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This article discusses historical medical language, including the word hysteria and conversion. Those terms can be considered outdated, imprecise and often stigmatising. It is used here only because it played a major role in the history of conditions now classified as functional neurological disorder.

Medical disclaimer: This article provides general educational information and is not a diagnosis or a substitute for individual medical advice. New or changing neurological symptoms—especially sudden weakness, speech difficulty, loss of consciousness or a first seizure—require appropriate medical assessment.

Introduction

Functional neurological disorder (FND) can sound like a new diagnosis. The name is relatively modern. The symptoms are not.

For thousands of years, people have experienced paralysis, tremors, seizures, loss of speech, blindness, numbness, abnormal movements and problems with walking that the biologists and medicine of the time could not explain.

Different societies tried to make sense of these symptoms using the ideas available to them. Explanations have included displaced organs, supernatural forces, disturbed “animal spirits”, nervous dysfunction, traumatic memories, dissociation, suggestion and subconscious conflict. Today, researchers are investigating changes in brain networks, attention, prediction and the sense of control over movement.

This history matters because some of the old assumptions still affect people with FND today. People may still be told that “nothing is wrong”, that their symptoms are “all psychological”, or that they must be producing them consciously. Those conclusions are wrong.

FND symptoms are real and involuntary.

FND is a genuine problem with how the nervous system is functioning.

The diagnosis should be supported by positive clinical features—not simply by normal scans or by failing to find another condition.

So this is more than a history of changing names. It is the story of medicine repeatedly trying to understand symptoms that do not fit comfortably into the artificial divisions between brain and mind, neurology and psychiatry, or body and experience.

A necessary warning about retrospective diagnosis

It is tempting to take every ancient account of unexplained paralysis, collapse or convulsion and call it FND. That would go too far.

Historical descriptions were written before modern neurological examinations, EEG, brain imaging, blood tests and contemporary diagnostic criteria. A person described as having “hysteria”, “possession”, “shell shock” or a “nervous disorder” might today receive a diagnosis of epilepsy, migraine, multiple sclerosis, Parkinson’s disease, PTSD, panic disorder, a dissociative disorder, FND—or more than one of these.

The safest conclusion is that FND-like symptoms have been recorded for a very long time, while recognising that old diagnostic categories do not map perfectly onto modern ones. Even “hysteria” was never a single stable disease. At different times it included symptoms now separated into FND, epilepsy, dissociative disorders, somatic symptom disorders, personality diagnoses and various recognised neurological or medical conditions.

The history at a glance

Period	Common explanation or label	Lasting significance
c. 1900 BCE	Uterine illness in Egyptian medical texts	Among the earliest surviving descriptions later linked—sometimes too confidently—to “hysteria”
Classical Greece and Rome	“Hysteria”, linked to the uterus; later broader bodily theories	Created a gendered label that persisted for centuries
Medieval and early modern Europe	Mixture of bodily illness, religious explanations, possession and witchcraft	Some ill people were moralised, punished or exorcised rather than treated
17th century	Brain and nervous-system explanations; “hysteria” also recognised in men	Willis and Sydenham helped move the disorder away from the uterus
18th century	Nervous disorder, animal magnetism, suggestion	Mesmerism inadvertently highlighted expectation, attention and therapeutic interaction
19th century	Neurosis, reflex disorder, dissociation, traumatic hysteria	Briquet, Charcot, Janet, Bernheim, Breuer and Freud created competing models
Early 20th century	Pithiatism, conversion, psychogenic symptoms; shell shock	Positive signs, suggestion, trauma and rehabilitation all became prominent
Mid-to-late 20th century	Conversion reaction/disorder, dissociative and somatoform diagnoses	FND became increasingly located within psychiatry and often neglected by neurology
21st century	Functional neurological symptom disorder / FND	Diagnosis by positive signs; integrated biological, psychological and social models; renewed research and treatment

Ancient Egypt: the earliest alleged ancestor of FND

Many histories begin with the Kahun Gynaecological Papyrus, usually dated to around 1900 BCE. The text described a range of illnesses in women and attributed some problems to the uterus. Later Egyptian writings, including the Ebers Papyrus, also described treatments intended to influence the position or behaviour of the womb.

