A girl believes she has been struck blind for stealing a kiss. A mother watches helplessly as each of her children is replaced by a changeling. A woman is haunted each month by the same four chords of a single song. In neurology, illness is inextricably linked with narrative, the clues to unraveling these mysteries hidden in both the details of a patient's story and the tells of their body.
Stories are etched into the very structure of our brains, coded so deeply that the impulse for storytelling survives and even surges after the most devastating injuries. But our brains are also porous—the stories they concoct shaped by cultural narratives about bodies and illness that permeate the minds of doctors and patients alike. In the history of medicine, some stories are heard, while others—the narratives of women, of Black and brown people, of displaced people, of disempowered people—are too often dismissed.
In The Mind Electric, neurologist Pria Anand reveals—through case study, history, fable, and memoir—all that the medical establishment has overlooked: the complexity and wonder of brains in health and in extremis, and the vast gray area between sanity and insanity, doctor and patient, and illness and wellness, each separated from the next by the thin veneer of a different story.
Moving from the Boston hospital where she treats her patients, to her childhood years in India, to Isla Providencia in the Caribbean and to the Republic of Guinea in West Africa, she demonstrates again and again the compelling paradox at the heart of neurology: that even the most peculiar symptoms can show us something universal about ourselves as humans.
A girl believes she has been struck blind for stealing a kiss. A mother watches helplessly as each of her children is replaced by a changeling. A woman is haunted each month by the same four chords of a single song. In neurology, illness is inextricably linked with narrative, the clues to unraveling these mysteries hidden in both the details of a patient's story and the tells of their body.
Stories are etched into the very structure of our brains, coded so deeply that the impulse for storytelling survives and even surges after the most devastating injuries. But our brains are also porous—the stories they concoct shaped by cultural narratives about bodies and illness that permeate the minds of doctors and patients alike. In the history of medicine, some stories are heard, while others—the narratives of women, of Black and brown people, of displaced people, of disempowered people—are too often dismissed.
In The Mind Electric, neurologist Pria Anand reveals—through case study, history, fable, and memoir—all that the medical establishment has overlooked: the complexity and wonder of brains in health and in extremis, and the vast gray area between sanity and insanity, doctor and patient, and illness and wellness, each separated from the next by the thin veneer of a different story.
Moving from the Boston hospital where she treats her patients, to her childhood years in India, to Isla Providencia in the Caribbean and to the Republic of Guinea in West Africa, she demonstrates again and again the compelling paradox at the heart of neurology: that even the most peculiar symptoms can show us something universal about ourselves as humans.
The Mind Electric: A Neurologist on the Strangeness and Wonder of Our Brains
288
The Mind Electric: A Neurologist on the Strangeness and Wonder of Our Brains
288Hardcover
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Overview
The human brain is still something of an enigma, but Pria Anand brings us closer to our consciousness with a thought-provoking combination of personal stories, neuroscience and medical history.
A girl believes she has been struck blind for stealing a kiss. A mother watches helplessly as each of her children is replaced by a changeling. A woman is haunted each month by the same four chords of a single song. In neurology, illness is inextricably linked with narrative, the clues to unraveling these mysteries hidden in both the details of a patient's story and the tells of their body.
Stories are etched into the very structure of our brains, coded so deeply that the impulse for storytelling survives and even surges after the most devastating injuries. But our brains are also porous—the stories they concoct shaped by cultural narratives about bodies and illness that permeate the minds of doctors and patients alike. In the history of medicine, some stories are heard, while others—the narratives of women, of Black and brown people, of displaced people, of disempowered people—are too often dismissed.
In The Mind Electric, neurologist Pria Anand reveals—through case study, history, fable, and memoir—all that the medical establishment has overlooked: the complexity and wonder of brains in health and in extremis, and the vast gray area between sanity and insanity, doctor and patient, and illness and wellness, each separated from the next by the thin veneer of a different story.
Moving from the Boston hospital where she treats her patients, to her childhood years in India, to Isla Providencia in the Caribbean and to the Republic of Guinea in West Africa, she demonstrates again and again the compelling paradox at the heart of neurology: that even the most peculiar symptoms can show us something universal about ourselves as humans.
Product Details
| ISBN-13: | 9781668064016 |
|---|---|
| Publisher: | Washington Square Press |
| Publication date: | 06/10/2025 |
| Pages: | 288 |
| Product dimensions: | 6.10(w) x 8.80(h) x 1.20(d) |
About the Author
Read an Excerpt
Chapter 1: The Theater of Illness CHAPTER 1 The Theater of Illness
THE STUDENT LOST HER vision so gradually, so insidiously, that not until days after the symptoms first began did she realize that she had been struck blind. First came the headache, a boring pain in her right temple. The pain was dull when she first woke, but later that morning, as she looked down at her folded hands during the liturgy at church, she felt as though someone had pierced her right eye with a sewing needle. At school, she realized that the pain seemed to swell and subside as her eye moved. She found herself turning her entire head as she read the pages of her textbooks, keeping her eyes as still as she could.
That night, she looked at the embroidered border of her new white nightgown and wondered how it had become so worn, wondered when the color of the thread—once maroon—had faded to pink. As she closed first her right eye and then the left, the border seemed by turns bright and dim. She was fasting for Lent, and she thought her symptoms—the headache, the fogginess—had been brought on by hunger. She went to bed early, and by the next morning, she could see only a sliver of the world through her right eye, a narrow crescent of preserved vision the shape of a fingernail clipping. By the afternoon, the vision in her left eye had begun to dim, too.
