INTRODUCTION Catatonia is a behavioral syndrome marked by an inability to

move normally, and is associated with many underlying psychiatric, neurologic, and
general medical disorders [ 1 ]. Within psychiatric nosology, catatonia is recognized
as a descriptive modifier of mood episodes (analogous to psychosis), a subtype of
schizophrenia, and a disorder due to a general medical condition [ 2,3 ].
Recognizing catatonia is important because it may be caused or exacerbated by
treatment of the underlying disorder (eg, antipsychotic drugs used for mood or
psychotic disorders may worsen catatonia)

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 ].
Starting, stopping, and planning movement can be impaired, and motor behavior may be
repetitive, purposeless, impervious to external stimuli, and contrary to intent [ 10 ].
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 [
1,2,10,25 ]:

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 (catalepsy)

Excessive motor activity (excitement)

Staring

Echophenomena (repeating another persons words or movements)

Onset of catatonia can be either acute or insidious [ 1,8 ]. Following remission, some patients
cannot recall their experience during the episode, whereas others describe an awareness of their
activity and the inability to communicate [ 26 ].
Catatonia occurs in patients who are severely ill with an underlying psychiatric or general
medical disorder, and is thus analogous to delirium [ 2,27 ]. (See 'Underlying disorders' below.)
Subtypes There are several subtypes of catatonia, based upon the specific nature of the
movement disturbance and other associated features [ 1,28,29 ]. The three principal forms 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 [ 30 ],
patients can exhibit signs of both subtypes concurrently [ 31 ]. Subtypes are not necessarily
stable during a catatonic episode, and patients may transition from retarded to excited catatonia
or vice versa [ 32,33 ]. In addition, retarded and excited catatonia can each progress to malignant
catatonia; alternatively, malignant catatonia can occur de novo.
Retarded catatonia The retarded form of catatonia is characterized by mutism, inhibited
movement, posturing, negativism, and staring [ 1,9 ]. 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 [ 33 ].
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 [ 1,15
]. The syndrome is typically fulminant and progresses rapidly within a few days [ 34 ]. Common
but nonspecific laboratory findings include leukocytosis, elevated creatine kinase, and low serum
iron [ 15,35 ]. Signs of malignant catatonia overlap with signs of the neuroleptic malignant
syndrome (NMS). (See 'Differential diagnosis' below.)
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, [ 1,9 ]. Delirium may occur in severe cases, and the excess motor
activity may cause self-injury or harm to others.
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 [ 28 ] or periods of retarded
catatonia alternating with excited catatonia [ 1 ].
Subtypes There are several subtypes of catatonia, based upon the specific nature of the
movement disturbance and other associated features [ 1,28,29 ]. The three principal forms 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 [ 30 ],
patients can exhibit signs of both subtypes concurrently [ 31 ]. Subtypes are not necessarily
stable during a catatonic episode, and patients may transition from retarded to excited catatonia
or vice versa [ 32,33 ]. In addition, retarded and excited catatonia can each progress to malignant
catatonia; alternatively, malignant catatonia can occur de novo.
Retarded catatonia The retarded form of catatonia is characterized by mutism, inhibited
movement, posturing, negativism, and staring [ 1,9 ]. 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 [ 33 ].
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 [ 1,15
]. The syndrome is typically fulminant and progresses rapidly within a few days [ 34 ]. Common
but nonspecific laboratory findings include leukocytosis, elevated creatine kinase, and low serum
iron [ 15,35 ]. Signs of malignant catatonia overlap with signs of the neuroleptic malignant
syndrome (NMS). (See 'Differential diagnosis' below.)
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, [ 1,9 ]. Delirium may occur in severe cases, and the excess motor
activity may cause self-injury or harm to others.
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 [ 28 ] or periods of retarded
catatonia alternating with excited catatonia [ 1
Partial, temporary relief of signs 5 to 10 minutes after IV administration of lorazepam is
consistent with a diagnosis of catatonia [ 1,28 ]. 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 [ 44 ]. In case reports, oral zolpidem 10 mg was useful

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 ) [ 1,11,25,38 ]. However,
neither the number of catatonic features required for the diagnosis nor their
duration is established, and no one sign is pathognomonic
Treatment:

Treatment algorithm First-line treatment for catatonia is a benzodiazepine or

electroconvulsive therapy (ECT), depending upon the subtype of catatonia, clinical urgency, and
availability of treatments [ 1,13,27-31 ]:

For patients with malignant catatonia, we recommend a benzodiazepine plus immediate

preparation to administer ECT as soon as possible. If the benzodiazepine provides a
substantive response during the first 24 to 48 hours, it can be continued in lieu of ECT.

