AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Background

Catatonia is not a diagnosis. Rather, catatonia is a descriptive term for a presentation observed in a wide variety of disorders. While there exists a vast differential diagnosis for catatonia, the identification of treatable causes, such as non-convulsive status epilepticus, is crucial to the administration of the needed interventions. When faced with a patient with catatonia, the clinician must first rule out treatable causes.

Catatonia (1) is a state of apparent unresponsiveness to external stimuli in a person who is apparently awake and (2) is difficult to differentiate from diffuse encephalopathy and nonconvulsive status epilepticus (see Epileptic and Epileptiform Encephalopathies and Focal Status Epilepticus).

This syndrome 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. Typically, the syndrome of catatonia is episodic, with periods of remission. The accurate prompt diagnosis of catatonia is crucial to prevent morbidity and death in a variety of emergency medicine, psychiatric, neurologic, medical, obstetric, and surgical settings and to institute effective interventions, including benzodiazepines (eg, clonazepam, lorazepam, midazolam), zolpidem, atypical neuroleptics, tricyclic antidepressants, muscle relaxants, amobarbital, reserpine, thyroid hormone, lithium carbonate, bromocriptine, and electroconvulsive treatments (ECT).

Catatonia likely has a similar pathophysiology as the neuroleptic malignant syndrome, ie, elevated temperature, rigidity, delirium, and dysregulation of the autonomic nervous system that occurs after exposure to antipsychotic medications, including typical and atypical antipsychotic medications. Although apparently uncommon, the neuroleptic malignant syndrome has been reported in up to 12.2% of people exposed to neuroleptic medication. Nielsen and Nielsen report the occurrence of the neuroleptic malignant syndrome after a single dose of neuroleptic medication.¹

Individuals with mental retardation, autism, other pervasive developmental disorders, or other developmental disabilities may be particularly vulnerable to developing catatonia.

Catatonia apparently has affected some well-known individuals, including Vaslav Nijinsky, the dancer and choreographer.²

Pathophysiology

Catatonia likely represents a heterogeneous group of etiologies. Some hypotheses have been proposed about the pathophysiology of catatonia.

• Deficits in fetal cortical development: Deficits in fetal cortical development may result in schizophrenia and other developmental disorders. These deficits in turn likely produce dysfunction in cortical and subcortical glutamatergic pathways, resulting in the symptoms and signs of catatonia.
• Imbalances in the excitatory:inhibitory ratio (EIR) model: Baguley proposes that alterations in interrelated networks at the spinal and brainstem level produce catatonia.³
• Dopaminergic blockade
• • 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, suggesting that these agents may be effective pharmacologic interventions. Additionally, the effectiveness of ECT for catatonia suggests that dopaminergic modulation may play a role in the development and amelioration of catatonia.
• Glutamatergic dysfunction
• • 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.⁴ Potentiation of the action of GABA by benzodiazepines suggests that some individuals with catatonia may have a functional deficit of GABA.
• Dysfunction in neurotransmission of noradrenaline and serotonin
  • In inbred rats with catalepsy, Alekhina and colleagues (1993) 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 reports that administration of a nonspecific inhibitor of nitric oxide synthase, NG-nitro-L-arginine methyl ester (L-NAME), to ethanol-dependent rats being withdrawn from ethanol precipitates catatonia.⁵ 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.
• Frontal anomalies: Kahlbaum noted lesions of the Sylvian fossa and the second and third frontal gyri on autopsy of his patients who died with catatonia.⁶ These regions modulate executive functions and the inhibition of voluntary acts.

Frequency

United States

The current frequency of catatonia in the United States is unknown. A few studies have noted a decrease in the frequency of catatonia in parts of the United States over the past century. A variety of biases may influence the results of the few epidemiological studies of catatonia.

In Iowa, a decrease in the prevalence of catatonia was reported from 1920-1966.⁷

In Monroe County, New York, the prevalence of catatonic schizophrenia was close to 1 per 1000 residents during the period 1960-1969.⁸

In a university hospital in New York in 1994, the incidence of catatonia was 7% of psychiatric inpatients.⁹ The study was performed at a tertiary care referral hospital known for the treatment of catatonia, so the population is likely not representative of the general population.

Recent anecdotal reports suggest that the prevalence of catatonia is decreasing in the United States.

International

The current frequency of catatonia in international populations is unknown. The few epidemiological studies report vastly different rates. These suggest that the occurrence of catatonia may differ greatly from one location to another. On the other hand, studies suggest that many cases of catatonia may be undiagnosed. Thus, results may be confounded by an ascertainment bias.

