Catatonia: Difference between revisions

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Catatonia is a neuropsychiatric syndrome most commonly seen in people with underlying mood disorders such as major depressive disorder, or psychotic disorders such as schizophrenia.^[1]^[2] People with catatonia exhibit abnormal movement and behaviors that vary from person to person, and which may fluctuate in intensity within a single episode.^[3]

People with catatonia appear withdrawn, with limited interaction with the outside world and difficulty processing information.^[4] They may be nearly motionless for days on end or perform repetitive, purposeless movements. People may exhibit very different sets of behaviors and still be diagnosed with catatonia. Treatment with benzodiazepines or electroconvulsive therapy is most effective and leads to remission of symptoms in most cases.^[2]

There are different subtypes of catatonia, which represent groups of symptoms that commonly occur together. These include stuporous/akinetic catatonia, excited catatonia, malignant catatonia, and periodic catatonia.^[5]

Catatonia has historically been related to schizophrenia, but is most often seen in mood disorders.^[2] It is now known that catatonic symptoms are nonspecific and may occur in other mental, neurological, and medical conditions. The prognosis of catatonia is typically good, with complete remission in some patients; however, outcomes vary depending on the underlying disorder.^[6]

Signs and symptoms

To properly diagnose catatonia, both the ICD-11 and DSM-5 require three or more of the symptoms defined in the table below. However, each person can have a different set of symptoms that may worsen, improve, and change in appearance throughout a single episode.^[3] Symptoms may develop in varying amounts of time, presenting in hours, days, or even weeks.^{[citation needed]}


Symptom	Definition
Stupor	A marked lack of psychomotor activity; the individual appears immobile and unresponsive
Catalepsy	Passive induction of a posture held against gravity
Waxy flexibility	Slight resistance to positioning by the examiner, allowing limbs to remain in imposed positions
Mutism	Lack of verbal response despite apparent alertness
Negativism	Resistance or no response to external instructions or stimulus
Posturing	Voluntary assumption of inappropriate or bizarre postures
Mannerism	Odd, exaggerated movements or behaviors
Stereotypy	Repetitive, non-goal-directed movements or gestures
Agitation	Restlessness or excessive motor activity without external stimulus
Grimacing	Facial contortions or expressions unrelated to emotional context
Echolalia	Mimicking or repeating another person's speech
Echopraxia	Mimicking or imitating another person's movements

Because most patients with catatonia have an underlying psychiatric illness, the majority will present with worsening depression, mania, or psychosis, followed by catatonia symptoms.^[2] Even when they are unable to interact, patients presenting with catatonia should not be assumed to be unaware of their surroundings, as some can recall their catatonic state and their actions in detail.^[7]

Subtypes

There are several subtypes of catatonia recognized: stuporous catatonia, excited catatonia, malignant catatonia, and periodic catatonia. Subtypes are defined by the group of symptoms and associated features that a person is experiencing or displaying. Although catatonia can be divided into subtypes, its presentation is often dynamic, and the same individual may exhibit different subtypes at different times.^[8]

Stuporous catatonia is characterized by immobility, mutism, and a lack of response to the world around them.^[1]^[2] They may appear frozen in one position for long periods of time unable to eat, drink, or speak.

Excited catatonia is characterized by odd mannerisms and gestures, purposeless or inappropriate actions, excessive motor activity, restlessness, stereotypy, impulsivity, agitation, and combativeness. Patients suffering from excited catatonia may have speech and actions that are repetitive or mimic another person's.^[1]^[2]^[7] This state is often characterized by hyperactivity, and the patient may have delusions and hallucinations.^[9]

Malignant catatonia is characterized by fever, dramatic and rapid changes in blood pressure, increased heart rate and respiratory rate, and excessive sweating.^[1]^[2] This condition is life-threatening, and the patient's laboratory tests may come back abnormal.^{[citation needed]}

Periodic catatonia is characterized by a person having recurrent episodes of catatonia. Individuals will experience multiple episodes over time, with no signs of catatonia between episodes. Historically, the Wernicke-Kleist-Leonhard school considered periodic catatonia a distinct form of "non-system schizophrenia", characterized by recurrent acute phases with hyperkinetic and akinetic features and often psychotic symptoms. There is also a residual state between these phases, characterized by low-level catatonic features and abulia of varying severity.^{[citation needed]}

Causes

Catatonia develops in the presence of an underlying condition, including psychiatric and neurological disorders, other medical conditions, and substance use.

Neuropsychiatric

Mood disorders like bipolar disorder and clinical depression are the most common conditions underlying catatonia.^[2] Other psychiatric conditions that can cause catatonia include schizophrenia and other primary psychotic disorders,^[10] autism spectrum disorder, ADHD,^[11] and post-traumatic stress disorder.^[12]

Psychodynamic theorists have historically interpreted catatonia as a psychological defense against the potentially destructive consequences of responsibility, with the passivity of the disorder providing relief.^[13]

Other conditions

Catatonia is also seen in many medical disorders, including encephalitis, meningitis, autoimmune disorders,^[14] focal neurological lesions (including strokes),^[15] alcohol withdrawal,^[16] abrupt or overly rapid benzodiazepine withdrawal,^[17]^[18]^[19] cerebrovascular disease, neoplasms, head injury,^[20] and some metabolic conditions (e.g.,homocystinuria, diabetic ketoacidosis, hepatic encephalopathy, and hypercalcaemia).^[20]

Neurological

Catatonia can occur due to several neurological conditions. For instance, certain types of encephalitis can cause catatonia. Anti-NMDA receptor encephalitis is a form of autoimmune encephalitis known to cause catatonia, albeit very rarely. Additionally, encephalitic catatonia has been reported in cases of severe HIV and herpes simplex virus infections. A small amount of evidence suggests that catatonia can develop after traumatic brain injury in the absence of a primary psychiatric disorder.^[21] Similarly, there are several case reports of catatonia after a stroke, with some having catatonia-associated symptoms that were unexplainable by stroke itself and which improved after treatment with benzodiazepines.^[22]^[23] Parkinson's disease can cause catatonia for some people by impairing their ability to produce and secrete dopamine, a neurotransmitter which is thought to contribute to motor dysfunction in people with catatonia.

Metabolic and endocrine

Abnormal thyroid function may result in the development of catatonia when the thyroid overproduces (hyperthyroidism) or underproduces thyroid hormones (hypothyroidism). This is thought to occur due to the impact of thyroid hormones on metabolism, including in the cells of the nervous system. Abnormal electrolyte levels have also been shown to cause catatonia in rare cases. Most notably, low blood sodium levels can cause catatonia in some people.^[24]^[25]^[26]^[27]

Infectious

Certain infections are known to cause catatonia, either by directly impairing brain function or by increasing a person's susceptibility to other diseases that can do so. HIV and AIDS can cause catatonia by predisposing one to infections in the brain, including different types of viral encephalitis.^[28]^[29] Borrelia burgdorferi causes Lyme disease, which has been shown to cause catatonia by infecting the brain and causing encephalitis.^[14]^[30]^[31]^[32]

Medications

Disulfiram, a drug used to treat alcoholism, can cause catatonia. It is theorized that the medication can cause alterations in dopamine metabolism, as it blocks dopamine beta-hydroxylase. Additionally, phencyclidine, corticosteroids, and antipsychotics, among other drugs, are known to cause catatonia.^[33]

Pathogenesis

The mechanisms underlying brain catatonia are poorly understood.^[7]^[34] Currently, there are two main categories of explanations for the brain pathology of catatonia. The first is a disruption of normal neurotransmitter production or release in certain brain areas, preventing normal cognitive function and leading to behavioral and motor symptoms associated with catatonia.^[35] The second claims that disruption of communication between different areas of the brain causes catatonia.^[36]

Neurotransmitters

The neurotransmitters that are most strongly associated with catatonia are GABA, dopamine, and glutamate. GABA is the primary inhibitory neurotransmitter of the brain, meaning it slows down the activity of the systems it acts on. In catatonia, people have low levels of GABA, which causes them to be overly activated, especially in areas of the brain that normally inhibit activity. This is thought to cause the behavioral symptoms associated with catatonia, including withdrawal.^[37] Dopamine can increase or decrease the activity of the area of the brain it acts on, depending on where in the brain it is. Dopamine is lower than normal in people with catatonia, which is thought to cause many of the motor symptoms, because dopamine is the main neurotransmitter that activates the parts of the brain responsible for movement.^[7] Glutamate is an excitatory neurotransmitter, meaning that it increases the activity of the areas of the brain it acts on. Notably, glutamate tells the neuron it acts on to fire by binding to the NMDA receptor. People with anti-NMDA receptor encephalitis can develop catatonia because their antibodies attack the NMDA receptor, reducing the brain's ability to activate different areas through glutamate.^[38]

Neurological pathways

Several brain pathways have been studied, and they seem to contribute to catatonia when they are not functioning properly.^[39] However, these studies were unable to determine if the abnormalities they observed were the cause of catatonia or if the catatonia caused the abnormalities. Furthermore, it has been hypothesized that pathways connecting the basal ganglia with the cortex and thalamus are involved in the development of catatonia.^[40]

Diagnosis

Catatonia is diagnosed when a person exhibits at least three key symptoms simultaneously.

These can include:

not moving or speaking (stupor or mutism)
unusual body positions
repeating words or actions
sudden restlessness
other, less common symptoms^[41]

The DSM-5 and ICD-11, global manuals for mental health conditions, describe catatonia and its various types. Catatonia can occur with other mental illnesses, like depression or schizophrenia. It may also be a reaction to certain drugs or a medical condition. While often linked to psychiatric disorders, about one in five cases of catatonia are due to medical conditions.^[42]

There is not a definitive consensus regarding diagnostic criteria. In the fifth edition of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM-5, 2013) and the eleventh edition of the World Health Organization's International Classification of Diseases (ICD-11, 2022), the classification is more homogeneous than in earlier editions. Prominent researchers in the field have other suggestions for diagnostic criteria.^[43] Still, diagnosing catatonia can be challenging. Evidence suggests that there is as high as a 15-day average delay to diagnosis for people with catatonia.

DSM-5

The DSM-5 does not classify catatonia as an independent disorder. Instead, it classifies it as:

catatonia associated with another mental disorder
due to another medical condition
unspecified catatonia.^[44]^[45] ^: 134–5

Diagnosis requires the presence of three or more of the following twelve psychomotor symptoms in association with a mental disorder, medical condition, or unspecified:^[44]^: 135

stupor: absence of psycho-motor activity; not actively relating to the environment
catalepsy: passive induction of a posture held against gravity
waxy flexibility: maintaining positions imposed by the examiner
mutism: minimal or absent verbal response (not due to aphasia)
negativism: resistance or lack of response to instructions or external stimuli
posturing: spontaneous and active maintenance of a posture against gravity
mannerisms: odd or exaggerated caricatures of normal actions
stereotypy: repetitive, abnormally frequent, non-goal-directed movements
agitation: excessive activity not influenced by external stimuli
grimacing: sustained facial expression
echolalia: mimicking another's speech
echopraxia: mimicking another's movements

Other disorders (additional code 293.89 [F06.1] to indicate the presence of the co-morbid catatonia):

Catatonia associated with autism spectrum disorder^[44]^: 57
Catatonia associated with schizophrenia spectrum and other psychotic disorders
- Catatonia associated with brief psychotic disorder^[44]^: 109
- Catatonia associated with schizophreniform disorder^[44]^: 111
- Catatonia associated with schizoaffective disorder^[44]^: 121
- Catatonia associated with a substance-induced psychotic disorder
Catatonia associated with bipolar and related disorders^[44]^: 142
Catatonia associated with major depressive disorder^[44]^: 185
Catatonic disorder due to another medical condition^[44]^: 136–7

If catatonic symptoms are present but do not form the catatonic syndrome, a medication- or substance-induced aetiology should be considered first.^[46]

ICD-11

The ICD-11 defines catatonia as a syndrome of psychomotor disturbances, characterized by the co-occurrence of several symptoms such as stupor, catalepsy, waxy flexibility, mutism, negativism, posturing, mannerisms, stereotypies, psychomotor agitation, grimacing, echolalia, and echopraxia. Catatonia may occur in the context of specific mental disorders, including mood disorders, schizophrenia or other primary psychotic disorders, and neurodevelopmental disorders. It may also be induced by psychoactive substances, including medications, or caused by a medical condition not classified under mental, behavioral, or neurodevelopmental disorders.

Table 1: **DSM-5 vs. ICD-11criteria:**
Features	DSM-5 (2013)	ICD-11 (2022)
Status of catatonia	Not an independent disorder; specified with another condition	Recognized as a syndrome that can occur across disorders
Required symptoms	≥3 of 12 psychomotor features	Several psychomotor features occurring simultaneously
Associated conditions	Mental disorders, medical conditions, unspecified	Mood disorders, schizophrenia, neurodevelopmental disorders, substance use, or medical conditions

Assessment and physical examination

Catatonia is often overlooked and under-diagnosed.^[47] Most patients present with an underlying psychiatric disorder, which can obscure recognition of catatonia. For example, psychotic symptoms may dominate the clinical picture, while classic catatonic features (such as mutism or posturing) are absent. Motor abnormalities can also be misleading; in mania, increased motor activity is typically goal-directed, whereas in excited catatonia, activity is non–goal-directed and repetitive.^[2] Careful observation of motor behavior is therefore crucial for diagnosis.

Catatonia remains a clinical diagnosis with no specific laboratory test to diagnose it. However, supportive investigations may help identify underlying causes:

EEG: usually shows diffuse slowing; can detect seizure activity if present
CT or MRI: do not demonstrate catatonia directly, but may reveal structural or metabolic causes
Laboratory tests (metabolic panels, inflammatory markers, autoantibodies): can identify reversible medical contributors^[2]

Vital signs should be frequently monitored as catatonia can progress to malignant catatonia, which is a life-threatening condition characterized by fever, hypertension, tachycardia, and tachypnea.^[2]

Rating scale

Several rating instruments have been developed, but their utility in clinical practice remains debated .^[48] The most commonly used scale is the Bush-Francis Catatonia Rating Scale (BFCRS).^[49] The scale consists of 23 items. The first 14 serve as a screening tool; if 2 of the 14 are positive, this prompts for further evaluation and completion of the remaining 9 items.

Diagnostic certainty may also be supported by:

lorazepam challenge^[50]
zolpidem challenge^[51]

Historically, barbiturates were used, but today benzodiazepines and electroconvulsive therapy (ECT) are the main options chosen for treatment.^{[citation needed]}

Laboratory findings

Laboratory abnormalities are most relevant in malignant catatonia rather that in other forms of catatonia, and may include:

elevated creatine kinase
leukocytosis
low serum iron

These findings overlap with neuroleptic malignant syndrome (NMS). Therefore, it is essential to make careful correlation with clinical history, medications, and physical findings.^{[citation needed]}

Table 2: Malignant catatonia vs. neuroleptic malignant syndrome (NMS)
Feature	Malignant catatonia	NMS
Trigger	Spontaneous or due to psychiatric illness	Typically after antipsychotics (esp. first-gen)
Motor	Posturing, stereotypy, echolalia possible	Rigidity, tremor
Labs	↑ CK, leukocytosis, low iron (variable)	↑ CK, leukocytosis, low iron (more consistent)
Treatment	Benzodiazepines, ECT	Stop antipsychotics, supportive care, benzodiazepines

Differential diagnosis

Because catatonia overlaps with many psychiatric and neurological conditions a careful and detailed history, medication review, and physical exam are key to diagnosing catatonia and differentiating it from other conditions. Furthermore, some of these conditions can themselves lead to catatonia. The differential diagnosis is as follows:

Neuroleptic malignant syndrome (NMS) and catatonia are both life-threatening conditions that share many of the same characteristics including fever, autonomic instability, rigidity, and delirium.^[52] Lab values of low serum iron, elevated creatine kinase, and white blood cell count are also shared by the two disorders, further complicating the diagnosis. There are features of malignant catatonia (posturing, impulsivity, etc.) that are absent from NMS and the lab results are not as consistent in malignant catatonia as they are in NMS. Some experts consider NMS to be a drug-induced condition associated with antipsychotics, particularly first generation antipsychotics,^[52] but it has not been established as a subtype.^[53] Therefore, discontinuing antipsychotics and starting benzodiazepines is a treatment for this condition, and similarly it is helpful in catatonia as well. (See table 2 above).
Anti-NMDA receptor encephalitis is an autoimmune disorder characterized by neuropsychiatric features and the presence of IgG antibodies.^[54] The presentation of anti-NMDA encephalitis has been categorized into 5 phases:
- prodromal phase.
- psychotic phase.
- unresponsive phase.
- hyperkinetic phase.
- recovery phase.

The psychotic phase progresses into the unresponsive phase characterized by mutism, decreased motor activity, and catatonia.^[54]

serotonin syndrome: Triggered by serotonergic drugs (ex: SSRI); features include delirium, hyperreflexia, myoclonus, GI symptoms (N/V/D), autonomic instability, hyperthermia, and rigidity.^[55]
Malignant hyperthermia: A hereditary disorder of skeletal muscle, triggered by anesthetics or muscle relaxants like succinylcholine.; associated with metabolic acidosis, hyperkalemia, and arrhythmias.^[56]
Akinetic mutism is a neurological disorder associated with structural damage in a variety of brain, it is characterized by immobility and mutism but intact awareness; lacks echolalia/echopraxia. Furthermore, it is unresponsive to benzodiazepines.^[57] Patients may present with apathy, and may seem indifferent to pain, hunger, or thirst.^[58]
Selective mutism has an anxious etiology but has also been associated with personality disorders.^[59] Patients with this disorder fail to speak with some individuals but will speak with others. Likewise, they may refuse to speak in certain situations; in another word it is anxiety-driven; speech restriction limited to certain contexts, without catatonic signs. for example, a child who refuses to speak at school but is conversational at home. This disorder is distinguished from catatonia by the absence of any other signs/symptoms.
Nonconvulsive status epilepticus is seizure activity with no accompanying tonic-clonic movements.^[60] It can present with stupor, similar to catatonia, and they both respond to benzodiazepines. Nonconvulsive status epilepticus is diagnosed by the presence of seizure activity seen on electroencephalogram (EEG).^[61] Catatonia, on the other hand, is associated with normal EEG or diffuse slowing.
Delirium is characterized by fluctuating disturbed perception and consciousness in the ill individual.^[62] It has hypoactive and hyperactive or mixed forms. People with hyperactive delirium present similarly to those with excited catatonia and have symptoms of restlessness, agitation, and aggression. Those with hypoactive delirium present with similarly to stuporous catatonia, withdrawn and quiet. However, catatonia also includes other distinguishing features including posturing and rigidity as well as a positive response to benzodiazepines.
Patients with locked-in syndrome present with immobility and mutism; however, unlike patients with catatonia who are unmotivated to communicate, patients with locked-in syndrome try to communicate with eye movements and blinking. Furthermore, locked-in syndrome is caused by damage to the brainstem.^[63]
Stiff-person syndrome and catatonia are similar in that they may both present with rigidity, autonomic instability, and a positive response to benzodiazepines.^[64] However, stiff-person syndrome may be associated with anti-glutamic acid decarboxylase (anti-GAD) antibodies^[65]^[66] and other catatonic signs such as mutism and posturing are not part of the syndrome.
Untreated late-stage Parkinson's disease may present similarly to stuporous catatonia with symptoms of immobility, rigidity, and difficulty speaking. Further complicating the diagnosis is the fact that many patients with Parkinson's disease will have major depressive disorder, which may be the underlying cause of catatonia. Parkinson's disease can be distinguished from catatonia by a positive response to levodopa. Catatonia, on the other hand, will show a positive response to benzodiazepines.
Extrapyramidal side effects of antipsychotic medication, especially dystonia and akathisia, can be difficult to distinguish from catatonic symptoms, or may confound them in the psychiatric setting. Extrapyramidal motor disorders usually do not involve social symptoms like negativism, while individuals with catatonic excitement typically do not have the physically painful compulsion to move that is seen in akathisia.^[7]
Certain stimming behaviors and stress responses in individuals with autism spectrum disorders can present similarly to catatonia. In autism spectrum disorders, chronic catatonia is distinguished by a lasting deterioration of adaptive skills from the background of pre-existing autistic symptomatology that cannot be easily explained. Acute catatonia is usually clearly distinguishable from autistic symptoms.^[67]
The diagnostic entities of obsessional slowness and psychogenic parkinsonism show overlapping features with catatonia, such as motor slowness, gegenhalten (oppositional paratonia), mannerisms, and reduced or absent speech. However, psychogenic parkinsonism involves tremor which is unusual in catatonia.^[68] Obsessional slowness is a controversial diagnosis, with presentations ranging from severe but common manifestations of obsessive compulsive disorder to catatonia.^[69]
Down syndrome disintegrative disorder (or Down Syndrome Regression Disorder, DSDD / DSRD) is a chronic condition characterized by loss of previously acquired adaptive, cognitive and social functioning occurring in persons with Down syndrome, usually during adolescence or early adulthood. The clinical picture is variable, but often includes catatonic signs, which is why it was called "catatonic psychosis" in initial reports in 1946.^[70] DSDD seems to phenotypically overlap with obsessional slowness (see above)^[71] and catatonia-like regression occurring in ASD.^[72]

Treatment

Treatment is most effective when it is early and aggressive.^[50] Patients may face issues such as poor nutrition, infections, and skin breakdown. Immobility can lead to pressure ulcers, muscle contractions, and the formation of blood clots in the legs (deep vein thrombosis) and the lungs (pulmonary embolism). Other complications also include the development of pneumonia and neuroleptic malignant syndrome.^[2]^[73]^[74]^[75]^[41]

The first choice of treatment for catatonia is benzodiazepines, particularly lorazepam, which may be used as a diagnostic tool via the "lorazepam challenge". Patients are given a dose of lorazepam and their condition monitored; if there is an improvement within minutes, catatonia is likely. Patients who require a rapid response or do not respond to benzodiazepines may undergo a course of electroconvulsive therapy.^[50] This has been shown to produce favorable response rates, particularly in patients with malignant catatonia, and often succeeds where medication does not.^[76]

Catatonia may be caused by external factors such as medical problems, side effects of certain medications, and psychiatric disorders such as depression and schizophrenia. The cause can affect treatment and outcomes: for example, catatonia associated with schizophrenia may respond less effectively to benzodiazepines.^[2]^[77]

Prognosis

Twenty-five percent of psychiatric patients with catatonia will have more than one episode throughout their lives.^[3] Treatment response for patients with catatonia is 50–70%, with treatment failure being associated with a poor prognosis. Many of these patients will require long-term and continuous mental health care. The prognosis for people with catatonia due to schizophrenia is much worse compared to other causes.^[2] In cases of malignant catatonia, the mortality rate is as high as 20%.^[78]

Epidemiology

Catatonia has been historically studied in psychiatric patients.^[79] Catatonia is under-recognized because the features are often mistaken for other disorders, including delirium or the negative symptoms of schizophrenia. The prevalence has been reported to be as high as 10% in those with acute psychiatric illnesses, and 9–30% in the setting of inpatient psychiatric care.^[3]^[80]^[7] The incidence of catatonia is 10.6 episodes per 100 000 person-years, which essentially means that in a group of 100,000 people, the group as a whole would experience 10 to 11 episodes of catatonia per year.^[81] Catatonia can occur at any age, but is most commonly seen in adolescence or young adulthood or in older adults with existing medical conditions. It occurs in males and females in approximately equal numbers.^[82]^[81] Around 20% of all catatonia cases can be attributed to a general medical condition.^[83]^[47]


Underlying condition	Proportion of catatonia cases
Mood disorders	20–40%
Major depressive disorder	15–20%
Bipolar disorder	15–20%
Psychotic disorders	20–30%
Schizophrenia	10–15%
Schizoaffective disorder	5–10%
Autism spectrum disorder	5–10%
Medical conditions	~20%

History

Ancient history

There have been reports of stupor-like and catatonia-like states in people throughout the history of psychiatry.^[84] In ancient Greece, the first physician to document stupor-like or catatonia-like states was Hippocrates, in his Aphorisms.^[85]^[86] He never defined the syndrome, but seemingly observed these states in people he was treating for melancholia. In ancient China, the first descriptions of people that appear in the Huangdi Neijing (The Yellow Emperor's Inner Canon),^[87] the book which forms the basis of Traditional Chinese Medicine. It is thought to have been compiled by many people over the course of centuries during the Warring States Period (475-221 BCE) and the early Han Dynasty (206 BCE-220 CE).^{[citation needed]}

Modern history

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The term "catatonia" was first used by German psychiatrist Karl Ludwig Kahlbaum in 1874, in his book Die Katatonie oder das Spannungsirresein, which translates to "Catatonia or Tension Insanity".^[88] He viewed catatonia as its own illness, which would get worse over time in stages of mania, depression, and psychosis leading to dementia. This work heavily influenced another German psychiatrist, Emil Kraeplin, who was the first to classify catatonia as a syndrome. Kraeplin associated catatonia with a psychotic disorder called dementia praecox, which is no longer used as a diagnosis, but heavily informed the development of the concept of schizophrenia.

