Hidden Valley Road: Inside the Mind of an American Family (20 page)

MARY HAD TRIED
to follow Margaret to the Kent School. When her seventh grade application was denied, she was furious.
I can’t get in to Kent?? My
sister
is at Kent. She didn’t even get Bs!

At the start of eighth grade, in 1978, Mary told her father that she wanted to go to boarding school. Don asked Sam Gary for advice. Sam asked Mary if a place like his alma mater, Hotchkiss, in Connecticut, might appeal to her. Technically, Sam had been kicked out of Hotchkiss, but all was forgiven now.

Mary didn’t hesitate. She’d already been doing whatever she could to stay out of the house. If she got into a celebrated, unimpeachably refined school two thousand miles away, there was a chance she might never have to come home again.

Mary applied to Andover, Exeter, Hotchkiss, and Taft. She got into them all. She chose Hotchkiss because it seemed like the prettiest, the one farthest away from a city. The Berkshires seemed like a reasonable substitute for the mountains of Colorado—the best that she could do.

Mary’s tuition was paid by a scholarship funded by another alumnus. The Garys picked up other costs, like transportation. After three years of looking for a way out, Mary had earned her ticket.

THIS NIGHT WOULD
be different. Mary knew it had to be.

She was thirteen years old. Jim was thirty-one, still married to Kathy, and still running the Manitou Incline. Behind the funicular station at the top of the hill was a musty cottage with a couple of old mattresses and sleeping bags. As the manager of the incline, Jim had unfettered use of this cottage. Sometimes, instead of hosting his younger brothers and sisters at home, he invited them there, at the top of the incline, where they could be alone.

This time, on a cool evening in the spring of 1979, Mary was there with Matt. Jim had invited them both to camp out and smoke pot and drink beer. When it got late, she fell asleep in one room of the cottage, the guys in the other. Matt was passed out, but the light was still on, so Mary pretended that she was asleep, just as she always did when she knew Jim would come to her—disassociating by pretending it wasn’t happening, at least not to her.

But she could not go through with it that night. Mary had gotten her period. She was more terrified of getting pregnant than she was of Jim’s fury at being refused.

For the first time, when Jim came over to her, she lost control, saying things she hadn’t expected to say.
Leave me alone. Get away from me. I hate you.

Jim attacked her anyway. He entered her, something he’d never accomplished with Mary’s sister. He came. And he never spoke to her about it after that. He avoided her altogether.

There were, of course, several weeks of terror that she might become pregnant. Once it became clear she wasn’t, Mary expected to feel relief. She’d done it: She’d fought him off, protected herself, made it so that he would never do it again. She was almost delirious with the thought of it.

But then, quite unexpectedly, part of her found Jim’s ability to disappear from her life to be utterly wrenching. She tried to ignore that feeling, but there was no mistaking it. She was heartbroken. Some part of her had truly believed, as a child does, that this was love.

SHE WAS ALMOST
free now. Jim was no longer in her life. Soon neither would Peter or Matt or Donald. Her future was her own. At the end of eighth grade, not long after she was accepted to Hotchkiss, Mary was invited to a high school party hosted by the older brother of a friend. She said yes right away.

Mary told her mother she was sleeping over at her friend’s house. She left out the part about the party. When she got there, the big brother was there, along with two other guys, drinking Seven and Sevens. She joined in.

The guys invited both girls out to a well-known make-out spot in town to drink some more. Her friend said no; she had to stay home to take care of her little sisters. But Mary said yes and got into a car with them. By the time they came back, Mary’s friend and her sisters were all asleep. Mary was so drunk she could barely stagger back inside.

The boys, seeking privacy, found a walk-in closet, opened the door, and directed Mary inside it. One at a time, they followed.

Mary woke up a few hours later with no idea of where she was. She opened the closet door and found her way to the living room. Daylight streamed through the windows. Mary shuddered. Her mother was supposed to pick her up. She stumbled outside and waited on the curb, holding her stomach, trying to sort out what had happened.

The plan had been for her mother to take her to a dentist appointment. “I can’t go,” Mary said, as soon as she got in the car. “I’m sick.” Mimi might have gathered that her daughter had been drinking—this was her twelfth teenager, after all—but she said nothing.