For patients with retarded or excited catatonia, we recommend treatment with a

benzodiazepine ( lorazepam is used most often).

No randomized trials have evaluated benzodiazepines or ECT for acute catatonia. However,
prospective open-label studies, cases series, and retrospective studies suggest that
benzodiazepines alone, or benzodiazepines followed by ECT, lead to recovery in approximately
60 to 80 percent of patients [ 1,13,24,32,33 ]. Treatment guidelines from the American
Psychiatric Association, United Kingdom National Institute for Health and Clinical Excellence,
and World Federation of Societies of Biological Psychiatry recommend treating catatonia with
either a benzodiazepine or ECT, depending upon the clinical urgency [ 27-31 ].
A review of open-label studies, case series, and case reports found that treatment of catatonia is
the same regardless of the underlying disorder [ 12 ].
Malignant catatonia ECT is first-line treatment for patients with malignant catatonia [
1,4,13,24 ]. We recommend that clinicians concurrently start a benzodiazepine and the process of
obtaining informed consent and medical consultation for ECT. If the patient does not measurably
respond to a benzodiazepine within the first day or two, ECT should commence. Reviews of case
reports have found that mortality for progressive malignant catatonia increases if ECT does not
begin within five days of symptom onset [ 24,34 ]. Another review of case reports found that in
patients with malignant catatonia, response to ECT occurred in 9 of 11 patients (89 percent),
whereas response to a benzodiazepine occurred in 2 of 5 patients (40 percent) [ 13 ]. During the
first week, daily ECT may be needed.
The safety and administration of benzodiazepines and ECT are discussed separately. (See
'Benzodiazepine safety and administration' below and 'Electroconvulsive therapy safety and
administration' below.)
Retarded or excited catatonia Based upon prospective open-label studies and case series, we
recommend initial treatment with a benzodiazepine for patients with retarded or excited catatonia
[ 1,13 ]. Lorazepam has been studied most frequently [ 1,10,13,32,35,36 ], but case reports also
describe successful treatment with diazepam , clonazepam , clorazepate , midazolam , and
alprazolam [ 37-46 ]. In a review of case reports of 104 catatonic episodes that were treated with
benzodiazepine monotherapy, 70 percent remitted; among the 72 episodes treated with
lorazepam, 79 percent remitted [ 13 ]. Other reviews estimate that 60 to 80 percent of patients
with catatonia respond to lorazepam monotherapy [ 4,37,47 ]. Although amobarbital was
significantly more effective than placebo in a randomized trial [ 48 ], most authorities consider
benzodiazepines as first-line pharmacotherapy because they are generally effective and safer than
barbiturates [ 1,3,4 ]. In addition, benzodiazepines have been studied more often, are familiar to
clinicians, and an antagonist ( flumazenil ) is available. (See 'Benzodiazepine safety and
administration' below.)

Clinical factors may be associated with response to a benzodiazepine. Successful benzodiazepine

