Fear, it seems at first, should be easy to identify and define. To borrow from that old judicial decision about the definition of obscenity: we know it when we feel it.
Putting that feeling into words can be harder. G. Stanley Hall, the nineteenth-century founder of the American Journal of Psychology and the first president of the American Psychological Association, described fear as “the anticipation of pain,” and that seems like a pretty good general definition to me. Fear of violence? Anticipatory pain. Fear of a breakup, the loss of someone you love? Anticipatory pain. Fear of sharks, of plane crashes, of falling off a cliff? Check, check, and check.
But what we need, really, isn’t just a solid catch-all definition. What we need, to understand the role of fear in our lives, is to examine the layers and varieties of fears that can afflict us.
There’s the sharp jab of alarm when you sense a clear, imminent threat: That car is going to hit me. There’s the duller, more dispersed foreboding, the feeling of malaise whose source you can’t quite pinpoint: Something is wrong here. I don’t feel safe. There are spiralling, sprawling existential fears: I am going to flunk this exam, tank this interview, fail at life. And there are precise, even banal, ones: Pulling this Band-Aid off is going to hurt. How do they all fit together? Or, put differently, to what extent does each stand apart?
According to Greek mythology, Ares, the god of war, had two sons, who accompanied him into battle: Phobos, the god of fear, and Deimos, the god of dread. That seems like a useful distinction to start with—fear versus dread—and it’s one that’s echoed today by our distinction between fear and anxiety. Fear, generally speaking, is regarded as being prompted by a clear and present threat: you sense danger and you feel afraid. Anxiety, on the other hand, is born from less tangible concerns: it can feel like fear but without a clear cause. Simple enough, at least in theory.
In Fear: A Cultural History, author Joanna Bourke gamely attempts to parse the distinctions between fear and anxiety. “In one case a frightening person or dangerous object can be identified: the flames searing patterns on the ceiling, the hydrogen bomb, the terrorist,” she writes. Whereas “more often, anxiety overwhelms us from some source ‘within’: there is an irrational panic about venturing outside, a dread of failure, a premonition of doom…. Anxiety is described as a more generalized state, while fear is more specific and immediate. The ‘danger object’ seems to be in front of us in fear states, while in anxiety states the individual is not consciously aware of what endangers him or her.”
But as Bourke points out, that distinction has serious limitations. It’s entirely dependent on the ability of the fearful person to identify the threat. Is it legitimately, immediately dangerous? Or is the fear abstract, “irrational”? She offers the hydrogen bomb and the terrorist as examples of potentially clear and present threats, but both can also serve as anxiety-inducing spectres, ominous even when absent.
Consider my meltdown on that ice-climbing trip. I was convinced, utterly convinced, that the frozen creek represented a legitimate and potentially lethal threat to my safety. And sure, one could theoretically slide down a frozen creek to one’s death, right? An ice-covered mountain isn’t the world’s safest environment, and that’s objective fact. But in context, on that sunny but cold afternoon, was my fear—my fierce conviction, my paralyzed reaction, my refusal to move—a reasonable reply to an immediate threat? It very clearly was not.
The distinction between fear and anxiety, then, can be murky, even as it can also be a useful and even necessary line to draw. Many of the fear episodes discussed in this book might also be described as containing at least some elements of anxiety.
Then, setting the issue of a threat’s clear presence aside, there’s the matter of our “fear” response.
The scientists who study our emotional lives make distinctions between different categories of feelings. There are the primary emotions, our most basic and near-universal responses, found across cultures and even appearing, or at least seeming to us to appear, in other species: fear, anger, disgust, surprise, sadness, and happiness. Think of them like primary colours, the foundational elements of a whole rainbow of emotion. Just as red and blue in combination can be used to create all the shades of purple, you can imagine some more precise feelings as being built by the primary emotions. Horror, for instance, is fear mixed with disgust—and, maybe, some shadings of anger and surprise. Delight could be happiness with a bit of surprise stirred in. And so on.
There are also the social emotions, the feelings that don’t stand alone like the primary emotions but are generated by our relationships to others: sympathy, embarrassment, shame, guilt, pride, jealousy, envy, gratitude, admiration, contempt, and more.
Of all these, fear is perhaps the most studied. But what does it really mean to study fear? What do we even mean, exactly, when we say “fear” in the context of scientific research? That’s a more complicated question than you might expect.
