REVIEW ARTICLE

PSYCHIATRY
published: 09 December 2014
doi: 10.3389/fpsyt.2014.00181

A clinical review of the treatment of catatonia

Pascal Sienaert 1,2 *, Dirk M. Dhossche 3 , Davy Vancampfort 4 , Marc De Hert 4 and Gábor Gazdag 5,6
1
Department of Mood Disorders and Electroconvulsive Therapy, University Psychiatric Center, KU Leuven, Leuven, Belgium
2
Department of Neurosciences, KU Leuven, Leuven, Belgium
3
Department of Psychiatry, University of Mississippi Medical Center, Jackson, MS, USA
4
University Psychiatric Center, KU Leuven, Leuven, Belgium
5
Center for Psychiatry and Addiction Medicine, Szent István and Szent László Hospitals, Budapest, Hungary
6
Department of Psychiatry and Psychotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary

Edited by: Catatonia is a severe motor syndrome with an estimated prevalence among psychiatric
Mihaly Hajos, Yale University School
inpatients of about 10%. At times, it is life-threatening especially in its malignant form
of Medicine, USA
when complicated by fever and autonomic disturbances. Catatonia can accompany many
Reviewed by:
Mihaly Hajos, Yale University School different psychiatric illnesses and somatic diseases. In order to recognize the catatonic syn-
of Medicine, USA drome, apart from thorough and repeated observation, a clinical examination is needed.
Sebastian Walther, University Hospital A screening instrument, such as the Bush-Francis Catatonia Rating Scale, can guide the
of Psychiatry, Switzerland
clinician through the neuropsychiatric examination. Although severe and life-threatening,
Manuel Morrens, University Antwerp,
Belgium catatonia has a good prognosis. Research on the treatment of catatonia is scarce, but there
*Correspondence: is overwhelming clinical evidence of the efficacy of benzodiazepines, such as lorazepam,
Pascal Sienaert , Department of Mood and electroconvulsive therapy.
Disorders and Electroconvulsive
Keywords: catatonia, benzodiazepines, electroconvulsive therapy, glutamate antagonists, zolpidem, transcranial
Therapy, University Psychiatric Center,
magnetic stimulation
KU Leuven (University of Leuven),
Campus Kortenberg,
Leuvensesteenweg 517, Kortenberg
3070, Belgium
e-mail: pascal.sienaert@
uc-kortenberg.be

