Updated: Dec 20, 2017
  • Author: James Robert Brasic, MD, MPH; Chief Editor: Selim R Benbadis, MD  more...
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Practice Essentials

Catatonia is a state of apparent unresponsiveness to external stimuli in a person who is apparently awake. There are 3 types: (1) catatonia associated with another mental disorder (catatonia specifier), (2) catatonic disorder due to another medical condition, and (3) unspecified catatonia.

Signs and symptoms

Individuals with catatonia often cannot provide a coherent history; however, collateral sources can often relate relevant historical information. A history of behavioral responses to others usually includes the presence of the following:

  • Mutism
  • Negativism
  • Echopraxia (repeating the movements of others)
  • Echolalia (repeating the words of others)
  • Waxy flexibility
  • Withdrawal

The alternative presentation of catatonia is an excited state, possibly with impulsivity, combativeness, and autonomic instability.

The history should inquire into the following:

  • Possible precipitating events, including infection, trauma, and exposure to toxins and other substances
  • Previous similar episodes of catatonia
  • Exposure to neuroleptics and other substances associated with catatonia
  • Comorbid disorders, including schizophrenia, mood disorders, psychological stressors, medical conditions, and obstetric conditions

In an emergency setting, treatable common causes of catatonia must be rapidly considered and ruled out. In addition, the following must be considered:

  • Neuroleptic malignant syndrome (NMS)
  • Encephalitis
  • Nonconvulsive status epilepticus
  • Acute psychosis

The physical examination should include evaluation of the patient for the following:

  • Excited and immobile states
  • Negativistic phenomena (eg, gegenhalten and mitgehen)
  • Automatic obedience
  • Stereotypies (eg, nose wrinkling; repetitive movements of the mouth and the jaw; repetitive eye movements; repetitive tapping of the foot, the finger, or the hand; and repetitive abdomen patting, shoulder shrugging, or body rocking)
  • Preservation (the inappropriate repetition of acts)
  • Echophenomena (echolalia and echopraxia)
  • Inappropriate verbal usage (eg, in France,vous for tu)
  • Comorbid conditions (eg, schizophrenia, mood disorders, and neurologic and medical conditions)
  • Psychogenic movement disorders (eg, somatoform disorders, factitious disorders, and malingering)

See Presentation for more detail.


Laboratory studies that may be useful include the following:

  • Complete blood count (CBC)
  • Electrolyte concentrations
  • Chemical analyses of blood
  • Fibrin D-dimer
  • Serum creatine kinase level
  • Liver function tests
  • Serum ceruloplasmin level

Imaging is mainly useful for ruling out other treatable disorders. Modalities that may be helpful include the following:

  • Magnetic resonance imaging (MRI)
  • Computed tomography (CT)
  • Single-photon emission CT (SPECT)
  • Positron emission tomography (PET) with fluorodeoxyglucose (FDG)

Electroencephalography (EEG) is indicated to rule out a seizure disorder.

See Workup for more detail.


Prompt treatment in the early phases of catatonic states is crucial to obtaining a lasting abatement of symptoms. Treatable conditions must be identified immediately.

Medications that have been used to treatment catatonia include the following:

  • Benzodiazepines (eg, clonazepam, lorazepam, and midazolam)
  • Carbamazepine
  • Zolpidem
  • Tricyclic antidepressants
  • Muscle relaxants
  • Amobarbital
  • Reserpine
  • Thyroid hormone
  • Lithium carbonate
  • Bromocriptine
  • Neuroleptics - Traditional neuroleptics are generally avoided; second-generation (atypical) antipsychotics should be used with caution

When nonconvulsive status epilepticus, diffuse encephalopathy, and other neurologic disorders are ruled out, electroconvulsive treatment (ECT) is indicated for patients who do not respond to pharmacotherapy within 5 days or who manifest malignant catatonia.

See Treatment and Medication for more detail.



Catatonia is a state of apparent unresponsiveness to external stimuli in a person who is apparently awake. It occurs in children, adolescents, and adults; is associated with a heterogeneous group of comorbid conditions; and is characterized by a variety of symptoms and signs of impairment of the expression of voluntary thoughts and movements.

