American Journal of Medicine Open 10 (2023) 100059

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American Journal of Medicine Open

journal homepage: www.elsevier.com/locate/ajmo

Review

Catatonia: A Narrative Review for Hospitalists

Alyssa C. Smith∗, Emily G. Holmes
Department of Psychiatry, Indiana University School of Medicine, Indianapolis

a r t i c l e i n f o a b s t r a c t

Keywords: Background: Catatonia is a complex psychomotor syndrome commonly associated with psychiatric disorders.
Catatonia However, hospitalists encounter this condition on medical floors, where it is typically due to an underlying med-
Diagnosis ical, especially neurological, etiology. Delays in the diagnosis of catatonia are common and lead to worsened
Management
outcomes for patients, including a multitude of medical complications, such as venous thromboembolism and
Neuroleptic malignant syndrome
stasis ulcers. Catatonia due to a medical condition is less likely to respond to benzodiazepine therapy; identifica-
tion and treatment of the underlying cause is crucial.
Methods: This article provides a practical review of the catatonia literature, with a focus on diagnosis, workup,
and management of catatonia for patients admitted to medical hospitals.
Conclusions: With greater knowledge about catatonia, internists are uniquely positioned to recognize and initiate
treatment.

Introduction can be helpful and can play a crucial role in detection of this syndrome.3
However, psychiatric services are not universally available, so it can be
Catatonia is a complex syndrome, characterized by abnormalities of helpful for the hospitalist to be comfortable understanding the differen-
movement and behavior. Most commonly, physicians associate catato- tial diagnosis, workup, and treatment of catatonia. Additionally, some
nia with extreme withdrawal and vegetative symptoms, but agitated aspects of the management of catatonia are paradoxical, so even if psy-
and hyperkinetic states also exist.1 , 2 Catatonia is most often associated chiatry is providing recommendations, it can be helpful for internists
with psychiatric conditions, with a prevalence of 10%-25% in acute psy- to understand the standard treatments. Finally, the internist has an im-
chiatric patients.1-4 However, neurological and medical etiologies also portant role in monitoring for the development of the adverse sequelae
cause catatonia; 3% of acute neurology patients and 4% of patients in associated with catatonia and preventing further morbidity. Here we
intensive care units have catatonia.2 , 3 Still, this condition is underdiag- present a narrative review of catatonia, with practical guidance targeted
nosed, by both psychiatrists and internists.3 A recent study within a for the internist.
general medical hospital found that 59% of patients who retrospectively
met criteria for catatonia were not diagnosed, underscoring the need for
greater recognition of this condition.3 Catatonia Subtypes
Catatonia can result in several medical complications including
malnutrition, stasis ulcers, contractures, rhabdomyolysis, and venous Catatonia, for much of history, has been separated into ex-
thromboembolisms.2 , 4 , 5 Additionally, catatonia can progress to a lethal cited/hyperkinetic or withdrawn/hypokinetic subtypes2 , 6 ; however, pa-
variant called malignant catatonia (MC), with a mortality rate of up to tients may experience symptoms of both hyperkinetic and hypokinetic
20%.6 , 7 Unfortunately, delays in diagnosis and treatment are common, states, and switching from one subtype to another is possible within
with a 2010 study reporting an average delay in treatment of 15 days.8 the course of the syndrome.7 , 9 Examples of hyperkinetic symptoms in-
Early diagnosis and treatment are of critical importance because delays clude excitement and combativeness; examples of hypokinetic symp-
have been shown to worsen outcomes. toms include mutism, immobility, staring, negativism, and withdrawal;
Internists, especially hospitalists, are likely to encounter patients and examples of parakinetic (abnormal) symptoms include posturing,
with catatonia. Therefore, it is valuable for the internist to be familiar automatic obedience, waxy flexibility, and grasp reflex.2 , 6 , 7 , 10 These
with this syndrome so that they can recognize concerning signs, consider symptoms are summarized and defined in Table 1. Generalized anal-
psychiatric consultation, and begin treatment. Psychiatric consultation gesia and bowel and bladder incontinence and/or retention may also

∗
Corresponding Author. Alyssa Ciera Smith MD, Indiana University School of Medicine, Department of Psychiatry, 355 West 16th Street, Suite 2364, Indianapolis,
46202
E-mail address: acs13@iu.edu (A.C. Smith).

https://doi.org/10.1016/j.ajmo.2023.100059
Received 9 May 2023; Accepted 19 September 2023
Available online 28 September 2023
2667-0364/© 2023 The Author(s). Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license
(http://creativecommons.org/licenses/by-nc-nd/4.0/)
A.C. Smith and E.G. Holmes American Journal of Medicine Open 10 (2023) 100059

Table 1
Catatonic Symptoms on the Bush Francis Catatonia Rating Scale.

