Prisoner of the Brain: Recognizing the Serious Implications of Catatonia

Psychiatric TimesVol 40, Issue 3

Catatonia is thought to be significantly underrecognized, and it is important to routinely screen for it among hospitalized patients. Here's how to recognize and treat.




-Series Editor Nidal Moukaddam, MD, PhD

In this installment of Tales From the Clinic: The Art of Psychiatry, we discuss catatonia, originally described by Karl Kahlbaum, MD, a German psychiatrist. At the time, and as we understand it now, catatonia was described as a diagnostic label that combines different clinical presentations and often presents as an add-on to other psychiatric or medical illnesses. Catatonic symptoms range from motoric immobility and mutism to purposeless excitement, which makes diagnosis challenging. Our understanding of the neurobiology and physiological underpinnings of this disease is woefully incomplete, and we hope this installment helps shed light on catatonia and draws readers’ attention to early diagnosis of this intriguing entity.

Case Study 

“Mr Shear” is a 40-year-old male patient seen by the general hospital psychiatric consultation service after being admitted for abdominal pain, laboratory derangements, and failure to thrive. His chart mentions history of childhood physical abuse as well as military sexual trauma while serving in the US Army during his early 20s. After an honorable discharge, he suffered a traumatic brain injury due to a motorcycle accident. Following a lengthy hospitalization and subsequent rehabilitation, he worked as a janitor in an office complex and was noted for his impeccable diligence and perfect attendance. He lived with a girlfriend in his early 30s and had 2 children with her. His behavior started becoming more erratic around his 35th birthday. He began disappearing from the home for increasingly lengthy periods and reported auditory hallucinations of music and “babies crying.” He became more withdrawn and started missing work, leading to his termination as a janitor. One day, he left home and did not return. His girlfriend dropped off their 2 children with Mr Shear’s mother and left town as well.

Four years later, his mother received a call from Mr Shear. He had been staying with a friend from high school for unknown reasons, and now that the friend had been diagnosed with Huntington disease, Mr Shear could no longer stay there and needed to return home. Since arriving home, his mother reported that “he is like a different person.” Once a highly attentive father, he almost completely ignored his young children and spent most of his time watching TV or on his phone. During the past 6 months, his behavior became even more withdrawn, so that he was no longer watching TV but just sitting and staring. He refused to bathe or use the restroom, often urinating and defecating on himself. When he did get up to use the restroom after multiple requests by his mother, he would spend increasingly lengthy periods in the bathroom. A few weeks before admission, he spent nearly 3 days locked in the bathroom. He stopped eating and drinking, citing abdominal pain, and spoke only in 1-to-3-word sentences. His mother eventually called 911 when he became unresponsive after not eating anything for 1 week.

Upon arrival at the emergency department, he was found to be hypothermic with hypernatremia, leukocytosis, rhabdomyolysis, and an acute kidney injury. He was warmed and resuscitated with intravenous (IV) fluids and admitted to the general hospital floor, where his electrolytes were slowly corrected. An esophagogastroduodenoscopy was performed, and he received a diagnosis of gastric ulcers and H. pylori and started on triple antibiotic therapy. Throughout this treatment and work-up, he remained minimally responsive. The psychiatric consultation service noted immobility, staring, and mutism, although he did not show signs of posturing or rigidity suggestive of catatonia.

Despite low clinical suspicion for catatonia, a 2-mg IV lorazepam trial was nevertheless attempted, to which he demonstrated remarkable improvement in length of speech, engagement, and responsiveness. He was able to express that he was still having considerable abdominal pain, at which time pain medication regimen was optimized by the pain medicine service. He underwent daily assessments by the psychiatry service and was noted to be more withdrawn when IV lorazepam had to be delayed due to receiving coinciding opioid pain medications or due to a staffing shortage. He was started on a regimen of IV lorazepam 4 times daily, which was successfully transitioned to oral formulation. On lorazepam, he was noted to start using the restroom independently, expressing his needs, eating and drinking appropriately, and having brief conversations with his medical teams. Due to concerns about caregiver burnout from frequent dosing of lorazepam, he was transitioned to oral diazepam twice daily. At outpatient psychiatric follow-up several weeks after discharge from the hospital, he was noted to maintain the improvements in speech and behavior and began slowly to taper off diazepam under psychiatrist supervision.


Catatonia is a distinct syndrome marked by a heterogeneous constellation of hallmark signs and symptoms. It is associated with both psychiatric etiologies, known as primary catatonia, and other neuromedical conditions, or secondary catatonia.1 Catatonia was first described by Karl Kahlbaum in 1874, and unfortunately it was nosologically associated primarily with schizophrenia syndromes until as recently as the 1990s.2,3 We now know that, among primary psychiatric causes of catatonia, mood disorders such as bipolar disorder and major depressive disorder are much more commonly associated. In general, catatonia is associated with a primary psychiatric etiology in about 75% of cases and with secondary causes in about 25%.4 In the DSM-5, catatonia is a specifier for psychosis and mood disorders.

