Catatonic stupor: signs and treatment

Catatonic stupor is a form of catatonia characterized by marked motor retardation, immobility, silence, lack of initiative, and minimal reactions to the environment. This is not "laziness" or "stubbornness," but an acute psychomotor disorder requiring urgent diagnosis, as without treatment, deterioration is possible, leading to life-threatening complications. Modern classifications consider catatonia a syndrome that can accompany various mental and physical illnesses. [1]

The syndrome includes a set of characteristic symptoms: stupor, waxy flexibility, catalepsy, mutism, negativism, fixed postures, stereotypies, echolalia, and echopraxia. For clinical diagnosis, it is not the individual symptoms that are important, but their combination, persistence, and marked impairment of daily functioning. In this context, "catatonic stupor" is a state dominated by immobility and silence, often accompanied by a refusal to eat or drink. [2]

Catatonia is not unique to schizophrenia. It is often observed in mood disorders, autoimmune, infectious, and metabolic diseases, as well as during medication use or withdrawal. The correct treatment strategy and prognosis critically depend on the underlying cause, so early recognition and a targeted search for the etiology are essential. [3]

Key treatment methods include benzodiazepines using the "lorazepam test" and electroconvulsive therapy (ECT). In severe or malignant cases, as well as in cases of inadequate response to medication, ECT has been shown to be highly effective, including in pediatric patients when life-threatening conditions arise. [4]

Code according to ICD-10 and ICD-11

In the International Classification of Diseases, Tenth Revision, catatonia can be coded in two ways: as "catatonic schizophrenia" F20.2 or as "catatonic disorder due to a known physiological condition" F06.1 if a somatic cause is identified. In some situations, catatonic stupor is coded R40.1 "stupor," but this is only acceptable as a symptom of a primary somatic diagnosis. [5]

In the International Classification of Diseases, Eleventh Revision, catatonia is classified separately: “catatonia associated with another mental disorder” 6A40, “catatonia due to substances or drugs” 6A41, and “catatonia, unspecified” 6A4Z if the cause cannot be determined. This approach reflects modern clinical reality and facilitates the indication of etiology in the diagnosis. [6]

Table 1. Correspondence of codes for catatonia and catatonic stupor

Classification	Chapter	Code	When to apply
ICD-10	Catatonic schizophrenia	F20.2	When catatonia is a manifestation of schizophrenia
ICD-10	Catatonic disorder due to a physiological condition	F06.1	When a somatic or neurological cause is identified
ICD-10	Stupor	R40.1	As a symptom within the framework of the main somatic diagnosis
ICD-11	Catatonia in other mental disorder	6A40	For mood disorders, psychosis, etc.
ICD-11	Substance- or drug-induced catatonia	6A41	In case of intoxication, withdrawal or side effects
ICD-11	Catatonia, unspecified	6A4Z	When the causal diagnosis has not yet been established
[7]

Epidemiology

According to meta-analyses and reviews, catatonia is detected in 9%–20% of acute psychiatric inpatients, and in some samples, the frequency reaches 27% or higher with active screening. This discrepancy is explained by different criteria, instruments, and populations. [8]

In the UK general population, the estimated incidence is about 4.34 episodes per 100,000 person-years, and the mean point-in-time prevalence is about 4.39 per 100,000. These estimates are lower than hospital estimates, reflecting the predominantly hospital-based nature of severe catatonia manifestations.[9]

An analysis of the United States National Inpatient Sample for 2016–2020 found that catatonia was diagnosed in approximately 0.035% of all hospitalizations, with 3,255 cases recorded in children. In adolescents and young adults, psychiatric etiology was more common, and some patients had a medical etiology. [10]

Overall data indicate a significant prevalence of catatonia in mood disorders and psychoses, but the syndrome also occurs in autoimmune, metabolic, infectious, and toxic conditions. This justifies the mandatory evaluation of a somatic cause, especially in catatonic stupor. [11]

Reasons

Catatonic stupor can occur in mental disorders, most commonly mood disorders and schizophrenia, as well as in neurological and somatic diseases, including autoimmune encephalitis, metabolic disorders, infections, vitamin deficiencies, and endocrine disorders. Drug effects and withdrawal of certain medications have also been described as causes.[12]

The pathogenesis involves dysfunctions of the gammogenic, glutamatergic, and dopaminergic systems, as well as disruptions in the regulation of networks including the amygdala, insular cortex, and prefrontal regions. Stressors and inflammatory processes can serve as triggers. [13]

Adverse reactions to neuroleptic drugs and malignant catatonia syndrome partially overlap clinically with neuroleptic malignant syndrome, which creates risks of diagnostic error and erroneous prescription of antipsychotic drugs in acute stupor. [14]