Traditionally, scientists have studied “fear” in animals by measuring their reactions to threatening or unpleasant stimuli—a rat’s freezing response when it is subjected to a small electric shock, for instance. In studying humans, scientists have more options and a broader array of tools. Most importantly, humans can self-report, verbally or in writing: Yes, I felt afraid.
The complicating factor is that those two responses—the freezing and the feeling—are separate and distinct. As the neuroscientist Joseph LeDoux, an expert on the brain circuitry of fear, emphasizes in his book Anxious, we know that the physical fear response and the emotional feeling of fear are produced by two different mechanisms in the body.
My interest is in both the physical fear response and the feeling.
One night when I was eleven or twelve years old, I had a terrible nightmare. The dream, as I remember it, was like a film shot in grainy black and white: I was in the ground-floor apartment that I shared with my mom, and, somehow, I knew that we were not alone. There were intruders in the house, though I couldn’t see them, only the apartment’s dim, grey hallways, the candelabras silhouetted on the walls. I knew that the intruders meant to kill us.
I woke up in my bed with the dream unfinished, my mind still filled with dread. I got up, walked across the hall to my mom’s room to climb in with her, and fell back to sleep.
A couple of hours later, I was ripped awake again by a tearing, stabbing, burning pain in my left knee. I woke up screaming, convinced that someone was putting my leg through a meat grinder. I only had a moment to understand that my leg was fine, that the pain was in my mind, and to register my mom’s fear and confusion, before I began to convulse. My legs and arms thrashed wildly, my spine arced and released, arced and released. It felt weirdly rhythmic; my body was throwing a party that my mind had not been invited to. Somehow I wound up on my stomach, and I can still so clearly remember the feeling of my neck jerking my head back and then forward again, over and over. I kept trying to scream but always wound up with a mouthful of pillow.
I faded in and out of consciousness for that first seizure, but at some point—after thirty seconds, maybe, or a minute at most, though it felt far longer—I became aware that the convulsions had stopped.
I seized twice more before I received a formal diagnosis of epilepsy. The next two came in the same night, one after the other, with the same pattern: the primal scream that woke my mom in the next room, the convulsions, and then a brief, lucid paralysis after my body had stopped heaving. Slowly, slowly, while my mom hovered over me, I was able to open my eyes again, and then move my lips, my fingers, my hands, my legs. I was conscious for the third one, the shorter of the two, and out cold for the second. My mom told me about that one after I came to.
Eventually a neurologist explained what I had experienced. The stabbing pain had been what epileptics call an “aura,” a sort of sensory warning shot from the brain before it all goes haywire. An aura could be a burst of light or colours, or a sound, or a sudden smell, like burning toast. Mine happened to be excruciating, but that had its uses: my screams meant that there would always be an adult awake and prepared to call an ambulance if my convulsions failed to stop within a minute or two.
I guess I was lucky in that way. I was lucky, too, that I only ever seized at night, so I never fell down a flight of stairs or collapsed in traffic. And I was luckiest because I grew out of the disease, as child epileptics sometimes do. The misfiring neurons that were causing my seizures were sidelined as I grew, I suppose, and I was given the all-clear by the time I was old enough to learn to drive. Still, even counting my blessings, those seizures were among the scariest experiences of my life. There was something deeply wrong about feeling my conscious self shunted to a far corner of my own brain, forced to watch my body act out without my permission.
Later, during the decade that I played rugby, I saw a couple of athletes lie convulsing on the field after hits to the head. I looked away, as I still do from depictions of seizures on TV medical dramas. I don’t like to watch the thrashing and the twisting, knowing that’s how I must have looked to my mom, my horrified audience of one.
The epilepsy left me with something else besides an occasional discomfort while watching Grey’s Anatomy. For years after that first night, the nightmare and the seizure were linked in my mind, one seeming to have caused the other. There was a time when I genuinely believed that another nightmare could cause me to seize, that standard childhood fare like campfire horror stories or scary movies would trigger the convulsions that could kill me.
I avoided scaring myself at all costs. I was convinced that fear itself could hurt me. It was a child’s illogical leap, but there was an intuitive truth at its core. Brains and bodies, nightmares and scary stories, these can’t be easily divided into separate categories, like the peas and carrots that must never touch each other on a fastidious eater’s plate. Our physical brains and our emotional minds—in other words, the brain cells that caused my seizures, and my own feelings of fear—are inextricably linked. Scientists are only just beginning to understand the ways in which our feelings, fear among them, are products of our physical brains.
