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Catatonia in adults: Epidemiology, clinical features, assessment, and diagnosis

Author: M Justin Coffey, MD


Section Editors: Peter P Roy-Byrne, MD, Stephen Marder, MD
Deputy Editor: David Solomon, MD

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2018. | This topic last updated: Nov 22, 2017.

INTRODUCTION — Catatonia is a behavioral syndrome marked by an inability to move normally, which can
occur in the context of many underlying psychiatric and general medical disorders [1]. Within psychiatric
nosology, catatonia is not conceptualized as a separate diagnostic entity [2,3]. Rather, the term catatonia is
used to specify a subtype of the underlying disorder, similar to the term “psychotic features.” (However, some
experts view catatonia as a syndrome that warrants a stand-alone diagnosis [4].)

Recognizing catatonia is important because it may be caused or exacerbated by treatment of the underlying
disorder. As an example, antipsychotic drugs used for bipolar or psychotic disorders may worsen catatonia
[5].

This topic reviews the epidemiology, pathogenesis, clinical features, assessment, and diagnosis of catatonia,
as well as the disorders that can progress to catatonia. The treatment and prognosis of catatonia are
discussed separately. (See "Catatonia: Treatment and prognosis".)

EPIDEMIOLOGY — The estimated incidence of catatonia has been studied primarily in acutely ill psychiatric
inpatients [2]. The incidence is approximately 10 percent, but estimates range from 5 to 20 percent, based
upon prospective studies conducted for one to twelve months at individual psychiatric units [6-14]. The range
is probably due in part to differences in study methods, including how catatonia was defined. The syndrome
may go unrecognized, leading to the false conclusion that it is rare. In a Dutch study of 139 acutely psychotic
inpatients, the treatment team diagnosed catatonia nine times less often than the research team (2 versus 18
percent of patients) [8].

It is not clear if there are any sociodemographic risk factors for catatonia. Catatonia seems to occur more
commonly in patients with unipolar major depression or bipolar disorder, compared with other disorders [6]. In
addition, catatonia may perhaps occur more often in patients with prior episodes. (See 'Underlying disorders'
below and 'Recurrence' below.)

PATHOGENESIS — Catatonia occurs in the context of an underlying psychiatric or general medical disorder,
and treatments that are used for these underlying disorders may cause or exacerbate catatonia. As an
example, antipsychotic drugs used for bipolar or psychotic disorders may worsen catatonia [5]. (See
"Catatonia: Treatment and prognosis", section on 'Avoid dopamine blocking drugs'.)

The pathophysiology of catatonia is unknown. Neurobiologic correlates of catatonia have been identified, but
it is not clear if these findings represent etiologic causes or sequelae of the disorder [15].

Neurobiologic studies have led to a hypothesis that catatonia involves pathways that connect the basal
ganglia with the cortex and thalamus [16]. Neuropathologic studies of patients with catatonic schizophrenia
have found alterations in the basal ganglia (caudate nucleus, nucleus accumbens, and pallidum) and
thalamus [17]. Neuroimaging studies suggest that catatonia may possibly involve functional alterations in the

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prefrontal, orbitofrontal, and parietal cortices [18,19]. In addition, neuropsychologic tests of remitted catatonic
patients found a deficit in visual-spatial abilities that may involve right parietal cortex function [17,20].
Neurotransmitter studies suggest that catatonia may be associated with decreased activity at gamma-
aminobutyric acid A and dopamine D2 receptors, and increased activity at N-methyl-D-aspartate receptors
[19,21].

Some patients may possibly have a genetic predisposition to catatonia. Preliminary evidence suggests that
genes on chromosomes 15 and 22 may be linked to the periodic form of catatonia [22-25]. (See 'Other forms'
below.)

CLINICAL FEATURES — The core feature of catatonia is a motor disturbance in which patients are unable
to move normally despite full physical capacity in the limbs and trunk [1]. The disturbance can range from
marked reduction in movements to marked agitation. Starting, stopping, and planning movement can be
impaired, and motor behavior may be repetitive, purposeless, impervious to external stimuli, and contrary to
intent [11].

Small prospective studies of catatonia and case series have found that catatonia is marked by
heterogeneous signs that are observed or elicited (table 1 and table 2); the most common are [1,11,26]:

● Immobility (hypokinesis or akinesis)

● Mutism

● Stupor (decreased alertness and response to stimuli)

● Negativism (resistance to all instructions or all attempts to be moved)

● Waxy flexibility

● Posturing

● Excessive, purposeless motor activity (excitement)

● Staring

● Echophenomena

• Echolalia – Senseless repetition of another person's utterances

• Echopraxia – Senseless repetition of another person's movements

Onset of catatonia can be either acute or insidious [1,9]. Following remission, some patients cannot recall
their experience during the episode, whereas others describe an awareness of their activity and the inability
to communicate [27].

Catatonia occurs in patients who are severely ill with an underlying psychiatric or general medical disorder
[2,28] (see 'Underlying disorders' below). Thus, catatonia is typically seen in hospitalized patients.

