Also In This Special Report
James A. Bourgeois, OD, MD
Sofia Matta, MD; and Patrick T. Triplett, MD
Melissa P. Bui, MD
Learn how to spot catatonia quickly, use BFCRS screening, and safely treat with lorazepam or ECT while preventing complications.
SPECIAL REPORT: CONSULTATION-LIAISON PSYCHIATRY
Following the American Psychiatric Association (APA)’s recent approval of its first Catatonia Resource Document,1 The American Journal of Psychiatry published a summary highlighting its key concepts.2 The following article provides a clinically focused review of catatonia, drawing upon these publications, and considers next steps for advancing the practice and science of catatonia.
Catatonia has long been a clinical curiosity, and it is little wonder why.3 A patient with catatonia may stand completely still for hours or even days, like a statue, unresponsive to the world. Then, suddenly, the stasis can be interrupted by periods of bizarre, often frenetic activity in which they may remove clothing or engage in other strange behaviors with little to no awareness or recollection of the event. A person with catatonia may mirror the examiner, echoing both words and actions, or they may summarily refuse to answer questions, perform basic motor instructions, or even allow examination. Moreover, catatonia may be accompanied by autonomic disturbances, a condition known as malignant catatonia, which can prove fatal without prompt attention and assertive treatment.4
Among the greatest curiosities of catatonia, at least from a clinical perspective, is its diverse range of potential presentations. As currently understood, the phenotype of catatonia is heterogeneous,5 with presentations characterized by inappropriately decreased, increased, or odd activity. These 3 presentations are commonly described as hypokinetic, hyperkinetic, and parakinetic, respectively. Despite the diversity of catatonia presentations, one feature that appears to cut across all cases is that of a peculiar disconnect between a person’s will and their actions. This is what is meant when catatonia is described as a psychomotor syndrome6: namely, that there is a disturbance not only of mind and motor but also a fundamental disturbance in the integration between the two, manifesting in abnormal behavior.
James A. Bourgeois, OD, MD
Sofia Matta, MD; and Patrick T. Triplett, MD
Melissa P. Bui, MD
The primary obstacle preventing the optimal care of patients with catatonia is under-recognition. Yet, even among those physicians who might otherwise consider catatonia on the differential, it is not uncommon that a diagnosis of catatonia is delayed, contributing to complications such as muscular atrophy, contractures, decubitus ulcers, deep vein thromboses, pulmonary emboli, aspiration events, rhabdomyolysis, and malnutrition. As a rule, catatonia should be included on the differential for any patient who presents with markedly decreased, increased, or odd activity, in line with its 3 motoric variants.
The Catatonia Resource Document approved by the APA in 2025 recommends that the Bush-Francis Catatonia Rating Scale (BFCRS) be used to characterize the features of catatonia when a diagnosis of catatonia is suspected.1 The first 14 items of the BFCRS may be used as a stand-alone screener known as the Bush-Francis Catatonia Screening Instrument (BFCSI), as they include all 12 items in Criterion A of the DSM-5-TR diagnostic criteria (
Epidemiological studies on catatonia prevalence across clinical settings report a broad range of estimates8 with underdiagnosis often confounding population-level data.9 Moreover, for those who have limited hands-on training in diagnosing catatonia, it can prove to be somewhat of a Rorschach test trying to differentiate mannerisms from stereotypy, or to decipher terms such as ambitendency, mitgehen, and gegenhalten. Therefore, videographic educational materials are recommended to illustrate catatonia’s varied motoric and behavioral presentations. Readers are referred to a free suite of catatonia assessment videos to learn how to identify each item on the BFCRS (
Catatonia should be recognized quickly to prevent medical and functional complications.1,4 A recent retrospective study using electronic medical record documentation found that using only 4 of the first 14 items of the BFCRS—excitement, mutism, staring, and posturing—detected catatonia with 97% sensitivity.10 Although this instrument, the Catatonia Quick Screen, awaits prospective validation, brief approaches such as this screening instrument stand to make catatonia diagnosis far more efficient.
