Key words
catatonia - electroconvulsive therapy - bush francis catatonia rating scale - grasp reflex
Introduction
Catatonia is a multifactorial psychomotor syndrome associated with motor and
behavioral abnormalities, disturbances of volition, and autonomic dysregulation
[1]
[2]. A recent meta-analysis indicated a mean prevalence of catatonia at
9% among patients with different psychiatric and medical conditions across
all continents [3]. The largest analysis of
clinical electronic health records showed an incidence of 11 episodes per 100,000
person-years and a much longer hospitalization in the catatonia group, indicating
high morbidity and enormous economic costs related to catatonia [4]. Traditionally, catatonia has been linked
either to schizophrenia (later also bipolar disorder) or organic brain disorders.
However, modern classification systems allow the diagnosis of catatonia with
comorbidity to multiple mental disorders or medical conditions. Thus, with the
introduction of the novel International Classification of Diseases, Eleventh
Revision (ICD-11) criteria, catatonia will likely be recognized more frequently
[52].
Catatonia may become a life-threatening condition in the form of malignant catatonia
(MC) that presents with autonomic dysregulation, severe rigidity, and altered mental
status, including high fever, sweating, confusion, and rhabdomyolysis. MC diagnosis
is often missed in severely ill patients, contributing to a high mortality rate
[5].
To ensure the correct diagnosis of catatonia, the use of standardized rating scales
is recommended [6]
[7]. The Bush-Francis Catatonia Rating Scale
(BFCRS) is the most frequently used rating scale for screening and evaluating
catatonia symptom severity [8]. Nevertheless,
specific training is required as many psychiatrists lack an understanding of
catatonia signs, and catatonia is often neglected by clinicians [9].
Currently, the first-line treatment of acute catatonia is the administration of
benzodiazepines, primarily lorazepam [5]
[6]
[10]
[11]
[12]. The response rates of benzodiazepines
range from 66% to 100% [13],
and a 2 mg lorazepam dose has proven effective for treating most catatonia
signs [14]. However, a considerable proportion
of catatonia patients fail to remit following benzodiazepine administration [15]
[16]
[17]. Importantly, in chronic
catatonia, benzodiazepines were not more effective than placebo [18].
The second-line treatment of catatonia is electroconvulsive therapy (ECT), with
proven efficacy for treating life-threatening conditions such as MC or in case of
non-response to benzodiazepines [6]
[7]
[11]
[19]
[20]. Both acute and persistent catatonia, as
well as treatment-resistant cases, respond to ECT [10]
[16]
[17]
[21]
[22]
[23] with response rates ranging from
59% to 100% [13]. Still, a
recent meta-analysis including 564 patients from 28 studies challenges the evidence
of effectiveness for ECT in catatonia, given the lack of high-quality studies [24]. Indeed, several potential factors may
reduce response rates to ECT in catatonia, such as illness duration, the type of the
underlying disorder, catatonia symptom severity, and the presence of specific
catatonia signs.
For example, a small retrospective study reported the lowest response rates to ECT so
far, with 59%, most likely due to heterogeneous diagnoses, a high rate of
comorbid neurological disorders, chronicity, and treatment delay [25]. In general, predictors of poor or slow ECT
response have been equivocal. Chronicity, non-affective catatonia, and the presence
of echophenomena seem to indicate poor response, while other signs, such as waxy
flexibility, have been found in patients with fast or slow responses [16]
[23]
[26].
Clinical reasoning clearly favors early detection of catatonia and rapid treatment
onset to improve outcomes. However, the use of ECT is often postponed because of
procedural obstacles, stigmatization of ECT, anticipated side effects, or a lack of
knowledge about catatonia pathophysiology. Inconsistencies in the literature call
for identifying predictors of treatment response. Particularly, some catatonia signs
may respond better than others to ECT.
The objective of this retrospective study is to explore the effect of ECT on specific
catatonia symptoms in a naturalistic sample of patients with catatonia due to
schizophrenia spectrum disorders or bipolar disorder. Furthermore, we aim to
identify predictors of treatment response in subjects receiving ECT for
catatonia.
