Practice Essentials

Catatonia is a state of apparent unresponsiveness to external stimuli and apparent inability to move normally in a person who is apparently awake.[1] 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

Catatonia can be acute and occur in severely ill patients with underlying psychiatric or other medical disorders.[2, 3] Individuals with catatonia often cannot provide a coherent history; however, collateral sources are crucial sources of relevant historical information. Thorough review of old records is needed to figure out possible causes of the behaviors of people with catatonia. A history of behavioral responses to others usually includes the presence of the following:

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

The history should inquire into the following:

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

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

See Presentation for more detail.


Laboratory studies that may be useful include the following:

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

Electroencephalography (EEG) is indicated to rule out a seizure disorder, a space-occupying lesion, and generalized abnormalities.

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:

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 and apparent inability to move normally in a person who is apparently awake.[1] 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,[6] as analyzed by latent class techniques, have been divided into the following 4 classes[7] :

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[8] :

It can be difficult to differentiate catatonia from diffuse encephalopathy, nonconvulsive status epilepticus, neuroleptic malignant syndrome (NMS), acute psychosis, somatization disorder, conversion disorder,[9] 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 and anti-NMDA receptor encephalitis[4] ) 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[8] :

  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[8] :

Case report

Typical patients entering the child psychiatry clinic have markedly increased activity. Their parents often chase them while they are bouncing off the walls. By contrast, a tall youth with an immobile facies slowly descended the stairs to the clinic. Although he walked when instructed by his parents, the actions were careful and deliberate. His behavior was so unusual in this setting that factitious disorders were suggested. Was this adolescent deliberately feigning the markedly reduced pace of his movements? Another striking aspect of this patient was the presence of continuous grimacing. He repeatedly blinked his eyes and frowned his face.

On examination he was immobile. He did not speak; he demonstrated mutism. He exhibited negativism. There were no apparent responses to questions. His mother explained that he communicated with her through his eye blinks. However, there was no apparent communication from the patient to the examiner. When he was asked by the examiner to stand still and he was given a slight push forward by the examiner, he walked forward. He exhibited negativism.[10, 11, 12, 13]

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.

Comorbid psychiatric disorders

Deficits in fetal cortical development may result in schizophrenia and other developmental disorders.[14] These deficits, in turn, likely produce dysfunction in cortical and subcortical glutamatergic pathways, resulting in the symptoms and signs of catatonia.[15, 16]

Individuals with developmental disability, autism, or other developmental disabilities may be particularly vulnerable to developing catatonia.[17, 10, 11, 18, 19, 12, 13]

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.[20]

Catatonia may represent an outward manifestation of severe anxiety. Many patients with catatonia reported feeling extremely anxious before and during the catatonic episode.[21]

Dysfunction of neurotransmission

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.[22] 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.[23]

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. 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.[24] These regions modulate executive functions and the inhibition of voluntary acts.

Inherited influences

Genetic predisposition may characterize individuals who are vulnerable to developing catatonia. Genes on chromosomes 15 and 22 may be linked to the periodic form of catatonia.[25, 26]

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).[17, 10, 11, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39]

Table. Causes of Catatonia by Category

View Table

See Table

Neuroleptic malignant syndrome (NMS)

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.[27] 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.[40]

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.[41] 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[42] and Tanner and Chamberland[43] 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

In general, the incidence of catatonia is estimated to be 10%, ranging from 5%–20% of acute psychiatrically ill patients.[44, 2, 45]

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 mostly due to different methods of the studies and various definitions of catatonia.[46] In 1994, the incidence of catatonia among psychiatric inpatients in a university hospital in New York was 7%.[47] 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,[48] 13.5% in India,[49] 16.9% in Spain,[50] and 9.6% in Wales.[49] In a forensic psychiatric hospital in France, the prevalence of catatonia was 13.1%.[51] 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.[52]

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.[53]

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.[54] 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.[55] 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.[56]

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.[57]


Carroll noted that studies of catatonia have reported recovery rates from 12% to more than 40%, regardless of the treatment administered.[58] 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.[59]

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.[60] 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.[60]

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.[55]

People with catatonia apparently are at increased risk for death from thromboembolic diseases.[61] Adults with catatonia and schizophrenia have a more prolonged course than those with catatonia without schizophrenia.[62]


Catatonia is a syndrome—typically episodic, with periods of remission—characterized by the presence of a variety of behavioral and motoric traits. Accurate, prompt diagnosis of catatonia is crucial for preventing morbidity and death in a variety of settings (including emergency medical, psychiatric, neurologic, medical, obstetric, and surgical ones) and for instituting effective interventions.