Modern authors have sometimes presented these passages as the first recorded cases of hysteria and therefore the first FND. That is possible only in a very broad historical sense. The papyri do not contain a modern neurological diagnosis, and the familiar phrase “wandering womb” is more directly associated with later Greek medicine. What the Egyptian material clearly demonstrates is an early tendency to explain varied bodily and behavioural symptoms through female reproductive anatomy.

That idea had an extraordinarily long life. It also planted the seed of one of the most damaging themes in this history: the assumption that puzzling illness was especially female and somehow arose from female biology.

Classical Greece: hysteria and the “wandering womb”

The word hysteria comes from the Greek hystera, meaning uterus. Writings in the Hippocratic corpus, produced by several authors around the fifth and fourth centuries BCE, described the womb as capable of moving within the body and causing symptoms by pressing on other organs. Breathlessness, choking, faintness, pain and other disturbances were interpreted within this model. Marriage, pregnancy, sexual activity, fumigation and scented or unpleasant substances near different parts of the body were among the proposed remedies.

It would be misleading to say that Hippocrates “discovered FND”. The reported symptoms were mixed and the theory was anatomical, reproductive and incorrect. Nevertheless, later medicine repeatedly connected the Hippocratic tradition with hysteria.

The Greek physician Galen (129–c.216 CE) rejected the literal idea of a womb roaming freely through the body. However, he continued to associate hysterical symptoms with reproductive processes, including retained sexual fluids. The organ may have stopped wandering, but the gendered explanation remained.

There were also descriptions outside this female framework. Herodotus told the story of Epizelus, an Athenian soldier who became blind during the Battle of Marathon despite apparently receiving no physical eye injury. Some modern writers have wondered whether this could be an early account of functional blindness following trauma. It is an intriguing parallel, not a diagnosis that can now be established.

The Middle Ages: illness, religion and possession

The idea that medieval Europe explained every unusual symptom as witchcraft is an oversimplification. Classical medical theories, including humoral and uterine explanations, continued alongside Christian and folk beliefs. Physicians, clergy and communities could interpret convulsions, paralysis, altered awareness, unusual movements or loss of speech in very different ways.

Some experiences that might now prompt neurological and psychiatric assessment were attributed to demonic possession, sin, spiritual testing or witchcraft. Prayer, pilgrimage and exorcism could therefore sit beside herbal and physical treatments. In the worst cases, vulnerable people were accused, punished or killed.

We cannot know how many of these people had FND. The historical importance lies in the moralisation of unexplained symptoms. When medicine could not explain an illness, responsibility was often transferred to the sufferer—an attitude that, in less overt forms, has survived into modern healthcare.

The 17th century: moving hysteria from the womb to the brain

The seventeenth century produced an important change. Thomas Willis (1621–1675), a founding figure in neurology, argued that hysteria arose from the brain and nerves rather than a wandering uterus. His proposed physiology was still based on period concepts such as “animal spirits”, but the shift was fundamental: symptoms could be understood as disturbances of nervous-system function.

Thomas Sydenham (1624–1689) then gave a remarkably broad clinical description of hysteria. He recognised that it could imitate many diseases and affect many parts of the body. Crucially, he also described a related condition in men, commonly called hypochondriasis. Although he retained separate gendered labels, the uterus was no longer an adequate explanation.

Sydenham’s observation that hysteria could mimic almost any bodily disease had two legacies. It encouraged careful clinical observation, but it also helped create the stereotype of a deceptive or protean illness. The patient’s symptoms were real; the danger lay in treating variability as dishonesty.

The 18th century: nerves, mesmerism and the power of suggestion

During the eighteenth century, “nervous” explanations became fashionable. The nervous system offered a way to connect emotion, bodily sensation and behaviour without relying solely on the uterus or the supernatural.