At nineteen, she still lived with her mother and grandmother while she took classes at the local community college, but she did not tell them about the blindness. She had grown up attending an insular Ethiopian Orthodox church, had quietly been taught since she was a teenager never to enter the church or take the Eucharist when she was on her period, to instead pray alone outside, and she was certain that the blindness was a form of divine punishment, levied against her for a secret sin: one week earlier, she’d had her first kiss, snuck in the church parking lot.
She stayed home from school that day, unsure whether the fragments of vision she had remaining would allow her to navigate the two city buses she took to the college. She had initially pleaded a headache and then a stomachache, but when she bumped into the wall walking from her bedroom into the bathroom, her grandmother brought her to the emergency room to find out what was wrong.
I was a medical student barely older than she was, one week into my first neurology rotation. The student told me about her vision—the pain, the fading colors—and then, after visiting hours ended and her grandmother had reluctantly left her bedside, she told me, weeping, about the kiss.
I had never seen a person suddenly struck blind. I still understood nearly nothing about the fragility of bodies and brains, but I had already started to absorb cynicism from the doctors around me, started to learn that the appropriate response to emotion was skepticism. Watching her cry, I wondered whether the blindness was imagined, a sort of self-flagellation for the sin of the kiss.
But the blindness was not imagined. Rather, it was the result of an inflammation of her optic nerves, the bundle of fibers that travel like an extension cord from the back of the eye to the visual centers of the brain. On an MRI of her brain, these nerves glowed ghostly white, tumescent with inflammation. In their quest to find the cause of the inflammation, the doctors tested her for every possible infection. Only one came back positive: a blood test for Epstein-Barr virus, which causes mononucleosis, that adolescent plague of exhaustion that spreads through saliva—“the kissing disease.” To her, it felt like incontrovertible proof: the kiss caused the blindness, and the blindness was punishment for her sin, divinely ordained rather than the random failure of a body assembled of parts as prone to malfunction as the gaskets of a car engine. In a way I, too, thought that the kiss caused the blindness, although my explanation was both more vague and less satisfying: a dysregulated immune system, somehow inflamed by the virus.
Unmoored by her loss of sight, the student began to have visions. Every night, she saw her own body rising up and hovering above her bed, suspended in her hospital purgatory with the seams of her gray cotton infirmary gown floating beneath her like angel wings. I told her that the visions, too, were something quotidian, an illusion manufactured by the misfiring of neurons in her visual cortex, robbed of actual sight. Secretly, though, I knew that my explanations, like hers, were grounded only in faith, in my own unshakable belief in things I could not see—viruses, neurons, electrical impulses.
A DECADE LATER, while teaching my own students the ways someone could be struck blind and then have their sight restored, I would come across the story of a fourteenth-century Dutch saint, Lidwina of Schiedam. At sixteen, Lidwina fell while ice-skating, breaking a rib and tearing into her skin a wound that would not heal. Weeks after she fell, she began to have violent pains in her teeth that kept her from eating, then a paralysis of the face that left her lips hanging open. In the years that followed, she struggled to walk, first reaching for furniture to keep herself upright, then being carried like an infant from room to room. In her twenties, she, like the student, began to float over her bed among angels. Her right arm became paralyzed, then mobile, her right eye blind, then sight restored. By the end of her life, Lidwina struggled to swallow.
Lidwina of Schiedam became a spectacle, physicians traveling from across Holland to see the girl who had been struck blind and then regained sight, who had been paralyzed and then limber. The disease, they said, came from God. “Even Hippocrates and Galenus would not be able to be of any help here,” said one physician. “The Lord’s hand had touched this woman.”
Like my patient, Lidwina was young and religious, had prayed to the Virgin Mary since her earliest childhood. She was immobilized, infantilized, haunted by excruciating pain. She would eventually believe that she had been chosen to suffer for the sins of humanity. After she died, her grave became a pilgrimage site, a chapel built upon it so that other sufferers could pray for deliverance. Centuries later, she was canonized—the patron saint of ice-skating, and of chronic pain.
In 1947, Lidwina’s body was exhumed and her skeleton examined. The bones of her legs and right arm bore the stigmata of years of paralysis, of muscles in spasm. The diagnosis was likely multiple sclerosis, the scientists speculated, which would make hers one of the first recorded cases. Her blindness and restored sight were neither curse nor miracle, but rather an affliction as ordinary as a failing nerve.
MUCH ABOUT MULTIPLE sclerosis—what renders someone susceptible to it, for instance, or even what determines whether a predisposed person will begin having symptoms at fourteen or twenty-four—remains mysterious, as inscrutable to doctors now as the causes of Saint Lidwina’s suffering were in her day. What little we do know suggests that the immune system plays a key role.I Our immune system is armed for warfare, designed to neutralize and even physically devour anything it deems a threat. Most often, these threats are invaders from outside the body: viruses and bacteria, which the immune system recognizes as foreign by the telltale proteins and genetic sequences that mark their surfaces, different from the ones that make up the human body. Sometimes, these threats are from within: the dying cells filling a wound, for instance, which the immune system consumes so that they can be replaced with healthy tissue. In autoimmune diseases, including multiple sclerosis, something goes awry in the finely tuned machinery that distinguishes the body’s own healthy cells from a potential threat. Instead of rooting out invading pathogens and cleaning up the debris of trauma, the immune system begins to devour the body it was designed to protect. At their core, these diseases represent a sort of civil war, the systems of the body in combat with one another.