Psychomotor manifestations of catatonia, [1] as analyzed by latent class techniques, have been divided into the following 4 classes [2] :

  • Automatic
  • Repetitive/echo
  • Withdrawal
  • Agitated/resistive

The American Psychiatric Association's Diagnostic Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), categorizes catatonia as belonging to schizophrenia spectrum and other psychotic disorders and divides it into the following 3 categories [3] :

  • Catatonia associated with another mental disorder (catatonia specifier)
  • Catatonic disorder due to another medical condition
  • Unspecified catatonia

It can be difficult to differentiate catatonia from diffuse encephalopathy, nonconvulsive status epilepticus, neuroleptic malignant syndrome (NMS), acute psychosis, somatization disorder, conversion disorder, factitious disorder, malingering, and psychogenic movement disorders. (See Presentation, DDx, and Workup.)

The vast differential diagnosis for catatonia notwithstanding, identification of treatable causes (eg, nonconvulsive status epilepticus) is crucial to the administration of the needed interventions. When faced with a patient with catatonia, the clinician's first task is always to rule out treatable causes. (See Etiology, Presentation, Workup, Treatment, and Medication.) For more information on catatonia, see the presentation below.

Diagnostic criteria (DSM-5)

For both catatonia associated with another mental disorder (catatonia specifier) and catatonic disorder due to another medical condition, DSM-5 notes that the clinical picture is dominated by the presence of 3 or more of the following 12 features [3] :

  1. Stupor (no psychomotor activity; not actively relating to environment)
  2. Catalepsy (passive induction of a posture held against gravity)
  3. Waxy flexibility (slight, even resistance to positioning by examiner)
  4. Mutism (no, or very little, verbal response) – This is not applicable if there is established aphasia
  5. Negativism (opposition or no response to instructions or external stimuli)
  6. Posturing (spontaneous and active maintenance of a posture against gravity)
  7. Mannerism (odd, circumstantial caricature of normal actions)
  8. Stereotypy (repetitive, abnormally frequent, non-goal-directed movements)
  9. Agitation, not influenced by external stimuli
  10. Grimacing
  11. Echolalia (mimicking another's speech)
  12. Echopraxia (mimicking another's movements)

Catatonia associated with another mental disorder (catatonia specifier) is indicated when the 3 or more features are present during the course of a neurodevelopmental, psychotic, bipolar, depressive, or other mental disorder. Catatonia appears in 35% of individuals with schizophrenia, but the majority of catatonia cases are associated with depressive or bipolar disorders.

In addition, DSM-5 lists the following criteria as specific for catatonic disorder due to another medical condition [3] :

  • There is evidence from the history, physical examination, or laboratory findings that the disturbance is the direct pathophysiologic consequence of another medical condition
  • The disturbance is not better explained by another mental disorder (eg, a manic episode)
  • The disturbance does not occur exclusively during the course of delirium
  • The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning

Pathophysiology and Etiology

Theories of pathogenesis

Catatonia is likely to be the consequence a heterogeneous group of etiologies. Various hypotheses have been proposed about the pathogenesis of catatonia, including the following.

Deficits in fetal cortical development may result in schizophrenia and other developmental disorders. [4] These deficits, in turn, likely produce dysfunction in cortical and subcortical glutamatergic pathways, resulting in the symptoms and signs of catatonia. [5]

Individuals with mental retardation, autism, or other developmental disabilities may be particularly vulnerable to developing catatonia. [6, 7, 8, 9, 10]

Imbalances in the excitatory-to-inhibitory ratio (EIR) may play a role. Baguley proposed that alterations in interrelated networks at the spinal and brainstem level produce catatonia. [11]

The administration of agents that block postsynaptic dopamine receptors is associated with the onset of catatonia in some individuals. Agonists of dopamine D1 and D2 receptors relieve catalepsy, a sign of catatonia in rats; this suggests that these agents may be effective pharmacologic interventions. In addition, the effectiveness of electroconvulsive treatment (ECT) for catatonia suggests that dopaminergic modulation may play a role in the development and amelioration of catatonia.

