CONTENTS

• Basics
• Pathophysiology
• Epidemiology
• Clinical presentation
• Differential diagnosis
• Diagnostic criteria
• Diagnostic challenge with lorazepam or ketamine
• Causes of catatonia
• Investigation for underlying cause
• Management
• Podcast
• Questions & discussion
• Pitfalls

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basics

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core concepts of catatonia

• Catatonia is a motor dysregulation syndrome involving difficulty initiating or terminating actions.(19884605) Most commonly this causes periods of physical rigidity, negativism, or stupor (although psychomotor hyperactivity may also occur).
• Catatonia is more common than generally realized. It is often misdiagnosed as delirium.
• Although catatonia is traditionally associated with schizophrenia, it is more often triggered by acute medical illness or affective disorders (e.g., bipolar disorder). The diagnosis of catatonia in the context of psychiatric disorders can be challenging, as there may be overlapping features of both conditions.
• Recognition of catatonia is essential because it is a highly treatable condition which responds to specific interventions. Alternatively, provision of nonspecific supportive care may often fail (especially in malignant catatonia).
• Catatonia is a spectrum disorder which varies in severity (rather than a binary, dichotomous condition).(33896535) More extreme cases will be more easily recognizable.

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pathophysiology

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general conceptualization

• The precise mechanism(s) of catatonia remains unclear. Overall, catatonia seems to reflect an abnormality of neural circuitry that regulates movement (involving the basal ganglia, thalamus, and cortex; figure below). This shares some similarities with Parkinson's disorder.
• Catatonia is closely related to neuroleptic malignant syndrome (NMS). Indeed, neuroleptic malignant syndrome is arguably a subset of malignant catatonia that is induced by neuroleptics.(28144147, 24275514, 19884605)
• Although catatonia may appear similar to delirium, these are fundamentally distinct processes:
  • Delirium is predominantly an abnormality of attention, which largely reflects dysfunction of the cerebral cortex.
  • Catatonia is predominantly an abnormality of motor regulation, which largely reflects dysfunction of the basal ganglia.

neurotransmitter imbalances

• Catatonia seems to involve several neurotransmitter imbalances (perhaps with different imbalances occurring in different patients). These include the following:
• (#1) Inadequate dopamine activity at D2-receptors:
  • D2-receptor inhibition by typical antipsychotics may exacerbate catatonia.
  • Dopamine augmentation (e.g., by levodopa, bromocriptine, or amantadine) may improve catatonia.
• (#2) Inadequate GABA signaling:
  • Deficient GABA activity due to withdrawal of benzodiazepines may trigger catatonia.
  • Administration of benzodiazepines (GABA-A agonists) generally improves catatonia.
• (#3) Excessive signaling via glutaminergic NMDA receptors:
  • Inhibition of NMDA signaling may improve catatonia (e.g., by ketamine or memantine).

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epidemiology

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• The precise incidence of catatonia is debatable (due to lack of any uniform, simple clinical diagnostic criteria). However, catatonia appears to be common and generally overlooked – especially within the critical care arena.
  • Catatonia may be seen in ~10% of acutely hospitalized psychiatric or medical patients.(26162545, 19884605, 31147176)
  • Among patients being evaluated for possible delirium, 12-37% may have catatonia (depending on the criteria used).(26162545)
• Catatonia may be more common in elderly patients.
• Individual patients may have repeated episodes of catatonia. In some cases this may represent a genetically mediated form of periodic catatonia.

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clinical presentation

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clues in the clinical history

• Patients with catatonia due to a psychiatric condition may experience a behavioral prodrome for weeks involving psychosis, agitation, insomnia, anorexia, or apathy.(28144147)
• A useful pattern to recognize is patients who present with agitation, receive treatment with antipsychotic medications, and subsequently deteriorate. Thus, catatonia should be considered in patients who appear to have “medication refractory psychosis” or “refractory agitation.”(34619813)