In the Bible, God regularly commands his followers not to be afraid. According to Rabbi Harold Kushner, the admonishment to “fear not” appears more than eighty times in the text, directed at Abraham, Jacob, Moses, and each of the prophets, among others. Its occurrence is so frequent that Kushner refers to it as an eleventh commandment. But whether we are religious or not, obedience to that command is usually far beyond most people. The fear response system is built into the human body. Fear is, for most of us, simply a part of being alive.
Not everyone experiences fear the same way: some of us, it seems, have a surplus of it. And managing that surplus, or at least its effects, has been a matter of medical concern for thousands of years. As early as 400 BCE, the Greek doctor Hippocrates was attempting to provide medical treatment to people whose symptoms we would recognize today as phobias: men who, in a perfect phrase that appears to have survived from ancient times, “feared that which need not be feared.” Hippocrates and his disciples treated otherwise healthy people who never went to parties or large gatherings, or avoided groups of other people altogether, so convinced were they that they would be mocked and scrutinized or would somehow humiliate themselves. They saw men who were afraid to leave their houses in daylight, and others who were terrified to go near a cliff edge or a bridge. Today we call these conditions social phobia, agoraphobia, and acrophobia.
Unlike many of his peers, Hippocrates did not believe that fear was injected into us by the gods. He believed, instead, that our neuroses had physical causes—specifically, a buildup of black bile in our brains that created overheating and resulted in fits of baseless fear. He treated his patients with improved diet and exercise, to purge the bile from their systems. If that didn’t work, he administered a poison that would induce diarrhea and vomiting, presumably purging the bile in the process.
His diagnoses and treatments had their limitations, but at least he was grappling with the problem. After the fall of the Roman Empire, the curtain of the Middle Ages closed over European science and medicine, and Hippocrates’s ideas—among those of many others—were swept aside by the Church. Through those centuries, phobics were often assumed to be possessed.
Then came the Enlightenment and a return to a search for more temporal causes. But black bile was out, and individual experiences were in. In 1649, Descartes wrote,
It is easy to conceive that the strange aversions of some, who cannot endure the smell of roses, the sight of a cat, or the like, come only from hence, that when they were but newly alive they were displeased with some such objects…. The smell of roses may have caused some great headache in the child when it was in the cradle; or a cat may have affrighted it and none took notice of it, nor the child so much as remembered it; though the idea of that aversion he then had to roses or a cat remain imprinted in his brain to his life’s end.
This idea, that our long-lasting fears stem from unpleasant early-childhood experiences, is still in play nearly four centuries later.
The end of the nineteenth century and the beginning of the twentieth saw key developments in the history of our understanding of fear. The first came from the Russian researcher Ivan Pavlov, who, while studying dog digestion, noticed that his canine subjects began to salivate not only when their food arrived but also in the presence of their usual feeder. To test his suspicion that he had inadvertently trained the dogs to associate the feeder with the food so closely that they responded to one as if it were the other, Pavlov devised a famous experiment: he began pairing the arrival of the food with the unrelated sound of a metronome, and then, after some repetition of the pairing, he presented the dogs with the sound but no food. On cue, they salivated, responding to the conditioned stimulus with a conditioned response. This process, now known as Pavlovian, or classical, conditioning, would become a cornerstone of modern psychology. And it played an essential role in future studies of fear and phobias.
After the First World War, the American psychologist John B. Watson decided to build on Pavlov’s work. He wanted to know if a seemingly natural human fear reaction, such as a child crying in response to a loud noise, might grow to encompass fear in other circumstances too. His test subject was Albert B., a baby whose mother worked as a wet nurse at a Baltimore hospital. Albert was reported to be an emotionally stable infant. “No one had ever seen him in a state of fear and rage,” Watson and his graduate student Rosalie Rayner wrote later. He “practically never cried.”
First, they determined that the baby was afraid, as is natural, of sudden loud noises. Then, after exposing Little Albert, as he became known, to the presence of a number of small animals and ensuring that he showed no fear of them, Watson and Rayner began the experiment proper. When the baby was just over eleven months old, one of the researchers presented him with a white lab rat. When Albert touched the animal, the other researcher, positioned behind their subject, slammed a hammer into a long steel bar, producing a loud crash. “The infant jumped violently and fell forward,” Watson and Rayner wrote, “burying his face in the mattress.”