Kraeplin's work influenced two other notable German psychiatrists, Karl Leonhard and Max Fink, and their colleagues to expand the concept of catatonia as a syndrome which could occur in the setting of many mental illnesses, not just psychotic disorders. They also laid the groundwork to describe different subtypes of catatonia still used today, including Stuporous Catatonia, Excited Catatonia, Malignant Catatonia, and Periodic Catatonia. Additionally, Leonhard and his colleagues categorized catatonia as either systematic or unsystematic, based on whether or not symptoms happened according to consistent and predictable patterns. These ways of thinking shaped the way that psychologists and psychiatrists thought of catatonia well into the 20th century. In fact, catatonia was a subtype of schizophrenia as recently as the DSM-III, and was not revised to be able to be applied to mood disorders until 1994 with the release of the DSM-IV.

In the latter half of the 20th century, clinicians observed that catatonia occurred in various psychiatric and medical conditions, not exclusively in schizophrenia. Max Fink and colleagues advocated for recognizing catatonia as an independent syndrome, highlighting its frequent association with mood disorders and responsiveness to treatments like benzodiazepines and ECT.

Society and culture

Popular conceptions and origins

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Catatonia has been subject to shifting perceptions in society. Since the 19th century, it was often linked exclusively to schizophrenia, perpetuating misconceptions. These historical misunderstandings have shaped the public opinion on catatonia. This has contributed to a lack of understanding about catatonia, and its broader association with other mental disorders and medical conditions.

Popular culture and media have played a significant role in shaping societal perceptions of catatonia. In many cases, media portrayals reduce it to a stereotypical "frozen state," similar to a coma, failing to capture the complexity of symptoms like stupor, agitation, and mutism. These oversimplifications have greatly affected the public perception of catatonia.

References

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↑ ^2.00 ^2.01 ^2.02 ^2.03 ^2.04 ^2.05 ^2.06 ^2.07 ^2.08 ^2.09 ^2.10 ^2.11 ^2.12 ^2.13 Burrow, Jeffrey P.; Spurling, Benjamin C.; Marwaha, Raman (2022). "Catatonia". StatPearls. StatPearls Publishing. PMID 28613592.
↑ ^3.0 ^3.1 ^3.2 ^3.3 Heckers, Stephan; Walther, Sebastian (9 November 2023). "Catatonia". New England Journal of Medicine. 389 (19): 1797–1802. doi:10.1056/NEJMra2116304. PMID 37937779 Check |pmid= value (help). S2CID 265673511 Check |s2cid= value (help).
↑ Edinoff, Amber N.; Kaufman, Sarah E.; Hollier, Janice W.; Virgen, Celina G.; Karam, Christian A.; Malone, Garett W.; Cornett, Elyse M.; Kaye, Adam M.; Kaye, Alan D. (8 November 2021). "Catatonia: Clinical Overview of the Diagnosis, Treatment, and Clinical Challenges". Neurology International. 13 (4): 570–586. doi:10.3390/neurolint13040057. ISSN 2035-8385. PMC 8628989. PMID 34842777.
↑ "Catatonia treatment and prognosis". UpToDate. Retrieved 22 November 2024.
↑ Hirjak, Dusan; Rogers, Jonathan P.; Wolf, Robert Christian; Kubera, Katharina Maria; Fritze, Stefan; Wilson, Jo Ellen; Sambataro, Fabio; Fricchione, Gregory; Meyer-Lindenberg, Andreas; Ungvari, Gabor S.; Northoff, Georg (18 July 2024). "Catatonia". Nature Reviews Disease Primers. 10 (1): 49. doi:10.1038/s41572-024-00534-w. ISSN 2056-676X.
↑ ^7.0 ^7.1 ^7.2 ^7.3 ^7.4 ^7.5 Rasmussen, Sean A; Mazurek, Michael F; Rosebush, Patricia I (22 December 2016). "Catatonia: Our current understanding of its diagnosis, treatment and pathophysiology". World Journal of Psychiatry. 6 (4): 391–8. doi:10.5498/wjp.v6.i4.391. PMC 5183991. PMID 28078203.
↑ Shorter, Edward; Fink, Max (2018). The Madness of Fear: A History of Catatonia. Oxford University Press. ISBN 978-0-19-088119-1.
↑ Nolen-Hoeksema, Susan (2014). Abnormal Psychology. McGraw-Hill Education. p. 224. ISBN 978-1-259-06072-4.
↑ Fink, Max; Taylor, Michael Alan (2003). Catatonia: A Clinician's Guide to Diagnosis and Treatment. Cambridge University Press. ISBN 978-0-521-82226-8.^{[page needed]}
↑ Dhossche, Dirk Marcel; Rout, Ujjwal (2006). "Are Autistic and Catatonic Regression Related? A Few Working Hypotheses Involving Gaba, Purkinje Cell Survival, Neurogenesis, and ECT". International Review of Neurobiology. 72. pp. 55–79. doi:10.1016/S0074-7742(05)72004-3. ISBN 978-0-12-366873-8. PMID 16697291.
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↑ Arieti, Silvano (1994). Interpretation of schizophrenia. Jason Aronson. ISBN 1-56821-209-7. OCLC 472906047.
↑ ^14.0 ^14.1 Rogers, Jonathan P; Pollak, Thomas A; Blackman, Graham; David, Anthony S (July 2019). "Catatonia and the immune system: a review". The Lancet Psychiatry. 6 (7): 620–630. doi:10.1016/S2215-0366(19)30190-7. PMC 7185541. PMID 31196793.
↑ Haroche, Alexandre; Rogers, Jonathan; Plaze, Marion; Gaillard, Raphaël; Williams, Steve CR; Thomas, Pierre; Amad, Ali (July 2020). "Brain imaging in catatonia: systematic review and directions for future research". Psychological Medicine. 50 (10): 1585–97. doi:10.1017/S0033291720001853. PMID 32539902. S2CID 219704600.
↑ Geoffroy, Pierre Alexis; Rolland, Benjamin; Cottencin, Olivier (1 May 2012). "Catatonia and Alcohol Withdrawal: A Complex and Underestimated Syndrome". Alcohol and Alcoholism. 47 (3): 288–290. doi:10.1093/alcalc/agr170. PMID 22278315.
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↑ Kanemoto K, Miyamoto T, Abe R (September 1999). "Ictal catatonia as a manifestation of de novo absence status epilepticus following benzodiazepine withdrawal". Seizure. 8 (6): 364–6. doi:10.1053/seiz.1999.0309. PMID 10512781. S2CID 17454162.
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↑ Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
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↑ Mehta, Vishal; Sharma, Akhya; Sharma, Chandra Bhushan; Guria, Rishi Tuhin (December 2021). "Cerebral Salt Wasting Induced Hyponatraemia Presenting as Catatonia". Journal of the Royal College of Physicians of Edinburgh. 51 (4): 377–9. doi:10.4997/jrcpe.2021.413. ISSN 1478-2715. PMID 34882138.
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↑ Walther, Sebastian; Stegmayer, Katharina; Wilson, Jo Ellen; Heckers, Stephan (July 2019). "Structure and neural mechanisms of catatonia". The Lancet Psychiatry. 6 (7): 610–9. doi:10.1016/S2215-0366(18)30474-7. PMC 6790975. PMID 31196794.
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↑ Rogers, Jonathan P.; Pollak, Thomas A.; Blackman, Graham; David, Anthony S. (1 July 2019). "Catatonia and the immune system: a review". The Lancet Psychiatry. 6 (7): 620–630. doi:10.1016/S2215-0366(19)30190-7. ISSN 2215-0366. PMC 7185541. PMID 31196793.
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External links

Catatonia in DSM-5
Encyclopedia of Mental Disorders — Catatonic Disorders
"Schizophrenia: Catatonic Type" video by Heinz Edgar Lehmann, 1952
Bush-Francis Catatonia Rating Scale

Template:Medical condition classification and resources

Template:Mental and behavioral disorders

[Fink_&_Taylor_2009-1] 1.0 ^1.1 ^1.2 ^1.3 Fink, Max; Taylor, Michael Alan (1 November 2009). "The Catatonia Syndrome: Forgotten but Not Gone". Archives of General Psychiatry. 66 (11): 1173–7. doi:10.1001/archgenpsychiatry.2009.141. PMID 19884605.

[Catatonia_StatPearls-2] 2.00 ^2.01 ^2.02 ^2.03 ^2.04 ^2.05 ^2.06 ^2.07 ^2.08 ^2.09 ^2.10 ^2.11 ^2.12 ^2.13 Burrow, Jeffrey P.; Spurling, Benjamin C.; Marwaha, Raman (2022). "Catatonia". StatPearls. StatPearls Publishing. PMID 28613592.

[Heckers_2023-3] 3.0 ^3.1 ^3.2 ^3.3 Heckers, Stephan; Walther, Sebastian (9 November 2023). "Catatonia". New England Journal of Medicine. 389 (19): 1797–1802. doi:10.1056/NEJMra2116304. PMID 37937779 Check |pmid= value (help). S2CID 265673511 Check |s2cid= value (help).

[4] Edinoff, Amber N.; Kaufman, Sarah E.; Hollier, Janice W.; Virgen, Celina G.; Karam, Christian A.; Malone, Garett W.; Cornett, Elyse M.; Kaye, Adam M.; Kaye, Alan D. (8 November 2021). "Catatonia: Clinical Overview of the Diagnosis, Treatment, and Clinical Challenges". Neurology International. 13 (4): 570–586. doi:10.3390/neurolint13040057. ISSN 2035-8385. PMC 8628989. PMID 34842777.

[5] "Catatonia treatment and prognosis". UpToDate. Retrieved 22 November 2024.

[6] Hirjak, Dusan; Rogers, Jonathan P.; Wolf, Robert Christian; Kubera, Katharina Maria; Fritze, Stefan; Wilson, Jo Ellen; Sambataro, Fabio; Fricchione, Gregory; Meyer-Lindenberg, Andreas; Ungvari, Gabor S.; Northoff, Georg (18 July 2024). "Catatonia". Nature Reviews Disease Primers. 10 (1): 49. doi:10.1038/s41572-024-00534-w. ISSN 2056-676X.

[Rasmussen_Mazurek_Rosebush_2016-7] 7.0 ^7.1 ^7.2 ^7.3 ^7.4 ^7.5 Rasmussen, Sean A; Mazurek, Michael F; Rosebush, Patricia I (22 December 2016). "Catatonia: Our current understanding of its diagnosis, treatment and pathophysiology". World Journal of Psychiatry. 6 (4): 391–8. doi:10.5498/wjp.v6.i4.391. PMC 5183991. PMID 28078203.

[8] Shorter, Edward; Fink, Max (2018). The Madness of Fear: A History of Catatonia. Oxford University Press. ISBN 978-0-19-088119-1.

[9] Nolen-Hoeksema, Susan (2014). Abnormal Psychology. McGraw-Hill Education. p. 224. ISBN 978-1-259-06072-4.

[Fink_&_Taylor-10] Fink, Max; Taylor, Michael Alan (2003). Catatonia: A Clinician's Guide to Diagnosis and Treatment. Cambridge University Press. ISBN 978-0-521-82226-8.^{[page needed]}

[11] Dhossche, Dirk Marcel; Rout, Ujjwal (2006). "Are Autistic and Catatonic Regression Related? A Few Working Hypotheses Involving Gaba, Purkinje Cell Survival, Neurogenesis, and ECT". International Review of Neurobiology. 72. pp. 55–79. doi:10.1016/S0074-7742(05)72004-3. ISBN 978-0-12-366873-8. PMID 16697291.

[12] Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.

[13] Arieti, Silvano (1994). Interpretation of schizophrenia. Jason Aronson. ISBN 1-56821-209-7. OCLC 472906047.

[Rogers19-14] 14.0 ^14.1 Rogers, Jonathan P; Pollak, Thomas A; Blackman, Graham; David, Anthony S (July 2019). "Catatonia and the immune system: a review". The Lancet Psychiatry. 6 (7): 620–630. doi:10.1016/S2215-0366(19)30190-7. PMC 7185541. PMID 31196793.

[15] Haroche, Alexandre; Rogers, Jonathan; Plaze, Marion; Gaillard, Raphaël; Williams, Steve CR; Thomas, Pierre; Amad, Ali (July 2020). "Brain imaging in catatonia: systematic review and directions for future research". Psychological Medicine. 50 (10): 1585–97. doi:10.1017/S0033291720001853. PMID 32539902. S2CID 219704600.

[Geoffroy-2012-16] Geoffroy, Pierre Alexis; Rolland, Benjamin; Cottencin, Olivier (1 May 2012). "Catatonia and Alcohol Withdrawal: A Complex and Underestimated Syndrome". Alcohol and Alcoholism. 47 (3): 288–290. doi:10.1093/alcalc/agr170. PMID 22278315.

[17] Rosebush PI; Mazurek MF (August 1996). "Catatonia after benzodiazepine withdrawal". Journal of Clinical Psychopharmacology. 16 (4): 315–9. doi:10.1097/00004714-199608000-00007. PMID 8835707.

[18] Deuschle M, Lederbogen F (January 2001). "Benzodiazepine withdrawal-induced catatonia". Pharmacopsychiatry. 34 (1): 41–42. doi:10.1055/s-2001-15188. PMID 11229621. S2CID 260241781 Check |s2cid= value (help).

[19] Kanemoto K, Miyamoto T, Abe R (September 1999). "Ictal catatonia as a manifestation of de novo absence status epilepticus following benzodiazepine withdrawal". Seizure. 8 (6): 364–6. doi:10.1053/seiz.1999.0309. PMID 10512781. S2CID 17454162.

[DSM-5-introduction-20] 20.0 ^20.1 American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (Fifth ed.). Arlington, VA: American Psychiatric Publishing. pp. 119–121. ISBN 978-0-89042-555-8.

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Catatonia: Difference between revisions