We expect a high effectiveness of ECT in the treatment of catatonia, with rapid
treatment response achieved within five ECT sessions. Furthermore, we aimed to
explore which signs of catatonia are associated with time to treatment response.
Given that there is insufficient data on the predictive value of single catatonia
signs on ECT outcome, this part of the analysis remains exploratory.
Materials and Methods
Study design
We retrospectively examined clinical case files of patients diagnosed with
catatonia due to schizophrenia or bipolar affective disorder according to the
International Classification of Diseases, Tenth Revision (ICD-10), who were
treated with ECT at the University Hospital of Psychiatry and Psychotherapy in
Bern between 01/01/2008 and 31/12/2021.
According to the ICD-10 criteria, catatonia is defined as a subtype of
schizophrenia with the simultaneous occurrence of at least two of the following
psychomotor symptoms: mutism, negativism, stupor, catalepsy, waxy flexibility,
agitation, and posturing for at least two weeks. Therefore, the majority of the
patients in our sample suffer from schizophrenia spectrum disorders, according
to DSM-5-TR. Furthermore, we included two patients diagnosed with bipolar
disorder, with the signs necessary for catatonia but a schizophrenia diagnosis.
This decision was based on work in catatonia by Northoff et al., Krüger
et al., and Taylor et al., who demonstrated that patients with major mood
disorders could also have severe catatonia [27]
[28]
[29]. We did not, however, diagnose
catatonia according to the DSM-IV. This would have resulted in a very different
catatonia sample. We based the selection of cases on clinical diagnoses
exclusively, which at the time were established using ICD-10 criteria.
The main outcome measure for clinical outcome was the BFCRS that was assessed
before, during, and after ECT. The scoring of the BFCRS was carried out by the
treating psychiatric resident and supervised by a senior psychiatrist according
to clinical routine.
The BFCRS is a 23-item rating scale with high validity and reliability for
catatonia screening and rating of catatonia symptom severity (7). The BFCRS is a
highly reliable and sensitive instrument to diagnose catatonia with a
sensitivity of 100% and specificity ranging between 75% and
100% [8]
[30]
[31]. Because of its great validity and reliability, as well as the
ease of administration, the BFCRS is considered the gold standard to evaluate
catatonia. Thus, the BFCRS is preferred for routine use among multiple catatonia
rating scales, such as the Northoff Catatonia Rating Scale [30]
[32]
[33].
In case of incomplete or missing BFCRS-single items or BFCRS-total scores, one
researcher (SB) assessed medical and nurses` reports of the clinical
course to determine if patients responded to ECT. These cases were not included
in the statistical analysis.
The study was approved by the local cantonal ethics committee (Ethics Commission
of the Canton of Bern, KEK-Number 2020–00432).
Statistical analysis
Data analysis was performed using the SPSS Statistics version 28.0. To
investigate the effect of the ECT procedure, BFCRS-total scores and BFCRS-single
items were compared before and after ECT using t-tests for paired samples. Due
to our directed hypothesis of BFCRS symptom reduction, we chose a one-tailed
t-test with a significance level of p<0.05.
Clinical response was determined as a 50% reduction in the BFCRS score
from baseline. In line with previous studies, we defined early response as a
response within five ECT sessions and late response as a response following six
or more ECT sessions [17]. To determine
which demographic and clinical parameters predict time to response to ECT, we
ran stepwise linear regression analyses with early or late responder status as
dependent and the following independent variables: baseline BFCRS-total scores,
baseline 23 BFCRS-single items, age, and sex.
Missing data
Only patients with complete BFCRS scores before and after an ECT-series were
included in the paired t-tests (BFCRS-total score and BFCRS-single items), and
only patients with completed BFCRS-single items at baseline were included in the
stepwise linear regression.