Movement category Symptom Definition

Immobility/stupor Decreased activity, minimal response to stimuli

Mutism Decreased verbal output, ranging from only a few words to total
silence
Staring Minimal gaze movement; decreased blinking
Hypokinetic Posturing/catalepsy Maintenance of a posture for a prolonged period
Rigidity (Gegenhalten) Maintenance of a rigid position, or resistance or stiffness with
passive range of motion
Withdrawal Decreased oral intake; decreased eye contact
Muscle resistance Resistance to passive movement of limb to repositioning, with
increased resistance to increased pressure
Ambitendency Appearance of being stuck in motor movements
Negativism Refusal to follow instructions or other oppositional behavior

Excitement Excessive motor activity

Hyperkinetic Impulsivity Sudden inappropriate behavior (ie, suddenly running down
hallway, taking off clothing)
Combativeness Sudden aggression or agitation without explanation or provocation

Grimacing Contracting the face into odd facial expressions; can be episodic or
maintained
Echopraxia Mimicking examiner’s movement
Echolalia Mimicking examiner’s speech
Stereotypy Repetitive non-goal-directed motor activity (ie, fiddling thumbs,
Parakinetic patting leg)
Mannerisms Repetitive purposeful motor activity (ie, waving hand, combing
hair); the act is unusual either in its context or its persistence
Verbigeration Repetition of words or phrases, “like a broken record”
Waxy flexibility Initial resistance to repositioning, then allowing repositioning (like
a wax candle bending)
Automatic obedience Exaggerated cooperation with examiner (ie, continues shaking
hand when told to stop; sticks tongue out if told, “stick your tongue
out for me, I’m going to stick a pin in it”)
Passive obedience Raises arm in response to light pressure of finger, even if told not to
(Mitgehen) raise arm
Grasp reflex Grasps the examiner’s fingers when the palm is rubbed
Perseveration Repetition of the same topic or motor movement

be present; while not part of the diagnostic criteria, these features may Though internists would not be expected to administer the BFCRS,
raise concern for catatonia.10-13 they may encounter the scale in consultation with psychiatry or neu-
MC is any form of catatonia with vital sign instability.6 , 10 , 14 Prior rology. Therefore, it is helpful for the internist to have a general un-
to the development of treatment of MC with benzodiazepines and elec- derstanding of BFCRS terms and scoring. Similarly, while the internist
troconvulsive therapy (ECT), the mortality rate was 75%-100%; now, would not be expected to memorize these terms, it is useful to have a
mortality has dropped to 9%-20%.6 , 7 general understanding and to consider psychiatric consultation for fur-
ther examination and diagnostic clarity when these findings are present
(Table 1).
Pathophysiology
The most common symptoms of the BFCRS in hospitalized patients
are staring, immobility/stupor, mutism (decreased verbal output), and
While the pathophysiology of catatonia is not fully understood, ab-
withdrawal.19 Underdiagnosis has been reported to be more common if
normal motor pathways and alterations in neurotransmitter systems
agitation, echolalia, and/or grimacing are present.3 When these symp-
have been implicated. These alterations include reduction in GABA ac-
toms are present, catatonia should be considered, especially if the pa-
tivity, increased glutamate activity (particularly at the NMDA recep-
tient’s status is a departure from baseline. Collateral information from
tor), and decreased dopamine activity.2 , 4 , 15 , 16 Pharmacologic treat-
family, friends, caregivers, or prior medical records will be critical when
ment aims to restore balance to these neurotransmitter systems.
the patient’s baseline is unknown.
The most common misidentified items on the BFCRS are immobil-
Diagnosis ity/stupor, posturing/catalepsy, negativism, withdrawal, and poor eye
contact.20 As such, these terms warrant increased attention and discus-
There are 2 generally accepted criteria for diagnosing catatonia. The sion. Immobility/stupor may present as decreased physical activity or
first is the criteria set in the Diagnostic and Statistical Manual, Fifth Edi- decreased responsiveness to environmental stimuli. Posturing/catalepsy
tion Text Revision (DSM-5 TR), with diagnosis of catatonia made in the may present as holding a physical position (such as a raised arm or leg)
presence of any 3 of the following 12 features: stupor, catalepsy, waxy for an extended period of time and can be assessed by moving the pa-
flexibility, mutism, negativism, posturing, mannerisms, stereotypy, agi- tient’s limb; if posturing is present, patients may not retract the limb
tation, grimacing, echolalia (verbal repetition), and echopraxia.17 to a resting position after examination. Negativism may present as op-
The second is the Bush Francis Catatonia Rating Scale (BFCRS) (see positional behavior; as only answering “no” to yes/no questions; or as
supplemental), which consists of 23 items; a diagnosis of catatonia is persistent refusal to follow instructions, without clear reason or explana-
made with the presence of 2 or more positives on the first 14 items.16 , 18 tion. Withdrawal may present as decreased oral intake, or as decreased
The BFCRS can also be helpful when used regularly to assess response eye contact with interviewers. Poor eye contact, which is considered
of symptoms to treatment. under both “staring” and “withdrawal,” may also include decreased vi-