One of the strangest chapters began with Franz Anton Mesmer (1734–1815). Mesmer claimed that illness resulted from disturbances in an invisible universal fluid called “animal magnetism”. His dramatic treatments involved magnets, iron rods, group rituals and intense therapeutic attention. Some patients developed convulsions or “crises” and then reported relief.

In 1784, a French royal commission that included Benjamin Franklin and Antoine Lavoisier investigated Mesmer’s claims. Its controlled demonstrations found no evidence for a magnetic fluid and concluded that effects were better explained by imagination, imitation and expectation.

Mesmer’s theory was wrong, but the episode was historically important. It showed that symptoms and bodily experiences could change through attention, expectation, social context and suggestion—processes that modern neuroscience investigates without assuming that symptoms are imaginary.

In the nineteenth century, “animal magnetism” gradually developed into the more psychologically framed study of hypnosis. This would become central to arguments about hysteria and later FND.

The 19th century: hysteria becomes a clinical research subject

Briquet’s detailed observations

In 1859, French physician Paul Briquet published Traité clinique et thérapeutique de l’hystérie, based on hundreds of patients. Briquet rejected a simple uterine theory and treated hysteria as a neurosis involving the nervous system. His work was more systematic than many earlier accounts and acknowledged heredity, environment, emotion and adverse experiences.

However, Briquet’s broad category included a large range of symptoms that would not all be called FND today. “Briquet’s syndrome” later became associated with somatisation rather than specifically with functional neurological symptoms.

Charcot and the Salpêtrière

The most famous nineteenth-century figure in this history is Jean-Martin Charcot (1825–1893), often described as a founder of modern neurology. At the Salpêtrière hospital in Paris, Charcot applied neurological observation to women diagnosed with hysteria and later to men with similar symptoms.

Charcot made several important advances:

• He treated hysteria as a legitimate illness rather than simple malingering.
• He demonstrated that men could be affected.
• He distinguished hysterical symptoms from epilepsy and structural neurological diseases.
• He described paralysis, sensory loss, abnormal movements and dramatic seizure-like episodes.
• He recognised that accidents and fright could precipitate symptoms—what he called traumatic hysteria.
• He proposed a “dynamic” or functional lesion: a real physiological disturbance without the structural tissue damage seen at post-mortem in other neurological diseases.

That last concept has an unexpectedly modern ring. Current FND is not defined by tissue destruction visible on routine scans; it concerns abnormal functioning within brain systems. Charcot did not have today’s neuroscience, but he recognised that a disorder could be genuine without a conventional anatomical lesion.

Charcot also linked hysteria with susceptibility to hypnosis and presented patients in famous public teaching demonstrations. These displays made hysteria scientifically visible, but they remain controversial. The symptoms shown by some patients may have been shaped by expectation, rehearsal, suggestion and the institutional environment. His rival Hippolyte Bernheim and the Nancy School argued that hypnosis was a normal psychological state produced by suggestion, not a pathological state unique to hysteria.

The debate still feels relevant. It concerned how symptoms are influenced by attention, relationships, expectations and social learning—without resolving where involuntary experience ends and interpersonal influence begins.

Pierre Janet: trauma, dissociation and subconscious processes

Pierre Janet (1859–1947) developed one of the most sophisticated early psychological models. In L’Automatisme psychologique (1889) and later work, Janet proposed that overwhelming experiences could narrow or disrupt the integration of consciousness. Memories, sensations and actions might become dissociated from ordinary awareness and voluntary control.

Janet used hypnosis both to investigate symptoms and, in some cases, to treat them. He did not simply claim that hidden thoughts were deliberately acted out. His model concerned automatic psychological processes outside normal conscious control. Modern ideas about dissociation, disrupted agency and trauma owe a substantial debt to Janet, although contemporary FND cannot be reduced to his theory.