INTRODUCTION EVALUATION, DIFFERENTIAL DIAGNOSIS, AND TREATMENT

Catatonia is a severe motor syndrome with an estimated preva- An effective treatment starts with a swift and correct diagnosis. In
lence among psychiatric inpatients of about 10% (1, 2). Catatonia any patient exhibiting marked deterioration in psychomotor func-
can accompany many different psychiatric illnesses and somatic tion and overall responsiveness, catatonia should be considered.
diseases. A minority of catatonic patients suffers from schizo- Moreover, any patient that is admitted to a psychiatric ward with a
phrenia (30%), while a majority has a bipolar disorder (43%) severe psychiatric disorder, such as depression, bipolar disorder, a
(1, 3, 4). Catatonia has also been linked to other psychiatric dis- psychotic disorder, or autism spectrum disorder, should be exam-
orders, such as obsessive-compulsive disorder (5), post-traumatic ined routinely (19). Some signs and symptoms are evident upon
stress disorder (6, 7), or withdrawal from alcohol (8) or benzo- observation of the patient during a psychiatric interview. Other
diazepines (9, 10). In up to 25% of cases, catatonia is related specific symptoms, however, such as automatic obedience, ambi-
with general medical or neurologic conditions (1, 11). Recently, tendency, negativism should be elicited during a neuropsychiatric
it was shown repeatedly that catatonic symptoms are observable examination (19, 20). A rating scale can be used as a screening
in most patients diagnosed with anti-N -methyl-d-aspartate recep- instrument and aid in the detection and quantification of catato-
tor (anti-NMDAR) encephalitis (12, 13). In adolescents and young nia. A number of rating scales have been found reliable, sensitive
adults with autism, catatonia is found in 12–17% (14). Pediatric and specific: the Rogers Catatonia Scale, the Bush-Francis Catato-
catatonia also emerges in patients with tic disorders, and a variety nia Rating Scale (BFCRS) (and its revised version), the Northoff
of other (developmental) disorders (15). The same principles of Catatonia Rating Scale, and the Braunig Catatonia Rating Scale
evaluation and treatment seem to apply to pediatric patients as in (19). Early detection of catatonia is of great importance, since the
adult patients (15, 16). presence of catatonic signs possesses significant prognostic and
A life-threatening situation occurs when catatonia is accompa- therapeutic value (19).
nied by fever and autonomic abnormalities. Malignant catatonia, Unfortunately, no laboratory test specifically defines catato-
coined as “lethal catatonia” by Stauder in 1934 (17), presents as nia. The “diagnostic weight” of several proposed laboratory and
a constellation of catatonia, stuporous exhaustion, autonomic imaging tests is limited (21). Possible laboratory tests, primar-
instability, respiratory failure, collapse, coma, and often death ily to assess various underlying conditions, include a complete
if left untreated. This clinical picture is very close to what is blood count and metabolic panel, erythrocyte sedimentation
observed in neuroleptic malignant syndrome (NMS), which is rate, blood urea nitrogen, creatinine, serum iron, and creatinine-
considered by several experts to be a drug-induced form of phosphokinase, antinuclear antibodies, and urinalysis, and mag-
catatonia (18). netic resonance imaging, electroencephalogram, cerebrospinal

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Sienaert et al. Treatment of catatonia