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A.C. Smith and E.G. Holmes American Journal of Medicine Open 10 (2023) 100059

Table 2
Differential Diagnosis of Catatonia.

Diagnosis Similarities to catatonia How it differs from catatonia

Neuroleptic malignant syndrome Vital sign instability Requires exposure to newly started dopaminergic
Altered mental status agent, or recent change in dose
Low serum iron
Elevated CPK
Serotonin syndrome Altered mental status GI distress
Rigidity Hyperreflexia
Vital sign instability Clonus
Delirium Hypoactive and hyperactive types Worsened by benzodiazepines
Decreased attention
Withdrawal from environment Other psychomotor abnormalities (echolalia,
echopraxia, rigidity, etc.) not present
Coma Hypoactivity Reflexes lost in coma
Mutism Parakinetic symptoms not present
Incontinence No response to benzodiazepine challenge
Extrapyramidal side-effects (EPS) Akathisia No altered mental status
Dystonia (may look like rigidity or No other motor symptoms present; no impaired
posturing) volition
No negativism
Hypoactivity not present
Parkinsonism Rigidity No other motor symptoms present
Motor freezing Tremor present in Parkinsonism
Staring Patients generally interactive
Status epilepticus Immobility Specific EEG findings
Withdrawal

sual scanning of the environment, or difficulty in switching attention Patients with catatonia who primarily exhibit hypokinetic symp-
between different examiners. toms, such as withdrawal, mutism, and stupor, may be misdiagnosed
with coma, especially those who also have incontinence and general-
ized analgesia.12 Reflexes may be used to distinguish between these; in
Differential Diagnosis
catatonia, reflexes are preserved, whereas they may be lost in coma.12
Additionally, parakinetic symptoms such as waxy flexibility, posturing,
Differential diagnoses to consider along with catatonia are broad and
and automatic obedience would not be expected in comatose patients.
include neuroleptic malignant syndrome (NMS), serotonin syndrome
A benzodiazepine challenge, discussed in detail under treatment, would
(SS), delirium, coma, extrapyramidal side effects from medications,
be expected to differentiate between these 2 states, as one would expect
Parkinsonism, and status epilepticus. These diagnoses may be challeng-
a positive response in catatonia but not coma.
ing to differentiate from catatonia and will be discussed further and
Extrapyramidal symptoms (EPS) are motor side effects, such as
summarized in Table 2.
akathisia, dystonia, or tardive dyskinesia, associated with the use of
NMS is particularly challenging to distinguish from MC. Some au-
first- and second-generation antipsychotics.26 These movement side ef-
thors consider NMS, MC, and SS to be on a spectrum of illnesses, and
fects may appear similar to the movement abnormalities seen in cata-
some consider SS and NMS to be drug-induced forms of MC.6 , 10 , 14 , 16
tonia; however, patients with EPS alone are unlikely to present with
When viewed as separate entities, NMS is more likely than MC to have
other signs and symptoms of catatonia including negativism, impaired
lead-pipe rigidity (although it can occur in both), and NMS requires re-
volition, AMS, withdrawal, echolalia, posturing, or vital sign abnormal-
cent exposure to a change in dopaminergic agent (eg, newly started or a
ities.26
change in dose).14 However, both conditions may have altered mental
Parkinsonism—which includes forms of Parkinson’s disease, as well
status (AMS), vital sign instability, low serum iron, and elevated creatine
as EPS—can include rigidity, motor freezing, and staring, sharing over-
phosphokinase (CPK).14
lap with catatonia. Patients with Parkinsonism are generally interactive
Like NMS and MC, SS commonly presents with elevated tempera-
and are unlikely to present with other signs of catatonia. In addition,
ture, rigidity, and AMS.21 SS requires recent exposure to a serotoner-
patients with Parkinsonism usually have a characteristic tremor, further
gic agent; however, serotonergic agents are common and include an-
distinguishing this diagnosis from catatonia.27
tidepressants, antiemetic agents, first- and second-generation antipsy-
Status epilepticus can present with immobility and withdrawal like
chotics, antiepileptics, St. John’s wort, antimicrobials (particularly line-
hypokinetic catatonia; an EEG can differentiate the two.15 , 26
zolid), and illicit substances (amphetamines, lysergic acid diethylamide,
ecstasy, etc.).22 , 23 SS is less likely to present with elevated CPK, LFT al-
terations, or low serum iron and is more likely to present with gastroin-
testinal distress, hyperreflexia, and clonus.22 , 23 Etiologies of Catatonia
Delirium is defined by a fluctuating sense of orientation and atten-
tion and, like catatonia, has both hypoactive and hyperactive subtypes.6 Medical Etiologies of Catatonia
Both syndromes may present with withdrawal and decreased attention.
The other psychomotor abnormalities seen in catatonia, such as waxy When catatonia is due to an underlying medical cause, it is less likely
flexibility, rigidity, echolalia, and echopraxia, are not present in delir- to respond to standard catatonia treatments; therefore, it is crucial that
ium alone.24 The distinction between the two is important, as benzodi- medical causes are identified and treated.28 , 29 Catatonia due to a psy-
azepine therapy is likely to worsen delirium but improve catatonia, and chiatric illness should be considered a diagnosis of exclusion.16 The
antipsychotic management of agitation in delirium may worsen catato- mnemonic MINDSET (Miscellany, Inflammation of the CNS, Neural In-
nia.6 Complicating matters, delirium and catatonia may coexist in some jury, Developmental disorder, Structural CNS pathology, Epilepsy, Toxin
patients24 , 25 ; a recent paper found that catatonia is present in 12%-30% or medication) may be of benefit to help clinicians recall the most com-
of patients with delirium.25 mon etiologies.30 Additional medical etiologies of catatonia are summa-

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A.C. Smith and E.G. Holmes American Journal of Medicine Open 10 (2023) 100059