clinical clues – bizarre features

• Catatonia may be suggested by bizarre features that aren't generally seen in the context of medical illness (e.g., due to delirium). However, psychiatric disorders can also cause some of these features (e.g., grimacing, echolalia, perseveration). More prominent features include the following:
• Posture & tone
  • Catalepsy (passive induction of a posture held against gravity).
  • Waxy flexibility (slight, even resistance to positioning by the examiner – as if bending a candle).
  • Posturing (spontaneous and active maintenance of a posture against gravity).
  • Gegenhalten (resistance to movement with force equal and opposite to that applied by the examiner; must be motiveless).
  • Mitgehen (even very slight pressure causes the patient to move in that direction, even if instructed not to move).
  • Ambitendency (patient seems to get stuck in indecisive movements).
• Negative symptoms
  • Negativism (opposition or no response to instructions or external stimuli).
  • Mutism (verbally unresponsive, without evidence of aphasia).
• Positive symptoms
  • Mannerism (odd, circumstantial caricature of normal actions).
  • Grimacing (maintenance of odd facial expressions).
  • Stereotypy (Repetitive, abnormally frequent, non-goal-directed movements. Examples include rocking, biting, sniffing, chewing, or tapping.).
  • Verbigeration (form of verbal stereotypy that involves continual repetition of meaningless phrases).
  • Echophenomena:
    • Echolalia (mimicking another's speech).
    • Echopraxia (mimicking another's movements).
    • Automatic obedience (exaggerated cooperation with request or excessive continuation of a requested movement).
  • Impulsivity (suddenly behaves inappropriately for no apparent reason, unable to explain behavior).

three types of catatonia

• Catatonia can generally be described as either hypokinetic catatonia (causing stupor) or hyperkinetic catatonia (causing agitation). Hypokinetic catatonia is the most common. However, individual patients can transition back and forth between these two extremes.
• Either hypokinetic or hyperkinetic catatonia may lead to autonomic instability, if severe enough. Catatonia which causes autonomic instability is defined as malignant catatonia.

hypokinetic catatonia (aka akinetic catatonia, stuporous catatonia)

• Overall patients generally appear obtunded, rather than completely comatose.(Posner 2019)
  • In the context of acute medical illness this may be misdiagnosed as “hypoactive delirium.”
  • This may sometimes manifest in elderly patients as “failure to thrive.”
• The most common symptoms include:
  • Immobility (~97%).
  • Mutism (no or very little verbal response)(~97%).
  • Withdrawal and refusal to eat (~91%).
  • Staring is common (~87%)(but some patients may have closed eyes that are resistant to passive eye opening).(33896535)
  • Motor symptoms (e.g., rigidity, posturing) may occur less commonly (~50%).
• Patients may fail to respond to painful stimuli.(19884605)
• Patients may be incontinent of urine or stool, or may retain urine and require catheterization.(Posner 2019)

hyperkinetic catatonia (aka, excited catatonia)

• Patients experience prolonged periods of psychomotor agitation.
• These are marked by nonpurposeful hyperactivity or motor unrest.(Posner 2019)
  • Unlike mania, activity is not goal-oriented.
• Disorganized, overproductive speech may be repetitive (verbigeration).(24275514; 32067538)
• Combativeness may occur.

malignant catatonia (aka lethal catatonia)

• Malignant catatonia may complicate either hypokinetic catatonia or hyperkinetic catatonia. The key finding in malignant catatonia is catatonia plus autonomic instability (especially hyperthermia, which is required for the diagnosis of malignant catatonia).
• Autonomic instability:
  • Hyperthermia is an especially important component.
  • Diaphoresis.
  • Labile blood pressure and/or tachycardia.
  • Tachypnea.
• Rigidity is a central feature, seen in ~80% of patients.(Frucht 2022)
• Altered consciousness.
• (Neuroleptic malignant syndrome (NMS) is a subtype of malignant catatonia which is induced by neuroleptics.(28144147, 24275514) Similar to neuroleptic malignant syndrome, malignant catatonia may be life-threatening due to hyperthermia, rhabdomyolysis, and acute kidney injury.)(26162545)

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differential diagnosis

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differential diagnosis of hypokinetic catatonia

• This may closely mimic:
  • Hypoactive delirium.
  • Akinetic mutism.
  • Locked-in syndrome.
  • Nonconvulsive status epilepticus.
  • Extrapyramidal/movement disorders (e.g., Parkinson's disease, acute dystonia, tardive dyskinesia).
  • Meningitis.
  • Major depression (with or without psychotic features).
  • Functional coma, aka “pseudocoma” (although there is probably considerable overlap between catatonia and patients diagnosed with functional coma).
• More on the approach to stupor/coma here: 📖

differential diagnosis of hyperkinetic catatonia

• This may tend to closely mimic:
  • Agitated delirium.
  • Acute mania.
  • Complex partial seizures / nonconvulsive status epilepticus (NCSE).
  • Akathisia.
• More on the differential diagnosis of delirium here: 📖

differential diagnosis of malignant catatonia

• Neuroleptic malignant syndrome (NMS) 📖 is important to consider, especially as many patients with psychiatric disorders may be receiving neuroleptics.
• CNS infection (e.g., meningitis).
• More on the differential diagnosis of the hyperthermia component here: 📖

