Catatonia

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.<ref name="Fink & Taylor 2009"/><ref name="Catatonia StatPearls"/> People with catatonia exhibit abnormal movement and behaviors that vary from person to person and may fluctuate in intensity within a single episode.<ref name="Heckers 2023"/>

People with catatonia appear withdrawn, meaning that they do not interact with the outside world and have difficulty processing information.<ref>Template:Cite journal</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 benzodiazepines or electroconvulsive therapy is most effective and leads to remission of symptoms in most cases.<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>Template:Cite web</ref>

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 be observed in other mental, neurological, and medical conditions.

Classification

Modern classifications

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<ref>Template:Cite journal</ref>

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>Template:Cite journal</ref>

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.<ref name="Heckers 2023">Template:Cite journal</ref> Symptoms may develop in a variable amount of time, and can take hours, days, or even weeks.

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.<ref name="Catatonia StatPearls">Template:Cite book</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">Template:Cite journal</ref>

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. Notably, while catatonia can be divided into various subtypes, the presentation of catatonia is often dynamic, and the same individual may exhibit different subtypes at different times.<ref>Template:Cite book</ref>

Stuporous catatonia is characterized by immobility, mutism, and a lack of response to the world around them.<ref name="Fink & Taylor 2009">Template:Cite journal</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 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 delusions and hallucinations.<ref>Template:Cite book</ref>

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.

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 build-up of a residual state between these phases, which is characterized by low-level catatonic features and aboulia of varying severity.

Causes

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

Psychiatric conditions

Mood disorders like 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">Template:Cite bookTemplate:Page needed</ref> autism spectrum disorder, ADHD,<ref>Template:Cite book</ref> and post-traumatic stress disorder.<ref>Template:Cite journal</ref>

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>Template:Cite book</ref>

Medical conditions

Catatonia is also seen in many medical disorders, including encephalitis, meningitis, autoimmune disorders,<ref name=Rogers19>Template:Cite journal</ref> focal neurological lesions (including strokes),<ref>Template:Cite journal</ref> alcohol withdrawal,<ref name="Geoffroy-2012">Template:Cite journal</ref> abrupt or overly rapid benzodiazepine withdrawal,<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> cerebrovascular disease, neoplasms, head injury,<ref name="DSM-5-introduction">Template:Cite book</ref> and some metabolic conditions (e.g.,homocystinuria, diabetic ketoacidosis, hepatic encephalopathy, and hypercalcaemia).<ref name="DSM-5-introduction"/>

Neurological disorders

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 evidence suggests that catatonia can develop after traumatic brain injury in the absence of a primary psychiatric disorder.<ref>Template:Cite journal</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 benzodiazepines.<ref>Template:Cite journal</ref><ref>Template:Cite journal</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.

Metabolic and endocrine disorders

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 levels of sodium in the blood can cause catatonia in some people.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref>

Infectious diseases

Certain types of infections are known to cause catatonia, either by directly impairing brain function or by increasing a person's susceptibility to diseases that can impair brain function. HIV and AIDS can cause catatonia by predisposing one to infections in the brain, including different types of viral encephalitis.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> Borrelia burgdorferi causes Lyme disease, which has been shown to cause catatonia by infecting the brain and causing encephalitis.<ref name=Rogers19/><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref>

Pharmacological causes

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 the dopamine beta-hydroxylase enzyme. Additionally, phencylidine, corticosteriods, and antipsychotics, among other drugs, are known to cause catatonia.<ref>Template:Cite book</ref>

Pathogenesis

The mechanisms in the brain that cause catatonia are poorly understood.<ref name="Rasmussen Mazurek Rosebush 2016"/><ref>Template:Cite journal</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 cognitive function, leading to behavioral and motor symptoms associated with catatonia.<ref>Slavnic, B. (2023). Methamphetamine-associated catatonia: Case series and systematic review of the literature from 1943-2020. Annals of Clinical Psychiatry, 35(3). https://doi.org/10.12788/acp.0116</ref> The second claims that disruption of communication between different areas of the brain causes catatonia.<ref>Rogers, J. P. et al. (2023). Evidence-based consensus guidelines for the management of catatonia: Recommendations from the British Association for Psychopharmacology. Journal of Psychopharmacology, 37(4), 327-369. https://doi.org/10.1177/02698811231158232</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.<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 which activates the parts of the brain responsible for movement.<ref> Rasmussen SA, Mazurek MF, Rosebush PI. Catatonia: Our current understanding of its diagnosis, treatment and pathophysiology. World Journal of Psychiatry 2016;6:391–1. https://doi.org/10.5498/wjp.v6.i4.391.‌</ref> 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.<ref> Rogers JP, Pollak TA, Blackman G, David AS. Catatonia and the immune system: a review. The Lancet Psychiatry 2019;6:620–30. https://doi.org/10.1016/s2215-0366(19)30190-7.</ref>

Neurological pathways

Several pathways in the brain have been studied which seem to contribute to catatonia when they are not functioning properly.<ref>Template:Cite journal</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>Template:Cite journal</ref>

Diagnosis

There is not yet a definitive consensus regarding diagnostic criteria of catatonia. 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.<ref>Template:Cite bookTemplate:Page needed</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.