The prevalence of catatonia among inpatients of psychiatric hospitals is 11.4% in Colombia¹⁰, 13.5% in India¹¹, and 16.9% in Spain¹², and 9.6% in Wales¹¹. In a forensic psychiatric hospital in France, the prevalence of catatonia was 13.1%.¹³ In Colombia, treatment apparently is not administered to many patients with catatonia until they have reached an advanced stage of the condition.

Benegal and colleagues report that catatonia appears to be more common in India than in Europe and North America.¹⁴

In contrast to those in Colombia, India, and Spain, studies in several other locations suggest 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.¹⁵ In a psychiatric clinic in Chile, a decrement in the proportion of patients with schizophrenia who manifest catatonia was observed from 1964-1984. In Finland, the percentage of patients with schizophrenia displaying catatonia decreased from 37% in 1933-1935 to 11% in 1953-1955.¹⁶ In Canada, catatonia was present in 10% of inpatient psychiatric admissions in 1993 (Rosebush and Gaind, 1993).

Mortality/Morbidity

In Monroe County, New York, the age-adjusted relative risk of death for people with catatonic schizophrenia was thrice that of the county population during the period 1960-1969. However, the risk of death was no higher than for other forms of schizophrenia or other types of mental illness.⁸

Race

The frequency of catatonia in specific races is unknown. Ungvari and colleagues note the need to investigate the role of ethnic, cultural, and social influences on the development of catatonia.¹⁷

Sex

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 1960-1969.⁸ In 1972-1973, a female-to-male ratio of 1.3:1 was observed among inpatients with catatonia admitted to two psychiatric units of a municipal hospital in New York City.¹⁸

Age

Although rare in children, catatonia has been reported in adolescents and adults.

CLINICAL

Section 3 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

History

Catatonia is a syndrome characterized by the presence of a variety of behavioral and motoric traits. While individuals with catatonia often cannot provide a coherent history, collateral sources of information 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 mutism, negativism, echopraxia, echolalia, waxy flexibility, and withdrawal. A history of stereotypies, mannerisms, and verbigeration is often elicited from people who are close to the patient.

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

During the initial interview of the patient and the family, elicit a history of possible precipitating events, including infection, trauma, and exposure to toxins and other substances.

• 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, encephalitis, nonconvulsive status epilepticus, and acute psychosis.
• • A history of exposure to traditional and atypical neuroleptics must be sought. While malignant neuroleptic syndrome often follows the initiation of neuroleptic therapy or an increase in neuroleptic dose, the exposure to neuroleptics may be minimal in some susceptible individuals. For example, Nielsen and Nielsen report the occurrence of the neuroleptic malignant syndrome after a single dose of neuroleptic medication.¹
  • A history of encephalitis should be sought. Determine whether the patients has had sudden onset of headache, fever, and deterioration in mental functioning.
  • Nonconvulsive status epilepticus must be ruled out (see Epileptic and Epileptiform Encephalopathies and Focal Status Epilepticus). Determine whether the patient has a history of seizures. Determine whether the patient has been prescribed antiepileptic drugs. Determine whether electroencephalograms (EEGs) have been performed and, if so, review the findings. (See Medscape's Epilepsy Resource Center for more information.)
  • Acute psychosis must be ruled out (see Schizophrenia and Alcohol-Related Psychosis). Determine whether the patient has exhibited evidence of delusions and hallucinations. Determine whether the patient has exhibited suicidal or homicidal threats or actions. Record any history of prior psychiatric hospitalization and treatment.
• A history of similar episodes is important to elicit. Determine whether the precipitating events of the earlier episode are present in the current episode. Record any interventions that relieved catatonia previously.
• Catatonia and the related condition, neuroleptic malignant syndrome, may follow the administration of neuroleptic medications. Question the patient and family to elicit a history of exposure to neuroleptics and the other substances associated with catatonia (see Differentials and Causes).
• Clinicians must identify comorbid disorders (see Differentials), including schizophrenia, mood disorders, psychological stressors, medical conditions, and obstetrical conditions.
• Chouinard and colleagues have reported the development of catatonia after treatment with levetiracetam.¹⁹

Physical

Assessment of a person with possible catatonia should include an unstructured observation of the person indirectly 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. Instead, conditions characterized by the presence of medical symptoms and signs without physical illness must be considered. Therefore, 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 exhibiting abnormal movements are commonly classified "psychogenic movement disorders."

Patients with somatoform disorders, such as somatization disorder, conversion disorder, and hypochondriasis, report symptoms and signs that they truly believe 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, typically an infant unable to communicate, fabricates symptoms and signs in the patient. Unlike patients with factitious disorders, patients with malingering deliberately report false symptoms and signs for specific gain, eg, to obtain disability benefits and to be excused from work.