It was then, on the way back home, it all came flooding back—two boys taking turns, a third halfheartedly trying to stop them. Mary almost threw up all over herself. A fitting punishment, she thought at the time, for a girl who had been so bad. She had lied to her mother, and she had gotten drunk, and she had failed to run away.

Too clouded by shame to place the blame on anyone but herself, Mary told no one what happened. She figured everyone she knew would know sooner or later. She made herself a promise that day: Once she left for Hotchkiss, she would never live in Colorado Springs again.

No more teenage boys in closets.

No more Jim in the cottage, at the top of the Manitou Incline.

No more Donald or Matt or Peter or anyone but her and her alone.

It was still orientation. Too soon to be pigeonholed, she hoped. All she wanted was to be the last person anyone at Hotchkiss would ever think was unusual. Then a teacher she’d just met read her name tag and scowled.

“There is already a Mary Galvin at this school,” she said. “What’s your middle name?”

Mary did not answer right away. She knew that her name said more about her than she wanted anyone to know. Forget, for the moment, how being called Mary Christine had helped to make her, in her brother Donald’s eyes, the sacred virgin mother of Christ. Sitting there with all of those sons and daughters of privilege, feeling the East Coast WASP-iness of the place, Mary sensed that her Catholic name screamed
not one of us
.

In a flash, she thought of another name. Thomas Lindsey Blayney was her great-grandfather on her mother’s side. Lindsey was a scholar and an eminence for the family—the kindly and wise Don Galvin of his generation. Lindsey had remained in close touch, writing Don and Mimi and doting on his great-grandchildren.

Lindsey
seemed like a prep school name to Mary—a better name, a Hotchkiss name. She flubbed the spelling, a mistake that had the virtue of making the name all hers. She had to do something, to make some sort of gesture that would wipe away everything that had happened to her in the first thirteen years of her life.

“Lindsay,” Mary said.

And from that moment on, Lindsay was her name.

1979

University of Colorado Medical Center, Denver, Colorado

Robert Freedman and Lynn DeLisi never worked in the same lab or even the same research institution or hospital. They were just two of hundreds of researchers around the world who were investigating schizophrenia. Their specialties were different, too—two disparate approaches to the same problem. While DeLisi wanted to track down the genetic components of schizophrenia, Freedman was on the hunt for a physiological understanding of the illness. She wanted to learn where it came from; he wanted to learn how it worked.

Neither of them knew that their paths one day would merge in the study of one extraordinary family—and that what they would learn from that family would help them both unearth new knowledge about the disease.

While DeLisi’s path to a career in medicine was riddled with detours, Freedman’s had been more or less seamless. He graduated from Harvard in 1968, two years after DeLisi graduated from the University of Wisconsin, and entered Harvard Medical School right away. As an undergraduate, Freedman had been drawn to the idea that the human mind could synthesize its own, entirely separate reality. “It just seemed to me if there was ever a disease that was uniquely human and philosophical, it was having schizophrenia,” he said. At the same time, Freedman was fascinated by the physical body, particularly the workings of the central nervous system. After medical school, he directed his career toward the study of the brain, starting off with the belief that there must be a better way to learn why neuroleptic drugs like Thorazine did what they did.

Freedman understood from a new flurry of research that people with schizophrenia might have difficulty processing all the information sensed by the central nervous system in an efficient way. This “
vulnerability hypothesis”—
an update, or elaboration, of Irving Gottesman’s 1967 diathesis-stress hypothesis, introduced by a team of researchers from Harvard and Columbia in 1977—sought a middle ground between nature and nurture by suggesting that certain genetic traits directly compromised the brain’s sensory and information-processing functions, making the brain especially vulnerable to any number of environmental triggers. To these researchers, those triggers—anything from everyday heartbreak, to chronic poverty, to traumatic child abuse—didn’t cause schizophrenia as much as provide “
an opportunity for vulnerability to germinate into disorder.” And that vulnerability, many thought, was really an issue with “
sensory gating,” or the brain’s ability (or inability) to correctly process incoming information. A sensory gating disorder was the most common
explanation for the schizophrenia experienced by John Nash—the Nobel Laureate mathematician depicted in
A Beautiful Mind
—who was able to detect patterns no one else could, and yet also was prone to delusions and visions of beings who were out to get him. Both of those aspects of Nash’s personality were said to be products of the same hypersensitivity.