It didn’t take many combinations of the noise and the rat for Albert to learn to associate the two. Before too much longer, Watson and Rayner were able to induce whimpering, tears, and an effort to escape from the rat without the use of the noise stimulus at all. Even more than that, they found that Little Albert also now cried and shrank away from a rabbit, dog, and fur coat he’d been exposed to earlier and hadn’t feared. Watson and Rayner had successfully created a phobia, or at least a pattern of fear, in a child where there had previously been none.
It’s not known what became of poor Little Albert after the experiment and whether he carried his fear of furry creatures with him for life. But we do know something about the fate of Pavlov’s dogs. Years after his initial study, a devastating flood in his laboratory nearly drowned many of the animals. For the rest of their lives, the surviving dogs showed signs of being afraid of water.
Around the same time that Pavlov was inducing his dogs to drool on command, Sigmund Freud was launching the field of psychoanalysis. Where Descartes had pondered the possibility that a child with a fear of cats might have had an early negative encounter with a cat, Freud took a different, more opaque, route. In his 1909 study of Little Hans, a child who had seen a carriage horse’s violent collapse in the street and had thereafter been afraid of horses, Freud posited that Hans suffered from a variation on what he called the Oedipus complex. The boy actually feared his father, not horses at all, Freud wrote, and that fear stemmed from the child’s sexual attraction to his mother. (It’s hard not to wonder what Freud would have made of my own hang-ups. Was my hesitation at the top of that escalator about something more than a small child’s sense of vulnerability when stepping onto a large and in-motion machine? Maybe I’d rather not hear his answer.)
Today, Freud remains famous for these sorts of theories, and his influence on the fields of psychology and psychiatry has been enormous. But his career nearly took a very different track. Initially, after he graduated from medical school, Freud worked in neurology. He studied the nervous systems of fish and crayfish and became involved in the then-ongoing debate over how, exactly, our brain cells communicate. Freud argued (correctly, as it turned out) for the existence of a physical gap between neurons, and in 1895 he wrote that “the nervous system consists of distinct and similarly constructed neurones…which terminate upon one another.” The neuroscientist Joseph LeDoux credits Freud with coining the phrase “contact barriers” to describe the connection points between neurons. “Although these notions were amazingly sophisticated for their time,” LeDoux writes, “Freud felt that progress in understanding the brain would be too slow for his taste and so abandoned a neural theory of the mind in favor of a purely psychological one. The rest is history.”
Freud wasn’t wrong: a lot of significant advances in neurology were still decades away. But luckily for those of us who suffer from phobias and other afflictions of fear and anxiety, our understanding of the physical mechanisms of the brain has advanced a long way since Freud gave up on it.
I remember when I first learned about classical conditioning. It was Grade 6, around the same time that I had my first seizure. I had been given Gordon, the Barenaked Ladies’ debut album, on a cassette tape for Christmas. The lyrics for each song were dense, layered with references I didn’t fully understand, and the second verse of the fourth track on side A, “Brian Wilson,” included a mention of Pavlov’s dogs.
I can still picture the evening darkness in our living room, the antique wooden armoire that held our stereo, me popping the tape into the tape deck and then unfurling the liner notes from the cassette case and poring over the lyrics in their tiny type. As I usually did when I couldn’t understand something, I turned to my mom, and she explained the basics of Pavlov’s work.
It didn’t make much sense to me then. Why would you want to make a dog drool for no reason? But I filed the information away, and I still can’t think about classical conditioning without hearing lead singer Steven Page’s voice singing softly in my head. Call it a conditioned response!
Everything I did that evening—listening to language and processing its meaning, learning and storing new information, forming an enduring memory of the whole event—was thanks to the remarkable properties of the human brain. There’s a lot going on up there. But until recently, I took it all entirely for granted. I never thought to wonder, How does the human brain work? What is actually happening when I’m feeling afraid?
Our brains receive, process, and transmit information using specialized cells called neurons, or nerve cells. Neurons have two sorts of appendages, or branches, dangling from the main cell body: axons, which transmit information; and dendrites, which receive it. The connections at the gaps between the two—the gaps correctly predicted by a young Freud, where one neuron’s axon passes information to another neuron’s dendrite—are called synapses.
The brain contains more than eighty billion neurons and trillions of synapses. When a neuron “fires”—that is, when it receives a stimulus and sends that information down its axon to another neuron—it can pass its message along at more than one hundred miles an hour; a good thing, considering that while most axons are microscopic, some measure several feet in length, traversing our bodies from brain to limbs. One neurobiologist has estimated that an adult human’s axons could measure a cumulative distance of several hundred thousand miles.
