Catatonia in the medically ill and dying: a review for palliative care clinicians

Introduction

Catatonia is a complex neuropsychiatric syndrome that can be life-threatening if not recognized and treated promptly. Although frequently encountered by psychiatrists and commonly linked to mental disorders, catatonia is not limited to psychiatric illness. While mood disorders remain the most common underlying cause, catatonia can also occur in the context of medical illness, including neurological disease, malignancy, autoimmune disease, or systemic infection (1,2). As a result, it may present across a wide range of clinical settings, including general medical wards, intensive care units (ICUs), and palliative care (PC) clinics (2-4).

PC is specialized medical care focused on relieving the symptoms and stress of serious illness through multidisciplinary management of physical, psychological, and spiritual needs (5). Evidence shows that PC improves quality of life, reduces caregiver burden, and may even prolong survival across a range of serious illnesses (6,7).

The interface between PC and psychiatry is expanding in both directions, with palliative psychiatry advancing ethical debate and clinical psychiatry increasingly adopting palliative approaches (8). PC psychiatry, in turn, is an emerging subspecialty that integrates the principles of both fields to address complex needs—expanding PC access for medically ill patients in psychiatric settings, applying palliative approaches to treatment-refractory mental illness, and providing specialized psychiatric care for serious medical conditions such as catatonia (9).

The evaluation and management of catatonia is directly relevant to PC practice, as illustrated by case studies in Table 1. Catatonia is a potentially life-threatening syndrome associated with substantial morbidity, including autonomic instability, venous thromboembolism (VTE), malnutrition, dehydration, pressure injuries, infection, and death (10). In addition to its physical consequences, catatonia often impairs communication and decision-making capacity, limiting patients’ ability to express goals and values in the setting of serious illness and increasing caregiver burden (1,10). Qualitative studies of individuals who recover from catatonia describe the experience as profoundly distressing and frightening, with lasting effects on quality of life (QOL) (11-14). It also commonly occurs in conjunction with other serious conditions, such as advanced cancer, progressive neurologic disease, or systemic infections, and may signify disease progression or the dying process (15-17). Although often reversible, catatonia has important implications for symptom management, prognostication, and patient-centered care, making it a critical syndrome for PC clinicians to recognize and address (16,18,19).

This clinically focused review examines the current literature at the intersection of PC and catatonia. We explore the epidemiology and diverse clinical presentations of catatonia in both adults and children with and without serious illness, review its underlying pathophysiology and common etiologies relevant to PC settings, and consider its impact on prognosis, QOL, medical decision-making capacity, and caregiver burden. Treatment approaches are discussed with attention to the unique considerations in patients with serious illness, and we highlight opportunities for PC involvement in the recognition and management of this complex and often underdiagnosed condition. The goal of this review is to enhance PC clinicians’ knowledge and confidence in identifying and treating catatonia across care settings, while also identifying areas where further research and advocacy could advance clinical care.

Part 1: catatonia in the general population

Epidemiology

Catatonia is a frequently underdiagnosed psychomotor syndrome that can be mistaken for a range of medical or psychiatric conditions. Its varied presentation, overlap with delirium, and lack of confirmatory laboratory or imaging tests contribute to diagnostic uncertainty and missed recognition in both psychiatric and general medical settings (20-24). A review of hospitalized patients found that among 133 individuals who retrospectively met diagnostic criteria for catatonia, only 41% had been recognized during their admission, suggesting that more than half of cases may go undetected (23). Therefore, true prevalence rates are likely underestimated, especially outside psychiatric settings (2,21,25,26).

Reported prevalence rates vary widely across settings. In psychiatric populations, catatonia is found in 5–18% of inpatients, with higher rates observed among those with mood disorders (27-32). On general medical wards, estimates range from 1.6% to 9%, with higher detection in older adults (20,33-36). In critical care settings, reported rates range from 3.8% up to 23%, depending on the population studied and the diagnostic methods used (17,20,37,38). Among children, prevalence estimates range from 0.01% of all pediatric discharges, to 0.6% in adolescent psychiatric inpatients, and up to 17% in children and adolescents with neurodevelopmental disorders, particularly those with autism spectrum disorder (39,40). Often conceptualized as a condition of acute hospitalization, catatonia is also encountered in outpatient care, though its recognition remains limited (37).