Results
Demographics
We included 20 patients with catatonia syndrome. Eighteen patients had
schizophrenia as an underlying diagnosis, and 2 patients were diagnosed with
bipolar disorder. During the time span from 2008 to 2021, 9 of these 20 patients
were included twice because they received two ECT-series, and 1 patient was
included thrice because he underwent three ECT-series. This resulted in a total
of 31 ECT-series. The mean age of participants was 47.9±18.3 years,
ranging from 15 to 75 years. The sex distribution was balanced, with 9 males and
11 females. Ten of the ECT sessions started during the acute phase of illness
within the first 2 weeks after illness onset, 18 ECT sessions were administered
during the chronic phase of illness after 1 month of illness onset, and three
ECT sessions started between 2 weeks and 1 month after illness onset. Seventeen
of the patients and 25 of the 31 ECT-series were assessed with the BFCRS before
and after treatment, and the BFCRS-total scores at baseline and at the end of
treatment were available. In 18 of 31 ECT-series, the single BFCRS items were
available. During the treatment, the BFCRS scores were also recorded, but not on
a daily basis, and in most cases, the pattern followed the clinical course and
thus lacked a standard frequency. The mean duration of the ECT-series was
31.1±17.3 days (min. 6 days, max. 89 days). The patients received a mean
of 12.2±4.9 ECT sessions (min. 4 sessions, max. 27 sessions). The mean
number of ECT sessions to response was 4.2±3.4 (min. 1 session, max. 12
sessions).
Psychotropic drugs
All patients were on antipsychotic medication during ECT. Eleven patients
received monotherapy, and 9 patients were on multiple antipsychotics. All
patients except 1 were on clozapine, and all other psychotropic drugs were used
as an add-on treatment to clozapine. In many patients, dose adjustments of
clozapine were necessary, and 6 patients underwent fluvoxamine augmentation.
Before starting ECT, 11 patients were treated with haloperidol; however, in 6
patients, it was discontinued due to lack of efficacy. In addition to clozapine,
other antipsychotics were administered during ECT: haloperidol in 5 patients,
aripiprazole in 2 patients, brexpiprazole in 1, levomepromazine in 1, and
pipamperone in 1. Four patients were additionally treated with an antidepressant
to treat comorbid depressive or anxiety symptoms: 1 with escitalopram, 1 with
venlafaxine, 1 with clomipramine, and 1 with venlafaxine and mirtazapine.
Benzodiazepines were not routinely administered during ECT. Twelve patients were
continued on lorazepam during ECT, as it led to a slight improvement in
catatonia severity. Lorazepam was tapered off after the remission from
catatonia. In 8 patients, lorazepam had no sufficient effect and was therefore
discontinued before starting ECT.
Electroconvulsive therapy procedure
ECT was performed according to the clinical routine. At the first ECT session,
the age method was used to determine the stimulation strength. Adjustments were
then made based on the quality of the seizures and the clinical course. ECT was
administered using a Thymatron IV system. The patients received, on average,
12.2±4.9 ECT sessions in the course of 4 to 5 weeks, i. e.,
three sessions per week and bilateral electrode placement, except for 1 patient
who was treated with right unilateral stimulation. The duration of treatment
depended on the clinical course and continued until no further improvement was
expected. Treatment in the acute phase of illness was defined as the start of
the ECT sessions within the first 2 weeks after catatonia onset, and treatment
in the chronic phase of illness was defined as the start of the ECT sessions
after 1 month of catatonia onset.
Anesthetics
In 27 ECT-series, etomidate was used for general anesthesia, and in 4 ECT-series,
propofol was utilized. In addition, most patients received alfentanil as an
additional analgesic. Some patients received remifentanil. In 25 ECT-series,
succinylcholine was administered for muscle relaxation, and in 6 ECT-series,
rocuronium was used for muscle relaxation in bedridden patients. Dosages were
chosen and modified according to the clinical routine procedures of the
anaesthesiologist. Patients treated with benzodiazepines were antagonized with
flumazenil.
Electroconvulsive therapy response
Response has been achieved in 19 of 20 patients and in 30 of 31 ECT-series (see
[Table 1]). The patient who did not
recover showed at least a moderate improvement in catatonia symptom severity of
44% on the BFCRS score.