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diagnostic criteria

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The two major psychiatric manuals (DSM-5 and ICD-11) have defined catatonia very similarly. Based on the more recent ICD-11 definition, catatonia is defined as displaying at least three of the following symptoms (if not better accounted for by another movement disorder): (the following text is copied from the ICD-11)

• Decreased psychomotor activity:
  • Staring: fixed gaze, decreased blinking, often with widely opened eyes.
  • Ambitendency: appearance of being ‘motorically stuck’ in indecisive or hesitant movement.
  • Negativism: opposing or behaving contrary to requests or instructions, which may lead to withdrawal from interaction with others (turning away) or refusal to take food or drink when offered.
  • Stupor: immobility; no or markedly reduced psychomotor activity; minimally responsive to external stimuli.
  • Mutism: no or very little verbal response; speech may be hushed or whispered to the point of being unintelligible. (Note: Do not count if speech symptoms are due to a Disease of the Nervous System, Developmental Speech or Language Disorder, or other disease or disorder affecting speech.)
• Increased psychomotor activity: Any of the following: extreme hyperactivity or agitation for no reason with non-purposeful movements and/or uncontrollable, extreme emotional reactions; impulsivity (sudden engagement in inappropriate behavior without provocation); combativeness (striking out against others usually in an undirected manner, with or without the potential for injury).
• Abnormal psychomotor activity:
  • Grimacing: odd or distorted facial expressions; often inappropriate and irrelevant to the situation.
  • Mannerisms: odd, purposeful movements that are not appropriate to the individual’s cultural context; exaggerated caricatures of mundane movements.
  • Posturing: spontaneous and active maintenance of a posture against gravity; sitting or standing for long periods without reacting.
  • Stereotypy: repetitive, non-goal-directed motor activity (e.g., finger-play, repeatedly touching, patting or rubbing self); the abnormality is not inherent in the action but relates to its frequency
  • Rigidity: resistance by way of increased muscle tone. May range in severity from mildly increased tone to severe ‘lead pipe’ rigidity.
  • Echophenomena: mimicking examiner’s speech (echolalia) or movements (echopraxia).
  • Verbigeration: continuous and directionless repetition of words, phrases, or sentences.
  • Waxy flexibility: slight and even resistance to positioning by examiner.
  • Catalepsy: passive induction of a posture (typically examiner passively moves patient’s extremity) which remains held against gravity.

Satisfying these criteria doesn't necessarily guarantee a diagnosis of catatonia – so alternative differential diagnoses must still be considered. Nonetheless, diagnostic criteria may be useful to provide some objective criteria for a diagnosis.

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diagnostic challenge of GABA-A or NMDA receptor inhibitors

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Traditionally, lorazepam has been used as a diagnostic/therapeutic challenge to help determine whether patients have catatonia. With increasing interest in ketamine, it's conceivable that ketamine might be utilized in a similar fashion.

lorazepam challenge

• This involves administration of 2 mg IV lorazepam (or ~1 mg IV lorazepam in patients at high risk of side effects, such as frail elderly patients, or patients at risk of respiratory depression).(26162545)
• Look for some improvement in symptoms within ~30 minutes (which may range from mild to dramatic).
• The diagnostic sensitivity is unclear, but might be ~80%.(26162545)
• Improvement following lorazepam is not entirely specific for catatonia (e.g., similar responses may be seen in patients with nonconvulsive status epilepticus or alcohol withdrawal).
  • In a patient with agitation, try not to be confused by the effects of nonspecific sedation. Ideally, an improvement in catatonic features should be seen following lorazepam administration.
  • Patients with catatonia are generally resistant to the sedating effects of lorazepam, so if nonspecific sedation occurs this could argue against the diagnosis of catatonia.
• Lorazepam may be continued if the patient improves, or if there continues to be a very high suspicion of catatonia (more on this below).