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, particularly in emergency settings. In particular, rigidity, gegenhalten, and a grasp reflex are readily apparent signs of catatonia in an emergency setting.

Examination should include checking for cogwheeling at the wrist and elbow. Instruct patients to keep their arms loose and limp (like a dead fish) and move the arms of the patients with varying degrees of force. Rigidity is commonly elicited in the extremities of patients with catatonia. The particular phenomenon of gegenhalten is characteristic in catatonia. Patients with gegenhalten demonstrate increasing resistance to passive movement of the limbs. The patient appears to be deliberately opposing the movements of the examiner.

Test for the presence of a grasp reflex, a secondary feature of catatonia.

• Diagnostic criteria for catatonia include "motoric immobility, excessive motor activity, extreme negativism or mutism, peculiarities of voluntary movement, and echolalia or echopraxia."²⁰ Two of the items are required to diagnose catatonia in schizophrenia and mood disorder. Only one item is required to diagnose catatonia in general medical conditions.
• The predominant activity level of the individual is either markedly slow or extremely high. The behavior of the patients 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 of 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 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 are observed typically in catatonia. These include gegenhalten and mitgehen. Gegenhalten is when the patient resists movement of his or her extremities by the examiner. Mitgehen is when the patient moves 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, the maintenance of a posture when commanded to not maintain the posture, 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.
• 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, 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, repetitive performing of apparently meaningless activities, are common. These may take the form of repetitive actions or sounds. Verbigeration refers to the presence of repetitive apparently meaningless utterances.
• • Common motor stereotypies include 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. Other movements associated with catatonia include mannerisms, postures, gaze fixation, and choreoathetoid movements of the trunk and extremities.
  • Verbigeration, or verbal stereotypies, include sniffing, clicking, snorting, and nonmeaningful sounds.
  • Patients with catatonia may also display preservation, the inappropriate repetition of acts.
• Echophenomena are typical in catatonia. Echolalia, the repetition of the words spoken by the examiner, and echopraxia, the repetition of the motor acts performed by the examiner, are common.
• In France, the inappropriately formal use of vous [ie, the formal form of "you"] to address the patient's spouse has been identified as a finding in catatonia.
• Peralta and Cuesta hypothesized that a sufficient condition to diagnose catatonia is the presence of 3 of the classic motor signs of catatonia as follows: immobility/stupor, mutism, negativism, oppositionism, posturing, catalepsy, automatic obedience, echophenomena, rigidity, verbigeration, and withdrawal.²¹
• Clinicians must identify comorbid disorders including schizophrenia, mood disorders, and neurological and medical conditions (see Causes).
• Neuroleptic-induced parkinsonism may also be associated with catatonia.
• The presence of severe muscle rigidity, autonomic dysregulation, and hyperthermia suggests the possibility of a neuroleptic malignant syndrome.
• Headache, fever, and a stiff neck in an acutely ill patient suggest the presence of encephalitis. See Encephalitis for further information about the physical examination of patients with encephalitis.
• Acute psychosis is suggested by the presence of hallucinations, delusions, and suicidal and homicidal threats and behaviors.

Causes

To facilitate assessment of the cause of catatonia, associated conditions are categorized as neurological, psychiatric, psychological, medical, and obstetrical.

Causes of Catatonia by Category

*See Neuroleptic Malignant Syndrome, Neuroleptic Malignant Syndrome, and Neuroleptic Malignant Syndrome.

† The administration of agents that block postsynaptic dopamine receptors is associated with the onset of catatonia in some individuals.

‡See Encephalitis.

§See Epileptic and Epileptiform Encephalopathies and Focal Status Epilepticus.

• Neuroleptic malignant syndrome: Neuroleptic malignant syndrome is characterized by introduction or increased dose of a neuroleptic medication, a temperature greater than 38 degrees centigrade, and heart rate greater than 100 beats per minute or diastolic blood pressure greater than 100 mm Hg. The triad of fever, tachycardia, and rigidity is typical of the syndrome, which is associated with death in about one fifth of cases.
• Latah betul or "real latah" or "true latah" is a phenomenon present in Malaysia characterized by the apparent loss of control over behavior and by echolalia, echopraxia, and automatic obedience.
• • Winzeler surveyed ethnic groups in different regions of Malaysia to present demographic and epidemiologic data about the condition. None of the individuals under 10 years of age exhibited latah in any of the groups examined. Latah was much more common in women. Mature women were the most common group to exhibit latah. People who developed latah exhibited it for the rest of their lives. People who developed latah in Malaysia often associated the onset with frightening experiences, both in life and in dreams, and with sorcery.²⁴ Simons²⁵ and Tanner and Chamberland²⁶ have published videotapes of individuals with latah to facilitate its recognition by individuals of 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 have a vulnerability to develop the condition. This is reminiscent of other neuropsychiatric disorders with a genetic basis. The histories of persons with latah betul suggest that extreme stress may precipitate the onset of the disorder in some individuals. 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 categorize 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.

