandfather would be eliminating them. The risks to Henry were as inarguable as they were unimaginable.
The risks to my grandfather, on the other hand, were not.
At that moment, the riskiest possible option for his patient was the one with the most potential rewards for him. After years of straddling the line between medical practice and medical research in the back wards of asylums, of attempting to both cure insanity and gain an understanding of various brain structures, he was about to perform one of his medial temporal lobotomies on a man who was not mentally ill at all, whose only dysfunction was epilepsy. In the language of scientific research, Henry was a “normal,” or at least much closer to being a normal than anyone who’d previously received one of my grandfather’s limbic lobe operations. For four years, my grandfather had been conducting “a study of the limbic lobe in man,” and so far he had only “small bits of passing data” to show for it. That afternoon, however, my grandfather’s study was expanding to include a whole different class of research subject.
Imagine my grandfather peering into that second trephine hole, guiding his suction catheter deeper and deeper, his headlamp illuminating the intricate corrugations of the structures he was in the process of destroying. It’s impossible to say exactly what thoughts drove him at that moment, what stew of motives. He had reason to believe his operation might help alleviate Henry’s epilepsy. He also had reason to believe his operation might provide new insight into the functions of some of the most mysterious structures in the human brain. It’s quite possible that he wasn’t thinking much at all, at least not consciously. Years later, during a rare moment of introspection, he described himself as follows: “I prefer action to thought, which is why I am a surgeon. I like to see results.”
He pressed the trigger on the suction catheter, and the remaining hemisphere of Henry’s medial temporal lobes vanished into the vacuum.
—
As my grandfather made that final cut, Henry lay there, looking up at him. He could catch glimpses of his mask, of his surgical cap, of his headlamp. He could see his glasses, those thick-rimmed surgical loupes with th
eir magnifiying lenses. He could hear my grandfather’s breathing, feel his warm exhalations.
And maybe, just maybe, some sweat or blood or condensation accumulated on a lense of those glasses, and maybe my grandfather asked a nurse to reach over and wipe it clean. Maybe that sight, which would have been one of the last ones ever processed by Henry’s vanishing medial temporal lobes, somehow stuck with him, blurred and dreamlike and of indeterminate origin. Maybe that’s why, for the rest of his life, Henry would tell people that he’d once dreamed of being a brain surgeon but had decided against it, because he wore glasses, and what if his glasses got dirty and a nurse attempting to clean them knocked them askew, causing him to make the wrong move, to cut too far, to go too deep.
If so, that meant that Henry was mistaken about what he’d seen, just as he was mistaken when he told people that he believed something had gone wrong with his own operation, that his own surgeon, Scoville, had made a mistake, had made the wrong move, and that was why he was the way he was. Because even if my grandfather did get something on his glasses, and even if they were then knocked askew by a nurse, that had no impact on the way the operation played out.
My grandfather didn’t make any mistakes that day.
He took exactly what he wanted to from Henry.
—
He finished the operation.
He removed the tools.
He replaced the bone and stitched the flesh.
Six weeks later, he sent off a print version of his Harvey Cushing Society presentation to the Journal of Neurosurgery for publication. The paper contained one major addition to the remarks he’d made onstage back in April. His limbic lobe operations, he now wrote, had “resulted in no marked physiologic or behavioral changes, with the one exception of a very grave, recent memory loss, so severe as to prevent the patient from remembering the locations of the rooms in which he lives, the names of his close associates, or even the way to toilet or urinal.”
The italics were his, and that italicized clause transformed a forgettable, modest paper into one that will continue to be referenced for as long as we remain interested in how we hold on to the past. It became a cornerstone of the skyscraper that is modern memory science.
It was the birth announcement of Patient H.M.
It was also the obituary of Henry Molaison.
PART IV
DISCOVERY
TWENTY
WHERE ANGELS FEAR TO TREAD
“It’s terrible how things accrue.”
Those are the first words in the transcript of my first interview with Brenda Milner. When I read the transcript, I hear her voice, a crisp British accent, words tightly spaced, while a hazy picture of her office forms in my mind. That’s what she was referring to: her office, and the clutter in it, how it had accrued over the years. The stacks of papers, the overstuffed bookshelves, the boxes full of files. It was one of those offices where it must be a struggle each morning to clear space for the new day’s work. There were posters on the walls, and I think one of them had an animal on it, a National Geographic–style nature photo, though I can’t remember what type of animal it was. There was one framed photograph on her desk, near her computer: a headshot of my grandfather in his light green surgical scrubs.
Our interview took place in 2010, and by that time things had been accruing in Milner’s office for more than a half century. She was ninety-three years old, still a full professor at McGill, still teaching classes, still doing research, still living the messy, striving life of an active scientist.
Milner greeted me warmly. Somebody from McGill public relations accompanied me to her office, and before the interview began a photographer arrived and led us to another room, to take a quick shot of the two of us for a Montreal Neurological Institute newsletter. “Does he look like Scoville?” somebody asked Milner. She appraised me—I’m taller than my grandfather, with a bigger nose, closer-set eyes, and a lot less hair.
“No,” she said, “not really.”
