The n e w e ng l a n d j o u r na l of m e dic i n e

Review Article

Allan H. Ropper, M.D., Editor

Catatonia
Stephan Heckers, M.D., and Sebastian Walther, M.D.​​

C
atatonia has been well described but is poorly understood.1 From the Department of Psychiatry and
Many physicians incorrectly believe that catatonia is a rare form of schizo- Behavioral Sciences, Vanderbilt Univer-
sity Medical Center, Nashville (S.H.,
phrenia, with bizarre abnormalities of motor behavior. Consequently, the S.W.); and the Translational Research
diagnosis is often missed, and a person with catatonia may be inappropriately Center, University Hospital of Psychiatry
treated. In 2013, the Diagnostic and Statistical Manual of Mental Disorders, fifth edition and Psychotherapy, University of Bern,
Bern, Switzerland (S.W.). Dr. Heckers can
(DSM-5)2 removed catatonia as a subtype of schizophrenia and listed it as a feature be contacted at ­stephan​.­heckers@​­vumc​
of several psychiatric and medical conditions. In 2022, the International Classification .­org or at Vanderbilt Psychiatric Hospital,
of Diseases, 11th revision (ICD-11),3 went further, recognizing catatonia as an inde- 1601 23rd Ave. South, Rm. 3060, Nash-
ville, TN 37212.
pendent diagnostic entity, on par with mood disorders and schizophrenia. Recog-
nizing the need for more neuroscientific research and clinical trials addressing N Engl J Med 2023;389:1797-802.
DOI: 10.1056/NEJMra2116304
catatonia, the National Institute of Mental Health added a sensorimotor domain Copyright © 2023 Massachusetts Medical Society.
in 2019 to its Research Domain Criteria, which are meant to provide a framework
to study abnormal motor behaviors, including catatonia, and advance transla- CME
at NEJM.org
tional research in the field.4
Despite these recent changes, there are several reasons why catatonia is often not
recognized.5 First, its severity ranges from subtle behavioral abnormalities, lasting
only hours, to malignant, at times lethal, forms. Second, the clinical features may
fluctuate over variable periods of time between stupor and severe agitation, or a
patient may shift from comfortable conversation to mutism that persists for hours.
Patients with catatonia do not engage with their surroundings or with other people,
making it difficult for the clinician to obtain a history and complete a mental
status examination.6,7 This inconstant and unpredictable presentation has contrib-
uted to varying prevalence estimates. Catatonia is common in psychiatric emer-
gency rooms and inpatient units, but prevalence estimates range from 9 to 30%.8-11
Among medical patients, the estimated prevalence of catatonia is less than 10%.12,13

Signs of C atat oni a

Among the many signs of catatonia, 12 are recognized as diagnostic criteria in the
DSM-5, text revision.15 All 12, plus 4 additional signs, are recognized as diagnostic
criteria in ICD-11 (Table 1). Any 3 of the 12 signs are sufficient for the DSM diag-
nosis of catatonia. Some signs are found in most patients: staring, stupor, mutism,
and posturing. Other signs, some considered almost pathognomonic, are found in
less than 20% of patients: echophenomena (imitation of words or actions), waxy
flexibility (slight and even resistance to positioning), and catalepsy (passive induc-
tion of a posture that is then held by the patient against gravity)16 (Table 1).
Catatonic signs may emerge rapidly, reaching a maximum level within hours
(in acute catatonia), or may develop slowly, over a period of days or weeks. Cata-
tonic episodes may recur periodically, or they may persist for years, as seen in
some patients with schizophrenia spectrum disorders17 or neurodevelopmental
disorders, including autism spectrum disorder.18 The course of catatonia due to
intoxication or to other medical conditions depends on the course of the underlying

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 The n e w e ng l a n d j o u r na l of m e dic i n e