DIFFERENTIALS

Section 4 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Other Problems to be Considered

Acute stress disorder
Astrocytoma
Autistic disorder
Brief reactive psychosis with catatonia
Carotid disease and stroke
Central pontine myelinolysis
Conversion disorder
Cortical basal ganglionic degeneration
Dystonia
Encephalopathy - HIV infection
Extrapontine myelinolysis
Fibromuscular dysplasia with dissection of basilar artery
Inherited neurometabolic disorders
Latah betul
Major depression, single episode with catatonic features
Medication adverse effect - Levetiracetam, zotepine
Mood disorders
Neuroleptic malignant syndrome
Posttraumatic stress disorder
Progressive multifocal leukoencephalopathy
Progressive supranuclear palsy
Renal failure
Schizophrenia
Stroke
Stupor
Substance intoxication - Cyclosporine, phencyclidine
Subdural hematoma
Syphilis
Systemic lupus erythematosus
Tay-Sachs disease
Thermal injury
Tuberculosis
Vegetative states
Von Economo encephalitis

WORKUP

Section 5 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Lab Studies

• Complete blood counts, electrolytes, and chemical analyses of blood are appropriate. In particular, hyponatremia and other metabolic abnormalities must be ruled out.
• Because elevations of serum creatine kinase, white blood cell counts, and liver function test results are common laboratory manifestations of catatonia, immediately measuring serum creatine kinase, white blood cell count, and liver function tests is appropriate to rule out neuroleptic malignant syndrome.
• Serum ceruloplasmin is needed to rule out Wilson disease.
• Encephalitis must be ruled out. See Encephalitis for additional information about the laboratory studies for encephalitis.

Imaging Studies

• Imaging of the head by means of MRI or CT is indicated to rule out treatable mass lesions. If no evidence of increased intracranial pressure is noted, 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 scan. However, CT scans cannot be used to establish the diagnosis of catatonia. The main value of CT scans in patients with catatonia is to rule out other treatable disorders.
• Single-photon emission computed tomography (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 ECT. However, SPECT scans cannot be used to establish the diagnosis of catatonia. The main value of SPECT scans in patients with catatonia is to rule out other treatable disorders.
• 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 scans cannot be used to establish the diagnosis of catatonia. The main value of PET scans in patients with catatonia is to rule out other treatable disorders.

Other Tests

• 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 may quickly confirm the presence of nonconvulsive status epilepticus. For further information on nonconvulsive status epilepticus, see Epileptic and Epileptiform Encephalopathies and Focal Status Epilepticus.

TREATMENT

Section 6 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Medical Care

Prompt treatment in the early phases of catatonic states is crucial to obtain a lasting abatement of symptoms.

Treatable conditions must be identified immediately. Specifically, neuroleptic malignant syndrome, encephalitis, nonconvulsive status epilepticus, and acute psychosis must be diagnosed and treated.

Neuroleptic malignant syndrome, encephalitis, and nonconvulsive status epilepticus constitute neurologic emergencies that merit admission to a neurological or medical intensive care unit. Acute psychosis merits admission for intensive psychiatric inpatient evaluation and treatment.

• Because of the possible development of neuroleptic malignant syndrome, the use of traditional neuroleptics is avoided.
• Successful treatment of catatonia has been reported with several medications, including dantrolene.
• When nonconvulsive status epilepticus, diffuse encephalopathy, and other neurological disorders are ruled out, ECT is indicated for patients who do not respond to pharmacotherapy in 5 days or who manifest malignant catatonia. ECT is effective for many patients with catatonia, especially those with catatonia secondary to mood disorders. Slooter and colleagues have reported the improvement of an adolescent with malignant catatonia apparently due to viral encephalitis treated with ECT.²⁷
• The onset of catatonia merits hospitalization to accomplish the workup and to provide intervention for assaultiveness. Refusal to eat requires parenteral nutrition. Autonomic instability requires intravenous fluids and monitoring of vital signs.

