A Critical Catch: Catatonia Due to Multiple General Medical Conditions

CATEGORY 1 CME

Premiere Date: October 20, 2025

Expiration Date: April 20, 2027

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1. Physicians (CME)

2. Other

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ACTIVITY GOAL

To distinguish catatonia despite overlapping symptomatology with other acute neuropsychiatric presentations.

LEARNING OBJECTIVES

1. Discuss a case presentation of malignant catatonia.

2. Increase awareness of the risk factors and presentation of catatonia outside of the classic association with depressive and psychotic disorders.

TARGET AUDIENCE

This accredited continuing education (CE) activity is intended for psychiatrists, psychologists, primary care physicians, physician assistants, nurse practitioners, and other health care professionals who seek to improve their care for patients with mental health disorders.

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Catatonia is a potentially fatal comorbidity of other illnesses, including antecedent and comorbid psychiatric illnesses such as depressive, bipolar, psychotic, and neurocognitive disorders, as well as neurological and general medical conditions.¹ Catatonia can also occur comorbidly with other acute neuropsychiatric presentations such as delirium and neuroleptic malignant syndrome (NMS).² Not only can it be difficult to distinguish which malady the patient is experiencing due to overlapping symptomatology, but the differential diagnosis may include illnesses with diametrically opposed treatments. Nowhere is this clinical puzzle highlighted more than in the critical care setting, where patients have acute medical fragility and may have restrictions on what treatment formulations they can receive (eg, inability to take oral medications, cumbersome or lack of local access to electroconvulsive therapy [ECT]). Catatonia and its mimics are frequently underappreciated, overlooked, and/or misdiagnosed in the inpatient medical setting.³ As such, the consult-liaison psychiatrist plays a vitally important role in identification, diagnosis, quantitative symptom ascertainment, and treatment of catatonia in this vulnerable patient population.

We present a case of a 66-year-old woman who developed malignant catatonia during a complicated and prolonged hospital course that required intensive care unit (ICU) level of care and included several barriers to treatment. This case presentation aims to increase awareness for the general psychiatrist of the risk factors and presentation of catatonia outside of the classic association with depressive and psychotic disorders. We also endeavor to highlight the need to regularly and reciprocally communicate with other physicians caring for patients at high risk for neuropsychiatric complications.

Case Report

“Ms Elisa” is a 66-year-old woman with a history of bipolar II disorder who had been under the care of a community outpatient psychiatrist and had stability for many years on divalproex sodium 1000 mg daily, lamotrigine 250 mg daily, and quetiapine 25 mg daily. Ms Elisa had a cancer diagnosis of myelofibrosis and was treated with a mismatched unrelated donor stem cell transplant (SCT), complicated by acute graft-vs-host disease (GVHD). During her admission for SCT, the psychiatry consultation- liaison (C-L) service was consulted to assist with management of Ms Elisa’s psychotropics in the setting of severe mucositis/esophagitis and subsequent inability to take medications orally. For treatment of mucositis/esophagitis, Ms Elisa was prescribed dexamethasone 4 mg twice daily for 3 days. At the recommendation of the C-L psychiatry team, Ms Elisa’s lamotrigine and quetiapine were held. Divalproex sodium was recommended to continue at 1000 mg daily with change to intravenous (IV) formulation; however, Ms Elisa declined this, and all psychotropics were held for the remainder of the admission for SCT. At discharge, psychotropics were not restarted based on patient preference. Recommendations were made to have Ms Elisa follow up with her outpatient psychiatrist and to involve psychiatry for assistance and monitoring if she required future corticosteroids (either as an inpatient or outpatient); she was discharged after a 29-day admission and had psychiatric stability.