On the battleground of the body, the brain and spinal cord exist in a privileged space, protected from even the blood coursing through them by a microscopic barrier of tightly bound cells that rings every capillary like stones in a fortress wall. The barrier is intended to keep infections of the blood from drifting into the brain. In people with multiple sclerosis, this barrier becomes leaky, the immune cells that circulate in the blood breaching the fortress wall and invading the nervous system.
In some ways, the nervous system is unfathomable; in others, it is remarkably banal. In our brains and spinal cords, the stuff of strength, sensation, and consciousness travels across vast distances—from cortex to extremities—as electricity, carried by the long, filamentous axons of each of our neurons. Each axon is encased in a fatty sheath of insulation, corralling the electrical signals it carries to keep them from leaking out before they reach their intended target. Attacked by an overactive immune system, this insulation begins to fray, gnawed and degraded like the faulty, mouse-bitten wiring of an old house, the signal ebbing from bare patches of wire so that it grows weaker with each millimeter of the journey. Multiple sclerosis is the most common of a family of illnesses called demyelinating diseases for the way they erode the particles of protein and fat that make up this insulation—myelin, the name derived from the Greek for “marrow,” because of its abundance at the heart of the brain.
On an MRI, multiple sclerosis is luminous, the gadolinium contrast injected into the blood vessels spilling out through the broken blood-brain barrier into the inflamed tissues of the brain and spinal cord in bright white patches. Under the microscope, multiple sclerosis is ruin, axons stripped of their myelin, surrounded by the ravenous cells of the immune system, particles of digested myelin still visible within their distended bellies. These are the scars—the scleroses—for which the disease is named.
Given equal weight in its name is that the disease is “multiple,” striking the nervous system with geographic abandon and leaving innumerable scleroses in its wake. In part, this multiplicity means that the manifestations of multiple sclerosis and other demyelinating diseases are protean, determined by where in the nervous system the immune cells land. A rift in the fibers of the brain that support the sensory system can lead to a symptom as minor as numbness, for instance, while one in the slender rope of spinal cord, high-value real estate where every millimeter is of consequence, can paralyze both legs. In the case of my patient—the student—the target was her optic nerves. Instead of traveling intact to her brain, the information about the world that entered her eyes was becoming lost in the journey, leaking from each unprotected fiber, the bridge between her brain and her eyes severed by her overactive immune system. Eventually, we would diagnose her with a rare type of demyelinating disease, called neuromyelitis optica for the structures it destroys: the tightly packed fibers of the brain stem, the spinal cord, and the optic nerve. The optic neuritis that had struck her blind would be a harbinger of future attacks; untreated, neuromyelitis optica inexorably causes blindness, paralysis, and sometimes even death, ravaging the nuclei in the brain stem that support the muscles of breath.
IN THEIR MOST common forms, demyelinating diseases are called relapsing and remitting, striking at any time with symptoms that range from double vision to incontinence. In the weeks that follow, these symptoms often reverse, but not all the way, the result of a thin layer of myelin beginning to form on once-bare axons, not quite as robust as the original insulation. This is the “remitting” phase of the disease: a leg paralyzed for weeks before it begins to move again, never quite as strong as it was before, vision returning to an eye once struck blind, always a little dimmer than it once was. Some sufferers report that this uncertainty is one of the cruelest parts of their disease: not knowing whether the symptoms will reverse, and if so, to what degree—will the world remain entirely obscured, or only a little less bright, red fading into pink and darkness lapping at the edge of vision? The medications we use to treat relapses can hasten this recovery, but none seem to change the end point—how much vision someone recovers, for instance, or whether someone is able to walk again.
The student was treated for her blindness, first with steroids to quiet her immune system and then with a procedure to cleanse her blood of excess antibodies, to remove the parts of her immune system that were attacking her optic nerves. Her vision began to recover, the crescent of vision in her right eye expanding like a waxing moon, colors returning to her once-dim left eye.
I told her the recovery was the result of something ordinary—the regrowth of myelin clinging to a naked axon. I talked about fraying insulation being repaired as if some minute electrician were at work on her brain, as confidently as if it were something I had seen with my own eyes. She was certain that it was instead a miracle: she had been struck blind for her sin, and just as powerfully, her vision had been restored. My faith was in the infinitesimal, in proteins and lipids, even in the treatments we gave her, though I knew they only half worked. Hers was in divine revelation.
Her waxing vision didn’t end the nightly visitations. She saw flames licking the hospital walls, the slither of scales on the floor beneath her. Always, she floated above her bed, removed and protected. Some nights, other gowned angels floated beside her, their feet robed in the same rubber-soled, candy-colored hospital socks as hers.
UNLIKE MANY NEUROLOGIC diseases that strike late in life—dementia and stroke, for instance—demyelinating diseases are afflictions of the young, their earliest symptoms often manifesting when patients are in their twenties. For reasons that are still unfathomable, autoimmune diseases such as multiple sclerosis and neuromyelitis optica are also much more often a blight of women than of men—blamed on everything from the X chromosome to sex hormones with no clear resolution. Neuromyelitis optica is four times more common in women than men,II while multiple sclerosis is more than thrice as common in women as men.III The gap is growing ever wider: the incidence of multiple sclerosis in women continues to climb, while the incidence in men has remained steady in recent decades, a mysterious observation that has been attributed to causes ranging from twenty-first-century changes in diet and lifestyle to the decreasing number of pregnancies the average woman will carry in her lifetime.IV
Perhaps because they primarily afflict young women, perhaps because of the way the symptoms seem to migrate—an eye afflicted, then an arm—or perhaps because of the way in which they relapse and remit, I was not the first ill-informed would-be doctor to want to dismiss the symptoms of a demyelinating disease as imagined, nor would I be the last. In the years since that first patient, I have cared for other women who were struck blind, for women who developed intractable nausea and violent hiccups, or a potent, narcoleptic sleepiness that seemed to lift as quickly as it befell them, who have described the weight of an illusory boa constrictor coiling around their ribs or the sensation that they were walking on broken glass, all symptoms of multiple sclerosis or neuromyelitis optica. All of these women were dismissed as hysterical by their doctors before they were diagnosed.