Consultations

• Medical consultation is recommended to rule out treatable medical disorders.
• Consultation with a neurologist is recommended to rule out treatable neurological conditions. Specifically, neuroleptic malignant syndrome, encephalitis, and focal status epilepticus must be ruled out.
• For information about locating a neurologist, please contact the American Academy of Neurology as follows:

  American Academy of Neurology
  1080 Montreal Avenue
  Saint Paul, Minnesota 55116
  Telephone: (651) 695-1940
  Facsimile: (651) 695-2791

• Consultation with a psychiatrist is indicated to rule out acute psychosis.
• Consultation with a movement disorders specialist may help to clarify the diagnosis and treatment. For information about locating movement disorder experts, please contact The Movement Disorder Society as follows:
• The Movement Disorder Society
  611 East Wells Street
  Milwaukee, Wisconsin 53202
  United States of America
  Telephone: (414) 276-2145
  Facsimile: (414) 276-3349

Diet

Refusal to eat requires parenteral nutrition.

Activity

Supervised activity is indicated. Prompt intervention may be needed to prevent collapse from exhaustion.

MEDICATION

Section 7 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

The goals of pharmacotherapy for catatonia are to reduce morbidity and prevent complications.

Drug Category: Benzodiazepines

By binding to specific receptor sites, these agents appear to potentiate the effects of GABA and facilitate inhibitory GABA neurotransmission and other inhibitory transmitters. Krivoy and colleagues recommend the addition of benzodiazepines to antipsychotics in the treatment of catatonia.¹²⁷

Drug Category: Antiepileptic drugs

Use of certain antiepileptic drugs has proven helpful in some cases of catatonia.

FOLLOW-UP

Section 8 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Further Inpatient Care

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

Further Outpatient Care

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 may require weekly ECT on an outpatient basis.

In/Out Patient Meds

If a patient fully recovers from catatonia, the gradual reduction and discontinuation of medications, one by one, is reasonable. Return of symptoms and signs of catatonia may necessitate maintenance of pharmacologic interventions.

Transfer

The need to administer parenteral nutrition and fluids and to monitor vital signs may require transfer of a patient from a psychiatric unit to a neurologic or medical unit. If the patient poses a risk of injury to self or staff, then a one-on-one psychiatric attendant at all times is indicated.

Complications

• During an excited state, patients with catatonia may cause serious, even fatal, injuries to self and others. They may cause marked destruction of property.
• Patients with catatonia may refuse to eat. Death may result unless parenteral nutrition and fluids are administered on an involuntary basis.
• Patients with catatonia may experience autonomic instability manifested by hyperthermia, hypertension, and tachycardia. Medical intervention is required.
• Neuroleptic malignant syndrome may occur in catatonia. In these cases, medical consultation is appropriate.
• Risk of fatal pulmonary embolism is increased in catatonia.
• Patients with catatonia are at risk of complications from the underlying neurological, psychiatric, medical, and obstetrical causes of catatonia (see Causes).

Prognosis

• Carroll noted that studies of catatonia have reported recovery rates from 12% to more than 40% regardless of the treatment administered.²⁸ 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 the condition is associated with a poor prognosis.
• Bonnot and colleagues reported that children with childhood schizophrenia and catatonia have more severe symptoms and a longer duration of illness then children with childhood schizophrenia without catatonia. They conclude that catatonia has deleterious effects beyond mere motor symptoms in children with schizophrenia.²⁹

MISCELLANEOUS

Section 9 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Medical/Legal Pitfalls

• Because neuroleptic malignant syndrome may occur in patients with symptoms and signs of catatonia, prudent clinicians avoid the use of neuroleptics if possible. Although success has been reported in cases of catatonia treated with a combination of lithium and a neuroleptic, the risk of adverse effects probably outweighs the chance of benefits.
• Generally, the onset of catatonia merits hospitalization, on an involuntary basis if necessary, for the diagnostic workup and initiation of treatment.
• Since treatment of the underlying disorder relieves the catatonia, Lahutte and colleagues recommend the prompt diagnosis and therapy of the comorbid disorders to avoid morbidity and mortality.³⁰

ACKNOWLEDGMENTS

Section 10 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

This research for this article is 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.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Media file 1:  Catatonia. PowerPoint presentation by James Robert Brasic, MD, MPH.
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Media type:  Presentation