A few weeks following discharge, Ms Elisa developed significant nausea and diarrhea and was diagnosed with gastrointestinal (GI) GVHD and subsequently started on high-dose corticosteroids in the outpatient setting; she initiated prednisone at 2 mg/kg daily (160 mg/d) for 2 days and then continued on prednisone 1 mg/kg daily (80 mg/d) for 1 week, with dose reduction by half each subsequent week for the following 3 weeks. After tapering down prednisone to 0.25 mg/kg daily (20 mg/d), it was retitrated due to worsening symptoms to prednisone 1 mg/kg daily (80 mg/d) over the next 7 days. Following 3 days of symptom improvement, prednisone was then reduced to 30 mg daily and continued. During this time, Ms Elisa did not follow up with her outpatient psychiatrist, she did not restart any of her home psychotropic medications, and concern for possible worsening depressive symptoms was noted by her primary oncology medical team.

Ms Elisa was readmitted 8 weeks after her initial discharge with dehydration and failure to thrive, and was still on prednisone 30 mg daily for GI GVHD. C-L psychiatry was consulted several days into her hospitalization due to “intermittent confusion, flat affect, and acting ‘odd’ per caregiver.” On C-L evaluation, she was able to converse and provide a full, detailed medical and psychiatric history. Mental status examination (MSE) results were notable for slow, monotonous speech with increased latency, flat affect, and difficulty with backward sequencing that required cueing (with the patient subsequently answering correctly). She was alert and fully oriented, with otherwise unremarkable MSE results. During the initial physical examination, she was able to follow all commands, could complete a brief cranial nerve examination, and was able to perform extraocular movements but was noted to have horizontal nystagmus, which her spouse reported noticing for the first time that day.

Ms Elisa’s examination results were concerning for hypoactive delirium and possible nonepileptiform seizures, with lower suspicion for catatonia. Scoring of the 3-minute diagnostic interview for Confusion Assessment Method–defined delirium was negative for delirium. Head CT and brain MRI results showed no acute abnormality, and EEG results showed diffuse generalized slowing with no epileptiform discharges, increasing concern for delirium. Ms Elisa received high-dose thiamine replacement at 500 mg IV 3 times a day, with an initial reduction in nystagmus but not consistent improvement. The primary team reduced prednisone to 20 mg daily, with a plan to taper by 50% weekly. After 6 days, Ms Elisa developed bloody diarrhea; prednisone was discontinued, and she started on methylprednisolone 70 mg IV every 12 hours (equivalent to prednisone 175 mg/d) for worsening GVHD and started broad-spectrum antibiotics to cover possible infection.

Over the next few days, Ms Elisa had a profound cognitive decline and her spouse took over as medical decision maker. On examination, she was minimally responsive to painful stimuli, with only whispered, unintelligible words; closed eyes; flat affect; and near mutism, scoring 13 on the Bush-Francis Catatonia Rating Scale (BFCRS). At this time, her vital signs were notable for hypertension and tachycardia. To treat this emergent catatonia, a lorazepam challenge was initiated with 1 mg IV, with subsequent 3-point reduction in BFCRS score. Lorazepam 0.5 mg IV every 12 hours was scheduled, and a positive response was noted. Ms Elisa spontaneously opened her eyes, grimaced from pain, turned her head toward sounds, and moved her arms away from painful stimuli.

The following day, Ms Elisa was notably improved; she was now responding to all questions appropriately (though with soft, whispered speech), and she was oriented to person, place, and time. Vital sign instability improved but had not resolved. The following day, Ms Elisa experienced regression; she was nonverbal, her eyes remained closed, and she did not respond to painful stimuli. No rigidity or cogwheeling was noted. On review, it appeared that nursing staff had held a dose of lorazepam due to concerns for somnolence. Vital sign instability remained unchanged. Lorazepam was titrated to 1 mg IV every 8 hours. The following day, Ms Elisa showed improvement; she was now opening her eyes spontaneously, though with poor eye contact and negativism. She remained mute and minimally engaged. Vital sign instability persisted with continued hypertension but normal heart rate. Lorazepam was titrated to 1 mg IV every 6 hours. Ms Elisa had now been on methylprednisolone 70 mg every 12 hours for 8 days and was tapered to methylprednisolone 35 mg IV every 12 hours (equivalent to prednisone 87.5 mg/24 h).

