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Catatonia

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(Redirected from Catatonic stupor)
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
SpecialtyPsychiatry, neurology
SymptomsImmobility, mutism, staring, posturing, rigidity, low consciousness, etc.
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 complex syndrome, most commonly seen in people with underlying mood (e.g major depressive disorder) or psychotic disorders (e.g schizophrenia).[2][3] People with catatonia have abnormal movement and behaviors, which vary from person to person and fluctuate in intensity within a single episode. People with catatonia appear withdrawn, meaning that they do not interact with the outside world and have difficulty processing information. They may be nearly motionless for days on end or perform repetitive purposeless movements. Two people may exhibit very different sets of behaviors and both still be diagnosed with catatonia. There are different subtypes of catatonia, which represent groups of symptoms that commonly occur together. These include akinetic catatonia, excited catatonia, malignant catatonia, and delirious mania.

Catatonia has historically been related to schizophrenia (catatonic 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.

Catatonia is commonly mistaken for a condition delirium, which can present similarly to catatonia, but requires very different treatment. Treatment with benzodiazepines or ECT are most effective and lead to remission of symptoms in most cases.[3]

Classification

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Modern Classifications

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The ICD-11 is the most common manual used globally to define and diagnose illness, including mental illness.[4] It diagnoses catatonia in someone who has three different symptoms associated with catatonia at one time. These symptoms are stupor, catalepsy, waxy flexibility, mutism, negativism, posturing, mannerisms, stereotypies, psychomotor agitation, grimacing, echolalia, and echopraxia. It divides catatonia into three groups based on the underlying cause; Catatonia associated with another mental disorder, catatonia induced by psychoactive substance, and secondary catatonia.

The DSM-5 is the most common manual used by mental health professionals in the United States to define and diagnose different mental illnesses. The DSM-5 defines catatonia as, “a syndrome characterized by lack of movement and communication, along with three or more of the following 12 behaviors; stupor, catalepsy, waxy flexibility, mutism, negativism, posturing, mannerism, stereotypy, agitation, grimacing, echolalia, or echopraxia.”[5] As a syndrome, catatonia can only occur in people with an existing illness. The DSM-5 divides catatonia into 3 diagnoses. The most common of the three diagnoses is Catatonia Associated with Another Mental Disorder. Around 20% of cases are caused by an underlying medical condition, and known as Catatonic Disorder Due to Another Medical Condition[6]. When the underlying condition is unknown it is considered Unspecified Catatonia.

Historical Classifications

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The term “catatonia” was first used by, German psychiatrist, Karl Ludwig Kahlbaum in 1874. 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. These include Stuporous Catatonia, Excited Catatonia, Malignant Catatonia, and Periodic Catatonia, which will be described in more detail later in this article. 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.

Signs and symptoms

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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 may worsen, improve, and change in appearance throughout a single episode.[7] Symptoms may develop over hours or days to 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 stimuli
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 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.[8]

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.[9]

Stuporous Catatonia: This form of 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: 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.[2][3][8] People in this state are extremely hyperactive and may have delusions and hallucinations.[10]

Malignant Catatonia: This form of catatonia is a life threatening. It is characterized by fever, dramatic and rapid changes in blood pressure, increased heart rate and respiratory rate, and excessive sweating.[2][3] Laboratory tests may be abnormal.

Periodic Catatonia: This form of catatonia is characterized by only 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.

Causes

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Catatonia can only exist if a person has another underlying illness, and can be associated with a wide range of illnesses including psychiatric disorders, medical conditions, and substance use.

Psychiatric Conditions

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Mood disorders such as a 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,[11] autism spectrum disorders, ADHD,[12] and Post-traumatic Stress Disorder.