Table 1. Signs of Catatonia.*

Included in Included in Psychomotor Setting in Which Sign

Sign DSM-5-TR ICD-11 Activity Definition Is Likely to Occur
High frequency
Staring No Yes Mildly decreased Fixed gaze, decreased blinking ED, medical unit, psychiat-
ric setting
Stupor Yes Yes Severely decreased No motor activity, not responsive ED, medical unit, psychiat-
to external stimuli ric setting
Mutism Yes Yes Severely decreased Incomprehensible speech or none ED, medical unit, psychiat-
ric setting
Posturing Yes Yes Abnormal Spontaneous maintenance of a ED, psychiatric setting
posture for minutes or hours
Moderate frequency
Ambitendency No Yes Decreased Indecisive, hesitant movements Psychiatric setting
due to conflicting goals; pa-
tient appears to be stuck
Negativism Yes Yes Abnormal Contrary behavior to that re- Psychiatric setting
quested
Stereotypy Yes Yes Abnormal Repetitive, non–goal-directed mo- ED, psychiatric setting
tor behavior
Rigidity No Yes Moderately abnormal Resistance through increased ED, medical unit
muscle tone, from mild resis-
tance to lead-pipe rigidity
Agitation Yes Yes Severely increased Nonpurposeful movements, hy- ED, medical unit
peractivity, or uncontrollable
emotional reactions
Grimacing Yes Yes Abnormal Distorted facial expressions, inap- Psychiatric setting
propriate and irrelevant to the
situation
Mannerisms Yes Yes Moderately abnormal Odd, purposeful movements, Psychiatric setting
inappropriate to the patient’s
cultural context
Low frequency
Echolalia Yes Yes Severely abnormal Imitating examiner’s words Unlikely in any of the three
settings
Echopraxia Yes Yes Severely abnormal Imitating examiner’s actions Unlikely in any of the three
settings
Verbigeration No Yes Severely abnormal Continuous and directionless Psychiatric setting
repetition of words, phrases,
or sentences
Waxy flexibility Yes Yes Severely abnormal Slight and even resistance to po- Unlikely in any of the three
sitioning by examiner settings
Catalepsy Yes Yes Severely abnormal Passive induction of a posture, Unlikely in any of the three
which remains held against settings
gravity

* DSM-5-TR denotes Diagnostic and Statistical Manual of Mental Disorders, fifth edition, text revision; ED emergency department; and ICD-11
International Classification of Diseases, 11th revision.

condition. The complex, and at times confusing,
psychomotor behaviors have been classified as
decreased, increased, or qualitatively abnormal,
because this classification may improve identifi-
cation of the syndrome and guide neuroscientific
exploration — similar to the categorization of
movement disorders that was developed in the
early 20th century in neurology19 (Table 1).
Several clinician-administered rating scales
have been validated for catatonia.20 Among them,

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 Catatonia

the 23-item Bush−Francis Catatonia Rating Scale21 Table 2. Clinical Scenarios of Catatonia.*
is widely accepted, and teaching modules for its
implementation are available.22 Measures of Clinical Setting Diagnosis, Testing, and Treatment
physical activity such as actigraphy are increas- Emergency department
ingly being used to monitor catatonia.23 Differential diagnosis Acute psychosis
Because there are numerous clinical presenta- Intoxication (cannabis, cocaine) and with-
tions and underlying disorders associated with drawal (alcohol, opioids, benzodiaz-
epines)
catatonia, we have chosen to review the syn- Neuroleptic malignant syndrome
drome in three clinical settings (Table 2): the Serotonin syndrome
emergency department, where prompt identifi- Autoantibody encephalitis
cation guides initial stabilization and disposition; Treatment Lorazepam challenge
medical settings, where catatonia informs the Hold dopamine antagonist
workup and management of the underlying con- Medical unit
dition; and the psychiatric setting, where catato- Differential diagnosis Epilepsy
nia is most common, may appear in subtle forms Delirium (may co-occur with catatonia)
and last for months or years, and can be aggra- Rule out medical causes Autoantibody encephalitis
Encephalopathy
vated by treatment with dopamine antagonists. Focal cerebral lesions
Medications
C atat oni a in the Emergenc y Treatment Adequate nutrition and hydration
Depa r tmen t Benzodiazepines
Electroconvulsive therapy
The most common presentation of catatonia in Psychiatric setting
the emergency department is failure to respond Disorders with catatonic Mood disorders
to questioning (mutism) and very little spontane- features Schizophrenia
Autism spectrum disorder
ous movement (stupor). These psychomotor be- Dementia
haviors, which are essential elements of catato- Intoxication (cannabis, cocaine) and with-
nia, can be distinguished from quiet and agitated drawal (alcohol, opioids, benzodiaz-
epines)
delirium, characterized by fluctuating but gener-
ally decreased levels of alertness and cognition. Treatment Benzodiazepines, electroconvulsive therapy
Valproic acid, NMDA receptor antagonist
When other causes of poor interaction are ruled Antipsychotic drug
out (e.g., anger, language difficulties, trauma- Repetitive transcranial magnetic stimulation
related dissociation, and failure to thrive), catato- Monitoring and workup                                                                       
nia should be considered as the underlying dis- Monitor in all settings Symptom severity (e.g., Bush–Francis
order. Catatonia Rating Scale)
A second presentation of catatonia in this Vital signs
Creatine kinase†
setting is characterized by rapidly fluctuating
levels of psychomotor behavior, ranging from Workup in medical setting Laboratory tests to rule out medical causes
Neuroimaging
mutism and stupor to posturing and agitation. EEG
This form of catatonia may be due to ingested
substances (especially cannabis or cocaine) or to * The main clinical scenarios are shown. For a more extensive list, see Rogers
et al.14 EEG denotes electroencephalography, and NMDA N-methyl-d-aspartate.
another medical condition. In such cases, a care- † Creatine kinase is monitored to rule out neuroleptic malignant syndrome and
ful assessment of the patient’s medical and because it is often elevated in catatonia.
mental health history is required, including col-
lateral information from family and other ob-
servers. If muscle rigidity is present, two impor- A third catatonic presentation is rigidity ac-
tant disorders in the differential diagnosis are companied by repetitive, purposeless movements,
the serotonin syndrome (triggered by serotoner- such as rocking back and forth (stereotypies).
gic drugs, often with severe sweating, fever, and This form is usually encountered in persons
hyperreflexia) and the neuroleptic malignant with autism or schizophrenia spectrum disor-
syndrome (triggered by dopamine antagonists, ders. Catatonic episodes can occur at the onset
usually with hyperthermia and autonomic dys- of these disorders or may indicate a deteriora-
function) (Table 2). tion of chronic mental illness.