Pathophysiology

Catatonia arises from a convergence of complex and interacting biological processes. While its precise pathophysiology remains incompletely understood, evidence suggests it reflects widespread disruptions across neurochemical, structural, and genetic systems. Rather than stemming from a single lesion or neurotransmitter deficit, catatonia likely represents a final common pathway of dysfunction involving motor control, affect regulation, and arousal (17,25,41-45). Although subtypes discussed below share overlapping features, each may arise from distinct mechanisms.

Neurotransmitter imbalance is central to catatonia’s neurobiology. Reductions in gamma-aminobutyric acid (GABA), excess glutamate activity at N-methyl-D-aspartate (NMDA) receptors, and decreased dopamine have all been implicated (25,43-45). This model is supported by the clinical response to benzodiazepines which enhance GABA, and by the observation that dopamine-2-receptor (D2) blocking antipsychotics can trigger or worsen catatonia (17,25,41-43). Functional imaging studies also show disrupted connectivity and abnormalities in motor circuits, reinforcing the role of diffuse network dysfunction (25,43-45).

Genetic and structural abnormalities may further predispose individuals. Variants in neurotransmitter-related genes and familial clustering support a heritable risk, with first-degree relatives showing significantly higher incidence (46). Malignant catatonia, marked by autonomic instability, may involve disrupted pathways between the orbitofrontal cortex, hypothalamus, and brainstem (25,43,45). Core motor features such as rigidity, mutism, and posturing likely reflect dysfunction in the basal ganglia, thalamus, supplemental motor area, and motor cortex (43,45,46). Evidence of glial activation and impaired blood-brain barrier function further supports a neuroinflammatory contribution (43,45,46).

Psychological and developmental factors also shape vulnerability. Dysregulation in limbic pathways, particularly between the orbitofrontal cortex and amygdala, may underlie behavioral arrest and emotional withdrawal (12-14). Some have likened this to tonic immobility, a primitive defense response to extreme threat (17,43,46). Individuals with early trauma or chronic stress exposure may be especially susceptible (17,43).

Catatonia subtypes and descriptors

Catatonia encompasses a range of psychomotor disturbances and is often classified by both underlying etiology and clinical presentation. The initial distinction is whether catatonia occurs in the context of a psychiatric or medical condition. The Diagnostic and Statistical Manual of Mental Disorders, fifth edition, text revision (DSM-5-TR) classifies catatonia as a syndrome marked by at least three of twelve characteristic signs, and into two primary types: (I) catatonia associated with another mental disorder (CAMD) and (II) catatonia due to a medical condition (CAMC) (1). The International Classification of Diseases (ICD-11) similarly recognizes catatonia as a distinct clinical syndrome that can arise in the setting of various mental or medical illnesses (17,47). While mood disorders are the most common psychiatric cause, medical contributors—such as seizures, autoimmune encephalitis, infections, strokes, and neoplasms (especially ovarian teratomas)—account for over half of all cases (1,2,4,17,47,48). Compared to adults, children with catatonia are more likely to develop catatonia due to encephalitis, psychotic disorders, and neurodevelopmental disorders (49). For both adults and children, identifying the underlying etiology is essential, as effective treatment hinges on addressing contributing medical and psychiatric comorbidities.

Beyond etiology, catatonia has also been subdivided by motor presentation. Though not formally codified in DSM-5-TR or ICD-11, catatonia is commonly described as hyperkinetic, hypokinetic, or parakinetic, reflecting a spectrum of psychomotor activity (Table 2) (50). Presentations may shift over time or even within a single episode. Descriptive terms like “excited”, “stuporous”, “retarded”, “periodic”, or “malignant” are frequently used to convey clinical severity and phenomenology (44). Any form can evolve into malignant catatonia, a life-threatening variant characterized by autonomic instability and high mortality risk.

Assessment and diagnosis

The diagnosis of catatonia draws on a combination of structured clinical observation and validated assessment tools. A thorough evaluation involves physical examination, patient interview, chart review, and collateral input from family or caregivers (1,17,44). Among available instruments, the Bush-Francis Catatonia Rating Scale (BFCRS) remains the most widely used. It includes a 14-item screening tool and a 23-item comprehensive scale that captures a range of psychomotor abnormalities—including hypoactivity, hyperactivity, and bizarre behaviors suggestive of catatonia (1,17,44,47,51,52). The screening version has shown high sensitivity in both psychiatric and medical settings, and Table 3 outlines the signs included (53). In addition to aiding diagnosis, the BFCRS is commonly used to track symptom severity and monitor response to treatment (51).