Latest revision as of 21:44, 30 May 2026

Contents

Signs and symptoms

Subtypes

Causes

Neuropsychiatric

Other conditions

Neurological

Metabolic and endocrine

Infectious

Medications

Pathogenesis

Neurotransmitters

Neurological pathways

Diagnosis

DSM-5

ICD-11

Assessment and physical examination

Rating scale

Laboratory findings

Differential diagnosis

Treatment

Prognosis

Epidemiology

History

Ancient history

Modern history

Society and culture

Popular conceptions and origins

See also

References

External links

Navigation menu

@@ Line 2: / Line 2: @@
 {{About|the catatonic state}}
 {{Distinguish|Katatonia|cataplexy|catalepsy|Catalonia|Cataonia}}
+{{copy-paste|date=May 2026}}
 {{cs1 config|name-list-style=vanc}}
 {{Use dmy dates|date=February 2020}}
-{{copy edit|date=December 2024}}
+{{Infobox medical condition
-{{Infobox medical condition (new)
 | name = Catatonia
 | synonyms = Catatonic syndrome
 | image = Сatatonic stupor3.jpg
 | caption = A patient in catatonic [[stupor]], 1914
+| pronunciation = {{IPAc-en|ˌ|k|æ|t|ə|ˈ|t|oʊ|n|i|ə}}
 | field = [[Psychiatry]], [[neurology]]
-| complications = Physical trauma, malignant catatonia (autonomic instability, life-threatening), dehydration, pneumonia, pressure ulcers due to immobility, muscle contractions, [[deep vein thrombosis]] (DVT)<ref name=Balaguer-Rivero2021>{{Cite journal |last1=Balaguer |first1=Ana Pérez |last2=Rivero |first2=Irene Sánchez |date=2021-12-22 |title=Electroconvulsive therapy, catatonia, deep vein thrombosis and anticoagulant treatment: a case report |journal=General Psychiatry |volume=34 |issue=6 |pages=e100666 |doi=10.1136/gpsych-2021-100666 |issn=2517-729X |pmc=8705197 |pmid=35028525}}</ref> and [[pulmonary embolism]] (PE)<ref name=Balaguer-Rivero2021 />
+| complications = Physical trauma, malignant catatonia (autonomic instability, life-threatening), dehydration, pneumonia, pressure ulcers due to immobility, muscle contractions, [[deep vein thrombosis]] (DVT)<ref name=Balaguer-Rivero2021>{{Cite journal |last1=Pérez-Balaguer |first1=Ana |last2=Sánchez-Rivero |first2=Irene |date=2021-12-22 |title=Electroconvulsive therapy, catatonia, deep vein thrombosis and anticoagulant treatment: a case report |journal=General Psychiatry |language=en |volume=34 |issue=6 |article-number=e100666 |doi=10.1136/gpsych-2021-100666 |issn=2517-729X |pmc=8705197 |pmid=35028525}}</ref> and [[pulmonary embolism]] (PE)<ref name=Balaguer-Rivero2021/>
 | onset =
 | duration =
@@ Line 19: / Line 20: @@
 | differential =
 | prevention =
-| treatment = Benzodiazepines ([[lorazepam challenge]]), [[electroconvulsive therapy]] (ECT)<ref name=Balaguer-Rivero2021 />
+| treatment = [[Benzodiazepine]]s ([[lorazepam challenge]]), [[electroconvulsive therapy]] (ECT)<ref name=Balaguer-Rivero2021/>
 | prognosis =
 | medication =
@@ Line 25: / Line 26: @@
 | deaths =
 | alt =
-| symptoms = Immobility, mutism, staring, posturing, rigidity, low consciousness, etc.
+| symptoms = Immobility, mutism, staring, posturing, rigidity, low consciousness
 }}
-'''Catatonia''' is a [[neuropsychiatric]] [[syndrome]] characterized by a range of psychomotor disturbances. It is most commonly observed in individuals with underlying [[mood disorder]]s, such as [[major depressive disorder]], and [[psychotic disorder]]s, including [[schizophrenia]].<ref name="Fink & Taylor 2009">{{cite journal |last1=Fink |first1=Max |last2=Taylor |first2=Michael Alan |title=The Catatonia Syndrome: Forgotten but Not Gone |journal=Archives of General Psychiatry |date=1 November 2009 |volume=66 |issue=11 |pages=1173–7 |doi=10.1001/archgenpsychiatry.2009.141 |pmid=19884605 }}</ref><ref name="Catatonia StatPearls">{{cite book |last1=Burrow |first1=Jeffrey P. |last2=Spurling |first2=Benjamin C. |last3=Marwaha |first3=Raman |title=StatPearls |date=2022 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK430842/ |chapter=Catatonia |pmid=28613592 }}</ref>
+'''Catatonia''' is a [[Neuropsychiatry|neuropsychiatric]] [[syndrome]] most commonly seen in people with underlying [[mood disorder]]s such as [[major depressive disorder]], or [[psychosis|psychotic disorders]] such as [[schizophrenia]].<ref name="Fink & Taylor 2009"/><ref name="Catatonia StatPearls"/> People with catatonia exhibit abnormal movement and behaviors that vary from person to person, and which may fluctuate in intensity within a single episode.<ref name="Heckers 2023"/>
-The condition involves abnormal motor behavior that can range from immobility (stupor) to excessive, purposeless activity. These symptoms may vary significantly among individuals and can fluctuate during the same episode.<ref name="Heckers 2023" /> Affected individuals often appear withdrawn, exhibiting minimal response to external stimuli and showing reduced interaction with their environment.<ref>{{Cite journal |last1=Edinoff |first1=Amber N. |last2=Kaufman |first2=Sarah E. |last3=Hollier |first3=Janice W. |last4=Virgen |first4=Celina G. |last5=Karam |first5=Christian A. |last6=Malone |first6=Garett W. |last7=Cornett |first7=Elyse M. |last8=Kaye |first8=Adam M. |last9=Kaye |first9=Alan D. |date=2021-11-08 |title=Catatonia: Clinical Overview of the Diagnosis, Treatment, and Clinical Challenges |journal=Neurology International |volume=13 |issue=4 |pages=570–586 |doi=10.3390/neurolint13040057 |doi-access=free |issn=2035-8385 |pmc=8628989 |pmid=34842777}}</ref> Some may remain motionless for extended periods, while others exhibit repetitive or stereotyped movements. Despite the diversity in clinical presentation, these features are part of a defined diagnostic syndrome.
+People with catatonia appear withdrawn, with limited interaction with the outside world and difficulty processing information.<ref>{{Cite journal |last1=Edinoff |first1=Amber N. |last2=Kaufman |first2=Sarah E. |last3=Hollier |first3=Janice W. |last4=Virgen |first4=Celina G. |last5=Karam |first5=Christian A. |last6=Malone |first6=Garett W. |last7=Cornett |first7=Elyse M. |last8=Kaye |first8=Adam M. |last9=Kaye |first9=Alan D. |date=2021-11-08 |title=Catatonia: Clinical Overview of the Diagnosis, Treatment, and Clinical Challenges |journal=Neurology International |volume=13 |issue=4 |pages=570–586 |doi=10.3390/neurolint13040057 |doi-access=free |issn=2035-8385 |pmc=8628989 |pmid=34842777}}</ref> They may be nearly motionless for days on end or perform repetitive, purposeless movements. People may exhibit very different sets of behaviors and still be diagnosed with catatonia. Treatment with [[benzodiazepine]]s or [[electroconvulsive therapy]] is most effective and leads to remission of symptoms in most cases.<ref name="Catatonia StatPearls" />
-Effective treatment options include [[benzodiazepine]]s and [[electroconvulsive therapy]] (ECT), both of which have shown high rates of symptom remission.<ref name="Catatonia StatPearls" />
+There are different subtypes of catatonia, which represent groups of symptoms that commonly occur together. These include stuporous/akinetic catatonia, excited catatonia, malignant catatonia, and periodic catatonia.<ref>{{Cite web |title=Catatonia treatment and prognosis |publisher=UpToDate |url=https://www.uptodate.com/contents/catatonia-treatment-and-prognosis |access-date=2024-11-22}}</ref>
-Several subtypes of catatonia are recognized, each defined by characteristic symptom patterns. These include:
+Catatonia has historically been related to schizophrenia, but is most often seen in mood disorders.<ref name="Catatonia StatPearls"/> It is now known that catatonic symptoms are nonspecific and may occur in other mental, neurological, and medical conditions. The prognosis of catatonia is typically good, with complete remission in some patients; however, outcomes vary depending on the underlying disorder.<ref>{{Cite journal |last=Hirjak |first=Dusan |last2=Rogers |first2=Jonathan P. |last3=Wolf |first3=Robert Christian |last4=Kubera |first4=Katharina Maria |last5=Fritze |first5=Stefan |last6=Wilson |first6=Jo Ellen |last7=Sambataro |first7=Fabio |last8=Fricchione |first8=Gregory |last9=Meyer-Lindenberg |first9=Andreas |last10=Ungvari |first10=Gabor S. |last11=Northoff |first11=Georg |date=2024-07-18 |title=Catatonia |url=https://www.nature.com/articles/s41572-024-00534-w |journal=Nature Reviews Disease Primers |language=en |volume=10 |issue=1 |pages=49 |doi=10.1038/s41572-024-00534-w |issn=2056-676X|url-access=subscription }}</ref>
-* '''Stuporous/akinetic catatonia''': marked by immobility, mutism, and withdrawal;
-* '''Excited catatonia''': characterized by excessive motor activity and agitation;
-* '''Malignant catatonia''': a severe form involving autonomic instability and fever;
-* '''Periodic catatonia''': involving episodic or cyclical symptom presentation.<ref>{{Cite web |title=Catatonia treatment and prognosis |publisher=UpToDate |url=https://www.uptodate.com/contents/catatonia-treatment-and-prognosis |access-date=2024-11-22 }}</ref>
-Although catatonia was historically classified as a subtype of schizophrenia (''catatonic schizophrenia''), it is now more frequently associated with mood disorders.<ref name="Catatonia StatPearls" /> Catatonic features are considered nonspecific and may also occur in a variety of other psychiatric, neurological, or general medical conditions.
-== Classification ==
-=== Modern classifications ===
-In both the [[DSM-5]] and the [[ICD-11]], catatonia is diagnosed if an individual has at least three different symptoms associated with catatonia at once. These symptoms are stupor, [[catalepsy]], [[waxy flexibility]], [[mutism]], negativism, posturing, [[mannerisms]], [[Stereotypy|stereotypies]], [[psychomotor agitation]], grimacing, [[echolalia]], and [[echopraxia]].<ref>{{Cite journal |last1=Reed |first1=Geoffrey M. |last2=First |first2=Michael B. |last3=Kogan |first3=Cary S. |last4=Hyman |first4=Steven E. |last5=Gureje |first5=Oye |last6=Gaebel |first6=Wolfgang |last7=Maj |first7=Mario |last8=Stein |first8=Dan J. |last9=Maercker |first9=Andreas |last10=Tyrer |first10=Peter |last11=Claudino |first11=Angelica |last12=Garralda |first12=Elena |last13=Salvador-Carulla |first13=Luis |last14=Ray |first14=Rajat |last15=Saunders |first15=John B. |date=2019-01-02 |title=Innovations and changes in the ICD-11 classification of mental, behavioural and neurodevelopmental disorders |journal=World Psychiatry |language=en |volume=18 |issue=1 |pages=3–19 |doi=10.1002/wps.20611 |pmc=6313247 |pmid=30600616}}</ref><ref name="DSM-5-introduction">{{Cite book |last=American Psychiatric Association |url=https://archive.org/details/diagnosticstatis0005unse/page/119 |title=Diagnostic and Statistical Manual of Mental Disorders |publisher=American Psychiatric Publishing |year=2013 |isbn=978-0-89042-555-8 |edition=Fifth |location=Arlington, VA |pages=[https://archive.org/details/diagnosticstatis0005unse/page/119 119–121]}}</ref> The ICD-11 divides catatonia into three types based on the underlying cause: catatonia associated with another mental disorder, catatonia induced by psychoactive substance, and secondary catatonia.{{Citation needed|date=April 2025}}
-Like the ICD-11, the DSM-5 divides catatonia into three diagnoses, Catatonia Associated with Another Mental Disorder, Catatonic Disorder due to Another Medical Condition, and Unspecified Catatonia (when the underlying cause is unknown). The most common of the three diagnoses is Catatonia Associated with Another Mental Disorder.{{Citation needed|date=April 2025}} Around 20% of cases are caused by an underlying medical condition.<ref name="Oldham 333–340">{{Cite journal |last=Oldham |first=Mark A. |date=2018-07-01 |title=The Probability That Catatonia in the Hospital has a Medical Cause and the Relative Proportions of Its Causes: A Systematic Review |url=https://linkinghub.elsevier.com/retrieve/pii/S0033318218301828 |journal=Psychosomatics |volume=59 |issue=4 |pages=333–340 |doi=10.1016/j.psym.2018.04.001 |pmid=29776679 |issn=0033-3182|url-access=subscription }}</ref>
 ==Signs and symptoms==
-As discussed previously, the ICD-11 and DSM-5 both require 3 or more of the symptoms defined in the table below in order to diagnose catatonia. However, each person can have a different set of symptoms that may worsen, improve, and change in appearance throughout a single episode.<ref name="Heckers 2023">{{cite journal |last1=Heckers |first1=Stephan |last2=Walther |first2=Sebastian |date=9 November 2023 |title=Catatonia |journal=New England Journal of Medicine |volume=389 |issue=19 |pages=1797–1802 |doi=10.1056/NEJMra2116304 |pmid=37937779 |s2cid=265673511}}</ref> Symptoms may develop over hours or days to weeks.
+To properly diagnose catatonia, both the ICD-11 and DSM-5 require three or more of the symptoms defined in the table below. However, each person can have a different set of symptoms that may worsen, improve, and change in appearance throughout a single episode.<ref name="Heckers 2023">{{cite journal |last1=Heckers |first1=Stephan |last2=Walther |first2=Sebastian |date=9 November 2023 |title=Catatonia |journal=New England Journal of Medicine |volume=389 |issue=19 |pages=1797–1802 |doi=10.1056/NEJMra2116304 |pmid=37937779 |s2cid=265673511}}</ref> Symptoms may develop in varying amounts of time, presenting in hours, days, or even weeks.{{cn|date=April 2026}}
 {| class="wikitable"
 |+
@@ Line 66: / Line 50: @@
 |Passive induction of a posture held against gravity
 |-
-|Waxy Flexibility
+|Waxy flexibility
 |Slight resistance to positioning by the examiner, allowing limbs to remain in imposed positions
 |-
@@ Line 73: / Line 57: @@
 |-
 |Negativism
-|Resistance or no response to external instructions or stimuli
+|Resistance or no response to external instructions or stimulus
 |-
 |Posturing
@@ Line 96: / Line 80: @@
 |Mimicking or imitating another person's movements
 |}
-Because most patients with catatonia have an underlying psychiatric illness, the majority will present with worsening depression, mania, or psychosis followed by catatonia symptoms.<ref name="Catatonia StatPearls" /> Even when unable to interact, it should not be assumed that patients presenting with catatonia are unaware of their surroundings as some patients can recall in detail their catatonic state and their actions.<ref name="Rasmussen Mazurek Rosebush 2016">{{cite journal |last1=Rasmussen |first1=Sean A |last2=Mazurek |first2=Michael F |last3=Rosebush |first3=Patricia I |date=2016 |title=Catatonia: Our current understanding of its diagnosis, treatment and pathophysiology |journal=World Journal of Psychiatry |volume=6 |issue=4 |pages=391–8 |doi=10.5498/wjp.v6.i4.391 |pmc=5183991 |pmid=28078203 |doi-access=free}}</ref>
+Because most patients with catatonia have an underlying psychiatric illness, the majority will present with worsening depression, [[mania]], or psychosis, followed by catatonia symptoms.<ref name="Catatonia StatPearls">{{cite book |last1=Burrow |first1=Jeffrey P. |url=https://www.ncbi.nlm.nih.gov/books/NBK430842/ |title=StatPearls |last2=Spurling |first2=Benjamin C. |last3=Marwaha |first3=Raman |date=2022 |publisher=StatPearls Publishing |chapter=Catatonia |pmid=28613592}}</ref> Even when they are unable to interact, patients presenting with catatonia should not be assumed to be unaware of their surroundings, as some can recall their catatonic state and their actions in detail.<ref name="Rasmussen Mazurek Rosebush 2016">{{cite journal |last1=Rasmussen |first1=Sean A |last2=Mazurek |first2=Michael F |last3=Rosebush |first3=Patricia I |date=2016-12-22 |title=Catatonia: Our current understanding of its diagnosis, treatment and pathophysiology |journal=World Journal of Psychiatry |volume=6 |issue=4 |pages=391–8 |doi=10.5498/wjp.v6.i4.391 |pmc=5183991 |pmid=28078203 |doi-access=free}}</ref>
+<gallery>
+File:Image from page 110 of "Mental medicine and nursing - for use in training-schools for nurses and in medical classes and a ready reference for the general practitioner" (1915).jpg|
+File:Image from page 219 of "A treatise on mental diseases" (1900).jpg|
+File:Image from page 719 of "Diseases of the nervous system - a text-book of neurology and psychiatry" (1915).jpg|
+</gallery>
 === Subtypes ===
-There are several subtypes of catatonia which are used currently: stuporous catatonia, excited catatonia, malignant catatonia, and periodic catatonia. Subtypes are defined by the group of symptoms and associated features that a person is experiencing or displaying. Notably, while catatonia can be divided into various subtypes, the appearance of catatonia is often dynamic and the same individual may have different subtypes at different times.<ref>{{Cite book |last1=Shorter |first1=Edward |url=https://books.google.com/books?id=K_tdDwAAQBAJ&q=fink+catatonia+%22alternation%22&pg=PA119 |title=The Madness of Fear: A History of Catatonia |last2=Fink |first2=Max |date=2018 |publisher=Oxford University Press |isbn=978-0-19-088119-1 |language=en}}</ref>
+There are several subtypes of catatonia recognized: stuporous catatonia, excited catatonia, malignant catatonia, and periodic catatonia. Subtypes are defined by the group of symptoms and associated features that a person is experiencing or displaying. Although catatonia can be divided into subtypes, its presentation is often dynamic, and the same individual may exhibit different subtypes at different times.<ref>{{Cite book |last1=Shorter |first1=Edward |url=https://books.google.com/books?id=K_tdDwAAQBAJ&q=fink+catatonia+%22alternation%22&pg=PA119 |title=The Madness of Fear: A History of Catatonia |last2=Fink |first2=Max |date=2018 |publisher=Oxford University Press |isbn=978-0-19-088119-1 |language=en}}</ref>
-'''Stuporous catatonia''': This form of catatonia is characterized by immobility, mutism, and a lack of response to the world around them.<ref name="Fink & Taylor 2009" /><ref name="Catatonia StatPearls" /> They may appear frozen in one position for long periods of time unable to eat, drink, or speak.
+'''Stuporous catatonia''' is characterized by immobility, mutism, and a lack of response to the world around them.<ref name="Fink & Taylor 2009">{{cite journal |last1=Fink |first1=Max |last2=Taylor |first2=Michael Alan |date=1 November 2009 |title=The Catatonia Syndrome: Forgotten but Not Gone |journal=Archives of General Psychiatry |volume=66 |issue=11 |pages=1173–7 |doi=10.1001/archgenpsychiatry.2009.141 |pmid=19884605}}</ref><ref name="Catatonia StatPearls"/> They may appear frozen in one position for long periods of time unable to eat, drink, or speak.
-'''Excited catatonia''': This form of catatonia is characterized by odd mannerisms and gestures, purposeless or inappropriate actions, excessive motor activity, restlessness, stereotypy, impulsivity, agitation, and combativeness. Speech and actions may be repetitive or mimic another person's.<ref name="Fink & Taylor 2009" /><ref name="Catatonia StatPearls" /><ref name="Rasmussen Mazurek Rosebush 2016" /> People in this state are extremely hyperactive and may have delusions and hallucinations.<ref>{{cite book |last1=Nolen-Hoeksema |first1=Susan |title=Abnormal Psychology |date=2014 |publisher=McGraw-Hill Education |isbn=978-1-259-06072-4 |page=224 }}</ref>
+'''Excited catatonia''' is characterized by odd mannerisms and gestures, purposeless or inappropriate actions, excessive motor activity, restlessness, stereotypy, impulsivity, agitation, and combativeness. Patients suffering from excited catatonia may have speech and actions that are repetitive or mimic another person's.<ref name="Fink & Taylor 2009"/><ref name="Catatonia StatPearls"/><ref name="Rasmussen Mazurek Rosebush 2016"/> This state is often characterized by hyperactivity, and the patient may have [[delusion]]s and [[hallucination]]s.<ref>{{cite book |last1=Nolen-Hoeksema |first1=Susan |title=Abnormal Psychology |date=2014 |publisher=McGraw-Hill Education |isbn=978-1-259-06072-4 |page=224}}</ref>
-'''Malignant catatonia''': This form of catatonia is life-threatening. It is characterized by fever, dramatic and rapid changes in blood pressure, increased heart rate and respiratory rate, and excessive sweating.<ref name="Fink & Taylor 2009" /><ref name="Catatonia StatPearls" /> Laboratory tests may be abnormal.
+'''Malignant catatonia''' is characterized by fever, dramatic and rapid changes in blood pressure, increased heart rate and respiratory rate, and excessive sweating.<ref name="Fink & Taylor 2009"/><ref name="Catatonia StatPearls"/> This condition is life-threatening, and the patient's laboratory tests may come back abnormal.{{cn|date=April 2026}}
-'''Periodic catatonia:''' This form of catatonia is characterized by a person having recurrent episodes of catatonia. Individuals will experience multiple episodes over time, without signs of catatonia in between episodes. Historically, the Wernicke-Kleist-Leonhard School considered periodic catatonia a distinct form of "non-system schizophrenia" characterized by recurrent acute phases with hyperkinetic and akinetic features and often psychotic symptoms, and the build-up of a residual state in between these acute phases, which is characterized by low-level catatonic features and [[aboulia]] of varying severity.
+'''Periodic catatonia''' is characterized by a person having recurrent episodes of catatonia. Individuals will experience multiple episodes over time, with no signs of catatonia between episodes. Historically, the Wernicke-Kleist-Leonhard school considered periodic catatonia a distinct form of "non-system schizophrenia", characterized by recurrent acute phases with hyperkinetic and akinetic features and often psychotic symptoms. There is also a residual state between these phases, characterized by low-level catatonic features and [[aboulia|abulia]] of varying severity.{{cn|date=April 2026}}
 == Causes ==
+Catatonia develops in the presence of an underlying condition, including psychiatric and neurological disorders, other medical conditions, and substance use.
-Catatonia can only develop if a person has another underlying condition – the most common causes being psychiatric disorders, medical conditions, and substance use.
+=== Neuropsychiatric ===
