Wikipedia

Catatonia

This article is about the catatonic state. For other uses, see Catatonia (disambiguation).
Not to be confused with Katatonia, cataplexy, catalepsy, Catalonia, or Cataonia.

Catatonia
Other namesCatatonic syndrome
A patient in catatonic stupor, 1914
SpecialtyPsychiatry, neurology
SymptomsImmobility, mutism, staring, posturing, rigidity, low consciousness
ComplicationsPhysical trauma, malignant catatonia (autonomic instability, life-threatening), dehydration, pneumonia, pressure ulcers due to immobility, muscle contractions, deep vein thrombosis (DVT)[1] and pulmonary embolism (PE)[1]
CausesUnderlying illness (psychiatric, neurologic, or medical), brain injury/damage, certain drugs/medications
Diagnostic methodClinical, lorazepam challenge
TreatmentBenzodiazepines (lorazepam challenge), electroconvulsive therapy (ECT)[1]

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.[2][3] People with catatonia exhibit abnormal movement and behaviors, which vary from person to person and may fluctuate in intensity within a single episode.[4]

People with catatonia appear withdrawn, meaning that they do not interact with the outside world and have difficulty processing information.[5] They may be nearly motionless for days on end or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 are most effective and lead to remission of symptoms in most cases.[3]

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.[6]

Catatonia has historically been related to schizophrenia, but is most often seen in mood disorders.[3] It is now known that catatonic symptoms are nonspecific and may be observed in other mental, neurological, and medical conditions.

Classification

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Modern classifications

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Catatonia is diagnosed when a person shows at least three key symptoms at once.

These can include:

  • not moving or speaking (stupor or mutism).
  • unusual body positions
  • repeating words or actions
  • sudden restlessness
  • other, less common effects[7]

The DSM-5 and ICD-11, global manuals for mental health condition, 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.[8]

Signs and symptoms

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To properly diagnose catatonia, the ICD-11 and DSM-5 both require 3 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.[4] 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.[3] 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.[9]

Subtypes

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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.[10]

Stuporous catatonia is characterized by immobility, mutism, and a lack of response to the world around them.[2][3] 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.[2][3][9] This state is often characterized by hyperactivity, and the patient may have delusions and hallucinations.[11]

Malignant catatonia is characterized by fever, dramatic and rapid changes in blood pressure, increased heart rate and respiratory rate, and excessive sweating.[2][3] 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, 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. 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

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Catatonia can only develop if a person has a previous underlying condition, such as a psychiatric disorder, medical conditions, or substance use.

Psychiatric conditions

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Mood disorders such as bipolar disorder and depression are the most common conditions underlying catatonia.[3] Other psychiatric conditions that can cause catatonia include schizophrenia and other primary psychotic disorders,[12] autism spectrum disorders, ADHD,[13] and post-traumatic stress disorder.[14]

Psychodynamic theorists have interpreted catatonia as a defense against the potentially destructive consequences of responsibility, with the passivity of the disorder providing relief.[15]

Medical conditions

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Catatonia is also seen in many medical disorders, including encephalitis, meningitis, autoimmune disorders,[16] focal neurological lesions (including strokes),[17] alcohol withdrawal,[18] abrupt or overly rapid benzodiazepine withdrawal,[19][20][21] cerebrovascular disease, neoplasms, head injury,[22] and some metabolic conditions (homocystinuria, diabetic ketoacidosis, hepatic encephalopathy, and hypercalcaemia).[22]

Neurological disorders

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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.[23] 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 benzodiazepines.[24][25] 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

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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 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.[26][27][28][29]

Infectious diseases

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Certain types of infections are known to cause catatonia, either by directly impairing brain function or by making a person more likely to catch a disease 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.[30][31] Borrelia burgdorferi causes Lyme disease, which has been shown to cause catatonia by infecting the brain and causing encephalitis.[16][32][33][34]

Pharmacological causes

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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.[35]

Pathogenesis

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The mechanisms in the brain that cause catatonia are poorly understood.[9][36] 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.[37] The second claims that disruption of communication between different areas of the brain causes catatonia.[38]

Neurotransmitters

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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.[39] 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.[40] 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.[41]

Neurological pathways

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Several pathways in the brain have been studied which seem to contribute to catatonia when they are not functioning properly.[42] 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.[43]