The next day, Ms Elisa continued to show improvement. She was now following simple commands to open or close her eyes. She remained nonverbal but with more affective responsiveness. Vital signs now showed increasing hypertension and continued normal heart rate. Lorazepam was titrated to 1 mg IV every 4 hours, and cardiology was consulted with recommendation for telemetry and amiodarone drip. Overnight, Ms Elisa developed a temperature of 101.3 °F (38.5 °C), and the following morning, she was again nonverbal and nonresponsive to painful stimuli. Ms Elisa’s hypertension remained unchanged. Lorazepam was titrated to 1.5 mg every 4 hours. The next day, Ms Elisa remained unchanged on examination results, with worsening vital sign instability, now with tachycardia (ranging from 80-174 beats per minute [BPM]) and hypertension (ranging from 159-198 mm Hg for systolic blood pressure and 77-102 mm Hg for diastolic blood pressure). Ms Elisa was transferred to the ICU for intubation for airway protection and lorazepam drip and diagnosed with malignant catatonia. On ICU day 1, her vital signs stabilized with lorazepam drip IV at 2 mg hourly, which was decreased the following day to 1 mg hourly and then to 0.5 mg hourly on ICU day 3, with resulting reemergence of vital sign instability and change in arousal and motor status ranging from –5 to +2 on the Richmond Agitation-Sedation Scale (RASS), including opening her eyes and violently shaking her head. Lorazepam drip was increased to 2 mg hourly, with resulting vital sign stability and RASS score of –5. She was continued on lorazepam 2 mg per hour for 6 hours, which was then reduced to 1 mg hourly with a RASS score of –4, as she was attempting to open her eyes to physical stimuli on ICU day 4.

Lumbar puncture was completed at this time with no significant findings. Repeat brain MRI results showed no acute abnormality, and EEG results showed diffuse generalized slowing with no epileptiform discharges. Creatine kinase (CK) levels were monitored and remained within normal limits. Serum iron levels were within normal limits. On ICU day 1, tacrolimus was discontinued due to concern that it may have been contributing to her neuropsychiatric status. On ICU day 4, she was alternatively started on 6-mg sirolimus loading dose, then 2 mg daily via nasogastric tube (NGT). She remained on methylprednisolone 35 mg every 12 hours till her sirolimus levels were therapeutic on ICU day 8, at which point methylprednisolone was tapered to 25 mg every 12 hours (equivalent to prednisone 62.5 mg/24 h). Throughout this time, she continued antibiotics, antivirals, and antifungals.

On ICU day 20, lorazepam was reduced to 0.75 mg hourly and tapered daily to 0.25 mg hourly on ICU day 22 without change in RASS score or reemergence of vital sign instability. On ICU day 23, Ms Elisa was arousable and able to follow simple commands to squeeze hands and wiggle her toes, though with slow processing. She was successfully extubated on ICU day 23. The C-L team recommended continued taper of lorazepam to 0.25 mg IV every 4 hours for any potential benzodiazepine withdrawal and to monitor for reemergence of catatonia; however, the ICU team decided to hold lorazepam. Ms Elisa was discharged from the ICU and moved to the general medical unit after 25 days.

Ms Elisa had stability off lorazepam and in the general medical unit for 2 days; methylprednisolone was further tapered to 35 mg daily (equivalent to prednisone 43.8 mg). During this time, her cognitive status remained unchanged; she continued to be nonverbal and only followed simple commands. Ms Elisa developed tachycardia and somnolence with initial concern for reemergence of catatonia, but after workup, she was found to have acute GI bleeding and was transferred back to the ICU for close monitoring. Ms Elisa was quickly stabilized and transferred out of the ICU within 48 hours. At this time, her cognitive status improved and she was able to respond to her name, briefly offer yes or no answers on occasion, follow simple commands to complete hand gestures, and briefly visually track clinicians across the room. She remained unable to answer orientation questions or participate in decisions regarding her care.