Although the BFCRS is a robust clinical tool, formal diagnostic criteria are defined by the DSM-5-TR and ICD-11, which differ in important ways (1,17,47). Both systems require at least three catatonic features for diagnosis. The DSM-5-TR lists 12 features but does not allow a diagnosis of catatonia in the context of delirium. In contrast, the ICD-11 includes 15 signs and permits diagnosis when catatonia co-occurs with delirium or substance use (17,47). Unique to the ICD-11 are signs such as verbigeration, ambitendency, staring, rigidity, and psychomotor agitation. It also combines echolalia and echopraxia into a single category, while the DSM-5-TR separates them (17,47).

Beyond these frameworks, many clinically important features of catatonia fall outside formal diagnostic systems but are included in the BFCRS. Signs such as impulsivity, automatic obedience, mitgehen, gegenhalten, perseveration, grasp reflex, withdrawal, and autonomic instability can offer critical diagnostic clues, particularly in complex or atypical presentations (51). Their inclusion in the BFCRS makes the scale particularly valuable in settings where catatonia is underdiagnosed (51,53).

In situations where the diagnosis remains uncertain, a positive treatment response may help clarify the clinical picture. The lorazepam challenge—typically involving 1–2 mg of intravenous (IV) or intramuscular (IM) lorazepam—can lead to rapid and sometimes dramatic improvement of catatonic features in adults and children. A response, defined as at least a 50% reduction in BFCRS score, is considered confirmatory and guides further treatment (43). The test is most useful as a rule-in measure and a negative challenge does not rule out catatonia, as some patients improve only after repeated doses or alternative interventions. Careful monitoring for sedation and other adverse effects is essential, particularly in medically complex patients (43).

Catatonia in children and medically ill individuals may present atypically, making recognition even more challenging. In pediatric populations, symptoms like incontinence, negativism, or apparent volitional hyperactivity may obscure diagnosis (54,55). In critically ill children, signs of dysautonomia or neurostorming should raise concern for malignant catatonia (43). Similar caution applies in adults, where hypokinetic catatonia may be misattributed to neurologic disease, delirium, or dementia (26).

Management

The management of catatonia rests on three essential principles: confirming the diagnosis, identifying and treating contributing causes, and alleviating catatonic symptoms. When clinical features raise concern for catatonia, structured assessment tools such as the BFCRS and lorazepam challenge can assist in diagnosis and symptom quantification.

Once recognized and diagnosed, a thorough assessment should investigate potential psychiatric, medical, and pharmacologic etiologies. Particular attention should be paid to recently initiated or discontinued medications, as catatonia has been associated with D2 receptor antagonists, including antipsychotics like haloperidol and antiemetics such as metoclopramide, as well as withdrawal from benzodiazepines and clozapine (56).

Although randomized trials are lacking, three clinical guidelines and an American Psychiatric Association resource document offer consistent recommendations for initial treatment (2,3,50,56). Benzodiazepines, most commonly lorazepam, are considered the first-line intervention. Lorazepam has demonstrated response rates of 66–100% across multiple studies, including retrospective reviews and case series (56). Initial dosing typically ranges from 1 to 4 mg per day, with reduced doses (1–2 mg daily) recommended for older adults (2,3,56,57). In more refractory cases, doses as high as 24 mg daily have been reported (2,3,50,56). While some patients experience rapid improvement within hours, others require several days of treatment before a response becomes evident. Once the syndrome resolves and any underlying drivers are adequately addressed, lorazepam can be tapered. In many cases where the underlying etiology has been identified and resolved, a rapid taper may be tolerated; however, symptom recurrence in some patients may necessitate a slower reduction over several weeks (56).

In cases where lorazepam provides only partial benefit or is limited by sedation or other adverse effects, alternative treatments may be considered. NMDA receptor antagonists, such as memantine and amantadine, have been used with some success and are supported by expert consensus (2,3,56,58). In selected cases—particularly in older adults or where mutism is a prominent feature—zolpidem may be useful, though its short half-life and lack of parenteral forms restrict its broader application (56).