Of the many paradoxes of the disease, perhaps the most ironic is this: the characteristic microscopic scars of multiple sclerosis—the first incontrovertible proof that the disease was one of the brain and not the mind—were first described by the famed neurologist Jean-Martin Charcot, a doctor who made his name in part as a curator of hysterical women.
In 1852, Charcot spent a year of his medical internship at the Salpêtrière, a Parisian hospital that had once been a gunpowder factory but had been converted into a women’s asylum in the seventeenth century.V The Salpêtrière was a place to consign women who were deemed mad or crippled, who were pregnant out of wedlock or simply old, all of whom were confined to low-lying rooms routinely flooded by the rising waters of the Seine. The grounds housed a prison for prostitutes, heretics, and other convicts awaiting execution. It was, as Charcot called it, “a grand asylum of human misery,” one to which he was inexorably drawn to return a decade after his internship ended. “We are in possession of some sort of museum of living pathology of great resources,” he wrote, the women housed at the Salpêtrière no different to him from a lepidopterist’s specimens, netted and suffocated to later be cataloged and dissected.
The earliest inklings of hysteria—the idea that physical symptoms could result from an emotional excess and that this sort of excess was uniquely an affliction of women—first emerged millennia before Charcot arrived at the Salpêtrière, in one of our oldest surviving medical texts: the piecemeal fragments of an Egyptian papyrus. The symptoms these fragments describe are manifold, ranging from aching pains of the entire body to an inability to speak, but all are attributed to the womb. The uterus, the fragments suggest, is a ravenous organ that migrates within the body in search of nourishment. When it rises too high above the pelvis, it crowds the other organs, and from this displacement, strange symptoms arise. The papyrus treats the uterus as if it were an animal to be herded and corralled, with desires and needs distinct from those of its woman host. To treat the symptoms of a lost uterus, the papyrus suggests luring it back into the pelvis with sweet fragrances, yellow ocher and myrrh, applied to the vulvae, or driving it back from the chest and abdomen with foul odors such as valerian and asafetida held at the nose and mouth. Hysteria was named for the uterus, hystera in Greek, by the ancient Greek physician Hippocrates, his own name immortalized in the Hippocratic oath taken by new doctors. In the Egyptian tradition, Hippocrates’s version of hysteria was also exclusively a disease of women, to be treated by herding a misbehaving womb back in place.VI His texts were translated first into Latin and then Arabic, diffusing through the Roman Empire and the Ottoman Empire, the idea of a wandering womb persisting until well into the Middle Ages, and the notion of femaleness itself as a pathology lasting much longer.
In the seventeenth century, two thousand years after Hippocrates and two hundred before Charcot, Thomas Sydenham, the British physician whose corpus includes some of the earliest descriptions of gout and chorea, also wrote on hysteria, which he called the most common of all chronic diseases. In his telling, hysteria afflicted nearly all women, while men were “less subject to it than women because of their more robust habit of body.” Like the wandering uterus, Sydenham’s hysteria wandered within the body, masquerading as virtually any other disease. “In whatever part it seats itself, it presently produces symptoms as belong to it, and unless the physician is very skillful, he will be mistaken and will think those symptoms come from some essential distemper of this or that part and not from any hysteric disease,” he wrote—in short, physicians should be careful not to misdiagnose a hysteric with a “real” disease, a prelude to the skepticism I would later absorb in my own training. Sydenham’s hysteria could cause everything from paralysis to convulsions, palpitations to coughing to phantom kidney stones.
Although Sydenham’s version of hysteria was intimately entwined with the uterus, most often striking after childbirth, he believed that it was a disease caused not by a physical organ, but rather strong emotion. “It is known to everyone that hysterical women sometimes laugh excessively, and sometimes cry as much, without cause for either,” he wrote. Rather than a uterus wandering too high, he believed that these strong emotions—“psychic pneuma,” the breath of the soul—might wander too low and by “rushing down upon the various organs of the body, excite pain and spasm and create the symptoms of that part.” To comfort these spirits, he prescribed bloodletting and laudanum, wormwood and water impregnated with iron and steel, along with a caveat: “But nothing does so much comfort and strengthens the blood and spirits as much as riding horseback every day for a long while.”
Unlike his predecessors, Charcot believed that hysteria was caused not by a wandering uterus or a discomfited soul but rather by a lesion within the nervous system, no different from the host of other neurologic diseases on display in his museum of curiosities.VII Hysteria, Charcot reported, was a performative disease, one characterized by violent fits and acrobatic contortions, attitudes passionnelles of terror and ecstasy and sensory disturbances that he termed hysterical “stigmata.” Although he, too, thought that hysteria was more often a plague of women than men, Charcot was so certain that it could afflict men as well that he began admitting male patients to a small ward in the women’s hospital—at first twenty beds, then fifty—to further his studies.
