One Sunday morning in January 2018, Eric McLaughlin was putting on his shoes while helping his son get ready for hockey practice. Suddenly, he felt he’d been “turned off,” McLaughlin says, and when his wife asked him what was wrong, he found he couldn’t speak. At the skating rink, the attacks of paralysis continued and became more intense. When parents of other kids approached, McLaughlin could hear them but was unable to respond.

At the time, McLaughlin’s job was doing road maintenance in southern New Hampshire. He had never before had any physical or mental health problems that seemed serious. He had injured his ankle at a worksite, he suffered periodic migraines and some people described him as anxious—“I hate that word,” McLaughlin says—but generally he was fine.

His primary care physician sent him to the local hospital, and he was admitted with a racing heart and monitored for cardiac arrhythmia. Yet the doctors found no clear reason for what he was experiencing. They described his condition as “mental,” his racing heart as “psychosomatic.” After McLaughlin was discharged, his doctor referred him to the Massachusetts General Hospital Emergency Department, where his inpatient team of physicians cataloged the symptoms: the tensing up, an increase in heart rate, confusion, sudden episodes of paralysis and his sense of a “fat tongue.” Everything in his nervous system appeared to be structurally sound, yet it was nevertheless malfunctioning. Impulses in his brain were somehow being diverted or hijacked by certain neural pathways, causing seizures—so-called functional (psychogenic, non-epileptic) seizures­­—and other symptoms. They were the hallmark of a condition now known as functional neurological disorder, or FND.

FND, under various names, has perplexed physicians since ancient times. Many know it as conversion disorder, a term still in use, which frames the condition as a psychological illness—stress or neurosis expressed, or converted, into physical symptoms. But patients with FND aren’t, by conventional standards, necessarily mentally ill, although many also suffer from anxiety, depression or post-traumatic stress disorder. Nor are these patients necessarily physically ill, though functional neurological symptoms may be observed in patients with strokes, epilepsy or Parkinson’s disease.

Until very recently, FND remained largely mysterious. It wasn’t a “rule in” diagnosis, something that test results might reliably point to. Often, in its many guises, it mimicked better known conditions. It was frequently a last resort, a diagnosis based on medically unexplained symptoms, arrived at only after ruling out everything else.

That confusion about the diagnosis and causes of FND has long been accompanied by a reluctance by physicians in various specialties to treat it. As recently as a few decades ago, and for a half century before that, neurologists had argued that symptoms such as those now associated with FND weren’t real—the problems were entirely mental, performative, “all in your head.” But while these patients may be more likely to have psychological trauma in their backgrounds, not all of them do, and the idea that this is the root cause of the disease is drastically changing. 

With his diagnosis of FND, McLaughlin was referred to David Perez, a neurologist and psychiatrist who leads the Functional Neurological Disorder Unit at MGH. Perez is part of a pioneering international group of scientists who, helped by increasing sophistication in brain-scanning technology and other diagnostic tools, are beginning to solve the mystery of FND. Perez can help McLaughlin and patients like him with an expanding range of treatments that bridge the gap between neurology and psychiatry—a therapeutic approach which, like the disease itself, exists “at the intersection of the mind and brain.”

Since the beginning of medical history, physicians have recorded symptoms such as McLaughlin’s—falling into seizures; losing the ability to stand, walk, talk, hear or see; or becoming paralyzed, all without apparent connections to muscles or the nervous system. In early Greek medical texts, such dysfunction was pinned on reproductive organs—a “wandering womb”—and it was then that the notion of “hysteria,” from the Greek word for uterus, first became attached to the condition. (The historic connection to women persists, and today, about two or three times as many women as men are affected by FND.) In later eras, demonic possession was blamed. Although there was progress in diagnosing similar neurological conditions such as epilepsy and Parkinson’s disease that had more visible organic symptoms, these cases continued to be mysterious. In the late 19th century, Pierre Janet, an influential French psychologist, physician and hypnotist, characterized functional neurologic symptoms as a matter of “suggestion,” a too strong idea that overcame the patient. Jean-Martin Charcot, Janet’s teacher and the father of modern neurology, looked for “dynamic lesions” in the brains of his patients that might be the source of these inexplicable breakdowns.   

In the early 20th century, Sigmund Freud—who explored the phenomenon with physician Josef Breuer in his 1895 book Studies on Hysteria—argued that these conditions resulted from repression and were a physical expression of unspeakable traumatic memories. In his view, patients who were unable to name their emotional pain found their bodies involuntarily signaling it. Treatment, in his view, would come from psychoanalysis that could help identify patients’ hidden trauma.