fluid analysis (4, 11). Given the frequent association with anti- of catatonia responded swiftly to the administration of lorazepam
NMDAR-encephalitis, detection of IgG antibodies to NMDAR in (35); a 15-year-old girl with catatonic lupus, resistant to several
cerebrospinal fluid or serum is advisable (22). Since serum iron treatments was successfully treated with ECT after 3 months (36).
was found to be reduced in NMS compared to catatonia (23), some A man developing catatonia after myocardial infarction remained
authors see low serum iron as a risk factor for developing NMS catatonic for 1.5 years until he was treated with ECT (37). A men-
after using antipsychotics in a catatonic patient (24). A drug screen tally retarded boy with catatonia of 5 year’s duration improved
to detect common illicit and prescribed substances is necessary. with lorazepam (38). Both Ripley and Millson (39) and Salam
et al. (40) reported positive response to lorazepam in two patients
PROGNOSIS with psychogenic catatonia that lasted 2 1/2 years and 3 months,
Prognosis of catatonia is good, especially with early and aggressive respectively. A long treatment delay should, however, be avoided
treatment. In mood disorders, prognosis is probably better than in since it can lead to a variety of serious medical complications,
psychotic disorders. Kraepelin, who classified catatonia as a type some of which may be lethal (41).
of dementia praecox, wrote, in the 9th edition of his textbook, In the above mentioned retrospective lorazepam-study in 107
that almost half of catatonic attacks begin with a depressive phase inpatients (30), predictors of response to lorazepam were exam-
and that these patients had a better prognosis. Hoch, in a mono- ined. A longer illness duration, the presence of mutism, third-
graph on benign stupors, reports good outcomes (‘remission and person auditory hallucinations and ‘made phenomena’ (in which
return to the community’) in 13 patients with manic-depressive the individual feels he is being made to do something) predicted a
illness, and a poor outcome in 12 schizophrenics (25). In more poor response, whereas the presence of waxy flexibility predicted
recent studies, results are conflicting. Most of the available data a good response (30). It should be noted that low lorazepam doses
confirm a worse prognosis in the context of schizophrenia. In a (3–6 mg/day) were used. A longer illness duration also seemed to
randomized double-blind, placebo-controlled trial in 18 patients predict a worse outcome in the first 11 patients treated by László
with chronic schizophrenia, who also displayed enduring catatonic Meduna, who invented convulsive therapy in 1934 (42, 43). In a
features, 6 mg lorazepam per day for 12 weeks did not have any 1912 monograph, Urstein reports on 30 patients with catatonia,
effect on catatonic symptoms (26). In another recent study, 73% of with various underlying conditions and a variable prognosis, being
24 patients with catatonia remitted within 6 days after starting ben- worse in patients with a higher number of episodes (44). Fink states
zodiazepines: partial responders (6/24) all had schizophrenia (27). that prognosis is especially favorable when the syndrome is dom-
In a retrospective study ECT was only partially efficacious in 2 of 4 inated by stupor, hyperactivity, rapid, and pressured speech, and
patients with schizophrenic catatonia, whereas 5 out of 5 patients lability of mood, or if there is a previous episode with recovery, a
with mood disorder fully recovered (28). In a small open study, rapid onset of the episode, and good social functioning prior to
however, lorazepam (4–12.5 mg/day) was reported ineffective in 5 the episode (45, 46). Van Waarde and co-workers have examined
of 20 patients; all 5 with mood disorders (29). In a recent retro- predictors of response to ECT in 27 catatonic patients and found
spective chart study on the effects of lorazepam in 107 inpatients improvement to be significantly associated with younger age, and
with a primary diagnosis of catatonia, there was no significant the presence of autonomic dysregulation, especially higher body
difference between patients with mood disorder and those with temperature (47). There is anecdotal evidence that organic catato-
a non-affective psychotic disorder (30, 31). Similarly, in an ECT- nia is less responsive, or does not respond at all, to ECT. Swartz and
study in 22 patients, 13 (59%) of which had a mood disorder, no colleagues described four patients with a variety of neurological
statistically significant difference was found in the effectiveness of impairment (Alzheimer’s disease, post-encephalitic mental retar-
the resolution of catatonic symptoms in persons with mood dis- dation, cerebellar atrophy, epilepsy, and spinal injury). Patients
order versus schizophrenia (32), although the authors stress that showed only transient and partial improvement to ECT. The
in the patients with mood disorders more catatonic symptoms authors suggest that advanced pathological changes of the CNS
resolved with ECT than in the other group. might explain a diminished response and that these states require
A factor that might complicate the difference in reported a particularly intensive treatment (48).
response rates of affective versus schizophrenic catatonia is Raffin and coworkers (16) recently reported treatments used
chronicity. At least part of the studies showing a worse response in in 66 consecutively hospitalized children and adolescents between
the context of schizophrenia have included patients with chronic the ages 9–19 with catatonia. The most frequent comorbid condi-
catatonia (4, 26, 33). Some authors have suggested that “chronic tions were schizophrenia (N = 38, 58%), pervasive developmental
catatonia” in the context of schizophrenia is phenomenologically disorder (N = 17, 26%), medical conditions (N = 16, 24%), bipo-
different and less responsive to either benzodiazepines or ECT lar disorder (N = 11, 17%), and intellectual disability (N = 8,
(34), and thus carries a less favorable prognosis then the acute 12%). The naturalistic design of the study lists a wide range
forms of catatonia. The fact that a longer duration of the episode of treatments in various combinations. Average catatonia scores
has been reported to predict a worse response should not be seen decreased and level of function increased during the admission.
as a reason to withhold adequate treatment in patients presenting Fifty-one (77%) patients received benzodiazepines, in doses up to
with longstanding or resistant catatonic symptoms. Catatonia that 15 mg of lorazepam per day, which were effective in 65% of cases.
is not effectively treated may persist for years, but should never- Twelve (18%) received ECT, in three cases as first-line treatment
theless be promptly treated upon detection. A number of cases (of which two cases had malignant catatonia). One patient with
are illustrative of the overall good prognosis, even in chronic and schizophrenia received maintenance ECT. There was no associa-
longstanding catatonic symptoms. A man with a 17-year history tion between sociodemographic variables, except gender (males