Individuals with catatonia often cannot provide a coherent history; however, collateral sources can often relate relevant historical information. Family members can confirm the presence of typical primary features of catatonia, including immobility, stupor, posturing, rigidity, staring, grimacing, and withdrawal.

A history of behavioral responses to others usually includes the presence of the following:

A history of stereotypies, mannerisms, and verbigeration (uttering gibberish) is often elicited from people who are close to the patient. Priapism was reported in a 20-year-old man with paranoid schizophrenia and catatonia.[63]

The alternative presentation of catatonia is an excited state, possibly with impulsivity, combativeness, and autonomic instability. A history of an excited state should be sought from the family of a person with catatonia, but it is often denied by the family. When excited episodes are present, they are typically short-lived and may precipitate collapse with exhaustion. An excited state of catatonia is usually associated with bipolar disorder.

The history-taking process should include the following:

Catatonia has occurred in patients after treatment with levetiracetam[64] and levofloxacin.[65] Catatonia developed in a 55-year-old woman with schizophrenia who was treated with rimonabant, a cannabinoid receptor (CB1) antagonist.[66]

Emergency settings

In an emergency setting, treatable common causes of catatonia must be rapidly considered and ruled out. The emergency physician must quickly consider the presence of neuroleptic malignant syndrome (NMS),[27] encephalitis, including anti-NMDA receptor encephalitis,[4] nonconvulsive status epilepticus, and acute psychosis. Catatonia has occurred in intensive care units (ICUs).[67] Given that the patients all had serious disorders leading to ICU placement, it is possible that the underlying disorders contributed to the development of catatonia in the units.

A history of exposure to traditional and atypical neuroleptic agents must be sought. Although NMS often follows the initiation of neuroleptic therapy or an increase in the neuroleptic dosage, exposure to neuroleptics may be minimal in some susceptible individuals. For example, Nielsen and Nielsen report the occurrence of NMS after a single dose of neuroleptic medication.[40]

In addition, the patient’s history must be evaluated for the following conditions:

Physical Examination

Assessment of a person with possible catatonia should include unstructured, indirect observation, as well as a direct interview. Patients with catatonia exhibit the same general behaviors whether or not the examiner is present. If a patient demonstrates behaviors consistent with catatonia only in the presence of the examiner, then catatonia is unlikely.

Because patients with catatonia may be unable to cooperate with the requests of the examiner, specific neurologic signs characteristic of catatonia must be quickly elicited, especially in emergency settings. In particular, rigidity, gegenhalten (passive resistance of the patient to the active movement of the patient's extremities by the examiner[5] ), and a grasp reflex are readily apparent signs of catatonia in such settings. During the physical examination, it is also important to test for the presence of a grasp reflex, a secondary feature of catatonia.

Commonly observed signs in catatonia include the following:

Excited and immobile states

The predominant activity level is either markedly slow or extremely high, and the patient’s behavior may shift suddenly and unpredictably from one state to the other.

In the excited state, people with catatonia may injure themselves and assault others. They may also experience autonomic instability manifested by hyperthermia, tachycardia, and hypertension. Individuals in the excited state are at risk for collapse from exhaustion.

In the immobile state, the individual may not move. Akinesia and stupor are synonyms for this state. The patient may appear unresponsive to external stimuli. He or she may be unable to eat and therefore may die unless parenteral nutrition and fluids are administered. People with catatonia may exhibit catalepsy, the persistent maintenance of spontaneous or imposed postures.

Negativistic phenomena

Negativistic phenomena (eg, gegenhalten [“to hold against” in German; the apparent resistance of the movement of the extremities by the examiner], and mitgehen [“to go along with” in German; movement in the direction of a slight push from the examiner in spite of the command to remain still]) are typically observed in catatonia.

Examination should include checking for cogwheeling at the wrist and elbow. Patients should be instructed to keep their arms loose and limp (like a dead fish), and the arms should be moved with varying degrees of force. Rigidity is commonly elicited in the extremities of patients with catatonia.

The particular phenomenon of gegenhalten is characteristic. Patients with gegenhalten demonstrate increasing resistance to passive movement of the limbs. The patient appears to be deliberately opposing the movements of the examiner. Mitgehen is characterized by the patient moving in the direction of a slight push from the examiner in spite of the command to remain still. The physical examination should include tests for these.