Electroconvulsive therapy (ECT) is the definitive treatment for catatonia when symptoms are life-threatening, progressive, or refractory to pharmacologic interventions (2,3,56,58,59). Expert consensus suggests that ECT should be considered a co-first-line treatment alongside benzodiazepines; however, access is often limited by legal restrictions, stigma, and availability of trained personnel (50,60). Although the precise mechanism of action is not fully understood, ECT is believed to modulate GABAergic, glutamatergic, and dopaminergic neurotransmission and promote neuroplasticity and cortical connectivity changes (45,60). Despite limited controlled data, the efficacy of ECT in catatonia is well established in clinical practice. Response rates of 80–100% have been consistently reported across pediatric, adult, and geriatric populations (2,3,56,58,59). Early initiation is associated with better outcomes and a reduced risk of complications, as delayed treatment may lead to diminished responsiveness over time (43,56,60-62).

ECT is also generally well tolerated. Serious complications are rare, and the risk-benefit ratio is generally favorable, particularly in cases of severe or treatment-refractory catatonia (2,3,26,50,56,63). Where available, ECT may be administered in ICU or general medical ward settings when indicated by severity and supported by institutional resources and legal frameworks (2,3,50,56). Clinical improvements are often observed after four to six sessions over one to two weeks (43,56,60,61).

ECT is particularly indicated in malignant catatonia and should be employed as a first-line intervention (50,56,64-66). In recognition of its utility, the US Food and Drug Administration (FDA) reclassified ECT devices in 2018 as class II (moderate risk) for the treatment of catatonia in individuals aged 13 years and older who are treatment-resistant or require urgent symptom control. Notably, the FDA did not define “treatment resistance” or “severity”, leaving these determinations to clinical judgment (65,67).

Morbidity and mortality

Catatonia is associated with medical complications, many of which are preventable with timely recognition and intervention. Approximately one in four patients with catatonia develops medical sequelae, including deep vein thrombosis (DVT), pulmonary emboli (PE), rhabdomyolysis, malnutrition, pressure injuries, and significant physical deconditioning (10,68). Immobility in hypokinetic forms of catatonia is a key driver of these risks, particularly for thromboembolic events and pressure ulcers (68). Notably, the risk of VTE in catatonia has been shown to exceed that of patients in prolonged physical restraints (68). Malnutrition and dehydration are particularly common in patients with prolonged withdrawal or mutism and may necessitate enteral or parenteral support (10,68). Rhabdomyolysis, driven by prolonged immobility or severe agitation, can progress to renal failure (25).

Malignant catatonia is especially severe, representing a medical emergency with a high risk of mortality if not treated promptly. This form of catatonia includes autonomic instability—such as hyperthermia, tachycardia, and labile blood pressure—that can progress to myocardial infarction, multiorgan failure, and cardiopulmonary arrest (17,25). Malignant catatonia has been studied in both adults and children, with mortality rates for untreated cases estimated to be as high as 75–100% (17,25,38,69,70). The urgency of early intervention is underscored by evidence that treatment delays are associated with reduced response to treatment and increased risk of death (56,62). Catatonia may become increasingly treatment refractory over time, reinforcing the need for rapid identification and treatment initiation.

Beyond physical complications, catatonia inflicts significant psychological and existential suffering. Catatonic symptoms often impair voluntary movement, verbal communication, and responsiveness, creating barriers to assessing and meeting basic needs (71). Patients may be unable to report pain, discomfort, or preferences, which can lead to goal-discordant care (26). Despite these outward signs of unresponsiveness, emerging evidence suggests that many patients with catatonia remain cognitively aware. In qualitative studies, individuals described the experience as frightening and isolating with common themes of feelings of abandonment, intense longing for loved ones, and preoccupation with death and fear (11). Even in the absence of primary mood disorders, depression is frequently reported (12-14).

Part 2: catatonia in patients with serious illness

While nearly a century of clinical experience, robust diagnostic frameworks, structured assessment tools, treatment algorithms, randomized trials, and outcome data exist to guide the care of patients with catatonia, there is a striking lack of evidence to inform the assessment and management of catatonia in the context of serious medical illness or the dying process (17). In this second part of our review, we aim to provide guidance grounded in available evidence, supported by clinical experience, and supplemented with anecdotal insight where necessary. Where possible, we cite relevant research and clarify which recommendations are evidence-based, which are extrapolated from existing data, and which reflect expert consensus. We also identify key challenges and gaps in the literature, as well as propose areas for future research to improve care for patients with serious illness and catatonia.