+Mood disorders like [[bipolar disorder]] and clinical depression are the most common conditions underlying catatonia.<ref name="Catatonia StatPearls"/> Other psychiatric conditions that can cause catatonia include [[schizophrenia]] and other primary psychotic disorders,<ref name="Fink & Taylor">{{cite book |last1=Fink |first1=Max |title=Catatonia: A Clinician's Guide to Diagnosis and Treatment |last2=Taylor |first2=Michael Alan |date=2003 |publisher=Cambridge University Press |isbn=978-0-521-82226-8}}{{page needed|date=June 2022}}</ref> [[autism spectrum disorder]], [[ADHD]],<ref>{{cite book |last1=Dhossche |first1=Dirk Marcel |last2=Rout |first2=Ujjwal |chapter=Are Autistic and Catatonic Regression Related? A Few Working Hypotheses Involving Gaba, Purkinje Cell Survival, Neurogenesis, and ECT |title=International Review of Neurobiology |date=2006 |volume=72 |pages=55–79 |doi=10.1016/S0074-7742(05)72004-3 |pmid=16697291 |isbn=978-0-12-366873-8}}</ref> and [[post-traumatic stress disorder]].<ref>{{Cite journal |last1=Ahmed |first1=Gellan K. |last2=Elbeh |first2=Khaled |last3=Karim |first3=Ahmed A. |last4=Khedr |first4=Eman M. |date=2021 |title=Case Report: Catatonia Associated With Post-traumatic Stress Disorder |journal=Frontiers in Psychiatry |volume=12 |article-number=740436 |doi=10.3389/fpsyt.2021.740436 |doi-access=free |issn=1664-0640 |pmc=8688766 |pmid=34950066}}</ref>
-=== Psychiatric conditions ===
+[[Psychodynamics|Psychodynamic theorists]] have historically interpreted catatonia as a psychological defense against the potentially destructive consequences of responsibility, with the passivity of the disorder providing relief.<ref>{{Cite book |last=Arieti |first=Silvano |title=Interpretation of schizophrenia |date=1994 |publisher=Jason Aronson |isbn=1-56821-209-7 |oclc=472906047}}</ref>
-Mood disorders such as bipolar disorder and depression are the most common conditions underlying catatonia.<ref name="Catatonia StatPearls" /> Other psychiatric conditions that can cause catatonia include [[schizophrenia]] and other primary psychotic disorders,<ref name="Fink & Taylor">{{cite book |last1=Fink |first1=Max |title=Catatonia: A Clinician's Guide to Diagnosis and Treatment |last2=Taylor |first2=Michael Alan |date=2003 |publisher=Cambridge University Press |isbn=978-0-521-82226-8}}{{page needed|date=June 2022}}</ref> [[autism spectrum disorders]], [[ADHD]],<ref>{{cite book |last1=Dhossche |first1=Dirk Marcel |last2=Rout |first2=Ujjwal |chapter=Are Autistic and Catatonic Regression Related? A Few Working Hypotheses Involving Gaba, Purkinje Cell Survival, Neurogenesis, and ECT |title=International Review of Neurobiology |date=2006 |volume=72 |pages=55–79 |doi=10.1016/S0074-7742(05)72004-3 |pmid=16697291 |isbn=978-0-12-366873-8 }}</ref> and [[post-traumatic stress disorder]].<ref>{{Cite journal |last1=Ahmed |first1=Gellan K. |last2=Elbeh |first2=Khaled |last3=Karim |first3=Ahmed A. |last4=Khedr |first4=Eman M. |date=2021 |title=Case Report: Catatonia Associated With Post-traumatic Stress Disorder |journal=Frontiers in Psychiatry |volume=12 |pages=740436 |doi=10.3389/fpsyt.2021.740436 |doi-access=free |issn=1664-0640 |pmc=8688766 |pmid=34950066}}</ref>
-Psychodynamic theorists have interpreted catatonia as a defense against the potentially destructive consequences of responsibility, with the passivity of the disorder providing relief.<ref>{{Cite book |last=Arieti |first=Silvano |title=Interpretation of schizophrenia |date=1994 |publisher=Jason Aronson |isbn=1-56821-209-7 |oclc=472906047}}</ref>
+=== Other conditions ===
+Catatonia is also seen in many medical disorders, including [[encephalitis]], [[meningitis]], [[autoimmune disorder]]s,<ref name=Rogers19>{{cite journal |last1=Rogers |first1=Jonathan P |last2=Pollak |first2=Thomas A |last3=Blackman |first3=Graham |last4=David |first4=Anthony S |date=July 2019 |title=Catatonia and the immune system: a review |journal=The Lancet Psychiatry |volume=6 |issue=7 |pages=620–630 |doi=10.1016/S2215-0366(19)30190-7 |pmc=7185541 |pmid=31196793}}</ref> focal neurological lesions (including [[stroke]]s),<ref>{{cite journal |last1=Haroche |first1=Alexandre |last2=Rogers |first2=Jonathan |last3=Plaze |first3=Marion |last4=Gaillard |first4=Raphaël |last5=Williams |first5=Steve CR |last6=Thomas |first6=Pierre |last7=Amad |first7=Ali |date=July 2020 |title=Brain imaging in catatonia: systematic review and directions for future research |url=https://discovery.ucl.ac.uk/id/eprint/10110277/ |journal=Psychological Medicine |volume=50 |issue=10 |pages=1585–97 |doi=10.1017/S0033291720001853 |pmid=32539902 |s2cid=219704600}}</ref> [[alcohol withdrawal]],<ref name="Geoffroy-2012">{{cite journal |last1=Geoffroy |first1=Pierre Alexis |last2=Rolland |first2=Benjamin |last3=Cottencin |first3=Olivier |date=1 May 2012 |title=Catatonia and Alcohol Withdrawal: A Complex and Underestimated Syndrome |journal=Alcohol and Alcoholism |volume=47 |issue=3 |pages=288–290 |doi=10.1093/alcalc/agr170 |pmid=22278315 |doi-access=free}}</ref> abrupt or overly rapid [[Benzodiazepine withdrawal syndrome|benzodiazepine withdrawal]],<ref>{{cite journal |author=Rosebush PI |author2=Mazurek MF |date=August 1996 |title=Catatonia after benzodiazepine withdrawal |journal=Journal of Clinical Psychopharmacology |volume=16 |issue=4 |pages=315–9 |doi=10.1097/00004714-199608000-00007 |pmid=8835707}}</ref><ref>{{cite journal |vauthors=Deuschle M, Lederbogen F |date=January 2001 |title=Benzodiazepine withdrawal-induced catatonia |journal=Pharmacopsychiatry |volume=34 |issue=1 |pages=41–42 |doi=10.1055/s-2001-15188 |pmid=11229621 |s2cid=260241781}}</ref><ref>{{cite journal |vauthors=Kanemoto K, Miyamoto T, Abe R |date=September 1999 |title=Ictal catatonia as a manifestation of de novo absence status epilepticus following benzodiazepine withdrawal |journal=Seizure |volume=8 |issue=6 |pages=364–6 |doi=10.1053/seiz.1999.0309 |pmid=10512781 |s2cid=17454162 |doi-access=free}}</ref> [[cerebrovascular disease]], [[neoplasm]]s, [[head injury]],<ref name="DSM-5-introduction">{{Cite book |last=American Psychiatric Association |url=https://archive.org/details/diagnosticstatis0005unse/page/119 |title=Diagnostic and Statistical Manual of Mental Disorders |publisher=American Psychiatric Publishing |year=2013 |isbn=978-0-89042-555-8 |edition=Fifth |location=Arlington, VA |pages=[https://archive.org/details/diagnosticstatis0005unse/page/119 119–121]}}</ref> and some metabolic conditions (e.g.,[[homocystinuria]], [[diabetic ketoacidosis]], [[hepatic encephalopathy]], and [[hypercalcaemia]]).<ref name="DSM-5-introduction"/>
-=== Medical conditions ===
+==== Neurological ====
-Catatonia is also seen in many medical disorders, including encephalitis, [[meningitis]], [[autoimmune disorder]]s,<ref name=Rogers19>{{cite journal |last1=Rogers |first1=Jonathan P |last2=Pollak |first2=Thomas A |last3=Blackman |first3=Graham |last4=David |first4=Anthony S |date=July 2019 |title=Catatonia and the immune system: a review |journal=The Lancet Psychiatry |volume=6 |issue=7 |pages=620–630 |doi=10.1016/S2215-0366(19)30190-7 |pmc=7185541 |pmid=31196793}}</ref> focal neurological lesions (including [[stroke]]s),<ref>{{cite journal |last1=Haroche |first1=Alexandre |last2=Rogers |first2=Jonathan |last3=Plaze |first3=Marion |last4=Gaillard |first4=Raphaël |last5=Williams |first5=Steve CR |last6=Thomas |first6=Pierre |last7=Amad |first7=Ali |date=July 2020 |title=Brain imaging in catatonia: systematic review and directions for future research |url=https://discovery.ucl.ac.uk/id/eprint/10110277/ |journal=Psychological Medicine |volume=50 |issue=10 |pages=1585–97 |doi=10.1017/S0033291720001853 |pmid=32539902 |s2cid=219704600}}</ref> alcohol withdrawal,<ref name="Geoffroy-2012">{{cite journal |last1=Geoffroy |first1=Pierre Alexis |last2=Rolland |first2=Benjamin |last3=Cottencin |first3=Olivier |date=1 May 2012 |title=Catatonia and Alcohol Withdrawal: A Complex and Underestimated Syndrome |journal=Alcohol and Alcoholism |volume=47 |issue=3 |pages=288–290 |doi=10.1093/alcalc/agr170 |pmid=22278315 |doi-access=free}}</ref> abrupt or overly rapid [[Benzodiazepine withdrawal syndrome|benzodiazepine withdrawal]],<ref>{{cite journal |author=Rosebush PI |author2=Mazurek MF |date=August 1996 |title=Catatonia after benzodiazepine withdrawal |journal=Journal of Clinical Psychopharmacology |volume=16 |issue=4 |pages=315–9 |doi=10.1097/00004714-199608000-00007 |pmid=8835707}}</ref><ref>{{cite journal |vauthors=Deuschle M, Lederbogen F |date=January 2001 |title=Benzodiazepine withdrawal-induced catatonia |journal=Pharmacopsychiatry |volume=34 |issue=1 |pages=41–42 |doi=10.1055/s-2001-15188 |pmid=11229621 |s2cid=260241781}}</ref><ref>{{cite journal |vauthors=Kanemoto K, Miyamoto T, Abe R |date=September 1999 |title=Ictal catatonia as a manifestation of de novo absence status epilepticus following benzodiazepine withdrawal |journal=Seizure |volume=8 |issue=6 |pages=364–6 |doi=10.1053/seiz.1999.0309 |pmid=10512781 |s2cid=17454162 |doi-access=free}}</ref> [[cerebrovascular disease]], [[neoplasm]]s, [[head injury]],<ref name="DSM-5-introduction" /> and some metabolic conditions ([[homocystinuria]], [[diabetic ketoacidosis]], [[hepatic encephalopathy]], and [[hypercalcaemia]]).<ref name="DSM-5-introduction" />
+Catatonia can occur due to several neurological conditions. For instance, certain types of encephalitis can cause catatonia. [[Anti-NMDA receptor encephalitis]] is a form of [[autoimmune encephalitis]] known to cause catatonia, albeit very rarely. Additionally, encephalitic catatonia has been reported in cases of severe [[HIV]] and [[herpes simplex virus]] infections. A small amount of evidence suggests that catatonia can develop after traumatic brain injury in the absence of a primary psychiatric disorder.<ref>{{Cite journal |last1=Berthelot |first1=Jessica |last2=Cambre |first2=Jacob |last3=Erwin |first3=Madeline |last4=Phan |first4=Jennifer |date=2024-03-06 |editor-last=Inada |editor-first=Toshiya |title=Catatonia as a Result of a Traumatic Brain Injury |journal=Case Reports in Psychiatry |language=en |volume=2024 |pages=1–3 |doi=10.1155/2024/5184741 |doi-access=free |issn=2090-6838 |pmc=10937075 |pmid=38482162}}</ref> Similarly, there are several case reports of catatonia after a stroke, with some having catatonia-associated symptoms that were unexplainable by stroke itself and which improved after treatment with [[benzodiazepine]]s.<ref>{{Cite journal |last1=Koprucki |first1=Shawna |last2=Morcos |first2=Roy |date=2024-09-18 |title=Acute Catatonia Following a Cerebellar Stroke: A Case Report |journal=Cureus |volume=16 |issue=9 |article-number=e69645 |language=en |doi=10.7759/cureus.69645 |doi-access=free |issn=2168-8184 |pmc=11488475 |pmid=39429282}}</ref><ref>{{Cite journal |last1=Hasan |first1=H. |last2=Abdo |first2=M. |last3=Rabei |first3=S. |date=March 2023 |title=Post Cerebrovascular Stroke Catatonic Psychosis: A Case Report |journal=European Psychiatry |language=en |volume=66 |issue=S1 |pages=S1058 |doi=10.1192/j.eurpsy.2023.2245 |issn=0924-9338 |pmc=10479261}}</ref> [[Parkinson's disease]] can cause catatonia for some people by impairing their ability to produce and secrete [[dopamine]], a neurotransmitter which is thought to contribute to motor dysfunction in people with catatonia.
-==== Neurological disorders ====
+==== Metabolic and endocrine ====
-Catatonia can occur due to a number of neurological conditions. For instance, certain types of [[encephalitis]] can cause catatonia. Anti-NMDA receptor encephalitis is a form of autoimmune encephalitis which is known to cause catatonia in some people. Additionally, encephalitis has been reported to cause catatonia in people who have encephalitis due to [[HIV]] and [[herpes simplex virus]] (HSV). The research is limited, but some evidence suggests that people can develop catatonia after traumatic brain injury without a primary psychiatric disorder.<ref>{{Cite journal |last1=Berthelot |first1=Jessica |last2=Cambre |first2=Jacob |last3=Erwin |first3=Madeline |last4=Phan |first4=Jennifer |date=2024-03-06 |editor-last=Inada |editor-first=Toshiya |title=Catatonia as a Result of a Traumatic Brain Injury |journal=Case Reports in Psychiatry |language=en |volume=2024 |pages=1–3 |doi=10.1155/2024/5184741 |doi-access=free |issn=2090-6838 |pmc=10937075 |pmid=38482162}}</ref> Similarly, there are several case reports suggesting that people have experienced catatonia after a stroke, with some people having catatonia-associated symptoms that were unexplainable by their stroke itself, and which improved after treatment with [[benzodiazepine]]s.<ref>{{Cite journal |last1=Koprucki |first1=Shawna |last2=Morcos |first2=Roy |date=2024-09-18 |title=Acute Catatonia Following a Cerebellar Stroke: A Case Report |journal=Cureus |volume=16 |issue=9 |pages=e69645 |language=en |doi=10.7759/cureus.69645 |doi-access=free |issn=2168-8184 |pmc=11488475 |pmid=39429282}}</ref><ref>{{Cite journal |last1=Hasan |first1=H. |last2=Abdo |first2=M. |last3=Rabei |first3=S. |date=March 2023 |title=Post Cerebrovascular Stroke Catatonic Psychosis: A Case Report |journal=European Psychiatry |language=en |volume=66 |issue=S1 |pages=S1058 |doi=10.1192/j.eurpsy.2023.2245 |issn=0924-9338 |pmc=10479261}}</ref> [[Parkinson's disease]] can cause catatonia for some people by impairing their ability to produce and secrete [[dopamine]], a neurotransmitter which is thought to contribute to motor dysfunction in people with catatonia.
+Abnormal [[thyroid]] function may result in the development of catatonia when the thyroid overproduces ([[hyperthyroidism]]) or underproduces thyroid hormones ([[hypothyroidism]]). This is thought to occur due to the impact of thyroid hormones on metabolism, including in the cells of the nervous system. Abnormal [[electrolyte]] levels have also been shown to cause catatonia in rare cases. Most notably, low blood sodium levels can cause catatonia in some people.<ref>{{Cite journal |last1=McGuire |first1=Eimear |last2=Yohanathan |first2=Mythily |last3=Lally |first3=Leona |last4=McCarthy |first4=Geraldine |date=2017-07-14 |title=Hyponatraemia-associated catatonia |journal=BMJ Case Reports |language=en |pages=bcr–2017–219487 |doi=10.1136/bcr-2017-219487 |issn=1757-790X |pmc=5534696 |pmid=28710304}}</ref><ref>{{Cite journal |last1=Peritogiannis |first1=Vaios |last2=Rizos |first2=Dimitrios V. |date=2021-05-24 |title=Catatonia Associated with Hyponatremia: Case Report and Brief Review of the Literature |url=https://clinical-practice-and-epidemiology-in-mental-health.com/VOLUME/17/PAGE/26/ |journal=Clinical Practice & Epidemiology in Mental Health |language=en |volume=17 |issue=1 |pages=26–30 |doi=10.2174/1745017902117010026 |issn=1745-0179 |pmc=8227445 |pmid=34249136}}</ref><ref>{{Cite journal |last1=Mehta |first1=Vishal |last2=Sharma |first2=Akhya |last3=Sharma |first3=Chandra Bhushan |last4=Guria |first4=Rishi Tuhin |date=December 2021 |title=Cerebral Salt Wasting Induced Hyponatraemia Presenting as Catatonia |url=https://journals.sagepub.com/doi/10.4997/jrcpe.2021.413 |journal=Journal of the Royal College of Physicians of Edinburgh |language=en |volume=51 |issue=4 |pages=377–9 |doi=10.4997/jrcpe.2021.413 |pmid=34882138 |issn=1478-2715|url-access=subscription}}</ref><ref>{{Cite journal |last1=Krueger |first1=Anna |last2=Shebak |first2=Shady S. |last3=Kavuru |first3=Bush |date=2015-11-12 |title=Catatonia in the Setting of Hyponatremia |url=https://www.psychiatrist.com/pcc/catatonia-setting-hyponatremia/ |journal=The Primary Care Companion for CNS Disorders |language=English |volume=17 |issue=6 |page=26803 |doi=10.4088/PCC.15l01808 |pmid=27057405 |pmc=4805406 |issn=2155-7780}}</ref>
-==== Metabolic and endocrine disorders ====
+==== Infectious ====
-Abnormal [[thyroid]] function can cause catatonia when the thyroid overproduces or underproduces thyroid hormones. This is thought to occur due to thyroid hormones impact on metabolism including in the cells of the nervous system. Abnormal electrolyte levels have also been shown to cause catatonia in rare cases. Most notably, low levels of sodium in the blood can cause catatonia in some people.<ref>{{Cite journal |last1=McGuire |first1=Eimear |last2=Yohanathan |first2=Mythily |last3=Lally |first3=Leona |last4=McCarthy |first4=Geraldine |date=2017-07-14 |title=Hyponatraemia-associated catatonia |journal=BMJ Case Reports |language=en |pages=bcr–2017–219487 |doi=10.1136/bcr-2017-219487 |issn=1757-790X |pmc=5534696 |pmid=28710304}}</ref><ref>{{Cite journal |last1=Peritogiannis |first1=Vaios |last2=Rizos |first2=Dimitrios V. |date=2021-05-24 |title=Catatonia Associated with Hyponatremia: Case Report and Brief Review of the Literature |url=https://clinical-practice-and-epidemiology-in-mental-health.com/VOLUME/17/PAGE/26/ |journal=Clinical Practice & Epidemiology in Mental Health |language=en |volume=17 |issue=1 |pages=26–30 |doi=10.2174/1745017902117010026 |issn=1745-0179 |pmc=8227445 |pmid=34249136}}</ref><ref>{{Cite journal |last1=Mehta |first1=Vishal |last2=Sharma |first2=Akhya |last3=Sharma |first3=Chandra Bhushan |last4=Guria |first4=Rishi Tuhin |date=December 2021 |title=Cerebral Salt Wasting Induced Hyponatraemia Presenting as Catatonia |url=https://journals.sagepub.com/doi/10.4997/jrcpe.2021.413 |journal=Journal of the Royal College of Physicians of Edinburgh |language=en |volume=51 |issue=4 |pages=377–9 |doi=10.4997/jrcpe.2021.413 |pmid=34882138 |issn=1478-2715|url-access=subscription }}</ref><ref>{{Cite journal |last1=Krueger |first1=Anna |last2=Shebak |first2=Shady S. |last3=Kavuru |first3=Bush |date=2015-11-12 |title=Catatonia in the Setting of Hyponatremia |url=https://www.psychiatrist.com/pcc/catatonia-setting-hyponatremia/ |journal=The Primary Care Companion for CNS Disorders |language=English |volume=17 |issue=6 |pages=26803 |doi=10.4088/PCC.15l01808 |pmid=27057405 |pmc=4805406 |issn=2155-7780}}</ref>
+Certain infections are known to cause catatonia, either by directly impairing brain function or by increasing a person's susceptibility to other diseases that can do so. [[HIV]] and [[AIDS]] can cause catatonia by predisposing one to infections in the brain, including different types of [[viral encephalitis]].<ref>{{Cite journal |last1=Volkow |first1=N D |last2=Harper |first2=A |last3=Munnisteri |first3=D |last4=Clother |first4=J |date=1987-01-01 |title=AIDS and catatonia. |journal=Journal of Neurology, Neurosurgery & Psychiatry |language=en |volume=50 |issue=1 |page=104 |doi=10.1136/jnnp.50.1.104-a |issn=0022-3050 |pmc=1033262 |pmid=3819740}}</ref><ref>{{Cite journal |last1=Hisamoto |first1=Yoshimi |last2=Gabriel |first2=Genevieve |last3=Verma |first3=Sonam |last4=Karakas |first4=Cemal |last5=Chari |first5=Geetha |date=2017-04-18 |title=Catatonia as a rare manifestation of HIV associated psychosis in adolescents. (P6.208) |url=https://www.neurology.org/doi/10.1212/WNL.88.16_supplement.P6.208 |journal=Neurology |language=en |volume=88 |issue=16_supplement |article-number=P6.208 |doi=10.1212/WNL.88.16_supplement.P6.208 |issn=0028-3878|url-access=subscription}}</ref> ''[[Borrelia burgdorferi]]'' causes [[Lyme disease]], which has been shown to cause catatonia by infecting the brain and causing encephalitis.<ref name=Rogers19/><ref>{{Cite journal |last1=Pfister |first1=H.-W. |last2=Preac-Mursic |first2=V. |last3=Wilske |first3=B. |last4=Rieder |first4=G. |last5=Förderreuther |first5=S. |last6=Schmidt |first6=S. |last7=Kapfhammer |first7=H.-P. |date=February 1993 |title=Catatonic syndrome in acute severe encephalitis due to Borrelia burgdorferi infection |url=https://www.neurology.org/doi/10.1212/WNL.43.2.433 |journal=Neurology |language=en |volume=43 |issue=2 |pages=433–5 |doi=10.1212/WNL.43.2.433 |pmid=8437717 |issn=0028-3878|url-access=subscription}}</ref><ref>{{Cite journal |last1=Neumärker |first1=K. J. |last2=Dudeck |first2=U. |last3=Plaza |first3=P. |date=February 1989 |title=[Borrelia encephalitis and catatonia in adolescence] |journal=Der Nervenarzt |volume=60 |issue=2 |pages=115–9 |issn=0028-2804 |pmid=2716930}}</ref><ref>{{Cite journal |last1=Ford |first1=Lenzie |last2=Tufts |first2=Danielle M. |date=2021-06-15 |title=Lyme Neuroborreliosis: Mechanisms of B. burgdorferi Infection of the Nervous System |journal=Brain Sciences |volume=11 |issue=6 |page=789 |doi=10.3390/brainsci11060789 |doi-access=free |issn=2076-3425 |pmc=8232152 |pmid=34203671}}</ref>
-==== Infectious diseases ====
+=== Medications ===
-Certain types of infections are known to cause catatonia either through directly impairing brain function or by making a person more likely to contract diseases that impair brain function. HIV and [[AIDS]] can cause catatonia, most likely by predisposing one to infections in the brain, including different types of viral encephalitis.<ref>{{Cite journal |last1=Volkow |first1=N D |last2=Harper |first2=A |last3=Munnisteri |first3=D |last4=Clother |first4=J |date=1987-01-01 |title=AIDS and catatonia. |journal=Journal of Neurology, Neurosurgery & Psychiatry |language=en |volume=50 |issue=1 |pages=104 |doi=10.1136/jnnp.50.1.104-a |issn=0022-3050 |pmc=1033262 |pmid=3819740}}</ref><ref>{{Cite journal |last1=Hisamoto |first1=Yoshimi |last2=Gabriel |first2=Genevieve |last3=Verma |first3=Sonam |last4=Karakas |first4=Cemal |last5=Chari |first5=Geetha |date=2017-04-18 |title=Catatonia as a rare manifestation of HIV associated psychosis in adolescents. (P6.208) |url=https://www.neurology.org/doi/10.1212/WNL.88.16_supplement.P6.208 |journal=Neurology |language=en |volume=88 |issue=16_supplement |doi=10.1212/WNL.88.16_supplement.P6.208 |issn=0028-3878|url-access=subscription }}</ref> ''[[Borrelia burgdorferi]]'' causes [[Lyme disease]], which has been shown to cause catatonia by infecting the brain and causing encephalitis.<ref name=Rogers19/><ref>{{Cite journal |last1=Pfister |first1=H.-W. |last2=Preac-Mursic |first2=V. |last3=Wilske |first3=B. |last4=Rieder |first4=G. |last5=Förderreuther |first5=S. |last6=Schmidt |first6=S. |last7=Kapfhammer |first7=H.-P. |date=February 1993 |title=Catatonic syndrome in acute severe encephalitis due to Borrelia burgdorferi infection |url=https://www.neurology.org/doi/10.1212/WNL.43.2.433 |journal=Neurology |language=en |volume=43 |issue=2 |pages=433–5 |doi=10.1212/WNL.43.2.433 |pmid=8437717 |issn=0028-3878|url-access=subscription }}</ref><ref>{{Cite journal |last1=Neumärker |first1=K. J. |last2=Dudeck |first2=U. |last3=Plaza |first3=P. |date=February 1989 |title=[Borrelia encephalitis and catatonia in adolescence] |journal=Der Nervenarzt |volume=60 |issue=2 |pages=115–9 |issn=0028-2804 |pmid=2716930}}</ref><ref>{{Cite journal |last1=Ford |first1=Lenzie |last2=Tufts |first2=Danielle M. |date=2021-06-15 |title=Lyme Neuroborreliosis: Mechanisms of B. burgdorferi Infection of the Nervous System |journal=Brain Sciences |volume=11 |issue=6 |pages=789 |doi=10.3390/brainsci11060789 |doi-access=free |issn=2076-3425 |pmc=8232152 |pmid=34203671}}</ref>