Subtypes — There are several subtypes of catatonia, based upon the specific nature of the movement
disturbance and other associated features [1,29,30]. The behavioral phenotype of catatonia exists on a
continuum between retarded and excited subtypes, depending upon the motor disturbance. In addition, the
severity of catatonia exists on a continuum between nonmalignant and malignant, depending upon other
associated features. The three principal forms of catatonia in order of incidence are retarded, excited, and
malignant. While a factor-analytic study of 314 psychotic patients supported separation of retarded and
excited catatonia as subtypes [31], patients can exhibit signs of both subtypes concurrently [32]. Subtypes
are not necessarily stable during a catatonic episode, and patients may transition from retarded to excited
catatonia or vice versa [33,34]. In addition, retarded and excited catatonia can each progress to malignant
catatonia; alternatively, malignant catatonia can occur de novo.
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Retarded catatonia — The retarded form of catatonia is characterized by mutism, inhibited movement,
posturing, negativism, and staring [1,10]. Postures may be mundane (eg, sitting or standing in the same
position for hours) or unusual (eg, head raised above the bed as if on a pillow). Response to voice and
noxious stimuli is decreased. Although speech and spontaneous movements are reduced, some patients
appear to be alert and aware of the environment. In more severe cases, eating and drinking may cease and
stupor and incontinence may occur [34].

Excited catatonia — Excited catatonia is characterized by excessive and purposeless motor activity in
both the upper and lower limbs (hyperkinesis), restlessness, stereotypy, impulsivity, frenzy, and
combativeness [1,10]. Delirium may occur in severe cases, and the excess motor activity may cause self-
injury or harm to others.

Malignant catatonia — Malignant catatonia (also called lethal catatonia) is a life-threatening condition
that is characterized by fever (less likely in older patients), autonomic instability (labile or elevated blood
pressure, tachycardia, tachypnea, and diaphoresis), delirium, and rigidity [1,16]. The syndrome is typically
fulminant and progresses rapidly within a few days [35]. Common but nonspecific laboratory findings include
leukocytosis, elevated creatine kinase, and low serum iron [16,36]. Signs of malignant catatonia overlap with
signs of the neuroleptic malignant syndrome (NMS). (See 'Differential diagnosis' below.)

Other forms — Other, infrequent forms of catatonia may occur [1]. One example is periodic catatonia,
which is marked by waxing and waning of catatonic signs [29] or periods of retarded catatonia alternating
with excited catatonia [1].

Underlying disorders — Psychiatric nosology does not conceptualize catatonia as a specific disease;
rather, catatonia is a syndrome that occurs in the context of an underlying psychiatric or general medical
illness [2,3,16]. Multiple underlying conditions may be present in the same catatonic patient [32,37,38].
However, it is not known if comorbidity increases the risk of catatonia. None of the underlying disorders
appear to be associated with a specific catatonic sign or subtype [9,32].

Although catatonia can occur in the context of many mental disorders, it is most often found in [2,39-42]:

● Bipolar I disorder

● Bipolar II disorder

● Unipolar major depression (major depressive disorder)

● Psychotic disorders

• Schizophrenia

• Schizoaffective disorder

• Brief psychotic disorder

• Schizophreniform disorder

● Autism spectrum disorder

● Delirium

Many general medical disorders can also lead to catatonia. A review of case reports found that catatonia
occurred in more than 100 general medical conditions [32]; these included infectious, metabolic, neurologic,
and rheumatologic disorders [1,2,43,44]. In addition, a study of 136 patients treated on an intensive care unit
with mechanical ventilation and/or vasopressors found that catatonia was present in approximately 35
percent [45].

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On acute inpatient psychiatric units, catatonia most frequently occurs in the context of bipolar disorder or
unipolar major depression [6,30,39]. A study of 148 patients with catatonia found that the underlying condition
was bipolar disorder or unipolar major depression in 46 percent of patients, psychotic disorder in 26 percent,
general medical condition in 20 percent, and another psychiatric disorder in 8 percent of patients [46]. Other
reviews have found a similar distribution of underlying diagnoses [47].

The presence of catatonia reflects the severity of the patient’s underlying illness. As an example, a study of
148 catatonic patients found that nearly 75 percent were concurrently psychotic [46].

Treatments that are used for the underlying disorder may cause or exacerbate catatonia (eg, antipsychotic
drugs used for bipolar or psychotic disorders may worsen catatonia) [5]. (See "Catatonia: Treatment and
prognosis", section on 'Avoid dopamine blocking drugs'.)

Recurrence — Patients who recover from catatonic episodes may suffer recurrences. A retrospective study
of patients with bipolar disorder and catatonia (n = 26) found that a prior history of catatonia was present in
38 percent [48].

ASSESSMENT — Signs of catatonia can be observed or elicited (table 1 and table 2) [28]. Clinicians may
overlook these signs because of the severity of associated psychopathology (eg, psychosis). In addition,
common signs of catatonia such as mutism, posturing, and rigidity may be absent; many catatonic patients
speak and move about. Thus, patients exhibiting only one apparent catatonic sign should be examined for
others.

For patients with an underlying psychiatric disorder, the motor dysregulation of catatonia can be similar to the
underlying psychopathology. As an example, the increased motor activity and impulsivity observed in mania
may progress to excited catatonia. Mania uncomplicated by catatonia is marked by goal-directed activity and
intact cognition. By contrast, activity in catatonia is often repetitive and not goal-directed. As another
example, the psychomotor retardation, anergia, anhedonia, and anorexia observed in major depression may
resemble retarded catatonia. The hypokinesis and refusal to eat or drink that characterize severe depression
may be catatonic signs, and should prompt an assessment for other catatonic signs. Clinical features that
often occur in depression not complicated by catatonia include suicidality, sleep disturbance, and feelings of
worthlessness, guilt, helplessness, and hopelessness. In addition, catatonia can be distinguished by
additional motor signs, such as posturing, rigidity, and negativism, as well as a positive response to the
lorazepam challenge test. (See 'Underlying disorders' above and 'Lorazepam challenge' below.)