treatment may be more likely in patients with a significant reduction of catatonic signs after the
first dose of lorazepam or other benzodiazepine (positive lorazepam challenge test) [ 34 ].
Acutely catatonic patients with an underlying mood disorder may respond more favorably to a
benzodiazepine than schizophrenic patients [ 11,49 ]. In addition, benzodiazepines at low doses
do not appear to benefit chronic catatonia in schizophrenic patients. A randomized trial compared
adjunctive lorazepam with placebo for treating slow-onset, long-standing (4 years) catatonic
signs in severely disabled and treatment-resistant chronic schizophrenic patients; lorazepam 6
mg daily provided no benefit [ 50 ]. It is not clear whether a longer duration of catatonia prior to
treatment is associated with a poorer response to treatment, due to contradictory study results [
11,32 ]. Age, sex, and the number and pattern of catatonic signs do not appear to be associated
with response to a benzodiazepine [ 4,9,24,32 ]. The lorazepam challenge test is discussed
separately. (See "Catatonia in adults: Epidemiology, clinical features, assessment, and diagnosis",
section on 'Lorazepam challenge' .)
For patients with retarded or excited catatonia that does not respond to a benzodiazepine, ECT is
the treatment of choice [ 1,4,24,32 ]. In addition, if the underlying cause of catatonia is a mood
disorder, or for patients requiring a rapid treatment response, ECT is the most effective treatment
option. Based upon open-label studies, case series, and retrospective studies, it is estimated that
approximately 60 percent or more of catatonic patients achieve remission with ECT, including
patients unresponsive to a benzodiazepine [ 4,27,32,33,35,51-53 ]. As an example, a review of
case reports of 55 catatonic episodes that were treated with ECT alone found that 85 percent
remitted [ 13 ]. A subsequent chart review of 27 catatonic patients treated with ECT found that
59 percent improved [ 33 ]. For patients with a mood disorder or acute psychosis, ECT can
relieve both the catatonic syndrome and the underlying psychopathology [ 4,24 ]. (See
'Electroconvulsive therapy safety and administration' below.)
There are no established predictors of response to ECT for patients with catatonia [ 3 ]. However,
acutely catatonic patients with an underlying mood disorder may respond more favorably to ECT
than schizophrenic patients [ 49 ], and ECT does not appear to benefit chronic catatonia in
schizophrenic patients [ 54 ].
Benzodiazepine safety and administration Benzodiazepines are generally safe and well
tolerated in this setting. At doses used for treating catatonia, benzodiazepines are not associated
with respiratory depression in otherwise healthy adults. However, clinicians should be cognizant
of concomitant drugs that can cause sedation or respiratory depression, eg, opioids. In addition,
benzodiazepines cause varying degrees of motor incoordination and increase the risk of falls [ 10
].
Benzodiazepines can be administered intravenously, intramuscularly, or orally ( lorazepam is
available in all three formulations) [ 4,32 ]. Intravenous administration is preferred to assure
adherence and rapid, complete absorption (intravenous access also permits administration of
fluids for dehydration). Intravenous benzodiazepines should be injected or infused slowly. As
patients improve, they should be switched to oral medication.