+[[Disulfiram]], a drug used to treat [[alcoholism]], can cause catatonia. It is theorized that the medication can cause alterations in dopamine metabolism, as it blocks [[dopamine beta-hydroxylase]]. Additionally, [[phencyclidine]], [[corticosteroid]]s, and [[antipsychotic]]s, among other drugs, are known to cause catatonia.<ref>{{Cite book |url=https://books.google.com/books?id=4cPp3Uj_xlYC |title=Catatonia: From Psychopathology to Neurobiology |date=3 May 2007 |publisher=American Psychiatric Pub |isbn=978-1-58562-712-7 |editor-last=Carrof |editor-first=Stanley N. |pages=133–136 |editor-last2=Mann |editor-first2=Stephan C. |editor-last3=Francis |editor-first3=Andrew |editor-last4=Fricchione |editor-first4=Gregory L.}}</ref>
-==== Pharmacological causes ====
-[[Disulfiram]], used to treat [[alcoholism]], can cause catatonia. It is theorized that the medication can cause the dopamine metabolism to be altered, as it blocks the [[dopamine beta-hydroxylase]] enzyme. Additionally, [[Phencyclidine|phencylidine]], [[Corticosteroid|corticosteriods]], and [[Antipsychotic|antipsychotics]], among other drugs, are known to cause catatonia.<ref>{{Cite book |url=https://books.google.com/books?id=4cPp3Uj_xlYC |title=Catatonia: From Psychopathology to Neurobiology |date=3 May 2007 |publisher=American Psychiatric Pub |isbn=9781585627127 |editor-last=Carrof |editor-first=Stanley N. |pages=133–136 |editor-last2=Mann |editor-first2=Stephan C. |editor-last3=Francis |editor-first3=Andrew |editor-last4=Fricchione |editor-first4=Gregory L.}}</ref>
 == Pathogenesis ==
-The mechanisms in the brain that cause catatonia are poorly understood.<ref name="Rasmussen Mazurek Rosebush 2016" /><ref>{{cite journal |last1=Walther |first1=Sebastian |last2=Stegmayer |first2=Katharina |last3=Wilson |first3=Jo Ellen |last4=Heckers |first4=Stephan |title=Structure and neural mechanisms of catatonia |journal=The Lancet Psychiatry |date=July 2019 |volume=6 |issue=7 |pages=610–9 |doi=10.1016/S2215-0366(18)30474-7 |pmid=31196794 |pmc=6790975 }}</ref> Currently, there are two main categories of explanations for what may be happening in the brain to cause catatonia. The first is that there is disruption of normal neurotransmitter production or release in certain areas of the brain preventing normal function of those areas of the brain, leading to behavioral and motor symptoms associated with catatonia. The second claims that disruption of communication between different areas of the brain causes catatonia.
+The mechanisms underlying brain catatonia are poorly understood.<ref name="Rasmussen Mazurek Rosebush 2016"/><ref>{{cite journal |last1=Walther |first1=Sebastian |last2=Stegmayer |first2=Katharina |last3=Wilson |first3=Jo Ellen |last4=Heckers |first4=Stephan |title=Structure and neural mechanisms of catatonia |journal=The Lancet Psychiatry |date=July 2019 |volume=6 |issue=7 |pages=610–9 |doi=10.1016/S2215-0366(18)30474-7 |pmid=31196794 |pmc=6790975}}</ref> Currently, there are two main categories of explanations for the brain pathology of catatonia. The first is a disruption of normal neurotransmitter production or release in certain brain areas, preventing normal cognitive function and leading to behavioral and motor symptoms associated with catatonia.<ref>{{Cite web |title=Sage Journals: Discover world-class research |url=https://journals.sagepub.com/action/cookieAbsent |access-date=2026-04-05 |website=Sage Journals |language=en |doi=10.12788/acp.0116}}</ref> The second claims that disruption of communication between different areas of the brain causes catatonia.<ref>{{Cite web |title=Sage Journals: Discover world-class research |url=https://journals.sagepub.com/action/cookieAbsent |access-date=2026-04-05 |website=Sage Journals |language=en |doi=10.1177/02698811231158232 |pmc=10101189 |pmid=37039129}}</ref>
 === Neurotransmitters ===
-The neurotransmitters that are most strongly associated with catatonia are GABA, dopamine, and glutamate. GABA is the main inhibitory neurotransmitter of the brain, meaning that it slows down the activity of the systems of the brain it acts on. In catatonia, people have low levels of GABA which causes them to be overly activated, especially in the areas of the brain that cause inhibition. This is thought to cause the behavioral symptoms associated with catatonia including withdrawal. Dopamine can increase or decrease the activity of the area of the brain it acts on depending on where in the brain it is. Dopamine is lower than normal in people with catatonia, which is thought to cause many of the motor symptoms, because dopamine is the main neurotransmitter which activates the parts of the brain responsible for movement. Glutamate is an excitatory neurotransmitter, meaning that it increases the activity of the areas of the brain it acts on. Notably, glutamate increases tells the neuron it acts on to fire, by binding to the NMDA receptor. People with anti-NMDA receptor encephalitis can develop catatonia because their own antibodies attack the NMDA receptor, which reduces the ability of the brain to activate different areas of the brain using glutamate.
+The neurotransmitters that are most strongly associated with catatonia are [[GABA]], [[dopamine]], and [[glutamate]]. GABA is the primary inhibitory neurotransmitter of the brain, meaning it slows down the activity of the systems it acts on. In catatonia, people have low levels of GABA, which causes them to be overly activated, especially in areas of the brain that normally inhibit activity. This is thought to cause the behavioral symptoms associated with catatonia, including withdrawal.<ref>
+Daniels J. Catatonia: Clinical Aspects and Neurobiological Correlates. The Journal of Neuropsychiatry and Clinical Neurosciences 2009;21:371–80. https://doi.org/10.1176/jnp.2009.21.4.371.‌</ref> Dopamine can increase or decrease the activity of the area of the brain it acts on, depending on where in the brain it is. Dopamine is lower than normal in people with catatonia, which is thought to cause many of the motor symptoms, because dopamine is the main neurotransmitter that activates the parts of the brain responsible for movement.<ref name="Rasmussen Mazurek Rosebush 2016"/> Glutamate is an excitatory neurotransmitter, meaning that it increases the activity of the areas of the brain it acts on. Notably, glutamate tells the neuron it acts on to fire by binding to the NMDA receptor. People with anti-NMDA receptor encephalitis can develop catatonia because their antibodies attack the NMDA receptor, reducing the brain's ability to activate different areas through glutamate.<ref>
+{{Cite journal |last=Rogers |first=Jonathan P. |last2=Pollak |first2=Thomas A. |last3=Blackman |first3=Graham |last4=David |first4=Anthony S. |date=2019-07-01 |title=Catatonia and the immune system: a review |url=https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(19)30190-7/fulltext |journal=The Lancet Psychiatry |language=English |volume=6 |issue=7 |pages=620–630 |doi=10.1016/S2215-0366(19)30190-7 |issn=2215-0366 |pmid=31196793|pmc=7185541 }}</ref>
 === Neurological pathways ===
-Several pathways in the brain have been studied which seem to contribute to catatonia when they are not functioning properly.<ref>{{cite journal |last1=Dhossche |first1=Dirk M. |last2=Stoppelbein |first2=Laura |last3=Rout |first3=Ujjwal K. |date=December 2010 |title=Etiopathogenesis of Catatonia: Generalizations and Working Hypotheses |journal=The Journal of ECT |volume=26 |issue=4 |pages=253–8 |doi=10.1097/YCT.0b013e3181fbf96d |pmid=21076339}}</ref> However, these studies were unable to determine if the abnormalities they observed were the cause of catatonia or if the catatonia caused the abnormalities. Furthermore, it has also been hypothesized that pathways that connect the [[basal ganglia]] with the cortex and [[thalamus]] is involved in the development of catatonia.<ref>{{cite journal |last1=Northoff |first1=Georg |title=What catatonia can tell us about 'top-down modulation': A neuropsychiatric hypothesis |journal=Behavioral and Brain Sciences |date=October 2002 |volume=25 |issue=5 |pages=555–577 |doi=10.1017/s0140525x02000109 |pmid=12958742 |s2cid=20407002 }}</ref>
+Several brain pathways have been studied, and they seem to contribute to catatonia when they are not functioning properly.<ref>{{cite journal |last1=Dhossche |first1=Dirk M. |last2=Stoppelbein |first2=Laura |last3=Rout |first3=Ujjwal K. |date=December 2010 |title=Etiopathogenesis of Catatonia: Generalizations and Working Hypotheses |journal=The Journal of ECT |volume=26 |issue=4 |pages=253–8 |doi=10.1097/YCT.0b013e3181fbf96d |pmid=21076339}}</ref> However, these studies were unable to determine if the abnormalities they observed were the cause of catatonia or if the catatonia caused the abnormalities. Furthermore, it has been hypothesized that pathways connecting the [[basal ganglia]] with the cortex and [[thalamus]] are involved in the development of catatonia.<ref>{{cite journal |last1=Northoff |first1=Georg |title=What catatonia can tell us about 'top-down modulation': A neuropsychiatric hypothesis |journal=Behavioral and Brain Sciences |date=October 2002 |volume=25 |issue=5 |pages=555–577 |doi=10.1017/s0140525x02000109 |pmid=12958742 |s2cid=20407002}}</ref>
-[[File:Image from page 110 of "Mental medicine and nursing - for use in training-schools for nurses and in medical classes and a ready reference for the general practitioner" (1915).jpg|thumb|upright]]
-[[File:Image from page 219 of "A treatise on mental diseases" (1900).jpg|thumb|upright]]
-[[File:Image from page 719 of "Diseases of the nervous system - a text-book of neurology and psychiatry" (1915).jpg|thumb|upright]]
 ==Diagnosis==
+Catatonia is diagnosed when a person exhibits at least three key symptoms simultaneously.
-There is not yet a definitive consensus regarding diagnostic criteria of catatonia. In the fifth edition of the [[American Psychiatric Association|American Psychiatric Association's]] ''[[Diagnostic and Statistical Manual of Mental Disorders]]'' ([[DSM-5]], 2013) and the eleventh edition of the [[World Health Organization|World Health Organization's]] ''[[International Classification of Diseases]] (''[[ICD-11]], 2022), the classification is more homogeneous than in earlier editions. Prominent researchers in the field have other suggestions for diagnostic criteria.<ref>{{Cite book|last=Fink|first=Max|title=Catatonia : a clinician's guide to diagnosis and treatment|date=2003|publisher=Cambridge University Press|others=Michael Alan Taylor|isbn=0-511-06198-6|location=Cambridge|oclc=57254202}}{{page needed|date=August 2022}}</ref> Still, diagnosing catatonia can be challenging. Evidence suggests that there is as high as a 15-day average delay to diagnosis for people with catatonia.
+These can include:
+* not moving or speaking (stupor or mutism)
+* unusual body positions
+* repeating words or actions
+* sudden restlessness
+* other, less common symptoms<ref name="Smith Holmes 2023">{{Cite journal |last1=Smith |first1=Alyssa C. |last2=Holmes |first2=Emily G. |date=2023-12-01 |title=Catatonia: A Narrative Review for Hospitalists |journal=American Journal of Medicine Open |volume=10 |article-number=100059 |doi=10.1016/j.ajmo.2023.100059  |doi-access=free|pmid=39035239 |issn=2667-0364|pmc=11256243 }}</ref>
-'''DSM-5 classification'''
+The [[DSM-5]] and [[ICD-11]], global manuals for mental health conditions, describe catatonia and its various types. Catatonia can occur with other mental illnesses, like depression or schizophrenia. It may also be a reaction to certain drugs or a medical condition. While often linked to psychiatric disorders, about one in five cases of catatonia are due to medical conditions.<ref>{{Cite journal |last1=Rogers |first1=Jonathan P |last2=Zandi |first2=Michael S |last3=David |first3=Anthony S |date=May 2023 |title=The diagnosis and treatment of catatonia |journal=Clinical Medicine |language=en |volume=23 |issue=3 |pages=242–245 |doi=10.7861/clinmed.2023-0113 |pmc=11046566 |pmid=37236789}}</ref>
-The [[DSM-5]] does not classify catatonia as an independent disorder, but rather it classifies it as catatonia associated with another mental disorder, due to another medical condition, or as unspecified catatonia.<ref name=":9">{{Cite book |last=American Psychiatric Association |title=Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision |publisher=American Psychiatric Association |year=2022 |isbn=978-0-89042-575-6 |location=Washington, DC |doi=10.1176/appi.books.9780890425787|s2cid= 249488050}}</ref><ref>{{cite book|last1=Jeste|first1=Dilip V. |last2=Lieberman|first2=Jeffrey A.|last3=Benson|first3=R Scott|last4=Young|first4=Melinda L.|last5=Akaka|first5=Jeffrey|last6=Bernstein|first6=Carol A.|last7=Crowley|first7=Brian|last8=Everett|first8=Anita S|last9=Geller|first9=Jeffrey|last10=Graff|first10=Mark David|last11=Greene|first11=James A.|last12=Kashtan|first12=Judith F.|last13=Mcvoy|first13=Molly K.|last14=Nininger|first14=James E.|last15=Oldham|first15=John M.|last16=Schatzberg|first16=Alan F.|last17=Widge|first17=Alik S.|last18=Vanderlip|first18=Erik R.|url=https://archive.org/details/dsm-5_202110/mode/2up |title=Diagnostic and Statistical Manual of Mental Disorders Fifth Edition DSM-5<sup><sup><small>TM</small></sup></sup> |date=2013|publisher=[[American Psychiatric Association]] |access-date=8 December 2023 |quote=}}</ref> {{Rp|pages=134–5}}
+There is not a definitive consensus regarding diagnostic criteria. In the fifth edition of the [[American Psychiatric Association|American Psychiatric Association's]] ''[[Diagnostic and Statistical Manual of Mental Disorders]]'' ([[DSM-5]], 2013) and the eleventh edition of the [[World Health Organization|World Health Organization's]] ''[[International Classification of Diseases]] (''[[ICD-11]], 2022), the classification is more homogeneous than in earlier editions. Prominent researchers in the field have other suggestions for diagnostic criteria.<ref>{{Cite book|last=Fink|first=Max|title=Catatonia: a clinician's guide to diagnosis and treatment|date=2003|publisher=Cambridge University Press|others=Michael Alan Taylor|isbn=0-511-06198-6|location=Cambridge|oclc=57254202}}{{page needed|date=August 2022}}</ref> Still, diagnosing catatonia can be challenging. Evidence suggests that there is as high as a 15-day average delay to diagnosis for people with catatonia.
-Catatonia is diagnosed by the presence of three or more of the following 12 psychomotor symptoms in association with a mental disorder, medical condition, or unspecified:<ref name=":9" />{{Rp|pages=|page=135}}
+===DSM-5 ===
-* [[stupor]]: no psycho-motor activity; not actively relating to the environment
+The [[DSM-5]] does not classify catatonia as an independent disorder. Instead, it classifies it as:
+* catatonia associated with another mental disorder
+* due to another medical condition
+* unspecified catatonia.<ref name="DS">{{Cite book |last=American Psychiatric Association |title=Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision |publisher=American Psychiatric Association |year=2022 |isbn=978-0-89042-575-6 |location=Washington, DC |doi=10.1176/appi.books.9780890425787|s2cid= 249488050}}</ref><ref>{{cite book|last1=Jeste|first1=Dilip V. |last2=Lieberman|first2=Jeffrey A.|last3=Benson|first3=R Scott|last4=Young|first4=Melinda L.|last5=Akaka|first5=Jeffrey|last6=Bernstein|first6=Carol A.|last7=Crowley|first7=Brian|last8=Everett|first8=Anita S|last9=Geller|first9=Jeffrey|last10=Graff|first10=Mark David|last11=Greene|first11=James A.|last12=Kashtan|first12=Judith F.|last13=Mcvoy|first13=Molly K.|last14=Nininger|first14=James E.|last15=Oldham|first15=John M.|last16=Schatzberg|first16=Alan F.|last17=Widge|first17=Alik S.|last18=Vanderlip|first18=Erik R.|url=https://archive.org/details/dsm-5_202110/mode/2up |title=Diagnostic and Statistical Manual of Mental Disorders Fifth Edition DSM-5<sup><sup><small>TM</small></sup></sup> |date=2013|publisher=[[American Psychiatric Association]] |access-date=8 December 2023 |quote=}}</ref> {{Rp|pages=134–5}}
+Diagnosis requires the presence of '''three or more''' of the following twelve psychomotor symptoms in association with a mental disorder, medical condition, or unspecified:<ref name="DS"/>{{Rp|pages=|page=135}}
+* [[stupor]]: absence of psycho-motor activity; not actively relating to the environment
 * [[catalepsy]]: passive induction of a posture held against gravity
-* [[waxy flexibility]]: allowing positioning by an examiner and maintaining that position
+* [[waxy flexibility]]: maintaining positions imposed by the examiner
-* [[mutism]]: no, or very little, verbal response (exclude if known [[aphasia]])
+* [[mutism]]: minimal or absent verbal response (not due to [[aphasia]])
-* negativism: opposition or no response to instructions or external stimuli
+* negativism: resistance or lack of response to instructions or external stimuli
 * [[Abnormal posturing|posturing]]: spontaneous and active maintenance of a posture against gravity
-* mannerisms that are odd, circumstantial caricatures of normal actions
+* mannerisms: odd or exaggerated caricatures of normal actions
 * [[stereotypy]]: repetitive, abnormally frequent, non-goal-directed movements
-* agitation, not influenced by external stimuli
+* agitation: excessive activity not influenced by external stimuli
-* grimacing: keeping a fixed facial expression
+* grimacing: sustained facial expression
 * [[echolalia]]: mimicking another's speech
 * [[echopraxia]]: mimicking another's movements
 Other disorders (additional code 293.89 [F06.1] to indicate the presence of the [[Comorbidity|co-morbid]] catatonia):
-* Catatonia associated with [[autism spectrum disorder]]<ref name=":9" />{{Rp|pages=|page=57}}
+* Catatonia associated with [[autism spectrum disorder]]<ref name="DS"/>{{Rp|pages=|page=57}}
 * Catatonia associated with [[schizophrenia]] spectrum and other psychotic disorders
-** Catatonia associated with [[brief psychotic disorder]]<ref name=":9" />{{Rp|pages=|page=109}}
+** Catatonia associated with [[brief psychotic disorder]]<ref name="DS"/>{{Rp|pages=|page=109}}
-** Catatonia associated with [[schizophreniform disorder]]<ref name=":9" />{{Rp|pages=|page=111}}
+** Catatonia associated with [[schizophreniform disorder]]<ref name="DS"/>{{Rp|pages=|page=111}}
-** Catatonia associated with [[schizoaffective disorder]]<ref name=":9" />{{Rp|pages=|page=121}}
+** Catatonia associated with [[schizoaffective disorder]]<ref name="DS"/>{{Rp|pages=|page=121}}
 ** Catatonia associated with a substance-induced psychotic disorder
-* Catatonia associated with [[Bipolar disorder|bipolar]] and related disorders<ref name=":9" />{{Rp|pages=|page=142}}
+* Catatonia associated with [[Bipolar disorder|bipolar]] and related disorders<ref name="DS"/>{{Rp|pages=|page=142}}
-* Catatonia associated with [[major depressive disorder]]<ref name=":9" />{{Rp|pages=|page=185}}
+* Catatonia associated with [[major depressive disorder]]<ref name="DS"/>{{Rp|pages=|page=185}}
-* Catatonic disorder due to another medical condition<ref name=":9" />{{Rp|pages=136–7}}
+* Catatonic disorder due to another medical condition<ref name="DS"/>{{Rp|pages=136–7}}
-If catatonic [[symptom]]s are present but do not form the catatonic [[syndrome]], a medication- or substance-induced aetiology should first be considered.<ref name="DSM-5Differential">{{cite book |author=Michael B. First |title=DSM-5® Handbook of Differential Diagnosis |url=https://books.google.com/books?id=haOvBAAAQBAJ&pg=PA49 |date=2013 |publisher=American Psychiatric Publishing |isbn=978-1-58562-998-5 |page=49}}</ref>
+If catatonic [[symptom]]s are present but do not form the catatonic [[syndrome]], a medication- or substance-induced aetiology should be considered first.<ref name="DSM-5Differential">{{cite book |author=Michael B. First |title=DSM-5® Handbook of Differential Diagnosis |url=https://books.google.com/books?id=haOvBAAAQBAJ&pg=PA49 |date=2013 |publisher=American Psychiatric Publishing |isbn=978-1-58562-998-5 |page=49}}</ref>
-'''ICD-11 classification'''
+===ICD-11===
-In the [[ICD-11]], catatonia is defined as a syndrome of primarily psychomotor disturbances that is characterized by the simultaneous occurrence of several symptoms such as stupor, catalepsy, waxy flexibility, mutism, negativism, posturing, mannerisms, stereotypies, psychomotor agitation, grimacing, echolalia, and echopraxia. Catatonia may occur in the context of specific mental disorders, including mood disorders, schizophrenia or other primary psychotic disorders, and neurodevelopmental disorders, and may be induced by psychoactive substances, including medications. Catatonia may also be caused by a medical condition not classified under mental, behavioral, or neurodevelopmental disorders.
+The [[ICD-11]] defines catatonia as a syndrome of psychomotor disturbances, characterized by the co-occurrence of several symptoms such as stupor, catalepsy, waxy flexibility, mutism, negativism, posturing, mannerisms, stereotypies, psychomotor agitation, grimacing, echolalia, and echopraxia. Catatonia may occur in the context of specific mental disorders, including mood disorders, schizophrenia or other primary psychotic disorders, and neurodevelopmental disorders. It may also be induced by psychoactive substances, including medications, or caused by a medical condition not classified under mental, behavioral, or neurodevelopmental disorders.
+{| class="wikitable"
+|+Table 1: '''DSM-5 vs. ICD-11criteria:'''
+!Features
+!DSM-5 (2013)
+!ICD-11 (2022)
+|-
+|Status of catatonia
+|Not an independent disorder; specified with another condition
+|Recognized as a syndrome that can occur across disorders
+|-
+|Required symptoms
+|≥3 of 12 psychomotor features
+|Several psychomotor features occurring simultaneously
+|-
+|Associated conditions
+|Mental disorders, medical conditions, unspecified
+|Mood disorders, schizophrenia, neurodevelopmental disorders, substance use, or medical conditions
+|}
-=== Assessment/physical ===
+=== Assessment and physical examination ===