Breuer, Freud and “conversion”

Josef Breuer and Sigmund Freud’s Studies on Hysteria appeared in 1895. Their best-known cases included patients with paralysis, sensory changes, pain, visual disturbance, speech problems and other symptoms. They proposed that unbearable ideas or affects could be excluded from conscious awareness while their emotional energy was “converted” into bodily symptoms. This is the origin of the later term conversion disorder.

Early in his career, Freud studied with Charcot and also visited Bernheim. He experimented with hypnosis and suggestion, but Freud did not seem to be very good at hypnosis at all. Freud found his hypnosis skills to be unreliable: not every patient entered the desired state, and symptom relief could be temporary. He gradually moved to alternative approaches such as pressure techniques, free association and psychoanalysis.

Freud’s historical influence was enormous, but it was mixed. He helped establish that symptoms could be involuntary, meaningful and connected to experiences outside conscious awareness. Yet the success of psychoanalysis also narrowed much twentieth-century thinking around a specific model: repressed psychological conflict converted into physical symptoms. Evidence of such a conflict was too often assumed even when it could not be demonstrated.

Freud’s failure to develop adequate hypnosis skills has resulted in the serious failure to adopt hypnosis and hypnotherapy widely through medical services, even though modern research reports that it can be highlight effective to conditions such as FND, chronic pain, IBS, anxiety and more.

Freud did not single-handedly advanced the field and may have actually hindered its progress. Nor did Freud simply prove that hysteria was caused by trauma. His theories changed over time, and later psychoanalytic accounts were not the same as modern evidence-based models of FND. Janet, Bernheim, Breuer and many patients themselves made essential contributions.

Babinski, positive signs and “pithiatism”

After Charcot’s death, his pupil Joseph Babinski (1857–1932) tried to make the category more precise. In the early 1900s he proposed the term pithiatism, derived from Greek words relating to persuasion and cure. He defined these disorders as symptoms that could be produced by suggestion and relieved by persuasion.

The label did not last, and “curable by persuasion” sounds simplistic today. FND is not normally resolved by telling someone to stop having symptoms. Nevertheless, Babinski highlighted two enduring ideas:

1. Diagnosis should depend on characteristic clinical features rather than merely the absence of disease.
2. A symptom’s capacity to change under particular conditions can reveal preserved nervous-system function.

In 1908, American physician Charles Franklin Hoover described the sign that now bears his name. In functional leg weakness, apparently weak hip extension may return automatically when the opposite hip flexes against resistance. Hoover’s sign is not a trick designed to catch a patient out. It demonstrates a difference between attempted voluntary movement and automatic movement, providing positive evidence of functional weakness.

Modern examination uses the same general principle in signs such as tremor entrainment, distractibility and internal inconsistency. These findings show how symptoms work; they do not show that they are deliberate.

The First World War: shell shock changes the gendered story

The First World War produced vast numbers of soldiers with tremor, paralysis, mutism, blindness, gait disturbance, seizure-like attacks, memory problems and states of altered awareness. Some had direct brain injuries, blast exposure or other physical disease; others had no detectable structural injury. The term shell shock, introduced by Charles Myers in The Lancet in 1915, initially suggested physical damage caused by exploding shells.

Hypnosis was used extensively through the first world war to help soldiers overcome “shell shock”.

Although the name “shell shock” was inadequate when similar symptoms appeared in soldiers who had not been close to an explosion. Doctors used overlapping labels including shell shock, war neurosis, traumatic neurosis, neurasthenia and hysteria.

A modern review of records from the National Hospital at Queen Square examined 462 servicemen admitted with functional neurological disorders between 1914 and 1919. The case notes contain recognisable descriptions of functional movement symptoms, weakness and seizure-like episodes. They also show a wide range of treatments, from rest and rehabilitation to hypnosis, suggestion and harsh electrical procedures.

The war decisively demonstrated that dramatic functional symptoms were not confined to women. Unfortunately, the female stereotype was often replaced by another moral judgement: affected soldiers might be labelled weak, cowardly or motivated by escape from duty or compensation. Some treatments were explicitly disciplinary.