In children and adolescents, the proportion of psychiatric etiology is approximately 75%, with psychotic disorders dominating, but medical causes are also significant and require a targeted search. [15]

Risk factors

Risk factors include the presence of severe affective and psychotic disorders, previous episodes of catatonia, recent changes in psychopharmacotherapy, acute somatic and neurological conditions, and autoimmune processes. Identification of these factors increases the physician's alertness to stupor in vulnerable patients. [16]

Sleep deprivation, dehydration, hyponatremia, folate and vitamin B12 deficiency, thyroid dysfunction, and systemic infection increase the risk of stupor. In the presence of such conditions, the diagnostic algorithm is supplemented by laboratory and instrumental tests. [17]

The risk of relapse is higher in patients with the 'inhibited' form of catatonia and in those who have previously demonstrated a good response to benzodiazepines, which requires the development of an individualized prevention plan and training in recognizing early signs. [18]

Table 2. Risk factors for catatonic stupor

Group	Examples	Clinical significance
Mental disorders	Mood disorders, schizophrenia, autism	High probability of catatonia syndrome
Medicinal factors	Recent prescription or escalation of doses of psychotropic medications	Risk of catatonia and neuroleptic malignant syndrome-like phenomena
Somatic causes	Encephalitis, infections, metabolic and endocrine disorders	They require targeted search and treatment of the cause.
Nutrition and metabolism	Folate deficiency, vitamin B12 deficiency, electrolyte imbalances	They worsen the severity and increase the risk of complications
[19]

Pathogenesis

Current data indicate an imbalance in neurotransmitter systems. A decrease in GABAergic transmission and an increase in glutamatergic activity increase the excitability of neural networks responsible for motor initiative and reactivity, which manifests as stupor and negativism. [20]

Disruption of the interaction between cortical regulatory areas and the basal ganglia and amygdala leads to the "sticking" of behavioral programs and a loss of response flexibility. This explains the phenomena of waxy flexibility, stereotypies, and echophenomena. [21]

The response to benzodiazepines is interpreted as indirect confirmation of the role of GABAergic deficit. Studies of memantine and amantadine as modifiers of glutamatergic transmission are based on the same logic, although the evidence base here is still limited and inconsistent. [22]

The overlap of clinical features of malignant catatonia and neuroleptic malignant syndrome is explained through common stress reactions at the level of dopaminergic systems and autonomic regulation, which requires careful differential diagnosis and caution with antipsychotic drugs until catatonia is relieved. [23]

Symptoms

The main signs of catatonic stupor are immobility, mutism, lack of response to stimuli while maintaining a waking posture, negativism, and refusal to engage in contact. Waxy flexibility and postural rigidity are often observed. Prolonged stupor rapidly increases the risk of dehydration and thromboembolism. [24]

Echolalia, echopraxia, mannerisms, stereotypies, and grimacing are also observed, which in some patients precede stupor. Lability of the autonomic nervous system is often observed: tachycardia, fluctuations in blood pressure, and increased sweating. [25]

Basic behavioral functions such as eating, drinking, hygiene, and sleep are impaired. This leads to rapid somatic decompensation, emphasizing the need for early hospitalization if catatonic stupor is suspected. [26]

Standardized assessments are performed using scales, particularly the Bush-Francis scale. It has a 14-item screening version and a 23-item expanded version, which helps not only confirm the syndrome but also monitor its progress under the influence of therapy. [27]

Classification, forms and stages

Clinically, a distinction is made between an "inhibited" form, where stupor, mutism, and negativism predominate, and an "excited" form with motor agitation and possible impulsive actions. In real-life practice, mixed and fluctuating variants are possible. [28]

According to the course, a distinction is made between acute episodes developing against the background of mental and somatic illnesses and chronic, protracted forms. Malignant catatonia is described separately, in which catatonic symptoms are accompanied by hyperthermia, severe autonomic instability, and increased creatine kinase. [29]

In children and adolescents, catatonia is increasingly recognized and may be associated with psychotic, affective, and neuroimmune disorders. In these groups, rapid diagnosis and targeted treatment are particularly important due to the high rate of somatic complications. [30]

Table 3. Clinical variants of catatonia

Option	Main features	Clinical risks
Slowed down	Stupor, mutism, waxy flexibility	Dehydration, thrombosis, bedsores
Excited	Motor restlessness, impulsivity	Injuries, interruption of treatment, exhaustion
Malignant	Catatonia plus hyperthermia and autonomic instability	Life-threatening condition requiring intensive care
[31]

Complications and consequences

Left untreated, catatonic stupor quickly leads to dehydration, electrolyte imbalance, thromboembolic complications, rhabdomyolysis, aspiration pneumonia, and pressure ulcers. Mortality increases in malignant forms and with late initiation of therapy. [32]