ketamine challenge

• Two case studies describe ketamine as being rapidly effective in catatonia at very low doses (e.g., 10 or 12.5 mg).(32001125, Kobayashi 2021) The sensitivity or specificity of a ketamine challenge for catatonia is unknown.
• The efficacy of ketamine makes sense for the following reasons:
  • The pathophysiology of catatonia is thought to involve excessive glutaminergic activity (more on this above).
  • Memantine (an oral NMDA-receptor antagonist with a mechanism of action similar to ketamine) has been used to treat catatonia.
• The exact role of ketamine challenge in the diagnosis of catatonia currently remains unclear. However, a ketamine challenge offers several advantages:
  • (1) Ketamine is generally extremely safe, even in patients who are somnolent (who may be at increased risk of airway suppression following a lorazepam challenge).
  • (2) Ketamine is very rapid-acting, allowing precise dose titration.
  • (3) Ketamine is short-acting, so if ketamine exacerbates symptoms then this will be a short-lived effect.
• The optimal way to perform a ketamine challenge is unclear. However, administering small doses of ketamine with careful observation seems reasonable (e.g., ~3 mg IV every few minutes up to a maximal dose of ~15-20 mg).(32001125)
• If a patient responds favorably to ketamine, it might be expected that they would also respond favorably to memantine or amantadine (since these agents also inhibit NMDA receptors).

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causes of catatonia

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Caution: Due to variation in the clinical definition of catatonia, it's difficult to precisely define which patients have catatonia. Furthermore, establishing causality with underlying etiologies is often impossible. The following list is based on several sources, but ultimately this is doomed to be both incomplete and excessively broad. (Posner 2019, 33896535)

medications/toxins

• Anti-dopaminergic medications:
  • Antipsychotics: Typical antipsychotics in particular may exacerbate catatonia and potentially precipitate malignant catatonia. (However, withdrawal of chronically utilized antipsychotics may also cause catatonia.)
  • Metoclopramide, prochlorperazine, promethazine.
• Lithium toxicity.
• Steroid.
• Tacrolimus, cyclosporine.
• Baclofen.
• Antibiotics (fluoroquinolones, cephalosporins, azithromycin).(33896535)
• Alcoholism, disulfiram.
• Levetiracetam.
• Substances of abuse, especially: cannabis, amphetamines, MDMA (aka extasy), cocaine withdrawal, phencyclidine (PCP).
• Withdrawal from alcohol, benzodiazepines, dopaminergic medications (including amantadine), or atypical antipsychotics (especially clozapine).

metabolic disorders

• Adrenal insufficiency or Cushing's disease.
• Diabetic ketoacidosis.
• Hyponatremia.
• Hypercalcemia.
• Uremia.
• Wernicke encephalopathy.
• B12 deficiency.
• Wilson's disease.

structural CNS disease

• Cerebral tumors.
• Intracranial hemorrhage (including subdural hemorrhage, subarachnoid hemorrhage).
• Ischemic stroke.
• Traumatic brain injury.
• Multiple sclerosis.
• Parkinsonism.

infection or inflammation

• Meningitis or encephalitis, especially viral encephalitis.(34842777)
• Non-CNS infection (e.g., urinary tract infection).(31011075)
• Anti-NMDA receptor encephalitis is increasingly recognized as a common cause of severe catatonia.(Freucht 2022)
• GABA-A receptor encephalitis.
• LGI1 receptor encephalitis.
• Lupus, Sjogren's syndrome.
• Hashimoto's encephalopathy.

seizure disorder

• Catatonia may occur during ictal states or postictal states (e.g., following status epilepticus).(31147176; 31011075)
• Catatonia may result from antiepileptic medications (e.g., levetiracetam).(31011075)

psychiatric

• Affective disorders are the most common psychiatric causes (especially bipolar disorder or depression with psychotic features).
• Psychotic disorders (including schizophrenia, schizoaffective disorder, and brief psychotic disorder due to acute stress).
• Autism spectrum disorder.

idiopathic

• Idiopathic catatonia is common (comprising half of patients in some series).(Posner 2019)

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investigation for underlying cause