Recognition of catatonia in patients with serious illness matters

Catatonia is both common and impactful in patients with serious illness, with well-documented morbidity, mortality, and psychological toll (10-14,17,25,26,38,56,62,68-70). Catatonia compromises communication, often impairs decision-making capacity, and adds a substantial burden on caregivers (10-14,17,25,26,38,56,62,68-70). Taken together, these effects disrupt autonomy, diminish QOL, and increase suffering—not just for patients, but for those who care for them. For all these reasons, we would argue that catatonia itself could be considered a serious illness (12-14,16,18,19,26,72).

Despite its relevance, catatonia occurring in the setting of serious illness is frequently mistaken for progressive dementia or the dying process itself (26). These misinterpretations can obscure prognosis, redirect goals of care (GOC) conversations, and lead to premature decisions about hospice referral or withdrawal of treatment (26). With some studies citing nearly one in four ICU patients meeting criteria for catatonia, PC providers are likely encountering catatonia in their daily practice, although it often goes unrecognized (17,20,21).

To our knowledge, no studies have specifically examined whether treating catatonia improves QOL or reduces caregiver distress in patients with serious illness. Still, clinical experience suggests that restoring function and communication, especially near the end of life (EOL), can shift the trajectory of care in meaningful ways.

For all of these reasons, recognizing and managing catatonia directly aligns with the goals of PC, which seeks to relieve suffering, preserve dignity, promote autonomy, and improve QOL for patients and caregivers through interdisciplinary, holistic support (72).

Missed opportunities and diagnostic challenges

Underdiagnosis of catatonia is not unique to PC. Driven by a combination of unfamiliarity, diagnostic complexity, and subtle presentation, catatonia underdiagnosis is the norm (17,20,23,29,51,52,56,66,73). This is particularly true for CAMC, which is likely the more common form encountered in PC (66). In a case series involving neurological patients ultimately diagnosed with catatonia, none were initially recognized as having the condition; instead, they received alternative diagnoses, including extrapyramidal symptoms, meningitis, conversion disorder, acute psychosis, encephalopathy, and non-convulsive status epilepticus (74). Retrospective studies in hospital and ICU settings have shown similar trends (20,23,29,73). A systematic review found that while medical causes were identified in only 20% of catatonia cases overall, this rose to over 50% in acute medical-surgical settings and approached 100% in elderly, critically ill patients (4). A milestone New England Journal of Medicine review underscored this diagnostic challenge by outlining a broad differential diagnosis for catatonia across clinical contexts—including delirium, neuroleptic malignant syndrome, serotonin syndrome, substance intoxication or withdrawal, autoimmune encephalitis, and structural brain lesions. Notably, however, that review did not address catatonia in the PC or hospice setting (59). For PC clinicians, clinical suspicion for a medical cause should be high, especially in the absence of a prior psychiatric diagnosis (66).

Phenomenological studies outside of serious illness suggest some differences in presentation between medical and psychiatric catatonia. Psychiatric catatonia is more likely to involve posturing, stereotypy, mannerisms, waxy flexibility, impulsivity, and perseveration, whereas medical catatonia is more commonly associated with autonomic instability, comorbid delirium, grasp reflex, hyperactivity, and a history of neurologic illness or seizures (4,75). These patterns may help guide diagnostic thinking, though overlap is frequent.

Catatonia also rarely presents as the stereotypical stuporous or florid akinetic state often depicted in textbooks (74). More often, it appears subtly—through purposeless agitation, mutism, urinary retention, rigidity, or unexplained diaphoresis—and is easily misattributed to hypoactive delirium, depression, or withdrawal (17,51,52,56,76). This is especially relevant in PC, where the manifestation of catatonia may be shaped by cognitive impairment, polypharmacy, and overlapping medical conditions (17,51,52,56). In this context, catatonia can closely resemble terminal delirium, progressive dementia, or even EOL anorexia (20,25,77-79).

Screening and assessment: a role for PC clinicians

PC clinicians are often the first to notice subtle changes in mental status, especially in patients with serious illness or functional decline (80). This places PC clinicians in a unique position to recognize features of catatonia, perform bedside screening, initiate a lorazepam challenge when appropriate, and advocate for further diagnostic workup or psychiatric consultation. Just as importantly, they can help ensure that care remains goal-concordant, aligned with the patient’s values, and guided by the overall prognosis.

