CHPR: Clinicians often associate catatonia with psychiatric illness. What should prompt us to step back and consider a medical cause?

Dr. Espí Forcén: It’s the million-dollar question, and the honest answer is that we often don’t know for sure at the outset. DSM-5-TR lets us diagnose catatonia when a patient has at least three catatonic signs, such as mutism, stupor, posturing, or echolalia, but those signs aren’t specific to any one cause. So, diagnosing catatonia is not the end of the workup. Rather, it’s the beginning of the next question: Why does this patient have catatonia? Medical causes may be urgent, treatable, and easy to miss if we assume the presentation is psychiatric. We have to ask what is driving it—psychiatric illness, medical illness, medication effects, withdrawal, seizures, delirium, or more than one of these at the same time. The task is to identify all the contributors, and medical contributors are common. One review found an associated medical disorder in more than half of acute medical or surgical cases, as well as in nearly 80% of older-adult cases (Oldham MA, Psychosomatics 2018;59(4):333–340).

CHPR: What clinical clues should make us suspect a medical cause of catatonia?

Dr. Espí Forcén: Delirium is one of the most important clues. If a patient with catatonic signs also has waxing and waning alertness, inattention, disorientation, or signs of medical illness, you have to think hard about an underlying medical or neurologic cause. The tricky part is that catatonia and delirium can coexist. If we focus only on the delirium, we may miss the catatonia, but if we focus only on the catatonic signs, we may miss the medical problem driving the presentation. Seizure history is another major flag. Nonconvulsive status epilepticus can look indistinguishable from catatonia.

“Catatonia and delirium can coexist. If we focus only on the delirium, we may miss the catatonia, but if we focus only on the catatonic signs, we may miss the medical problem driving the presentation.” - Fernando Espí Forcén, MD, PhD

CHPR: What else is on the differential for medically driven catatonia?

Dr. Espí Forcén: I think in broad categories: brain inflammation, metabolic disturbance, neurodegenerative disease like Parkinson’s disease or dementia with Lewy bodies, seizures, and medication toxicity. Within that differential, anti-NMDA receptor encephalitis deserves special attention because it can start with prominent psychiatric symptoms, so it may initially look like a primary psychiatric illness (Guasp M and Dalmau J, Med Clin (Barc) 2018;151(2):71–79). It can occur in patients of any age or sex, but it is more common in young women and is often associated with ovarian teratomas (Dalmau J et al, Ann Neurol 2007;61(1):25–36). Susannah Cahalan’s book helped bring attention to this problem (Cahalan S. Brain on Fire: My Month of Madness. Simon & Schuster; 2012). She has also suggested that some historical cases interpreted as demonic possession may have reflected anti-NMDA receptor encephalitis.

CHPR: That’s an interesting idea.

Dr. Espí Forcén: Those cases were shaped by the medical, cultural, and religious frameworks of their time, making retrospective diagnosis inherently uncertain. What history does remind us, however, is that medicine is always evolving. Disorders we now recognize as neurologic or autoimmune have often been mistaken for psychiatric illness, and that still happens today. The clinical lesson is to keep autoimmune encephalitis and other medical causes in the differential when evaluating catatonia or atypical psychiatric presentations.

CHPR: What other medical contributors do you look for?

Dr. Espí Forcén: I also explore whether benzodiazepines were recently reduced or stopped, because abrupt discontinuation or rapid tapering after prolonged use can precipitate catatonia or cause previously treated catatonia to recur. Catatonia has also been reported during alcohol withdrawal, although it appears to be uncommon (Rogers JP et al, J Psychopharmacol 2023;37(4):327–369). The larger point is that catatonia does not always have a single clean cause. So rather than asking, “Is this psychiatric or medical?” I keep asking, “What factors might be contributing to this patient’s catatonia?”

CHPR: Please elaborate on the workup you recommend to uncover those contributors.

Dr. Espí Forcén: Start with a careful medication and substance history, and look for autonomic instability, signs of infection, metabolic problems, seizure risk, and any focal neurologic findings. Also, order an EEG when there is concern for seizures, and MRI or CT if you’re worried about a stroke, tumor, or other structural lesion. Keep encephalitis in your differential (eg, in a patient with new-onset psychiatric symptoms that are accompanied by abnormal movements, autonomic instability, or fluctuating consciousness), and in those cases, do an autoimmune encephalitis workup, including lumbar puncture and anti-NMDA receptor antibody testing. At the same time, don’t let the workup delay treatment. If the patient has catatonia, you want to begin treating the catatonia while you continue looking for the cause. Waiting for every lab, scan, or consult to come back can be dangerous, especially if the patient is not eating, not drinking, immobile, or medically deteriorating.

CHPR: Good point. Does the Bush-Francis Catatonia Rating Scale (BFCRS) help distinguish underlying causes of catatonia, such as through differences in specific symptoms?