DSM-5 classification

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">Template:Cite book</ref><ref>Template:Cite book</ref> Template:Rp

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"/>Template:Rp

• 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<ref name="DS"/>Template:Rp
• Catatonia associated with schizophrenia spectrum and other psychotic disorders
  • Catatonia associated with brief psychotic disorder<ref name="DS"/>Template:Rp
  • Catatonia associated with schizophreniform disorder<ref name="DS"/>Template:Rp
  • Catatonia associated with schizoaffective disorder<ref name="DS"/>Template:Rp
  • Catatonia associated with a substance-induced psychotic disorder
• Catatonia associated with bipolar and related disorders<ref name="DS"/>Template:Rp
• Catatonia associated with major depressive disorder<ref name="DS"/>Template:Rp
• Catatonic disorder due to another medical condition<ref name="DS"/>Template:Rp

If catatonic symptoms are present but do not form the catatonic syndrome, a medication- or substance-induced aetiology should be considered first.<ref name="DSM-5Differential">Template:Cite book</ref>

ICD-11 classification

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.<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 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 .<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

Several rating instruments have been developed, but their utility in clinical practice remains debated .<ref>Template:Cite journal</ref> The most commonly used scale is the Bush-Francis Catatonia Rating Scale (BFCRS).<ref>Template:Cite journal</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">Template:Cite journal</ref>
• zolpidem challenge.<ref>Template:Cite journal</ref>

Historically, barbiturates were used, but today benzodiazepines and electroconvulsive therapy (ECT) are the main options chosen for treatment.

Laboratory findings

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

• leukocytosis
• elevated creatine kinase
• 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.

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.<ref name="Neuroleptic Malignant Syndrome StatPearls">Template:Cite book</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 antipsychotics, particularly first generation antipsychotics,<ref name="Neuroleptic Malignant Syndrome StatPearls"/> but it has not been established as a subtype.<ref>Template:Cite journal</ref> 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.<ref name="Anti-NMDA Receptor Encephalitis StatPearls">Template:Cite book</ref> 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.<ref name="Anti-NMDA Receptor Encephalitis StatPearls" />

• serotonin syndrome: Triggered by serotonergic drugs (ex: SSRI); features include delirium, hyperreflexia, myoclonus, GI symptoms (N/V/D), autonomic instability, hyperthermia, and rigidity.<ref>Template:Cite journal</ref>
• Malignant hyperthermia: A hereditary disorder of skeletal muscle, triggered by anesthetics or muscle relaxants like succinylcholine.; associated with metabolic acidosis, hyperkalemia, and arrhythmias.<ref>Template:Cite book</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 benzodiazepines.<ref>Template:Cite journal</ref> Patients may present with apathy, and may seem indifferent to pain, hunger, or thirst.<ref>Template:Cite journal</ref>
• Selective mutism has an anxious etiology but has also been associated with personality disorders.<ref>Template:Cite journal</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>Template:Cite book</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 electroencephalogram (EEG).<ref>Template:Cite journal</ref> 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.<ref>Template:Cite book</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>Template:Cite book</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>Template:Cite journal</ref> However, stiff-person syndrome may be associated with anti-glutamic acid decarboxylase (anti-GAD) antibodies<ref>Template:Cite journal</ref><ref>Template:Cite journal</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>Template:Cite journal</ref>
• 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.<ref name="Vaquerizo-Serrano Salazar De Pablo Singh Santosh 2022">Template:Cite journal</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>Template:Cite book</ref> Obsessional slowness is a controversial diagnosis, with presentations ranging from severe but common manifestations of obsessive compulsive disorder to catatonia.<ref>Template:Cite journal</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>Template:Cite journal</ref> DSDD seems to phenotypically overlap with obsessional slowness (see above)<ref>Template:Cite web</ref> and catatonia-like regression occurring in ASD.<ref>Template:Cite journal</ref>

Treatment

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 the development of pressure ulcers, muscle contractions, and the formation of blood clots in the legs (deep vein thrombosis) and lungs (pulmonary embolism). Other complications also include the development of pneumonia and neuroleptic malignant syndrome.<ref name="Catatonia StatPearls" /><ref name="CC">Template:Cite journal</ref><ref>Template:Cite journal</ref><ref name="EB">Template:Cite journal</ref><ref>Template:Cite journal</ref>

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 that 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>Template:Cite journal</ref>

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>Template:Cite journal</ref>

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 malignant catatonia, the mortality rate is as high as 20%.<ref>Template:Cite journal</ref>

Epidemiology

Catatonia has been historically studied in psychiatric patients.<ref>Template:Cite bookTemplate:Page needed</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>Template:Cite journal</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">Template:Cite journal</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>Template:Cite journal</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">Template:Cite journal</ref><ref name="Serra-Mestres & Jaimes-Albornoz 2018">Template:Cite journal</ref>

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.<ref>Template:Cite journal</ref> In ancient Greece, the first physician to document stupor-like or catatonia-like states was Hippocrates, in his Aphorisms.<ref>Template:Citation</ref><ref>Template:Cite journal</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>Template:Cite book</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).

Modern history

Template:More citations needed section 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>Template:Cite web</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.

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

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.

See also

• Acquiescence
• Akinetic mutism
• Autistic catatonia
• Awakenings (1990 biopic about catatonic patients, based on Oliver Sacks's book of the same name)
• Blank expression
• Botulism
• Clouding of consciousness
• Disorganized schizophrenia
• Homecoming (features catatonia as a main plot point)
• Karolina Olsson
• Oneiroid syndrome
• Vegetative state
• Resignation syndrome
• Sensory overload
• Tonic immobility
• Sleep paralysis

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