Diagnosis

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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.[44] 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.[45][46] : 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:[45]: 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):

If catatonic symptoms are present but do not form the catatonic syndrome, a medication- or substance-induced aetiology should be considered first.[47]

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

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Catatonia is often overlooked and under-diagnosed.[48] 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.[3] 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 .[3]

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.[3]

Rating scale

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Several rating instruments have been developed, but their utility in clinical practice remains debated .[49] The most commonly used scale is the Bush-Francis Catatonia Rating Scale (BFCRS).[50] 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:

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

Laboratory findings

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

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

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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.[53] 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,[53] but it has not been established as a subtype.[54] 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.[55] 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.[55]

  • serotonin syndrome: Triggered by serotonergic drugs (ex: SSRI); features include delirium, hyperreflexia, myoclonus, GI symptoms (N/V/D), autonomic instability, hyperthermia, and rigidity.[56]
  • Malignant hyperthermia: A hereditary disorder of skeletal muscle, triggered by anesthetics or muscle relaxants like succinylcholine.; associated with metabolic acidosis, hyperkalemia, and arrhythmias.[57]
  • 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.[58] Patients may present with apathy, and may seem indifferent to pain, hunger, or thirst.[59]
  • Selective mutism has an anxious etiology but has also been associated with personality disorders.[60] 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.[61] 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).[62] 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.[63] 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.[64]
  • Stiff-person syndrome and catatonia are similar in that they may both present with rigidity, autonomic instability, and a positive response to benzodiazepines.[65] However, stiff-person syndrome may be associated with anti-glutamic acid decarboxylase (anti-GAD) antibodies[66][67] 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.[68]
  • 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.[69]
  • 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.[70] Obsessional slowness is a controversial diagnosis, with presentations ranging from severe but common manifestations of obsessive compulsive disorder to catatonia.[71]
  • 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.[72] DSDD seems to phenotypically overlap with obsessional slowness (see above)[73] and catatonia-like regression occurring in ASD.[74]

Treatment

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Treatment is most effective when it is early and aggressive.[51] 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.[3][75][76][77][78]

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.[51] This has been shown to produce favorable response rates, particularly in patients with malignant catatonia, and often succeeds where medication does not.[79]

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.[3][80]

Prognosis

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Twenty-five percent of psychiatric patients with catatonia will have more than one episode throughout their lives.[4] 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.[3] In cases of malignant catatonia, the mortality rate is as high as 20%.[81]

Epidemiology

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Catatonia has been historically studied in psychiatric patients.[82] 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.[4][83][9] 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.[84] 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.[85][84] Around 20% of all catatonia cases can be attributed to a general medical condition.[86][48]

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

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Ancient history

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There have been reports of stupor-like and catatonia-like states in people throughout the history of psychiatry.[87] In ancient Greece, the first physician to document stupor-like or catatonia-like states was Hippocrates, in his Aphorisms.[88][89] 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),[90] 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

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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".[91] 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

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[edit]