The effectiveness of amantadine in the treatment of catatonia suggests that at least some individuals with catatonia manifest glutamatergic dysfunction.

Decreased binding to gamma-aminobutyric acid (GABA)–A receptors in the left sensorimotor cortex has been observed in some subjects with catatonia. The favorable responses of some patients with catatonia to benzodiazepines and zolpidem, agonists of GABA-A, suggest that this is a likely site of dysfunction in some cases of catatonia. [12] Potentiation of the action of GABA by benzodiazepines suggests that some individuals with catatonia may have a functional deficit of GABA.

Some patients may have dysfunction in the neurotransmission of noradrenaline and serotonin. In inbred rats with catalepsy, Alekhina et al reported decreases of noradrenaline and increases of serotonin in the striatum and diencephalon.

Animal models have been developed to study the pathophysiology of catatonia. Uzbay reported that administration of a nonspecific inhibitor of nitric oxide synthase, N(G)-nitro-L-arginine methyl ester (L-NAME), to ethanol-dependent rats being withdrawn from ethanol precipitated catatonia. [13]

Moreover, L-arginine, a precursor of nitric oxide, does not reverse the catatonia precipitated by L-NAME. Therefore, nitric oxide does not mediate the production of the catatonia. These findings suggest that dysfunction of dopaminergic, serotonergic, and glutamatergic systems may play a role in the production of catatonia in ethanol-dependent rats.

Kahlbaum noted lesions of the sylvian fossa and the second and third frontal gyri on autopsy of patients who died with catatonia. [14] These regions modulate executive functions and the inhibition of voluntary acts.

Disorders associated with catatonia

Numerous neurologic, psychiatric, psychological, medical, and obstetric conditions and factors have been associated with the development of catatonia (see the Table below). [6, 7, 8, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27]

Table. Causes of Catatonia by Category (Open Table in a new window)

Category Causes
Neurologic conditions Neuroleptic malignant syndrome [15]

Administration of agents that block postsynaptic dopamine receptors*

Administration of sibutramine [16] (withdrawn from US market October 8, 2010)

Withdrawal of lorazepam and other sedatives

Akinetic-rigid syndrome

Arachnoid cyst in right parietal region


Atrophy of left amygdala [17]

Autistic disorder [6, 7, 8, 18, 19, 20, 21, 22, 23]

Basilar artery thrombosis

Bilateral hemorrhagic lesions of temporal lobes

Cerebellar catalepsy

Cerebral hemorrhage

Cerebral infarct

Cerebrovascular disease

Cortical venous thrombosis

Central pontine myelinolysis

Cortical basal ganglionic degeneration


Encephalitis (herpesvirus, Trypanosoma cruzi)

Encephalopathy (Borrelia burgdorferi, HIV infection, Wernicke encephalopathy)

Familial fatal insomnia [24]

Fibromuscular dysplasia with dissection of basilar artery

Frontal lobotomy

Head injury

Huntington disease


Hypopituitarism secondary to postpartum hemorrhage

Idiopathic recurring stupor

Inherited neurometabolic disorders

Locked-in syndrome

Meningitis, tuberculous


Multiple sclerosis [25, 26]


Nonconvulsive status epilepticus

Pervasive developmental disorders [7, 8, 22]

Pallidoluysian atrophy

Paraneoplastic encephalitis [27]


Postencephalitic parkinsonism

Progressive multifocal leukoencephalopathy

Progressive supranuclear palsy


Seizures (complex with partial symptomatology)

Stiff-man syndrome



Subarachnoid hemorrhage

Subdural hematoma

Substance intoxication (alcohol, disulfiram, organic fluorides, phencyclidine)

Subthalamic mesencephalic tumor

Surgical removal of cerebellar tumor

Tay-Sachs disease

Temporal lobe epilepsy

Tuberous sclerosis

Tumors (corpus callosum, glioma of third ventricle, supraventricular diffuse pinealoma)