Motor persistence (ie, maintenance of a posture when commanded not to maintain it) is a manifestation of catatonia that is associated with right hemispheric strokes. Other negativistic phenomena are withdrawal from all usual activities and refusal to eat.

Automatic obedience

In addition to negativistic phenomena, individuals with catatonia may display other behaviors, indicating inability to appropriately modulate the inhibition of impulses. For example, patients with catatonia may demonstrate automatic obedience, meaning the performance of tasks at the command of the examiner even though the tasks are inappropriate or dangerous.


Peculiarities of movement are common in catatonia. Stereotypies, in which the patient repetitively performs apparently meaningless activities, are common. These may take the form of repetitive actions or sounds. Verbigeration (verbal stereotypies) refers to the presence of repetitive, apparently meaningless utterances, such as sniffing, clicking, snorting, and nonmeaningful sounds.

Common motor stereotypies include the following:

Other movements associated with catatonia include mannerisms, postures, gaze fixation, and choreoathetoid movements of the trunk and extremities.


Patients with catatonia may also display preservation (ie, the inappropriate repetition of acts).


Echophenomena are typical in catatonia. Echolalia (repetition of the words spoken by the examiner) and echopraxia (repetition of the motor acts performed by the examiner) are common.

Verbal findings

In France, the inappropriately formal use of vous (the formal form of “you”) by the patient to address his or her spouse has been identified as a finding in catatonia. Normally, tu (the informal form of “you”) is used by an individual to address a spouse.

Comorbid conditions

Clinicians must identify comorbid disorders, including schizophrenia, mood disorders, and neurologic and medical conditions. Neuroleptic-induced parkinsonism may also be associated with catatonia. Headache, fever, and a stiff neck in an acutely ill patient suggest encephalitis. The presence of severe muscle rigidity, autonomic dysregulation, and hyperthermia suggests neuroleptic malignant syndrome (NMS). Acute psychosis is suggested by the presence of hallucinations, delusions, and suicidal and homicidal threats and behaviors.

Psychogenic movement disorders

Patients with catatonia exhibit the same general behaviors whether or not the examiner is present. If a patient demonstrates behaviors consistent with catatonia only in the presence of the examiner, then catatonia is unlikely, and conditions characterized by the presence of medical symptoms and signs without physical illness must be considered.

More specifically, catatonia that occurs only when the patient is directly observed by the examiner suggests the presence of somatoform disorders, factitious disorders, or malingering. In the movement disorders literature, somatoform disorders, factitious disorders, and malingering in patients exhibiting abnormal movements are commonly classified as psychogenic movement disorders.

Patients with somatoform disorders (eg, somatization disorder, conversion disorder, and hypochondriasis) report symptoms and signs that they truly believe they have, despite the absence of confirmation on physical examination. Patients with factitious disorders and malingering deliberately report symptoms and signs that they know to be false.

Patients with Munchausen syndrome and other factitious disorders fabricate symptoms and signs because they want to be patients. In Munchausen syndrome by proxy, the parents of the patient (who is typically an infant unable to communicate) fabricate symptoms and signs in the patient.

Unlike patients with factitious disorders, patients with malingering deliberately report false symptoms and signs for specific gain—for example, to obtain disability benefits and to be excused from work.


The following complications are associated with catatonia:

Approach Considerations

On the grounds that treatment of the underlying disorder relieves the catatonia, Lahutte et al recommended prompt diagnosis and therapy of the comorbid disorders to prevent morbidity and mortality.[81] This process includes appropriate use of laboratory tests, imaging modalities, and electroencephalography (EEG). EEG is performed to rule out underlying causes.[82] While an EEG often reveals focal abnormalities or generalized slowing, an EEG may be normal in catatonia.

Lorazepam challenge can also help the diagnosis of catatonia. Patients who respond to the first or two doses of IV lorazepam (1 to 2 mg) are likely to have catatonia. Partial or temporary relief of symptoms and signs of catatonia after 5 to 10 minutes of injection is consistent with catatonia.[83, 1]

An effort should be made to assess the degree of catatonia present. Of the several scales that have been developed to measure catatonia, the Bush-Francis Catatonia Rating Scale (BFCRF) is favored, owing to its demonstrated reliability and validity in clinical settings.[84, 85]

Laboratory Studies

A complete blood count (CBC), measurement of electrolyte concentrations, and chemical analyses of blood are appropriate. In particular, hyponatremia and other metabolic abnormalities must be ruled out.