It is not just psychiatrists who need to identify catatonia. Instead, because catatonia can be the chief manifestation of many medical and neurological conditions, acute care clinicians in hospital medicine and neurology should also be aware of it, as they are often the first to evaluate these patients.11 As one might suspect, the results of an online survey of clinicians in medicine and neurology found that they were less accurate in scoring the BFCRS than clinicians in psychiatry.11,12 Promoting awareness among acute care clinicians, additionally including clinicians in critical care and emergency medicine, is a pressing next step in educational efforts.
Both the DSM-5-TR and the latest version of the International Statistical Classification of Diseases, Eleventh Revision allow for the diagnosis of unspecified catatonia, agnostic of any associated psychiatric condition or secondary cause. This allows for prompt diagnosis, workup, and treatment of the syndrome even when it cannot yet be attributed to an associated condition. Although these 2 diagnostic systems differ slightly in which criteria qualify for catatonia diagnosis, they both require the presence of 3 features as the diagnostic threshold. Once the syndrome of catatonia has been diagnosed, a workup is indicated to identify whether catatonia is the result of a previously established psychiatric condition (eg, bipolar disorder, schizophrenia, etc), or is due to the physiological effects of a comorbid systemic medical condition (eg, autoimmune encephalitis) or a psychoactive substance (eg, cannabinoids).
The APA Catatonia Resource Document notes that, for every patient presenting with a first-lifetime episode of catatonia, “the clinician should consider conducting a workup for a range of potential psychiatric and nonpsychiatric causes.” Roughly two-thirds of secondary causes of catatonia are conditions with direct central nervous system involvement,13 so a workup should prioritize electroencephalography14 with consideration of brain MRI or cerebrospinal fluid studies as indicated by the clinical presentation.1
Catatonia management typically involves 3 domains: targeting the syndrome of catatonia, addressing associated conditions or contributory substances, and preventing medical and functional complications (
Targeting the Syndrome of Catatonia
The primary approach to the syndrome of catatonia is lorazepam, beginning with the lorazepam challenge in which 2 mg (1 mg in children, older adults, or those at risk of respiratory compromise) is administered intravenously (IV). The initial challenge should be regarded as a diagnostic test for catatonia.15 A 50% reduction in total BFCRS score is a positive challenge and typically occurs within 15 minutes of administration, though delayed responses may occur and require additional doses. Reports suggest that up to 85% of catatonia is responsive to lorazepam16; however, response rates may be closer to 50% in catatonia associated with systemic medical conditions17 and among older adults.18 Intramuscular or oral administration, typically via nasogastric tube, may be used if IV access is unavailable.
Acute phase management of the syndrome of catatonia following a lorazepam challenge typically consists of scheduled lorazepam, such as 2 mg IV administered every 8 hours.1 Reports indicate that high-dose lorazepam, up to 30 mg in a day, may be necessary for maximal effect in lysing the catatonia syndrome in select patients. Electroconvulsive therapy is indicated for malignant catatonia, which is a medical emergency, or where catatonia is severe and unresponsive to lorazepam, especially in cases at elevated risk for additional morbidity (eg, malnutrition, aspiration events, etc). Second-line treatments to target the syndrome of catatonia include zolpidem, glutamate antagonists (eg, amantadine), antiseizure drugs (eg, valproic acid), or low-potency antipsychotics, specifically for patients with a previous psychotic disorder. The APA Catatonia Resource Document recommends that, when antipsychotics are administered to patients with catatonia, low dopamine blocking agents are preferred (eg, quetiapine, clozapine), and that lorazepam be given concurrently.1
Pending improvement of catatonia’s clinical features, acute phase treatments may be tapered off cautiously, monitoring for the recurrence of catatonic signs. Occasionally, maintenance therapy with benzodiazepines or other catatonia-specific treatments is necessary for durable clinical improvement,19 especially in severe or relapsing presentations.