Lorazepam has been studied most often, and is typically initiated at 1 to 2 mg three times per
day. Close observation for a clinical response can substantiate the diagnosis of catatonia. The
dose is then increased by 3 mg per day every one to two days, depending upon patient response,
tolerability, and clinical urgency. A dose of 6 to 21 mg daily is effective for most patients, but a
dose of 30 mg per day is occasionally necessary [ 1 ]. For patients with excited catatonia,
lorazepam 1 to 2 mg is given at more frequent intervals until the patient is calm but awake. A
more cautious approach is suggested for patients at risk of cardiorespiratory compromise or
oversedation (eg, older, obese, or volume depleted patients; patients with cardiovascular or
respiratory disease; patients receiving opioid analgesics). For patients with these risk factors, the
initial dose may be reduced to 0.5 mg three times per day and closer monitoring provided [ 10,35
]. (See "Catatonia in adults: Epidemiology, clinical features, assessment, and diagnosis", section
on 'Lorazepam challenge' .)
The duration of treatment required to achieve remission of catatonia with a benzodiazepine is
typically 4 to 10 days [ 34 ]. The benzodiazepine is usually continued at the effective dose for
three to six months to maintain recovery and is then slowly tapered and discontinued, although
longer maintenance treatment may be necessary [ 55 ].
Additional information about the clinical use and pharmacology of benzodiazepines is discussed
separately. (See "Sedatives and hypnotics abuse and dependence: Pharmacology and
epidemiology" .)
Electroconvulsive therapy safety and administration ECT is generally safe, even in patients
whose general medical status is compromised [ 56 ]. However, safety concerns necessitate
preprocedure medical consultation. ECT is typically administered with the same technique used
for other indications. (See "Medical consultation for electroconvulsive therapy" and "Technique
for performing electroconvulsive therapy (ECT) in adults" .)
There are no absolute contraindications to ECT [ 57-61 ]. Underlying general medical conditions
may increase the risk of adverse effects of ECT or general anesthesia, but modern ECT technique
and preprocedure consultation to optimize the patients general medical status reduce these risks.
As an example, catatonic patients with motor immobility and muscle damage are at increased
risk for transient hyperkalemia associated with the muscle relaxant succinylcholine [ 3,12 ]. This
increased risk is eliminated by using a nondepolarizing muscle relaxant (eg, rocuronium ) [ 62 ].
Electrode placement and other aspects of ECT technique for treating catatonia have not been
standardized [ 12 ]. However, bilateral electrode placement and brief pulse current are generally
preferred [ 1 ]. ECT is generally given three times per week on alternating days. However,
clinical urgency may necessitate daily treatments for malignant catatonia until the patient is
physiologically stable, which often occurs within two to five treatments [ 1 ]. At least six
treatments are given regardless of the catatonia subtype to reduce the risk of sudden relapse.
Most patients receiving ECT regardless of the indication remit with 6 to 12 treatments, but some
patients may require 20 or more [ 56 ]. ECT is usually terminated after the acute catatonic
episode has remitted, but one case report described maintenance ECT for a patient with recurrent
catatonia [ 63 ]. Additional information about ECT is discussed separately. (See "Overview of

electroconvulsive therapy (ECT) for adults" and "Technique for performing electroconvulsive
therapy (ECT) in adults" .)
Case reports describe catatonic patients who responded to ECT plus lorazepam [ 60,61 ]. The
decision to continue a benzodiazepine during ECT is determined by the patients initial response
to the medication and the modifications in ECT technique that are required. For patients with a
partial but incomplete response to lorazepam, the drug may be continued during ECT to maintain
the drugs therapeutic benefit. However, the benzodiazepine should be discontinued if it
interferes with ECT (increases seizure threshold and shortens seizure duration) despite
adjustments in the ECT technique. (See "Overview of electroconvulsive therapy (ECT) for
adults", section on 'Concurrent medications' .)
Other treatments Alternative treatments may be available for patients with catatonia who do
not respond to benzodiazepines and either decline ECT or do not have access to it [ 4 ]. Case
reports describe other treatments that were added to an existing pharmacotherapy regimen and
may possibly be beneficial. These other treatments include carbamazepine [ 64 ], topiramate [ 65
], valproate [ 66,67 ], zolpidem [ 4,68,69 ], memantine [ 70-73 ], and bromocriptine [ 74 ].
Amantadine has also been used, but has dopamine agonist activity that can potentially worsen an
underlying psychosis [ 73 ]. Additional case reports describe treatment of catatonia with repeated
transcranial magnetic stimulation [ 12 ].
LONG-TERM PROGNOSIS Although the long-term outcome of catatonia has not been
rigorously studied, catatonia appears to have a generally favorable prognosis, especially the
retarded and excited subtypes [ 4,75 ]. Long-term prognosis appears to be linked to the nature
and severity of the underlying psychiatric or general medical disorder [ 3,24 ]. Retarded or
excited catatonia in patients with an underlying mood disorder or toxic-metabolic disorder
usually resolves with treatment of the catatonic syndrome plus the underlying condition [ 24 ].
However, catatonia may persist for years, particularly in patients with schizophrenia [ 50 ]. In
addition, patients with malignant catatonia may be left with permanent morbidity (eg, cognitive
deficits, apathy syndromes, and limb strictures), and death rates of up to 20 percent have been
reported [ 34 ].
Case reports describe recurrent catatonic episodes [ 13,63 ]. One case series of five patients
reported that the mean interval between consecutive episodes was 11 months (range 5 to 20
months) [ 76 ]. The motor signs were generally consistent across each patients two episodes. For
cases with complete information, the same treatment worked in the two episodes