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The optimal evaluation will depend on patient specifics, but the following investigations may be considered:

neurological examination

• Catatonia itself should not affect cranial nerve reflexes (e.g. pupillary reflexes).
• Oculocephalic reflexes are often absent (since these may be suppressed by the cortex in the absence of structural neurological damage). However, stronger stimulation via cold calorics is preserved (the vestibulo-ocular reflex) – and this should elicit a pattern of nystagmus identical to that seen in an awake and normal person (more on the vestibulo-ocular reflex here 📖).
• Optokinetic responses are usually present (if present, this implies that the brainstem and visual cortex are functioning).
• Deep tendon reflexes are usually present.(Posner 2019)

medication review

• See the list of implicated medications above.
• Evaluate also for any recently discontinued medications.

laboratory studies

• Electrolytes, including Ca/Mg/Phos.
• Cortisol level and thyroid stimulating hormone (TSH) level.
• Creatine kinase (to evaluate for rhabdomyolysis).
• Liver function tests.
• Additional toxicological workup as appropriate, based on the context.

neuroimaging (preferably MRI)

• Neuroimaging should be normal (unless there is an underlying structural neurological cause of the catatonia).

lumbar puncture

• Evaluation for infection.
• Consider sending autoimmune encephalitis panels (both from CSF and from serum).

EEG

• EEG should be considered, especially in patients displaying bizarre behaviors (e.g., staring, grimacing, repeated movements). Some of these symptoms could occur in patients with complex partial seizures or nonconvulsive status epilepticus.
• EEG might also be helpful in sorting out catatonia versus delirium.(Posner 2019) EEG findings in delirium may include the following
  • (1) Perhaps the most common finding may be slowing of the background EEG rhythm. This is especially seen with delirium due to hepatic encephalopathy or sedatives. Of course, this pattern may be nonspecific among patients who have been treated with exogenous sedatives.)
  • (2) Delirium due to withdrawal usually causes low-voltage, fast activity.
  • (3) GRDA (generalized rhythmic delta activity) is frequently associated with delirium, especially if it is frontally predominant. 📖
  • (4) GPDs (generalized periodic discharges), especially with triphasic morphology, may be associated with various forms of delirium. However, in some cases the GPDs may themselves be causing encephalopathy, thereby lying within the ictal-interictal continuum. 📖
• A normal EEG supports catatonia rather than delirium. (However, catatonia due to an underlying medical condition may not have a normal EEG). A normal EEG in a patient who is unable to follow commands has a limited differential diagnosis (e.g., severe neuromuscular weakness, locked-in syndrome, catatonia, neuroleptic malignant syndrome).(LaRoche 2018)

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management of catatonia

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overview of management

• Meticulous supportive care along with management of any triggers of catatonia is fundamental.
• The only therapies supported by substantial evidence are lorazepam and electroconvulsive therapy (ECT). For patients in whom catatonia is causing critical illness (e.g., malignant catatonia), early ECT should be considered.
• The role of other medical therapies is less clear (e.g., amantadine and dopaminergic agents). These agents are discussed below, but please note that they are not supported by high-level evidence.
• Chronic catatonia in patients with schizophrenia may be treatment resistant (including to benzodiazepine and ECT).

supportive care

• Treat any underlying cause.
• Avoid anti-dopaminergic agents, especially antipsychotics.(24275514) These may worsen the condition and potentially precipitate neuroleptic malignant syndrome (NMS). Typical antipsychotics are more problematic than atypical antipsychotics, but both should usually be avoided. Other medications which inhibit dopamine signaling should also be avoided (e.g., metoclopramide and prochlorperazine). Some exceptions to this are as follows:
  • Withdrawal of chronic therapy with atypical antipsychotics may precipitate catatonia (especially clozapine withdrawal). In this scenario, antipsychotic resumption may be helpful. Clozapine's effect on other neurotransmitters (e.g., glutamate modulation) may outweigh its effects on dopamine signaling.
  • Aripiprazole is another potential exception to this, given its unique partial agonist activity at the D2 receptor. Aripiprazole might be helpful to treat catatonia in the context of underlying psychosis.(28917389)
• Restart dopamine agonists if these were recently discontinued (e.g., Parkinson's medications).
• Management of hyperthermia (if present).📖
• Diagnosis and management of rhabdomyolysis.📖
• Fluid resuscitation may be needed in patients with reduced oral intake and/or profuse diaphoresis, with monitoring of electrolytes and hemodynamics.
• Nasoenteral tube placement to provide nutritional support.📖 Among patients with subacute catatonia and poor intake for several days, attention is required to avoid refeeding syndrome.📖
• DVT prophylaxis is important, especially among immobile patients.
• Foley catheter placement may be needed in patients with urinary retention.
• Meticulous skin care may be needed to prevent pressure ulceration.
• Dexmedetomidine may be especially useful in nonintubated patients with catatonia and agitation.(34619813) In refractory agitation, valproic acid may also be considered (see below).
• In malignant catatonia, high-quality supportive care resembles the management of neuroleptic malignant syndrome (discussed further here 📖).