Which brings up another point. We tend to think of the brain as distinct, separate from our bodies, of the wrinkled lump in our skulls as the conductor alone on his stand, directing the orchestra. But our bodies and our brains are intricately linked in every possible way; the brain is no more neatly separable from our bodies than our skulls are from the rest of our skeletons, or our hearts are from our arteries and veins.
Together, the brain and the spinal cord make up what we call the central nervous system. Its partner, the peripheral nervous system, is the entire collection of nerves and nerve cells that fall outside of those two core structures: the axons that carry information and instructions out from the central nervous system to our every muscle, and the sensory neurons that carry information from every part of the body back to the centre. It’s this system that gathers everything we know about the state of our bodies: hot and cold, pressure, pain, and so on. That sensory information gets passed up the spinal cord to the brain for further processing. It’s bringing you the image of these words right now.
In the brain proper, our neurons organize themselves into groups and systems, called nuclei, and form structures to complete certain tasks. One key structure for our purposes is the thalamus (or thalami, since, as is the case for most brain structures, there are two, one in each hemisphere of the brain). It’s a sort of gatekeeper, regulating the flow of sensory information from the body to the cerebral cortex. The hypothalamus is another regulatory structure. It works alongside parts of the brain stem, the most evolutionarily ancient, bottom-most portion of our brain, in governing our autonomic nervous system, the involuntary, invisible system that regulates our internal organs: heart, guts, lungs, bladder, and so on.
The hypothalamus’s neighbour, the amygdala, is a critical structure for any discussion of fear—so critical, in fact, that Joseph LeDoux, who has made a career out of the study of fear, named his science-rock band the Amygdaloids. The amygdala’s job, in highly simplified terms, is to receive sensory input and to subject that information to a threat assessment. If it finds a threat, it lets the hypothalamus know that it’s time to fire up the autonomic nervous system’s “fight-or-flight” response. The amygdala can operate without bothering to check in “upstairs” with the cerebral cortex for permission. It can even be triggered by stimuli of which we are not consciously aware.
Above and surrounding all these smaller structures is the big guy: the cerebral cortex, that heavily crevassed dome of soft matter that will dominate in a child’s drawing of the brain. It is believed to be the key to our whole array of higher-order mental functions, from perception and consciousness—in the philosophical sense rather than in the raw sense of whether you are awake or comatose—to skilled movements, memory, and intelligence. It’s the reason why we have Steph Curry’s three-point shot, Picasso’s Guernica, and the classic New Yorker cartoon by Charles Barsotti of an affable piece of rigatoni saying on the phone, “Fusilli, you crazy bastard! How are you?” It’s also the reason why we can carry grudges, nurse insecurities, and stew for years about the mistakes we’ve made.
So let’s say you get scared. What does that actually look like, in physical terms?
Picture something like the vision I experienced in that nightmare a couple of hours before my first seizure. You wake up suddenly in the night. You’re alone in your home, but you hear a strange noise in the darkness—maybe a footstep, a door opening or closing. That auditory input is first carried from the ear’s receptor cells to a major cranial nerve and then directly to the brain itself. There, it’s presented with various pathways and options, but for simplicity’s sake, let’s assume that in this case we have a straightforward journey from gatekeeper to fear trigger. The thalamus sends an alert straight to the amygdala, which in turn alerts the hypothalamus, and then the sympathetic nervous system is fired up. Messages race along the axons throughout your body, from synapse to synapse to synapse, carrying the news of potential danger to your organs, to your skin. Your heart rate accelerates; its loud pounding seems to fill the dark room. Maybe your breath comes faster and shorter too, and your flesh prickles with sweat beads or goosebumps. Your pupils dilate; your muscles flood with blood, preparing for action. You feel afraid: a sickness in your gut, tightness in your chest. Fear is a full-body emotion.
The physical reactions—the blood flow, the pupil dilation, and so on—can all be traced at the neural level. But what about the feeling of fear, which is distinct, as we know, from the physical fear response. Where does it come from?
For a long time, the working theory held that the feeling came first, in response to the fear stimulus, and then the physical response followed from the feeling. This is what’s known as the commonsense, or Darwinian, school of thought. But that was more an assumption than a proven mechanism, and these days it has fallen out of favour. Instead, as science has turned its attention to working out that elusive mechanism more concretely, the neuroscientist Antonio Damasio has come up with an answer that, while provocative, ultimately feels right to me. The feeling, he argues in a pair of funny and wise books, Descartes’ Error and Looking for Spinoza, is actually derived from that same menu of physical reactions that we would typically view as accessories of, or adjacent to, our emotions.