Fibrin D-dimer levels must be obtained to rule out early coagulation activation.[61] Patients with catatonia typically have fibrin D-dimer levels higher than 500 ng/mL.[61] Prompt identification and treatment of pulmonary embolism in people with catatonia are crucial for minimizing morbidity and mortality.[86]

To rule out neuroleptic malignant syndrome (NMS), immediate evaluation of the serum creatine kinase level, white blood cell (WBC) counts, and liver function test results is warranted. Measurement of serum ceruloplasmin is needed to rule out Wilson disease. In addition, encephalitis must be ruled out.

Magnetic Resonance Imaging and Computed Tomography

Imaging of the head by means of magnetic resonance imaging (MRI) or computed tomography (CT) is indicated to rule out treatable mass lesions. If no evidence of increased intracranial pressure is noted on imaging, lumbar puncture is appropriate to rule out encephalitis and other infections, hemorrhages, and tumors.

People with catatonia may exhibit increased ventricle-to-brain ratios on CT scans. However, CT cannot be used to establish the diagnosis of catatonia. The main value of CT in patients with catatonia is to rule out other treatable disorders.

Single-photon emission CT (SPECT) has demonstrated increased cerebral blood flow in the parietal, temporal, and occipital regions of some patients with catatonia secondary to mood disorders after treatment with electroconvulsive treatment (ECT). However, SPECT cannot be used to establish the diagnosis of catatonia. The main value of SPECT in patients with catatonia, like that of CT, is to rule out other treatable disorders.

Positron Emission Tomography

Positron emission tomography (PET) with fluorodeoxyglucose (FDG) reveals bitemporal hypometabolism in catatonia. Patients with various vegetative states have demonstrated decrements in regional cerebral blood flow in the prefrontal and the parietotemporal association areas. However, PET cannot be used to establish the diagnosis of catatonia. The main value of PET in patients with catatonia is to rule out other treatable disorders.[10, 11]


EEG is indicated to rule out a seizure disorder. Nonconvulsive status epilepticus can readily be identified on EEG. Obtaining a portable EEG in the emergency department (ED) may quickly confirm the presence of nonconvulsive status epilepticus.

EEG changes in catatonia typically include focal abnormalities or generalized slowing.[4] However, a normal EEG may occur in a patients with the excited state of catatonia due to anti-NMDA receptor encephalitis.[4] Therefore, a normal EEG in a patient with catatonia does not rule out the presence of cerebral pathology.

During the psychotic episodes of periodic catatonia, alpha rhythm is characterized by an increase in frequency and a decrease in amplitude. In a patient with periodic catatonia, increased urinary excretion of 4-hydroxy-3-methoxy-mandelic acid (VMA) and of normetadrenaline correlated with increased frequences of alpha rhythm.[87, 88]

Other Tests

Transcranial magnetic stimulation (TMS) is a procedure under investigation for patients with catatonia.

Approach Considerations

Treatment modalities include pharmacotherapy and electroconvulsive treatment (ECT). Prompt treatment in the early phases of catatonic states is crucial to obtaining a lasting abatement of symptoms.

Treatable conditions must be identified immediately. Specifically, neuroleptic malignant syndrome (NMS), encephalitis, including anti-NMDA receptor encephalitis, nonconvulsive status epilepticus, and acute psychosis must be diagnosed and treated. The first 3 constitute neurologic emergencies that merit admission to a neurologic or medical intensive care unit (ICU); acute psychosis merits admission for intensive psychiatric inpatient evaluation and treatment.

Refusal to eat necessitates the institution of parenteral nutrition. Supervised activity is indicated. Prompt intervention may be needed to prevent collapse from exhaustion.

The need to administer parenteral nutrition and fluids and to monitor vital signs may require a patient to be transferred from a psychiatric unit to a neurologic or medical unit. If the patient poses a risk of injury to himself or herself or to staff members, then the use of a 1-on-1 psychiatric attendant at all times is indicated.

Regular outpatient follow-up visits are advisable to check for the recurrence of catatonia. In some patients, catatonia remits only in response to ECT. Some patients may require weekly ECT on an outpatient basis.