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Sienaert et al. Treatment of catatonia

improved less than females) or co-morbid (medical or psychi- notion to discontinue neuroleptics because of their inefficacy
atric) condition, and treatment response. Lower catatonia scores and their potential of aggravating the catatonic symptoms. Once
on admission and acute onset were associated with better clinical treatment with benzodiazepines or ECT is started and catatonia
response. Cases with posturing and mannerisms were found to improves, there may be a role for SGA to target residual psy-
have less improvement than other cases. chotic symptoms such as delusions or hallucinations, especially
in patients with schizophrenia (69), or as a prophylactic treat-
TREATMENT OF CATATONIA ment in psychotic disorders and mood disorders. SGA with low
SUPPORTIVE MEASURES D2 blockade (quetiapine, olanzapine) or with D2 partial agonism
A broad range of complications of catatonia can occur, such as (aripiprazole) should be favored in these situations (54).
aspiration pneumonia, dehydration, muscle contractures, pres- Patients presenting with both delirium and catatonia warrant
sure ulcers, nutritional deficiencies, severe weight loss, thiamine special consideration (73, 74). Catatonia is a frequent feature of
deficiency, electrolyte disturbances, urinary tract infections, and delirious mania, a severe syndrome characterized by the rapid
venous thromboembolism (11, 49, 50), some of which can lead onset of delirium, mania, and psychosis. Symptoms of catato-
to life-threatening situations. Some patients will require a high nia and delirium overlap, complicating diagnosis. Moreover, DSM
level of nursing care, and IV fluids and/or nasogastric tube feeds, states that catatonia should not be diagnosed if it occurs during the
in order to reduce the risk of morbidity and mortality caused course of a delirium. The issue is important because treatments
by immobility, poor nutrition and dehydration (11). Antico- for catatonia and delirium are different, albeit with overlap. While
agulant therapies can be used to prevent deep vein thrombo- delirium is typically treated with (typical or atypical) antipsy-
sis/pulmonary embolism in immobile patients (50). Medical com- chotics, the emergence of catatonia may caution against the use
plications should be treated lege artis. Given the often dramatic of antipsychotics (75, 76). Moreover, if catatonia is not recognized
and prompt improvement of motor immobility after treatment, in a delirious patient, the withdrawal or withholding of benzo-
the major measure in preventing complications is a prompt diag- diazepines sometimes thought to worsen delirium may induce
nosis, and a rapid initiation of an adequate treatment of the catatonia or leave catatonia untreated. Further studies in delirious
catatonic state. patients are needed to aid these treatment dilemmas (77).

