The Woman Who Saw Zombies
Discovering the molecule that drove her madness.
By Sara M Peskin M.D. published March 8, 2022 - last reviewed on April 25, 2022
In the spring of 2016, Lauren Kane graduated from an elite college and moved back to her mother’s house to apply for graduate school in creative writing. She read for pleasure, savoring the unstructured, almost endless days.
Then, on a humid morning that summer, something went wrong in Lauren’s brain.
She woke up early and went downstairs, where her mother poured her a mug of coffee. Sausage and eggs hissed from the frying pan. The women settled into the barstools at their tall kitchen table and ate breakfast over small talk, neither aware that it would be the last normal conversation they would have with each other for months.
After eating, Lauren returned to her bedroom and fell asleep.
“What’s for breakfast?” she asked her mother an hour later.
“We already ate,” her mother replied. She considered the strangeness of her daughter’s comment, then let the concern slip from her mind; time had become irrelevant without the didactics and deadlines of college courses. Lauren had been engrossed in The Walking Dead, a post-apocalyptic zombie horror show that she watched episode after episode, like chain-smoking.
Lauren went to sleep again, then woke up midday. “What’s for breakfast?” she asked.
By early evening, her forehead was warm and her steps were unsteady. She stumbled in the carpeted hallway. Descending the stairs, she gripped the banister so tightly that her fingertips turned white. Frightened, her mother helped her to the car and drove her to the hospital.
Sitting in the emergency room, Lauren recognized she was surrounded by nurses and doctors but could not remember why they had come. “Mom, what happened that we had to take you to the hospital?” she asked, not realizing that she was the one on the gurney. “I’m losing time,” she repeated every few minutes, as if the statement was novel each time. “Do you think this could be a virus in my head?” she asked her mother.
The curtain opened and a scrubs-clad doctor came in. “What year is it?” he asked. Lauren answered correctly.
“What state do you live in?”
“Can you count backward from one hundred?”
Suddenly, as if occupied by a spirit, Lauren reached for the doctor’s chest and gripped his shirt. She thrust him across the room, then dug her fingernails into the arm of a startled nurse. Her mother moved to calm her, but Lauren pushed her to the floor. The beat of footsteps echoed across the emergency department as nine security guards rushed like a tidal wave toward the room. They burst in loudly, each draping himself on one part of Lauren’s body or another.
“Don’t you see it, she’s a walker,” Lauren yelled, pointing at one of the guards. An announcement rang out overhead, calling for reinforcements.
“Is she on PCP?” one guard yelled to Lauren’s mother, who was still struggling to stand up from the floor.
“Oh my god,” said another guard, placing Lauren’s words into context. “She thinks she’s in The Walking Dead.”
Subdued with sedatives, Lauren was admitted to the hospital’s neurology ward, where she became increasingly unpredictable. At times, she seethed with aggression. At other moments, she was calm but confused. She drifted in and out of the world of The Walking Dead, mistaking hospital staff, friends, and family for characters from the show. Occasionally, there were lucid moments. She would recognize her mother and talk of feeling worried about her. She would remember that her cat had died recently and start to cry. But within a few hours, the confusion would invariably set in again.
Days passed with little progress toward making a diagnosis. Lauren’s doctors tested her for seizures, strokes, and infections. Everything was negative. According to blood tests and brain scans, she was normal.
Lauren’s mother began recording their conversations, hoping the audio files might yield a diagnosis. She captured the snippets on her phone and gave the collection the bland title “Lauren Hospital Audio 2016.” In one clip, labeled “Feeding Time; Zombie Apocalypse,” she captured her efforts to nourish Lauren:
“Want some more melon?” she asked.
“Look for supplies, or look for families or friends we used to know,” Lauren said. She spoke quickly, like a film being played at double speed.
“You mean because of the zombie apocalypse?” Lauren’s mother asked, having learned that it was better to meet her daughter in the fictional world than to try to convince her that she had lost hold of reality.
“Yeah,” Lauren confirmed.
“OK, well, let’s have some fruit first.”
“I can hear them.”
“Who are they?”
“OK, well, it was nice to meet you, Rick,” Lauren said after a delay, calling her mother by the name of a character in The Walking Dead. “I guess I’m just going to run out and try to shoot shit. I’ve got to go because I got some walkers that are stuck to my arm. Nice seeing you.”
“It was nice seeing you, too.”
“There’s so many of them attached to me now. It’s hard for me to move.”