Table 3 held on admission. Fortunately, this type of catatonia is highly respon-

Summary of More Common Medical Etiologies of Catatonia. sive to reinitiation of home benzodiazepine regimen.36
Neurological Poisoning Many other medications have also been implicated in causing
catatonia, including disulfiram, aspirin, lithium, baclofen, steroids,
Encephalitis Carbon monoxide
anticonvulsants, antibiotics, antiretrovirals, bupropion, chemotherapy
Seizures Ethylene
Structural abnormalities Organophosphates agents (particularly tacrolimus), and the discontinuation of clozap-
Vascular insults Endocrine ine.4 , 6 , 15 , 32 , 33 , 36 Poisonings, including carbon monoxide, ethylene, and
TBI Hypothyroidism organophosphates, may also cause catatonia.33 It is crucially important
Hydrocephalus Hyperthyroidism to obtain a detailed history and home medication list and obtain appro-
Narcolepsy Hyperparathyroidism
Hypoxia
priate lab work when catatonia is diagnosed.
DKA
PRES Hypoglycemia Endocrine etiologies of catatonia include both hypo- and hy-
Substance Use Wilson’s disease perthyroidism, hyperparathyroidism, diabetic ketoacidosis, hypo-
Benzodiazepine intoxication or Cushing’s disease glycemia, Wilson’s disease, Cushing’s disease, and adrenal abnormali-
withdrawal Adrenal abnormalities ties.4 , 6 , 15 , 29 , 30 , 32 , 33
Alcohol intoxication or withdrawal Infectious Infections of various etiologies may cause catatonia, including those
Stimulant intoxication UTI
Hallucinogen intoxication
of the urinary tract, respiratory system, cellulitis, and systemic infec-
Respiratory infections (esp. COVID)
Inhalant intoxication tions.6 , 15 , 30 , 32 Examples of systemic infectious that may lead to catato-
Cellulitis
Medications Systemic infections nia include HIV, syphilis, CMV, and EBV.32 Recently, COVID-19 has led
Disulfiram HIV/AIDS to catatonia in a portion of affected patients.37
Aspirin Autoimmune Autoimmune conditions to consider include systemic lupus (with
Baclofen SLE or without cerebral involvement), demyelinating conditions, Crohn’s
Bupropion Demyelinating conditions
Discontinuation of clozapine disease, paraneoplastic syndromes, and Pediatric Autoimmune Neu-
Crohn’s disease
Steroids Paraneoplastic syndrome ropsychiatric Disorders Associated with Streptococcal infections (PAN-
Anticonvulsants PANDAS DAS).6 , 15 , 30 , 32 , 33
Antibiotics Metabolic Metabolic abnormalities to consider include hyponatremia, hyperna-
Antiretrovirals Hyponatremia
Chemotherapy
tremia, hypercalcemia, hyperammonemia, porphyria, renal failure, and
Hypercalcemia
Developmental hepatic failure.4 , 30 , 33 Interestingly, recent transplantation, particularly
Hyperammonemia
Autism spectrum disorder Porphyria of the liver, has also been implicated as the precipitating factor in some
Down’s syndrome Renal failure cases.33 Nutritional deficiencies to consider include vitamin B1, vitamin
Mitochondrial abnormalities Hepatic failure B3, vitamin B12, and niacin deficiencies.15 , 32 , 33
22q11.2 deletion syndrome
Nutritional Deficiencies Developmental causes of catatonia include autism spectrum disorder
Tay-Sachs’ disease
Vitamin B1
Tuberous sclerosis (ASD), Down’s syndrome, mitochondrial abnormalities, 22q11.2 dele-
Vitamin B3
Vitamin B12 tion syndrome, Tay-Sachs’ disease, tuberous sclerosis, and Prader-Willi’s
Niacin syndrome.16 , 30 , 32 , 33 , 38

Psychiatric Etiologies of Catatonia