For the purposes of his argument, Damasio makes an unusual distinction between “emotions”—by which, in this context, he specifically means the physical, measurable reactions of the body in response to an emotional stimulus, the physical fear response—and “feelings,” the intangible expressions of emotion in our minds. That may seem odd, or even nonsensical, but it’s a key to his case, so keep it in mind.
“We tend to believe that the hidden is the source of the expressed,” he writes in Looking for Spinoza. But he argues, instead, for a counterintuitive reversal of that order: “Emotions”—again, meaning the physical reactions here—“and related phenomena are the foundation for feelings, the mental events that form the bedrock of our minds.”
All organisms have varying abilities to react to stimuli, from a simple startle reflex or withdrawal movement all the way up to more complex multipart responses, like the description of our physical fear processes above, which are Damasio’s “emotions.” Some of the more basic responses might sometimes look, to our eyes, like expressions of the feeling of fear, and in fact the machinery that governs them is also implicated in the more complex processes. (My startle reflex, one of our oldest and simplest reactions, has certainly come into play at times when I’ve also felt afraid. Hello, raptors in the kitchen in Jurassic Park!) But the “emotions” are at the top of the heap in terms of complexity, and as such not all organisms are capable of generating them.
Unlike some of the simpler “fear” reactions in simpler organisms (poke a “sensitive plant,” watch its leaves curl up), our emotions can be generated by stimuli both real, in the moment, and remembered—or even imagined. That’s the gift and the burden of the human mind. But for now, let’s stick with an in-the-moment example, like the noise heard in the night. The fact of the noise is captured by the sensory nerves in the ear and is relayed to the brain structures involved in triggering and then executing a response—that’s the amygdala and the hypothalamus again. Now your body is reacting in all the ways described above.
So far, so good? The next step, in Damasio’s formulation, is the creation of the feeling itself.
We know that our bodies are laced with neurons, and that they not only send out information from the brain, they also receive it. So after the outgoing messages have gotten our hearts pumping, our sweat beading, and so on, a series of incoming messages returns to the brain, bearing all of that information about our physical state. Our brains, Damasio explains, maintain incredibly complex maps of the state of the body, from our guts to our fingertips, at all times. And here’s the core of his argument: when the incoming messages bearing news of the body’s physical fear-state alter these maps, that’s when the feeling itself arises.
Your brain learns from your body that your heart is pounding, your pupils are dilated, your goosebumps are standing at attention. Your brain does the math and says, Aha! I am afraid!
In his 1884 essay, “What is an emotion?” the philosopher and psychologist William James wrote,
If we fancy some strong emotion and then try to abstract from our consciousness of it all the feelings of its bodily symptoms, we find we have nothing left behind, no “mind-stuff” out of which the emotion can be constituted, and that a cold and neutral state of intellectual perception is all that remains…. What kind of an emotion of fear would be left if the feeling neither of quickened heart-beats nor of shallow breathing, neither of trembling lips nor of weakened limbs, neither of gooseflesh nor of visceral stirrings, were present, it is quite impossible for me to think.
Damasio picks up where James left off. But he doesn’t just draw on Victorian-era philosophizing to make his argument. He also works from case studies and his own research; for instance, the case of a Parkinson’s patient in Paris. The woman, who was sixty-five years old and had no history of depression or other mental illness, was undergoing an experimental treatment for her Parkinson’s symptoms. It involved the use of an electrical current to stimulate motor-control areas of the brain stem via tiny electrodes.
Nineteen other patients had undergone the treatment successfully. But when the current entered the woman’s brain, she stopped chatting with the doctors, lowered her eyes, and her face slumped. Seconds later, she began to cry, and then to sob. “I’m fed up with life,” she said, through her tears. “I’ve had enough…I don’t want to live anymore…I feel worthless.” The team, alarmed, stopped the current, and within ninety seconds the woman had stopped crying. Her face perked up again, the sadness melting away. What had just happened? she asked.
It turned out, according to Damasio, that instead of stimulating the nuclei that controlled her tremors, the electrode, infinitesimally misplaced, had activated the parts of the brain stem that control a suite of actions by the facial muscles, mouth, larynx, and diaphragm—the actions that allow us to frown, pout, and cry. Her body, stimulated not by a sad movie or bad news, had acted out the motions of sadness, and her mind, in turn, had gone to a dark, dark place. The feeling arose from the physical; her mind followed her body.