Other clinicians took more humane approaches. W. H. R. Rivers, working with traumatised officers including Siegfried Sassoon, argued against simply suppressing painful war memories. Arthur Hurst used explanation, demonstration, suggestion and rapid physical retraining in some motor cases. His films appear to show spectacular recoveries, although historians have questioned their staging and selection.

Shell shock is not simply an old name for FND. The category also contained what would now be called PTSD, traumatic brain injury, depression, anxiety and other conditions. It nevertheless forced medicine to confront neurological-looking symptoms in men exposed to extreme physical and psychological stress.

Between the wars and after 1945: neurology and psychiatry divide the territory

As structural neurology advanced, diseases such as epilepsy, multiple sclerosis and movement disorders became better differentiated. Symptoms without a recognised lesion were increasingly handed to psychiatry. Psychoanalytic conversion became a dominant explanation, particularly in the United States.

The first Diagnostic and Statistical Manual of Mental Disorders (DSM-I, 1952) used conversion reaction within “psychoneurotic disorders”. DSM-II (1968) retained hysterical neurosis, conversion type. DSM-III (1980) removed “hysteria” from the formal label and introduced conversion disorder, locating it among somatoform disorders. DSM-IV continued the diagnosis and required psychological factors to be judged associated with the symptom.

These classifications reduced some of the old language but preserved Freud’s causal theory inside the name and criteria. The diagnosis often depended on two weak foundations: tests had not revealed an “organic” disease, and a clinician believed that psychological conflict or stress must be responsible.

This encouraged a damaging clinical gap. Neurologists sometimes felt their job ended once structural disease was excluded; psychiatrists could be reluctant to accept a patient who did not identify a psychological problem. Patients were left between specialties, sometimes after years of tests and contradictory explanations.

Misdiagnosis, stigma and the meaning of “psychogenic”

The mid-twentieth-century literature also created lasting fear about misdiagnosis. A highly influential 1965 follow-up by Eliot Slater and Maurice Glithero reported that many patients previously labelled hysterical later developed neurological disease. The paper encouraged the view that hysteria was a dangerous diagnostic mistake.

Later reappraisal showed important methodological problems: early cohorts lacked modern investigations, diagnostic criteria were loose, and the original “hysteria” category was very broad. More recent studies find that diagnostic revision can occur in both directions—FND mistaken for neurological disease and neurological disease mistaken for FND—but rates are much lower when diagnosis is based on recognised positive signs and appropriate assessment.

FND can also coexist with neurological disease. A person can have epilepsy and functional seizures, Parkinson’s disease and functional movement symptoms, or multiple sclerosis and functional weakness. The presence of one must not automatically exclude the other.

The word psychogenic became increasingly unpopular because it claimed a psychological cause that might not have been established. It also invited patients to hear “imagined” or “made up”, even though that was not its technical meaning. Likewise, “medically unexplained symptoms” defined people by what doctors had failed to find rather than by what clinicians could positively identify.

The return of “functional”

The word functional has had several meanings in medicine. At its best, it describes a problem in how a system operates rather than visible destruction of its structure. A computer analogy is often used: a software rather than hardware problem. That can be useful, although the brain is not literally a computer and research increasingly finds measurable differences in network activity, connectivity, attention, perception and sense of agency.

During the late twentieth and early twenty-first centuries, neurologists and psychiatrists including Jon Stone, Michael Sharpe, Alan Carson, Mark Edwards, Mark Hallett, Selma Aybek, David Perez and many others helped rebuild FND as a positive, interdisciplinary diagnosis.

Research showed that:

• functional symptoms are common in neurological practice;
• experienced neurologists can identify characteristic positive signs;
• symptoms are genuinely experienced and not equivalent to malingering or factitious disorder;
• psychological trauma or stress is relevant for some people but absent or not identifiable in others;
• physical injury, illness, pain, migraine, panic, fatigue and other physiological events can precipitate or perpetuate symptoms;
• attention, expectation, learned movement patterns, threat processing and altered sense of agency may all contribute;
• specialised physiotherapy, occupational therapy, psychological therapy, speech therapy and multidisciplinary rehabilitation can help selected patients.