rized in Table 3, although this table is also not all-inclusive, given the
breadth of conditions that may cause catatonia. A prior history of psychiatric illness makes the diagnosis of primary
Symptoms that favor a primary diagnosis of medical catatonia rather psychiatric catatonia, rather than medical catatonia, more likely; how-
than psychiatric catatonia include presence of delirium, autonomic ab- ever, a prior history of psychiatric illness does not exclude an underlying
normalities, excitement, presence of the grasp reflex, and a history of medical cause.30 Careful history, exam, and appropriate workup remain
a neurological condition including seizures.30 As such, when these are important in these patients.
present, suspicion of an underlying medical cause should be especially Historically, catatonia was regarded as a subtype of schizophrenia,
high. and this has resulted in a misconception that persists today.4 , 7 , 15 The
Around 70% of cases of medical catatonia are due to a neurologi- most common causes of psychiatric catatonia are the affective (mood)
cal etiology, most commonly encephalitis, particularly NMDA receptor disorders, predominately bipolar disorder and major depressive disor-
encephalitis.4 , 6 , 30 , 31 Other neurological causes include seizures, struc- der.4 , 7 , 9 , 10
tural abnormalities or space-occupying lesions, vascular insults (such
as strokes, hematomas, venous thrombosis, and aneurysms), traumatic Workup
brain injury, hydrocephalus, narcolepsy, hypoxia, and posterior re-
versible encephalopathy syndrome.4 , 6 , 15 , 30-33 Initial workup should include a complete blood count, comprehen-
Dementia, including Alzheimer’s disease, dementia with Lewy bod- sive metabolic panel, ammonia, TSH with reflex T3 and T4, urine tox-
ies, frontotemporal dementia, Creutzfeldt-Jakob’s disease, and dementia icology, iron, creatine phosphokinase, and vitamin B12 and folate lev-
due to medical conditions such as AIDS, may also present with catato- els.7 , 9 , 10 , 16 , 32 Brain imaging, ideally MRI, and an EEG should be consid-
nia.15 , 34 , 35 However, patients with catatonia may also be mistakenly ered in most cases.16 , 32 Additional workup to consider based on history
diagnosed with dementia instead of catatonia; it is important to obtain and presentation may include HIV, RPR, COVID-19, ANA, CRP, serum
a careful history including collateral, perform longitudinal assessments, copper, and ceruloplasmin, as well as a lumbar puncture with serolo-
and assess for response to benzodiazepine therapy to distinguish be- gies for encephalitis.16 , 32 , 33 , 37 A detailed history of recent exposures,
tween these diagnoses.34 , 35 including medications, should be obtained.7
Intoxication or withdrawal from various substances of abuse may
cause catatonia. Examples include alcohol or benzodiazepine intox- Management
ication or withdrawal, and intoxication with stimulants, opioids,
hallucinogens (including LSD, PCP, MDMA, and cannabis), and in- Treatment
halants.4 , 6 , 15 , 30 , 33 , 36 Benzodiazepine withdrawal precipitating catato-
nia typically occurs when the benzodiazepine use is chronic and may It is worth reiterating that if the underlying cause of catatonia is
occur when a benzodiazepine is tapered too quickly or inadvertently medical, patients are less likely to respond to treatments described be-