Rating scales have been used for research purposes to systematically examine patients at the initial
assessment and quantify progress during treatment, but their utility for routine clinical care is not well-
established [26,46,49]. The most widely used measure is the Bush-Francis Catatonia Rating Scale, which is
a 23-item rating scale with good inter-rater reliability (0.93) and construct validity; the first 14 items can be
used to screen for catatonia [50]. Each item is defined, the procedure for rating each item is described, and
the scale appears to be sensitive to clinical change [30]. The Northoff Catatonia Scale and the Kanner
Catatonia Scale are reasonable alternatives [51,52].

There is no laboratory test specific for catatonia. However, malignant catatonia is associated with non-
specific test results that include leukocytosis, increased creatine kinase, and low serum iron (table 3) [36,53-
55].

The underlying disorder may be unknown in some patients with catatonia, in which case the initial clinical
evaluation should include the following [9,32,46]:

● Psychiatric and general medical history

● Mental status and physical examination

● Laboratory tests – Tests should be guided by the symptoms, history, and findings on the physical
examination. Patients with an established underlying disorder (eg, unipolar major depression with
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psychotic features) may not need any tests.

Catatonic stupor and mutism may preclude assessing the patient for symptoms of the underlying disorder.
However, family and friends can often compensate for the patient’s inability to provide a history. After
catatonia resolves, the patient should be re-evaluated for psychopathology or a general medical disorder.
(See "Unipolar depression in adults: Assessment and diagnosis" and "Bipolar disorder in adults: Clinical
features" and "Schizophrenia in adults: Clinical manifestations, course, assessment, and diagnosis".)

Lorazepam challenge — Nearly every catatonic patient is treated initially with lorazepam or another
benzodiazepine (patients with malignant catatonia may be quickly switched to electroconvulsive therapy); the
response to the first one or two doses can help make the diagnosis of catatonia. Case series suggest using
an intravenous (IV) bolus of lorazepam 1 to 2 mg [32]. IV administration allows for rapid, complete
absorption, although intramuscular (IM) injections and oral administration have also been used [30,56].
Intravenous benzodiazepines should be injected or infused slowly. In addition, clinicians should be cognizant
of concomitant drugs that can cause sedation or respiratory depression, eg, opioids. Benzodiazepines cause
varying degrees of motor incoordination and increase the risk of falls [12].

Partial, temporary relief of signs 5 to 10 minutes after IV administration of lorazepam is consistent with a
diagnosis of catatonia [1,29]. If there is no change and the patient remains awake with stable vital signs, a
second dose is given, and the patient is examined within 5 to 10 minutes, although observation can continue
for longer periods. A negative response does not rule out catatonia, and occurs in approximately 20 percent
or more of catatonic patients.

Reasonable alternatives to lorazepam are available. A randomized trial that compared a single dose of oral
oxazepam 60 mg with a single dose of oral lorazepam 2 mg in 17 patients found that the benefit of each drug
was comparable [57]. In case reports, oral zolpidem 10 mg was useful [26,37,58-60].

The treatment of catatonia is discussed separately. (See "Catatonia: Treatment and prognosis".)

DIAGNOSIS — A minimum of two to four signs for at least several hours is required to make the diagnosis of
catatonia (table 1 and table 2) [1,12,26,50]. However, neither the number of catatonic features nor their
duration is established, and no one sign is pathognomonic [47]. A positive lorazepam challenge test can help
verify the diagnosis. (See 'Lorazepam challenge' above.)

Psychiatric nosology — According to psychiatric nosology, catatonia is not a separate, specific disease;
rather, catatonia is a behavioral syndrome that is diagnosed in patients who are ill with an underlying
psychiatric and/or general medical disorder [2,3]. In the American Psychiatric Association's Diagnostic and
Statistical Manual, Fifth Edition (DSM-5), the term catatonia is used to specify a subtype of the underlying
disorder, similar to the term “psychotic features” [2]. The underlying psychiatric disorders that can give rise to
catatonia include autism spectrum disorder, bipolar disorders, psychotic disorders, and unipolar major
depression.

In DSM-5, criteria for catatonia are met when the clinical picture is dominated by at least three of the
following [2]:

● Stupor (decreased psychomotor activity or decreased reactivity to the environment)

● Catalepsy (passively allowing the examiner to position the body or a body part)

● Waxy flexibility (slight, even resistance to positioning by the examiner, as in bending a candle)

● Mutism (lack of verbal response; not applicable to patients with an established aphasia)

● Negativism (motiveless resistance to instructions or external stimuli)

● Posturing (voluntarily maintaining a position of the body or a body part against gravity for a long time)

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● Mannerisms (odd movements)

● Stereotypy (repetitive movements that are not goal directed and often are awkward or stiff)

● Agitation or excessive motor activity that is purposeless and not influenced by external stimuli

● Grimacing

● Echolalia (mimicking another person’s speech)

● Echopraxia (mimicking another person’s movements)

DIFFERENTIAL DIAGNOSIS — Signs of catatonia can overlap with signs of other disorders; in particular,
malignant catatonia may resemble the neuroleptic malignant syndrome (NMS) [5,61]. Both disorders present
with fever, autonomic instability, rigidity, and delirium. Patients who present with these signs should be
assessed with neuroimaging and a lumbar puncture to rule out central nervous system and systemic
infection.

The differential diagnosis of catatonia includes a number of conditions, some of which can cause catatonia
(eg, delirium, stroke, and nonconvulsive status epilepticus) [6]:

● Neuroleptic malignant syndrome – The neuroleptic malignant syndrome (NMS) and malignant
catatonia are life-threatening disorders with similar clinical features. Both disorders can present with
delirium, autonomic instability, fever, and rigidity [61,62]. In addition, an elevated creatinine kinase and
white blood count and low serum iron are common to NMS and malignant catatonia. A review of 292
cases of malignant catatonia found that the clinical features were indistinguishable from NMS in more
than 20 percent of cases [63]. (See "Neuroleptic malignant syndrome", section on 'Clinical
manifestations'.)