DSM-5: a major conceptual change

DSM-5, published in 2013, adopted the combined label functional neurological symptom disorder (conversion disorder). Its most important changes were not merely cosmetic.

The diagnosis no longer required a preceding psychological stressor or conflict. Instead, clinical findings had to provide evidence that the symptom was incompatible with recognised neurological or medical conditions. In practical terms, this supported a rule-in diagnosis based on positive signs.

The removal of mandatory psychological causation corrected a century-old assumption. It did not claim that psychology is irrelevant. Rather, it recognised that FND is heterogeneous: trauma, stress, anxiety or dissociation may be central for one person, contributory for another and not evident in a third.

DSM-5 and its text revision, DSM-5-TR, retain “conversion disorder” in brackets, partly for continuity. Many clinicians and patients prefer simply FND because it is less tied to an unproven mechanism.

The World Health Organization’s ICD-11 uses dissociative neurological symptom disorder within the dissociative disorders grouping. That difference shows that classification remains unsettled. Neurology often prefers “functional”; psychiatry’s international classification retains “dissociative”. Neither name fully captures every patient.

Modern neuroscience: from a hidden lesion to altered networks

Modern research does not support a single “FND centre” in the brain. Nor has it found one universal scan or blood test that diagnoses FND. Instead, studies point to altered interactions among systems involved in movement, sensation, attention, emotion, threat, bodily awareness, memory and the sense that “I am causing this movement”.

Functional neuroimaging studies have reported group-level differences involving regions and networks such as the amygdala, insula, supplementary motor area, temporoparietal junction, anterior cingulate and prefrontal cortex. For example, a 2010 study by Voon and colleagues found altered amygdala responses and connectivity with motor regions during emotional stimuli in people with motor conversion symptoms. Such findings suggest possible mechanisms through which arousal or salience may influence motor control in some patients.

These studies need careful interpretation:

• They usually compare groups and cannot yet diagnose an individual.
• Findings vary across FND subtypes and study designs.
• A difference in brain activity does not establish a single cause.
• Brain changes can be causes, consequences, maintaining factors or adaptations.
• Psychological and biological explanations are not opposites; psychological experience is implemented through brain and body systems.

Predictive processing and active inference

One influential modern account uses predictive processing. The brain does not passively receive information; it continually predicts what sensations mean and updates those predictions using incoming signals. Perception and movement depend on the balance—or “precision”—given to prior expectations and current sensory evidence.

In a 2012 paper titled A Bayesian account of ‘hysteria’, Edwards and colleagues proposed that overly strong symptom-related expectations, combined with attention directed towards the body, could outweigh contradictory sensory information. A movement, sensation or seizure-like episode could then be generated and experienced as involuntary.

This model helps explain several clinical features:

• why attention can amplify a symptom;
• why distraction can temporarily restore movement;
• why symptoms can be triggered by an injury, panic episode, migraine or frightening medical event;
• why a person genuinely experiences loss of control even though the basic movement machinery remains available;
• why rehabilitation often focuses on automatic movement, redirected attention, retraining and changed expectations.

Predictive processing is a framework, not a finished answer. It should not be simplified into “you expected it, so you caused it”. Predictions are largely automatic brain processes, not conscious choices.

An integrated biopsychosocial model

Current thinking usually considers several interacting levels:

• Predisposing factors: biological vulnerability, previous illness, pain, migraine, adverse experiences, learned responses or other individual factors.
• Precipitating factors: injury, infection, surgery, panic, acute stress, medication effects, sleep deprivation or sometimes no identifiable event.
• Perpetuating factors: abnormal attention, fear of symptoms, avoidance, deconditioning, pain, fatigue, disrupted sleep, misunderstanding of the diagnosis, social stress and unhelpful healthcare experiences.
• Protective and recovery factors: a clear diagnosis, trust, understanding, preserved automatic function, graded retraining, useful psychological strategies, supportive relationships and coordinated care.