But the rise of the Freudian paradigm was accompanied by a loss of interest among neurologists. In 1908, prominent New York neurologist Bernard Sachs wrote that “while hysterical patients … are numerous enough,” their suffering was “less important than the sufferings of those afflicted with various forms of organic spinal disease.” Soon, psychiatrists, too, backed away from the problem, which turned out not to be easily resolved with drugs or traditional psychoanalysis. In the mid-1960s, the book Hysteria: The History of a Disease announced “the near total disappearance” of hysteria as a diagnosis. In 1965, eminent British neurologist and psychiatrist Eliot Slater went further, arguing in a seminal paper that hysteria had never existed, but rather was the result of misdiagnosis. In the 1980s and 1990s, most doctors wanted little to do with these patients—who had become “almost literally invisible to medicine,” according to historian Andrew Scull, who called them “modern medicine’s untouchables.”

Yet the years wore on, and their numbers could not be ignored. With clearer statistics, it became evident that FND touches about as many people as Parkinson’s disease or multiple sclerosis. Functional neurological symptoms are the second most common reason for outpatient visits to neurology clinics. A turning point in acknowledging the condition came in 2000, when Sean A. Spence of the University of Sheffield in England published a study in The Lancet.  Using positron emission tomography, Spence found distinctly different patterns of activation in the brains of diagnosed conversion patients compared with the brains of a control group—in this case, actors hired to feign the same symptoms. 

Then in 2007, Jon Stone—a neurologist at the Centre for Clinical Brain Sciences at the University of Edinburgh and one of the leading global voices in FND diagnosis and treatment—published an article in which he and his colleagues built on Spence’s results. Through MRI scans, Stone and his team looked at patients with functional ankle and leg weakness and discovered unusual patterns in several brain regions, involving the basal ganglia, insula, lingual gyri and inferior frontal cortex. Those brain patterns differed from those in people who faked the same conditions and suggested that motor control in the brains of people with FND might be somehow impaired. 

Later research brought this into clearer focus, revealing abnormal functional connections in certain brain networks. For example, irregularities appeared in the salience network—a collection of neurons in the cortical and subcortical parts of the brain that help process and determine the relevance of sensory information—and the limbic network, the deep brain connections involved in emotion processing. In a 2010 study published in Neurology, Valerie Voon, a neuropsychiatrist at the University of Cambridge, suggested that people with FND have reduced activity at the right temporal parietal junction, a crucial node in the network that controls self-agency, or the sense people have of directing their own bodies.

One idea to come out of this research is that, for people with FND, unusual interactions between brain networks—between prediction and response—lead to impairments in feedback and feed-forward loops. These may make it difficult to perceive or predict threats or to respond to them. So Eric McLaughlin felt perfectly calm while his heart raced and his limbs froze. 

Today the condition straddles two terms in the DSM-5, the chief taxonomic tool of the American Psychiatric Association. Conversion disorder remains on the books, albeit in a secondary position to functional neurological disorder. The latter is a newer and overlapping description of nearly identical symptoms. It is the result of an effort by Stone and colleagues to correct the judgment implied by “conversion disorder” and the term’s connection with the older ideas of hysterical conversion, which posits a singular cause almost entirely within the mind. The new model proposed by Stone, Perez and others suggests a “biopsychosocial” origin—a problem with multiple roots in brain biology, patient history and the social context of their lives.

In his work, David Perez brings all of these factors together. In addition to leading the FND Unit at MGH, Perez is director of the MGH Functional Neurological Disorder Research Group, and for much of the past decade he has published extensively on FND, leaning into his training as a psychiatrist, neurologist and neuroscientist. The pressure to distinguish too neatly between physical and mental health in FND may not be necessary. “Some patients with FND that I encounter may have important psychological disturbances,” he says, “yet when they have trouble walking or have convulsions, their symptoms are every bit as real, and every bit as brain-based, as those of patients with stroke or Parkinson’s disease.”

Some of those symptoms—seizures that aren’t easily explained by electrical storms in the brain (functional seizures) and difficulty in controlling movements (functional movement disorder, or FMD)—have been at the heart of his research. In terms of sheer numbers, these two conditions represent a crisis in neurology. “In epilepsy and movement disorder subspecialties, upwards of 20% to 30% of patients admitted to the epilepsy monitoring units and 20% of patients seen in movement disorder clinics” have functional seizures or FMD, he wrote in a 2015 paper. Yet despite the frequency with which neurologists encounter these conditions, most have “limited comfort” in caring for them.

