Abstract
Catatonia is a syndrome of disturbed movement, volition, and behaviour in which a person may become immobile and unresponsive, hold abnormal postures, repeat the words or actions of others, or swing into agitated, purposeless excitement. First delineated by Karl Ludwig Kahlbaum in 1874, it was absorbed for most of the twentieth century into schizophrenia and so overlooked, until a sustained argument that it is an independent, recognisable, and highly treatable syndrome restored it to its own diagnostic standing in DSM-5. The clinical stakes are high: catatonia responds dramatically to benzodiazepines and electroconvulsive therapy, yet its most dangerous form can be fatal if missed. This article sets out what catatonia is, how it is identified with the Bush-Francis scale, its GABAergic and top-down cortical mechanisms, and its transdiagnostic reach, with interactive demonstrations of its signs, screening, and treatment response.
Keywords: catatonia, psychomotor, schizophrenia, mutism, electroconvulsive therapy
Few syndromes in psychiatry are as visually arresting, or as frequently missed, as catatonia. A patient may lie motionless for hours, mute and apparently unreachable, yet resist the slightest attempt to move a limb; another may hold an arm aloft for an uncomfortably long time, or mould into whatever posture an examiner leaves them in, like wax. For most of the last century these signs were read as a severe variant of schizophrenia and little more. The modern account is both humbler and more useful: catatonia is a distinct motor-behavioural syndrome that can arise on top of many different illnesses, that can be scored at the bedside in a few minutes, and that lifts, often completely, in response to a simple benzodiazepine. The cost of not knowing this is measured in lives.
- Catatonia is a syndrome, not a disease. It is a recognisable cluster of motor, volitional, and behavioural signs — immobility, mutism, posturing, negativism, echophenomena, and excitement — that sits on top of a wide range of psychiatric and medical conditions (Fink, 2013). - It was hidden inside schizophrenia for a century. Kahlbaum described it as its own entity in 1874, but it was later filed as a subtype of schizophrenia, and only a sustained argument that it is independent restored it to standalone status in DSM-5 (Kahlbaum, 1874; Taylor & Fink, 2003). - It is recognised with a standardised exam. The Bush-Francis Catatonia Rating Scale turned a subjective impression into a reproducible bedside count, and its screening instrument flags the syndrome from the presence of just two of fourteen signs (Bush et al., 1996). - It is highly treatable. Catatonia responds, often dramatically, to benzodiazepines such as lorazepam and to electroconvulsive therapy — a responsiveness so reliable it is itself a diagnostic hallmark (Rosebush & Mazurek, 2010; Sienaert et al., 2014). - Its malignant form is a medical emergency. When catatonia is accompanied by fever and autonomic instability it can be fatal if untreated, which is why recognising it quickly matters (Rogers et al., 2023).
What Catatonia Is
Catatonia is a neuropsychiatric syndrome defined by a characteristic disturbance of movement and volition — the capacity to initiate, sustain, and stop voluntary action. The person with catatonia is not paralysed and not unconscious; the machinery of movement is intact, but its voluntary control is derailed. The result is a paradoxical picture in which a patient can be at once profoundly immobile and yet actively resistant, mute and yet responsive to a whispered instruction, apparently absent and yet later able to recount what happened around them (Fink, 2013).
The syndrome is built from a set of cardinal signs that recur across cases. Some are signs of too little movement: stupor (a state of unresponsive immobility), mutism, posturing (spontaneously adopting and maintaining a posture against gravity), catalepsy (passive holding of a posture the examiner imposes), and waxy flexibility (a slow, even, candle-like resistance as a limb is moved). Others are signs of disordered volition: negativism (motiveless resistance to instructions or to attempts to be moved), automatic obedience (its mirror image, exaggerated cooperation), mitgehen (moving a body part with light pressure despite instructions to resist), and ambitendency (appearing stuck between acting and not acting). A third group is repetitive and imitative: stereotypy, mannerisms, echolalia (repeating another's speech), and echopraxia (copying another's movements). And at the opposite pole from stupor is excitement — severe, purposeless motor agitation unrelated to the environment (Bush et al., 1996).