Pharmacologic Therapy

The following medications have been used in the treatment of patients suffering from catatonia[89] :

Because of the possible development of NMS, the use of traditional neuroleptics is avoided; second-generation (atypical) antipsychotics may be helpful in some cases but should still be used with caution.[90, 91] Because catatonia was reported in a 47-year-old woman treated with levofloxacin, prudent clinicians exercise caution when treating patients with fluoroquinolones.[65]

In particular, successful treatment of catatonia has been reported with carbamazepine,[92] clonazepam,[92] olanzapine,[93] and dantrolene,[89] as well as for lorazepam and diazepam.[94, 95] Cyclooxygenase (COX) inhibitors have been reported to protect against the development of perphenazine-induced catatonia in rats.[96]

Krivoy et al recommended the addition of benzodiazepines to antipsychotics in the treatment of catatonia.[97] Lorazepam has been reported to reduce the serum levels of brain-derived neurotrophic factor and to ameliorate the symptoms and signs of catatonia in patients with schizophrenia.[98] A 38-year-old woman with idiopathic catatonia required maintenance treatment with 6 mg lorazepam orally daily.[99]

If a patient fully recovers from catatonia, the gradual reduction and discontinuance of medications, one drug at a time, is reasonable. A return of symptoms and signs of catatonia may necessitate maintenance of pharmacologic interventions.

Electroconvulsive Treatment

When nonconvulsive status epilepticus, diffuse encephalopathy, and other neurologic disorders are ruled out, ECT is indicated for patients who do not respond to pharmacotherapy within 5 days or who manifest malignant catatonia. ECT is effective for many patients with catatonia,[100, 101, 89] including those with catatonia secondary to mood disorders, autistic disorder,[102] or another pervasive developmental disorder.[32, 33] Efficacy may be hindered by coexisting alcohol or drug abuse.[103]

ECT is beneficial for adolescents with catatonic schizophrenia.[104, 89] Slooter et al reported improvement in an adolescent with malignant catatonia (apparently due to viral encephalitis) after ECT.[105] One study found right unilateral ultrabrief ECT to be an effective treatment for catatonia in adolescents and adults.[106]

Indications for Hospitalization and ICU Admission

Because of the risk of serious complications of catatonia, admission to an ICU is the treatment of choice for a patient with this condition. Although placement in an ICU may itself precipitate the development of catatonia,[67] an ICU is nevertheless the appropriate location for monitoring a patient with catatonia until the symptoms have improved sufficiently to allow transfer to a less restrictive setting.

The onset of catatonia merits hospitalization to accomplish the workup and provide intervention for assaultiveness; refusal to eat necessitates parenteral nutrition. Vitamin K deficiency may result from inadequate nutrition.[107] Vitamin K deficiency must be identified and treated in people with catatonia.[107] Autonomic instability requires intravenous (IV) administration of fluids and monitoring of vital signs.

Because catatonia is often periodic, a patient who has recovered from one episode of catatonia is at risk for further episodes. A recurrence of catatonia is an indication for hospitalization to perform a diagnostic workup and initiate therapeutic interventions.


Medical consultation is recommended to rule out treatable medical disorders. The following consultations may be required:


Moving an immobile patients from side to side, mattresses with air cushions, and vigilant nursing care may prevent development of pressure ulcers.


A regular diet may be adminstered as tolerated. Patients may require assistance with feeding. Refusal to consume food may require the utilization of a nasogastric tube to feed the patient.


Physical therapy, occupational therapy, and speech pathology may facilitate the development of appropriate actions.

Since excitement may lead to collapse from exhaustion, measures may be required to sedate an agitated patient.


Avoid the administration of agents known to precipitate the development of catatonia in individuals.

Medication Summary

Medications that may be used in the treatment of patients suffering from catatonia include benzodiazepines, carbamazepine, zolpidem, tricyclic antidepressants (TCAs), muscle relaxants, amobarbital, reserpine, thyroid hormone, lithium carbonate, bromocriptine, and neuroleptics.[108]

Because neuroleptic malignant syndrome (NMS) may occur in patients with symptoms and signs of catatonia, prudent clinicians use neuroleptics, including atypical neuroleptics, with caution. Although success has been reported in cases of catatonia treated with a combination of lithium and a neuroleptic, the risk of adverse effects must be considered when this combination is given, even if an atypical neuroleptic is used.

Lorazepam (Ativan)

Clinical Context:  Lorazepam is a sedative hypnotic with a short onset of effects and a relatively long half-life. By increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, it may depress all levels of the central nervous system (CNS), including the limbic and reticular formations. After a lorazepam dose is administered, the patient's blood pressure should be monitored. The dose is adjusted as necessary.