This whole thing seemed counterintuitive to me at first, reversing as it does the “commonsense” view. But then I sat back and really thought about my experience of fear. How do I recall it in my memory? How do I try to explain it to other people? The fact is that I think of it mostly in physical terms: that sick feeling in my gut, the tightness in my chest, maybe some dizziness or shortness of breath. (Appropriately, the ancient Greeks’ angh, the root of the Latin anxietas and the ancestor of modern terms like “anxiety” and “anguish,” was originally used to mean tightness, restriction.) The conscious thoughts about how I am feeling—I am not okay; I am afraid—are decidedly secondary.
Think about how you actually experience the feeling of happiness, of contentment, or ease. For me, it manifests in the loosening of the eternally tense muscles in my forehead and jaw, in my neck and shoulders. My eyes open wider, losing the worried squint. I breathe more deeply.
Or think about the sheer physicality of deep grief, how it wrecks your body as well as your mind. When I look back on the worst of my grief after my mom’s death, I remember it as headaches, exhaustion, a tight chest, a sense of heaviness, and lethargy. I felt sad, yes—sadder than I’ve ever been—and it was my body that told me how sad I was.
One morning, a few months after my epilepsy diagnosis, I woke up with the memory of another vivid dream lodged in my mind. The dream was straightforward: I’d had a seizure. The usual pain, screaming, and convulsions; the same waking paralysis after the thrashing stopped. It seemed so real that I began to wonder if it was a dream at all.
And here was the thing: I’d been home alone the night before. So if I had been screaming and convulsing, there would have been no one around to hear.
My mom and I mentioned the phantom seizure to my neurologist at our next appointment, and she was concerned enough to up my drug dosage on the basis of that dream-memory alone. I never seized again, either awake or in dreams.
Dreams and nightmares are one of the stranger manifestations of our brain’s ability to make pictures in our minds. They’re a phenomenon that remains somewhat imperfectly understood, although humans have been throwing a variety of explanations at them for millennia. Dreams have been messages from the gods or the ancestors, warnings of danger, or glimpses of the future. Hippocrates and Aristotle believed that dreams could be used as a diagnostic tool, that they were telltale mental symptoms of a physical illness. Aristotle wrote, “Beginnings of diseases and other distempers which are about to visit the body must be more evident in the sleeping than in the waking state.” A couple of millennia later, Freud posited that dreams were all about wish fulfillment: our minds acted out the desires that were not permitted to us in waking life.
These days, we have a pretty specific understanding of the mechanism of dreaming—the how, even if not always the why. “Neurochemical changes that occur during REM sleep prime our brains to not only generate but also trust extraordinary visions,” the science journalist Alice Robb writes in Why We Dream. In simple terms, the chemicals and structures involved in emotion and memory are activated, while the parts of our brain that deal with reasoning and self-control quiet down. “The result,” writes Robb, “is a perfect chemical canvas for dramatic, psychologically intense visions.”
Still, even with a basic grasp of the chemical processes involved, we find it hard to let go of our sense of the significance of dreams. It’s something about the way they cling to your mind after waking, the way they take command of your mood even after their details have faded away. It feels powerful. Of course, my nightmare that first night didn’t actually cause my seizure—but still, for me, dreams and seizures remained all bound up together. The phantom dream-seizure only cemented the connection.
According to the psychologist Richard Wiseman, statistics can explain away most of the perceived potency of dreams, their symbolism and their seemingly predictive powers. Wiseman estimates that between age fifteen and seventy-five, an average person might have nearly ninety thousand dreams over thousands of nights of sleep. “You have lots of dreams and encounter lots of events,” Wiseman writes in his book Paranormality. “Most of the time the dreams are unrelated to the events, and so you forget about them. However, once in a while one of the dreams will correspond to one of the events. Once this happens, it is suddenly easy to remember the dream…. In reality, it is just the laws of probability at work.” Would I even remember that one nightmare if it hadn’t been followed by my first seizure? Or would it have just slipped away like all the rest?
