eMedicine Specialties > Neurology > Movement and Neurodegenerative Diseases

Catatonia: Treatment & Medication

Author: James Robert Brasic, MD, MPH, Research Associate, Division of Nuclear Medicine, Russell H Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine
Contributor Information and Disclosures

Updated: Sep 25, 2008

Treatment

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.28
  • 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

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

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.29


Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and 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 CNS, including limbic and reticular formation.
Monitor patient's blood pressure after administering dose. Adjust as necessary.

Adult

2 mg IM recommended dose; if symptoms and signs of catatonia persist for 48 h after initial dose, consider additional dose
Starting dose: 1 mg PO bid; if symptoms do not remit fully after a few days, may increase to 1 mg PO tid
If symptoms of catatonia do not remit with PO lorazepam, then parenteral administration is appropriate; 1 mg IV may be administered to ameliorate symptoms; 1-2 mg IV bid/tid may be administered for a few days to produce therapeutic effect60
Daily doses may be increased to 16 mg for persistent symptoms of catatonia by experienced clinicians in inpatient settings where parenteral fluids are administered and vital signs are monitored91 ; lack of response to this regimen is indication for ECT

Pediatric

1 mg/d PO reasonable starting dose for adolescent
For children, proportionate reductions in dose are suitable

Toxicity increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs

Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease; may cause birth defects (administration to pregnant women or to women who are likely to become pregnant is unwise); sedation and incoordination may be transient effects of initiation of treatment and each increment in dose (patients are advised to avoid driving car or operating dangerous machinery with each increase in dose)

Antiepileptic drugs

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


Carbamazepine (Tegretol, Carbatrol, Epitol)

Antiepileptic drug. Mechanism of action may include modulation of voltage-dependent sodium channels.

Adult

300 mg PO bid initial; if symptoms do not remit fully after a few days, may increase to 600 mg PO bid

Pediatric

Administer dose proportionately to weight

Serum levels may increase significantly within 30 d of danazol coadministration (avoid whenever possible); do not coadminister with MAOIs; cimetidine may increase toxicity, especially if taken in first 4 wk of therapy; carbamazepine may decrease primidone and phenobarbital levels (their coadministration may increase carbamazepine levels)

Documented hypersensitivity; history of bone marrow depression; administration of MAOIs within last 14 d

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Do not use to relieve minor aches or pains; caution with increased intraocular pressure; obtain CBC counts and serum-iron baseline prior to treatment, during first 2 mo, and yearly or every other year thereafter; can cause drowsiness, dizziness, and blurred vision; caution while driving or performing other tasks requiring alertness; may cause birth defects (administration to pregnant women or to women who are likely to become pregnant is unwise); sedation and incoordination may be transient effects of initiation of treatment and each increment in dose (patients are advised to avoid driving a car or operating dangerous machinery with each increase in dose)

More on Catatonia

Overview: Catatonia
Differential Diagnoses & Workup: Catatonia
Treatment & Medication: Catatonia
Follow-up: Catatonia
Multimedia: Catatonia
References
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Further Reading

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Keywords

catatonia, unresponsiveness, deficits in fetal cortical development, dopaminergic blockade, glutamatergic dysfunction, dysfunction in neurotransmission of noradrenaline, dysfunction in neurotransmission of serotonin, frontal anomalies, motoric immobility, excessive motor activity, extreme negativism, mutism, peculiarities of voluntary movement, echolalia, echopraxia, stupor, oppositionism, posturing, catalepsy, automatic obedience, echophenomena, rigidity, verbigeration, withdrawal, akinesia, stupor

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Contributor Information and Disclosures

Author

James Robert Brasic, MD, MPH, Research Associate, Division of Nuclear Medicine, Russell H Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine
James Robert Brasic, MD, MPH is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Academy of Neurology, and Movement Disorders Society
Disclosure: Taylor and Francis Royalty Independent contractor

Medical Editor

Joseph Quinn, MD, Assistant Professor, Department of Neurology, Portland VA Medical Center, Oregon Health Sciences University
Joseph Quinn, MD is a member of the following medical societies: American Academy of Neurology, Society for Neuroscience, and Society for Pediatric Radiology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

 
 
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