People with different underlying conditions may be more likely than others to present with different symptoms. For instance, people with major depressive disorder may present with catatonia during a severe depressive episode and be more likely to present with slow movement, mutism, and withdrawal. On the other hand, a person with bipolar disorder may appear similarly to a person with major depressive disorder if their catatonia occurs during a depressive episode, but may be more likely to present with excited catatonia symptoms like agitation and hyperactivity during a manic episode.

Medical Conditions

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Catatonia is also seen in many medical disorders, encephalitis, meningitis, autoimmune disorders,[13], focal neurological lesions (including strokes),[14] alcohol withdrawal,[15] abrupt or overly rapid benzodiazepine withdrawal,[16][17][18] cerebrovascular disease, neoplasms, head injury,[5] and some metabolic conditions (homocystinuria, diabetic ketoacidosis, hepatic encephalopathy, and hypercalcaemia).[5]

Neurological Disorders

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Metabolic and Endocrine Disorders

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Autoimmune Disorders

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Infectious Diseases

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Substance Use

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Use of NMDA receptor antagonists including ketamine and phencyclidine (PCP) can lead to catatonia-like states. Information about these effects has improved scientific understanding of the role of glutatmate in catatonia. High dose and chronic use of stimulants like Cocaine and Amphetamines can lead to cases of catatonia, typically associated with psychosis. This is thought to be due to changes in the function of circuits of the brain associated with dopamine release.


Psychodynamic theorists have interpreted catatonia as a defense against the potentially destructive consequences of responsibility, and the passivity of the disorder provides relief.[19]

Pathogenesis

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The pathophysiology that leads to catatonia is still poorly understood and a definite mechanism remains unknown.[8][20] Neurologic studies have implicated several pathways; however, it remains unclear whether these findings are the cause or the consequence of the disorder.[21]

Abnormalities in GABA, glutamate signaling, serotonin, and dopamine transmission are believed to be implicated in catatonia.[3][8][22]

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.[23]

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 World Health Organization's eleventh edition of the 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.[24]

DSM-5 classification

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.[25][26] : 134–135 

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:[25]: 135 

  • stupor: no 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
  • mutism: no, or very little, verbal response (exclude if known aphasia)
  • negativism: opposition or no response to instructions or external stimuli
  • posturing: spontaneous and active maintenance of a posture against gravity
  • mannerisms that are odd, circumstantial caricatures of normal actions
  • stereotypy: repetitive, abnormally frequent, non-goal-directed movements
  • agitation, not influenced by external stimuli
  • grimacing: keeping a fixed 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 first be considered.[27]

ICD-11 classification

In 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.

Assessment/Physical

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Catatonia is often overlooked and under-diagnosed.[28] 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 that may progress to exciting catatonia. 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.[3]

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.[3]

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.[3]

Rating scale

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Various rating scales for catatonia have been developed, however, their utility for clinical care has not been well established.[29] The most commonly used scale is the Bush-Francis Catatonia Rating Scale (BFCRS) (external link is provided below).[30] 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.

A diagnosis can be supported by the lorazepam challenge[31] or the zolpidem challenge.[32] While proven useful in the past, barbiturates are no longer commonly used in psychiatry; thus the option of either benzodiazepines or ECT.

Laboratory Findings

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Certain lab findings are common with this 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.

Differential diagnosis

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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:

  • 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.[33] 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,[33] but it has not been established as a subtype.[34] Therefore, discontinuing antipsychotics and starting benzodiazepines is a treatment for this condition, and similarly it is helpful in catatonia as well.
  • Anti-NMDA receptor encephalitis is an autoimmune disorder characterized by neuropsychiatric features and the presence of IgG antibodies.[35] The presentation of anti-NMDAR 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.[35]
  • 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: SSRI). These patients will also present with hyperreflexia, myoclonus, nausea, vomiting, and diarrhea.[36]
  • 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.[37] 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.
  • 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.[38] 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.[39] 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.
  • Elective mutism has an anxious etiology but has also been associated with personality disorders.[40] 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.
  • Nonconvulsive status epilepticus is seizure activity with no accompanying tonic-clonic movements.[41] 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).[42] 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.[43] 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 retarded 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.[44]
  • Stiff-person syndrome and catatonia are similar in that they may both present with rigidity, autonomic instability and a positive response to benzodiazepines.[45] However, stiff-person syndrome may be associated with anti-glutamic acid decarboxylase (anti-GAD) antibodies[46][47] 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 retarded 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.[48]
  • 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.[49]
  • 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.[50] Obsessional slowness is a controversial diagnosis, with presentations ranging from severe but common manifestations of obsessive compulsive disorder to catatonia.[51]
  • 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.[52] DSDD seems to phenotypically overlap with obsessional slowness (see above)[53] and catatonia-like regression occurring in ASD.[54]