Many authorities consider NMS a drug-induced form of malignant catatonia, based upon their
overlapping clinical features as well as similarities in the hypothesized pathophysiology for each disorder
[1,5,9,11,16,21,26,62,64]. In addition, discontinuing antipsychotics and starting benzodiazepines can be
helpful for both NMS and malignant catatonia, and electroconvulsive therapy can benefit patients with
either disorder even after failed pharmacotherapy [1,61].

However, it is not established that NMS is a subtype of catatonia [18,46]. Malignant catatonia can
present with signs (eg, impulsivity, posturing, and repetitive stereotypic movements) that are not
generally observed in NMS [46,65,66], affective symptoms that can occur in catatonia do not seem to be
as prominent in NMS [18], and laboratory abnormalities that occur in NMS may not occur as consistently
in patients with malignant catatonia [46]. Some authorities hypothesize that NMS and malignant
catatonia have overlapping but distinct pathophysiologic mechanisms [18]. Establishing the diagnosis of
NMS can lead to treatment that differs in some respects from that of catatonia [61,63], although some
authorities recommend a common and consistent therapeutic approach [64]. (See "Neuroleptic
malignant syndrome", section on 'Treatment'.)

● Serotonin syndrome – Serotonin syndrome and malignant catatonia can both present with delirium,
autonomic instability, hyperthermia, and rigidity. Distinguishing features of the serotonin syndrome
include ingestion of a serotonergic drug such as an SSRI, and the prominence of hyperreflexia,
myoclonus, nausea, vomiting, and diarrhea. Some authorities view the serotonin syndrome as a form of
catatonia, due to similarities in presenting signs and response to specific treatments [67]. (See
"Serotonin syndrome (serotonin toxicity)".)

● Malignant hyperthermia – Malignant hyperthermia and malignant catatonia can both present with
autonomic instability, hyperthermia, and rigidity. Malignant hyperthermia is a rare genetic disorder that
occurs in susceptible patients exposed to an inhalational anesthetic (eg, halothane) or a depolarizing
muscle relaxant (eg, succinylcholine). The distinguishing feature of malignant hyperthermia is its clinical

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setting, and various procedures are used to diagnose it (muscle contracture testing, muscle biopsy, and
genetic testing). (See "Malignant hyperthermia: Clinical diagnosis and management of acute crisis".)

● Akinetic mutism – Akinetic mutism and catatonia may both manifest with immobility, mutism, and waxy
flexibility. However, akinetic mutism does not include posturing, echolalia, or echopraxia; is not
responsive to benzodiazepines; and the lesions to the prefrontal or premotor areas that cause akinetic
mutism should be detectable with neuroimaging. (See "Stupor and coma in adults", section on 'Akinetic
mutism'.)

● Nonconvulsive status epilepticus – Nonconvulsive status epilepticus and catatonia can both present
with stupor and respond positively to benzodiazepines. Nonconvulsive status epilepticus may be
distinguished by the presence of subtle rhythmic twitching and ocular movement abnormalities, and is
diagnosed by epileptic activity on the electroencephalogram (EEG). By contrast, catatonia is associated
with either a normal EEG or diffuse, nonspecific changes (eg, slowing). (See "Nonconvulsive status
epilepticus".)

● Locked-in syndrome – Locked-in syndrome is characterized by immobility and mutism. However, no


other signs of catatonia are present, neuroimaging typically reveals brainstem lesions, and locked-in
patients usually attempt to communicate with eye movements and blinking, whereas catatonic patients
are not motivated to communicate. (See "Locked-in syndrome".)

● Stiff-person syndrome – Stiff-person syndrome is marked by rigidity and a positive response to a


benzodiazepine, and autonomic instability may occur as well, all of which may occur in catatonia.
However, stiff-person syndrome is generally accompanied by a fixed deformity of the spine and anti-
glutamic acid decarboxylase antibodies, which are not observed in catatonia. In addition, catatonic signs
such as mutism and posturing are not part of stiff-person syndrome. (See "Stiff-person syndrome".)

● Parkinson disease – Retarded catatonia and late-stage untreated Parkinson disease may both present
with immobility, rigidity, and decreased speech output. In addition, major depression can occur in
Parkinson disease and may underlie catatonia. However, catatonia often includes odd postures and a
positive response to benzodiazepines, whereas distinguishing features of Parkinson disease include rest
tremor, postural instability, and a positive response to levodopa. (See "Clinical manifestations of
Parkinson disease".)

● Stroke – Stroke can manifest with mutism, but focal neurologic signs and positive findings on
neuroimaging are often present as well, and other signs of catatonia are absent. (See "Overview of the
evaluation of stroke".)

● Delirium – Catatonia may include periods of delirium, and delirium may include some features of
catatonia. A study of 136 critically ill patients on mechanical ventilation and/or vasopressors found that
catatonia plus delirium were both present in approximately 30 percent [45].

Patients with delirium and catatonia present with both stupor (decreased alertness and response to
stimuli), hypokinesis or hyperkinesis, and limited speech output, but catatonia is usually accompanied by
other distinguishing features, including posturing, rigidity, and negativism, as well as a positive response
to the lorazepam challenge test. (See "Diagnosis of delirium and confusional states".)