The thing is, laws of probability aside, dreams actually can affect our waking lives, and they can even have a measurable impact on our health. When our real-life partners or family members play the villain in a bad dream, our negative dream-perceptions of them can persist once we are awake. (A 2013 study found that dreamland “slights and betrayals” from participants’ partners lingered into the daytime.) Nightmares have been shown to play a role in triggering migraines and asthma attacks, and even, in very rare cases, heart attacks and other potentially fatal events. Here’s Alice Robb again:
A man in his late thirties—a nonsmoker with no family history of heart disease—dreamed that he died in a car crash and woke up vomiting; two hours later, he was at the hospital describing the unbearable pressure in his chest. A twenty-three-year-old woke at six A.M. from a nightmare in which he was murdered alongside his father and had a heart attack at seven. The early-morning and the final hours of sleep—when REM cycles are longest and nightmares are most intense—is the most dangerous period for cardiovascular patients; heart attacks are most frequent, and most severe, between the hours of six A.M. and noon.
I’d like, for the sake of my own ability to sleep comfortably through the night, to believe that these kinds of cases are utterly freak events, rare as an asteroid strike or a jackpot-winning lottery ticket. But unfortunately they’re not quite so unimaginable. And while the two men in Robb’s anecdotes ultimately survived, others weren’t so lucky.
In 1980, a medical examiner in Portland, Oregon, contacted the Centers for Disease Control. The examiner had noticed that two recent unexplained deaths seemed to have similar properties. Soon enough, more similarly mysterious American deaths were added to the list, and by the end of the decade, more than one hundred of them had been noted. Here’s what the deaths had in common. The dead were mostly male and mostly of Southeast Asian origin—a majority of them, in fact, Hmong refugees from Laos. They had all died in their sleep, had generally been healthy, and autopsies turned up no physiological causes of the deaths. Researchers scrambled to understand, seeking out genetic or cardiovascular explanations. “We drew a complete blank,” one medical examiner said at the time. “In each case we asked ourselves what they had died from and the answer was ‘Nothing.’ ” With little to go on, the authorities slapped a name on the phenomenon: sudden unexplained nocturnal death syndrome, or SUNDS.
In 1991, Shelley Adler, a doctoral candidate at UCLA, published a theory about the SUNDS deaths in The Journal of American Folklore. Adler was a folklorist, perhaps an unlikely source of insight into a bizarre medical crisis. But, as she explained in her paper, “Sudden Unexplained Nocturnal Death Syndrome among Hmong Immigrants: Examining the Role of the ‘Nightmare,’ ” her training was crucial to the formation of her hypothesis. She’d been taught, after all, to listen to the stories of ordinary people—the kinds of people medical experts can sometimes overlook—and to build a more universal truth from their specific stories.
Her bona fides established, Adler got down to her theory. Across cultures, there is an enduring story, or legend, of an event that she calls “the nightmare”: a force, often perceived as an evil spirit, that presses down on its sleeping victims’ chests, squeezing the life out of them as they lie helpless, conscious but dreaming. In Hmong culture, the nightmare spirit is called the dab tsog. Ordinarily, attacks by the dab tsog aren’t necessarily fatal, but Adler argued that a combination of factors had changed that. The Hmong had seen staggering casualties in the war that swept Vietnam, Laos, and Cambodia from the late 1950s to the 1970s; the Hmong, who worked in cooperation with the US’s Central Intelligence Agency, died at ten times the rate at which American soldiers were killed in Vietnam, and by the time it was all over, it was estimated that one-third of the Laotian Hmong population had been lost. Then came more danger: death or re-education at the hands of the victorious Communists or a risky flight across the Mekong River to refugee camps in Thailand. By the time the Hmong refugees made it to the United States, they had suffered trauma, hunger, loss of loved ones on an almost unimaginable scale, and the disorientation and alienation that comes when you are wrenched from tight-knit communities and tradition.
Adler argued that it was the stress of all these social factors, combined with the power of the Hmong men’s own belief in the dab tsog, that turned a terrifying nightmare into a fatal event. The images in the men’s minds had acted upon their bodies, as we increasingly understand they can do. Their feelings were not neatly separable from their physical existence; their fears were not neatly separable from reality. In some ways, it was almost as though their fears had called the nightmare into reality. It was my fear-caused tumble down the escalator, but on a deadly scale.
Sometimes, on my worst days after my mom died, I wondered if all my worrying about her death, my dread of losing her the way she had lost Janet, had called her fatal stroke into being. I felt as though, maybe, I had summoned the nightmare through my own terror.
Of course, that isn’t rational, just my grieving mind making connections after the fact. My childhood belief that a nightmare could trigger my seizures may not have been rational or scientific either. But nightmares, it turns out, can come true.