Addressing Any Associated Conditions or Contributory Substances
Targeting the syndrome of catatonia alone is usually inadequate, as catatonia is generally the complication of a premorbid psychiatric condition or due to a secondary systemic cause. Any associated primary or secondary condition should be treated accordingly. Depressive and bipolar disorders account for 40% to 50% of catatonia, psychotic disorders 25% to 30%, general medical and neurological disorders 25%, and other psychiatric and neurodevelopmental conditions, such as autism-spectrum disorder and Down syndrome regression disorder, are associated with the remaining few cases.20 Drug effects should also be considered, including both the direct effects of substances such as cannabis and stimulants and the effects of substance withdrawal, including from clozapine and benzodiazepines.1
Preventing Medical and Functional Complications
The APA Catatonia Resource Document also describes potential complications of catatonia, categorized by organ system.1 For instance, pulmonary complications may include atelectasis and pneumonia; cardiovascular complications may include venous thromboembolism; urinary complications may include urinary retention and urinary tract infections; neuromuscular complications can include deconditioning and contractures; and skin complications can include decubitus ulcers.
Catatonia is a proverbial phoenix, frequently forgotten and then rediscovered. However, the growing interest in catatonia over the past few years is much broader than in previous eras, which we take as a favorable omen for continued discovery.21 Despite the advances in catatonia awareness and expanding recognition, there are several areas of needed progress. Chief among these is the absence of randomized, controlled trials of benzodiazepines or any other treatment for lysing catatonia.22 There remains a dearth of evidence to guide lorazepam dosing, second-line treatments, or the continuation vs discontinuation of acute phase treatments.
Additionally, catatonia awareness needs to expand beyond the boundaries of psychiatry to our colleagues in acute care settings, including hospital medicine, neurology, emergency medicine, and critical care, given that clinicians in such settings are on the front lines. If they do not identify catatonia or request psychiatric consultation, catatonia will often remain undiagnosed, which could lead to untoward outcomes and missed opportunities for effective treatment.
Dr Oldham is a consultation-liaison psychiatrist based in Rochester, New York, and an associate professor of psychiatry at the University of Rochester Medical Center.
Dr Wilson is a consultation liaison psychiatrist, epidemiologist, and associate professor of psychiatry and behavioral sciences at Vanderbilt University Medical Center, and a physician scientist at the Veterans Affairs Geriatric Research, Education, and Clinical Center.
References
1. Wilson JE, Oldham MA, Francis A, et al.
2. Wilson JE, Oldham MA, Francis A, et al.
3. Hirjak D, Foucher JR, Ams M, et al.
4. Connell J, Oldham M, Pandharipande P, et al.
5. Wilson JE, Niu K, Nicolson SE, et al.
6. Walther S, Stegmayer K, Wilson JE, Heckers S.
7. Bush G, Fink M, Petrides G, et al.
8. Solmi M, Pigato GG, Roiter B, et al.
9. Luccarelli J, Smith JR, Kalinich M, et al.
10. Luccarelli J, Kalinich M, Wilson JE, et al.
11. Kaur J, Maeng DD, Wortzel JR, Oldham MA.
12. Wortzel JR, Maeng DD, Francis A, Oldham MA.
13. Oldham MA.
14. Hosseini P, Whincup R, Devan K, et al.
15. Bush G, Fink M, Petrides G, et al.
16. Hirjak D, Fricchione G, Wolf RC, Northoff G.
17. Smith JH, Smith VD, Philbrick KL, Kumar N.
18. Jaimes-Albornoz W, Serra-Mestres J.
19. Brown O, McLay L, Glue P, Barak Y.
20. Coid F, Rogers JP, Saini A, Oldham MA.
21. Oldham MA.
22. Zaman H, Gibson RC, Walcott G.
4 months ago
Prior Auth Parasite4 months ago
DSM-5-TR: Where Should We Go From Here?4 months ago
An Invitation for Video Insights