● Dementia – End-stage dementia and catatonia may both manifest with mutism and hypokinesis.
However, catatonia is usually accompanied by other distinguishing features, including posturing, rigidity,
negativism, and a positive response to the lorazepam challenge test. (See "Evaluation of cognitive
impairment and dementia", section on 'Dementia syndromes'.)

● Elective mutism – Elective mutism is the failure to speak in an otherwise vigilant patient, who may
selectively refuse to speak with some individuals and speak with others. The disorder is usually
accompanied by a personality disorder, preexisting stressor, and no other signs of catatonia.

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● Anti-N-methyl-D-aspartate (NMDA) receptor encephalitis – Anti-N-methyl-D-aspartate (NMDA)


receptor encephalitis is an autoimmune disorder with prominent neuropsychiatric symptoms, including
catatonia in approximately 40 percent of patients [68]. This form of encephalitis may rapidly progress to
seizures, hypoventilation, and coma.

Anti-NMDA receptor encephalitis and catatonia both can include stupor and motor disturbances; in
addition, both anti-NMDA receptor encephalitis and the malignant subtype of catatonia can present with
autonomic instability. However, catatonia can be distinguished from this form of encephalitis by the
presence of other features, including waxy flexibility, staring, and negativism, as well as a positive
response to the lorazepam challenge test. (See "Paraneoplastic and autoimmune encephalitis", section
on 'Anti-NMDA receptor encephalitis'.)

SUMMARY

● Catatonia is a behavioral syndrome that is marked by an inability to move normally despite full physical
capacity to do so. The syndrome occurs in the context of an underlying psychiatric and/or general
medical disorder. The most common underlying psychopathology is bipolar disorder, unipolar major
depression, psychotic disorder, and autism spectrum disorder. Recognizing catatonia is important
because it may be caused or exacerbated by treatment of the underlying disorder. (See 'Clinical features'
above.)

● The estimated incidence of catatonia in acutely ill psychiatric inpatients is approximately 10 percent.
(See 'Epidemiology' above.)

● Signs of catatonia can be either observed (table 1) or elicited (table 2). (See 'Clinical features' above.)

● The three principal subtypes of catatonia are retarded, excited, and malignant. Patients can exhibit signs
of more than one subtype, and subtypes are not necessarily stable during a catatonic episode. (See
'Subtypes' above.)

● The initial clinical evaluation for determining the underlying disorder should include a history, mental
status and physical examination, and laboratory tests guided by symptoms and findings on examination.
(See 'Assessment' above.)

● An intravenous (IV) bolus of lorazepam 1 to 2 mg can help diagnose catatonia. Partial, temporary relief
of signs 5 to 10 minutes after IV administration of lorazepam is consistent with a diagnosis of catatonia. If
there is no change, a second dose is given. A negative response does not rule out catatonia, and occurs
in approximately 20 percent or more of catatonic patients. (See 'Lorazepam challenge' above.)

● The diagnosis of catatonia requires a minimum of two to four signs (table 1 and table 2) for at least
several hours. However, neither the number of catatonic features nor their duration is established. (See
'Diagnosis' above.)

● Signs of catatonia can overlap with signs of other disorders; in particular, malignant catatonia resembles
the neuroleptic malignant syndrome (NMS). Both of these life-threatening disorders can present with
delirium, autonomic instability, fever, and rigidity. The differential diagnosis of catatonia also includes the
serotonin syndrome, malignant hyperthermia, akinetic mutism, nonconvulsive status epilepticus, locked-
in syndrome, stiff-person syndrome, Parkinson disease, stroke, delirium, dementia, elective mutism, and
anti-N-methyl-D-aspartate receptor encephalitis. (See 'Differential diagnosis' above.)