lorazepam

• Lorazepam is generally considered a front-line agent for catatonia (including both hypokinetic catatonia and hyperkinetic catatonia).
• The usual dose is initially 6-8 mg daily (e.g., 2 mg IV q8hr). This may be up-titrated if necessary and well-tolerated (up to 30 mg total daily dose).(24275514)
• Lorazepam monotherapy may be effective in ~75% of patients with catatonia. Resolution usually occurs over ~4-10 days, after which lorazepam may be very gradually tapered off.
• Lorazepam is usually a cornerstone of the medical regimen, with ECT or other agents being added to it as necessary. However, for patients with coexisting schizophrenia or delirium, lorazepam may be less helpful.
• Among intubated patients, propofol may be useful in providing sedation and potentially treating the catatonia. Note that propofol's mechanism of action is similar to benzodiazepines (with GABA-A receptor augmentation).(Frucht 2022)

electroconvulsive therapy (ECT)

• ECT is effective in ~90% of patients with catatonia.(26162545) In malignant catatonia, daily ECT often achieves physiological stability within 2-5 days.(19884605) ECT appears to be effective regardless of the cause of catatonia.(Frucht 2022)
• ECT requires the availability of this therapy within the hospital as well as some form of consent (which may be problematic among patients who are altered).
• Potential indications for ECT include:
  • Malignant catatonia.
  • Inadequate response to medical treatment for ~2-5 days (depending on severity).
  • Patients requiring a rapid treatment response (e.g., inability to safely provide supportive care).
  • Patients with underlying depression or bipolar disorder may benefit especially from ECT (since it also treats these disorders).

amantadine or memantine

• The use of these agents is supported by small case series.(26162545) Both agents inhibit NMDA receptor signaling. Amantadine also augments dopamine signaling (which may be beneficial for catatonic symptoms – but could risk exacerbating psychotic features in patients with underlying psychosis).
• Theoretically, ketamine could be utilized to determine which patients would benefit most from these agents (since ketamine, amantadine, and memantine all inhibit NMDA receptors). More on the ketamine challenge above 📖.
• Amantadine:
  • The starting dose is 100 mg daily or BID. This may be increased over 3-4 days to a maximal dose of 200-300 mg BID.(28917389)
  • Amantadine may reduce seizure threshold, so it should be used with caution in patients with a history of seizure.(28917389)
• Memantine:
  • Starting dose 5 mg BID. This may be increased over 3-4 days to 10 mg BID.(28917389)

dopaminergic agents

• Dopaminergic agents may be considered in refractory catatonia, especially if catatonia was precipitated by the use of neuroleptics. This is essentially identical to the use of bromocriptine in neuroleptic malignant syndrome. Dopaminergic agents may exacerbate any underlying psychosis, so caution is required in the context of underlying psychotic disorders.
• Bromocriptine is discussed further in the chapter on neuroleptic malignant syndrome here.📖
• Carbidopa/levodopa may also be considered in refractory catatonia, at doses ranging from 25-100 mg/day.(33896535; 28917389)

valproic acid

• Some cases suggest that valproic acid could be useful in catatonia, possibly by potentiation of GABA signaling.
• Valproic acid could be useful pragmatically as a treatment of agitation in catatonic patients, who may have limited treatment options for agitation (since antipsychotic agents are generally avoided).(17431072) Valproate may be especially useful in patients with underlying bipolar or schizophrenia-spectrum disorder, as it provides treatment for these conditions.(28917389)
• More on the use of valproic acid for agitation here: 📖

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questions & discussion

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To keep this page small and fast, questions & discussion about this post can be found on another page here.

• Avoid misdiagnosis and treatment with antipsychotics, since this may actually exacerbate the catatonia.
• Don't assume that catatonia is due to a psychiatric diagnosis (e.g., schizophrenia). Similar to delirium, catatonia requires an evaluation to exclude an underlying medical or neurological cause.
• During a catatonic episode, some patients retain awareness but are unable to communicate. Treat patients compassionately, given the possibility that they have preserved awareness.

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