ANTIPSYCHOTICS DIAGNOSTIC TEST

All prescribed medications should be evaluated for their poten- Benzodiazepines are the mainstay of the treatment of catatonia and
tial to induce catatonic symptoms and discontinued if possible. are also helpful as a diagnostic probe. A positive Lorazepam Chal-
There is some ambiguity about the role of antipsychotics but it lenge Test validates the diagnosis of catatonia. After the patient is
is generally encouraged to discontinue antipsychotic treatment examined for signs of catatonia, 1 or 2 mg of lorazepam is admin-
in patients presenting with catatonia (46). In the presence of a istered intravenously. After 5 minutes, the patient is re-examined.
catatonic state, both first and second generation antipsychotics If there has been no change, a second dose is given, and the
(SGA) may contribute to maintaining or worsening the cata- patient is again reassessed (46, 78). A positive response is a marked
tonic state and increase the risk of developing NMS (51–54). reduction (e.g., at least 50%) of catatonic signs and symptoms, as
During a prospective follow-up of 82 patients that had received measured with a standardized rating scale. Favorable responses
antipsychotics at some point when catatonic, NMS developed usually occur within 10 min (46). If lorazepam is given intramus-
in three cases (3.6%) (4), a substantially higher incidence than cularly or per os, the interval for the second dose should be longer:
the estimated incidence of 0.07–1.8% in all antipsychotics-treated 150 and 300 , respectively. Many clinicians will share the experi-
patients (55). The risk of worsening catatonia appears greater with ence that a “lorazepam test” not only confirms the diagnosis of
neuroleptics and antipsychotics with higher D2-blockade and a catatonia but that it also makes the underlying psychopathology
higher potential of causing extrapyramidal side effects (56), but apparent “by permitting mute patients to speak” (79). Analogous to
a worsening of catatonia and precipitation of NMS has also been the lorazepam test, a Zolpidem Challenge Test was proposed (80,
reported in association with, e.g., olanzapine (57, 58). 81). In this test 10 mg of zolpidem is administered per os and after
Although it is generally accepted that neuroleptics are inef- 30 min the patient is examined. A positive response is a reduc-
fective in catatonia (59), the role of the SGA in the treatment tion of at least 50% of the BFCRS-score. After a positive response,
of catatonia is more ambiguous, and based on cases mostly with treatment can be initiated.
schizophrenia (21). SGA have weak GABA-agonist activity and
5HT2-antagonism that could stimulate dopamine release in the BENZODIAZEPINES
prefrontal cortex and thus alleviate catatonic symptoms (11). Benzodiazepines are the first-choice treatment for catatonia,
Several authors have reported a beneficial effect of SGA, such regardless of the underlying condition. Benzodiazepines are pos-
as clozapine (60–63), olanzapine (64–66), risperidone (67–70), itive allosteric modulators of GABA-A receptors and will correct
and quetiapine (71). In one randomized controlled trial, in 14 deficient GABA-ergic function in the orbitofrontal cortex (11).
stuporous psychotic patients, risperidone (4–6 mg/day) was com- Following a positive Lorazepam Challenge Test, repeated doses of
pared to ECT. ECT-treated patients showed significantly greater benzodiazepines can be used as a treatment. Their use is safe,
improvement than those receiving risperidone (72). easy and effective, with remission rates reported to be as high
The use of antipsychotics in the presence of catatonia should be as 70–80% (4, 27, 82–87). In a naturalistic study of 66 children
evaluated in any individual case. We support, however, the general and adolescents with catatonia, it was found that benzodiazepines

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Sienaert et al. Treatment of catatonia