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REFERENCES

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1. Fink M, Taylor MA. The catatonia syndrome: forgotten but not gone. Arch Gen Psychiatry 2009;
66:1173.
2. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition
(DSM-5), American Psychiatric Association, Arlington 2013.
3. The ICD-10 Classification of Mental and Behavioural Disorders: Clinical descriptions and diagnostic gui
delines. World Health Organization. http://www.who.int/classifications/icd/en/bluebook.pdf (Accessed on
October 29, 2013).
4. Fink M. Catatonia from its creation to DSM-V: Considerations for ICD. Indian J Psychiatry 2011; 53:214.
5. Lee JW. Neuroleptic-induced catatonia: clinical presentation, response to benzodiazepines, and
relationship to neuroleptic malignant syndrome. J Clin Psychopharmacol 2010; 30:3.
6. Taylor MA, Fink M. Catatonia in psychiatric classification: a home of its own. Am J Psychiatry 2003;
160:1233.
7. Francis A, Fink M, Appiani F, et al. Catatonia in Diagnostic and Statistical Manual of Mental Disorders,
Fifth Edition. J ECT 2010; 26:246.
8. van der Heijden FM, Tuinier S, Arts NJ, et al. Catatonia: disappeared or under-diagnosed?
Psychopathology 2005; 38:3.
9. Freudenreich O, Nejad SH, Francis A, Fricchione GL. Psychosis, mania, and catatonia. In: Textbook of
Psychosomatic Medicine: Psychiatric Care of the Medically Ill, Second Edition, Levenson JL (Ed), Ameri
can Psychiatric Publishing, Washington, DC 2011. p.219.
10. Chalasani P, Healy D, Morriss R. Presentation and frequency of catatonia in new admissions to two
acute psychiatric admission units in India and Wales. Psychol Med 2005; 35:1667.
11. Zisselman MH, Jaffe RL. ECT in the treatment of a patient with catatonia: consent and complications.
Am J Psychiatry 2010; 167:127.
12. Rosebush PI, Hildebrand AM, Furlong BG, Mazurek MF. Catatonic syndrome in a general psychiatric
inpatient population: frequency, clinical presentation, and response to lorazepam. J Clin Psychiatry
1990; 51:357.
13. Ungvari GS, Leung CM, Wong MK, Lau J. Benzodiazepines in the treatment of catatonic syndrome.
Acta Psychiatr Scand 1994; 89:285.
14. Seethalakshmi R, Dhavale S, Suggu K, Dewan M. Catatonic syndrome: importance of detection and
treatment with lorazepam. Ann Clin Psychiatry 2008; 20:5.
15. Dhossche DM, Stoppelbein L, Rout UK. Etiopathogenesis of catatonia: generalizations and working
hypotheses. J ECT 2010; 26:253.
16. Mann SC, Caroff SN, Campbell EC, et al. Malignant catatonia. In: Current Clinical Neurology: Movemen
t Disorder Emergencies: Diagnosis and Treatment, Frucht SI, Fahn S (Eds), Humana Press, Totowa, NJ
2005. p.53.
17. Northoff G. What catatonia can tell us about "top-down modulation": a neuropsychiatric hypothesis.
Behav Brain Sci 2002; 25:555.
18. Northoff G. Catatonia and neuroleptic malignant syndrome: psychopathology and pathophysiology. J
Neural Transm (Vienna) 2002; 109:1453.
19. Northoff G. Brain imaging in catatonia: current findings and a pathophysiologic model. CNS Spectr
2000; 5:34.
20. Northoff G, Steinke R, Nagel DCzerwenka C, et al. Right lower prefronto-parietal cortical dysfunction in
akinetic catatonia: a combined study of neuropsychology and regional cerebral blood flow. Psychol Med
2000; 30:583.
21. Carroll BT. The universal field hypothesis of catatonia and neuroleptic malignant syndrome. CNS Spectr
2000; 5:26.
https://bibvirtual.upch.edu.pe:2148/contents/catatonia-in-adults-epidemiology-clinical-features-assessment-and-diagnosis/print?search=neurolep… 9/15
6/3/2018 Catatonia in adults: Epidemiology, clinical features, assessment, and diagnosis - UpToDate

22. Meyer J, Huberth A, Ortega G, et al. A missense mutation in a novel gene encoding a putative cation
channel is associated with catatonic schizophrenia in a large pedigree. Mol Psychiatry 2001; 6:302.
23. Stöber G. Genetic predisposition and environmental causes in periodic and systematic catatonia. Eur
Arch Psychiatry Clin Neurosci 2001; 251 Suppl 1:I21.
24. Stöber G, Pfuhlmann B, Nürnberg G, et al. Towards the genetic basis of periodic catatonia: pedigree
sample for genome scan I and II. Eur Arch Psychiatry Clin Neurosci 2001; 251 Suppl 1:I25.
25. Stöber G, Seelow D, Rüschendorf F, et al. Periodic catatonia: confirmation of linkage to chromosome 15
and further evidence for genetic heterogeneity. Hum Genet 2002; 111:323.
26. Francis A. Catatonia: diagnosis, classification, and treatment. Curr Psychiatry Rep 2010; 12:180.
27. Lewis S, Escalona PR, Keith SJ. Phenomenology of schizophrenia. In: Kaplan & Sadock's Comprehens
ive Textbook of Psychiatry, Ninth Edition, Sadock BJ, Sadock VA, Ruiz P (Eds), Lippincott Williams & Wi
lkins, Philadelphia 2009. Vol I, p.1433.
28. Fink M, Taylor MA. Catatonia: subtype or syndrome in DSM? Am J Psychiatry 2006; 163:1875.
29. Fink M, Taylor MA. The many varieties of catatonia. Eur Arch Psychiatry Clin Neurosci 2001; 251 Suppl
1:I8.
30. Bush G, Fink M, Petrides G, et al. Catatonia. II. Treatment with lorazepam and electroconvulsive
therapy. Acta Psychiatr Scand 1996; 93:137.
31. Peralta V, Cuesta MJ, Serrano JF, Martinez-Larrea JA. Classification issues in catatonia. Eur Arch
Psychiatry Clin Neurosci 2001; 251 Suppl 1:I14.
32. Daniels J. Catatonia: clinical aspects and neurobiological correlates. J Neuropsychiatry Clin Neurosci
2009; 21:371.
33. Penland HR, Weder N, Tampi RR. The catatonic dilemma expanded. Ann Gen Psychiatry 2006; 5:14.
34. Fink M. Catatonia: a syndrome appears, disappears, and is rediscovered. Can J Psychiatry 2009;
54:437.
35. Trigo M, Crippa J, Hallak J, et al. The complexity of the differential diagnosis in psychiatry exemplified
by a catatonic syndrome. Rev Psiquiatr Clin 2001; 28:144.
36. Northoff G, Wenke J, Pflug B. Increase of serum creatine phosphokinase in catatonia: an investigation
in 32 acute catatonic patients. Psychol Med 1996; 26:547.
37. Cottencin O, Warembourg F, de Chouly de Lenclave MB, et al. Catatonia and consultation-liaison
psychiatry study of 12 cases. Prog Neuropsychopharmacol Biol Psychiatry 2007; 31:1170.
38. Carroll BT, Anfinson TJ, Kennedy JC, et al. Catatonic disorder due to general medical conditions. J
Neuropsychiatry Clin Neurosci 1994; 6:122.
39. Taylor MA, Abrams R. Catatonia. Prevalence and importance in the manic phase of manic-depressive
illness. Arch Gen Psychiatry 1977; 34:1223.
40. Takaoka K, Takata T. Catatonia in high-functioning autism spectrum disorders: case report and review of
literature. Psychol Rep 2007; 101:961.
41. Wing L, Shah A. A systematic examination of catatonia-like clinical pictures in autism spectrum
disorders. Int Rev Neurobiol 2006; 72:21.
42. Oldham MA, Hochang BL. Catatonia vis-a-vis delirium: The significance of recognizing catatonia in
altered mental status. Gen Hosp Psychiatry 2015.
43. Grover S, Parakh P, Sharma A, et al. Catatonia in systemic lupus erythematosus: a case report and
review of literature. Lupus 2013; 22:634.
44. Smith JH, Smith VD, Philbrick KL, Kumar N. Catatonic disorder due to a general medical or psychiatric
condition. J Neuropsychiatry Clin Neurosci 2012; 24:198.