Now 4 days off lorazepam, the psychiatry team recommended not to restart lorazepam and to continue close observation. The following day, Ms Elisa’s mental status declined; she was no longer opening her eyes or responding to commands. After receiving 1 mg IV lorazepam, she was able to open her eyes (though with poor eye contact), squeeze the clinician’s hand when prompted, and nod her head in responses to questions but she remained nonverbal. Lorazepam 1 mg IV every 4 hours was scheduled. The following day, upon psychiatric examination, Ms Elisa did not respond to commands or open her eyes, but her family at her bedside and staff reported that earlier in the day, she had been following simple commands to squeeze their hands or flex her toes. Each reported period of increased engagement was within 45 to 90 minutes of receiving scheduled lorazepam. As such, lorazepam was increased in frequency to 1 mg IV every 3 hours. There was subsequent concern from family members that Ms Elisa appeared drowsier the following day, and lorazepam was subsequently tapered over the next 4 days to 0.5 mg every 3 hours. During this time, she improved to the point of responding to her name when asked, briefly offering yes or no answers on occasion, following simple commands to complete hand gestures, and briefly tracking providers visually across the room. She remained unable to answer orientation questions or participate in decisions regarding her care.

Ms Elisa remained on the scheduled dose of lorazepam for 6 days, during which time methylprednisolone was tapered to 20 mg daily (equivalent to prednisone 29 mg). Over this time, she had no further improvement. A 1-mg dose of lorazepam IV was trialed, and Ms Elisa became notably more engaged; she was able to provide 2-word answers at times to simple questions and complete 2-step commands. Lorazepam was titrated to 1 mg IV every 4 hours. The following day, Ms Elisa was reported to have had increased periods of wakefulness, lasting up to 5 hours. She remained on this dose of lorazepam for 4 days, with improved engagement each day. At this time, she was oriented to date and location, able to engage in brief conversation with staff, and could follow more complex commands, though she sometimes required repeated prompting. Methylprednisolone was reduced to 15 mg daily (equivalent to prednisone 18.8 mg).

At this point, Ms Elisa’s progress began to plateau without change for 1 week. Lorazepam was increased to 1 mg IV every 3 hours without further benefit. At this time, in the absence of available ECT, amantadine was initiated at 50 mg daily via NGT for 1 day and then increased to 50 mg twice daily via NGT while continuing lorazepam 1 mg IV every 3 hours. On the second day of amantadine dosing, Ms Elisa showed a marked improvement; she was able to remark to staff about a TV show she had watched that day, was oriented to person and place, and could again follow simple commands. Titration of amantadine was slowed as she developed increased sedation, fever, and shortness of breath, with increased oxygen demand within days of initiation. This was soon confirmed to be due to pneumonia secondary to human metapneumovirus infection. Once medical stability was attained with antivirals, amantadine was then titrated to 100 mg twice daily via NGT and lorazepam was reduced to 1 mg IV every 4 hours.

For the next 14 days, Ms Elisa remained on this regimen while slowly recovering from fluctuating delirium, with her care focused on infectious disease management, nutrition, and safety in the setting of altered mental status, which required mittens at times to prevent her from pulling out treatment lines. She then developed a superimposed bacterial pneumonia along with her viral pneumonia, leading to acute hypoxic respiratory failure and increasing oxygen demands. Lorazepam was reduced to 0.5 mg IV every 4 hours for 2 days and then to 0.5 mg IV every 6 hours with corresponding reduction in somnolence. Ms Elisa was now having periods of calm and cooperative behavior, was tracking providers visually, and was able to make single-word requests for “water” or “more,” but she remained unable to follow commands and was largely nonverbal. She had resolution of her catatonic symptoms. After 2 days, lorazepam was further reduced to 0.5 mg IV every 12 hours, with no change in amantadine dosing.