What unites this apparently miscellaneous list is that each is a disturbance of willed action rather than of the motor apparatus itself. This is why modern diagnostic systems require not any single sign but a cluster: DSM-5 defines catatonia by the presence of at least three of twelve such features, precisely because the syndrome is a pattern, not a symptom (Taylor & Fink, 2003).
The Forms Catatonia Takes
Although catatonia is a single syndrome, it presents in recognisably different clinical forms, and distinguishing them matters for urgency and treatment. The classic division is between a retarded (or stuporous) pole and an excited pole, with a malignant form as a dangerous escalation of either.
Retarded, or stuporous, catatonia is the textbook picture: immobility, mutism, staring, posturing, negativism, and waxy flexibility. The patient withdraws, stops eating and drinking, and may hold uncomfortable positions for long periods. It is the most commonly recognised form, and the one most often confused with depression, stupor of other causes, or an unresponsive medical state (Fink, 2013).
Excited catatonia is its opposite in surface appearance but the same syndrome underneath: severe psychomotor agitation, purposeless and often frenzied movement, combativeness, and rapid, repetitive speech or echophenomena, all unconnected to the surroundings. Because the patient is moving rather than still, it is easily mistaken for mania or agitated psychosis, and the catatonic nature of the excitement is missed (Fink, 2013; Ungvari et al., 2010).
Malignant catatonia is a medical emergency. Here the motor syndrome is accompanied by autonomic instability — fever, labile blood pressure and heart rate, and often rigidity — and can progress to multi-organ failure and death. It overlaps clinically and probably mechanistically with the neuroleptic malignant syndrome, a life-threatening reaction to antipsychotic drugs, and the two are now widely regarded as closely related conditions; recognising either as catatonia is what redirects treatment away from more antipsychotic and toward benzodiazepines and electroconvulsive therapy (Rogers et al., 2023).
Table 1
The principal clinical forms of catatonia
| Form | Core clinical picture | Most often mistaken for | Urgency |
|---|---|---|---|
| Retarded (stuporous) | Immobility, mutism, staring, posturing, negativism, and waxy flexibility; withdrawal and refusal of food and drink | Depression, stupor of other causes, or an unresponsive medical state | Serious but not immediately life-threatening unless prolonged |
| Excited | Severe psychomotor agitation, purposeless frenzied movement, combativeness, and repetitive speech or echophenomena | Mania or agitated psychosis | Can escalate to the malignant form; needs prompt recognition |
| Malignant | Catatonic signs plus autonomic instability — fever, labile blood pressure and heart rate, rigidity; overlaps neuroleptic malignant syndrome | Neuroleptic malignant syndrome or sepsis | Medical emergency; can be fatal if untreated |
From Kahlbaum to DSM-5
The history of catatonia is a cautionary tale about how a diagnostic framework can make a real phenomenon disappear. In 1874 the German psychiatrist Karl Ludwig Kahlbaum published Die Katatonie, describing a syndrome of motor and volitional disturbance — what he called a tension insanity — as a distinct clinical entity with its own course (Kahlbaum, 1874). Within a generation, however, Emil Kraepelin folded catatonia into dementia praecox, and Eugen Bleuler carried it into the new category of schizophrenia as one of its subtypes. For most of the twentieth century, to see catatonia was, by definition, to be looking at schizophrenia.
That classification had a self-fulfilling consequence. Because catatonia was defined as a form of schizophrenia, clinicians stopped looking for it in patients who did not fit the schizophrenia picture — in mood disorders, in medical and neurological illness, in the general hospital — and so it appeared rare and specifically schizophrenic, which reinforced the classification that produced the blindness (Fink & Taylor, 2009). The empirical reality, once people looked, was the opposite: catatonia is more often associated with mood disorders than with schizophrenia, and it occurs across a wide range of medical and neurological conditions.
The sustained argument that catatonia deserved a home of its own — advanced most prominently by Max Fink and Michael Alan Taylor — eventually prevailed (Taylor & Fink, 2003; Fink & Taylor, 2009). DSM-5, published in 2013, broke catatonia out of schizophrenia: it is now recognised as a specifier that can be applied across psychotic, mood, and other disorders, and as catatonic disorder due to another medical condition, and as an unspecified catatonia for cases whose underlying cause is not yet known. The reclassification was not a bureaucratic tidy-up. It was the correction of a century-long error that had cost patients a treatment that works.