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

1. Nielsen N, Nielsen NB. [Malignant neuroleptic syndrome in a 15-year old girl after a single injection of a high-dose neuroleptic]. Ugeskr Laeger. Aug 5 1991;153(32):2239-40. [Medline].
2. Ostwald P. The "God of the dance": treating Nijinsky's manic excitement and catatonia. Hosp Community Psychiatry. Oct 1994;45(10):981-5. [Medline].
3. Baguley IJ. The excitatory:inhibitory ratio model (EIR model): An integrative explanation of acute autonomic overactivity syndromes. Med Hypotheses. 2008;70(1):26-35. [Medline].
4. Coconcea C. Zolpidem in treatment resistant catatonia: 2 case reports and literature review [abstract]. Schizophrenia Res. 2008;98:134.
5. Uzbay IT. L-NAME precipitates catatonia during ethanol withdrawal in rats. Behav Brain Res. Feb 15 2001;119(1):71-6. [Medline].
6. Kahlbaum KL. Catatonia. Baltimore, Md: Johns Hopkins University Press; 1874/1973.
7. Morrison JR. Changes in subtype diagnosis of schizophrenia: 1920-1966. Am J Psychiatry. Jun 1974;131(6):674-7. [Medline].
8. Guggenheim FG, Babigian HM. Catatonic schizophrenia: epidemiology and clinical course. A 7-year register study of 798 cases. J Nerv Ment Dis. Apr 1974;158(4):291-305. [Medline].
9. Fink M, Bush G, Francis A. Catatonia: a treatable disorder, occasionally recognized. Directions in Psychiatry. 1993;13(3):1-8.
10. Escobar R, Rios A, Montoya ID, et al. Clinical and cerebral blood flow changes in catatonic patients treated with ECT. J Psychosom Res. Dec 2000;49(6):423-9. [Medline].
11. Chalasani P, Healy D, Morriss R. Presentation and frequency of catatonia in new admissions to two acute psychiatricadmission units in India and Wales. Psychol Med. Nov 2005;35(11):1667-75. [Medline].
12. Peralta V, Cuesta MJ, Serrano JF, Mata I. The Kahlbaum syndrome: a study of its clinical validity, nosological status, and relationship with schizophrenia and mood disorder. Compr Psychiatry. Jan-Feb 1997;38(1):61-7. [Medline].
13. Vorspan F, Cornic F, Mathis D, Cohen D, Lepine JP. Catatonia in a French forensic psychiatric facility: Frequency, prognosis and treatment [abstract]. European Psychiatry. 2008;23:S332-S333.
14. Benegal V, Hingorani S, Khanna S. Idiopathic catatonia: validity of the concept. Psychopathology. 1993;26(1):41-6. [Medline].
15. Johnson J. Catatonia: the tension insanity. Br J Psychiatry. Jun 1993;162:733-8. [Medline].
16. Rogers D. Catatonia: a contemporary approach. J Neuropsychiatry Clin Neurosci. Summer 1991;3(3):334-40. [Medline].
17. Ungvari GS, Leung SK, Ng FS, et al. Schizophrenia with prominent catatonic features ('catatonic schizophrenia'): I. Demographic and clinical correlates in the chronic phase. Prog Neuropsychopharmacol Biol Psychiatry. Jan 2005;29(1):27-38. [Medline].
18. Abrams R, Taylor MA. Catatonia. A prospective clinical study. Arch Gen Psychiatry. May 1976;33(5):579-81. [Medline].
19. Chouinard MJ, Nguyen DK, Clement JF, Bruneau MA. Catatonia induced by levetiracetam. Epilepsy Behav. Feb 2006;8(1):303-7. [Medline].
20. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association; 1994.
21. Peralta V, Cuesta MJ. Motor features in psychotic disorders. II. Development of diagnostic criteria for catatonia. Schizophr Res. Mar 1 2001;47(2-3):117-26. [Medline].
22. Lee J. Teoh T, Lee T-S. Catatonia and psychosis associated with sibutramine: A case report andpathophysiologic correlation. Journal of Psychosomatic Research. 2008;64:107-109.
23. Wachtel L. Catatonia in autism: Etiology, incidence and treatment [abstract]. European Psychiatry. 2008;23:S402-S402.
24. Winzeler RL. Latah in Southeast Asia: the history and ethnography of a culture-bound syndrome. Cambridge, Great Britain: Cambridge University Press; 1995.
25. Simons RC. Latah: a culture-specific elaboration of the startle reflex [film]. Bloomington, Indiana: Indiana University Audiovisual Center; 1983.