This framework is not a checklist that every patient must fit. It allows different routes into the same broad disorder and avoids treating “psychological” as the opposite of “real”.

Functional seizures and the problem of names

Seizure-like episodes without the electrical activity of epilepsy have acquired an especially long list of labels: hysterical seizures, pseudoseizures, psychogenic seizures, psychogenic nonepileptic seizures (PNES), nonepileptic attack disorder, dissociative seizures and functional seizures.

“Pseudoseizure” is now widely avoided because it can sound as though the event is fake. Functional seizures and dissociative seizures are increasingly used, while PNES remains common in research and clinical services.

Video-EEG can be important in diagnosis by recording a typical event without the epileptic electrical pattern expected for that event type. However, epilepsy and functional seizures can coexist. As with other FND symptoms, diagnosis and explanation require care rather than a dismissive “your EEG was normal”.

The changing terminology illustrates a broader lesson: names affect treatment. A label that implies deception or a single unproven cause can damage trust before therapy has begun.

What the history of FND teaches us

1. The symptoms are not new

Descriptions resembling FND appear across centuries and cultures. What changes most dramatically is the explanation applied to them.

2. “Hysteria” was never simply another word for modern FND

It was a changing umbrella category. Some historical cases probably resembled FND; others almost certainly represented different neurological, psychiatric or medical conditions.

3. Gender bias shaped the diagnosis

The uterine theory embedded women into the name itself. Women’s distress and bodily symptoms were too often sexualised, trivialised or treated as evidence of instability. The First World War proved that men could develop similar symptoms but did not eliminate moral judgement. Modern research must still be alert to sex, gender, race, class and cultural bias.

4. Freud was influential, but the history is much bigger than Freud

Freud supplied the term “conversion” and helped popularise an unconscious-conflict model. Charcot, Janet, Bernheim, Babinski, wartime neurologists and many others developed competing ideas. Some modern concepts—dissociation, altered agency, expectation, suggestion, attention and functional brain disturbance—have roots outside classical psychoanalysis.

5. Hypnosis and suggestion have played both helpful and harmful roles

Hypnosis helped demonstrate that perception, movement and bodily sensation can change without structural injury. It was also used in theatrical, coercive and theoretically overconfident ways. A response to suggestion does not mean a symptom is fake, and suggestibility is not unique to FND. Modern therapeutic use should be collaborative, evidence-informed and never a test of whether a patient “really” has the condition.

6. FND is no longer meant to be a diagnosis of exclusion

A normal scan alone does not diagnose FND. Clinicians should identify positive features such as Hoover’s sign, tremor entrainment, distractibility or characteristic features of functional seizures, considered alongside the full clinical picture.

7. Psychological factors are possible, not compulsory

Stress, trauma, anxiety and dissociation may matter greatly, but they are not required for diagnosis. Physical illness and injury can also trigger FND. Insisting on a hidden trauma recreates the same error as insisting on a wandering womb or repressed conflict: forcing every person into one theory.

8. Function can change—and that creates grounds for hope

Positive signs often demonstrate that normal movement or sensation is accessible under some conditions. This is not proof that recovery will be quick or easy. It does, however, provide a rational basis for retraining nervous-system function.

Where are we now?

FND now has a stronger scientific and clinical identity than at any previous point in its history. Major neurology journals publish research on its mechanisms and treatment. Specialist services increasingly bring neurology, physiotherapy, occupational therapy, psychology, psychiatry and speech and language therapy together. Patient organisations have made lived experience and stigma harder for healthcare systems to ignore.

Yet the historical problems have not disappeared. Many people still face delayed diagnosis, repeated emergency attendance, contradictory explanations and limited access to treatment. Others receive a correct label but no meaningful account of what it means. Research samples remain relatively small, biomarkers are not ready for routine diagnosis, and no single treatment works for everyone.