The DSM-5 criteria: three of twelve
DSM-5 diagnoses catatonia when at least three of twelve specified features are present — the syndrome is defined by the number of co-occurring signs, not by any single one. Toggle each feature and watch the count cross the diagnostic threshold.
4 of 12 — at or above the DSM-5 threshold of 3, by 1 feature.
Catatonia is identified by the count of co-occurring signs rather than any single pathognomonic one (after Taylor & Fink, 2003).
Assessing Catatonia
Before catatonia could be studied or reliably treated, it had to be measured, and for much of its history it could not be. The decisive instrument is the Bush-Francis Catatonia Rating Scale (BFCRS), introduced in 1996, which turned a clinician's gestalt impression into a reproducible, standardised bedside examination (Bush et al., 1996). The scale has two parts that serve two purposes.
The first fourteen items form the Bush-Francis Catatonia Screening Instrument (BFCSI): a rapid screen in which each sign is rated simply as present or absent, and the presence of two or more of the fourteen is a positive screen that should prompt a full evaluation. The complete scale rates twenty-three items, each from 0 (absent) to 3 (severe), yielding a severity score that can be tracked over time and used to measure response to treatment. Crucially, the examination is partly procedural: the examiner does not merely observe but actively probes — reaching to shake hands while instructing the patient not to, testing for the light resistance of mitgehen, moving a limb to feel for waxy flexibility — because several cardinal signs only appear when elicited (Bush et al., 1996).
DSM-5 uses a parallel but distinct rule: the diagnosis requires at least three of twelve specified features. The two systems are complementary — the BFCRS for screening, scoring, and tracking; the DSM-5 criteria for formal diagnosis — and both encode the same core idea that catatonia is identified by the number of co-occurring signs rather than by any single pathognomonic one (Taylor & Fink, 2003).
A second, confirmatory tool is diagnostic and therapeutic at once: the lorazepam challenge test. A small dose of intravenous lorazepam is given, and a marked reduction in catatonic signs within minutes to an hour both supports the diagnosis and points to the treatment. A positive challenge is strong evidence that the picture is catatonia and not another cause of immobility such as delirium (Sienaert et al., 2014; Oldham & Lee, 2015).
Worked Example
How does a bedside examination become a diagnosis? Consider a patient on a medical ward who is withdrawn and barely speaking. The clinician works through the fourteen screening items of the BFCSI and finds the following signs present: immobility/stupor, mutism, staring, posturing, negativism, and withdrawal — six of the fourteen. Each screening item counts once, present or absent, so the screen total is the simple count:
6 present out of 14.
The screening threshold is a count of 2 or more, so this patient screens positive — and by a wide margin, since 6 − 2 = 4 signs above the threshold. In proportional terms the six positive signs are 6 / 14 ≈ 0.43 of the screening items, already well past the 2 / 14 ≈ 0.14 cut-off. The patient also clears the separate DSM-5 rule of 3 of 12 features, since all six observed signs are among the twelve DSM-5 criteria and 6 ≥ 3.
The clinician then administers a 2 mg intravenous lorazepam challenge. Thirty minutes later the patient speaks, sits up, and the staring and posturing have resolved; a repeat examination finds only two signs still present. That fall — from six signs to two — is both a confirmation of the diagnosis and the start of treatment. On the full 23-item BFCRS, scored for severity, the same improvement would show as a drop in the total severity score, which is exactly how response is tracked over the days that follow. The demonstration below lets the reader toggle each of the fourteen screening items and watch the count, the proportion, and the screen verdict update.
Screen with the Bush-Francis instrument
The first fourteen items of the Bush-Francis scale form a rapid screen: each sign is rated simply present or absent, and two or more is a positive screen that should prompt a full evaluation. Toggle each item; the count, the proportion of the fourteen, and the verdict update.
6 of 14 — a positive screen, 4 signs above the threshold of 2 (6/14 ≈ 0.43).
Two or more of the fourteen screening signs is a positive screen (after Bush et al., 1996).