Recognizing catatonia at the bedside begins with clinical suspicion. While completing a full BFCRS may not be feasible in all settings, we suggest PC teams should at minimum be familiar with key signs that can be assessed quickly at the bedside, including staring, waxy flexibility, withdrawal, grasp reflex, and rigidity. PC teams can also consider use of the Catatonia Quick Screen, a four-item screening instrument derived from the BFCRS with high sensitivity (81). In settings where psychiatric consultation is unavailable, PC teams may need to recognize a broader range of BFCRS features and consider initiating a lorazepam challenge themselves, particularly when symptoms are distressing or rapidly progressing. Educational resources, including those from The Catatonia Foundation and video demonstrations from the University of Rochester, can support clinician confidence in bedside screening and assessment (51,52,82).

We recommend maintaining a high index of suspicion for catatonia in any patient with serious illness presenting with acute or subacute mental status changes from baseline, particularly those with motor features and/or underlying cognitive impairment, neurologic disease, significant psychiatric history, or unexplained weight loss and withdrawal.

Catatonia and delirium often wax and wane, share overlapping features, and commonly co-occur (17,76). Because benzodiazepines typically help in catatonia but may worsen delirium, distinguishing between the two is critical (17). Although DSM-5-TR excludes catatonia in the context of delirium, multiple studies have shown that co-occurrence is possible (1,56). In practice, a key clinical clue that should prompt consideration of catatonia is delirium that fails to improve or paradoxically worsens after antipsychotic treatment (21,27,57,83,84). Delirium that does not improve with standard treatment, or worsens after antipsychotic use, should prompt consideration of catatonia. Although clinicians may hesitate to use lorazepam in patients with altered mental status, a positive response to a diagnostic dose is generally interpreted as evidence that treating catatonia is likely to be more beneficial than harmful (2,3,56,85).

As with any intervention in serious illness, these decisions must be guided by clinical judgment and grounded in context. Factors such as age, frailty, comorbid substance use, overall prognosis, and patient values should all shape the approach. While not without risk, a single diagnostic dose of lorazepam is often well tolerated, and when clinical suspicion is moderate to high, the potential benefit of identifying and treating catatonia likely outweighs the risks (2,3,56,85).

Prognostication and medical decision-making

Prognostication is a core skill in PC, essential for guiding medical decisions and aligning treatments with patient values (72,86-89). However, the presence of catatonia can significantly complicate this process.

Although catatonia frequently represents a reversible condition, it may signal a turning point in the trajectory of serious illness, potentially heralding a new central nervous system lesion, systemic infection, psychiatric decompensation, or disease progression (4,17,26). In some cases, it reflects irreversible decline, such as cancer advancement or a new stroke, with major implications for prognosis.

Additionally, catatonia features may independently contribute to medical complications (17). These factors may worsen outcomes regardless of underlying etiology and should be thoughtfully integrated into prognostic conversations.

When catatonia is suspected, diagnostic evaluation should be tailored to the patient’s GOC. For patients pursuing full workup, appropriate studies may include neuroimaging, lumbar puncture with cerebrospinal fluid (CSF) analysis, electroencephalogram (EEG), and laboratory evaluation. For those near the EOL, clinical judgment should weigh the burden and invasiveness of testing against likely yield and therapeutic impact (see Figure 1). Shared decision-making, grounded in the patient’s values and informed by clinical context, should guide this process.

Figure 1 Medical workup of catatonia: a risk-benefit approach to diagnostic testing. CT, computed tomography; EEG, electroencephalogram; MRI, magnetic resonance imaging.

Ultimately, identifying catatonia—even in patients with limited life expectancy—can support prognostication, clearer communication and promote care that remains aligned with the patient’s goals.

Managing catatonia: guidance for PC clinicians

No specific guidelines are available for PC clinicians working at the intersection of catatonia and serious illness (2,3,50,56). Likewise, no published recommendations define the specific role of PC clinicians in the recognition, assessment, or management of catatonia. Figure 2 provides targeted guidance for PC clinicians on treating catatonia in patients with serious illness, with particular attention to the added complexity of factors such as older age, frailty, polypharmacy, substance use, and medical comorbidities—all of which can impact the risks and benefits of treatment (2,3,50,72,90).

Figure 2 Role of the PC clinician in the evaluation and management of catatonia in serious illness. BFCRS, Bush–Francis Catatonia Rating Scale; PC, palliative care.

PC clinicians are more likely to encounter CAMC, which may be less responsive than CAMD to standard treatments like benzodiazepines. When the underlying etiology is potentially treatable, PC clinicians can encourage early identification and intervention. When the cause requires complex interventions like artificial nutrition, dialysis, or surgery, PC teams can help patients and families navigate those decisions within a GOC framework (10,25,68,72).