The modern achievement is therefore not that medicine has found one final cause. It is that FND can now be approached positively and respectfully:

• the symptoms are real and involuntary;
• nervous-system function is disrupted;
• the diagnosis can often be demonstrated using positive clinical evidence;
• biological, psychological and social processes may interact differently in different people;
• treatment should be individualised and should explain, demonstrate and retrain function rather than blame the patient.

Conclusion: an old disorder with a new framework

The history of FND is full of wrong turns, but also recurring insights. Ancient physicians looked to the organs. Early neurologists looked to the brain and nerves. Hypnotists exposed the influence of expectation and attention. Janet examined dissociation and automatic processes. Freud proposed conversion of unconscious conflict. Wartime clinicians saw the effects of overwhelming experience and experimented with rehabilitation. Babinski and Hoover sought positive physical signs. Modern researchers study brain networks, agency, interoception, learning and prediction.

No single historical theory is sufficient. FND is not a wandering womb, possession, weak character, malingering or merely a hidden psychological conflict. It is a genuine and potentially disabling disorder at the intersection of movement, sensation, attention, expectation, emotion, bodily regulation and personal experience.

Perhaps the most important advance is not a new scan or a new label. It is a change in the question.

Instead of asking, “If there is no structural damage, is this real?”, we can ask:

“What has changed in the functioning of this person’s nervous system, how can we demonstrate it, and what may help it work differently?”

That is a much more useful question. It replaces blame with curiosity—and gives people with FND a more realistic basis for understanding their symptoms and working towards improvement.

Support for FND

If you live with FND, you do not need to identify one hidden psychological cause before you can begin helping your nervous system. Different approaches suit different people. These may include specialist physiotherapy, occupational therapy, psychological support, help with sleep or pain, stress regulation and carefully chosen complementary approaches.

EasingFND provides straightforward information and practical resources to help you understand FND and explore ways of calming and retraining the brain–body system. This should complement—not replace—appropriate medical and neurological care.

Explore EasingFND resources

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Selected research and further reading

The following sources include historical reviews, original historical works and major modern papers. Some older works use language that is now outdated.

1. Raynor G, Baslet G. A historical review of functional neurological disorder and comparison to contemporary models. Epilepsy & Behavior Reports. 2021;16:100489. Full text · DOI
2. Tasca C, Rapetti M, Carta MG, Fadda B. Women and hysteria in the history of mental health. Clinical Practice & Epidemiology in Mental Health. 2012;8:110–119. Full text · DOI
3. Koehler PJ. Sydenham on hysteria. European Neurology. 2016;76:175–181. Article · DOI
4. Brancaccio MT. Between Charcot and Bernheim: the debate on hypnotism in fin-de-siècle France. Notes and Records. 2017;71:157–177. Full text · DOI
5. Goetz CG. Charcot, hysteria, and simulated disorders. Handbook of Clinical Neurology. 2016;139:11–23. PubMed · DOI
6. van der Hart O, Brown P, van der Kolk BA. Pierre Janet’s treatment of post-traumatic stress. Journal of Traumatic Stress. 1989;2:379–395. DOI
7. Breuer J, Freud S. Studies on Hysteria. 1895. Digitised English edition
8. North CS. The classification of hysteria and related disorders: historical and phenomenological considerations. Behavioral Sciences. 2015;5:496–517. Full text · DOI
9. Allilaire JF. Babinski and hysteria. Bulletin de l’Académie Nationale de Médecine. 2007;191:1329–1339. PubMed
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14. Slater E, Glithero E. A follow-up of patients diagnosed as suffering from “hysteria”. Journal of Psychosomatic Research. 1965;9:9–13. DOI
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16. Stone J, LaFrance WC Jr, Brown R, Spiegel D, Levenson JL, Sharpe M. Conversion disorder: current problems and potential solutions for DSM-5. Journal of Psychosomatic Research. 2011;71:369–376. PubMed · DOI
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18. Voon V, Brezing C, Gallea C, et al. Emotional stimuli and motor conversion disorder. Brain. 2010;133:1526–1536. Article · DOI
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