The Neurobiology of Catatonia
The single most informative clue to the mechanism of catatonia is its treatment response. That a syndrome of profound motor and volitional shutdown lifts within minutes of a dose of lorazepam — a positive allosteric modulator of the GABA-A receptor — points directly at GABAergic signalling, the brain's principal inhibitory system. The leading pharmacological account holds that catatonia involves a hypofunction of GABA-A-mediated transmission in cortical circuits, which benzodiazepines transiently correct, and that this is why boosting GABA-A activity relieves the syndrome (Rosebush & Mazurek, 2010; Walther et al., 2019).
The most influential systems-level model is Georg Northoff's top-down modulation hypothesis, which locates catatonia not in the motor system proper but in the cortical regions that regulate it. On this account, dysfunction in the orbitofrontal and medial prefrontal cortex — regions that link emotion to action — disrupts the normal top-down control of motor and premotor areas, so that the translation of intention and affect into movement fails. The GABAergic deficit is the proposed molecular substrate of this cortical dysregulation, tying the pharmacology to the circuit (Northoff, 2002). Intense fear or an overwhelming affective state is, in this framing, one route into the motor shutdown — a connection that resonates with the old clinical observation that catatonia can look like a terminal freeze.
Figure 1
The top-down modulation model of catatonia and its correction by GABA-A agonists
Imaging and neurophysiological work has begun to fill in this picture, implicating altered activity and connectivity in orbitofrontal, prefrontal, and motor networks, though the field is clear that no single lesion or circuit fully accounts for a syndrome that so many different conditions can produce (Walther et al., 2019; Heckers & Walther, 2023). A separate and growing strand implicates the immune system: catatonia is a recognised feature of autoimmune encephalitides, most notably anti-NMDA-receptor encephalitis, which has reframed some cases as fundamentally inflammatory and treatable with immunotherapy (Rogers et al., 2019).
Treating Catatonia
Catatonia is, by the standards of psychiatry, remarkably treatable, and the treatment is counter-intuitive in a way that makes recognition essential. The first-line therapy is a benzodiazepine, usually lorazepam, which relieves catatonic signs in a large proportion of cases, often rapidly and sometimes completely. The same lorazepam challenge that confirms the diagnosis is the beginning of treatment, and doses are then titrated to effect (Rosebush & Mazurek, 2010; Sienaert et al., 2014).
When benzodiazepines are insufficient, or when the situation is urgent — as in malignant catatonia — the definitive treatment is electroconvulsive therapy (ECT), which is highly effective across catatonia of all causes and can be life-saving in the malignant form. The British Association for Psychopharmacology's consensus guidelines codify this stepped approach, lorazepam first and ECT for refractory or severe cases, and they emphasise a point that follows directly from the mechanism: antipsychotic drugs can worsen catatonia and may precipitate the malignant form, so they are used with great caution, if at all, while the catatonia is active (Rogers et al., 2023). Alongside the specific treatment, the underlying cause — a mood episode, a psychotic illness, an autoimmune encephalitis, a metabolic derangement — must be identified and addressed.
The lorazepam challenge, step by step
A small dose of intravenous lorazepam is given and the signs are re-counted over the next hour; a marked fall within minutes confirms the diagnosis and begins the treatment. Drag the time since a 2 mg dose and watch the six presenting signs resolve. The curve is a schematic illustration of the characteristic response, not patient data.
At 0 min: 6 of 6 signs still present — before the drug has taken effect.
A rapid fall in catatonic signs after intravenous lorazepam is diagnostic and therapeutic at once (after Sienaert et al., 2014).
A Transdiagnostic Syndrome
Once catatonia was freed from schizophrenia and could be looked for everywhere, it turned out to be far from rare. A meta-analysis of clinical samples put its pooled prevalence at roughly one in ten psychiatric inpatients, with substantial variation by setting and by the criteria used (Solmi et al., 2018). It is now understood as a transdiagnostic syndrome that occurs across mood disorders — with which it is most frequently associated — psychotic disorders, autism, and a long list of medical and neurological conditions, from autoimmune encephalitis to metabolic and infectious states (Ungvari et al., 2010; Rogers et al., 2019).
