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Catatonia Treatment & Management

  • Author: James Robert Brasic, MD, MPH; Chief Editor: Selim R Benbadis, MD  more...
Updated: Jul 09, 2015

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, 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[68] :

  • Benzodiazepines (eg, clonazepam, lorazepam, and midazolam)
  • Carbamazepine
  • Zolpidem
  • Tricyclic antidepressants
  • Muscle relaxants
  • Amobarbital
  • Reserpine
  • Thyroid hormone
  • Lithium carbonate
  • Bromocriptine
  • Neuroleptics [69, 70]

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.[69, 70] Because catatonia was reported in a 47-year-old woman treated with levofloxacin, prudent clinicians exercise caution when treating patients with fluoroquinolones.[50]

In particular, successful treatment of catatonia has been reported with carbamazepine,[71] clonazepam,[71] olanzapine,[72] and dantrolene,[68] as well as for lorazepam and diazepam.[73, 74] Cyclooxygenase (COX) inhibitors have been reported to protect against the development of perphenazine-induced catatonia in rats.[75]

Krivoy et al recommended the addition of benzodiazepines to antipsychotics in the treatment of catatonia.[76] 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.[77] A 38-year-old woman with idiopathic catatonia required maintenance treatment with 6 mg lorazepam orally daily.[78]

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,[79, 80, 68] including those with catatonia secondary to mood disorders, autistic disorder,[81] or another pervasive developmental disorder.[20, 21] Efficacy may be hindered by coexisting alcohol or drug abuse.[82]

ECT is beneficial for adolescents with catatonic schizophrenia.[83, 68] Slooter et al reported improvement in an adolescent with malignant catatonia (apparently due to viral encephalitis) after ECT.[84] One study found right unilateral ultrabrief ECT to be an effective treatment for catatonia in adolescents and adults.[85]


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,[52] 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.[86] Vitamin K deficiency must be identified and treated in people with catatonia.[86] 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:

  • Consultation with a neurologist is recommended to rule out treatable neurologic conditions; specifically, NMS, encephalitis, and focal status epilepticus must be ruled out
  • Ophthalmologic consultation is recommended to rule out Kayser-Fleischer rings (pigmented rings at the edge of the cornea that are characteristic of Wilson disease)
  • Hematologic consultation is appropriate to prevent thromboembolic disease if people with catatonia demonstrate evidence of early coagulation activation [46]
  • 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; information about locating movement disorder experts is available from the Movement Disorder Society
Contributor Information and Disclosures

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

James Robert Brasic, MD, MPH is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Academy of Neurology, International Parkinson and Movement Disorder Society

Disclosure: 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.

Chief Editor

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

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cyberonics; Eisai; Lundbeck; Sunovion; UCB; Upsher-Smith<br/>Serve(d) as a speaker or a member of a speakers bureau for: Cyberonics; Eisai; Glaxo Smith Kline; Lundbeck; Sunovion; UCB<br/>Received research grant from: Cyberonics; 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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Table. Causes of Catatonia by Category
Category Causes
Neurologic conditions Neuroleptic malignant syndrome[15]

Administration of agents that block postsynaptic dopamine receptors*

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

Withdrawal of lorazepam and other sedatives

Akinetic-rigid syndrome

Arachnoid cyst in right parietal region


Atrophy of left amygdala[17]

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

Basilar artery thrombosis

Bilateral hemorrhagic lesions of temporal lobes

Cerebellar catalepsy

Cerebral hemorrhage

Cerebral infarct

Cerebrovascular disease

Cortical venous thrombosis

Central pontine myelinolysis

Cortical basal ganglionic degeneration


Encephalitis (herpesvirus, Trypanosoma cruzi)

Encephalopathy (Borrelia burgdorferi, HIV infection, Wernicke encephalopathy)

Familial fatal insomnia[24]

Fibromuscular dysplasia with dissection of basilar artery

Frontal lobotomy

Head injury

Huntington disease


Hypopituitarism secondary to postpartum hemorrhage

Idiopathic recurring stupor

Inherited neurometabolic disorders

Locked-in syndrome

Meningitis, tuberculous


Multiple sclerosis[25, 26]


Nonconvulsive status epilepticus

Pervasive developmental disorders[7, 8, 22]

Pallidoluysian atrophy

Paraneoplastic encephalitis[27]


Postencephalitic parkinsonism

Progressive multifocal leukoencephalopathy

Progressive supranuclear palsy


Seizures (complex with partial symptomatology)

Stiff-man syndrome



Subarachnoid hemorrhage

Subdural hematoma

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

Subthalamic mesencephalic tumor

Surgical removal of cerebellar tumor

Tay-Sachs disease

Temporal lobe epilepsy

Tuberous sclerosis

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

Vegetative state

Von Economo (lethargic) encephalitis

Wilson disease

Psychiatric conditions Acute stress disorder

Anorexia nervosa

Autistic disorder[6]

Brief reactive psychosis with catatonia

Conversion disorder


Major depression, single episode with catatonic features

Mood disorders

Neuroleptic malignant syndrome[15]

Posttraumatic stress disorder


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

Psychological factors Immigration

Experiencing rejection of an expression of love

Feelings of alienation in an unfamiliar country

Medical conditions AIDS

Acute intermittent porphyria

Addison disease

Bacterial septicemia


Carcinoid tumors

Diabetic ketoacidosis

Encephalopathy (hepatic, HIV infection, Wernicke encephalopathy)

Fever of unknown cause

Heat stroke

Hepatic failure

Hereditary coproporphyria







Intestinal atony


Neuroleptic malignant syndrome[15]

Poisoning (carbon monoxide, tetraethyl lead)

Renal failure

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

Syndrome of inappropriate antidiuretic hormone (SIADH)


Systemic lupus erythematosus

Thermal injury

Thrombotic thrombocytopenic purpura


Typhoid fever


Von Economo (lethargic) encephalitis

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