Prolonged immobility leads to muscle loss and impaired glucose metabolism, which worsens the physical condition. Mutism can also hinder communication with medical staff and family members, increasing the risk of underestimating the severity of the condition. [33]

An erroneous tactic with the early administration of high doses of antipsychotic drugs before the relief of catatonia can increase the severity of the syndrome and contribute to the development of conditions similar to neuroleptic malignant syndrome. [34]

Table 4. Common complications of catatonic stupor

System	Complication	Why does it arise?
Cardiovascular	Deep vein thrombosis, pulmonary embolism	Immobilization, blood thickening
Kidneys and muscles	Rhabdomyolysis, acute renal failure	Physical inactivity, dehydration
Respiratory system	Aspiration pneumonia	Difficulty swallowing, decreased cough reflex
Leather	Bedsores	Prolonged lying down, impaired microcirculation
[35]

When to see a doctor

Immediate medical attention is required in the event of sudden immobility, cessation of speech, refusal to eat or drink, or unresponsiveness to treatment. These signs warrant an emergency inpatient evaluation. [36]

If the patient has severe mental disorders, autoimmune and endocrine diseases, or recent changes in psychopharmacotherapy, any episode of severe inhibition and mutism should be considered as a potential catatonic stupor. [37]

It's important for relatives to know that attempts to "revive" the patient by force are ineffective and dangerous. A medical assessment, monitoring of vital signs, and initiation of specialized therapy are necessary. [38]

Diagnostics

The diagnosis is clinical and based on the identification of at least three characteristic features, their persistence, and significant impairment of functioning. The Bush-Francis scale is used for standardization: first, a 14-item screening, followed by a detailed 23-item assessment to monitor progress. [39]

A parallel assessment of the patient's somatic status is performed, with mandatory monitoring of temperature, pulse, blood pressure, oxygen saturation, glucose levels, electrolytes, creatine kinase, and renal and liver function. This is necessary to detect malignant variants and a medical cause. [40]

If autoimmune genesis is suspected, neuroimaging, electroencephalography, and extensive laboratory testing, including N-methyl-D-aspartate receptor antibodies and other markers, are considered. The physician decides on the list of tests based on the clinical presentation and medical history. [41]

The therapeutic and diagnostic "lorazepam challenge" helps confirm catatonia: intravenous administration of 2 milligrams often results in a noticeable reduction in symptoms within a short time. Lack of response does not rule out the diagnosis and requires re-evaluation and alternative steps. [42]

Table 5. Step-by-step diagnostic tactics for suspected catatonic stupor

Step	Action	Task
1	Clinical assessment and screening according to the Bush-Francis scale	Confirmation of the syndrome and initial severity
2	Monitoring vital signs and basic tests	Exclusion of malignant course and complications
3	Advanced search for the cause of indications	Identification of autoimmune, infectious or metabolic nature
4	Lorazepam test	Confirmation and start of treatment
5	Risk-based and comorbidity-based treatment planning	Choosing between benzodiazepines and electroconvulsive therapy
[43]

Differential diagnosis

Malignant catatonia and neuroleptic malignant syndrome share common features: hyperthermia, muscle rigidity, autonomic instability, and elevated creatine kinase. Differences are related to medication history, dynamics, and the leading catatonic signs, so collecting a detailed history of psychotropic medication use is essential. [44]

Delirium can mimic catatonic stupor, but delirium is characterized by fluctuations in consciousness and marked attention deficits. In some cases, a combination of the two is possible, requiring parallel treatment of the underlying somatic disorder and the catatonia. [45]

Depressive stupor is characterized by the predominance of painful melancholy, severe mental pain and daily dynamics, whereas in catatonia, motor and behavioral signs with echophenomena and waxy flexibility dominate. [46]

Table 6. Differential landmarks

State	Key Features	Tips for the doctor
Catatonic stupor	Immobility, mutism, waxy flexibility, echophenomena	Response to lorazepam, Bush-Francis scale is positive
Neuroleptic malignant syndrome	Hyperthermia, rigidity, antipsychotic medication use	Recent prescription or dose increase of an antipsychotic
Delirium	Fluctuation of consciousness, impaired attention	Search for a somatic cause, infection, metabolic failure
Depressive stupor	Longing, mental pain, daily dynamics	Less echophenomena and waxy flexibility
[47]

Treatment

The basic strategy begins with ensuring safety: monitoring breathing, circulation, and temperature, preventing thrombosis, correcting dehydration and electrolyte imbalances, caring for the skin, and preventing aspiration. This is not "preparation" but a vital part of treatment, especially in stupor. [48]