This breadth is also why catatonia is so often missed on general medical and intensive-care wards, where it hides among the many causes of an altered, unresponsive, or agitated patient. The most consequential differential is delirium: both can present with a fluctuating, altered mental state, the two can co-occur, and the treatments pull in opposite directions, so distinguishing them — often with the lorazepam challenge — is a decision with real stakes (Oldham & Lee, 2015). The practical lesson of the modern literature is simple: catatonia should be actively screened for in any patient with unexplained immobility, mutism, or unresponsiveness, because the cost of recognising it is small and the cost of missing it can be fatal (Heckers & Walther, 2023).
Discussion
The story of catatonia is, more than anything, a demonstration of how classification shapes perception. A syndrome that Kahlbaum had described accurately in 1874 became nearly invisible for a century, not because the clinical phenomena changed but because the diagnostic map filed them under a heading — schizophrenia — that told clinicians where not to look (Kahlbaum, 1874; Fink & Taylor, 2009). The correction, when it came, depended on two unglamorous advances: a measurement instrument that made the syndrome countable and reproducible (Bush et al., 1996), and a sustained conceptual argument that it belonged in its own category rather than inside another illness (Taylor & Fink, 2003).
The payoff of getting the classification right is unusually direct. Because catatonia responds to specific treatments that differ from — and in the case of antipsychotics can be opposite to — the treatment of the disorders it accompanies, recognising it changes what is done at the bedside and, in the malignant form, whether the patient survives (Rogers et al., 2023). Few corrections in descriptive psychiatry have had so immediate a clinical consequence.
The open problems are correspondingly concrete. The mechanism is still only partly understood: the GABAergic and top-down cortical models are well supported by the treatment response and by imaging, but they do not yet explain why so many different insults converge on the same final syndrome (Northoff, 2002; Walther et al., 2019). The relationship between catatonia, the neuroleptic malignant syndrome, and autoimmune encephalitis is an active and clinically important question (Rogers et al., 2019). And the syndrome remains underdiagnosed in exactly the settings — medical and intensive-care wards — where its recognition matters most (Oldham & Lee, 2015).
Cognitive and Psychological Implications
Catatonia is, at its core, a disorder of volition — the translation of intention and affect into action — and that places it within cognitive psychology as well as clinical medicine. The person with catatonia reveals, by its failure, a process normally so automatic as to be invisible: the step between deciding to move and moving. In negativism and ambitendency the will seems to oppose itself; in automatic obedience and echopraxia it seems to be captured by the environment; in waxy flexibility the body holds whatever the world leaves it holding. Each is a window onto the ordinarily seamless coupling of motivation, action, and control (Northoff, 2002).
The syndrome also illustrates, as starkly as any condition can, that movement and its willed control are separable from consciousness and from the motor apparatus alike — a dissociation that bears on the psychology of consciousness and agency. And because catatonia appears across schizophrenia, bipolar disorder, and medical illness alike, it is a clear case of very different disorders converging on a shared disturbance of a single motor-volitional system — the excess-and-shutdown sibling of psychomotor agitation and a counterpart, on the side of action, to the reward-system flattening of anhedonia. A syndrome once dismissed as an endpoint of chronic psychosis turns out to be one of the most informative natural experiments on how the brain turns intention into movement.
Current Directions
Three threads dominate the recent literature. The first is mechanistic: neuroimaging and neurophysiology are mapping the altered cortical connectivity and GABAergic signalling that the treatment response has long implied, working toward a circuit-level account that could explain why so many conditions produce one syndrome (Walther et al., 2019; Heckers & Walther, 2023). The second is immunological: the recognition that catatonia can be a manifestation of autoimmune encephalitis, and more broadly that immune dysregulation may contribute to it, has opened a line of work on inflammatory mechanisms and on immunotherapy for a subset of cases (Rogers et al., 2019). The third is standardisation of care: evidence-based consensus guidelines now codify screening, the lorazepam challenge, and the stepped lorazepam-to-ECT treatment pathway, with the explicit aim of reducing the underdiagnosis that still characterises general-hospital settings (Rogers et al., 2023). Across all three, the unifying ambition is to convert a syndrome that was for a century defined by neglect into one that is routinely screened for, mechanistically understood, and reliably treated.
Common Misconceptions
- Catatonia is a type of schizophrenia.