Treatment

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The initial treatment of catatonia is to stop medication that could be potentially leading to the syndrome.[31] These may include steroids, stimulants, anticonvulsants, neuroleptics or dopamine blockers.[3] A "lorazepam challenge", in which patients are given 2 mg of IV lorazepam (or another benzodiazepine) may aid in the diagnosis.[55] Most patients with catatonia will respond significantly to this within the first 15–30 minutes. If no change is observed during the first dose, then a second dose is given and the patient is re-examined. If the patient responds to the lorazepam challenge, then lorazepam can be scheduled at interval doses until the catatonia resolves.[3] The lorazepam must be tapered slowly, otherwise, the catatonia symptoms may return. The underlying cause of the catatonia should also be treated during this time. ECT may also be used to resolve catatonia. The success rate of ECT and lorazepam in the treatment of catatonia is estimated to be 60-100%, with earlier treatment being associated with a greater likelihood of treatment success.[7] ECT is usually administered as multiple sessions over one-two weeks and is usually successful in those in which lorazepam fails.[7] ECT in combination with benzodiazepines is used to treat malignant catatonia. In France, zolpidem has also been used in diagnosis, and response may occur within the same time period. Ultimately the underlying cause needs to be treated.[11]

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 blood clot, and measures to prevent the development of pressure ulcers.[7]

Electroconvulsive therapy (ECT) is an effective treatment for catatonia that is well acknowledged.[31] ECT has also shown favorable outcomes in patients with chronic catatonia. However, it has been pointed out that further high quality randomized controlled trials are needed to evaluate the efficacy, tolerance, and protocols of ECT in catatonia.[56]

Antipsychotics 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.[11][7]

There is evidence that clozapine works better than other antipsychotics to treat catatonia.[57][7]

Excessive glutamate activity is believed to be involved in catatonia;[57] 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.[58]

Prognosis

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Twenty-five percent of psychiatric patients with catatonia will have more than one episode throughout their lives.[7] 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. For patients with catatonia with underlying schizophrenia, the prognosis is much poorer.[3]

Complications

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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.[28] Furthermore, if immobility is a symptom the patient is presenting with, then they may develop pressure ulcers, muscle contractions, and are at risk of developing deep vein thrombosis (DVT) and pulmonary embolus (PE).[28] 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.[3]

Epidemiology

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Catatonia has been historically studied in psychiatric patients.[59] Catatonia is underrecognized and the features may be mistaken for other disorders (such as negative symptoms of schizophrenia), leading to an underestimate of the prevalence. 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.[7][60][8] One large population estimate has suggested that the incidence of catatonia is 10.6 episodes per 100 000 person-years.[61] It occurs in males and females in approximately equal numbers.[62][61] 21-46% of all catatonia cases can be attributed to a general medical condition.[28]

History

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Reports of stupor-like and catatonia-like states abound in the history of psychiatry.[63] After the middle of the 19th century there was an increase of interest in the motor disorders accompanying madness,[64] culminating in the publication by Karl Ludwig Kahlbaum in 1874 of Die Katatonie oder das Spannungsirresein ("Catatonia or Tension Insanity").[65]

See also

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References

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