-Catatonia is often overlooked and under-diagnosed.<ref name="Serra-Mestres & Jaimes-Albornoz 2018" /> Patients with catatonia most commonly have an underlying psychiatric disorder. For this reason, physicians may overlook signs of catatonia due to the severity of the psychosis the patient is presenting with. Furthermore, the patient may not be presenting with the common signs of catatonia such as mutism and posturing. Additionally, the motor abnormalities seen in catatonia are also present in psychiatric disorders. For example, a patient with mania will show increased motor activity and may not be considered for a diagnosis of excited catatonia, even if symptoms are developing that are not associated with mania. One way in which physicians can differentiate between the two is to observe the motor abnormality. Patients with mania present with increased goal-directed activity. On the other hand, the increased activity in catatonia is not goal-directed and often repetitive.<ref name="Catatonia StatPearls" />
+Catatonia is often overlooked and under-diagnosed.<ref name="Serra-Mestres & Jaimes-Albornoz 2018" /> Most patients present with an underlying psychiatric disorder, which can obscure recognition of catatonia. For example, psychotic symptoms may dominate the clinical picture, while classic catatonic features (such as mutism or posturing) are absent. Motor abnormalities can also be misleading; in mania, increased motor activity is typically goal-directed, whereas in excited catatonia, activity is non–goal-directed and repetitive.<ref name="Catatonia StatPearls" /> Careful observation of motor behavior is therefore crucial for diagnosis.
-Catatonia is a clinical diagnosis and there is no specific laboratory test to diagnose it. However, certain testing can help determine what is causing the catatonia. An EEG will likely show diffuse slowing. If seizure activity is driving the syndrome, then an EEG would also be helpful in detecting this. CT or MRI will not show catatonia; however, they might reveal abnormalities that might be leading to the syndrome. Metabolic screens, inflammatory markers, or autoantibodies may reveal reversible medical causes of catatonia.<ref name="Catatonia StatPearls" />
+Catatonia remains a clinical diagnosis with no specific laboratory test to diagnose it. However, supportive investigations may help identify underlying causes:
-Vital signs should be frequently monitored as catatonia can progress to malignant catatonia which is life-threatening. Malignant catatonia is characterized by fever, hypertension, tachycardia, and tachypnea.<ref name="Catatonia StatPearls" />
+* EEG: usually shows diffuse slowing; can detect seizure activity if present
+* CT or MRI: do not demonstrate catatonia directly, but may reveal structural or metabolic causes
+* Laboratory tests (metabolic panels, inflammatory markers, autoantibodies): can identify reversible medical contributors<ref name="Catatonia StatPearls" />
+Vital signs should be frequently monitored as catatonia can progress to malignant catatonia, which is a life-threatening condition characterized by fever, hypertension, tachycardia, and tachypnea.<ref name="Catatonia StatPearls" />
 ===Rating scale===
-Various rating scales for catatonia have been developed, however, their utility for clinical care has not been well established.<ref>{{cite journal |last1=Sienaert |first1=Pascal |last2=Rooseleer |first2=Jonas |last3=De Fruyt |first3=Jürgen |title=Measuring catatonia: A systematic review of rating scales |journal=Journal of Affective Disorders |date=December 2011 |volume=135 |issue=1–3 |pages=1–9 |doi=10.1016/j.jad.2011.02.012 |pmid=21420736 }}</ref> The most commonly used scale is the Bush-Francis Catatonia Rating Scale (BFCRS) (external link is provided below).<ref>{{cite journal |last1=Bush |first1=G. |last2=Fink |first2=M. |last3=Petrides |first3=G. |last4=Dowling |first4=F. |last5=Francis |first5=A. |title=Catatonia. I. Rating scale and standardized examination |journal=Acta Psychiatrica Scandinavica |date=February 1996 |volume=93 |issue=2 |pages=129–136 |doi=10.1111/j.1600-0447.1996.tb09814.x |pmid=8686483 |s2cid=20752576 }}</ref> The scale is composed of 23 items with the first 14 items being used as the screening tool. If 2 of the 14 are positive, this prompts for further evaluation and completion of the remaining 9 items.
+Several rating instruments have been developed, but their utility in clinical practice remains debated .<ref>{{cite journal |last1=Sienaert |first1=Pascal |last2=Rooseleer |first2=Jonas |last3=De Fruyt |first3=Jürgen |title=Measuring catatonia: A systematic review of rating scales |journal=Journal of Affective Disorders |date=December 2011 |volume=135 |issue=1–3 |pages=1–9 |doi=10.1016/j.jad.2011.02.012 |pmid=21420736}}</ref> The most commonly used scale is the '''Bush-Francis Catatonia Rating Scale (BFCRS)'''.<ref>{{cite journal |last1=Bush |first1=G. |last2=Fink |first2=M. |last3=Petrides |first3=G. |last4=Dowling |first4=F. |last5=Francis |first5=A. |title=Catatonia. I. Rating scale and standardized examination |journal=Acta Psychiatrica Scandinavica |date=February 1996 |volume=93 |issue=2 |pages=129–136 |doi=10.1111/j.1600-0447.1996.tb09814.x |pmid=8686483 |s2cid=20752576}}</ref> The scale consists of 23 items. The first 14 serve as a screening tool; if 2 of the 14 are positive, this prompts for further evaluation and completion of the remaining 9 items.
+Diagnostic certainty may also be supported by:
+* [[lorazepam challenge]]<ref name="Sienaert Dhossche Vancampfort et al 2014">{{cite journal |last1=Sienaert |first1=Pascal |last2=Dhossche |first2=Dirk M. |last3=Vancampfort |first3=Davy |last4=De Hert |first4=Marc |last5=Gazdag |first5=Gábor |title=A Clinical Review of the Treatment of Catatonia |journal=Frontiers in Psychiatry |date=9 December 2014 |volume=5 |page=181 |doi=10.3389/fpsyt.2014.00181 |pmid=25538636 |pmc=4260674 |doi-access=free}}</ref>
+* zolpidem challenge<ref>{{cite journal |title=Catatonia in French Psychiatry: Implications of the Zolpidem Challenge Test |journal=Psychiatric Annals |date=January 2007 |volume=37 |issue=1 |pages=00485713–20070101–02 |article-number=00485713-20070101-02 |doi=10.3928/00485713-20070101-02}}</ref>
-A diagnosis can be supported by the [[lorazepam challenge]]<ref name="Sienaert Dhossche Vancampfort et al 2014">{{cite journal |last1=Sienaert |first1=Pascal |last2=Dhossche |first2=Dirk M. |last3=Vancampfort |first3=Davy |last4=De Hert |first4=Marc |last5=Gazdag |first5=Gábor |title=A Clinical Review of the Treatment of Catatonia |journal=Frontiers in Psychiatry |date=9 December 2014 |volume=5 |page=181 |doi=10.3389/fpsyt.2014.00181 |pmid=25538636 |pmc=4260674 |doi-access=free }}</ref> or the zolpidem challenge.<ref>{{cite journal |title=Catatonia in French Psychiatry: Implications of the Zolpidem Challenge Test |journal=Psychiatric Annals |date=January 2007 |volume=37 |issue=1 |pages=00485713–20070101–02 |doi=10.3928/00485713-20070101-02 }}</ref> While proven useful in the past, barbiturates are no longer commonly used in [[psychiatry]]; thus the option of either benzodiazepines or ECT.
+Historically, barbiturates were used, but today benzodiazepines and electroconvulsive therapy (ECT) are the main options chosen for treatment.{{cn|date=April 2026}}
 === Laboratory findings ===
-Certain lab findings are common with malignant catatonia that are uncommon in other forms of catatonia. These lab findings include: [[leukocytosis]], elevated [[creatine kinase]], low serum iron. The signs and symptoms of malignant catatonia overlap significantly with [[neuroleptic malignant syndrome]] (NMS). Therefore, the results of laboratory tests need to be considered in the context of clinical history, review of medications, and physical exam findings.
+Laboratory abnormalities are most relevant in malignant catatonia rather that in other forms of catatonia, and may include:
+* elevated [[creatine kinase]]
+* [[leukocytosis]]
+* low serum iron
+These findings overlap with [[neuroleptic malignant syndrome]] (NMS). Therefore, it is essential to make careful correlation with clinical history, medications, and physical findings.{{cn|date=April 2026}}
+{| class="wikitable"
+|+Table 2: Malignant catatonia vs. neuroleptic malignant syndrome (NMS)
+!Feature
+!Malignant catatonia
+!NMS
+|-
+|Trigger
+|Spontaneous or due to psychiatric illness
+|Typically after antipsychotics (esp. first-gen)
+|-
+|Motor
+|Posturing, stereotypy, echolalia possible
+|Rigidity, tremor
+|-
+|Labs
+|↑ CK, leukocytosis, low iron (variable)
+|↑ CK, leukocytosis, low iron (more consistent)
+|-
+|Treatment
+|Benzodiazepines, ECT
+|Stop antipsychotics, supportive care, benzodiazepines
+|}
 === Differential diagnosis ===
-The differential diagnosis of catatonia is extensive as signs and symptoms of catatonia may overlap significantly with those of other conditions. Therefore, a careful and detailed history, medication review, and physical exam are key to diagnosing catatonia and differentiating it from other conditions. Furthermore, some of these conditions can themselves lead to catatonia. The differential diagnosis is as follows:
+Because catatonia overlaps with many psychiatric and neurological conditions a careful and detailed history, medication review, and physical exam are key to diagnosing catatonia and differentiating it from other conditions. Furthermore, some of these conditions can themselves lead to catatonia. The differential diagnosis is as follows:
-* [[Neuroleptic malignant syndrome]] (NMS) and catatonia are both life-threatening conditions that share many of the same characteristics including fever, autonomic instability, rigidity, and delirium.<ref name="Neuroleptic Malignant Syndrome StatPearls">{{cite book |last1=Simon |first1=Leslie V. |last2=Hashmi |first2=Muhammad F. |last3=Callahan |first3=Avery L. |title=StatPearls |date=2022 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK482282/ |chapter=Neuroleptic Malignant Syndrome |pmid=29489248 }}</ref> Lab values of low serum iron, elevated creatine kinase, and white blood cell count are also shared by the two disorders, further complicating the diagnosis. There are features of malignant catatonia (posturing, impulsivity, etc.) that are absent from NMS and the lab results are not as consistent in malignant catatonia as they are in NMS. Some experts consider NMS to be a drug-induced condition associated with [[antipsychotic]]s, particularly [[first generation antipsychotic]]s,<ref name="Neuroleptic Malignant Syndrome StatPearls" /> but it has not been established as a subtype.<ref>{{cite journal |last1=Northoff |first1=G. |title=Catatonia and neuroleptic malignant syndrome: psychopathology and pathophysiology |journal=Journal of Neural Transmission |date=1 December 2002 |volume=109 |issue=12 |pages=1453–67 |doi=10.1007/s00702-002-0762-z |pmid=12486486 |s2cid=12971112 |citeseerx=10.1.1.464.9266 }}</ref> Therefore, discontinuing antipsychotics and starting [[benzodiazepine]]s is a treatment for this condition, and similarly it is helpful in catatonia as well.
+* [[Neuroleptic malignant syndrome]] (NMS) and catatonia are both life-threatening conditions that share many of the same characteristics including fever, autonomic instability, rigidity, and delirium.<ref name="Neuroleptic Malignant Syndrome StatPearls">{{cite book |last1=Simon |first1=Leslie V. |last2=Hashmi |first2=Muhammad F. |last3=Callahan |first3=Avery L. |title=StatPearls |date=2022 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK482282/ |chapter=Neuroleptic Malignant Syndrome |pmid=29489248}}</ref> Lab values of low serum iron, elevated creatine kinase, and white blood cell count are also shared by the two disorders, further complicating the diagnosis. There are features of malignant catatonia (posturing, impulsivity, etc.) that are absent from NMS and the lab results are not as consistent in malignant catatonia as they are in NMS. Some experts consider NMS to be a drug-induced condition associated with [[antipsychotic]]s, particularly [[first generation antipsychotic]]s,<ref name="Neuroleptic Malignant Syndrome StatPearls"/> but it has not been established as a subtype.<ref>{{cite journal |last1=Northoff |first1=G. |title=Catatonia and neuroleptic malignant syndrome: psychopathology and pathophysiology |journal=Journal of Neural Transmission |date=1 December 2002 |volume=109 |issue=12 |pages=1453–67 |doi=10.1007/s00702-002-0762-z |pmid=12486486 |s2cid=12971112 |citeseerx=10.1.1.464.9266}}</ref> Therefore, discontinuing antipsychotics and starting [[benzodiazepine]]s is a treatment for this condition, and similarly it is helpful in catatonia as well. (See table 2 above).
-* [[Anti-NMDA receptor encephalitis]] is an autoimmune disorder characterized by neuropsychiatric features and the presence of IgG antibodies.<ref name="Anti-NMDA Receptor Encephalitis StatPearls">{{cite book |last1=Samanta |first1=Debopam |last2=Lui |first2=Forshing |title=StatPearls |date=2022 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK551672/ |chapter=Anti-NMDA Receptor Encephalitis |pmid=31869136 }}</ref> The presentation of anti-NMDA encephalitis has been categorized into 5 phases: prodromal phase, psychotic phase, unresponsive phase, hyperkinetic phase, and recovery phase. The psychotic phase progresses into the unresponsive phase characterized by mutism, decreased motor activity, and catatonia.<ref name="Anti-NMDA Receptor Encephalitis StatPearls" />
+* [[Anti-NMDA receptor encephalitis]] is an autoimmune disorder characterized by neuropsychiatric features and the presence of IgG antibodies.<ref name="Anti-NMDA Receptor Encephalitis StatPearls">{{cite book |last1=Samanta |first1=Debopam |last2=Lui |first2=Forshing |title=StatPearls |date=2022 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK551672/ |chapter=Anti-NMDA Receptor Encephalitis |pmid=31869136}}</ref> The presentation of anti-NMDA encephalitis has been categorized into 5 phases:
-* Both [[serotonin syndrome]] and malignant catatonia may present with signs and symptoms of delirium, autonomic instability, hyperthermia, and rigidity. Again, similar to the presentation in NMS. However, patients with Serotonin syndrome have a history of ingestion of serotonergic drugs (ex: [[Selective serotonin reuptake inhibitor|SSRI]]). These patients will also present with [[hyperreflexia]], [[myoclonus]], nausea, vomiting, and diarrhea.<ref>{{Cite journal|last1=Foong|first1=Ai-Leng|last2=Grindrod|first2=Kelly A.|last3=Patel|first3=Tejal|last4=Kellar|first4=Jamie|author2-link=Kelly Grindrod|date=October 2018|title=Demystifying serotonin syndrome (or serotonin toxicity)|journal=Canadian Family Physician|volume=64|issue=10|pages=720–7 |pmc=6184959|pmid=30315014}}</ref>
+** prodromal phase.
-* [[Malignant hyperthermia]] and malignant catatonia share features of autonomic instability, hyperthermia, and rigidity. However, malignant hyperthermia is a hereditary disorder of skeletal muscle that makes these patients susceptible to exposure to halogenated anesthetics and/or depolarizing muscle relaxants like [[succinylcholine]].<ref>{{cite book |last1=Watt |first1=Stacey |last2=McAllister |first2=Russell K. |title=StatPearls |date=2022 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK430828/ |chapter=Malignant Hyperthermia |pmid=28613578 }}</ref> Malignant hyperthermia most commonly occurs in the intraoperative or postoperative periods. Other signs and symptoms of malignant hyperthermia include metabolic and respiratory acidosis, [[hyperkalemia]], and cardiac arrhythmias.
+** psychotic phase.
-* [[Akinetic mutism]] is a neurological disorder characterized by a decrease in goal-directed behavior and motivation; however, the patient has an intact level of consciousness.<ref>{{cite journal |last1=Arnts |first1=Hisse |last2=van Erp |first2=Willemijn S. |last3=Lavrijsen |first3=Jan C.M. |last4=van Gaal |first4=Simon |last5=Groenewegen |first5=Henk J. |last6=van den Munckhof |first6=Pepijn |title=On the pathophysiology and treatment of akinetic mutism |journal=Neuroscience & Biobehavioral Reviews |date=May 2020 |volume=112 |pages=270–8 |doi=10.1016/j.neubiorev.2020.02.006 |pmid=32044373 |doi-access=free |hdl=11245.1/c438b878-4d5b-4f13-887c-7f01df095324 |hdl-access=free }}</ref> Patients may present with apathy, and may seem indifferent to pain, hunger, or thirst. Akinetic mutism has been associated with structural damage in a variety of brain areas.<ref>{{cite journal |last1=Ackermann |first1=H. |last2=Ziegler |first2=W. |title=Akinetischer Mutismus – eine Literaturübersicht |journal=Fortschritte der Neurologie · Psychiatrie |date=February 1995 |volume=63 |issue=2 |pages=59–67 |doi=10.1055/s-2007-996603 |pmid=7705740 |s2cid=260156218 }}</ref> Akinetic mutism and catatonia may both manifest with immobility, mutism, and waxy flexibility. Differentiating both disorders is the fact that akinetic mutism does not present with echolalia, echopraxia, or posturing. Furthermore, it is not responsive to benzodiazepines as is the case for catatonia.
+** unresponsive phase.
-* [[Selective mutism]] has an anxious etiology but has also been associated with personality disorders.<ref>{{cite journal |last1=Holka-Pokorska |first1=Justyna |last2=Piróg-Balcerzak |first2=Agnieszka |last3=Jarema |first3=Marek |title=The controversy around the diagnosis of selective mutism – a critical analysis of three cases in the light of modern research and diagnostic criteria |journal=Psychiatria Polska |date=30 April 2018 |volume=52 |issue=2 |pages=323–343 |doi=10.12740/PP/76088 |pmid=29975370 |doi-access=free }}</ref> Patients with this disorder fail to speak with some individuals but will speak with others. Likewise, they may refuse to speak in certain situations; for example, a child who refuses to speak at school but is conversational at home. This disorder is distinguished from catatonia by the absence of any other signs/symptoms.
+** hyperkinetic phase.
-* Nonconvulsive [[status epilepticus]] is seizure activity with no accompanying tonic-clonic movements.<ref>{{cite book |last1=Wylie |first1=Todd |last2=Sandhu |first2=Divyajot S. |last3=Murr |first3=Najib |title=StatPearls |date=2022 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK430686/ |chapter=Status Epilepticus |pmid=28613459 }}</ref> It can present with stupor, similar to catatonia, and they both respond to benzodiazepines. Nonconvulsive status epilepticus is diagnosed by the presence of seizure activity seen on [[Electroencephalography|electroencephalogram]] (EEG).<ref>{{cite journal |last1=Sutter |first1=Raoul |last2=Kaplan |first2=Peter W. |title=Electroencephalographic criteria for nonconvulsive status epilepticus: Synopsis and comprehensive survey: EEG Criteria for NCSE |journal=Epilepsia |date=August 2012 |volume=53 |pages=1–51 |doi=10.1111/j.1528-1167.2012.03593.x |pmid=22862158 |s2cid=24014621 }}</ref> Catatonia, on the other hand, is associated with normal EEG or diffuse slowing.
+** recovery phase.
-* [[Delirium]] is characterized by fluctuating disturbed perception and consciousness in the ill individual.<ref>{{cite book |title=Delirium: prevention, diagnosis and management |series=National Institute for Health and Care Excellence: Guidelines |date=2019 |publisher=National Institute for Health and Care Excellence (NICE) |isbn=978-1-4731-2992-4 |url=https://www.ncbi.nlm.nih.gov/books/NBK553009/ |pmid=31971702 }}</ref> It has hypoactive and hyperactive or mixed forms. People with hyperactive delirium present similarly to those with excited catatonia and have symptoms of restlessness, agitation, and aggression. Those with hypoactive delirium present with similarly to stuporous catatonia, withdrawn and quiet. However, catatonia also includes other distinguishing features including posturing and rigidity as well as a positive response to benzodiazepines.
+The psychotic phase progresses into the unresponsive phase characterized by mutism, decreased motor activity, and catatonia.<ref name="Anti-NMDA Receptor Encephalitis StatPearls" />
-* Patients with [[locked-in syndrome]] present with immobility and mutism; however, unlike patients with catatonia who are unmotivated to communicate, patients with locked-in syndrome try to communicate with eye movements and blinking. Furthermore, locked-in syndrome is caused by damage to the brainstem.<ref>{{cite book |last1=M Das |first1=Joe |last2=Anosike |first2=Kingsley |last3=Asuncion |first3=Ria Monica D. |title=StatPearls |date=2022 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK559026/ |chapter=Locked-in Syndrome |pmid=32644452 }}</ref>
+* [[serotonin syndrome]]: Triggered by serotonergic drugs (ex: [[Selective serotonin reuptake inhibitor|SSRI]]); features include delirium, hyperreflexia, myoclonus, GI symptoms (N/V/D), autonomic instability, hyperthermia, and rigidity.<ref>{{Cite journal|last1=Foong|first1=Ai-Leng|last2=Grindrod|first2=Kelly A.|last3=Patel|first3=Tejal|last4=Kellar|first4=Jamie|author2-link=Kelly Grindrod|date=October 2018|title=Demystifying serotonin syndrome (or serotonin toxicity)|journal=Canadian Family Physician|volume=64|issue=10|pages=720–7 |pmc=6184959|pmid=30315014}}</ref>
-* [[Stiff-person syndrome]] and catatonia are similar in that they may both present with rigidity, autonomic instability, and a positive response to benzodiazepines.<ref>{{cite journal |last1=Balint |first1=Bettina |last2=Meinck |first2=Hans-Michael |title=Pragmatic Treatment of Stiff Person Spectrum Disorders: Pragmatic Treatment of SPSD |journal=Movement Disorders Clinical Practice |date=July 2018 |volume=5 |issue=4 |pages=394–401 |doi=10.1002/mdc3.12629 |pmid=30363317 |pmc=6174384 }}</ref> However, stiff-person syndrome may be associated with anti-glutamic acid decarboxylase (anti-GAD) antibodies<ref>{{cite journal |last1=Baizabal-Carvallo |first1=José Fidel |last2=Jankovic |first2=Joseph |title=Stiff-person syndrome: insights into a complex autoimmune disorder |journal=Journal of Neurology, Neurosurgery & Psychiatry |date=August 2015 |volume=86 |issue=8 |pages=840–8 |doi=10.1136/jnnp-2014-309201 |pmid=25511790 |s2cid=19981869 }}</ref><ref>{{cite journal |last1=Sarva |first1=Harini |last2=Deik |first2=Andres |last3=Ullah |first3=Aman |last4=Severt |first4=William L. |title=Clinical Spectrum of Stiff Person Syndrome: A Review of Recent Reports |journal=Tremor and Other Hyperkinetic Movements |date=4 March 2016 |volume=6 |pages=340 |doi=10.7916/D85M65GD |pmid=26989571 |pmc=4790195 }}</ref> and other catatonic signs such as mutism and posturing are not part of the syndrome.