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

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References

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  1. ^ a b c Balaguer AP, Rivero IS (22 December 2021). "Electroconvulsive therapy, catatonia, deep vein thrombosis and anticoagulant treatment: a case report". General Psychiatry. 34 (6) e100666. doi:10.1136/gpsych-2021-100666. ISSN 2517-729X. PMC 8705197. PMID 35028525.
  2. ^ a b c d Fink M, Taylor MA (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.
  3. ^ a b c d e f g h i j k l m n Burrow JP, Spurling BC, Marwaha R (2022). "Catatonia". StatPearls. StatPearls Publishing. PMID 28613592.
  4. ^ a b c d Heckers S, Walther S (9 November 2023). "Catatonia". New England Journal of Medicine. 389 (19): 1797–1802. doi:10.1056/NEJMra2116304. PMID 37937779. S2CID 265673511.
  5. ^ Edinoff AN, Kaufman SE, Hollier JW, Virgen CG, Karam CA, Malone GW, Cornett EM, Kaye AM, Kaye AD (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.
  6. ^ "Catatonia treatment and prognosis". UpToDate. Retrieved 22 November 2024.
  7. ^ Smith AC, Holmes EG (1 December 2023). "Catatonia: A Narrative Review for Hospitalists". American Journal of Medicine Open. 10 100059. doi:10.1016/j.ajmo.2023.100059. ISSN 2667-0364. PMC 11256243. PMID 39035239.
  8. ^ Rogers JP, Zandi MS, David AS (May 2023). "The diagnosis and treatment of catatonia". Clinical Medicine. 23 (3): 242–245. doi:10.7861/clinmed.2023-0113. PMC 11046566. PMID 37236789.
  9. ^ a b c d Rasmussen SA, Mazurek MF, Rosebush PI (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.
  10. ^ Shorter E, Fink M (2018). The Madness of Fear: A History of Catatonia. Oxford University Press. ISBN 978-0-19-088119-1.
  11. ^ Nolen-Hoeksema S (2014). Abnormal Psychology. McGraw-Hill Education. p. 224. ISBN 978-1-259-06072-4.
  12. ^ Fink M, Taylor MA (2003). Catatonia: A Clinician's Guide to Diagnosis and Treatment. Cambridge University Press. ISBN 978-0-521-82226-8.[page needed]
  13. ^ Dhossche DM, Rout U (2006). "Are Autistic and Catatonic Regression Related? A Few Working Hypotheses Involving Gaba, Purkinje Cell Survival, Neurogenesis, and ECT". International Review of Neurobiology. Vol. 72. pp. 55–79. doi:10.1016/S0074-7742(05)72004-3. ISBN 978-0-12-366873-8. PMID 16697291.
  14. ^ Ahmed GK, Elbeh K, Karim AA, Khedr EM (2021). "Case Report: Catatonia Associated With Post-traumatic Stress Disorder". Frontiers in Psychiatry. 12 740436. doi:10.3389/fpsyt.2021.740436. ISSN 1664-0640. PMC 8688766. PMID 34950066.
  15. ^ Arieti S (1994). Interpretation of schizophrenia. Jason Aronson. ISBN 1-56821-209-7. OCLC 472906047.
  16. ^ a b Rogers JP, Pollak TA, Blackman G, David AS (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.
  17. ^ Haroche A, Rogers J, Plaze M, Gaillard R, Williams SC, Thomas P, Amad A (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.
  18. ^ Geoffroy PA, Rolland B, Cottencin O (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.
  19. ^ 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.
  20. ^ 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.
  21. ^ 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.
  22. ^ a b 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.
  23. ^ Berthelot J, Cambre J, Erwin M, Phan J (6 March 2024). Inada T (ed.). "Catatonia as a Result of a Traumatic Brain Injury". Case Reports in Psychiatry. 2024: 1–3. doi:10.1155/2024/5184741. ISSN 2090-6838. PMC 10937075. PMID 38482162.
  24. ^ Koprucki S, Morcos R (18 September 2024). "Acute Catatonia Following a Cerebellar Stroke: A Case Report". Cureus. 16 (9) e69645. doi:10.7759/cureus.69645. ISSN 2168-8184. PMC 11488475. PMID 39429282.