Dr. Espí Forcén: For individual signs, some patterns emerge, but there is a lot of overlap. In our own research, mannerisms, stereotypies, waxy flexibility, and impulsivity appeared more often in catatonia associated with a psychiatric disorder, though the sample was small and there was substantial overlap (Espí Forcén F et al, Int J Psychiatry Med 2022;57(1):80–88). Patients with catatonia due to a medical condition appear more likely to exhibit negativism and to have higher BFCRS scores than patients with psychiatric catatonia (Duque L et al, General Hospital Psychiatry 2026;98:99–106). Thus, a more severe presentation should raise your level of concern, but no single sign is diagnostic. The BFCRS is also useful because it reminds you that catatonia is not always quiet—it can be hypokinetic, hyperkinetic, or parakinetic (with odd or abnormal movements). So, keep catatonia on the differential whenever a patient has a markedly altered level of motor activity or abnormal behavior. The practical point is that a patient can be very active and agitated and still be catatonic (Editor’s note: For more on the BFCRS, see: www.tinyurl.com/4anjptzf).

CHPR: Once you suspect catatonia, how much does the lorazepam challenge help, and does the response differ by etiology?

Dr. Espí Forcén: First, it’s important to point out that a positive response to a lorazepam challenge, typically 2 mg IV or IM, can support a diagnosis of catatonia, but nonresponse does not exclude catatonia. You also have to distinguish improvement from sedation, which is especially tricky in hyperkinetic presentations. If the patient falls asleep after lorazepam, that is not the same as catatonic signs resolving. What you want to see is improvement in catatonic signs without simply sedating the patient. That said, nonresponse to lorazepam appears to be more common in patients with medical catatonia. In the study I referred to earlier, 56% of psychiatric catatonia patients improved after initial lorazepam treatment, compared with 34% of medical catatonia patients (Duque et al, 2026).

CHPR: How do you approach antipsychotics, particularly when the patient has an underlying psychotic disorder?

Dr. Espí Forcén: You have to be cautious. Catatonia itself is a risk factor for neuroleptic malignant syndrome (NMS), and dopamine blockade can worsen catatonia or add to that risk. In most cases, I initially hold antipsychotics while treating the acute catatonia. Many patients have already received them because the presentation looked psychotic, manic, or severely agitated. If a patient develops fever, rigidity, or autonomic instability, especially after antipsychotic exposure, think about NMS rather than assuming the catatonia is simply progressing. Treatment of NMS requires avoiding further dopamine blockade, providing supportive medical care, and considering ECT in severe or refractory cases (Morcos N et al, J ECT 2019;35(4):225–230). The approach is more nuanced when the patient has an underlying psychotic disorder that also requires treatment. In those cases, you may still need to use an antipsychotic, but choose a second-generation agent, start at a low dose, titrate gradually, and monitor closely for worsening catatonia or signs of NMS.

CHPR: When catatonia appears medically driven, does that change how you think about ECT?

Dr. Espí Forcén: It changes the risk-benefit calculation, but it does not take ECT off the table. In fact, some medically complicated cases are exactly the patients for whom you need to think about ECT earlier, especially when a patient is deteriorating, not eating or drinking, or failing to respond to benzodiazepines. ECT is one of the two main evidence-supported treatments for catatonia, along with benzodiazepines. A medical cause does not rule out ECT. The challenge is often logistical and medical: These patients may have encephalitis, seizures, metabolic abnormalities, fever, pulmonary complications, or other active problems, so you need to collaborate closely with medicine, neurology, anesthesia, and the ECT team. In my experience, the response may be less immediately dramatic in medically complex consultation-liaison cases than in classic mood-associated or psychosis-associated catatonia. But the key point is that ECT is a critical treatment for severe, refractory, or medically dangerous catatonia and can in fact be lifesaving (Rogers JP et al, J Psychopharmacol 2023;37(4):327–369).

CHPR: What’s your bottom line for clinicians?

Dr. Espí Forcén: Five things. 1) Don’t assume catatonia is psychiatric, especially in medically ill or older patients. Delirium, fever, autonomic instability, neurologic findings, seizure history, and withdrawal risk should push you to look harder for a medical cause. 2) Don’t wait for the entire workup before treating. Start treating the catatonia while you continue looking for the cause. 3) Remember that a lorazepam response helps rule in catatonia, but lack of response does not rule it out. Medical forms of catatonia may be less likely to show a dramatic response. 4) Be careful with antipsychotics. They may be needed when an underlying psychotic disorder also requires treatment, but dopamine blockade can worsen catatonia or contribute to NMS. 5) Keep ECT on the table when catatonia is severe, refractory, or medically dangerous, even when the catatonia appears medically driven. And if you really want to understand catatonia, read the classic authors, especially Kahlbaum and Kraepelin. Their descriptions are richer than many modern summaries and remind us that catatonia is not just a checklist (Editor’s note: See box “Why Kahlbaum and Kraepelin Still Matter”). You have to step back and look at the whole patient.

From the Expert Q&A
“Distinguishing Medical From Psychiatric Catatonia”
by Fernando Espí Forcén, MD, PhD
The Carlat Hospital Psychiatry Report, Volume 6, Number 7 & 8
October/November/December 2026
www.thecarlatreport.com

CHPR: Thank you for your time, Dr. Espí Forcén.