- It is not — this is the century-long error that DSM-5 corrected. Catatonia is an independent syndrome that occurs most often with mood disorders and across many medical and neurological conditions, not only with schizophrenia (Taylor & Fink, 2003; Fink & Taylor, 2009).
- Catatonia just means being frozen and immobile.
- Immobility is only one pole. Excited catatonia presents as severe, purposeless agitation, and the syndrome also includes negativism, echophenomena, posturing, and automatic obedience — a cluster of volitional signs, not a single state of stillness (Bush et al., 1996).
- A catatonic patient is unconscious or unaware.
- Patients are typically not unconscious; many later recall events around them. Catatonia is a disorder of volition and movement, not of consciousness, which is one of the features distinguishing it from delirium and coma (Oldham & Lee, 2015).
- Antipsychotics are the treatment for catatonia.
- The opposite can be true: antipsychotics can worsen catatonia and may precipitate its malignant form. First-line treatment is a benzodiazepine, with electroconvulsive therapy for severe or refractory cases (Rogers et al., 2023; Sienaert et al., 2014).
Glossary
- Ambitendency.
- A catatonic sign in which the patient appears motorically stuck between acting and not acting, starting and stopping a movement as if caught between opposing impulses.
- Automatic obedience.
- Exaggerated, uncritical cooperation with an examiner's instructions or movements; the volitional mirror image of negativism.
- Bush-Francis Catatonia Rating Scale (BFCRS).
- The standard instrument for catatonia, comprising a 14-item screening exam and a 23-item severity scale, each sign elicited by a defined bedside procedure.
- Catalepsy.
- Passive maintenance of a posture into which the examiner has placed the patient, held against gravity.
- Catatonia.
- A neuropsychiatric syndrome of disturbed movement, volition, and behaviour, identified by a cluster of cardinal signs and highly responsive to benzodiazepines and electroconvulsive therapy.
- Echolalia.
- Automatic repetition of another person's speech.
- Echopraxia.
- Automatic imitation of another person's movements.
- Excited catatonia.
- The agitated pole of the syndrome: severe, purposeless motor excitement and often echophenomena, unrelated to the environment and easily mistaken for mania.
- GABA-A receptor.
- The main receptor for the inhibitory neurotransmitter GABA; benzodiazepines enhance its activity, and its hypofunction is a leading candidate mechanism for catatonia.
- Lorazepam challenge test.
- The administration of a small dose of intravenous lorazepam, whose rapid relief of catatonic signs both supports the diagnosis and indicates the treatment.
- Malignant catatonia.
- A life-threatening form in which the motor syndrome is accompanied by fever and autonomic instability; closely related to the neuroleptic malignant syndrome and a medical emergency.
- Mitgehen.
- A sign in which a body part moves in response to light pressure from the examiner despite an instruction to resist; an extreme form of cooperation.
- Mutism.
- Absence or marked poverty of verbal response, not attributable to aphasia, in an otherwise awake patient.
- Negativism.
- Motiveless resistance to instructions or to attempts to be moved, sometimes with action in the opposite direction.
- Posturing.
- Spontaneous adoption and maintenance of a posture, often uncomfortable, held against gravity.
- Stupor.
- A state of unresponsive immobility and markedly reduced reaction to the environment, with preserved arousal.
- Waxy flexibility (cerea flexibilitas).
- A slow, even, candle-like resistance as the examiner moves a limb, which then remains in the new position.