Perez notes that in more recent years, research has started to settle into a working model of how the condition probably takes shape in the brain. In a 2021 review article that focuses on functional motor symptoms, Perez and his co-authors outline possible mechanisms. When people need to make voluntary movements, the brain switches between consciously experiencing control of movement and the neural networks that perceive those movements and enable them to occur. Problems like speechlessness or paralysis may arise when nonconscious cognitive, perceptual and affective processes interfere with the sensory and motor parts of the process.

Sometimes that kind of problem may develop after an injury, Perez says. Focusing on what has been hurt—Eric McLaughlin thinking about his injured ankle, for example—could bring “heightened attention to the self and activation of bodily arousal systems.” An important implication of this and other recent work has been to support the idea that FND is a brain-based condition that bridges neurology and psychiatry, Perez says.

Indeed, as a wealth of research shows, FND can’t be understood exclusively as the result of either psychological or biological factors. For Freud, conversion disorders began in childhood trauma, with episodes of hysterical conversion happening when the memory was summoned and repressed. Experts in the field note that between 20% and 50% of patients with functional seizures have experienced sexual or physical abuse or neglect—but while traumatic childhood experiences can be seen as a risk factor, they are not a clear-cut cause.

Events during childhood can affect brain development, sometimes leading to over-activation of parts of the limbic system, including the amygdala and the hippocampus. And a study published in Epilepsy & Behavior in September 2021 explored one way in which such psychological factors might manifest themselves to promote functional seizures. The study compared fMRI brain scans of 23 people having functional seizures to 25 healthy controls. Noting the differences in several brain areas, the researchers concluded that emotion-processing regions in the patients experiencing the seizures inhibited the brain’s executive control areas and motor regions. That suggests emotional arousal could contribute to the problem, and that cognitive behavioral therapy might help those patients regulate their emotions and avoid seizures.

Social and cultural factors can play a role, too. In a 2021 article in JAMA Neurology, Perez and several colleagues noted that some adverse responses to the COVID-19 vaccine, such as seizures and abnormal movements, are “seemingly consistent with FND.” The patients aren’t faking their symptoms, yet it’s unlikely the chemistry of the vaccines plays a causative role in FND—a shot of saline water might have the same effect.

When Perez established his FND clinic at MGH in 2014, it was embedded across the neurology and psychiatry departments. It has since been elevated to its own unit, and its growing multidisciplinary and interdisciplinary staff includes five neurologists and two psychiatrists, as well as a speech therapist, a physical therapist, an occupational therapist and two psychotherapists.

New patients meet a physician for a 90-minute assessment and work collaboratively to put together a plan of action that can run the gamut—a personalized combination of talk therapy, speech therapy, physical therapy and occupational therapy. “One patient may have never seen a psychiatrist,” says Perez. “Another may have been psychiatrically hospitalized multiple times with a range of active mood-, anxiety- and trauma-related symptoms.” Even two patients with nearly identical physical symptoms may have divergent treatment needs. In working with his patients, Perez and his team look not only to understand the complex biopsychosocial factors contributing to disabilities but also to explain them in a way that promotes growth and recovery.

A plan of action for treatment can run the gamut—talk therapy, speech therapy, physical therapy and occupational therapy.

Kyla Kenney, a singer from Rhode Island, went to the FND Unit because she was experiencing crippling headaches and tremors. Other doctors had found no reasons for her condition. But Perez showed her that the likely diagnosis of FND meant that she was experiencing a common, diagnosable disorder that could be treated. He prescribed a combination of cognitive behavioral therapy and occupational therapy, and through that, she has learned a set of skills to help with her tremors. She keeps super sour candies (a “sensory snack”) in her purse, and when she feels symptoms coming on, she pops one in her mouth—the awful taste can distract her and prevent tremors. 

Meanwhile, Perez and his colleagues are contributing to a renewed scientific interest in FND. He recently received a $4.1 million grant from the National Institutes of Health to use fMRI imaging to better understand the brain network mechanisms underlying symptoms, disease risk and clinical outcomes. Separate, recently published work by another group explores the possible impact of stress-related systemic low-grade inflammation on patients with FND. The researchers discovered elevated levels of inflammation in patients with FND that could possibly mimic stroke-like symptoms, and microRNA levels in the blood also seemed to play a role, influencing the expression of genes.

One major advance Perez hopes to see in the next few years is the stigma of FND finally falling away—not only among the public but his colleagues across the clinical brain sciences. “For decades, these have been patients that we couldn’t help much, and so many of them were told that their disease was all in their minds,” he says. “But our job is to be doctors of the brain and mind. The science is finally catching up. And as the picture becomes clearer, we have so many people that we can help.”