Treatment in the outpatient PC setting poses several challenges. Outpatient access to IV lorazepam, ECT referral, or psychiatric referral is often limited. This may lead to the emergency department, which may not align with the stated GOC. In these cases, we suggest considering a short-term trial of oral lorazepam or amantadine, with dosing and duration guided by risk-benefit analysis, patient goals, and overall prognosis (37).

In older adults with serious illness, lower-dose lorazepam (1–2 mg/day in divided doses) is often effective and better tolerated (57). When benzodiazepines are inadequate or poorly tolerated, the PC clinician is encouraged to consider second-line options such as amantadine or memantine (2,3,56,91). Though evidence remains limited, the largest case series in older patients suggests both classes can be helpful when initiated conservatively, with attention to minimizing sedation and other adverse effects (57,91).

Prevalence of substance use disorders is high in patients with serious illnesses. Catatonia often presents in the context of substance intoxication or withdrawal, particularly with substances such as cannabis, cocaine, alcohol, opioids, or benzodiazepines. While no specific guidelines exist to guide management of catatonia in this setting, current guidance generally supports the use of benzodiazepines or ECT as first-line treatment, even in patients with active or recent substance use (2,3,56,59,91).

In patients with serious illness, there are multiple barriers to the use of ECT, including stigma, hospital infrastructure, legal frameworks, clinician comfort, and concerns about the impact of medical comorbidity. While ECT is safe and well-studied, stigma remains a powerful barrier (92-95). Furthermore, nearly every state imposes legal restrictions on ECT, many of which limit its use to adult patients who can consent for themselves (92-95). These statutes may prevent its use in patients with catatonia who lack decision-making capacity, even if they have surrogate decision-makers (96,97). Many hospitals lack the resources, trained staff, or policy frameworks to administer ECT in ICUs or general medical settings. Even where ECT is technically available, patients with serious illness may be excluded due to medical concerns such as brain metastases, recent stroke, or the medically imposed risks associated with general anesthesia. Because ECT works by inducing a seizure under anesthesia via electrical stimulation, these concerns are legitimate and warrant careful consideration. In some cases, protocols can be adapted—for example, modifying electrode placement to avoid tumor-involved areas—but feasibility and safety must always be considered in light of the patient’s overall prognosis and GOC (2,3,26,50,56,98).

Despite these challenges, a growing body of literature supports the use of “palliative ECT” for select patients. ECT’s rapid onset and effectiveness in treating catatonia, depression, and psychosis make it a compelling option in time-sensitive situations where other treatments have failed or are too slow-acting (26,99). One recent cohort study examined patients referred to both PC and ECT services for this indication. Most were treated for catatonia and had significant comorbidities, including cancer, advanced organ disease, and dementia. Among those who received ECT, outcomes included reduced mortality, reversal of life-threatening weight loss, correction of inappropriate dementia diagnoses later attributed to catatonia, cognitive improvement even in patients with coexisting dementia, and improved quality of life, including near the EOL (26,98).

Given that some forms of catatonia respond only to ECT, we suggest that in select cases, a time-limited treatment trial—an “ECT challenge” akin to a diagnostic lorazepam challenge—may help clarify both diagnosis and prognosis, particularly before considering hospice enrollment (60). If ECT is not available locally, referral to a center where it is available should be considered. Transcranial magnetic stimulation (TMS), a less invasive neuromodulation technique used primarily for mood disorders, is being explored as a potential alternative. However, evidence for its use in catatonia remains limited, and its role in the PC population is not yet well defined (100).

EOL and hospice considerations

Catatonia at the EOL is under-recognized and poorly studied (26,98,99). Given that terminal delirium affects nearly 90% of dying patients, we contend that catatonia—at a minimum, as a co-occurring condition—is likely far more common than currently recognized (101,102). In our clinical experience, the dying process and terminal delirium often share phenomenological features, and many patients exhibit signs consistent with catatonia in their final days. PC clinicians are uniquely positioned to identify catatonia in the hospice setting, differentiate potentially reversible presentations from irreversible decline, and guide appropriate hospice referrals and management (26).

