Consultation-Liaison Psychiatry

Medical Aspects of Catatonia

Vice-Chairman, Department of Psychiatry Professor of Psychiatry, Medicine, and Surgery, Chairman, Consultation/Liaison Psychiatry, Virginia Commonwealth University Medical Center

First published in Psychiatry Weekly, Volume 4, Issue 3, on February 9, 2009

The prognosis in catatonia, both in response to treatment and after multiple episodes, is determined by the nature and severity of the disease state of which catatonia is a manifestation. Classical catatonic signs, such as mutism, stupor, negativism, and excitement, do not by themselves indicate the etiology or determine the prognosis. The prognosis is better for catatonia occurring in a mood disorder than in schizophrenia. Among medical causes of catatonia, the prognosis is better in metabolic or substance-induced disorders than in those involving injury to the brain. The prognosis is poorer in very chronic cases, those with incomplete recovery after electroconvulsive therapy (ECT), those with early relapse, and when catatonia is accompanied by dementia.

Differential Diagnosis of Catatonia in Medical Settings

The evaluation and differential diagnosis in catatonia are challenging because medical history and those aspects of the physical examination requiring cooperation are usually not obtainable from a catatonic patient, requiring collateral sources of information. Other disease states can mimic catatonia and should be considered in the differential diagnosis,¹ including stiff-person syndrome,² akinetic Parkinson’s disease, malignant hyperthermia,³ locked-in syndrome,⁴ selective mutism, conversion disorder, and other hyperkinetic and hypokinetic states.⁵

Catatonia has been reported to result from a variety of medical conditions, including metabolic, neurologic, and substance-induced disorders. A review⁶ of 261 published cases of catatonia found that there was no relevant psychiatric disorder associated with the catatonic state in 75% of cases. The most common cause of “organic catatonia” (ie, catatonia resulting from a general medical condition) is injury to the central nervous system (CNS), whether from stroke, trauma, vasculitis, tumor, or anoxia.⁷ Strokes involving the anterior cerebral circulation may cause akinetic and apathetic states.^8,9

Metabolic disorders causing catatonia have included hypo- and hyperthyroidism, hypo- and hyperadrenalism, and vitamin B₁₂ deficiency.¹ Numerous drugs and toxins have been reported to cause catatonia, including neuroleptics, dopamine-blocking antiemetics, corticosteroids, cyclobenzaprine, disulfiram, and tetraethyl lead poisoning.^1,10

Hallucinogens can cause an excited catatonic state, including 3,4- methylenedioxymethamphetamine (ecstasy) and phencyclidine (angel dust). Carbon monoxide poisoning can cause catatonia due to damage to the basal ganglia. Neuroleptics can cause a parkinsonian catatonic state or catatonia as part of neuroleptic malignant syndrome as well as aggravate catatonia due to other causes.¹¹ If a patient with catatonia of any etiology is treated with a neuroleptic, it can be difficult, if not impossible, to discriminate the original catatonia from neuroleptic-induced catatonia, with a subsequent high risk of evolution into neuroleptic malignant syndrome. Neuroleptic malignant syndrome can be particularly difficult to distinguish from “acute lethal catatonia,” ie, severe agitatedprimary catatonia.¹² As if this were not diagnostically and therapeutically challenging enough, catatonia has also been reported as a result of withdrawal from clozapine,¹³ anticonvulants,¹⁴ and benzodiazepenes.¹⁵

References

1. Masand PS, Christopher E, Clary GL, et al. Mania, catatonia, and psychosis in the medically ill. In: Levenson JL, ed. The American Psychiatric Publishing Textbook of Psychosomatic Medicine. Washington, DC: American Psychiatric Publishing, Inc; 2005:235-250.

2. Lockman J, Burns TM. Stiff-person syndrome. Curr Treat Options Neurol. 2007;9(3):234-240.

3. Ali SZ, Taguchi A, Rosenberg H. Malignant hyperthermia. Best Pract Res Clin Anaesthesiol. 2003;17(4):519-533.

4. Smith E, Delargy M. Locked-in syndrome. BMJ. 2005;330(7488):406-409.

5. Fink M, Taylor MA. Catatonia: A Clinician’s Guide to Diagnosis and Treatment. New York, NY: Cambridge University Press; 2003.

6. Thorpe LU, Keegan DL, Veeman GA. Conversion mutism: case report and discussion. Can J Psychiatry. 1985;30(1):71-73.

7. Carroll BT, Anfinson TJ, Kennedy JC, Yendrek R, Boutros M, Bilon A. Catatonic disorder due to general medical conditions. J Neuropsychiatr. 1994;6(2):122-133.

8. Wolff V, Saint Maurice JP, Ducros A, Guichard JP, Woimant F. Akinetic mutism and anterior bicerebral infarction due to abnormal distribution of the anterior cerebral artery [French]. Rev Neurol (Paris). 2002;158(3):377-380.

9. Kumral E, Bayulkem G, Evyapan D, Yunten N. Spectrum of anterior cerebral artery territory infarction: clinical and MRI findings. Eur J Neurol. 2002;9(6):615-624.

10. Duggal HS, Singh I. Drug-induced catatonia. Drugs Today (Barc). 2005;41(9):599-607.

11. Caroff SN, Mann SC, Francis A, Fricchione GL. Catatonia: From Psychopathology to Neurobiology. Washington, DC: American Psychiatric Publishing; 2004.

12. Mann SC, Caroff SN, Bleier HR, Welz WK, Kling MA, Hayashida M. Lethal catatonia. Am J Psychiatry. 1986;143(11):1374-1380.

13. Yeh AW, Lee JW, Cheng TC, Wen JK, Chen WH. Clozapine withdrawal catatonia associated with cholinergic and serotonergic rebound hyperactivity: a case report. Clin Neuropharmacol. 2004;27(5):216-218.

14. Rosebush PI, MacQueen GM, Mazurek MF. Catatonia following gabapentin withdrawal. J Clin Psychopharmacol. 1999;19(2):188-189.

15. Deuschle M, Lederbogen F. Benzodiazepine withdrawal-induced catatonia. Pharmacopsychiatry. 2001;34(1):41-42.

Disclosure: Dr. Levenson is a consultant to Eli Lilly.