  25. ^ Hasan H, Abdo M, Rabei S (March 2023). "Post Cerebrovascular Stroke Catatonic Psychosis: A Case Report". European Psychiatry. 66 (S1): S1058. doi:10.1192/j.eurpsy.2023.2245. ISSN 0924-9338. PMC 10479261.
  26. ^ McGuire E, Yohanathan M, Lally L, McCarthy G (14 July 2017). "Hyponatraemia-associated catatonia". BMJ Case Reports: bcr–2017–219487. doi:10.1136/bcr-2017-219487. ISSN 1757-790X. PMC 5534696. PMID 28710304.
  27. ^ Peritogiannis V, Rizos DV (24 May 2021). "Catatonia Associated with Hyponatremia: Case Report and Brief Review of the Literature". Clinical Practice & Epidemiology in Mental Health. 17 (1): 26–30. doi:10.2174/1745017902117010026. ISSN 1745-0179. PMC 8227445. PMID 34249136.
  28. ^ Mehta V, Sharma A, Sharma CB, Guria RT (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.
  29. ^ Krueger A, Shebak SS, Kavuru B (12 November 2015). "Catatonia in the Setting of Hyponatremia". The Primary Care Companion for CNS Disorders. 17 (6): 26803. doi:10.4088/PCC.15l01808. ISSN 2155-7780. PMC 4805406. PMID 27057405.
  30. ^ Volkow ND, Harper A, Munnisteri D, Clother J (1 January 1987). "AIDS and catatonia". Journal of Neurology, Neurosurgery & Psychiatry. 50 (1): 104. doi:10.1136/jnnp.50.1.104-a. ISSN 0022-3050. PMC 1033262. PMID 3819740.
  31. ^ Hisamoto Y, Gabriel G, Verma S, Karakas C, Chari G (18 April 2017). "Catatonia as a rare manifestation of HIV associated psychosis in adolescents. (P6.208)". Neurology. 88 (16_supplement) P6.208. doi:10.1212/WNL.88.16_supplement.P6.208. ISSN 0028-3878.
  32. ^ Pfister HW, Preac-Mursic V, Wilske B, Rieder G, Förderreuther S, Schmidt S, Kapfhammer HP (February 1993). "Catatonic syndrome in acute severe encephalitis due to Borrelia burgdorferi infection". Neurology. 43 (2): 433–5. doi:10.1212/WNL.43.2.433. ISSN 0028-3878. PMID 8437717.
  33. ^ Neumärker KJ, Dudeck U, Plaza P (February 1989). "[Borrelia encephalitis and catatonia in adolescence]". Der Nervenarzt. 60 (2): 115–9. ISSN 0028-2804. PMID 2716930.
  34. ^ Ford L, Tufts DM (15 June 2021). "Lyme Neuroborreliosis: Mechanisms of B. burgdorferi Infection of the Nervous System". Brain Sciences. 11 (6): 789. doi:10.3390/brainsci11060789. ISSN 2076-3425. PMC 8232152. PMID 34203671.
  35. ^ Carrof SN, Mann SC, Francis A, Fricchione GL, eds. (3 May 2007). Catatonia: From Psychopathology to Neurobiology. American Psychiatric Pub. pp. 133–136. ISBN 978-1-58562-712-7.
  36. ^ Walther S, Stegmayer K, Wilson JE, Heckers S (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.
  37. ^ 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
  38. ^ 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
  39. ^ 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.‌
  40. ^ 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.‌
  41. ^ 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.
  42. ^ Dhossche DM, Stoppelbein L, Rout UK (December 2010). "Etiopathogenesis of Catatonia: Generalizations and Working Hypotheses". The Journal of ECT. 26 (4): 253–8. doi:10.1097/YCT.0b013e3181fbf96d. PMID 21076339.
  43. ^ Northoff G (October 2002). "What catatonia can tell us about 'top-down modulation': A neuropsychiatric hypothesis". Behavioral and Brain Sciences. 25 (5): 555–577. doi:10.1017/s0140525x02000109. PMID 12958742. S2CID 20407002.
  44. ^ Fink M (2003). Catatonia: a clinician's guide to diagnosis and treatment. Michael Alan Taylor. Cambridge: Cambridge University Press. ISBN 0-511-06198-6. OCLC 57254202.[page needed]
  45. ^ a b c d e f g h i American Psychiatric Association (2022). Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision. Washington, DC: American Psychiatric Association. doi:10.1176/appi.books.9780890425787. ISBN 978-0-89042-575-6. S2CID 249488050.