Perhaps in thrall to the prevailing narratives of the time, to the enduring image of the “hysterical woman,” even though Charcot had accumulated a collection of male hysterics, it was only the women he asked to perform. The hysterical women of his grand asylum were photographed and sculpted, painted and drawn, but the true dramatic spectacle of the disease, the doctor thought, was best demonstrated in live shows, attended by hordes of not only physicians and students but voyeuristic Parisians and tourists alike. Charcot had a flair for showmanship, beginning each performance with a silent entrance—the ringmaster, trailed by his protégés—before his hysterical women were brought onstage. The women were dressed in carnivalesque feathered hats that quivered with every movement to ensure that even those in the back rows of the theater could witness the spectacle. Onstage, in performances orchestrated by Charcot, they convulsed and arched, wailed and fainted. Among the crowd were famous dancers and actors, hoping to emulate the range of emotions displayed by the hysterical women.
In the Salpêtrière, medical care was a quid pro quo, given in exchange for a performance of one’s illness. In modern emergency departments and hospital rooms, I have seen quieter ways we ask our patients to perform their illness in exchange for their care. A woman arrives in the emergency department three times in as many weeks, first with hazy vision in one eye, then with a heaviness that weights her right foot like a winter boot. Each time, she is perfunctorily examined and sent home with no explanation for her symptoms; in the chaos of an emergency department flooded with overdoses and heart attacks, her symptoms are too subtle to merit attention. The third time she is examined, she says that she cannot move her right leg at all, refuses to lift it when the doctor asks. This time, she cannot walk out of the emergency room to return home. An MRI shows the unmistakable white lesions of multiple sclerosis, unfurling like flames from the center of her brain. Given a name for her disease, a reason for her symptoms, she will later walk to the bathroom, bearing weight on her right leg. The weakness has retreated to just her foot. This sort of unconscious exaggeration is common enough that it has a name: medicine calls it elaboration, the inadvertent performance of a weak leg to receive care for a weak foot that would otherwise be overlooked.
In the centuries since Charcot’s performances, the term hysteria has fallen out of favor, making way for an entirely new lexicon: functional neurologic symptoms, ones that impair someone’s ability to function with no clear lesion to explain them.
The most obvious of these functional neurologic disorders is malingering, in which symptoms are deliberately faked for secondary gain, for a financial payoff after a car accident or leave from work. Murkier is factitious disorder, where the only possible gain is medical care or attention, the cold comforts offered to the ill. Stranger still is conversion disorder, in which the pageantry of illness is not deliberate or even conscious. Like Sydenham’s hysteria, these symptoms can manifest in any part of the body, although there is often a terrible logic to the places they choose: the inability to speak after witnessing something unspeakable, a weak limb after an experience that robs you of agency. (I had briefly wondered whether my own patient had lost her vision in this way, because of something she did not want to see.)
Even now, the neurology literature is rife with studies offering ways to tease apart functional symptoms—hysterical symptoms—from “real” ones: a tuning fork pressed to each side of the forehead to discern whether someone’s numbness is genuine, or a hand placed beneath the strong leg to test whether it braces as the weak one attempts to lift, called the Hoover’s sign for the neurologist who first described it. The search for a way to distinguish these symptoms is born of necessity: one study estimated that one-third of hospital neurology consultations are for functional symptoms. In the hospital, functional is sometimes shorthand for “not my problem.” On busy days, neurology residents will often report that someone’s weakness is functional because of a “positive Hoover’s sign”—one leg failing to brace the other, offered as evidence that a patient is not truly weak. But when someone is weak in both legs, the Hoover’s sign fails no matter what—neither leg braces and neither lifts, a “positive Hoover’s sign” rendered meaningless, “hysterical” symptoms collapsing into “real” ones.
Charcot’s search for a physical wound to explain hysteria has continued in modern-day neurology, aided by imaging techniques that document the flow of energy coursing through living brains. In patients with functional weakness, these imaging studies show that the structures that suppress unpleasant memories of traumatic experiences are overactive. Perhaps the neurons of the motor cortex are suppressed, too, collateral damage from a haunted brain struggling to quiet itself. In patients with functional tremors—not the circumscribed tremors of Parkinson’s disease or a stroke, but rather a shaking born of emotional dysregulation—the networks of the brain that conceive of the self, that underlie a sense of agency and volition, are silent. Our studies seem to suggest that “real” symptoms and “functional” ones may not represent a binary at all, but rather a spectrum of bodily distress. The line between the two—between the neighboring territories of “psychiatry” and “neurology”—is faint, becoming fainter as we map the nervous system in greater detail. As Charcot surmised, perhaps functional symptoms are simply the result of a lesion we don’t yet have words to fully understand.
IN MEDICAL SCHOOL, thousands of miles and hundreds of years removed from the Salpêtrière, I learn that medicine is still a spectacle. In simulation rooms outfitted with cameras that project to a large-screen television, I playact as an empathetic doctor for an unseen audience of teaching doctors and fellow students, performing compassion as I deliver the news of an imagined ectopic pregnancy to a weeping actor, who calls the embryo growing in her fallopian tube a baby and asks whether it can be transplanted into her uterus. I shake my head: “It’s not a baby. It can’t ever grow into a baby. It’s a collection of cells, growing too big in a space that’s too small.” Half of my brain conjures these words while the other half tries to remember the checklist I’ve been given—points for eye contact, extra for furrowed brows to telegraph my concern. Like blood pressure and heart rate, empathy, we’re told, can be quantified. It is a technical skill that can be taught to future doctors as easily as placing IVs or reading EKGs. In school, I secretly roll my eyes at the idea that empathy can be reduced to a checklist of points, then crease my forehead for the performance.