Vegetative state

Von Economo (lethargic) encephalitis

Wilson disease

Psychiatric conditions Acute stress disorder

Anorexia nervosa

Autistic disorder [6]

Brief reactive psychosis with catatonia

Conversion disorder


Major depression, single episode with catatonic features

Mood disorders

Neuroleptic malignant syndrome [15]

Posttraumatic stress disorder


Substance intoxication (3,4-methylenedioxymethamphetamine [“ecstasy”], alcohol, amphetamine, phencyclidine, substance withdrawal, hypnotic-sedative, lorazepam)

Psychological factors Immigration

Experiencing rejection of an expression of love

Feelings of alienation in an unfamiliar country

Medical conditions AIDS

Acute intermittent porphyria

Addison disease

Bacterial septicemia


Carcinoid tumors

Diabetic ketoacidosis

Encephalopathy (hepatic, HIV infection, Wernicke encephalopathy)

Fever of unknown cause

Heat stroke

Hepatic failure

Hereditary coproporphyria







Intestinal atony


Neuroleptic malignant syndrome [15]

Poisoning (carbon monoxide, tetraethyl lead)

Renal failure

Substance intoxication (alcohol, cyclosporine, disulfiram, organic fluorides, phencyclidine)

Syndrome of inappropriate antidiuretic hormone (SIADH)


Systemic lupus erythematosus

Thermal injury

Thrombotic thrombocytopenic purpura


Typhoid fever


Von Economo (lethargic) encephalitis

Obstetric conditions Hypopituitarism secondary to postpartum hemorrhage
*Administration of agents that block postsynaptic dopamine receptors is associated with the onset of catatonia in some individuals.

Neuroleptic malignant syndrome

NMS is characterized by the introduction of a neuroleptic medication or an increase in its dosage, a temperature higher than 38° C, and a heart rate exceeding 100 beats/min or a diastolic blood pressure exceeding 100 mm Hg. [15] The triad of fever, tachycardia, and rigidity is typical of the syndrome, which is associated with death in about one fifth of cases.

A similar etiology for catatonia and NMS after exposure to antipsychotic medications, including typical and atypical neuroleptics, is suggested by the similar clinical presentation—that is, elevated temperature, rigidity, delirium, and dysregulation of the autonomic nervous system.

Although apparently uncommon, NMS has been reported in as many as 12.2% of people exposed to neuroleptic medication. Nielsen and Nielsen reported the occurrence of NMS after a single dose of neuroleptic medication. [28]

Latah betul

Latah betul ("real latah" or "true latah") is a phenomenon in Malaysia that is characterized by apparent loss of control over behavior, as well as by echolalia, echopraxia, and automatic obedience.

Winzeler surveyed ethnic groups in different regions of Malaysia to obtain demographic and epidemiologic data about the condition. [29] No one younger than 10 years exhibited latah in any of the groups examined. Latah was much more common in women; mature women were the group that most often exhibited latah. People who developed latah had it for the rest of their lives. The onset of the condition was often associated with frightening experiences (in life and in dreams) and with sorcery.

Simons [30] and Tanner and Chamberland [31] published videotapes of individuals with latah to facilitate its recognition by individuals from other cultures who are unfamiliar with the condition.

The occurrence of latah betul in older women in particular cultures in Southeast Asia suggests that some individuals in the affected ethnic groups may be more prone to this condition. This is reminiscent of other neuropsychiatric disorders with a genetic basis. The histories of persons with latah betul suggest that in some cases, extreme stress may precipitate the onset of the disorder. Thus, environmental influences may facilitate the development of latah betul in those with an inborn predisposition to express the phenotype of latah betul.

Evaluation of people with latah betul by clinicians experienced with movement disorders may facilitate the application of the standard nomenclature for movement disorders, mental disorders, and other medical conditions to latah betul. The published reports of latah betul suggest the diagnosis of catatonia. Research by individuals trained in the diagnosis of neuropsychiatric disorders will facilitate the understanding of latah betul and its place in a lexicon of diseases.