“So many of what—the walkers?” her mother asked. “They’re kind of restricting your movement?”
“Yeah.” A rustling ensued.
“Where are you going?”
“I’m pushing it out of the way. I’ll try not to lose my supplies.” Lauren paused. “Apparently my legs are tied to the—” her voice trailed off. Then, with more curiosity than fright, she remarked, “That’s so weird.”
As Lauren’s hospitalization stretched into a second week, her mother adopted the signature behavior of parents of children with unsolved diseases. When a doctor walked into the room each morning, she would be ready with a notebook of lined paper. She would jot down bits of what the physician said, asking for the spelling of unruly words like e-n-c-e-p-h-a-l-i-t-i-s—inflammation of the brain—and l-e-u-k-o-c-y-t-o-s-i-s, a flood of white cells. She would underline words she thought were important, making sure to look them up when the doctor left.
As Lauren’s world morphed into that of The Walking Dead, her mother’s universe narrowed to Lauren’s nine-foot-by-nine-foot hospital room. A plastic chair that had been crammed into the space became her official place in the world. Day and night, she kept watch over her daughter, hoping one of the always answerless doctors would burst into the room and announce the reason for Lauren’s illness.
The dramatic moment never happened. Increasingly discouraged, Lauren’s mother began looking for a diagnosis on the internet. She found an article about diseases that happen when the body creates a protein that attacks the brain. According to the article, there were several culprit proteins, each of which caused a particular constellation of symptoms. Some caused seizures. Others caused stiffness. One of the proteins—the first of its kind to be discovered—caused young women to have sudden bouts of psychosis. “That’s exactly it,” she thought, bookmarking the page to show the doctor the next day.
Before Lauren’s mother found the article, a guard in the emergency room had come closest to diagnosing the cause of her ills. As Lauren fought off imaginary zombies, the guard—who had seen many patients high on a variety of illicit drugs—asked if Lauren had used PCP(phenylcyclohexyl). Lauren had not, but her body had created a protein that had the same effect.
PCP was synthesized in the 1950s to solve a surgical problem. Until then, the only way to sedate patients for most surgeries was to administer general anesthesia. Doctors would wheel patients into the operating room and induce a coma with anesthetics that had the unfortunate side effect of stopping the natural drive to breathe. Quickly, a doctor would thread a hollow tube down a patient’s throat and begin delivering bursts of oxygen while a surgeon performed the operation—removing an appendix, fixing a hernia, or something else. Then, if everything went as planned, the sedating medications would wear off, a doctor would remove the breathing tube, and the patient would once again breathe independently.
Anesthesia was a minor nuisance for the young and healthy but could cause problems for the elderly, obese, and sickly—the people most likely to require surgery in the first place. Some patients took days to breathe on their own after sedatives wore off. Others became dependent on the breathing tube for life. Still, others died on the operating table as doctors failed to pinch-hit for the heart-and-lung system. Sometimes sedation was so risky that patients were deemed to be ineligible for surgery, not because the cutting and sewing was dangerous in itself, but because the anesthesia was likely to kill them.
In the 1950s, chemists at a drug company in Detroit began looking for a solution. They collected molecules they thought could be useful for sedating people, then set out to modify each compound and observe the effects. They added and subtracted carbon, hydrogen, and oxygen atoms. They stirred ingredients together, dried them under a vacuum, heated them, cooled them, and filtered them. Finally, they infused the modified substances into laboratory mice, cats, hamsters, dogs, and fish.
One of the molecules they synthesized, named PCP, caused an effect scientists had never observed before: it sedated the animals long enough to perform surgery, but it did not stop them from breathing on their own. After receiving an intravenous dose of PCP, the animals would fall unconscious. Scientists could then transfer pieces of skin, break bones, and even remove a stomach or gallbladder, all while their subjects continued to breathe on their own. When the anesthetic wore off, the animals would wake up and go about their usual laboratory activities.
Seeing what PCP could do, one scientist at the company called it, “the most unique compound he had ever examined.” With PCP, the scientists imagined, breathing tubes might become obsolete.
Triumphantly, the company marketed PCP as Sernyl, to evoke the serenity patients would feel while surgeons did their work. After small trials in humans, the drug gained approval from the Federal Drug Administration (FDA) in 1963. Shipments of the white powder made their way to hospitals across the country. Then—much to the company’s disappointment—tales of startling side effects made their way right back.