Benzodiazepines are the first line of drug treatment. Lorazepam is administered at an initial dose of approximately 2 milligrams intravenously, with reassessment at short intervals. If a partial response is observed, the dose is titrated based on the scale and clinical findings, while monitoring respiration and sedation. A significant proportion of patients experience a rapid clinical response. [49]

If the response is absent or incomplete, consideration is given to switching to electroconvulsive therapy. Current guidelines recommend bilateral stimulation at least twice a week in acute cases, and in malignant cases, accelerated regimens involving an anesthesiologist and resuscitation team. Efficacy is high even in severe and protracted episodes. [50]

Antipsychotics are used with caution in acute catatonic stupor, usually after the catatonia has been relieved. The exception is life-threatening situations where there is a confirmed psychotic driver with a significant threat. However, even then, benzodiazepines and electroconvulsive therapy remain the preferred treatment. [51]

If autoimmune encephalitis or another inflammatory cause is suspected, etiotropic and immunotherapeutic approaches are added to the basic therapy according to specialized standards. For patients with drug-induced catatonia, the key measure will be discontinuation of the offending agent under the supervision of a physician. [52]

Amantadine and memantine are considered potential adjuvants in patients with a partial response to benzodiazepines and who are not candidates for immediate electroconvulsive therapy. The evidence base is moderate, so decisions are made on an individual basis based on a benefit-risk assessment. [53]

In pediatric patients with life-threatening symptoms and benzodiazepine resistance, electroconvulsive therapy has proven safe and effective when used in a multidisciplinary setting. Informed communication with the family, a detailed explanation of the goals and risks, and careful monitoring are essential. [54]

Reintroduction to eating and drinking is gradual, with the assistance of a dietitian and a speech therapist if swallowing is impaired. Early initiation of physical therapy and gentle verticalization reduce the risk of thromboembolism and pressure ulcers. Families and staff are trained in appropriate communication techniques without pressure or threats. [55]

After catatonia has been relieved, a secondary prevention plan is developed: recognition of early signs, discussion of supportive psychotherapy, careful resumption and correction of psychopharmacotherapy, education of the patient and relatives, control of risk factors, including sleep, nutrition and somatic state. [56]

Table 7. Comparison of key treatment approaches

Approach	Role	Strengths	Restrictions
Lorazepam and other benzodiazepines	First line	Fast effect, diagnostic value	Risk of sedation, respiratory risks at high doses
Electroconvulsive therapy	Highly effective in the absence of response	Rapid reduction of severe symptoms	Requires anesthesia and infrastructure
Amantadine, memantine	Adjuvant	Possibility to enhance the effect with a partial response	The evidence base is limited
Supportive measures	Mandatory for everyone	Reduce mortality and complications	The syndrome does not resolve without specific therapy.
[57]

Prevention

Primary prevention involves early recognition of catatonia among patients with mental and physical illnesses. Physician training and the use of standardized scales increase detection rates and reduce the time to treatment. [58]

Secondary prevention is aimed at preventing relapses: monitoring sleep and nutrition, carefully adjusting psychopharmacotherapy, gradually titrating doses, and informing the patient and family about the first signs of deterioration. An action plan is developed in advance. [59]

Tertiary prevention is aimed at reducing the consequences of the past episode: supportive psychotherapy, rehabilitation, work with comorbid conditions and regular medical examinations in the first months after discharge. [60]

Forecast

With timely initiation of benzodiazepine therapy and electroconvulsive therapy, the prognosis is favorable, and full recovery is often observed. Delayed treatment and malignant variants worsen outcomes and increase the risk of complications. [61]

Relapses are possible, especially in patients with chronic mental disorders. Having an individualized prevention plan and family involvement reduces the likelihood of recurrence and improves quality of life. [62]

In pediatric practice, timely interdisciplinary care allows for the achievement of sustained remission even in severe episodes. When necessary, electroconvulsive therapy remains a reliable method for relieving resistant conditions. [63]

FAQ

Is this condition unique to schizophrenia?
No. Catatonia, including catatonic stupor, is often found in mood disorders and somatic illnesses. Therefore, a search for the cause is always performed, rather than limiting oneself to a single nosology. [64]

Why is a lorazepam test necessary and is it safe?
It helps confirm the diagnosis and initiate treatment. Typically, 2 milligrams are administered intravenously with repeated assessment. The procedure is performed by medical personnel with monitoring. [65]

When is electroconvulsive therapy needed?
If there is no response to benzodiazepines or the progression is threatening, as well as in malignant cases. The method is effective and safe with proper anesthetic preparation. [66]

Is it possible to start antipsychotics immediately?
In most cases, no. Catatonia is initially treated with benzodiazepines or electroconvulsive therapy. Exceptions are rare and are decided on an individual basis. [67]