I’d arrived in Montreal the night before and was disappointed to hear that I’d just missed a screening of the movie Memento that Milner had hosted for the McGill Film Society. Memento’s protagonist, an amnesic man attempting to solve a murder mystery, was inspired in part by Henry. I told Milner I liked the film, and she said she did, too, that in general it was one of the most realistic cinematic portrayals of amnesia she’d ever seen, even though, she pointed out, the script had bungled the definition of short-term memory. People like Henry and the man in Memento don’t have bad short-term memory, she said. On the contrary, short-term memory is all they have.
I remember Milner sitting there by her cluttered desk, a tiny woman in a woolen skirt.
“Now,” she said, “how can I help you?”
—
Until coming to the Neuro in 1950, Milner had not had a major interest in memory. She was deeply curious about the brain, of course, and all the mysterious ways its structure correlated with its functions. And she understood how lesion patients had contributed to our understanding of those functions: During her final examination in psychology at Cambridge University, as she sat in the historic Senate House, one of the questions asked for a summary of the current knowledge about the localization of function for sight and hearing and speech. That was in 1937, and though she doesn’t remember her precise answer, she imagines she would have written about Phineas Gage, Monsieur Tan, and all of those other fascinatingly broken men and women. She would have had no reason to mention memory, though. In 1937, the general consensus was the same as it would be more than a decade later, when Milner began working with Penfield’s patients: Memory was not associated with a particular structure in the brain but was instead distributed equally, equipotentially, across the whole cerebral landscape. According to that view, trying to find a seat of memory was the neurological equivalent of a snipe hunt: It didn’t exist. Milner’s own views on memory didn’t change much until she sat down with Patient P.B. and Patient F.C., those two men with their two unilateral medial temporal lobe lesions, and told them some stories, and asked them to repeat them back to her. When they looked at her blankly, when it was clear they weren’t retaining anything she told them, she realized that something significant was happening. She didn’t believe in the seat of memory, that is, until she found it.
But had she?
If removing the left hemispheres of the hippocampi of these two men had caused profound amnesia, which it clearly had, then it should have done the same to the other patients who had received the same operation, which it clearly hadn’t.
Milner and Penfield discussed that paradox at length. Eventually they arrived at some tentative conclusions.
Yes, Penfield had performed the same operation on the two amnesics that he’d performed on at least ninety other patients. And yes, the brains of those two patients, postoperatively, appeared to function very differently from the brains of the others who’d received the same lesions. And no, that didn’t make any sense. Unless the brains of the two amnesics had been different to begin with.
They concluded that the only reasonable explanation for such different results from the same procedure was that the medial temporal lobes of the two amnesics must have already been damaged prior to the operations. The hemispheres opposite to the hemispheres that Penfield targeted must have been dysfunctional. Perhaps this damage had taken place during birth, if tongs had been used to extract them from the womb, or maybe they’d suffered undetected strokes later in life. This would have meant that Penfield’s unilateral lesioning of their hippocampi would have been equivalent to bilateral lesioning. In effect, though Penfield had targeted only one hemisphere, he would have been destroying both.
If this turned out to be true, it meant that normal memory function depended on the hippocampus and other medial temporal lobe structures. Although Penfield and Milner both felt that they were on the verge of finally zeroing in on the seat of memory in the human brain, they also knew that they lacked proof. The brain imaging techno
logies of the day could not detect damage to the remaining hippocampi of the two amnesic patients. And even if Penfield had decided to reopen their skulls to look inside, the damage might not have been visible to the naked eye. To upend prevailing views of how memory worked would require more than just a hunch.
Were Penfield willing to test the theory by actually removing both hippocampi of a patient bilaterally and seeing what happened, he and Milner might have been able to obtain the evidence they needed. But Penfield would never do that. He was too wary of causing unnecessary harm. Despite having revolutionized the field of epilepsy surgery, he was fundamentally a conservative, cautious doctor. He viewed all novelty with skepticism. Psychosurgery, for example, appeared to him to be a technically interesting but therapeutically unsettling practice. In his long career Penfield had still never performed a lobotomy, and he sometimes obliquely criticized the doctors who did, making pronouncements about the “vainglory” of “young surgeons who have learned to use a scalpel so expertly that they can take anything out of anywhere without a fatality, to cut the pathways of the currents of intellect and leave a man who is still capable of walking.”
Penfield’s conservatism was both a boon to his patients and a barrier to progress. By the mid-1950s, several years had passed since Milner’s testing of Penfield’s first amnesic, and though they planned to write a paper based on these cases, they still hadn’t published their findings. Their data felt incomplete, their evidence too easy to dismiss. They were, in the scientific sense, stalled.
Then, during a neurosurgical conference in New Mexico in May 1954, Penfield ran into just the sort of young, ambitious, mechanically gifted psychosurgeon he often accused of vainglory. My grandfather and Penfield discussed their respective experiences operating on the medial temporal lobes. Despite the fact that these operations had mostly been done for very different reasons—my grandfather performed them almost exclusively on asylum patients, Penfield almost exclusively on epileptics—what they found interesting was not their differing motives but their similar results. Penfield told my grandfather about the amnesia he and Milner had documented in Patients P.B. and F.C. and about their hunch that the limbic region must therefore be crucial to memory. Penfield was repulsed by psychosurgery, but he was fascinated when my grandfather told him that he, too, had encountered cases of postoperative amnesia. Not only that, but the younger surgeon’s operations, unlike Penfield’s, had all targeted both hemispheres. When Penfield returned to Montreal he told Milner what he’d learned.
Patient H.M. Page 22