improved catatonia in 65% of cases, that there was no relation a prompt response (i.e., reduction of at least 50% of symptoms)
between dose and level of improvement, that the dose was higher in all patients 20 min after the administration of 10 mg zolpidem,
in some cases (up to 15 mg of lorazepam) than the dose recom- at a plasma level of 80–150 ng/L (29). These favorable results are
mended in pediatric patients, and that side effects were few (16). replicated in a few case reports (100–102). In some instances, the
In a recent trial in 107 adult inpatients (49% with a psychotic beneficial response to zolpidem occurred after treatment with ben-
disorder; 44% with a mood disorder), lower success rates were zodiazepines and/or ECT had failed (98, 101, 102). These data have
reported: two thirds responded but only one third of patients led to the proposition of a Zolpidem Challenge Test (see higher),
remitted (30). The authors argue that the lower remission rate and have urged some clinicians to continue treatment with zolpi-
could be explained by a delay between illness onset and treatment dem instead of benzodiazepines, using doses from 7.5 to 40 mg per
(30) but the doses used in the trial (3–6 mg per day) were inad- day, without noticeable adverse effects. Even though the short-half
equately low. As described above, it was shown repeatedly that life results in a transient effect on symptoms, long-term treatment
chronic catatonia associated with schizophrenia is less respon- with zolpidem has also been described (101, 102).
sive to benzodiazepines. Beckmann and colleagues, in a 5-year
follow-up study, found benzodiazepines ineffective in the treat- GLUTAMATE ANTAGONISTS
ment of chronic catatonic schizophrenia (33). A comparable poor Because of its N -methyl-d-aspartic acid (NMDA) antagonist
response (to lorazepam 6 mg per day) was shown in a randomized properties, amantadine (100–500 mg three times a day), and its
double-blind, placebo-controlled trial in 18 patients with chronic derivative memantine (5–20 mg/day), have been tried in catato-
catatonia in schizophrenia (26). nia. Carroll and coworkers identified 25 cases of amantadine and
Efficacy of benzodiazepines in catatonia is determined by memantine use in the treatment of catatonia (103). All cases (16/25
dosage (75), and doses from 8 to 24 mg lorazepam per day are com- were psychotic disorders) were substantially improved, mostly
mon and are tolerated without ensuing sedation, especially when after 1–7 days. It should be noted, however, that six of these cases
instituted using daily incremental dosages (77). Most authors sug- were unpublished, and that seven other were cases experiencing
gest starting at 1–2 mg of lorazepam every 4–12 h, and adjusting a “catatonia-parkinsonian syndrome” while under treatment with
the dose in order to relieve catatonia without sedating the patient the high-potency neuroleptic drugs haloperidol or fluphenazine.
(11). With an adequate dose, response is usually seen within 3– The symptoms diminished when neuroleptics were tapered and
7 days (75), but is some cases, response can be gradual and slow amantadine was added (104, 105). Since then, eleven additional
(38). If high dosages of lorazepam are used, patients should be cases describing the successful use of amantadine or memantine
monitored carefully for excessive sedation and respiratory com- in catatonia have been published (58, 105–110). In one case, in an
promise (77). The issue of whether some benzodiazepines are adolescent girl, catatonia that was resistant to ECT improved after
more efficacious in catatonia has not been cleared. Lorazepam is the addition of amantadine (58). Only in a review of Hawkins
generally accepted to be a first-choice drug, demonstrating a 79% and coworkers, a case is reported in which the use of amanta-
remission rate and the highest frequency of use (84). Successful use dine remained without effect (84). It should be acknowledged,
of diazepam (86–90), oxazepam (91), or clonazepam (27, 92–95) however, that negative cases are less likely to be published. Never-
has also been reported. There is no consensus on how long benzo- theless, given these positive signals in the published literature, and
diazepines are to be continued, and generally they are discontinued evidence of its efficacy in treating the negative and cognitive symp-
once the underlying illness has remitted. In a number of cases, toms of schizophrenia, amantadine should be further studied as a
however, catatonic symptoms will emerge each time lorazepam is possible treatment option for catatonia.
tapered off, urging the clinician to continue benzodiazepines for
an extended period of time (96, 97). OTHER AGENTS
There is anecdotal evidence from case-reports on the use of various
ZOLPIDEM other pharmacological agents, such as bromocriptine (111) and
Zolpidem, a positive allosteric modulator of GABA-A receptors, biperiden (112). Based on the GABA-hypothesis of catatonia, and
seems to be a safe and effective treatment alternative. To our the GABA-related working mechanism of several anti-convulsive
knowledge, Mastain and colleagues were the first to report a dra- mood stabilizers, these drugs have been proposed as a possible
matic durable improvement of catatonia, resistant to ECT and treatment option for the treatment of catatonia in bipolar patients.
benzodiazepines, with zolpidem in a 56-year-old woman that was Only a few case-reports have been published. Valproate was used in
in a catatonic state secondary to a subcortical stroke (98). Two several case reports (113–115), and found not only to have prophy-
years later, the same group presented an open study with zolpi- lactic effects but also“an ameliorating effect on the catatonic symp-
dem in seven catatonic patients, observing remission of catatonic toms” (116). In a single case report, levetiracetam was advocated as
symptoms in five of them within 15–30 min after ingestion, last- a treatment for catatonia in bipolar disorder (117), given its possi-
ing 2–5 h (99). They observed these therapeutic effects at a plasma ble mood stabilizing efficacy. It is of note, however, that levetirac-
concentration between 80 and 130 ng/L. They also published a etam has also been described to provoke catatonia (118). The use of
case report about catatonia in a 21-year-old woman, resolving topiramate (119) and carbamazepine (120) has also been reported.
15 min after administration of zolpidem as the plasma concentra- Although lithium has been anecdotally reported to have a bene-
tion reached a peak level of 90 ng/mL. Relapse occurred after 4 h ficial effect on acute catatonic symptoms (121, 122), it is mostly
when plasma concentrations fell below 90 ng/mL (80). In a subse- described to be of use in the prevention of recurrent catatonia
quent publication of the same French group, the authors confirm (121, 123–127), albeit with sometimes limited results (123).