The first standardized patient, in the sixties, was a model who usually worked in the art department at the University of Southern California. A neurology professor at the School of Medicine had the idea that he might be able to test his students’ mastery of the neurologic exam by having them examine her—in his own training, testing future doctors on their examination skills required recruiting patients from the surrounding hospitals with a prescribed set of diseases, curating a “museum of living pathology” like Charcot’s. “She was coached to have a paraplegia, bilateral Babinski’s,VIII dissociated sensory loss, and a blind eye. She learned to present with the anxiety and concern of the real patient she was modeled after,” the professor wrote of the model. Using standardized patients saved real patients the experience of “being experimented on by neophyte physicians,” allowing student doctors to learn on healthy bodies before plying their trade on sick ones. “It is far better that students make their mistakes in working with a dying patient, a comatose patient, or a sexually abused patient in a simulated setting rather than in the real setting,” he wrote.
Decades later, when I am a resident, I tell a man that his daughter is dead, her brain so turgid with blood and fluid after a car accident that it was crushed against her skull, irretrievably damaged. I have been awake for twenty hours. She is the third young woman who has died on my watch this week. I watch her father cry and can feel only a cold remove. Overcome with shame, I furrow my brows, lean forward, hold eye contact—a performance so concocted that I might as well be wearing a feathered hat onstage at the Salpêtrière. Not until I leave the hospital half a day later am I, too, able to weep.
Onstage at the Salpêtrière, Charcot used his captive patients in a sort of liturgy, demonstrating for his craning audiences the ways the tremors of Parkinson’s disease—called paralysis agitans by neurologists at the time—differed from the head-nodding tremors he termed senile titubation, how the haphazard gaits of alcoholics differed from the swaying of the vertiginous. Late in his career, he began to incorporate hypnotism into his performances. The show would begin with what he termed the “cataplectic” stage of hypnotism, which he induced by shining a bright light into his patient’s eyes, or by sounding a gong or a drum. The woman would become limp and pliable, her eyes frozen. Of this spectacle, one observer wrote, “Body and limbs now maintain any position in which they are placed.... If the arm is raised to a right angle, it remains so; if a leg is placed in a similar position, it does not fall. The patient may be moulded at will, like a waxen figure, into any pose one pleases.... She makes no response to questions, nor in any way gives any sign of being in communication with the external world.”
Charcot claimed that his performers were entirely anesthetized in this state, pricking their skin with pins to show that they did not flinch. In one engraving, he is shown piercing a woman’s entire forearm through and through with a long pin while she smiles beatifically. From cataplexy, he ushered his patients into lethargy, a deep, cadaveric sleep from which they could be aroused by pressure on an ovary, which Charcot had identified as a “hysterogenic zone.” In the final phase, somnambulism, the women would become suggestible, obeying Charcot’s orders. In this state, women could be induced to act the role of an army general barking orders or to stomp at imaginary snakes. Women who had once been blind could suddenly see, those who had been struck dumb could speak, those rendered paralyzed could walk, the power of suggestion as potent as any drug.
Charcot’s hysterics became famous, fictionalized in novels and mocked in newspaper columns. In one painting that still hangs in a Parisian university, a woman in a gauzy white blouse faints into Charcot’s arms before an audience of besuited doctors-in-training. The woman, Blanche Wittman, was his most popular diva, dubbed the Queen of Hysterics by the press. Her hysteria was reportedly cured by Charcot’s death, after which she never had another fit. Instead, she became an assistant in the asylum’s radiology department until her arms became riddled with cancer from the radiation exposure and had to be amputated. A second star hysteric, Louise Augustine Gleizes, entered the asylum at fourteen and escaped five years later, in the only way she could conceive of disappearing from the spectacle: disguised in men’s clothing. Charcot would continue his performances for more than a decade after her escape, one hysteric interchangeable with another.
In some ways, standardized patients are an attempt at privacy, a way of protecting actual patients from having to perform their illness for student after student, of saving students the embarrassment of a bumbling exam witnessed by a person who is genuinely suffering. But pageantry is as much a part of medicine as privacy. For decades after Charcot’s death, each medical department at most university hospitals hosted weekly grand rounds, in which a physician in white coat and tie—a “master clinician” in the image of Charcot—would examine a gowned patient before an auditorium of spectators in hierarchical tiers—faculty in the front rows, then residents, and finally medical students in the nosebleed seats.IX The performance often began with a resident giving a summary of the patient’s history, telling the story as if the patient were not present to tell it personally, before the teaching physician began his routine. When his turn arrived, the master clinician would ask probing questions—“How many miscarriages have you had?” or “How much do you drink?”—and examine the patient in detail, noting for his audience the drooping eyelid of myasthenia gravis, or the weak scapula, jutting from the back like a broken wing, of muscular dystrophy. In pediatrics departments, the patient would be a child or an infant, seated on a mother’s lap or held in her arms.
The patients were chosen because their diagnoses were esoteric or obscure, to test the diagnostic acumen of the teaching physicians and allow them to display the full extent of their clinical prowess. Sometimes, patients with particularly rare or illustrative conditions were kept in the hospital for a few extra days after they would otherwise have been discharged to ensure that they could be presented at grand rounds. Patients were at the center of grand rounds, but the teaching physicians were the stars, reveling in their showmanship, teasing the diagnosis, building suspense, saving the key physical-examination finding—the one that would crack the case wide open—for the final act.