  46. ^ Jeste DV, Lieberman JA, Benson RS, Young ML, Akaka J, Bernstein CA, Crowley B, Everett AS, Geller J, Graff MD, Greene JA, Kashtan JF, Mcvoy MK, Nininger JE, Oldham JM, Schatzberg AF, Widge AS, Vanderlip ER (2013). Diagnostic and Statistical Manual of Mental Disorders Fifth Edition DSM-5TM. American Psychiatric Association. Retrieved 8 December 2023.
  47. ^ Michael B. First (2013). DSM-5® Handbook of Differential Diagnosis. American Psychiatric Publishing. p. 49. ISBN 978-1-58562-998-5.
  48. ^ a b Serra-Mestres J, Jaimes-Albornoz W (29 June 2018). "Recognizing Catatonia in Medically Hospitalized Older Adults: Why It Matters". Geriatrics. 3 (3): 37. doi:10.3390/geriatrics3030037. PMC 6319219. PMID 31011075.
  49. ^ Sienaert P, Rooseleer J, De Fruyt J (December 2011). "Measuring catatonia: A systematic review of rating scales". Journal of Affective Disorders. 135 (1–3): 1–9. doi:10.1016/j.jad.2011.02.012. PMID 21420736.
  50. ^ Bush G, Fink M, Petrides G, Dowling F, Francis A (February 1996). "Catatonia. I. Rating scale and standardized examination". Acta Psychiatrica Scandinavica. 93 (2): 129–136. doi:10.1111/j.1600-0447.1996.tb09814.x. PMID 8686483. S2CID 20752576.
  51. ^ a b c Sienaert P, Dhossche DM, Vancampfort D, De Hert M, Gazdag G (9 December 2014). "A Clinical Review of the Treatment of Catatonia". Frontiers in Psychiatry. 5: 181. doi:10.3389/fpsyt.2014.00181. PMC 4260674. PMID 25538636.
  52. ^ "Catatonia in French Psychiatry: Implications of the Zolpidem Challenge Test". Psychiatric Annals. 37 (1) 00485713-20070101-02: 00485713–20070101–02. January 2007. doi:10.3928/00485713-20070101-02.
  53. ^ a b Simon LV, Hashmi MF, Callahan AL (2022). "Neuroleptic Malignant Syndrome". StatPearls. StatPearls Publishing. PMID 29489248.
  54. ^ Northoff G (1 December 2002). "Catatonia and neuroleptic malignant syndrome: psychopathology and pathophysiology". Journal of Neural Transmission. 109 (12): 1453–67. CiteSeerX 10.1.1.464.9266. doi:10.1007/s00702-002-0762-z. PMID 12486486. S2CID 12971112.
  55. ^ a b Samanta D, Lui F (2022). "Anti-NMDA Receptor Encephalitis". StatPearls. StatPearls Publishing. PMID 31869136.
  56. ^ Foong AL, Grindrod KA, Patel T, Kellar J (October 2018). "Demystifying serotonin syndrome (or serotonin toxicity)". Canadian Family Physician. 64 (10): 720–7. PMC 6184959. PMID 30315014.
  57. ^ Watt S, McAllister RK (2022). "Malignant Hyperthermia". StatPearls. StatPearls Publishing. PMID 28613578.
  58. ^ Arnts H, van Erp WS, Lavrijsen JC, van Gaal S, Groenewegen HJ, van den Munckhof P (May 2020). "On the pathophysiology and treatment of akinetic mutism". Neuroscience & Biobehavioral Reviews. 112: 270–8. doi:10.1016/j.neubiorev.2020.02.006. hdl:11245.1/c438b878-4d5b-4f13-887c-7f01df095324. PMID 32044373.
  59. ^ Ackermann H, Ziegler W (February 1995). "Akinetischer Mutismus – eine Literaturübersicht". Fortschritte der Neurologie · Psychiatrie. 63 (2): 59–67. doi:10.1055/s-2007-996603. PMID 7705740. S2CID 260156218.
  60. ^ Holka-Pokorska J, Piróg-Balcerzak A, Jarema M (30 April 2018). "The controversy around the diagnosis of selective mutism – a critical analysis of three cases in the light of modern research and diagnostic criteria". Psychiatria Polska. 52 (2): 323–343. doi:10.12740/PP/76088. PMID 29975370.
  61. ^ Wylie T, Sandhu DS, Murr N (2022). "Status Epilepticus". StatPearls. StatPearls Publishing. PMID 28613459.
  62. ^ Sutter R, Kaplan PW (August 2012). "Electroencephalographic criteria for nonconvulsive status epilepticus: Synopsis and comprehensive survey: EEG Criteria for NCSE". Epilepsia. 53: 1–51. doi:10.1111/j.1528-1167.2012.03593.x. PMID 22862158. S2CID 24014621.