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Sienaert et al. Treatment of catatonia

ELECTROCONVULSIVE THERAPY that catatonic symptoms remitted faster and to a greater extent in
Electroconvulsive therapy should be started in a patient with cata- the depressed patients (4/9) than in those with schizophrenia (5/9).
tonia that is not responding to benzodiazepines or when a decisive In seven retrospective chart reviews, with a total of 222 patients,
and rapid response is required in severe cases with life-threatening mostly benzodiazepine-non-responders, high response rates are
conditions such as malignant catatonia featuring high idiopathic confirmed (Table 1). The largest and most informative study
fevers, tachycardia, severe blood pressure changes. If the under- included a chart review of 250 patients with catatonic schizophre-
lying condition, e.g., psychotic depression, warrants ECT, this nia, and was part of the Iowa 500 project (134). Eighty-five (40%)
treatment may as well become the treatment of first choice. patients remitted (regardless of treatment used), while 53% of the
The excellent efficacy of ECT in catatonia is generally acknowl- 75 patients who had received ECT remitted. Another retrospec-
edged, even in the absence of randomized controlled evidence. tive chart review was conducted in a university-affiliated inpatient
The guidelines for the use of neurostimulation therapies in major unit. Seven of 19 patients presenting with catatonia were diagnosed
depressive disorder of the Canadian Network for Mood and Anxi- with schizophrenia and ECT was used in four of them, expe-
ety Treatments define catatonia as one of the indications in which riencing partial (N = 3) or considerable (N = 1) improvement.
ECT should be considered as a first-line treatment (128). In contrast, five out of five patients with mood disorder fully
Response rates in ECT are not systematically studied, but it is recovered after receiving ECT (28).
efficacy is described in hundreds of case reports and some small Rohland et al. reported ECT to be effective in 93% (26/28) of
studies. In a review paper, Hawkins et al. reported an 85% (47/55) patients with catatonia admitted to an inpatient psychiatric unit
complete response rate (84). To our knowledge, only one ran- (32). England et al. reported dramatic improvement in 10 of 12
domized controlled ECT trial has been published. In this trial, the (83%) patients with catatonia after 1–5 ECT sessions (63). In the
efficacy of ECT (BT, 3/W, N = 8) plus oral placebo was compared largest study to date, 63 patients with catatonia (30% schizophre-
with sham ECT plus risperidone in lorazepam non-responsive nia; 41% mood disorders) received bilateral ECT, thrice weekly,
non-affective catatonia. BFCRS scores reduced markedly, but the either as a first choice (n = 6), or after lorazepam had failed
reduction was significantly more profound in the ECT group (72). (n = 57). Fifty-six patients (89%) responded to ECT. Patients
Suzuki and co-workers studied both short- and long-term efficacy who responded in 4 sessions (31/56; 55%) had a lower duration
of ECT in intractable catatonic schizophrenia. In the acute phase, of catatonia, a higher BFCRS-score, more often waxy flexibility
100% of 11 patients responded to ECT. Relapse occurred in seven and Gegenhalten, the involuntary resistance to passive movement
cases, and all occurred within 6 months. The 1-year recurrence of the extremities. Echophenomena predicted a slower response
rate was 63.6%, despite continuation pharmacotherapy (129). (136). The lowest response rates were reported in a retrospective
Relapsers received a second course of ECT followed by mainte- study of 27 patients, treated with bitemporal ECT, often daily dur-
nance ECT for 1 year and four remained in remission (130). Those ing the first week (47). Response rates were 59%. Probably, the
who relapsed again could be treated successfully with adjusting the smaller proportion of patients with a primary mood disorder, a
frequency of treatment sessions (131). In another Japanese study, significant treatment delay (a mean time interval of 2 months)
the efficacy of ECT was shown very clearly (132). Fifty patients may have negatively influenced treatment response. Another pos-
presenting with catatonic symptoms, 23 of whom were diagnosed sible explanation is the fact that one third of the patients had been
with schizophrenia, received either ECT or a benzodiazepine as exposed to antipsychotics before ECT, which was reported earlier
first-line treatment. If benzodiazepines were ineffective, the next to be related to a decreased effectiveness (84).
step was either ECT or an antipsychotic drug; if the latter failed, The successful use of ECT in chronic catatonia has been
ECT was the last resort. Only 1 of 41 patients responded fully described in a few case reports (137–140). Duration of catato-
to benzodiazepines, and 19 responded partially. In contrast, all 17 nia varied from 3 months to 12 years, and in some cases protracted
patients who received ECT achieved remission. Payee and cowork- courses of bitemporal ECT (e.g., 17–68 treatments (138, 140) were
ers confirmed these favorable results: 8 of 9 (89%) lorazepam- needed to achieve a response. In several of these chronic cases, the
non-responders responded to ECT (85). In another small (N = 9) catatonic symptoms reappeared when ECT was stopped. Some
prospective comparative study Escobar and colleagues (133) noted patients with chronic catatonia in schizophrenia will respond to a