Clonazepam (Klonopin)

Clinical Context:  Clonazepam is a long-acting benzodiazepine that increases presynaptic GABA inhibition and reduces the monosynaptic and polysynaptic reflexes. It suppresses muscle contractions by facilitating inhibitory GABA neurotransmission and the action of other inhibitory transmitters.


Clinical Context:  Midazolam is an alternative for the termination of refractory status epilepticus. Because it is water-soluble, it takes approximately 3 times longer than diazepam to reach peak electroencephalographic (EEG) effects. Therefore, the clinician must wait 2-3 minutes to evaluate midazolam's sedative effects fully. Midazolam has twice the affinity for benzodiazepine receptors that diazepam does. It may be administered intramuscularly (IM) if intravenous (IV) access cannot be obtained.

Class Summary

By binding to specific receptor sites, benzodiazepines appear to potentiate the effects of gamma-aminobutyric acid (GABA) and facilitate inhibitory GABA neurotransmission and the action of other inhibitory transmitters.

Carbamazepine (Tegretol, Carbatrol, Epitol, Equetro)

Clinical Context:  Carbamazepine's mechanism of action may include modulation of voltage-dependent sodium channels.

Valproic acid (Depakote, Depakote ER)

Clinical Context:  Valproic acid may be helpful by increasing activity at GABA or modest antiglutaminergic effects.

Class Summary

The use of certain anticonvulsants has proven helpful in some cases of catatonia.

Amobarbital (Amytal)

Clinical Context:  Amobarbital is a sedative hypnotic with anticonvulsant properties that interfere with the transmission of impulses from the thalamus to the cortex.

Class Summary

The use of certain anticonvulsants has proven helpful in some cases of catatonia.

Zolpidem (Ambien, Edluar, ZolpiMist)

Clinical Context:  Zolpidem increases neural hyperpolarization by enhancing the activity of the inhibitory neurotransmitter GABA through selective agonist activity at the benzodiazepine-1 receptor.

Class Summary

The use of certain nonbenzodiazepine anxiolytics has been shown to be helpful in some cases of catatonia.

Dantrolene (Dantrium, Revonto, Ryanodex)

Clinical Context:  Dantrolene acts directly on skeletal muscle by interfering with the release of calcium ions from the sarcoplasmic reticulum.

Class Summary

The use of certain skeletal muscle relaxants has been shown to be helpful in some cases of catatonia.


Clinical Context:  Reserpine depletes norepinephrine and dopamine, and this depletion may result in reduced blood pressure and sedative effects.

Class Summary

The use of central monoamine-depleting agents has been shown in case reports to be helpful in some cases of catatonia.

Thyroid, Desiccated (Armour Thyroid, Nature Throid, Westhroid)

Clinical Context:  Thyroid hormone is involved in normal metabolism, gluconeogenesis, utilization and mobilization of glycogen, and stimulation of protein synthesis.

Class Summary

The use of thyroid products has been shown in case reports to be helpful in some cases of catatonia.

Lithium carbonate (Lithobid)

Clinical Context:  A case report has described successful lithium treatment in a patient with long-standing periodic catatonia. Although success has been reported in cases of catatonia treated with a combination of lithium and a neuroleptic, the risk of adverse effects must be considered when this combination is given, even if the neuroleptic is an atypical one.

Class Summary

The use of antipsychotic products has been shown in case reports to be helpful in some cases of catatonia.

Olanzapine (Zyprexa)

Clinical Context:  The effects of olanzapine are mediated through combined antagonism of dopamine and serotonin type 2 receptor sites.

Clozapine (Clozaril, FazaClo)

Clinical Context:  Clozapine has been reported to improve catatonia in psychosis, perhaps via a greater pass-though of dopamine to the D2 receptor.

Class Summary

The use of second-generation antipsychotic products has been shown in case reports to be helpful in some cases of catatonia.

Bromocriptine (Parlodel, Cycloset)

Clinical Context:  Bromocriptine activates postsynaptic dopamine receptors in the tuberoinfundibular and nigrostriatal pathways. A case report on a patient with catatonia described successful treatment with bromocriptine.

Class Summary

The use of ergot derivatives has been shown in case reports to be helpful in some cases of catatonia.

Amitriptyline hydrochloride

Clinical Context:  Amitriptyline is an analgesic indicated for certain chronic and neuropathic pain.