In neurology, patients’ stories, the stigmata of their bodies, are the very ground we walk on. The ability to construct a diagnosis from these scattered details—from the twitch of an eye, from the contents of someone’s most recent meals—is paramount, the neurologists who do this most astutely akin to heroes. To diagnose someone is an art, one students and residents learn by watching those who have mastered it. In some narratives, the pageantry of grand rounds is a way of centering patients, their stories and their bodies at the heart of the exercise. In others, patients and their privacy are sacrificed in the service of something else: elevating the art of diagnosis and, in doing so, lionizing the diagnosticians.
The practice of examining a patient at grand rounds fell out of favor sometime in the late twentieth century, replaced by visiting speakers who deliver PowerPoint slides about their research, but the performance remains a part of teaching hospitals in ways both subtle and overt. I spent my residency in the building where bedside rounds were first named: for the circular wards where patients were housed, teaching doctors sweeping around the wards flanked by their trainees, performing the rituals of the physical examination. I learned to press my fingers against a patient’s wrist even when I already knew their heart rate, to peer through their pupils to search for swelling even when I’d already seen it on their CT scan, to become a white-coated cleric performing the morning’s liturgy. With these maneuvers, we telegraph that we have access to privileged knowledge of our patients’ insides, that by finding their pulse we can know something about their heart, a performance of doctoring that, alongside the white coat, the dangling stethoscope, separates us from our patients. In fact, our diagnoses are a mix of evidence and belief, grounded in things that others have witnessed but we can only take on faith.
The art of performance in medicine—an understanding of the value of a dramatic show, the amplification of illness medicine still demands of its patients and the theatrics it demands of its doctors—would not be the only legacy Charcot would leave behind. In his quest to understand the neurologic basis of hysteria, Charcot meticulously documented the symptoms of each of the women in his asylum. When they died, he studied their corpses. He himself died before ever finding a lesion that caused hysteria, but his approach still yielded dividends, his name preserved in an interminable list of eponymous neurologic syndromes. Among them are Charcot joints, a deformation that Charcot first described in patients with syphilis who had lost sensation in their feet, bearing their weight so unevenly that they fractured their own bones (in the era of penicillin, Charcot joints are much more often an affliction of people living with diabetes than those with syphilis); and Charcot-Marie-Tooth disease, an inherited wasting of the nerves named for Charcot, one of his disciples, and a British contemporary, which Charcot studied in such careful detail that he observed that, although it often progressed over years to involve all four limbs, the disease nearly always seemed to begin in the nerves of the big toe.
Among these eponyms is Charcot’s triad, a constellation of multiple sclerosis symptoms that he observed in a maid who initially worked in his home before being hospitalized at the Salpêtrière: tremors of the eyes, voice, and hands that seemed to worsen with movement, the inverse of the resting tremors he had seen in older patients with Parkinson’s disease. After she died, he dissected her body. In her brain and spinal cord, he saw what he called sclérose en plaque disseminée—the wide-ranging scars of multiple sclerosis. Charcot was also an artist, had spent his life compulsively drawing landscapes and still lifes, portraits of his patients and anatomical deformities, and he drew the plaques as he saw them under the microscope: the myelin fraying from bundles of coarse nerve fibers and floating beside them in greasy droplets. In drawings of the brain, he showed diseased optic nerves like those of my patient’s, stripped bare in patches, exposed and fragile. He would go on to describe thirty-four patients—twenty-five of them women—with the disease. One of the strangest features of the disease, he noted even then, was that it was intermittent, with symptoms that could spontaneously remit and relapse.X
Even though Charcot described sclérose en plaque disseminée as a disease primarily of women, such as his wards in the Salpêtrière, his successors were convinced until the early twentieth century that it was an affliction of men: men who reported sudden, transient blindness or paralysis were given a diagnosis of multiple sclerosis, their symptoms assumed to be the result of a physical malady, a lesion of the brain or spinal cord, while women with the same fluctuating symptoms were dismissed as hysterical. Until even more recently, for perhaps the same reasons, multiple sclerosis was deemed an affliction of white women. We now understand that it affects Black and brown women just as often. Black women are still diagnosed much later in the course of their illness than white women, often with worse symptoms by the time a diagnosis is made. Centuries after Charcot died, I would read the paper “Multiple Sclerosis and Hysteria,” published in 1980. “Multiple sclerosis,” the authors explained, “shares with hysteria a common epidemiology (young patients and preponderantly women), prevalence, and frequency of equivocal, difficult-to-verify abnormal neurological signs.”
My patient, the student, found her vision improving in fits and starts. She left the hospital to reenter a world just slightly dimmer than it had been before. To keep the attacks at bay, she started a course of infusions designed to suppress her body’s immune system, to keep it from attacking her nerve fibers. In the winter, she caught every flu and cold, and when she burned her wrist pulling a baking dish from the oven, the wound—robbed of a functioning immune system—seemed as though it would never heal. But the hospital was the place where a miracle had once happened—the restoration of her sight—and the next year, when she had another attack, she returned. This time, the lesion was in her spinal cord; it left her incontinent and bedbound, her legs too weak to bear her weight.