A day later, Ms Elisa was noted to be more alert and engaged on examination, cooperating with staff in brushing her teeth, showing spontaneous movement of her head/neck and upper extremities, tracking providers around the entire room, and speaking simple but full sentences such as, “I’m good. How are you?” With the goal of maintaining awake status in the daytime, lorazepam was consolidated to 1 mg IV hourly, with no change in amantadine dosing. Over the following days, she became more verbal and was able to express her wishes and motivations. Lorazepam was reduced to 0.5 mg IV every night at bedtime and then to 0.25 mg IV every night at bedtime and continued at this dose for 1 week before discontinuation. At this time, Ms Elisa no longer exhibited symptoms of catatonia or delirium.

Her admission continued with a primary focus on physical rehabilitation. Approximately 4 days after discontinuation of lorazepam, an amantadine taper was initiated without recurrence of catatonia. Amantadine was reduced to 100 mg twice daily for 1 week, then to 75 mg twice daily for 2 weeks, and then to 50 mg twice daily, at which point divalproex sodium was resumed at 125 mg nightly given her history of bipolar II disorder, though at this time, she exhibited no symptoms of mood instability. Four days later, amantadine was further reduced to 25 mg twice daily and valproate was increased to 250 mg nightly. Another 4 days later, Ms Elisa reported feeling “sluggish” and fatigued, and valproate was discontinued at her request.

She remained on amantadine 25 mg twice daily throughout the remainder of her admission and was discharged 140 days after her admission. Toward the end of her admission, Ms Elisa’s outpatient psychiatrist was contacted to discuss continued outpatient care, but she decided to continue outpatient care with a C-L subspecialist who had access to her oncology records and treatment plan. Ms Elisa continued to follow up in a C-L psychiatry clinic for the next 2 years and had stability from a psychiatric perspective on 50 mg of amantadine daily. Her amantadine dose was consolidated to once daily and, despite patient education, she wished to continue on this dose due to fear of recurrent catatonia. Over these 2 years, she exhibited no symptoms of catatonia, bipolar disorder, or other psychiatric condition and remained off other psychotropics aside from low-dose amantadine.

The Figure shows an overview of this case report.

Discussion

Catatonia is a specific neuropsychiatric syndrome that can occur de novo or follow another neuropsychiatric syndrome that does not resolve and hence progresses to include catatonia. The catatonia syndrome features full alertness, mutism, increased muscle tone, odd/purposeless movements, posturing, and a variety of other distinguishing clinical features.⁴ It is most accurately diagnosed with a high level of suspicion in the appropriate clinical context with the use of standardized rating instruments, the best known of which is the BFCRS.⁴ In the context of suspected catatonia, 2 or more of the specified items on the BFCRS are enough to establish a case of catatonia whereas the full-scale items are scored to delineate specific symptoms and to gauge severity. Although the subject of active debate, the formal diagnosis of catatonia (DSM-5-TR) does not allow it to be diagnosed in the context of delirium. Nonetheless, physicians need to be alert for a catatonia diagnosis in a setting of high risk (eg, unresolved baseline psychiatric illness) where the patient manifests a clinical gestalt appearance (eg, alertness, mutism, aberrant motor movements, increased muscle tone) that raises the suspicion of catatonia.

The issue of catatonia in the setting of complex systemic illness remains unresolved. Many patients with chronic or severe illness will develop delirium, which can become persistent and even chronic if the associated medical illness is not reversed. The DSM-5-TR prohibition against concurrent diagnosis of delirium and catatonia is especially problematic in this regard. Semantically, a patient with established delirium who subsequently develops catatonic signs while still experiencing delirium will warrant separate clinical intervention (eg, a trial of IV lorazepam) to target specific catatonia symptoms whereas benzodiazepines are usually problematic in delirium. Additionally, the continuum of catatonia and malignant catatonia (which itself significantly overlaps with NMS) confers other challenges. Although malignant catatonia and NMS often overlap considerably (to the point where some clinicians regard them as essentially the same syndrome),² NMS is almost always precipitated by antipsychotics and thus antipsychotics must be held, pending recovery.⁵

Adding significant complexity to our case, this patient had an established illness of bipolar disorder (and thus was at risk for catatonia based on the chronic major psychiatric illness) and clearly had an episode of delirium requiring separate, specific management. She also received robust doses of corticosteroids as part of a cancer chemotherapy regimen, thus predisposing her further to corticosteroid-associated psychiatric adverse effects (which can include delirium, catatonia, mania, and numerous other clusters of psychiatric symptoms). Therefore, this case is one of high complexity, with overlapping (or even competing) psychiatric complications of her systemic illness and its treatments, and a baseline elevated risk of catatonia attributable to bipolar disorder.