While catatonia is often reversible, some patients experience treatment-refractory illness in which ECT and pharmacologic interventions fail to restore communication, function, or oral intake (17,20,43). In these cases, patients may meet hospice eligibility due to complications such as malnutrition or infection, even if catatonia itself is not the primary qualifying diagnosis. To our knowledge, no studies have examined the prevalence of catatonia at the time of hospice enrollment or the impact of treatment in hospice on patient outcomes, including the potential for hospice graduation.

In the hospice setting and, in an attempt to improve comfort and reduce suffering near the EOL, recognizing catatonia and trialing low-dose lorazepam is a high-yield, relatively low-risk intervention. In this setting, we recommend avoiding D2 blocking agents, which may worsen symptoms, and instead suggest considering benzodiazepines or NMDA antagonists to relieve distressing psychomotor features (17,26,103).

Hospice regulations may limit access to interventions that are both life-prolonging and palliative such as dialysis, transfusions, advanced heart failure therapies, and ECT (104). Some patients with chronic or relapsing catatonia require maintenance ECT on a spaced schedule (e.g., weekly), and recurrence of symptoms is often seen when treatment intervals are extended (17,59). A palliative ECT approach, prioritizing function and comfort, is consistent with hospice philosophy but may be financially or logistically restricted, and there is an opportunity for PC clinicians to advocate for continued access. Future research and advocacy are needed to explore how ECT and other psychiatric treatments might be incorporated into models of concurrent care in hospice (104).

Future directions

Despite growing awareness of catatonia in patients with serious illness, critical gaps remain in how best to assess and manage this condition in PC settings. Future work must aim to clarify the true prevalence and impact of catatonia among patients with serious illness. Prospective epidemiologic studies across care settings, including outpatient clinics, inpatient units, and long-term care facilities, are needed to capture the full scope of catatonia’s presentation and burden.

Further studies are needed to examine how catatonia affects QOL, caregiver burden, communication, decision-making, and overall clinical trajectory. Just as importantly, education and training for non-psychiatric clinicians could improve recognition and reduce diagnostic delays. Brief bedside tools that account for diagnostic uncertainty and overlap with delirium may support earlier identification and treatment. Decision aids developed with patients, caregivers, and clinicians could further guide conversations about interventions like ECT, especially when balancing symptom relief, prognosis, and treatment burden in the setting of serious illness.

Finally, further study is needed at the EOL. The experience and prevalence of catatonia in hospice settings remain almost entirely unexamined. Future work should focus on defining treatment approaches such as oral lorazepam protocols, expanding access to ECT where feasible, and developing outcomes focused on comfort, clarity, and dignity. Coordinated efforts in research, education, and advocacy are essential to improve care for catatonia across the spectrum of serious illness.

Conclusions

Catatonia is a severe but often reversible neuropsychiatric syndrome that can profoundly shape the course of serious illness. Though historically associated with psychiatric conditions, it is increasingly recognized in medically complex patients, where it may be misconstrued as other neuropsychiatric conditions, obscure prognosis, and disrupt communication and decision-making.

In PC, where symptom relief, communication, and aligning treatment with patient goals are central, the timely recognition and treatment of catatonia can meaningfully improve QOL. For PC clinicians, it must become a routine diagnostic consideration. Integrating catatonia into daily practice allows clinicians to navigate complexity with greater confidence and ensure care remains focused on what matters most to patients and families.

Acknowledgments

None.

Footnote

Provenance and Peer Review: This article was commissioned by the Guest Editor (Alexander Gamble) for the series “Integration of Palliative Care and Mental Health Services” published in Annals of Palliative Medicine. The article has undergone external peer review.

Peer Review File: Available at https://apm.amegroups.com/article/view/10.21037/apm-25-76/prf

Funding: This study was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development (No. 1P50-HD103537 to J.R.S.) and National Institute of Mental Health (No. R01-MH135028 to J.R.S.), and was supported in part by the Department of Veterans Affairs, Geriatric Research, Education, and Clinical Center (funding to J.W.).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://apm.amegroups.com/article/view/10.21037/apm-25-76/coif). The series “Integration of Palliative Care and Mental Health Services” was commissioned by the editorial office without any funding sponsorship. J.R.S. reporting receiving grants from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (No. 1P50-HD103537), National Institute of Mental Health (No. R01-MH135028), Roche, Axial, Vanda, Bristol Myer Squibb, Johnson and Johnson, and Otsuka; and payment or honoraria for research colloquium from American Academy of Child and Adolescent Psychiatry. The authors have no other conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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