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A.C. Smith and E.G. Holmes American Journal of Medicine Open 10 (2023) 100059

low.28 , 29 As such, underlying causes should be promptly identified and receptor encephalitis can be treated with benzodiazepines, ECT, and
treated appropriately. NMDA receptor antagonists; NMDA receptor antagonists may be par-
The first-line treatment for catatonia is benzodiazepines, most com- ticularly useful for catatonia in these cases, given the pathophysiol-
monly lorazepam. An initial treatment is referred to as a “benzodi- ogy.43 , 44 NMDA receptor encephalitis is particularly sensitive to an-
azepine challenge,” a positive response to which is considered diagnostic tipsychotics; when these agents are administered, they may cause pro-
of catatonia, although a negative response does not exclude the diagno- gression to MC and/or NMS. Antipsychotics must therefore be used with
sis.39 A positive response is denoted by rapid improvement in catatonic caution and discontinued if signs of MC or NMS become present.43 , 44
symptoms, typically measured by comparing a BFCRS both pre- and Treatment of the underlying encephalitis may include steroids, im-
post–benzodiazepine administration. The response to the challenge in munotherapy (intravenous immunoglobin, or IVIG), or plasma ex-
hypokinetic patients is somewhat paradoxical, as post-lorazepam, these change.43
patients tend to become more interactive and may even convert to a
hyperkinetic state. It is crucial to explain to nursing the counterintu-
itive response to benzodiazepines in these patients, as without educa- Complications
tion, they may hold the medication due to concerns for oversedation,
which can worsen the catatonia and prolong the course. The lorazepam Medical complications have been reported in up to 25% of patients
should be held for respiratory depression, but it should not be held when with catatonia.45 Possible complications include DVTs/PEs, nutritional
the patient is sleeping. deficiencies, rhabdomyolysis, pressure ulcers, deconditioning, and con-
A lorazepam challenge is administered as 0.5-2 mg for a first dose, tractures.5 , 6 , 33 , 46
with lower initial dosages used for medically frail patients. Most com- Patients with catatonia are at increased risk of developing DVTs and
monly, lorazepam is administered IV, as this formulation achieves the subsequent PEs, which may be fatal; the incidence of DVT has been re-
most effective response; however, PO and IM can also be given. A lower ported as up to 35% in hypokinetic catatonia.46 DVT prophylaxis should
dose can be repeated in 10 minutes if the initial results are equivocal. A be considered in any patient hospitalized with catatonia.5 , 46
positive response will typically be observed quickly, within minutes and Dermatologic and neuromuscular complications, such as contrac-
up to 30 minutes after administration. Subsequent treatment and dos- tures, deconditioning, and skin breakdown, are complications of cata-
ing are adjusted based on response, with a goal to improve symptoms tonic immobility.5 , 6 Early engagement in physical therapy and occu-
but avoid oversedation; doses usually vary from 2 to 24 mg/day, sched- pational therapy, as well as mobility protocols, should be utilized as
uled every 6-8 hours.6 , 15 , 16 , 26 , 40 Typically, the benzodiazepine will be preventative measures.5 , 6 Fall risk should be assessed, and appropri-
titrated to achieve full resolution of catatonia symptoms before con- ate precautions placed.33 Repositioning and skin assessments should be
verting from IV to oral, and then tapered slowly, over weeks to months performed regularly.5 , 6
if necessary. A recent review40 found that response rates to benzodi- Nutritional status, including electrolytes and hydration, in patients
azepines are in the range of 65%-100%, typically seen within a few days with catatonia should be assessed regularly, and when possible, dietician
of treatment initiation.7 , 39 support should be sought.5 , 6 Artificial nutrition may need to be consid-
In cases not responsive to benzodiazepine treatment, or if a ben- ered if spontaneous oral intake is insufficient for around 5 days. Care
zodiazepine is contraindicated (such as with respiratory depression or must be taken to avoid refeeding syndrome.5 Due to the risk of aspira-
co-occurring delirium), the NMDA receptor antagonists amantadine and tion pneumonia, there is a low threshold to engage in speech therapy.5 , 6