Key Researchers
Max Fink
(1923-2025). Professor Emeritus of Psychiatry and Neurology at Stony Brook University; with Michael Alan Taylor, the leading modern advocate for recognising catatonia as an independent, treatable syndrome, a central figure in the Bush-Francis examination tradition and the author of the field's defining reviews. Wikipedia - Google Scholar - Faculty
Karl Ludwig Kahlbaum
(1828-1899). German psychiatrist who first delineated catatonia as a distinct clinical syndrome in his 1874 monograph Die Katatonie; the historical founder of the construct. Wikipedia - Wikidata
Georg Northoff
(contemporary). Professor of Psychiatry and Mind, Brain Imaging and Neuroethics Research Chair at the University of Ottawa; author of the top-down modulation hypothesis linking catatonia to orbitofrontal-prefrontal cortical and GABAergic dysfunction. ORCID - Wikidata - Google Scholar - Faculty
Jonathan P. Rogers
(contemporary). Clinical Lecturer and Wellcome Trust Fellow in Psychiatry at University College London; lead author of the British Association for Psychopharmacology consensus guidelines for catatonia and of work on catatonia and the immune system. ORCID - Google Scholar - Faculty
Pascal Sienaert
(contemporary). Professor of Psychiatry at KU Leuven and head of its academic centre for electroconvulsive therapy and neurostimulation; author of a widely cited clinical review of the treatment of catatonia. ORCID - Google Scholar - Faculty
Sebastian Walther
(contemporary). Professor of Psychiatry at the University of Bern and a leading researcher on the motor domain of psychosis and the neural mechanisms of catatonia; co-author of the Lancet Psychiatry and New England Journal of Medicine reviews. Google Scholar - Faculty
Frequently Asked Questions
What is catatonia in simple terms?
Catatonia is a syndrome in which a person's movement and willed action become badly disturbed. Someone with catatonia might become immobile and silent, hold strange postures, resist being moved, copy what others say or do, or at the other extreme become severely agitated. It is not a single disease but a recognisable pattern of signs that can appear on top of many psychiatric and medical conditions, and it is highly treatable (Fink, 2013).
Is catatonia a form of schizophrenia?
No, although it was classified that way for most of the twentieth century. Catatonia occurs more often with mood disorders such as depression and bipolar disorder than with schizophrenia, and it also appears in autism and in many medical and neurological illnesses. DSM-5 reclassified it in 2013 as an independent syndrome that can accompany several different disorders (Taylor & Fink, 2003; Fink & Taylor, 2009).
How is catatonia diagnosed?
By a standardised bedside examination. The Bush-Francis Catatonia Rating Scale screens for fourteen signs, and the presence of two or more prompts a full evaluation; DSM-5 requires at least three of twelve features. A small dose of intravenous lorazepam that quickly relieves the signs, known as the lorazepam challenge, both supports the diagnosis and points to the treatment (Bush et al., 1996; Sienaert et al., 2014).
How is catatonia treated?
The first-line treatment is a benzodiazepine, usually lorazepam, which often relieves the syndrome rapidly. When that is not enough, or in urgent cases, electroconvulsive therapy is highly effective and can be life-saving. Importantly, antipsychotic drugs can worsen catatonia and are used cautiously, if at all, while it is active (Rosebush & Mazurek, 2010; Rogers et al., 2023).
Is catatonia dangerous?
It can be. Beyond the risks of not eating or drinking and prolonged immobility, its most severe form, malignant catatonia, adds fever and unstable blood pressure and heart rate and can be fatal if untreated. This is why recognising catatonia quickly matters, and why it should be screened for in any unexplained unresponsive or agitated patient (Rogers et al., 2023).
How common is catatonia?
More common than its century of neglect would suggest. A meta-analysis of clinical samples found a pooled prevalence of roughly one in ten psychiatric inpatients, varying with the setting and the criteria used. It is frequently missed, especially on general medical and intensive-care wards (Solmi et al., 2018).
What causes catatonia in the brain?
The leading accounts point to the brain's inhibitory GABA system and to the cortical regions that control movement. Because the syndrome lifts with lorazepam, which boosts GABA-A receptor activity, a GABA deficit is thought to be central, and a top-down model locates the problem in orbitofrontal and prefrontal cortex disrupting motor control. Some cases are caused by autoimmune encephalitis (Northoff, 2002; Rogers et al., 2019).
How is catatonia different from delirium?
Both can present as an altered, fluctuating mental state, and they can co-occur, but they are different syndromes with opposite treatments, so telling them apart matters. Catatonia is a disorder of volition and movement in an awake patient, often with preserved awareness, whereas delirium is a disturbance of attention and consciousness. The lorazepam challenge helps distinguish them (Oldham & Lee, 2015).
References
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Heckers, S., & Walther, S. (2023). Catatonia. New England Journal of Medicine, 389(19), 1797-1802. https://doi.org/10.1056/NEJMra2116304
Kahlbaum, K. L. (1874). Die Katatonie oder das Spannungsirresein. Berlin: Hirschwald.
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