Within months of the drug’s release, stories of Sernyl-induced hallucinations proliferated. Some patients felt they were floating in outer space without arms or legs. A third of patients experienced confusion and agitation as the drug wore off. Doctors described “maniacal excitement” as patients became “noisy and abusive.” People who had no predilection for violence became physically threatening to hospital staff and family members. While the best anesthetics wore off quickly, PCP stayed in the body for up to two days, yielding a trippy and prolonged recovery from operations. The purported miracle drug soon became one of the biggest failures in anesthetic history, and Sernyl became illegal in 1965—two years after it received approval from the FDA.
PCP intoxicates by causing the limbic system, which processes emotions, to function independently from perceptions of the outside world. It causes people to dissociate. Feelings that would normally be kept in check by reality instead become a part of it. Aggression bursts forth, unmitigated, from deep inside the brain. Fragmented memories, often scary and strange, feel convincingly real. At the same time, information about the outside world is muted. Neurons are meant to warn the brain when a body part is in pain instead fall quiet, sometimes permitting violent acts of self-mutilation.
At a molecular level, PCP disables a protein that floats at the outer edges of our neurons. The protein—called the NMDA receptor—has a remarkable job: it senses the environment, determines what is relevant, and then either opens or closes a tunnel between the neuron and the rest of the brain. In the process, the receptor helps us to gather information from our surroundings, to sort out what is salient, and to learn from experience.
When the tunnel in the NMDA receptor is open, connections between our neurons flourish and allow us to grasp new information. We become teachable. But the tunnel is a volatile structure. Open too long, and we can suffer relentless seizures, the product of neurons that are too interconnected for our own good. Open too little, and we can find ourselves in the grip of amnesia, dissociated from reality, or even comatose.
PCP works by sticking to the NMDA receptor and preventing the tunnel from opening. This is precisely why Sernyl was such an effective anesthetic; patients who received it stopped paying attention to the operating room around them. They could no longer learn that a scalpel was painful. They could not internalize the cutting and tugging of flesh. In the meantime, unbeknownst to anesthesiologists, the patients had been at the mercy of whatever reality sprouted from their minds—however violent and explosive that alternative experience was. “The profundity of PCP,” writes Marc Lewis, an ex-drug addict–cum–neuroscientist, “lies in the embellishment of the self.” With PCP, users inhabit only their own minds. Nothing else seems relevant.
Lauren Kane had not used PCP, but her body had created a protein—an antibody—that caused the same effect. The antibody stuck to her NMDA receptors and prevented the tunnels from opening. As a result, she was launched into the same dissociated reality that PCP users experience, with one notable exception: the effect of PCP wears off within a few days, but Lauren’s intoxication lasted for months. With her body chronically producing a supply of the offending antibodies, it was, molecularly speaking, as if she were hooked up to an intravenous drip of PCP.
Scientists now know that Lauren was afflicted with an autoimmune disease called anti-NMDA receptor encephalitis. The disorder, identified just a decade before Lauren became ill, is one of several conditions in which the human immune system makes antibodies that attack the brain.
Our immune systems have been honed for millions of years to prevent the condition that took hold of Lauren. The average person makes 10 billion distinct antibodies, each acting like an assassin with a particular molecular target. We make the antibodies prophylactically throughout our lives, before we are aware of what threats we will encounter. Lying in wait, the antibodies circulate in our blood and rest in our lymph nodes. Most antibodies will go unused; we do not come into contact with a molecule that sticks to them. But some antibodies will encounter a target that attaches to them perfectly, like a puzzle piece finally reunited with its neighbor. When a match is made between antibody and invader, the body sounds a cellular alarm, calling immune cells into action.
There is one ground rule that is essential for this process to happen: an antibody that targets a molecule native to the human body must be obliterated. We want antibodies to fight the enemy but leave our own cells alone. Since antibodies are produced by a random process, those that bind to native human molecules inevitably arise from time to time in all of us. In most cases—through mechanisms still incompletely understood—our bodies get rid of these self-targeting antibodies without our even noticing.
But sometimes this quality-control measure fails. Antibodies that put our own cells in the crosshairs are allowed to proliferate. When they stick to molecules that are critical to the brain, catastrophe ensues.
This is precisely what happened to Lauren. At some point in the months before she became sick, she had unknowingly developed a small tumor on her right ovary. The tumor contained many different types of cells, including neuron-like cells with NMDA receptors. Mistaking the receptors for something harmful, Lauren’s immune system produced millions of antibodies that stuck to the receptors and marked them for destruction. In response, her neurons began to gobble up their own NMDA receptors, leaving fewer of them for her mind to survive on.