+* [[Malignant hyperthermia]]: A hereditary disorder of skeletal muscle, triggered by anesthetics or muscle relaxants like [[succinylcholine]].; associated with metabolic acidosis, [[hyperkalemia]], and arrhythmias.<ref>{{cite book |last1=Watt |first1=Stacey |last2=McAllister |first2=Russell K. |title=StatPearls |date=2022 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK430828/ |chapter=Malignant Hyperthermia |pmid=28613578}}</ref>
+* [[Akinetic mutism]] is a neurological disorder associated with structural damage in a variety of brain, it is characterized by immobility and mutism but intact awareness; lacks echolalia/echopraxia. Furthermore, it is unresponsive to [[benzodiazepine]]s.<ref>{{cite journal |last1=Arnts |first1=Hisse |last2=van Erp |first2=Willemijn S. |last3=Lavrijsen |first3=Jan C.M. |last4=van Gaal |first4=Simon |last5=Groenewegen |first5=Henk J. |last6=van den Munckhof |first6=Pepijn |title=On the pathophysiology and treatment of akinetic mutism |journal=Neuroscience & Biobehavioral Reviews |date=May 2020 |volume=112 |pages=270–8 |doi=10.1016/j.neubiorev.2020.02.006 |pmid=32044373 |doi-access=free |hdl=11245.1/c438b878-4d5b-4f13-887c-7f01df095324 |hdl-access=free}}</ref> Patients may present with apathy, and may seem indifferent to pain, hunger, or thirst.<ref>{{cite journal |last1=Ackermann |first1=H. |last2=Ziegler |first2=W. |title=Akinetischer Mutismus – eine Literaturübersicht |journal=Fortschritte der Neurologie · Psychiatrie |date=February 1995 |volume=63 |issue=2 |pages=59–67 |doi=10.1055/s-2007-996603 |pmid=7705740 |s2cid=260156218}}</ref>
+* [[Selective mutism]] has an anxious etiology but has also been associated with personality disorders.<ref>{{cite journal |last1=Holka-Pokorska |first1=Justyna |last2=Piróg-Balcerzak |first2=Agnieszka |last3=Jarema |first3=Marek |title=The controversy around the diagnosis of selective mutism – a critical analysis of three cases in the light of modern research and diagnostic criteria |journal=Psychiatria Polska |date=30 April 2018 |volume=52 |issue=2 |pages=323–343 |doi=10.12740/PP/76088 |pmid=29975370 |doi-access=free}}</ref> Patients with this disorder fail to speak with some individuals but will speak with others. Likewise, they may refuse to speak in certain situations; in another word it is anxiety-driven; speech restriction limited to certain contexts, without catatonic signs. for example, a child who refuses to speak at school but is conversational at home. This disorder is distinguished from catatonia by the absence of any other signs/symptoms.
+* Nonconvulsive [[status epilepticus]] is seizure activity with no accompanying tonic-clonic movements.<ref>{{cite book |last1=Wylie |first1=Todd |last2=Sandhu |first2=Divyajot S. |last3=Murr |first3=Najib |title=StatPearls |date=2022 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK430686/ |chapter=Status Epilepticus |pmid=28613459}}</ref> It can present with stupor, similar to catatonia, and they both respond to [[benzodiazepine]]s. Nonconvulsive status epilepticus is diagnosed by the presence of seizure activity seen on [[Electroencephalography|electroencephalogram]] (EEG).<ref>{{cite journal |last1=Sutter |first1=Raoul |last2=Kaplan |first2=Peter W. |title=Electroencephalographic criteria for nonconvulsive status epilepticus: Synopsis and comprehensive survey: EEG Criteria for NCSE |journal=Epilepsia |date=August 2012 |volume=53 |pages=1–51 |doi=10.1111/j.1528-1167.2012.03593.x |pmid=22862158 |s2cid=24014621}}</ref> Catatonia, on the other hand, is associated with normal [[Electroencephalography|EEG]] or diffuse slowing.
+* [[Delirium]] is characterized by fluctuating disturbed perception and consciousness in the ill individual.<ref>{{cite book |title=Delirium: prevention, diagnosis and management |series=National Institute for Health and Care Excellence: Guidelines |date=2019 |publisher=National Institute for Health and Care Excellence (NICE) |isbn=978-1-4731-2992-4 |url=https://www.ncbi.nlm.nih.gov/books/NBK553009/ |pmid=31971702}}</ref> It has hypoactive and hyperactive or mixed forms. People with hyperactive delirium present similarly to those with excited catatonia and have symptoms of restlessness, agitation, and aggression. Those with hypoactive delirium present with similarly to stuporous catatonia, withdrawn and quiet. However, catatonia also includes other distinguishing features including posturing and rigidity as well as a positive response to benzodiazepines.
+* Patients with [[locked-in syndrome]] present with immobility and mutism; however, unlike patients with catatonia who are unmotivated to communicate, patients with locked-in syndrome try to communicate with eye movements and blinking. Furthermore, locked-in syndrome is caused by damage to the brainstem.<ref>{{cite book |last1=M Das |first1=Joe |last2=Anosike |first2=Kingsley |last3=Asuncion |first3=Ria Monica D. |title=StatPearls |date=2022 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK559026/ |chapter=Locked-in Syndrome |pmid=32644452}}</ref>
+* [[Stiff-person syndrome]] and catatonia are similar in that they may both present with rigidity, autonomic instability, and a positive response to benzodiazepines.<ref>{{cite journal |last1=Balint |first1=Bettina |last2=Meinck |first2=Hans-Michael |title=Pragmatic Treatment of Stiff Person Spectrum Disorders: Pragmatic Treatment of SPSD |journal=Movement Disorders Clinical Practice |date=July 2018 |volume=5 |issue=4 |pages=394–401 |doi=10.1002/mdc3.12629 |pmid=30363317 |pmc=6174384}}</ref> However, stiff-person syndrome may be associated with anti-glutamic acid decarboxylase (anti-GAD) antibodies<ref>{{cite journal |last1=Baizabal-Carvallo |first1=José Fidel |last2=Jankovic |first2=Joseph |title=Stiff-person syndrome: insights into a complex autoimmune disorder |journal=Journal of Neurology, Neurosurgery & Psychiatry |date=August 2015 |volume=86 |issue=8 |pages=840–8 |doi=10.1136/jnnp-2014-309201 |pmid=25511790 |s2cid=19981869}}</ref><ref>{{cite journal |last1=Sarva |first1=Harini |last2=Deik |first2=Andres |last3=Ullah |first3=Aman |last4=Severt |first4=William L. |title=Clinical Spectrum of Stiff Person Syndrome: A Review of Recent Reports |journal=Tremor and Other Hyperkinetic Movements |date=4 March 2016 |volume=6 |page=340 |doi=10.7916/D85M65GD |pmid=26989571 |pmc=4790195}}</ref> and other catatonic signs such as mutism and posturing are not part of the syndrome.
 * Untreated late-stage [[Parkinson's disease]] may present similarly to stuporous catatonia with symptoms of immobility, rigidity, and difficulty speaking. Further complicating the diagnosis is the fact that many patients with Parkinson's disease will have major depressive disorder, which may be the underlying cause of catatonia. Parkinson's disease can be distinguished from catatonia by a positive response to levodopa. Catatonia, on the other hand, will show a positive response to benzodiazepines.
-* Extrapyramidal side effects of antipsychotic medication, especially [[dystonia]] and [[akathisia]], can be difficult to distinguish from catatonic symptoms, or may confound them in the psychiatric setting. Extrapyramidal motor disorders usually do not involve social symptoms like negativism, while individuals with catatonic excitement typically do not have the physically painful compulsion to move that is seen in akathisia.<ref>{{cite journal |last1=Rasmussen |first1=Sean A |last2=Mazurek |first2=Michael F |last3=Rosebush |first3=Patricia I |title=Catatonia: Our current understanding of its diagnosis, treatment and pathophysiology |journal=World Journal of Psychiatry |date=2016 |volume=6 |issue=4 |pages=1875–9 |doi=10.5498/wjp.v6.i4.391 |pmid=8078203 |pmc=5183991 |doi-access=free }}</ref>
+* Extrapyramidal side effects of antipsychotic medication, especially [[dystonia]] and [[akathisia]], can be difficult to distinguish from catatonic symptoms, or may confound them in the psychiatric setting. Extrapyramidal motor disorders usually do not involve social symptoms like negativism, while individuals with catatonic excitement typically do not have the physically painful compulsion to move that is seen in akathisia.<ref name="Rasmussen Mazurek Rosebush 2016"/>
 * Certain [[stimming]] behaviors and stress responses in individuals with [[autism spectrum disorder]]s can present similarly to catatonia. In autism spectrum disorders, chronic catatonia is distinguished by a lasting deterioration of adaptive skills from the background of pre-existing autistic symptomatology that cannot be easily explained. Acute catatonia is usually clearly distinguishable from autistic symptoms.<ref name="Vaquerizo-Serrano Salazar De Pablo Singh Santosh 2022">{{cite journal |last1=Vaquerizo-Serrano |first1=J. |last2=Salazar De Pablo |first2=G. |last3=Singh |first3=J. |last4=Santosh |first4=P. |date=2022 |title=Catatonia in autism spectrum disorders: A systematic review and meta-analysis |journal=European Psychiatry |volume=65 |issue=1 |pages=e4 |doi=10.1192/j.eurpsy.2021.2259 |pmc=8792870 |pmid=34906264}}</ref>
-* The diagnostic entities of [[obsessional slowness]] and psychogenic [[parkinsonism]] show overlapping features with catatonia, such as motor slowness, gegenhalten (oppositional [[paratonia]]), mannerisms, and reduced or absent speech. However, psychogenic parkinsonism involves [[tremor]] which is unusual in catatonia.<ref>{{cite book |doi=10.1016/B978-0-12-801772-2.00022-9 |chapter=Psychogenic (Functional) parkinsonism |title=Functional Neurologic Disorders |series=Handbook of Clinical Neurology |year=2016 |last1=Thenganatt |first1=M.A. |last2=Jankovic |first2=J. |volume=139 |pages=259–262 |pmid=27719845 |isbn=978-0-12-801772-2 }}</ref> Obsessional slowness is a controversial diagnosis, with presentations ranging from severe but common manifestations of [[obsessive compulsive disorder]] to catatonia.<ref>{{cite journal |last1=Ganos |first1=Christos |last2=Kassavetis |first2=Panagiotis |last3=Cerdan |first3=Maria |last4=Erro |first4=Roberto |last5=Balint |first5=Bettina |last6=Price |first6=Gary |last7=Edwards |first7=Mark J. |last8=Bhatia |first8=Kailash P. |title=Revisiting the Syndrome of "Obsessional Slowness" |journal=Movement Disorders Clinical Practice |date=June 2015 |volume=2 |issue=2 |pages=163–9 |doi=10.1002/mdc3.12140 |pmid=30713890 |pmc=6353487 |s2cid=73414098 }}</ref>
+* The diagnostic entities of [[obsessional slowness]] and psychogenic [[parkinsonism]] show overlapping features with catatonia, such as motor slowness, gegenhalten (oppositional [[paratonia]]), mannerisms, and reduced or absent speech. However, psychogenic parkinsonism involves [[tremor]] which is unusual in catatonia.<ref>{{cite book |doi=10.1016/B978-0-12-801772-2.00022-9 |chapter=Psychogenic (Functional) parkinsonism |title=Functional Neurologic Disorders |series=Handbook of Clinical Neurology |year=2016 |last1=Thenganatt |first1=M.A. |last2=Jankovic |first2=J. |volume=139 |pages=259–262 |pmid=27719845 |isbn=978-0-12-801772-2}}</ref> Obsessional slowness is a controversial diagnosis, with presentations ranging from severe but common manifestations of [[obsessive compulsive disorder]] to catatonia.<ref>{{cite journal |last1=Ganos |first1=Christos |last2=Kassavetis |first2=Panagiotis |last3=Cerdan |first3=Maria |last4=Erro |first4=Roberto |last5=Balint |first5=Bettina |last6=Price |first6=Gary |last7=Edwards |first7=Mark J. |last8=Bhatia |first8=Kailash P. |title=Revisiting the Syndrome of "Obsessional Slowness" |journal=Movement Disorders Clinical Practice |date=June 2015 |volume=2 |issue=2 |pages=163–9 |doi=10.1002/mdc3.12140 |pmid=30713890 |pmc=6353487 |s2cid=73414098}}</ref>
-* [[Down Syndrome Disintegrative Disorder]] (or Down Syndrome Regression Disorder, DSDD / DSRD) is a chronic condition characterized by loss of previously acquired adaptive, cognitive and social functioning occurring in persons with [[Down Syndrome]], usually during adolescence or early adulthood. The clinical picture is variable, but often includes catatonic signs, which is why it was called "catatonic psychosis" in initial reports in 1946.<ref>{{cite journal|pmid=32471843 |date=2020 |last1=Rosso |first1=M. |last2=Fremion |first2=E. |last3=Santoro |first3=S. L. |last4=Oreskovic |first4=N. M. |last5=Chitnis |first5=T. |last6=Skotko |first6=B. G. |last7=Santoro |first7=J. D. |title=Down Syndrome Disintegrative Disorder: A Clinical Regression Syndrome of Increasing Importance |journal=Pediatrics |volume=145 |issue=6 |pages=e20192939 |doi=10.1542/peds.2019-2939 |s2cid=219104019 |doi-access=free }}</ref> DSDD seems to phenotypically overlap with obsessional slowness (see above)<ref>{{cite web |first=B. |last=Chicoine |title=Obsessional Slowness |date=December 2022 |publisher=Adult Down Syndrome Center, Advocate Medical Group |url=https://adscresources.advocatehealth.com/resources/obsessional-slowness/#:~:text=The%20persistent%20stress%20of%20the%20rapidly%20moving%20environment,slowness%2C%20which%20we%20have%20also%20labeled%20%E2%80%9CThe%20Pace.%E2%80%9D;}}</ref> and catatonia-like regression occurring in ASD.<ref>{{cite journal|pmid=31959555 |date=2020 |last1=Lyons |first1=A. |last2=Allen |first2=N. M. |last3=Flanagan |first3=O. |last4=Cahalane |first4=D. |title=Catatonia as a feature of down syndrome: An under-recognised entity? |journal=European Journal of Paediatric Neurology |volume=25 |pages=187–190 |doi=10.1016/j.ejpn.2020.01.005 |s2cid=210841869 |doi-access=free }}</ref>
+* [[Down syndrome disintegrative disorder]] (or Down Syndrome Regression Disorder, DSDD / DSRD) is a chronic condition characterized by loss of previously acquired adaptive, cognitive and social functioning occurring in persons with [[Down syndrome]], usually during adolescence or early adulthood. The clinical picture is variable, but often includes catatonic signs, which is why it was called "catatonic psychosis" in initial reports in 1946.<ref>{{cite journal|pmid=32471843 |date=2020 |last1=Rosso |first1=M. |last2=Fremion |first2=E. |last3=Santoro |first3=S. L. |last4=Oreskovic |first4=N. M. |last5=Chitnis |first5=T. |last6=Skotko |first6=B. G. |last7=Santoro |first7=J. D. |title=Down Syndrome Disintegrative Disorder: A Clinical Regression Syndrome of Increasing Importance |journal=Pediatrics |volume=145 |issue=6 |pages=e20192939 |doi=10.1542/peds.2019-2939 |s2cid=219104019 |doi-access=free}}</ref> DSDD seems to phenotypically overlap with obsessional slowness (see above)<ref>{{cite web |first=B. |last=Chicoine |title=Obsessional Slowness |date=December 2022 |publisher=Adult Down Syndrome Center, Advocate Medical Group |url=https://adscresources.advocatehealth.com/resources/obsessional-slowness/#:~:text=The%20persistent%20stress%20of%20the%20rapidly%20moving%20environment,slowness%2C%20which%20we%20have%20also%20labeled%20%E2%80%9CThe%20Pace.%E2%80%9D;}}</ref> and catatonia-like regression occurring in ASD.<ref>{{cite journal|pmid=31959555 |date=2020 |last1=Lyons |first1=A. |last2=Allen |first2=N. M. |last3=Flanagan |first3=O. |last4=Cahalane |first4=D. |title=Catatonia as a feature of down syndrome: An under-recognised entity? |journal=European Journal of Paediatric Neurology |volume=25 |pages=187–190 |doi=10.1016/j.ejpn.2020.01.005 |s2cid=210841869 |doi-access=free}}</ref>
 ==Treatment==
-Treating catatonia effectively requires treating the catatonia itself, treating the underlying condition, and helping them with their basic needs, like eating, drinking, and staying clean and safe, while they are withdrawn and incapable of caring for themselves.
-=== Catatonia-specific treatments ===
-The specifics of treating catatonia itself can vary from region to region, hospital to hospital, and individual to individual, but typically involves the use of benzodiazepines. In fact, in some cases it is unclear whether a person has catatonia or another condition which may present similarly. In these cases a "benzodiazepine challenge" is often done. During a "benzodiazepine challenge" a healthcare provider will give a moderate dose of a benzodiazepine to the patient and monitor them. If a person has catatonia they will often have improvements in their symptoms within 15 to 30 minutes. If the person does not improve within 30 minutes they are given a second dose and the process is repeated once more. If the person responds to either of the doses then they can be given benzodiazepines at a consistent dose and timing until their catatonia resolves. Depending on the person, a person may need to reduce their dosing slowly over time in order to prevent reoccurrence of their symptoms.
-ECT is also commonly used to treat catatonia in people who do not improve with medication alone or whose symptoms reoccur whenever the dose of medications are reduced. ECT is usually administered with multiple sessions per week over two to four weeks.<ref>{{Cite web |title=Catatonia treatment and prognosis: Search |publisher=UpToDate |url=https://www.uptodate.com/contents/catatonia-treatment-and-prognosis?search=catatonia&source=search_result&selectedTitle=1~63&usage_type=default&display_rank=1 |access-date=2024-11-15 }}</ref> ECT has a success rate of 80% to 100%.<ref name=Luchini15>{{cite journal |vauthors=Luchini F, Medda P, Mariani MG, Mauri M, Toni C, Perugi G |title=Electroconvulsive therapy in catatonic patients: Efficacy and predictors of response |journal=World J Psychiatry |volume=5 |issue=2 |pages=182–92 |date=June 2015 |pmid=26110120 |pmc=4473490 |doi=10.5498/wjp.v5.i2.182 |doi-access=free }}</ref> ECT is effective for all subtypes of catatonia, however people who have catatonia with an underlying neurological condition show less improvement with ECT treatment.<ref name=Luchini15 /><ref name="Sienaert Dhossche Vancampfort et al 2014" />
-Excessive [[glutamate]] activity is believed to be involved in catatonia;<ref name="sciencedirect.com">{{Cite journal |last1=Saini |first1=Aman |last2=Begum |first2=Nazifa |last3=Matti |first3=James |last4=Ghanem |first4=Dory Anthony |last5=Fripp |first5=Laurie |last6=Pollak |first6=Thomas A. |last7=Zandi |first7=Michael S. |last8=David |first8=Anthony |last9=Lewis |first9=Glyn |last10=Rogers |first10=Jonathan |date=2022-09-15 |title=Clozapine as a treatment for catatonia: A systematic review |url=https://discovery.ucl.ac.uk/10156362/1/Lewi_Clozapine%20as%20a%20treatment%20for%20catatonia_AOP.pdf |journal=Schizophrenia Research |language=en |volume=263 |pages=275–281 |doi=10.1016/j.schres.2022.09.021 |issn=0920-9964 |pmid=36117082 |s2cid=252276294 |doi-access=free}}</ref> when first-line treatment options fail, [[NMDA antagonists]] such as [[amantadine]] or [[memantine]] may be used. Amantadine may have an increased incidence of tolerance with prolonged use and can cause psychosis, due to its additional effects on the dopamine system. Memantine has a more targeted pharmacological profile for the glutamate system, reduced incidence of psychosis and may therefore be preferred for individuals who cannot tolerate amantadine. [[Topiramate]] is another treatment option for resistant catatonia; it produces its therapeutic effects by producing glutamate antagonism via modulation of AMPA receptors.<ref name="Carroll-2007">{{cite journal |last1=Carroll |first1=Brendan T. |last2=Goforth |first2=Harold W. |last3=Thomas |first3=Christopher |last4=Ahuja |first4=Niraj |last5=McDaniel |first5=William W. |last6=Kraus |first6=Marilyn F. |last7=Spiegel |first7=David R. |last8=Franco |first8=Kathleen N. |last9=Pozuelo |first9=Leopold |last10=Muñoz |first10=Camilo |date=October 2007 |title=Review of Adjunctive Glutamate Antagonist Therapy in the Treatment of Catatonic Syndromes |journal=The Journal of Neuropsychiatry and Clinical Neurosciences |volume=19 |issue=4 |pages=406–412 |doi=10.1176/jnp.2007.19.4.406 |pmid=18070843}}</ref>
-=== Non-specific aspects of treatment ===
-==== Treating the underlying condition ====
+Treatment is most effective when it is early and aggressive.<ref name="Sienaert Dhossche Vancampfort et al 2014"/> Patients may face issues such as poor nutrition, infections, and skin breakdown. Immobility can lead to pressure ulcers, muscle contractions, and the formation of blood clots in the legs ([[deep vein thrombosis]]) and the lungs ([[pulmonary embolism]]). Other complications also include the development of [[pneumonia]] and [[neuroleptic malignant syndrome]].<ref name="Catatonia StatPearls" /><ref name="CC">{{Cite journal |last1=Clinebell |first1=Kimberly |last2=Azzam |first2=Pierre N. |last3=Gopalan |first3=Priya |last4=Haskett |first4=Roger |date=2014-06-15 |title=Guidelines for Preventing Common Medical Complications of Catatonia: Case Report and Literature Review |url=https://www.psychiatrist.com/jcp/guidelines-preventing-common-medical-complications |journal=The Journal of Clinical Psychiatry |volume=75 |issue=6 |pages=644–651 |doi=10.4088/JCP.13r08870 |pmid=25004188 |issn=0160-6689}}</ref><ref name=Balaguer-Rivero2021/><ref name="EB">{{Cite journal |last1=Rogers |first1=Jonathan P. |last2=Oldham |first2=Mark A. |last3=Fricchione |first3=Gregory |last4=Northoff |first4=Georg |last5=Ellen Wilson |first5=Jo |last6=Mann |first6=Stephan C. |last7=Francis |first7=Andrew |last8=Wieck |first8=Angelika |last9=Elizabeth Wachtel |first9=Lee |last10=Lewis |first10=Glyn |last11=Grover |first11=Sandeep |last12=Hirjak |first12=Dusan |last13=Ahuja |first13=Niraj |last14=Zandi |first14=Michael S. |last15=Young |first15=Allan H. |date=April 2023 |title=Evidence-based consensus guidelines for the management of catatonia: Recommendations from the British Association for Psychopharmacology |journal=Journal of Psychopharmacology |volume=37 |issue=4 |pages=327–369 |doi=10.1177/02698811231158232 |issn=1461-7285 |pmc=10101189 |pmid=37039129}}</ref><ref name="Smith Holmes 2023"/>
-There are many medications that are known to cause catatonia in some people including steroids, stimulants, anticonvulsants, neuroleptics or dopamine blockers.<ref name="Catatonia StatPearls" /> If a person has catatonia and is on these medications, they should be considered as a potential cause if another cause is not apparent and discontinued if possible.
-[[Antipsychotic]]s are sometimes used in those with a co-existing psychosis, however they should be used with care as they may worsen catatonia and have a risk of [[neuroleptic malignant syndrome]], a dangerous condition that can mimic catatonia and requires immediate discontinuation of the antipsychotic.<ref name="Fink & Taylor" /><ref name="Heckers 2023" /> There is evidence that [[clozapine]] works better than other [[antipsychotic]]s to treat catatonia.<ref name="sciencedirect.com" /><ref name="Heckers 2023" />