26. Tanner CM, Chamberland J. Latah in Jakarta, Indonesia. Mov Disord. May 2001;16(3):526-9. [Medline].
27. Slooter AJ, Braun KP, Balk FJ, et al. Electroconvulsive therapy for malignant catatonia in childhood. Pediatr Neurol. Mar 2005;32(3):190-2. [Medline].
28. Carroll BT. Kahlbaum's catatonia revisited. Psychiatry Clin Neurosci. Oct 2001;55(5):431-6. [Medline].
29. Bonnot O, Tanguy ML, Consoli A, Cornic F, Graindorge C, Laurent C, et al. Does catatonia influence the phenomenology of childhood onset schizophrenia beyond motor symptoms?. Psychiatry Res. Apr 15 2008;158(3):356-62. [Medline].
30. Lahutte B, Cornic F, Bonnot O, Consoli A, An-Gourfinkel I, Amoura Z. Multidisciplinary approach of organic catatonia in children and adolescents may improve treatment decision making. Prog Neuropsychopharmacol Biol Psychiatry. Mar 7 2008;[Medline].
31. Abdullah S. Diagnostic guidelines and clinical realities. In: Synapse: The West Hudson Psychiatric Society Newsletter. Vol 3, 6, 7. 2002 July-August. [Full Text].
32. Adams RD, Victor M. Principles of Neurology. 5^th ed. New York, NY: McGraw-Hill; 1993.
33. Akhtar S, Ahmad H. Ciprofloxacin-induced catatonia. J Clin Psychiatry. Mar 1993;54(3):115-6. [Medline].
34. Akhtar S, Buckman J. The differential diagnosis of mutism: a review and a report of three unusual cases. Dis Nerv Syst. Jul 1977;38(7):558-63. [Medline].
35. Ambelas A. Preschizophrenics: adding to the evidence, sharpening the focus. Br J Psychiatry. Mar 1992;160:401-4. [Medline].
36. Amore M, Montanari M. [Neuroleptic malignant syndrome and related conditions]. Minerva Psichiatr. Oct-Dec 1992;33(4):259-83. [Medline].
37. Anfinson TJ, Cruse J. SIADH associated with catatonia: its resolution with ECT. Psychosomatics. 1995;36(2):212.
38. Arunodaya GR, Vani S, Shankar SK, et al. Fibromuscular dysplasia with dissection of basilar artery presenting as "locked-in-syndrome". Neurology. Jun 1997;48(6):1605-8. [Medline].
39. Ayd FJ Jr. Catatonia. Psychiatric Times;1994:31.
40. Barnes MP, Saunders M, Walls TJ, et al. The syndrome of Karl Ludwig Kahlbaum. J Neurol Neurosurg Psychiatry. Sep 1986;49(9):991-6. [Medline].
41. Benson DF, Cummings JL. Agraphia. In: Vinken PJ, Bruyn GW, Klawans HL, eds. Handbook of Clinical Neurology. Vol 1. Amsterdam, Netherlands: Elsevier Science; 1985:457-472.
42. Bernstein L, Levin R. Catatonia responsive to intravenous lorazepam in a patient with cyclosporine neurotoxicity and hypomagnesemia. Psychosomatics. Jan-Feb 1993;34(1):102-3. [Medline].
43. Bhatia MS, Salrabh, Shome S, Joshi G. Recurrent catatonia in Sheehan's syndrome (a case report). Indian J Med Sci. Feb 1994;48(2):43, 45. [Medline].
44. Black KJ, Kilzieh N. Severe imipramine-induced myoclonus in a patient with psychotic bipolar depression, catatonia, and schizencephaly. Ann Clin Psychiatry. Mar 1994;6(1):45-9. [Medline].
45. Blumer D. Catatonia and the neuroleptics: psychobiologic significance of remote and recent findings. Compr Psychiatry. Jul-Aug 1997;38(4):193-201. [Medline].
46. Bodkin JA. Emerging uses for high-potency benzodiazepines in psychotic disorders. J Clin Psychiatry. May 1990;51 Suppl:41-6; discussion 50-3. [Medline].
47. Boeve BF, Rummans TA, Philbrick KL, Callahan MJ. Electrocardiographic and echocardiographic changes associated with malignant catatonia. Mayo Clin Proc. Jul 1994;69(7):645-50. [Medline].
48. Bogousslavsky J, Ghika J. Catalepsy after stroke. Neurology. Apr 25 2000;54(8):1711-2. [Medline].
49. Boronow J, Stoline A, Sharfstein SS. Refusal of ECT by a patient with recurrent depression, psychosis, and catatonia. Am J Psychiatry. Sep 1997;154(9):1285-91. [Medline].
50. Brasic JR, Barnett JY, Will MV, et al. Dyskinesias differentiate autistic disorder from catatonia. CNS Spectrums. 2000;5(12):19-22.