Instead of protecting Lauren, antibodies had caused her downfall. Scenes from The Walking Dead and thoughts of her cat’s death—both memories from recent months—emerged in a distorted form and hijacked her reality. Fluorescent lights, white-coated doctors, and incessant recordings of blood pressures all failed to convince her that she was in the hospital.
Lauren’s mother, who had found a story about NMDA receptor antibodies on the internet, asked her daughter’s doctors to check for an autoimmune etiology for her illness. The request went unfulfilled. “It was as if they were saying, ‘You’re a mother, go away,’ ” she later recalled.
The rejection only made her more persistent. “If you won’t do it, send us someplace that will,” she said to the doctors. Bereft of diagnoses, the physicians acquiesced.
An ambulance took Lauren to a larger hospital, where results soon confirmed that her mother was right. Lauren’s brain was under siege by an antibody that attacked her NMDA receptors. An ultrasound showed the source of her ills, exposing the ovarian tumor that had probably been growing for months.
As soon as the abnormal test result appeared in red numbers on Lauren’s electronic chart, treatments began. Doctors prescribed high-dose steroids to quiet her immune system. Another medication helped her destroy the cells that made antibodies. A third medication served as a decoy, distracting her white blood cells so they spent less energy attacking her brain. Finally, surgeons addressed the origin of her ills; they took her to the operating room and removed the tumor from her ovary.
Days later, Lauren became reacquainted with reality. “What the hell is going on here?” she asked her mother. She looked at a whiteboard on the wall, where nurses had written and erased the date for weeks without her noticing. It was October. She had no memory of the prior two months.
There were setbacks on the way to recovery. Even after treatment, Lauren’s heart rate became unstable, at times soaring dangerously high, and at other moments falling so low that doctors worried the beating would stop altogether. She still had moments of confusion, partly because it took time to rid her body of toxic antibodies, but also because long stays in the hospital can themselves inflict fluctuating cycles of disorientation. She had not been outside in weeks. Aside from the small window in her room, there were few cues for when day turned to night and then back again.
In December of 2016, three months after her mother took her to the local emergency room, Lauren left the hospital for a rehabilitation center. Having spent so much time in bed, her muscles had weakened. She needed to do physical therapy to relearn how to walk. She had to develop tricks to keep facts planted in her mind. Her memory had improved, but it was not yet normal. It would happen at some point, doctors said—the quick-witted, academically savvy Lauren would return—but it would take months of medications and years of practice. What’s more, her disease could come back at any moment; one in five people with antibodies against NMDA receptors will suffer a relapse.
In 2020, one of Lauren’s short stories was selected for a national fiction contest—her first paid publication. She was considering writing a book. “I still don’t have any memories of that time,” she recalled of her hospitalization. “But I’m actually relieved about that. Based on things I’ve heard, I’m much happier not remembering any of it.”
In any other decade, before the molecular cause of her disease was discovered, Lauren would have been admitted to a psychiatric ward at the start of her symptoms. Doctors would have remarked that she was precisely the right age for a first psychotic break. They would have sent her home with prescriptions for antipsychotics, instructing her mother to retrieve the pills from a local pharmacy and to never miss a dose. Drugs would have failed to cure Lauren’s symptoms since they would not have treated the underlying cause of her disease. Antibodies against her NMDA receptors would have continued to surge in her brain, dominating her personality and erasing a woman who had accomplished so much.
Scientists now know that Lauren’s disease is one of several conditions in which the human immune system makes antibodies that attack the brain. The list of similar afflictions grows every year as new syndromes are identified and new antibodies are discovered in laboratories across the world. People who would previously have been untreatable—and even undiagnosable—have now become curable. Like Lauren, their minds and lives are saved.
* Name has been changed.
Sara Manning Peskin, M.D., is a professor at the University of Pennsylvania and author of A Molecule Away From Madness.
Reprinted from A Molecule Away From Madness by Sara Manning Peskin. Copyright © 2022 by Sarah Manning Peskin. With permission of W. W. Norton & Company, Inc. All rights reserved.
Submit your response to this story to email@example.com. If you would like us to consider your letter for publication, please include your name, city, and state. Letters may be edited for length and clarity.
Pick up a copy of Psychology Today on newsstands now or subscribe to read the rest of the latest issue.