  63. ^ Delirium: prevention, diagnosis and management. National Institute for Health and Care Excellence: Guidelines. National Institute for Health and Care Excellence (NICE). 2019. ISBN 978-1-4731-2992-4. PMID 31971702.
  64. ^ M Das J, Anosike K, Asuncion RM (2022). "Locked-in Syndrome". StatPearls. StatPearls Publishing. PMID 32644452.
  65. ^ Balint B, Meinck HM (July 2018). "Pragmatic Treatment of Stiff Person Spectrum Disorders: Pragmatic Treatment of SPSD". Movement Disorders Clinical Practice. 5 (4): 394–401. doi:10.1002/mdc3.12629. PMC 6174384. PMID 30363317.
  66. ^ Baizabal-Carvallo JF, Jankovic J (August 2015). "Stiff-person syndrome: insights into a complex autoimmune disorder". Journal of Neurology, Neurosurgery & Psychiatry. 86 (8): 840–8. doi:10.1136/jnnp-2014-309201. PMID 25511790. S2CID 19981869.
  67. ^ Sarva H, Deik A, Ullah A, Severt WL (4 March 2016). "Clinical Spectrum of Stiff Person Syndrome: A Review of Recent Reports". Tremor and Other Hyperkinetic Movements. 6: 340. doi:10.7916/D85M65GD. PMC 4790195. PMID 26989571.
  68. ^ Rasmussen SA, Mazurek MF, Rosebush PI (2016). "Catatonia: Our current understanding of its diagnosis, treatment and pathophysiology". World Journal of Psychiatry. 6 (4): 1875–9. doi:10.5498/wjp.v6.i4.391. PMC 5183991. PMID 8078203.
  69. ^ Vaquerizo-Serrano J, Salazar De Pablo G, Singh J, Santosh P (2022). "Catatonia in autism spectrum disorders: A systematic review and meta-analysis". European Psychiatry. 65 (1): e4. doi:10.1192/j.eurpsy.2021.2259. PMC 8792870. PMID 34906264.
  70. ^ Thenganatt M, Jankovic J (2016). "Psychogenic (Functional) parkinsonism". Functional Neurologic Disorders. Handbook of Clinical Neurology. Vol. 139. pp. 259–262. doi:10.1016/B978-0-12-801772-2.00022-9. ISBN 978-0-12-801772-2. PMID 27719845.
  71. ^ Ganos C, Kassavetis P, Cerdan M, Erro R, Balint B, Price G, Edwards MJ, Bhatia KP (June 2015). "Revisiting the Syndrome of "Obsessional Slowness"". Movement Disorders Clinical Practice. 2 (2): 163–9. doi:10.1002/mdc3.12140. PMC 6353487. PMID 30713890. S2CID 73414098.
  72. ^ Rosso M, Fremion E, Santoro SL, Oreskovic NM, Chitnis T, Skotko BG, Santoro JD (2020). "Down Syndrome Disintegrative Disorder: A Clinical Regression Syndrome of Increasing Importance". Pediatrics. 145 (6): e20192939. doi:10.1542/peds.2019-2939. PMID 32471843. S2CID 219104019.
  73. ^ Chicoine B (December 2022). "Obsessional Slowness". Adult Down Syndrome Center, Advocate Medical Group.
  74. ^ Lyons A, Allen NM, Flanagan O, Cahalane D (2020). "Catatonia as a feature of down syndrome: An under-recognised entity?". European Journal of Paediatric Neurology. 25: 187–190. doi:10.1016/j.ejpn.2020.01.005. PMID 31959555. S2CID 210841869.
  75. ^ Clinebell K, Azzam PN, Gopalan P, Haskett R (15 June 2014). "Guidelines for Preventing Common Medical Complications of Catatonia: Case Report and Literature Review". The Journal of Clinical Psychiatry. 75 (6): 644–651. doi:10.4088/JCP.13r08870. ISSN 0160-6689. PMID 25004188.
  76. ^ Pérez-Balaguer A, Sánchez-Rivero I (December 2021). "Electroconvulsive therapy, catatonia, deep vein thrombosis and anticoagulant treatment: a case report". General Psychiatry. 34 (6) e100666. doi:10.1136/gpsych-2021-100666. ISSN 2517-729X. PMC 8705197. PMID 35028525.
  77. ^ Rogers JP, Oldham MA, Fricchione G, Northoff G, Ellen Wilson J, Mann SC, Francis A, Wieck A, Elizabeth Wachtel L, Lewis G, Grover S, Hirjak D, Ahuja N, Zandi MS, Young AH (April 2023). "Evidence-based consensus guidelines for the management of catatonia: Recommendations from the British Association for Psychopharmacology". Journal of Psychopharmacology. 37 (4): 327–369. doi:10.1177/02698811231158232. ISSN 1461-7285. PMC 10101189. PMID 37039129.