+The first choice of treatment for catatonia is benzodiazepines, particularly lorazepam, which may be used as a diagnostic tool via the  "[[lorazepam challenge]]". Patients are given a dose of lorazepam and their condition monitored; if there is an improvement within minutes, catatonia is likely. Patients who require a rapid response or do not respond to benzodiazepines may undergo a course of [[electroconvulsive therapy]].<ref name="Sienaert Dhossche Vancampfort et al 2014"/> This has been shown to produce favorable response rates, particularly in patients with malignant catatonia, and often succeeds where medication does not.<ref>{{cite journal |last1=Hawkins |first1=John M |last2=Archer |first2=Katharine J |last3=Strakowski |first3=Stephen M |last4=Keck |first4=Paul E |title=Somatic Treatment of Catatonia |journal=The International Journal of Psychiatry in Medicine |date=December 1995 |volume=25 |issue=4 |pages=345–369 |doi=10.2190/X0FF-VU7G-QQP7-L5V7}}</ref>
-==== Supportive care ====
+Catatonia may be caused by external factors such as medical problems, side effects of certain medications, and psychiatric disorders such as depression and schizophrenia. The cause can affect treatment and outcomes: for example, catatonia associated with schizophrenia may respond less effectively to benzodiazepines.<ref name="Catatonia StatPearls"/><ref>{{cite journal |last1=Rosebush |first1=Patricia I |last2=Mazurek |first2=Michael F |title=Catatonia and Its Treatment |journal=Schizophrenia Bulletin |date=March 2010 |volume=36 |issue=2 |pages=239–242 |doi=10.1093/schbul/sbp141 |pmid=19969591 }}</ref>
-Supportive care is required in those with catatonia. This includes monitoring vital signs and fluid status, and in those with chronic symptoms; maintaining nutrition and hydration, medications to prevent a [[venous thromboembolism|blood clot]], and measures to prevent the development of pressure ulcers.<ref name="Heckers 2023" />
-==Prognosis==
+== Prognosis ==
-Twenty-five percent of psychiatric patients with catatonia will have more than one episode throughout their lives.<ref name="Heckers 2023" /> Treatment response for patients with catatonia is 50–70%, with treatment failure being associated with a poor prognosis. Many of these patients will require long-term and continuous mental health care. The prognosis for people with catatonia due to schizophrenia is much worse compared to other causes.<ref name="Catatonia StatPearls" /> In cases of catatonia that develop into malignant catatonia, the mortality rate is as high as 20%.<ref>{{Cite journal |last1=Smith |first1=Alyssa C. |last2=Holmes |first2=Emily G. |date=2023-12-01 |title=Catatonia: A Narrative Review for Hospitalists |journal=American Journal of Medicine Open |volume=10 |article-number=100059 |doi=10.1016/j.ajmo.2023.100059 |pmid=39035239 |pmc=11256243 |issn=2667-0364}}</ref>
-===Complications===
+Twenty-five percent of psychiatric patients with catatonia will have more than one episode throughout their lives.<ref name="Heckers 2023"/> Treatment response for patients with catatonia is 50–70%, with treatment failure being associated with a poor prognosis. Many of these patients will require long-term and continuous mental health care. The prognosis for people with catatonia due to schizophrenia is much worse compared to other causes.<ref name="Catatonia StatPearls"/> In cases of malignant catatonia, the mortality rate is as high as 20%.<ref>{{cite journal |last1=Park |first1=Julia |last2=Tan |first2=Josh |last3=Krzeminski |first3=Sylvia |last4=Hazeghazam |first4=Maryam |last5=Bandlamuri |first5=Meghana |last6=Carlson |first6=Richard W |title=Malignant Catatonia Warrants Early Psychiatric-Critical Care Collaborative Management: Two Cases and Literature Review |journal=Case Reports in Critical Care |date=30 January 2017 |volume=2017 |issue=1 |pages=1–4 |doi=10.1155/2017/1951965 |doi-access=free |pmc=5303832 }}</ref>
-Patients may experience several complications from being in a catatonic state. The nature of these complications will depend on the type of catatonia being experienced by the patient. For example, patients presenting with withdrawn catatonia may have refusal to eat which will in turn lead to malnutrition and dehydration.<ref name="Serra-Mestres & Jaimes-Albornoz 2018" /> Furthermore, if immobility is a symptom the patient is presenting with, then they may develop [[pressure ulcer]]s, [[muscle contraction]]s, and are at risk of developing [[Deep vein thrombosis|deep vein thrombosis (DVT)]] and [[Pulmonary embolism|pulmonary embolus]] (PE).<ref name="Serra-Mestres & Jaimes-Albornoz 2018" /> Patients with excited catatonia may be aggressive and violent, and physical trauma may result from this. Catatonia may progress to the malignant type which will present with autonomic instability and may be life-threatening. Other complications also include the development of pneumonia and neuroleptic malignant syndrome.<ref name="Catatonia StatPearls" />
 == Epidemiology ==
-Catatonia has been historically studied in psychiatric patients.<ref>{{cite book |title=Diagnostic and Statistical Manual of Mental Disorders |year=2022 |doi=10.1176/appi.books.9780890425787 |isbn=978-0-89042-578-7 |url=https://dsm.psychiatryonline.org/doi/book/10.1176/appi.books.9780890425787 |last1=American Psychiatric Association |s2cid=249488050 }}{{page needed|date=June 2022}}</ref> Catatonia is under-recognized because the features are often mistaken for other disorders including delirium or the negative symptoms of schizophrenia. The prevalence has been reported to be as high as 10% in those with acute psychiatric illnesses, and 9–30% in the setting of inpatient psychiatric care.<ref name="Heckers 2023" /><ref>{{cite journal |last1=Solmi |first1=Marco |last2=Pigato |first2=G Giorgio |last3=Roiter |first3=Beatrice |last4=Guaglianone |first4=Argentina |last5=Martini |first5=Luca |last6=Fornaro |first6=Michele |last7=Monaco |first7=Francesco |last8=Carvalho |first8=Andrè F |last9=Stubbs |first9=Brendon |last10=Veronese |first10=Nicola |last11=Correll |first11=Christoph U |title=Prevalence of Catatonia and Its Moderators in Clinical Samples: Results from a Meta-analysis and Meta-regression Analysis |journal=Schizophrenia Bulletin |date=20 August 2018 |volume=44 |issue=5 |pages=1133–50 |doi=10.1093/schbul/sbx157 |pmid=29140521 |pmc=6101628 }}</ref><ref name="Rasmussen Mazurek Rosebush 2016"/> The incidence of catatonia is 10.6 episodes per 100 000 person-years, which essentially means that in a group of 100,000 people, the group as a whole would experience 10 to 11 episodes of catatonia per year.<ref name="Rogers Pollak Begum et al 2021">{{cite journal |last1=Rogers |first1=Jonathan P. |last2=Pollak |first2=Thomas A. |last3=Begum |first3=Nazifa |last4=Griffin |first4=Anna |last5=Carter |first5=Ben |last6=Pritchard |first6=Megan |last7=Broadbent |first7=Matthew |last8=Kolliakou |first8=Anna |last9=Ke |first9=Jessie |last10=Stewart |first10=Robert |last11=Patel |first11=Rashmi |last12=Bomford |first12=Adrian |last13=Amad |first13=Ali |last14=Zandi |first14=Michael S. |last15=Lewis |first15=Glyn |last16=Nicholson |first16=Timothy R. |last17=David |first17=Anthony S. |title=Catatonia: demographic, clinical and laboratory associations |journal=Psychological Medicine |date=2 November 2021 |volume=53 |issue=6 |pages=2492–2502 |doi=10.1017/S0033291721004402 |pmid=35135642 |pmc=10123832 |s2cid=242076501 |doi-access=free }}</ref> Catatonia can occur at any age, but is most commonly seen in adolescence or young adulthood or in older adults with existing medical conditions. It occurs in males and females in approximately equal numbers.<ref>{{cite journal |last1=Parsanoglu |first1=Zozan |last2=Balaban |first2=Ozlem Devrim |last3=Gica |first3=Sakir |last4=Atay |first4=Ozge Canbek |last5=Altin |first5=Ozan |title=Comparison of the Clinical and Treatment Characteristics of Patients Undergoing Electroconvulsive Therapy for Catatonia Indication in the Context of Gender |journal=Clinical EEG and Neuroscience |date=May 2022 |volume=53 |issue=3 |pages=175–183 |doi=10.1177/15500594211025889 |pmid=34142904 |s2cid=235471133 }}</ref><ref name="Rogers Pollak Begum et al 2021"/> Around 20% of all catatonia cases can be attributed to a general medical condition.<ref name="Oldham 333–340"/><ref name="Serra-Mestres & Jaimes-Albornoz 2018">{{cite journal |last1=Serra-Mestres |first1=Jordi |last2=Jaimes-Albornoz |first2=Walter |title=Recognizing Catatonia in Medically Hospitalized Older Adults: Why It Matters |journal=Geriatrics |date=29 June 2018 |volume=3 |issue=3 |pages=37 |doi=10.3390/geriatrics3030037 |pmid=31011075 |pmc=6319219 |doi-access=free }}</ref>
+Catatonia has been historically studied in psychiatric patients.<ref>{{cite book |title=Diagnostic and Statistical Manual of Mental Disorders |year=2022 |doi=10.1176/appi.books.9780890425787 |isbn=978-0-89042-578-7 |url=https://dsm.psychiatryonline.org/doi/book/10.1176/appi.books.9780890425787 |last1=American Psychiatric Association |s2cid=249488050 |page=103}}</ref> Catatonia is under-recognized because the features are often mistaken for other disorders, including delirium or the negative symptoms of schizophrenia. The prevalence has been reported to be as high as 10% in those with acute psychiatric illnesses, and 9–30% in the setting of inpatient psychiatric care.<ref name="Heckers 2023" /><ref>{{cite journal |last1=Solmi |first1=Marco |last2=Pigato |first2=G Giorgio |last3=Roiter |first3=Beatrice |last4=Guaglianone |first4=Argentina |last5=Martini |first5=Luca |last6=Fornaro |first6=Michele |last7=Monaco |first7=Francesco |last8=Carvalho |first8=Andrè F |last9=Stubbs |first9=Brendon |last10=Veronese |first10=Nicola |last11=Correll |first11=Christoph U |title=Prevalence of Catatonia and Its Moderators in Clinical Samples: Results from a Meta-analysis and Meta-regression Analysis |journal=Schizophrenia Bulletin |date=20 August 2018 |volume=44 |issue=5 |pages=1133–50 |doi=10.1093/schbul/sbx157 |pmid=29140521 |pmc=6101628}}</ref><ref name="Rasmussen Mazurek Rosebush 2016"/> The incidence of catatonia is 10.6 episodes per 100 000 person-years, which essentially means that in a group of 100,000 people, the group as a whole would experience 10 to 11 episodes of catatonia per year.<ref name="Rogers Pollak Begum et al 2021">{{cite journal |last1=Rogers |first1=Jonathan P. |last2=Pollak |first2=Thomas A. |last3=Begum |first3=Nazifa |last4=Griffin |first4=Anna |last5=Carter |first5=Ben |last6=Pritchard |first6=Megan |last7=Broadbent |first7=Matthew |last8=Kolliakou |first8=Anna |last9=Ke |first9=Jessie |last10=Stewart |first10=Robert |last11=Patel |first11=Rashmi |last12=Bomford |first12=Adrian |last13=Amad |first13=Ali |last14=Zandi |first14=Michael S. |last15=Lewis |first15=Glyn |last16=Nicholson |first16=Timothy R. |last17=David |first17=Anthony S. |title=Catatonia: demographic, clinical and laboratory associations |journal=Psychological Medicine |date=2 November 2021 |volume=53 |issue=6 |pages=2492–2502 |doi=10.1017/S0033291721004402 |pmid=35135642 |pmc=10123832 |s2cid=242076501 |doi-access=free}}</ref> Catatonia can occur at any age, but is most commonly seen in adolescence or young adulthood or in older adults with existing medical conditions. It occurs in males and females in approximately equal numbers.<ref>{{cite journal |last1=Parsanoglu |first1=Zozan |last2=Balaban |first2=Ozlem Devrim |last3=Gica |first3=Sakir |last4=Atay |first4=Ozge Canbek |last5=Altin |first5=Ozan |title=Comparison of the Clinical and Treatment Characteristics of Patients Undergoing Electroconvulsive Therapy for Catatonia Indication in the Context of Gender |journal=Clinical EEG and Neuroscience |date=May 2022 |volume=53 |issue=3 |pages=175–183 |doi=10.1177/15500594211025889 |pmid=34142904 |s2cid=235471133}}</ref><ref name="Rogers Pollak Begum et al 2021"/> Around 20% of all catatonia cases can be attributed to a general medical condition.<ref name="Oldham 333–340">{{Cite journal |last=Oldham |first=Mark A. |date=2018-07-01 |title=The Probability That Catatonia in the Hospital has a Medical Cause and the Relative Proportions of Its Causes: A Systematic Review |url=https://linkinghub.elsevier.com/retrieve/pii/S0033318218301828 |journal=Psychosomatics |volume=59 |issue=4 |pages=333–340 |doi=10.1016/j.psym.2018.04.001 |issn=0033-3182 |pmid=29776679 |url-access=subscription}}</ref><ref name="Serra-Mestres & Jaimes-Albornoz 2018">{{cite journal |last1=Serra-Mestres |first1=Jordi |last2=Jaimes-Albornoz |first2=Walter |title=Recognizing Catatonia in Medically Hospitalized Older Adults: Why It Matters |journal=Geriatrics |date=29 June 2018 |volume=3 |issue=3 |page=37 |doi=10.3390/geriatrics3030037 |pmid=31011075 |pmc=6319219 |doi-access=free}}</ref>
 {| class="wikitable"
 |+
@@ Line 274: / Line 322: @@
 |~20%
 |}
 == History ==
 === Ancient history ===
-There have been reports of stupor-like and catatonia-like states in people throughout the history of psychiatry.<ref>{{cite journal | pmid=7034030 | date=1981 | last1=Berrios | first1=G. E. | title=Stupor: A conceptual history | journal=Psychological Medicine | volume=11 | issue=4 | pages=677–688 | doi=10.1017/s0033291700041179 | s2cid=26932116 }}</ref> In ancient Greece, the first physician to document stupor-like or catatonia-like states was Hippocrates, in his ''Aphorisms.<ref>{{Citation |last=Roccatagliata |first=Giuseppe |title=The Idea of Melancholia in Classical Culture |date=1985 |work=Psychiatry The State of the Art: Volume 8 History of Psychiatry, National Schools, Education, and Transcultural Psychiatry |pages=89–93 |editor-last=Pichot |editor-first=P. |url=https://link.springer.com/chapter/10.1007/978-1-4757-1853-9_12 |access-date=2024-11-18 |place=Boston, MA |publisher=Springer US |language=en |doi=10.1007/978-1-4757-1853-9_12 |isbn=978-1-4757-1853-9 |editor2-last=Berner |editor2-first=P. |editor3-last=Wolf |editor3-first=R. |editor4-last=Thau |editor4-first=K.|url-access=subscription }}</ref>''<ref>{{Cite journal |last=Scholtz |first=M. |date=December 1940 |title=Hippocrates' Aphorisms |journal=California and Western Medicine |volume=53 |issue=6 |pages=272 |issn=0093-4038 |pmc=1634189 |pmid=18745795}}</ref> He never defined the syndrome, but seemingly observed these states in people he was treating for melancholia. In ancient China, the first descriptions of people that appear in the Huangdi Neijing (The Yellow Emperor's Inner Canon),<ref>{{Cite book |last=Veith |first=Ilza |url=http://dx.doi.org/10.1525/9780520963245 |title=The Yellow Emperor's Classic of Internal Medicine |date=2015-12-15 |publisher=University of California Press |doi=10.1525/9780520963245 |isbn=978-0-520-96324-5}}</ref> the book which forms the basis of Traditional Chinese Medicine. It is thought to have been compiled by many people over the course of centuries during the Warring States Period (475-221 BCE) and the early Han Dynasty (206 BCE-220 CE).
+There have been reports of stupor-like and catatonia-like states in people throughout the history of psychiatry.<ref>{{cite journal | pmid=7034030 | date=1981 | last1=Berrios | first1=G. E. | title=Stupor: A conceptual history | journal=Psychological Medicine | volume=11 | issue=4 | pages=677–688 | doi=10.1017/s0033291700041179 | s2cid=26932116}}</ref> In ancient Greece, the first physician to document stupor-like or catatonia-like states was Hippocrates, in his ''Aphorisms.<ref>{{Citation |last=Roccatagliata |first=Giuseppe |chapter=The Idea of Melancholia in Classical Culture |date=1985 |title=Psychiatry: The State of the Art |volume=8 |pages=89–93 |editor-last=Pichot |editor-first=P. |chapter-url=https://link.springer.com/chapter/10.1007/978-1-4757-1853-9_12 |access-date=2024-11-18 |place=Boston, MA |publisher=Springer US |language=en |doi=10.1007/978-1-4757-1853-9_12 |isbn=978-1-4757-1853-9 |editor2-last=Berner |editor2-first=P. |editor3-last=Wolf |editor3-first=R. |editor4-last=Thau |editor4-first=K.|chapter-url-access=subscription}}</ref>''<ref>{{Cite journal |last=Scholtz |first=M. |date=December 1940 |title=Hippocrates' Aphorisms |journal=California and Western Medicine |volume=53 |issue=6 |page=272 |issn=0093-4038 |pmc=1634189 |pmid=18745795}}</ref> He never defined the syndrome, but seemingly observed these states in people he was treating for melancholia. In ancient China, the first descriptions of people that appear in the Huangdi Neijing (The Yellow Emperor's Inner Canon),<ref>{{Cite book |last=Veith |first=Ilza |title=The Yellow Emperor's Classic of Internal Medicine |date=2015-12-15 |publisher=University of California Press |doi=10.1525/9780520963245 |isbn=978-0-520-96324-5}}</ref> the book which forms the basis of Traditional Chinese Medicine. It is thought to have been compiled by many people over the course of centuries during the Warring States Period (475-221 BCE) and the early Han Dynasty (206 BCE-220 CE).{{cn|date=April 2026}}
 === Modern history ===
-The term "catatonia" was first used by German psychiatrist Karl Ludwig Kahlbaum in 1874, in his book ''Die Katatonie oder das Spannungsirresein'', which translates to "Catatonia or Tension Insanity".<ref>{{cite web |title=Zur Entwicklung der Psychiatrie - ein Internet-Atlas von Dr. Hans-Peter Haack |url=http://www.entwicklung-der-psychiatrie.de/seiten/24.1_kahlbaum_die_katatonie.htm |url-status=dead |archive-url=https://web.archive.org/web/20080209213229/http://www.entwicklung-der-psychiatrie.de/seiten/24.1_kahlbaum_die_katatonie.htm |archive-date=2008-02-09 |access-date=2017-06-29 |language=de}}</ref> He viewed catatonia as its own illness, which would get worse over time in stages of mania, depression, and psychosis leading to dementia. This work heavily influenced another German psychiatrist, Emil Kraeplin, who was the first to classify catatonia as a syndrome. Kraeplin associated catatonia with a psychotic disorder called [[dementia praecox]], which is no longer used as a diagnosis, but heavily informed the development of the concept of schizophrenia.
+{{More citations needed section|date=August 2025}}
+The term "catatonia" was first used by German psychiatrist Karl Ludwig Kahlbaum in 1874, in his book ''Die Katatonie oder das Spannungsirresein'', which translates to "Catatonia or Tension Insanity".<ref>{{cite web |title=Zur Entwicklung der Psychiatrie - ein Internet-Atlas von Dr. Hans-Peter Haack |url=http://www.entwicklung-der-psychiatrie.de/seiten/24.1_kahlbaum_die_katatonie.htm |archive-url=https://web.archive.org/web/20080209213229/http://www.entwicklung-der-psychiatrie.de/seiten/24.1_kahlbaum_die_katatonie.htm |archive-date=2008-02-09 |access-date=2017-06-29 |language=de}}</ref> He viewed catatonia as its own illness, which would get worse over time in stages of mania, depression, and psychosis leading to dementia. This work heavily influenced another German psychiatrist, Emil Kraeplin, who was the first to classify catatonia as a syndrome. Kraeplin associated catatonia with a psychotic disorder called [[dementia praecox]], which is no longer used as a diagnosis, but heavily informed the development of the concept of schizophrenia.
 Kraeplin's work influenced two other notable German psychiatrists, Karl Leonhard and Max Fink, and their colleagues to expand the concept of catatonia as a syndrome which could occur in the setting of many mental illnesses, not just psychotic disorders. They also laid the groundwork to describe different subtypes of catatonia still used today, including Stuporous Catatonia, Excited Catatonia, Malignant Catatonia, and Periodic Catatonia. Additionally, Leonhard and his colleagues categorized catatonia as either systematic or unsystematic, based on whether or not symptoms happened according to consistent and predictable patterns. These ways of thinking shaped the way that psychologists and psychiatrists thought of catatonia well into the 20th century. In fact, catatonia was a subtype of schizophrenia as recently as the DSM-III, and was not revised to be able to be applied to mood disorders until 1994 with the release of the DSM-IV.
@@ Line 290: / Line 340: @@
 === Popular conceptions and origins ===
-Catatonia, historically misunderstood, has been subject to shifting perceptions in society. As discussed previously, since the 19th century it was often linked exclusively to schizophrenia, perpetuating misconceptions. These historical misunderstandings have shaped the public opinions on catatonia. This has contributed to a lack of understanding about catatonia and its broader association with other mental disorders and medical conditions.
+{{Unreferenced section|date=April 2026}}
+Catatonia has been subject to shifting perceptions in society. Since the 19th century, it was often linked exclusively to schizophrenia, perpetuating misconceptions. These historical misunderstandings have shaped the public opinion on catatonia. This has contributed to a lack of understanding about catatonia, and its broader association with other mental disorders and medical conditions.
-Popular culture and media have played a significant role in shaping societal perceptions of catatonia. In many cases, media portrayals reduce it to a stereotypical "frozen state," similar to a coma, failing to capture the complexity of symptoms like stupor, agitation, and mutism. Such oversimplifications contribute to public misperceptions and get in the way of people receiving the care they need.
+Popular culture and media have played a significant role in shaping societal perceptions of catatonia. In many cases, media portrayals reduce it to a stereotypical "frozen state," similar to a coma, failing to capture the complexity of symptoms like stupor, agitation, and mutism. These oversimplifications have greatly affected the public perception of catatonia.
 ==See also==
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 * [[Karolina Olsson]]
 * [[Oneiroid syndrome]]
-* [[Paranoid schizophrenia]]
+* [[Vegetative state]]
-* [[Persistent vegetative state]]
 * [[Resignation syndrome]]
 * [[Sensory overload]]
@@ Line 319: / Line 369: @@
 == External links ==
+{{Commons}}
 * [https://web.archive.org/web/20171013152335/http://ccpweb.wustl.edu/pdfs/2013barchcatatonia.pdf Catatonia in DSM-5]
 * [http://www.minddisorders.com/Br-Del/Catatonic-disorders.html Encyclopedia of Mental Disorders — Catatonic Disorders]