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 The n e w e ng l a n d j o u r na l
Most forms of acute catatonia remit promptly
with appropriate treatment. The lorazepam chal-
lenge test for catatonia has been found to be an
effective treatment,24-27 and remission with the
challenge validates the diagnosis. Within minutes
after intravenous administration of 1 to 2 mg of
lorazepam, previously mute patients start talk-
ing, and immobile patients move and resume oral
intake. Typically, these effects wear off quickly
but can be reinstated with repeated administra-
tion. Intramuscular or oral administration is also
effective, albeit with a slower onset of action.
Lorazepam is effective in up to 90% of acute
catatonia cases.24,25
C atat oni a in the Medic a l Uni t
Catatonia in a patient in a medical unit requires
extensive diagnostic efforts because otherwise un-
usual underlying causes are common in such pa-
tients.12,13 First, anti–N-methyl-d-aspartate (NMDA)
receptor encephalitis may cause acute catatonia
before progressing to encephalopathy or sei-
zures.28 Second, several metabolic disorders and
focal cerebral lesions may be manifested as
catatonia. Third, catatonia may be due to pre-
scribed or illicitly used drugs, especially in pa-
tients withdrawing from benzodiazepines, alco-
hol, or opioids.12,29 Fourth, in critically ill patients,
catatonia may linger in the shadow of delirium30
because the psychomotor signs of catatonia are
often not recognized in a delirious patient with
fluctuating levels of attention and cognition.15 In
addition, certain conditions confer a predisposi-
tion to an acute episode of catatonia (e.g., post-
partum psychosis in the perinatal period31 and
urinary tract infections in older patients13).
Monitoring of vital signs and prevention or
treatment of catatonia complications, such as
inadequate nutrition, dehydration, and bed sores,
are often necessary.6,7 General medical services
may be called on to manage rare cases of severe,
malignant catatonia, which require monitoring
for and management of hyperthermia, tachycar-
dia, renal failure, pneumonia, and metabolic
disorders.32 Patients with severe catatonia typi-
cally present with prominent rigidity, mutism, or
stupor — and it is in these patients that death
may result. Differential diagnoses include the
above-mentioned neuroleptic malignant syndrome
and the serotonin syndrome.14,33
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of m e dic i n e
C atat oni a in Ps ychi at r ic
Se t t ings
Catatonia in psychiatric patients may be due to
a medical condition rather than an underlying
psychiatric disorder. For this reason, an assess-
ment for medical causes should be performed
not only during the initial presentation but
even after years of psychiatric illness. Once
medical causes have been ruled out, several
psychiatric disorders should be considered.
Psychiatric patients may present with less severe
forms of catatonia, such as elective mutism (re-
fusal to speak) or ambitendency (indecisive,
hesitant movements due to conflicting goals).
These presentations may be acute, periodic, or
chronic. Patients with depression, bipolar disor-
der, schizophrenia, or autism spectrum disorder
may pre­sent with staring, mutism, immobility,
or stereotypies (repetitive, non–goal-directed
movements).16,34 In schizophrenia, aberrant
speech production, such as echolalia (imitating
words) or verbigeration (repetition of words or
phrases), is seen. These episodes typically have
a prolonged course of weeks to months, with
less autonomic instability than in patients with
underlying medical conditions. Disturbances of
will are common in these circumstances, in-
cluding negativism (leading to refusal of oral
intake), odd mannerisms, or rituals (repetitive
action sequences such as repeatedly replacing
items on a shelf without purpose).16,34 A quarter
of psychiatric patients with catatonia have
more than one episode.11
At times, the signs of catatonia are not easily
distinguished from other features of psychiatric
illness.6,35 In neurodevelopmental disorders, for
example, periods of catatonia need to be distin-
guished from childhood-onset motor abnormali-
ties.36 In schizophrenia, the distinction between
catatonia and negative symptoms or disorganized
behavior can be challenging. Furthermore, signs
such as grimacing or engaging in rituals may be
mistaken for tics or compulsive symptoms.
A sse ssmen t of C atat oni a
Catatonia is a clinical diagnosis, the severity of
which can be captured with standardized rating
scales, such as the above-mentioned Bush–Fran-
cis Catatonia Rating Scale, which grades 23 items,
nejm.org November 9, 2023
 Catatonia

