Dustin Thomason: 12.21

“Dr. Thane, was it you who came up with the idea of testing the amylase levels?” They had arrived on the sixth floor.

“Yeah. Why?”

“Putting FFI on the differential diagnosis list isn’t something most residents would’ve considered.”

Thane shrugged. “Saw a homeless guy in the ER this morning who’d eaten eight bags of banana chips to make his potassium so high that we’d have to admit him. Spend a little more time in East L.A. You’ll see we have to consider just about everything.”

Stanton noticed that every staff member smiled or nodded or waved at Thane as they approached the nerve center of the floor. The reception area looked as if it hadn’t been updated in decades, complete with ancient computers. Nurses and interns scribbled notes in fading plastic binders. Orderlies finished their rounds, clearing scratched trays from patients’ rooms.

A security guard was posted outside room 621. He was middle-aged, with dark skin and a crew cut, and wore a pink mask over his face.

“Everything all right in there?” Thane asked.

“He’s not moving too much right now,” the guard said, closing his book of crossword puzzles. “Couple of short outbursts, but for the most part pretty quiet.”

“This is Mariano,” Thane said. “Mariano, this is Dr. Stanton. He’ll be working the John Doe with us.”

Mariano’s dark-brown eyes, the only part of his face visible above the mask, were trained on Stanton. “He’s been flailing around for most of the past three days. Gets pretty loud in there. He’s still saying vooge vooge vooge over and over.”

“Saying what ?” Stanton asked.

“Sounds like vooge to me. Hell if I know what it means.”

“I typed it in on Google and got nothing that made sense in any language,” Thane said.

Mariano pulled the strings of his mask firmly behind his ears. “Hey, Doc, if you’re the expert, can I ask you a question about this?”

Stanton glanced at Thane. “Of course.”

“What this guy has,” the guard said. “It’s not contagious, is it?”

“No, don’t worry,” Stanton said, following Thane into the room.

“He’s got like six kids, I think,” Thane whispered once they were out of earshot. “He’s always talking about how he doesn’t want to pass on anything from here. I’ve never seen him without a mask.”

Stanton pulled a fresh mask from a dispenser on the wall and fastened it to his face. “We should be following his lead,” he said, handing another mask to Thane. “Insomnia compromises the immune system, so we have to avoid infecting John Doe with a cold or anything else he won’t be able to fight off. Everyone needs masks and gloves when they go in. Post a sign on the door.”

Stanton had seen worse patient rooms, but not in the United States. Room 621 contained two metal beds, cracked night tables, two orange chairs, and curtains with worn edges. Dispensers of Purell clung loosely to the wall, and there was water damage on the ceiling. Lying in the bed closest to the window was their John Doe: about five-foot-six, thin, with dark skin and long black hair that draped over his shoulders. His head was covered with tiny stickers, from which wires extended toward an EEG machine, measuring brain waves. The patient’s gown clung to him like damp tissue paper, and he was groaning softly.

The doctors watched the patient tossing and turning. Stanton noted John Doe’s eye movements, the strange, staccato breathing, and the involuntary tremor in his hands. In Austria, Stanton had treated a woman with FFI who’d had to be chained to her bed because her tremor was so bad. By that time, her children were overcome by grief and helplessness and by the knowledge they might someday die the same way. It had been hard to watch.

Thane bent down to flip the pillow beneath John Doe’s head. “How long can you live without sleeping?” she asked.

“Twenty days max of total insomnia,” Stanton said.

Even most doctors knew virtually nothing about sleep. Medical schools spent less than one day out of four years on it, and Stanton himself had learned what he knew only through his FFI cases. Part of it was that no one knew why humans needed sleep in the first place: Its function and importance were as mysterious as the existence of prions. Some experts believed sleep recharged the brain, assisted in the healing of wounds, and aided in metabolism. Some suggested it protected animals against the dangers of night or that sleep was an energy-conservation technique. But no one had ever been able to explain why not sleeping killed Stanton’s FFI patients.

Suddenly John Doe’s bloodshot eyes went wide. “Vooge, vooge, vooge!” he moaned, more loudly than before.

At the monitor, Stanton studied the patient’s brain activity like a musician looking at sheet music he’d played a thousand times. The four stages of normal sleep ran in ninety-minute cycles, each with characteristic patterns, and, as expected, there was no evidence of any of them. No stage-one or -two slow-wave sleep, no REM, nothing. The machine confirmed what Stanton already knew from instinct and experience: This was no meth addiction.

“Vooge, vooge, vooge!”

“So what do you think?” asked Thane.

Stanton met her eyes. “This could be the first case of FFI in U.S. history.”

Though she’d been proven right, Thane didn’t look satisfi ed. “He’s going to the hundredth floor, isn’t he?”

“Probably.”

“There’s nothing we can do for him?”

It was the question Stanton had been asking for a decade. Before prions were discovered, scientists believed that food-borne diseases came from bacteria, viruses, or fungi and replicated themselves with DNA or RNA. Yet prions had neither: They were made of pure protein and they “replicated” by causing other nearby proteins to mutate their shape as well. All of which meant that none of the conventional cures for bacteria or viruses worked on prions. Not antibiotics or antivirals or anything else.

“I read about pentosan and quinacrine,” Thane said. “What about those?”

“Quinacrine is toxic to the liver,” Stanton explained. “And we can’t get pentosan into the brain without doing even more damage.” There were some highly experimental treatments, he told her, but none that were ready for human testing and none that were FDA approved.

But there were ways they could make John Doe more comfortable before the inevitable happened. “Where are the temperature controls?” Stanton asked.

“They’re all central, down in the basement,” Thane said.

He scanned the wall, started pulling back curtains and moving furniture. “Call down there and tell them to turn up the air-conditioning on this floor. We need to get the temperature in this room down as low as it’ll go.”

“You’ll freeze every other patient on the floor.”

“That’s what blankets are for. Let’s get fresh sheets and gowns for him too. He’ll keep sweating through them, so tell the nurses we need new ones every hour.”

Thane hurried out, and Stanton flipped off all the lights and shut the door. He pulled the curtain over the window, preventing any outside light from spilling in, then picked up a towel and tossed it over the EEG monitor, extinguishing its light.

The thalamus—a tiny collection of neurons in the midsection of the brain—was the body’s “sleep shield.” When it was time for sleep, it shut off “waking” signals from the outside world, like noise and light. In every FFI patient he’d treated, Stanton had seen the horrific effects of destroying this part of the brain. Nothing could be shut off or even tamped down, making victims painfully sensitive to light and sound. So while working with Clara, his Austrian patient, Stanton learned to relieve her distress in a small way by turning her room into a kind of cave.