memantine may be trialed.26 Amantadine can be started at 100 mg daily Low serum iron in patients with catatonia has been correlated with
and increased by 100 mg every few days up to a total daily dose of reduced response to benzodiazepines; as such, iron should be repleted
400 mg daily. Amantadine carries the risk of precipitating psychosis, if low.6
and it can lower the seizure threshold. Memantine, as a more selec-
tive NMDA antagonist, has less dopamine activity and therefore is not
thought to carry the risk of psychosis.41 Memantine is usually started Conclusion
at 5 mg twice a day and titrated up to 10 mg twice a day after a
few days. Catatonia is a complex psychomotor syndrome that is underdiag-
Antipsychotic therapy in catatonia is a matter of debate, as both first- nosed in hospital settings. Due to the significant morbidity, mortality,
and second-generation antipsychotics have the potential to worsen cata- and medical complications, early recognition of catatonia is crucial. An
tonia or even cause progression to MC or NMS.40 However, when cata- appropriate workup, identification of underlying medical comorbidities,
tonia is due to underlying psychosis, initiation of an antipsychotic may and treatment of these comorbidities is necessary.
be beneficial.27 Similarly, discontinuing an antipsychotic too rapidly in Catatonia is less likely to respond to catatonia therapy alone if the
these cases may cause clinical worsening. As such, careful consideration underlying cause is medical in nature; prognosis is improved by treat-
of these nuances is needed, and if psychiatry is not already involved, a ing the underlying medical cause. As the most common medical causes
consultation should be considered. In general, a second-generation an- of catatonia are neurologic, emphasized by the MINDSET mnemonic,
tipsychotic with lower D2 affinity, such as olanzapine or quetiapine, is workup should generally include consideration of neurological causes.
typically preferred over higher potency agents in the setting of catato- Treatment of catatonia most commonly consists of benzodiazepines,
nia, and if catatonia is not thought to be due to underlying psychosis, ECT, NMDA receptor antagonists, or a combination of these.
antipsychotics should generally be avoided.27 , 40 , 42 Medical complications due to catatonia can include DVTs/PEs, mal-
For life-threatening catatonia, such as when vital sign abnormalities nutrition, aspiration, and dermatologic and neuromuscular damage. As
(ie, MC) are present or nutritional status is gravely compromised, ECT these complications worsen morbidity and mortality, appropriate pre-
is first-line.2 , 6 ECT may also be considered in pharmacologic-resistant vention and treatment of these conditions when they occur is of utmost
catatonia.2 , 6 ECT is usually started at 3 times a week; scheduling may importance.
be adjusted subsequently based on response. Response rates are up to Psychiatric consultation can assist with diagnostic clarity and treat-
80%, even in treatment-resistant cases.4 , 6 , 7 ment recommendations and should be considered when catatonia is on
Given that NMDA receptor encephalitis is among the most common the differential and psychiatric services are available. However, even
causes of medical catatonia—and that catatonia presents with high fre- when psychiatric services are available, the internist has an invaluable
quency in NMDA receptor encephalitis—increased awareness of this role in medical workup, medical management of underlying comorbidi-
condition and its treatment is warranted.30 , 43 , 44 Catatonia due to NMDA ties, and prevention and treatment of complications.

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Disclosure 19. Wilson JE, Niu K, Nicolson SE, Levine SZ, Heckers S. The diagnostic criteria and
structure of catatonia. Schizophr Res. 2015;164(1):256–262.
20. Wortzel JR, Maeng DD, Francis A, Oldham MA. Prevalent gaps in understanding the
The authors do not have any financial relationships or conflicts to features of catatonia among psychiatrists, psychiatry trainees, and medical students.
disclose. Both authors were involved in the conceptualization, research, J Clin Psychiatry. 2021;82(5).
and writing of this manuscript. 21. Tormoehlen LM, Rusyniak DE. Neuroleptic malignant syndrome and serotonin syn-
drome. Handb Clin Neurol. 2018;157:663–675.
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