https://bibvirtual.upch.edu.pe:2148/contents/catatonia-in-adults-epidemiology-clinical-features-assessment-and-diagnosis/print?search=neurole… 10/15
6/3/2018 Catatonia in adults: Epidemiology, clinical features, assessment, and diagnosis - UpToDate

45. Wilson JE, Carlson R, Duggan MC, et al. Delirium and Catatonia in Critically Ill Patients: The Delirium
and Catatonia Prospective Cohort Investigation. Crit Care Med 2017; 45:1837.
46. Rosebush PI, Mazurek MF. Catatonia and its treatment. Schizophr Bull 2010; 36:239.
47. Ungvari GS, Caroff SN, Gerevich J. The catatonia conundrum: evidence of psychomotor phenomena as
a symptom dimension in psychotic disorders. Schizophr Bull 2010; 36:231.
48. Medda P, Toni C, Luchini F, et al. Catatonia in 26 patients with bipolar disorder: clinical features and
response to electroconvulsive therapy. Bipolar Disord 2015; 17:892.
49. Sienaert P, Rooseleer J, De Fruyt J. Measuring catatonia: a systematic review of rating scales. J Affect
Disord 2011; 135:1.
50. Bush G, Fink M, Petrides G, et al. Catatonia. I. Rating scale and standardized examination. Acta
Psychiatr Scand 1996; 93:129.
51. Northoff G, Koch A, Wenke J, et al. Catatonia as a psychomotor syndrome: a rating scale and
extrapyramidal motor symptoms. Mov Disord 1999; 14:404.
52. Carroll BT, Kirkhart R, Ahuja N, et al. Katatonia: a new conceptual understanding of catatonia and a
new rating scale. Psychiatry (Edgmont) 2008; 5:42.
53. Lee JW. Serum iron in catatonia and neuroleptic malignant syndrome. Biol Psychiatry 1998; 44:499.
54. Carroll BT, Goforth HW. Serum iron in catatonia. Biol Psychiatry 1995; 38:776.
55. Singerman B, Raheja R. Malignant catatonia--a continuing reality. Ann Clin Psychiatry 1994; 6:259.
56. Koek RJ, Mervis JR. Treatment-refractory catatonia, ECT, and parenteral lorazepam. Am J Psychiatry
1999; 156:160.
57. Schmider J, Standhart H, Deuschle M, et al. A double-blind comparison of lorazepam and oxazepam in
psychomotor retardation and mutism. Biol Psychiatry 1999; 46:437.
58. Zaw ZF, Bates GD. Replication of zolpidem test for catatonia in an adolescent. Lancet 1997; 349:1914.
59. Thomas P, Rascle C, Mastain B, et al. Test for catatonia with zolpidem. Lancet 1997; 349:702.
60. Cottencin O, Danel T, Goudemand M, et al. Catatonia recognition and treatment. Med Sci Monit 2009;
15:CS129.
61. Strawn JR, Keck PE Jr, Caroff SN. Neuroleptic malignant syndrome. Am J Psychiatry 2007; 164:870.
62. Fricchione GL. Neuroleptic catatonia and its relationship to psychogenic catatonia. Biol Psychiatry 1985;
20:304.
63. Caroff SN, Mann SC, Keck PE Jr. Specific treatment of the neuroleptic malignant syndrome. Biol
Psychiatry 1998; 44:378.
64. Fink M, Taylor MA. Neuroleptic malignant syndrome is malignant catatonia, warranting treatments
efficacious for catatonia. Prog Neuropsychopharmacol Biol Psychiatry 2006; 30:1182.
65. Castillo E, Rubin RT, Holsboer-Trachsler E. Clinical differentiation between lethal catatonia and
neuroleptic malignant syndrome. Am J Psychiatry 1989; 146:324.
66. Fleischhacker WW, Unterweger B, Kane JM, Hinterhuber H. The neuroleptic malignant syndrome and
its differentiation from lethal catatonia. Acta Psychiatr Scand 1990; 81:3.
67. Keck PE, Arnold LM. The serotonin syndrome. Psychiatr Ann 2000; 30:333.
68. Sarkis RA, Coffey MJ, Cooper JJ, et al. Anti-N-methyl-D-aspartate receptor encephalitis: a review of
psychiatric phenotypes and management considerations. A report of the American Neuropsychiatric
Association Committee on Research. J Neuropsychiatry Clin Neurosci 2017.

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GRAPHICS

Observed signs of catatonia

Feature Description and examples

Immobility Hypokinetic or akinetic behavior that is not influenced by external stimuli.

Stupor Decreased alertness, hypoactivity, and diminished responses to voice and painful stimuli.