United States statistics

The current frequency of catatonia in the United States is unknown. A few studies noted a decrease in the frequency of catatonia in parts of the United States over the past century. Various biases may influence the results of the few epidemiologic studies of catatonia. In 1994, the incidence of catatonia among psychiatric inpatients in a university hospital in New York was 7%. [32] However, the hospital was a tertiary care referral hospital known for treatment of catatonia; this, the population probably was not representative of the general population.

International statistics

The current frequency of catatonia in international populations is unknown. The few published epidemiologic studies have reported vastly different rates, suggesting that the frequency of catatonia may vary widely from one location to another. On the other hand, many cases of catatonia may remain undiagnosed. Results may be confounded by an ascertainment bias. In other words, catatonia may be diagnosed less frequently in developing countries than it is in industrialized countries, because clinicians fail to identify the condition in their patients.

The prevalence of catatonia among inpatients of psychiatric hospitals is 11.4% in Colombia, [33] 13.5% in India, [34] 16.9% in Spain, [35] and 9.6% in Wales. [34] In a forensic psychiatric hospital in France, the prevalence of catatonia was 13.1%. [36] In Colombia, treatment apparently is not administered to many patients with catatonia until they have reached an advanced stage of the condition. Benegal et al reported that catatonia appears to be more common in India than in Europe and North America. [37]

In contrast to studies from Colombia, India, and Spain, reports from several other locations have suggested that the occurrence of catatonia in the general population decreased dramatically in the past century. In Great Britain, the incidence of catatonia dropped from 6% of admissions to a hospital in the 1850s to 0.5% in the 1950s. [38]

In a psychiatric clinic in Chile, a decrement in the proportion of patients with schizophrenia who manifested catatonia was observed from 1964 to 1984. In Finland, the percentage of patients with schizophrenia displaying catatonia decreased from 37% in 1933-1935 to 11% in 1953-1955. [39] In Canada, catatonia was present in 10% of inpatient psychiatric admissions in 1993.

Age-, sex-, and race-related demographics

Catatonia is rare in preadolescent children; it has been reported in adolescents and adults.

In Monroe County, New York, the female-to-male ratio was 1.3:1 for catatonic schizophrenia and 1.1:1 for all forms of schizophrenia during the period 1960-1969. [40] In 1972-1973, a female-to-male ratio of 1.3:1 was observed among inpatients with catatonia admitted to 2 psychiatric units in a municipal hospital in New York City. [41]

The frequency of catatonia in different races is unknown. Ungvari et al noted the need to investigate the role of ethnic, cultural, and social influences in the development of catatonia. [42]



Carroll noted that studies of catatonia have reported recovery rates from 12% to more than 40%, regardless of the treatment administered. [43] A response to benzodiazepines has been reported in more than 70% of patients with catatonia who undergo treatment. Failure to institute treatment early in the course of catatonia is associated with a poor prognosis.

Bonnot et al reported that children with childhood schizophrenia and catatonia have more severe symptoms and a longer duration of illness than do children with childhood schizophrenia without catatonia. They concluded that catatonia has deleterious effects beyond mere motor symptoms in children with schizophrenia. [44]

Catatonia in adolescents also has a poor prognosis. In a prospective follow-up study of 35 people aged 12-18 years with catatonia, 20 of the 31 patients identified for follow-up had schizophrenia, 5 had major depression, 1 had bipolar disorder type 1, and 2 had brief psychiatric episodes. [45] At follow-up, 3 deaths were recorded, including 2 suicides. A causal organic disorder was identified for 6 at follow-up. At follow-up, 14 people needed continuous psychiatric care. [45]

In Monroe County, New York, the age-adjusted relative risk of death for people with catatonic schizophrenia was 3-fold greater that for the county population during the period 1960-1969. However, the risk of death was no higher than with other forms of schizophrenia or other types of mental illness. [40]

People with catatonia apparently are at increased risk for death from thromboembolic diseases. [46] Adults with catatonia and schizophrenia have a more prolonged course than those with catatonia without schizophrenia. [47]