Henry Gustave Molaison knew that he knew Suzanne Corkin. But he couldn’t know how.
Molaison had been visiting Corkin’s Massachusetts Institute of Technology lab for decades, often staying for a week or more. But the patient long known to the world as H.M. had been amnesic since a doctor removed portions of his brain in 1953 in an experimental surgery to treat severe seizures.
Molaison came to see Corkin as familiar. When prompted with her first name, he would remember her last. He called her “Doctress.” He fit her into his perception not as a researcher but as a former schoolmate.
“That’s where he put me,” Corkin said during an interview last week.
Corkin, emeritus professor of neuroscience at Massachusetts Institute of Technology, has just released a book about Molaison and the decades she and others spent defining what was lost or preserved after his surgery. Much of the book reads like a case study, detailing the various tests performed with Molaison and the parallel history of brain research. But it also provides a peek into the life of one of the world’s most famous research subjects.
“It’s a funny thing,” he told one researcher about this testing experience, Corkin recounted in the book. “You just live and learn. I’m living, and you’re learning.”
Molaison died in 2008 of respiratory failure. I spoke with Corkin a bit about his life and the impetus for the book, “Permanent Present Tense.” Our conversation, edited for length and clarity:
The book makes clear how concretely researchers viewed the brain at the time of Molaison’s surgery. Could you briefly describe what scientists understood then and how they see it now?
Before Henry, we didn’t understand that memory, the establishment of long-term memory was localized to a particular part of the brain. Obviously people going back centuries have observed that when something happens to your head, or something inside your head, the results could be very bad memory. There was never any strong evidence linking amnesia with a specific brain area. It was actually Henry’s case that clinched the deal, that clinched the association.
Now, the idea is to be reductionistic, to reduce our idea of how memory is formed at the cellular and molecular level. That’s really where neuroscience is now—researchers are working out the cellular and molecular mechanism of learning and consolidation and storage.
What is there left to learn from Molaison?
We want to know the precise limits of his lesion. We had high resolution MRI scans done when he was alive. Then, the night he died we scanned his brain for 9 hours. What we got then was a very clear picture of Henry’s brain.
We learned more about the characteristics of his lesion, but section by section. You could see how the dimensions changed front to back. Now we have the real thing to look at. Now we can define his lesion precisely, to help us pinpoint the underpinnings of what he could not learn after his lesion. The other thing that we can learn is about the telephone lines in his brain, the white matter. Looking at white matter is important because this tells us about the efficiency of neurotransmission.
There are a lot of things to look at and of course there are many neuroscientists that have their sort of favorite brain area. There are loads of people who are just dying to get their hands on this. The brain will be in a brain bank and we have a committee to review protocols and get the tissue sent out to people who have a good experiment in mind, a good question to answer.
You write toward the end of the book about keeping your distance from Henry to maintain your perspective as a researcher. Now that Henry is gone and the book is written, how do you see that Henry and this research shaped your life?
Henry and I became friends, and it happened quite naturally. He was a nice person, he was pleasant to interact with, and over the years he became part of my lab family.
But beyond that, Henry and I had a lot in common. I also grew up in the Hartford area. When he talked to me about his childhood, I recognized the names of the streets, the buildings, the parks he went to. I was born in the hospital where Henry had his operation.
We were sort of neighbors, but not really. We were sort of mental neighbors. But I also felt sorry for him.
Henry got a raw deal, and I wanted to help him make the best of a life that he was stuck with. I kept in close contact with his nursing home, and I saw to it that his medical needs were met. In addition to that, my lab sent him gifts for his birthday and Christmas. We sent him pictures of us and our dogs to put on his bulletin board, because the other patients [in his nursing home] had pictures to put on their bulletin boards.
He became demented around 2004. When I saw him in September of 2008, he couldn’t walk because of osteoporosis. I was visiting that day with a neurologist who did a neurologic exam. Henry was mute. He was basically sitting there not talking. I wanted to see if he was responsive at all. I stood on the right side, I bent down at eye level. I said, ‘Hi, Henry. It’s your friend from East Hartford High School.’ He kind of gave a faint smile. And I smiled back at him.
Why write this book now?
Years ago, off and on, people would invite me to give talks about H.M., and so I would. After the talk, there was always a Q&A. It would spill over into the hall afterward. People would keep asking me questions. Then I would get e-mails from people from all over the world. He really has captured the interest and imagination of thousands of people. They want to know about the science and about his everyday life.Chelsea Conaboy can be reached at email@example.com. Follow her on Twitter @cconaboy.