By then I had begun to understand the limitations of the treatments we had given her. I could see the way in which her body healing itself was as much miracle as it was medicine. We gave her the same steroids as we had before, cleansed her blood with the same machinery. When she left the hospital weeks later, she walked out, her legs only slightly heavier than they had been before.
In some ways, multiple sclerosis is as much a prison as the Salpêtrière once was, young women held hostage by the uncertainty of their haphazard symptoms. The disease is one of a body betraying itself, one’s own immune system stripping the brain and spinal cord of something essential until the whole is no longer greater than the sum of its parts.
Understanding this basic truth of invisible diseases—the way in which they turn a body on itself—requires both knowledge and faith. It is intensely private, the inverse of the dramatic performances given at the Salpêtrière. Years later, I can finally comprehend my own perfidy, that of a medical student still going through the motions of empathy with nothing beneath them, unable to grasp that which I could not see and that which I had not, in my brief training, already seen, stuck at the superficial spectacle of tears and prayer. The body, I know now, is capable of producing its own spectacles, as phenomenal as the shows at the Salpêtrière and infinitely more powerful.
- I. At the time my patient lost her vision, scientists suspected that there could be a link between Epstein-Barr virus and multiple sclerosis, but because Epstein-Barr virus is so common—90 percent of the world’s population has at some point been infected—the data were murky. More recently, a 2022 study of 10 million active-duty military personnel who were followed over two decades found that the incidence of multiple sclerosis increased more than thirty-six-fold after people contracted Epstein-Barr virus. Still, the nature of the relationship between the virus and the disease is opaque.
- II. Neuromyelitis optica is also three times as common in women of Asian descent and ten times as common in Black women as it is in white women. It is difficult to know the full geographic extent of most demyelinating diseases—in the twenty-first century, both neuromyelitis optica and multiple sclerosis are typically diagnosed with MRIs, which are not readily available in most of the world—but on a map shaded for those places where the prevalence of known cases of neuromyelitis optica is highest, two curving archipelagoes of islands—Japan, arcing south from the frigid Sea of Okhotsk, and the Antilles, spanning the warm waters of the Caribbean—would be the most densely colored.
- III. There are virtually no studies on demyelinating diseases—in fact, on any neurologic disease—in people of underrepresented genders; what limited information we have on the prevalence of multiple sclerosis in this group comes from a single British study using National Health Service data, which suggested that trans women suffer from multiple sclerosis more than six times as often as cis men.
- IV. Multiple sclerosis is a plague of women’s childbearing years, but it seems to remit during pregnancy. The third trimester of pregnancy is as potent at suppressing multiple sclerosis flares as most of our drugs, although the disease often returns with renewed vigor in the postpartum months, when one-third of women will experience a relapse.
- V. The Salpêtrière derives its name from saltpeter, a critical component of the gunpowder that was once manufactured on its grounds.
- VI. The documents that have survived don’t offer a complete picture of how ancient Egyptian medicine influenced the works of Hippocrates, but the gynecological treatises of the Hippocratic Corpus seem to echo those of the Egyptian papyri produced ten centuries earlier in both their structure and the particular tests and remedies they describe. Some of the treatments Hippocrates offered rely on pharmaceuticals first produced in Egypt, and the Greek historian Herodotus—a contemporary of Hippocrates’s—wrote of Egypt, “It is all full of doctors.”
- VII. Lesion is among neurology’s favorite words, a catchall term used to describe a physical wound within the nervous system. A neurologic lesion can arise from virtually any illness, from a tumor to a stroke to a demyelinating disease.
- VIII. The Babinski sign is named for Josef Babinski, a pupil of Charcot’s who practiced in the trenches of World War I and wrote on what he called hystérie-pithiatisme—symptoms that could be “reproduced by suggestion and disappear by persuasion,” often resulting from the traumas of war. His eponymous sign, elicited by stroking the sole of the foot and observing whether the toes fan upward (an abnormal response in adults) or curl down (a healthy one) was offered as a way to distinguish “hysterical” weakness from “real” weakness originating in the brain or spinal cord. Contemporary studies on the accuracy of the Babinski sign have found that roughly half the time a patient with weakness arising from an injury to the brain or spinal cord expected to cause a “positive Babinski reflex” will have a negative one, and that multiple neurologists examining the same patient often disagreed about whether the reflex was positive or negative depending on whether they had access to the rest of the patient’s medical file.
- IX. “The rear rows, some are cynical enough to suggest, also offer easy egress to those who wish to take care of other matters once their attendance has been recorded,” bemoaned one professor in a 1978 essay, “The Graying of Grand Rounds,” in the New England Journal of Medicine.
- X. On the subject of treatment, Charcot was terse. In one lecture, after demonstrating the tremor he saw as characteristic of the disease in one of his patient-performers, he asked his audience, “After what precedes, need I detain you long over the question of treatment? The time has not yet come when such a subject can be seriously considered. I can only tell you of some experiments which have been tried, the results of which have, unfortunately, not been very encouraging.”
In the era when many still prayed to the patron saint of chronic pain, the treatment was prayer, augmented by beefsteaks and fortified wine, by tepid baths and astringent plasters and ingestion of strychnine. One manuscript from the 1930s alphabetizes the treatments that had been tried to date—most still in use at that time—from antimony to X-ray, in a twenty-nine-page table. Fevers were induced by infecting patients with malaria, blood cleansed with injections of arsenic and silver, electrical impulses and leeches applied to the skin. Some hastened death, others palliated pain, still others were excruciating, but none stopped the plaques from forming or kept the inexorable symptoms from waxing and waning.