Catatonia is a neuropsychiatric syndrome in which the cluster of psychomotor signs and symptoms results in aberrations of movement and behavior. DSM-IV included new criteria for mood disorders with catatonic features, and for catatonic disorder secondary to a general medical condition. In DSM-5, catatonia is recognized as due to a medical or psychiatric condition, or unspecified, as, for example, in recurrent idiopathic catatonia. Mood disorders such as MDD and bipolar disorder are now recognized as more commonly associated with catatonia.
The diagnosis of catatonia relies on the recognition of its sometimes unusual symptoms. Three subtypes of catatonia are conceptualized in Figure 1: stuporous, excited, and malignant. Catatonic withdrawal or stuporous catatonia, includes motoric immobility, staring, mutism, rigidity, withdrawal and refusal to eat, along with more bizarre features such as posturing, grimacing, negativism, waxy flexibility, echophenomena, stereotypy, verbigeration, and automatic obedience. Excited catatonia is characterized by purposeless and excessive motor activity that includes disorganized pressured speech, flight of ideas, verbigeration, disorientation and/or confusion, and confabulation.
Catatonic signs of malignant subtype are accompanied by fever and dysautonomia. Malignant catatonia is associated with increased morbidity and mortality. A specific example of malignant catatonia is neuroleptic malignant syndrome, induced by dopamine-blocking agents or withdrawal of a dopamine or gamma-aminobutyric acidA (GABAA) agonist. Another variant, known as manic delirium or delirious mania, exists with features of both excited and malignant catatonia. Periodic catatonia can present with alternating stuporous and excited forms.
The prevalence of catatonia among psychiatric patients ranges from 7.6% to 38%.1 (See Table 1 for risk factors for catatonia.)
Catatonia has attracted neuroscientists interested in brain mediation of motivation and movement, leading to attention on neurotransmitters and circuits. Several models for the neuropathophysiology of catatonia focus on neurotransmitters. In 1985, it was hypothesized that pharmacotherapies for catatonia act on dopamine- GABA connections in the mesostriatal and mesocorticolimbic systems and in the hypothalamus.2 A restitutive dopamine system seeks rebalance through GABAA–mediated up- and down-regulation of dopamine.
When the restitutive system is dysfunctional, a vulnerability to catatonia emerges from dopamine antagonists. Carroll3 has described a “universal field theory” encompassing diverse neurotransmitter changes for catatonia. Their model postulates a reduced GABA activity in the frontal cortex, increased N-methyl-D-aspartate glutamatergic activity in the posterior parietal cortex, and a dampening of dopaminergic action in the basal ganglia.
Dr Beach is Assistant Professor of Psychiatry and Residency Training Director, Massachusetts General Hospital, Harvard Medical School; Dr Francis is Professor of Psychiatry, Associate Director of Residency Training, and Director of Neuromodulation Services, Penn State Medical School, Hershey Medical Center, Hershey, PA; Dr Fricchione is Professor of Psychiatry, Mind Body Medical Institute and Associate Chief of Psychiatry, Massachusettes General Hospital, Harvard Medical School, Boston, MA. Drs Fricchione and Beach have received funding through the David Judah Fund for catatonia research.
1. Taylor MA, Fink M. Catatonia in psychiatric classification: a home of its own. Am J Psychiatry. 2003;160:1233-1241.
2. Fricchione GL. Neuroleptic catatonia and its relationship to psychogenic catatonia. Biol Psychiatry. 1985;20:304-313.
3. Carroll BT. The universal field hypothesis of catatonia and neuroleptic malignant syndrome. CNS Spectr. 2000;5:26-33.
4. Fisher CM. Honored guest presentation: abulia minor vs. agitated behavior. Clin Neurosurg. 1983;31:9-31.
5. Northoff G. What catatonia can tell us about “top-down modulation”: a neuropsychiatric hypothesis. Behav Brain Sci. 2002;25:555-577.
6. Northoff G. Catatonia and neuroleptic malignant syndrome: psychopathology and pathophysiology. J Neural Transm. 2002;109:1453-1467.
7. Hirjak D, Kubera KM, Northoff G, et al. Cortical contributions to distinct symptom dimensions of catatonia. Schizophr Bull. February 2019; Epub ahead of print.
8. Fricchione G, Mann SC, Caroff SN. Catatonia, lethal catatonia, and neuroleptic malignant syndrome. Psychiatric Annals. 2000;30:347-355.
9. Tuerlings JH, van Waarde JA, Verwey B. A retrospective study of 34 catatonic patients: analysis of clinical care and treatment. Gen Hosp Psychiatry. 2010;32:631-635.
10. Fisher CM. “Catatonia” secondary to disulfiram toxicity. Arch Neurol. 1989;46:798-804.
11. Fricchione GL, Cassem NH, Hooberman D, Hobson D. Intravenous lorazepam in neuroleptic-induced catatonia. J Clin Psychopharmacol. 1983;3:338-342.
12. Bush G, Fink M, Petrides G, Dowling F, Francis A. Catatonia. II. Treatment with lorazepam and electroconvulsive therapy. Acta Psychiatr Scand. 1996;93:137-143.
13. Petrides G, Divadeenam KM, Bush G, Francis A. Synergism of lorazepam and electroconvulsive therapy in the treatment of catatonia. Biol Psychiatry. 1997;42:375-381.
14. Fink M, Taylor MA. Catatonia: A Clinician’s Guide to Diagnosis and Treatment. New York, NY: Cambridge University Press; 2003.
15. Levenson JL. Medical aspects of catatonia. Prim Psychiatry. 2009;16:23-26.
16. Philbrick KL, Rummans TA. Malignant catatonia. J Neuropsychiatry Clin Neurosci. 1994;6:1-13.
17. Bush G, Fink M, Petrides G, Dowling F, Francis A. Catatonia I: rating scale and standardized examination. Acta Psychiatr Scand. 1996;93:129-136.
18. Carroll BT, Goforth HW, Thomas C, et al: Review of adjunctive glutamate antagonist therapy in the treatment of catatonic syndromes. J Neuropsychiatry Clin Neurosci. 2007;19:406-412. ❒