such as excitement, immobility, staring, manner-
isms, and rigidity, each on a scale of 0 to 3. At a
minimum, assessment of catatonia requires phys-
ical examination, including measurement of
vital signs, a complete blood count, and a com-
prehensive blood metabolic panel. More specific
laboratory tests, neuroimaging, and electroen-
cephalography are needed if there is an indica-
tion of an underlying neurologic disorder, such
as clonic seizure movements, asterixis, or focal
neurologic signs.
T r e atmen t of C atat oni a
Management of catatonia includes specific treat-
ments, treatment of the underlying disorder, and
prevention of complications. The British Asso-
ciation for Psychopharmacology has published a
consensus guideline,14 which is an authoritative
compilation of evidenced-based approaches to
catatonia. However, much of the evidence is
anecdotal, and data from randomized, controlled
trials are lacking.24 Some measures apply to all
patients with catatonia: monitoring blood pres-
sure, temperature, and fluid balance and ensur-
ing hydration and nutrition. General measures
of care include prophylaxis for thromboembo-
lism, pressure ulcers, infections, and muscle
contractions.6,7
The primary treatment of catatonia should be
initiated as soon as possible after the condition
has been identified, since the likelihood of a
response declines with time. Both lorazepam
administration, as noted above, and electrocon-
vulsive therapy (ECT) lead to a response in 60 to
100% of patients, and ECT is also effective after
insufficient response to benzodiazepine admin-
istration.14,25 The lorazepam dose may be adjust-
ed, sometimes above the standard dose (up to
16 mg per day). ECT is administered bilaterally,
and effects can be expected after four to six ses-
sions, usually administered over the course of
1 to 2 weeks.14
Second-line treatment of catatonia includes
the NMDA receptor antagonists, amantadine and
memantine.14 In cases with coexisting psychosis,
the use of dopamine antagonists, which are of-
ten needed to treat psychotic symptoms, should
be considered carefully because of the poten-
tial for these agents to worsen catatonia. After
the neuroleptic malignant syndrome has been
ruled out, second-generation antipsychotic drugs
(particularly clozapine) are preferable to first-
generation antipsychotic drugs in patients with
catatonia and psychosis.14,37 Periodic forms of
catatonia require monitoring for early signs of
recurrence (e.g., slowed performance of stan-
dard motor tasks) in order to curtail another
episode. Treatment of chronic catatonia includes
maintenance ECT, clozapine at lower-than-typi-
cal doses (<150 mg per day), and psychothera-
peutic approaches.38 Especially in the context of
schizophrenia spectrum disorders, such treat-
ment may be required for months or years.17
F u t ur e Dir ec t ions
We do not understand the neural mechanisms of
catatonia. There have been few behavioral and
neuroimaging studies of patients with a history
of catatonia; even fewer studies of acute catato-
nia have been conducted.7,39 Investigations to test
treatments, including transcranial magnetic
stimulation and new pharmacologic agents, are
at early stages. Finally, genetic studies and ani-
mal models are sparse, but when better devel-
oped, they should aid our understanding of the
mechanisms underlying catatonia.40-42
Disclosure forms provided by the authors are available with
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