Table 1 | ECT in catatonia: retrospective chart reviews.

Author(s), year ECT EP/Schedule Mood (%)/psychotic disorder (%) N responders/N total Responders (%)

Morrison (134) NA/NA 0/100 40/75 53

Pataki (28) BT/NA 56/44 6/9 67
McCall (135) BT/NA 75/12 7/8 88
Rohland (33) BT/3*W 59/23 26/28 93
van Waarde (47) BT (93%)/daily [first week (56%)] 48/44 16/27 59
England (63) BT/NA NA 10/12 83
Raveendranathan (136) BT/3*W 41/30 56/63 89

EP, electrode position; BT, bitemporal; N, number; NA, not available.

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Sienaert et al. Treatment of catatonia

combination of ECT and clozapine. In a retrospective study, this CONCLUSION

combination resulted in sound clinical improvement as measured Catatonia is a severe psychomotor syndrome with an excellent
with the clinical global impression (CGI) in 22 patients (141). prognosis if recognized and treated appropriately. The treatment
A recent systematic review of treatment of (severe) autistic cata- of catatonia in children and adolescents should follow the same
tonia identified 12 cases with autism and catatonic symptoms of a principles as in adults. Great care should be taken to avoid (med-
few months to around 6 years’ duration, treated with ECT-courses ical) complications. Although a number of pharmacological agents
that ranged from 7 to 29 sessions. Almost all cases reported a dra- have been tried successfully in catatonia, rarely, if ever, the effect
matic improvement with ECT, usually after relatively few sessions. is as immediate and dramatic as seen with benzodiazepines. If
A few papers report a more mixed response to ECT. Several cases lorazepam is not available, zolpidem can be used as a diagnostic
reported rapid recurrence of symptoms when ECT was discontin- probe, and probably as a treatment alternative. If benzodiazepines
ued or suspended (142). Consoli et al collected 59 cases of children fail (inadequate or transient response, excessive sedation), ECT
and adolescents with catatonia treated with ECT. Response to ECT should be started without delay. If the underlying condition war-
was favorable for 45 patients (76%), with partial improvement rants ECT-treatment, or in life-threatening situations like malig-
noted in 3 (5%) and a lack of response in only one (143). nant catatonia or NMS, ECT is the treatment of first choice. It
Recently, several authors report on the successful use of uni- is advised to choose the most efficacious technique, i.e., bilat-
lateral ECT in a total number of 21 cases (36, 144), 15 of eral standard-pulse ECT with a stimulus dose that is substantially
which were treated with an ultra-brief pulse (UB) width (139, above the seizure threshold.
145, 146). In a case-series of 5 patients with catatonia, resistant
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