Clomipramine (Anafranil)

Clinical Context:  Clomipramine is a dibenzazepine compound belonging to the TCA family. It inhibits the membrane pump mechanism responsible for the uptake of norepinephrine and serotonin in adrenergic and serotonergic neurons. Clomipramine affects serotonin uptake and affects norepinephrine uptake when converted into its metabolite, desmethylclomipramine. These actions are believed to be responsible for clomipramine's antidepressant activity.


Clinical Context:  Doxepin increases the concentration of serotonin and norepinephrine in the CNS by inhibiting their reuptake by the presynaptic neuronal membrane. It inhibits histamine and acetylcholine activity and has proved useful in treatment of various forms of depression associated with chronic pain.

Nortriptyline (Pamelor)

Clinical Context:  Nortriptyline has demonstrated effectiveness in the treatment of chronic pain.

Desipramine (Norpramin)

Clinical Context:  Desipramine is the original TCA used for depression. It and similar agents appear to act by inhibiting reuptake of noradrenaline at synapses in central descending pain-modulating pathways located in the brainstem and spinal cord.

Class Summary

The use of TCAs has been shown in case reports to be helpful in some cases of catatonia.


James Robert Brasic, MD, MPH, Assistant Professor, Russell H Morgan Department of Radiology and Radiological Science, Division of Nuclear Medicine, Johns Hopkins University School of Medicine; Active Staff, Department of Radiology and Radiological Science, Division of Nuclear Medicine, Johns Hopkins Hospital; Courtesy Staff, Department of Radiology, Johns Hopkins Bayview Medical Center

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Johns Hopkins University School of Medicine<br/>Received research grant from: National Institutes of Health<br/>Received income in an amount equal to or greater than $250 from: Brand Institute, Inc.<br/>Received royalty from Medscape for other; Received royalty from Neuroscience-Net, LLC for other; Received grant/research funds from National Institutes of Health for other.


Farzaneh Farhadi, MD,

Disclosure: Nothing to disclose.

Chief Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida Morsani College of Medicine

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Acorda, Cyberonics, Eisai, Lundbeck, Sunovion, UCB, Upsher-Smith<br/>Serve(d) as a speaker or a member of a speakers bureau for: Cyberonics (Livanova), Eisai, Lundbeck, Neuropace, Sunovion, UCB<br/>Received research grant from: Acorda, Cyberonics, GW, Lundbeck, Sepracor, Sunovion, UCB, Upsher-Smith.


Nestor Galvez-Jimenez, MD, MSc, MHA Chairman, Department of Neurology, Program Director, Movement Disorders, Department of Neurology, Division of Medicine, Cleveland Clinic Florida

Nestor Galvez-Jimenez, MD, MSc, MHA is a member of the following medical societies: American Academy of Neurology, American College of Physicians, and Movement Disorders Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment


The research for this article was supported by the Essel Foundation; the National Alliance for Research on Schizophrenia and Depression (NARSAD); the Tourette Syndrome Association, Inc; the National Institutes of Health; and the Department of Psychiatry of Bellevue Hospital Center and the New York University School of Medicine, New York, New York. The cooperation of the Health and Hospitals Corporation of the City of New York is gratefully acknowledged.


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Category Causes
Neurologic conditionsNeuroleptic malignant syndrome[27]

Administration of agents that block postsynaptic dopamine receptors*

Administration of sibutramine[28] (withdrawn from US market October 8, 2010)

Withdrawal of lorazepam and other sedatives

Akinetic-rigid syndrome

Anti-NMDA receptor encephalitis[4]

Arachnoid cyst in right parietal region


Atrophy of left amygdala[29]

Autistic disorder[17, 10, 11, 30, 31, 32, 33, 34, 35, 12, 13]

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[36]

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[37, 38]


Nonconvulsive status epilepticus

Pervasive developmental disorders[10, 11, 34]

Pallidoluysian atrophy

Paraneoplastic encephalitis[39]


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 conditionsAcute stress disorder

Anorexia nervosa

Autistic disorder[17]

Brief reactive psychosis with catatonia

Conversion disorder


Major depression, single episode with catatonic features

Mood disorders

Neuroleptic malignant syndrome[27]

Posttraumatic stress disorder


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

Psychological factorsImmigration

Experiencing rejection of an expression of love

Feelings of alienation in an unfamiliar country

Medical conditionsAIDS

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[27]

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