Symptoms and Diagnosis

TABLE 1. Characteristic Signs and Symptoms of Catatonia

Table 1. Characteristic Signs and Symptoms of Catatonia

On inpatient psychiatric consultation services, catatonia is most diagnosed using the Bush-Francis Catatonia Rating Scale, although other diagnostic scales exist. Characteristic signs and symptoms are defined and can be found in Table 1. The exact number of positive diagnostic features needed to diagnose catatonia is controversial, with Bush-Francis requiring 2 of 14 “screening” symptoms, whereas the DSM-5 requires 3 of 12 symptoms. At any rate, catatonia is thought to be significantly underrecognized, and it is important to routinely screen for it among hospitalized patients.5


Causes of secondary catatonia are broad and include both direct central nervous system (CNS) insults as well as systemic conditions. Common causes include stroke, seizures, CNS lesions, infections, and systemic lupus erythematosus. Limbic encephalitis can also be responsible, with anti–NMDA receptor encephalitis being the most common form associated with catatonia.6 Other causes may include endocrinopathies, metabolic disorders, poisoning, or drug-related circumstances. Notably, dopamine antagonists such as antipsychotic medications may cause catatonia, although low-potency antipsychotics are sometimes used in specific cases of catatonia associated with psychotic conditions. Drugs of abuse—including hallucinogens, stimulants, alcohol, and synthetic cannabinoids—and withdrawal of GABA or dopamine agonists have also been implicated.

It is important to complete a thorough neuromedical work-up when catatonia is suspected to evaluate for a secondary cause. This might include a metabolic panel, toxicology screen, infectious screen, autoimmune screen (erythrocyte sedimentation rate, C-reactive protein, antinuclear antibodies, paraneoplastic panel), creatine kinase levels (to monitor for malignant form), iron studies, electroencephalogram, head CT or MRI, and possibly a lumbar puncture.4,7-10

Catatonia Subtypes

TABLE 2. Subtypes of Catatonia

Table 2. Subtypes of Catatonia

Various subtypes of catatonia have been described, including the classic stuporous catatonia, excited catatonia, delirious mania, and the potentially life-threatening lethal or malignant catatonia (Table 2). In the stuporous form, patients demonstrate severe withdrawal, immobility, and mutism, and inpatient services may have a hard time distinguishing between catatonic withdrawal and sedation. In contrast, the excited subtype is characterized by hyperactivity, with verbigeration, stereotyped movements, negativism, or impulsivity. Malignant catatonia, a psychiatric emergency, is marked by fever, autonomic instability, and elevated creatine kinase.11 Delirious mania is a specific form of excited catatonia that also overlaps with malignant catatonia, marked by features of mania (grandiosity, emotional lability, delusions, insomnia), altered arousal suggestive of delirium, and autonomic instability.4,10


The mainstays of treatment for catatonia involve pharmacologic treatment as well as supportive care to manage the physical complications associated with immobility and poor oral intake. The initial approach to nonmalignant forms of catatonia involves a challenge of 2 mg of IV lorazepam. If IV access is not available, an intramuscular route can be used, although this is not preferred given risks of iatrogenic harm. Though less effective than parenteral forms, sublingual lorazepam is also available and is more effective than the oral form. A positive response to the lorazepam challenge is often quickly apparent, with marked improvement in motor and speech symptoms within several minutes. In some cases, a more diminished improvement may be seen over a longer period, such as 30 to 120 minutes. Although sedation with benzodiazepines is decreased in catatonia, falling asleep after a lorazepam challenge does not necessarily rule out the syndrome. Similarly, a negative challenge does not rule it out in cases with high clinical suspicion.

Electroconvulsive therapy (ECT) is used in cases that fail to respond to benzodiazepines or in malignant catatonia, and delays in administration of ECT in malignant catatonia are associated with increased mortality. Amantadine, memantine, zolpidem, and topiramate have also been used in cases that do not respond fully to benzodiazepines.4,7,10

Dr Vijayvargiya is an assistant professor in the Department of Psychiatry at the University of Florida College of Medicine in Gainesville.


1. Taylor MA. Catatonia: a review of a behavioral neurologic syndrome. Neuropsychiatry Neuropsychol Behav Neurol. 1990;3(1):48-72.

2. Fink M, Taylor MA. Catatonia: a separate category in DSM-IV? Integr Psychiatr. 1991;7(1):2-10.

3. Kahlbaum K. Catatonia. Johns Hopkins University Press; 1973.

4. Hebert C. Psychosis III: Catatonia. American Physician Institute for Advanced Professional Studies; 2022.

5. Sienaert P, Rooseleer J, De Fruyt J. Measuring catatonia: a systematic review of rating scales. J Affect Disord. 2011;135(1-3):1-9.

6. Ali S, Welch CA, Park LT, et al. Encephalitis and catatonia treated with ECT. Cogn Behav Neurol. 2008;21(1):46-51.

7. Beach SR, Gomez-Bernal F, Huffman JC, Fricchione GL. Alternative treatment strategies for catatonia: a systematic review. Gen Hosp Psychiatry. 2017;48:1-19.

8. Bey T, Patel A. Phencyclidine intoxication and adverse effects: a clinical and pharmacological review of an illicit drug. Cal J Emerg Med. 2007;8(1):9-14.

9. Espi Forcen F, Respino M, Eloge J, et al. Catatonia in the medically ill: differences and parallels in etiology, phenomenology and management. Int J Psychiatry Med. 2022;57(1):80-88.

10. Fricchione GBS, Gross A, Huffman J, et al. Catatonia, neuroleptic malignant syndrome, and serotonin syndrome. In: Massachusetts General Hospital Handbook of General Hospital Psychiatry. Elsevier; 2018:253-261.

11. Desai S, Hirachan T, Toma A, Gerolemou A. Malignant catatonia versus neuroleptic malignant syndrome. Cureus. 2021;13(6):e15818.

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