Excitement Impulsive, frantic, and stereotypic behavior that may include sudden outbursts of talking,
singing, dancing, and tearing of clothes. Patients may be irritable and damage objects or injure
themselves or others. Excitement may suddenly alternate with stupor.

Mutism Patients are awake but verbally unresponsive. Mutism is not always associated with immobility
and may appear elective. Less severe forms of mutism include lack of spontaneous speech,
sluggish responses to questions with automatic answers such as "I don't know" (speech-prompt),
and speaking with progressively less volume until speech is an inaudible mumble (prosectic
speech).

Posturing Voluntarily maintaining a position of the body or a body part for a long time; eg, standing or lying
(catalepsy) down in the same position, an exaggerated pucker, lying in bed with the head elevated and
unsupported as if on a pillow, holding arms above the head or raised in a prayer-like manner, and
holding fingers and hands in odd positions.

Echophenomena Echolalia (senseless repetition of another person's utterances) and echopraxia (senseless
repetition of another person's movements).

Speech Robotic speech, feigned foreign accent, palilalia or verbigeration (involuntary repetition of words
mannerisms or phrases).

Behavioral Odd, purposeful movements, such as holding hands as if they were handguns or saluting
mannerisms passersby, or exaggerated or stilted caricatures of mundane movements.

Stereotypy Non-goal-directed, repetitive movements that often are awkward or stiff; examples include
grimacing, teeth/tongue clicking, rocking, sniffing, biting, or automatically touching or tapping.

Staring Fixed gaze with little or no scanning of the environment and decreased blinking.

Adapted from:
1. Fink M, Taylor MA. The catatonia syndrome: Forgotten but not gone. Arch Gen Psychiatry 2009; 66:1173.
2. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text
Revision. Washington, DC, American Psychiatric Association, 2000.
3. Bush G, Fink M, Petrides G, et al. Catatonia. I. Rating scale and standardized examination. Acta Psychiatr Scand
1996; 93:129.
4. Greenhalgh J, Knight C, Hind D, et al. Clinical and cost-effectiveness of electroconvulsive therapy for depressive
illness, schizophrenia, catatonia and mania: systematic reviews and economic modelling studies. Health Technol
Assess 2005; 9:1.

Graphic 53391 Version 3.0

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Elicited signs of catatonia

Feature Description and examples

Ambitendency The patient appears "stuck" in an indecisive, hesitant movement when the examiner verbally
contradicts his or her own nonverbal signal. As an example, the examiner offers his hand as if to
shake hands while stating, "Do not shake my hand."

Waxy The rigid patient's initial resistance to the examiner's manipulations is gradually overcome, allowing
flexibility re-positioning (as in bending a candle).

Automatic The patient moves with the examiner's light pressure into a new position despite instructions to the
obedience contrary. The new position may then be maintained despite instructions to the contrary. Test
bilaterally as this sign may result from contralateral brain lesions.

Negativism The patient resists the examiner's manipulations with strength equal to that applied (rigidity);
social negativism may include sleeping under the bed, turning away when addressed, refusing to
open the eyes, and closing the mouth when offered food or liquids.

Stimulus- The patient's behavior is tied to certain stimuli. As an example, the examiner states, "When I touch
bound my nose, you touch your chest," and the patient touches his nose in a mirrored behavior despite
behavior understanding the instruction.

Adapted from:
1. Fink M, Taylor MA. The catatonia syndrome: Forgotten but not gone. Arch Gen Psychiatry 2009; 66:1173.
2. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text
Revision. Washington, DC, American Psychiatric Association, 2000.
3. Bush G, Fink M, Petrides G, et al. Catatonia. I. Rating scale and standardized examination. Acta Psychiatr Scand
1996; 93:129.
4. Greenhalgh J, Knight C, Hind D, et al. Clinical and cost-effectiveness of electroconvulsive therapy for depressive
illness, schizophrenia, catatonia and mania: systematic reviews and economic modelling studies. Health Technol
Assess 2005; 9:1.

Graphic 66229 Version 2.0

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Laboratory findings in catatonia

Laboratory finding Implication

Leukocytosis Non-specific; levels between 15,000 and 25,000 per mL correlate with malignant
catatonia

Increased creatinine Non-specific; levels exceeding 1000 IU/L (normal range <150 IU/L) strongly correlate
kinase (CK) with malignant catatonia

Low serum iron Observed in 40 percent of persons with malignant catatonia

Data from:
1. Northoff G, Wenke J, Pflug B. Increase of serum creatine phosphokinase in catatonia: an investigation in 32 acute
catatonic patients. Psychol Med 1996; 26:547.
2. Lee JW. Serum iron in catatonia and neuroleptic malignant syndrome. Biol Psychiatry 1998; 44:499.
3. Carroll BT, Goforth HW. Serum iron in catatonia. Biol Psychiatry 1995; 38:776.
4. Singerman B, Raheja R. Malignant catatonia - a continuing reality. Ann Clin Psychiatry 1994; 6:259.

Graphic 57370 Version 1.0

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Contributor Disclosures
M Justin Coffey, MD Nothing to disclose Peter P Roy-Byrne, MD Employment: Mass Medical Society
(journal Watch); Wiley Lliss (Depression and Anxiety) [Editor in Chief]. Stock Options: Valant Medical
Solutions [behavioral health (EMR)]. Stephen Marder, MD Grant/Research/Clinical Trial Support: Forum;
Neurocrine [schizophrenia and tardive dyskinesia]. Consultant/Advisory Boards: Takeda, Gideon Richter,
Boeringer-Ingleheim, Otsuka; Allergan; Teva [schizophrenia (brexpiprazole, cariprazine)]. David Solomon,
MD Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
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