How best can we diagnose and manage such a case? An openness to diagnose and manage the various elements of the case as outlined is critical. Second is a willingness to treat the catatonia syndrome with lorazepam (and ECT for treatment failures), all while being attuned to delirium in a patient with high risk, the risk of decompensated bipolar disorder, and the induction of new psychiatric adverse effects from immunomodulators. Use of the BFCRS in a standard way allows separate attribution of the catatonia element while providing a baseline score by which to judge incremental improvement to catatonia-specific interventions. Similarly, one should search for signs more specific to NMS (eg, rigidity, hyperthermia, elevated CK, depleted serum ferrous iron), as this can help distinguish NMS from malignant catatonia.⁵ Finally, searching for a temporal association between onset of new corticosteroid use and subsequent new onset of psychiatric symptoms shortly thereafter is necessary to elucidate such an inferential causal connection between immunomodulators and their specific psychiatric adverse effects.

The ultimate outpatient management (once the patient is well enough to be discharged) would ideally include a full understanding of the complexities summarized above and vigilance for recurrence. Close, collaborative, multispecialty comanagement (at the very least among psychiatry, primary care, and oncology in this case) is essential. Clinical management requires regular surveillance for recurrence of catatonia, delirium, and psychiatric symptoms attributable to immunomodulation and recurrence of psychiatric symptoms attributable to her baseline bipolar disorder. Amantadine, a noncompetitive N-methyl-_D-aspartate (NMDA) antagonist, is considered one of the second-line options for treatment of catatonia. Through its different mechanism of action, it is able to work synergistically with γ-aminobutyric acid–ergic agents or, as highlighted here, as monotherapy maintenance treatment in some cases. There is emerging evidence supporting the use of NMDA antagonists in the treatment of catatonia, including amantadine, memantine, and ketamine.⁶

Concluding Thoughts

The case described here is certainly complicated but is not altogether uncommon to encounter. It behooves all psychiatrists, even those who practice outside a C-L role, to be knowledgeable about risk factors for and presenting symptoms of catatonia in those with medical illnesses. This is not a condition often considered by other specialties; thus, increased vigilance in patients at risk befits our role as specialists and advocates for our patients.

This case highlights several factors that can challenge management: diagnosing catatonia amid co-occurring delirium, oversedation in response to lorazepam requiring adjunctive agents, prolonged recovery with periods of perceived plateauing, and progression to malignant catatonia. Beyond reporting the specific approaches to management in this case, we hope to have made apparent the need for careful clinical assessment and close collaboration with other medical specialties when facing this potentially fatal neuropsychiatric syndrome.

Dr Taylor is an assistant professor and consult-liaison psycho-oncologist in the Department of Psychiatry at The University of Texas MD Anderson Cancer Center in Houston.

Dr Cumming is an associate staff psychiatrist in the Neurological Institute at the Cleveland Clinic in Ohio.

Dr Bourgeois is vice chair of hospital psychiatry services at the University of California, Davis Medical Center in Sacramento.

References

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4. Bush G, Fink M, Petrides G, et al. Catatonia. I. Rating scale and standardized examination. Acta Psychiatr Scand. 1996;93(2):129-136.

5. Fricchione G, Mann SC, Caroff SN. Catatonia, lethal catatonia, and neuroleptic malignant syndrome. Psychiatr Ann. 2013;30(5):347-355.

6. Caliman-Fontes AT, Vieira F, Leal GC, et al. Ketamine for catatonia: a novel treatment for an old clinical challenge? a systematic review of the evidence. Schizophr Res. 2024;271:355-370.