  78. ^ Smith AC, Holmes EG (1 December 2023). "Catatonia: A Narrative Review for Hospitalists". American Journal of Medicine Open. 10 100059. doi:10.1016/j.ajmo.2023.100059. ISSN 2667-0364. PMC 11256243. PMID 39035239.
  79. ^ Hawkins JM, Archer KJ, Strakowski SM, Keck PE (December 1995). "Somatic Treatment of Catatonia". The International Journal of Psychiatry in Medicine. 25 (4): 345–369. doi:10.2190/X0FF-VU7G-QQP7-L5V7.
  80. ^ Rosebush PI, Mazurek MF (March 2010). "Catatonia and Its Treatment". Schizophrenia Bulletin. 36 (2): 239–242. doi:10.1093/schbul/sbp141. PMID 19969591.
  81. ^ Park J, Tan J, Krzeminski S, Hazeghazam M, Bandlamuri M, Carlson RW (30 January 2017). "Malignant Catatonia Warrants Early Psychiatric-Critical Care Collaborative Management: Two Cases and Literature Review". Case Reports in Critical Care. 2017 (1): 1–4. doi:10.1155/2017/1951965.
  82. ^ American Psychiatric Association (2022). Diagnostic and Statistical Manual of Mental Disorders. doi:10.1176/appi.books.9780890425787. ISBN 978-0-89042-578-7. S2CID 249488050.[page needed]
  83. ^ Solmi M, Pigato GG, Roiter B, Guaglianone A, Martini L, Fornaro M, Monaco F, Carvalho AF, Stubbs B, Veronese N, Correll CU (20 August 2018). "Prevalence of Catatonia and Its Moderators in Clinical Samples: Results from a Meta-analysis and Meta-regression Analysis". Schizophrenia Bulletin. 44 (5): 1133–50. doi:10.1093/schbul/sbx157. PMC 6101628. PMID 29140521.
  84. ^ a b Rogers JP, Pollak TA, Begum N, Griffin A, Carter B, Pritchard M, Broadbent M, Kolliakou A, Ke J, Stewart R, Patel R, Bomford A, Amad A, Zandi MS, Lewis G, Nicholson TR, David AS (2 November 2021). "Catatonia: demographic, clinical and laboratory associations". Psychological Medicine. 53 (6): 2492–2502. doi:10.1017/S0033291721004402. PMC 10123832. PMID 35135642. S2CID 242076501.
  85. ^ Parsanoglu Z, Balaban OD, Gica S, Atay OC, Altin O (May 2022). "Comparison of the Clinical and Treatment Characteristics of Patients Undergoing Electroconvulsive Therapy for Catatonia Indication in the Context of Gender". Clinical EEG and Neuroscience. 53 (3): 175–183. doi:10.1177/15500594211025889. PMID 34142904. S2CID 235471133.
  86. ^ Oldham MA (1 July 2018). "The Probability That Catatonia in the Hospital has a Medical Cause and the Relative Proportions of Its Causes: A Systematic Review". Psychosomatics. 59 (4): 333–340. doi:10.1016/j.psym.2018.04.001. ISSN 0033-3182. PMID 29776679.
  87. ^ Berrios GE (1981). "Stupor: A conceptual history". Psychological Medicine. 11 (4): 677–688. doi:10.1017/s0033291700041179. PMID 7034030. S2CID 26932116.
  88. ^ Roccatagliata G (1985), Pichot P, Berner P, Wolf R, Thau K (eds.), "The Idea of Melancholia in Classical Culture", Psychiatry The State of the Art: Volume 8 History of Psychiatry, National Schools, Education, and Transcultural Psychiatry, Boston, MA: Springer US, pp. 89–93, doi:10.1007/978-1-4757-1853-9_12, ISBN 978-1-4757-1853-9, retrieved 18 November 2024
  89. ^ Scholtz M (December 1940). "Hippocrates' Aphorisms". California and Western Medicine. 53 (6): 272. ISSN 0093-4038. PMC 1634189. PMID 18745795.
  90. ^ Veith I (15 December 2015). The Yellow Emperor's Classic of Internal Medicine. University of California Press. doi:10.1525/9780520963245. ISBN 978-0-520-96324-5.
  91. ^ "Zur Entwicklung der Psychiatrie - ein Internet-Atlas von Dr. Hans-Peter Haack" (in German). Archived from the original on 9 February 2008. Retrieved 29 June 2017.
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