Neurons talk to one another through brain synapses, the junctions between nerve cells that are essential for sending messages through the central nervous system. Many researchers came to suspect that the John Nashes of the world weren’t able to prune their synapses in the same way as most people.
^*
Some people with schizophrenia, they thought, might become sensitive to distracting sounds and feel flooded by too much information—the way it sometimes seemed Peter Galvin felt, or Daniel Paul Schreber had back in 1894. Others might become hyper-reactive, guarded, even paranoid—like Donald Galvin, mysteriously inspired to move all the furniture out of the house on Hidden Valley Road. Still others might be unable to pick and choose what to focus on with any reliability and might become delusional—seeing hallucinations and hearing voices, like Jim Galvin.

Sensory gating was just a theory. But once Freedman came to the subject, in 1978, as a researcher at the University of Colorado Medical Center in Denver, he started to develop a deceptively simple method for measuring sensory gating—and, by extension, indirectly measuring the vulnerability of a brain to schizophrenia. Freedman realized that the other researchers who were studying sensory gating—measuring their test subjects’ reactions to various lights and sounds and such—were skipping right past an important part of the process. As a neurophysiologist, Freedman understood physical reflexes and their peculiar, even counterintuitive relationship with the brain. He knew there were neurons—brain cells—that ordered you to move your muscles, but also neurons that inhibited the movement of those same muscles. In order to walk, for example, your central nervous system needs both kinds of neurons, for action and inhibition. Otherwise, everyone would be falling down all over the place. Why wouldn’t it be the same, Freedman wondered, for thinking?

What if the problem with schizophrenia patients wasn’t that they lacked the ability to respond to so much stimuli, but that they lacked the ability
not
to? What if their brains weren’t overloaded, but lacked inhibition—forced to reckon with everything that was coming their way, every second of every day?

In 1979, working at his lab in Denver, a little more than an hour’s drive from the Galvin family’s home on Hidden Valley Road, Freedman developed a method of measuring inhibition that was painless for the patients: A small electrode was placed on the test subject’s scalp, and that electrode measured electrical activity in the form of waves. Bigger waves meant the brain was working harder to process information; smaller waves meant the brain was doing less. Freedman devised an experiment. He measured his test subjects’ reactions when they heard the same exact noise—a click—played twice, with just a short interval between them, usually half a second.

Any so-called “normal” brain, a brain without schizophrenia, recorded a large brain wave reacting to the first click, followed by a smaller wave reacting to the second click. The normal brain learns from what it perceives. It doesn’t have to start from zero if it hears the same thing twice. People with schizophrenia, however, couldn’t manage that. In test after test, conducted at Freedman’s lab in Denver, their brains showed two waves of equal size for the two clicks. It was as if they had to react all over again to the second click—even though they had just heard the same click a fraction of a second earlier.

The double-click test was not testing for schizophrenia itself. It was testing sensory gating, which was one potential aspect of schizophrenia. What made this result so exciting was that a sensory gating deficiency might well be genetic—and therefore could be traced through generations. Freedman felt as if he were on the cusp of a major breakthrough not just in understanding schizophrenia, but in treating it: What if he could isolate the gene irregularity that caused people to react this way to the double-click test? If he could do that, and if those people were indeed diagnosed with schizophrenia, then he would have proven the existence of a gene related to the illness and opened the door to a genetic remedy.

No one had ever done such a thing, though many dreamed of doing it. This was a common enough strategy for other diseases: With diabetes, for instance, there may be ten or twenty different genes in play, but the first generation of medicine treating diabetes targeted just one of those genes.

All it would take, Freedman thought, was the identification of one gene. What might help him in that search, he thought, was a large group—a family—with an extraordinarily large incidence of schizophrenia.

Where Freedman would find such a family, he had no idea. But they were out there somewhere. Probably closer than he thought.