51. Brasic JR, Zagzag D, Kowalik S, et al. Clinical manifestations of progressive catatonia. German Journal of Psychiatry [serial online]. 2000;[Full Text].
52. Brasic JR, Zagzag D, Kowalik S, et al. Progressive catatonia. Psychol Rep. Feb 1999;84(1):239-46. [Medline].
53. Brasic JR, Zagzag D, Kowalik S, et al. Progressive catatonia. Psychol Rep. Feb 1999;84(1):239-46. [Medline].
54. Brown MM, Swash M. Systemic lupus erythematosus. In: Vinken PJ, Bruyn GW, Klawans HL, eds. Handbook of Clinical Neurology, Revised Series: Vascular Diseases. Amsterdam, Netherlands: Elsevier Science; 1989:369-385.
55. Brust JC. Coma. In: Rowland LP, ed. Merritt's Textbook of Neurology. 8^th ed. Philadelphia: Lea & Febiger; 1989:21-28.
56. Burruss JW, Chacko RC. Episodically remitting akinetic mutism following subarachnoid hemorrhage. J Neuropsychiatry Clin Neurosci. Winter 1999;11(1):100-2. [Medline].
57. Bush G, Fink M, Petrides G, et al. Catatonia. I. Rating scale and standardized examination. Acta Psychiatr Scand. Feb 1996;93(2):129-36. [Medline].
58. Bush G, Fink M, Petrides G, et al. Catatonia. II. Treatment with lorazepam and electroconvulsive therapy. Acta Psychiatr Scand. Feb 1996;93(2):137-43. [Medline].
59. Bush G, Francis AJ, Fink M. Identification and classification of catatonia. San Francisco: American Psychiatric Association; 1993:184-185.
60. Carroll BT. Catatonia due to mixed sedative withdrawal. J Neuropsychiatry Clin Neurosci. Spring 1997;9(2):303-4. [Medline].
61. Carroll BT, Boutros NN. Clinical electroencephalograms in patients with catatonic disorders. Clin Electroencephalogr. Jan 1995;26(1):60-4. [Medline].
62. Carroll BT, Spetie L. Catatonia on the consultation-liaison service: a replication study. Int J Psychiatry Med. 1994;24(4):329-37. [Medline].
63. Carroll BT, Taylor RE. The nondichotomy between lethal catatonia and neuroleptic malignant syndrome. J Clin Psychopharmacol. Jun 1997;17(3):235-8. [Medline].
64. Castillo E, Rubin RT, Holsboer-Trachsler E. Clinical differentiation between lethal catatonia and neuroleptic malignant syndrome. Am J Psychiatry. Mar 1989;146(3):324-8. [Medline].
65. Chang GY. Arm levitation in progressive supranuclear palsy. Neurology. Feb 8 2000;54(3):774; discussion 774-5. [Medline].
66. Chaves-Carballo E. Detection of inherited neurometabolic disorders. A practical clinical approach. Pediatr Clin North Am. Aug 1992;39(4):801-20. [Medline].
67. Chern CH, Tsai WJ. [Acute amphetamine intoxication with catatonia: a case report]. Zhonghua Yi Xue Za Zhi (Taipei). Apr 1993;51(4):322-7. [Medline].
68. Cizadlo BC, Wheaton A. Case study: ECT treatment of a young girl with catatonia. J Am Acad Child Adolesc Psychiatry. Mar 1995;34(3):332-5. [Medline].
69. Climo LH. Treatment-resistant catatonic stupor and combined lithium-neuroleptic therapy: a case report. J Clin Psychopharmacol. Jun 1985;5(3):166-70. [Medline].
70. Cools AR. Clinical neuropharmacology of the basal ganglia. In: Vinken PJ, Bruyn GW, Klawans HL, eds. Handbook of Clinical Neurology, Extrapyramidal Disorders. Vol 5. Amsterdam, Netherlands: Elsevier Science; 1986:47-63.
71. Cooper AF, Schapira K. Case report: depression, catatonic stupor, and EEG changes in hyperparathyroidism. Psychol Med. Nov 1973;3(4):509-15. [Medline].
72. Cottencin O, Debien C, Vaiva G, et al. Catatonia and liver transplant. Psychosomatics. Jul-Aug 2002;43(4):338-9. [Medline].
73. Davis EJ, Borde M. Wilson's disease and catatonia. Br J Psychiatry. Feb 1993;162:256-9. [Medline].
74. DeQuardo JR, Liberzon I, Silk KR. Buproprion, ECT, and dopaminergic overdrive. Am J Psychiatry. 1991;148:1102.
75. Devanand DP, Shapira B, Petty F, et al. Effects of electroconvulsive therapy on plasma GABA. Convuls Ther. Mar 1995;11(1):3-13. [Medline].
76. Dhossche D, Bouman N. Catatonia in children and adolesce