Table 1 Catatonia symptom reduction of total
BFCRS-scores.
|
Patient #
|
BFCRS-Score before ECT
|
BFCRS-Score after ECT
|
Symptom Reduction
|
|
1a
|
19
|
1
|
95%
|
|
1b
|
17
|
1
|
94%
|
|
2a
|
17
|
0
|
100%
|
|
2b
|
14
|
0
|
100%
|
|
3
|
14
|
3
|
79%
|
|
4
|
9
|
5
|
44%
|
|
5a
|
15
|
4
|
68%
|
|
5b
|
25
|
8
|
73%
|
|
6
|
22
|
7
|
68%
|
|
7
|
24
|
2
|
92%
|
|
8a
|
24
|
0
|
100%
|
|
8b
|
25
|
0
|
100%
|
|
9
|
23
|
8
|
65%
|
|
10a
|
8
|
1
|
87%
|
|
10b
|
28
|
1
|
96%
|
|
11a
|
28
|
1
|
96%
|
|
11b
|
15
|
1
|
93%
|
|
12
|
17
|
7
|
59%
|
|
13
|
14
|
3
|
79%
|
|
14
|
20
|
7
|
66%
|
|
15
|
14
|
3
|
79%
|
|
16
|
23
|
3
|
87%
|
|
17a
|
9
|
2
|
78%
|
|
17b
|
19
|
7
|
63%
|
|
17c
|
19
|
4
|
79%
|
BFCRS: Bush Francis Catatonia Rating Scale; ECT: electroconvulsive
therapy.
In 3 patients with missing BFCRS-scores, we consulted the medical records. Before
ECT, these patients were characterized by the presence of pronounced immobility,
mutism, negativism, stereotypy, and mannerisms. In these patients, medical
records clearly indicated a clinical response with a substantial improvement in
catatonia symptoms.
A paired t-test of BFCRS scores indicated substantial reductions in catatonia
severity with ECT (T=12.4; P<0.001). The mean BFCRS-score before
the treatment was 18.5±5.6, and after the treatment, 3.2±2.7,
resulting in an 82.8% reduction from baseline.
Single Bush-Francis Catatonia Rating Scale-item response and predictors of
late response
Paired t-tests of the single-item response to ECT revealed a better response to
ECT for motor inhibition symptoms such as stupor and mutism, while
echophenomena, dyskinesia, stereotypy, and perseveration responded less well
(see [Table 2]).
Table 2 Results of paired t-tests of single BFCRS-items in
15 ECT-series (level of significance one-tailed).
|
Items with good response
|
Significance (p-value)
|
Item-value ≥1 before ECT
|
BFCRS-Items not responding well
|
Significance (p-value)
|
Item value ≥1 before ECT
|
|
Immobility
|
T(14)=4.525
p< 0.001
|
89%
|
Excitement
|
T(14)=1.468
p=0.082
|
22%
|
|
Mutism
|
T(14)=5.237
p< 0.001
|
83%
|
Grimacing
|
T(14)=1.146
p=0.136
|
22%
|
|
Staring
|
T(14)=2.256
p=0.02
|
83%
|
Echopraxia
|
T(14)=0.367
p=0.360
|
33%
|
|
Catalepsy
|
T(14)=3.623
p=0.001
|
72%
|
Mannerism
|
T(14)=1.000
p=0.167
|
22%
|
|
Stereotypy
|
T(14)=1.848
p=0.043
|
44%
|
Verbigeration
|
T(14)=1.000
p=0.167
|
22%
|
|
Rigidity
|
T(14)=3.292
p=0.003
|
56%
|
Impulsivity
|
T(14)=0.000
p=0.500
|
17%
|
|
Negativism
|
T(14)=2.646
p=0.010
|
39%
|
Autonomic Obedience
|
T(14)=0.000
p=0.500
|
17%
|
|
Waxy flexibility
|
T(14)=2.092
p=0.028
|
22%
|
Ambitendency
|
T(14)=1.705
p=0.055
|
17%
|
|
Withdrawal
|
T(14)=5.047
p<0.001
|
78%
|
Perseveration
|
T(14)=0.000
p=0.500
|
22%
|
|
Mitgehen
|
T(14)=2.092
p=0.028
|
28%
|
Combativeness
|
T(14)=0.716
p=0.243
|
17%
|
|
Gegenhalten
|
T(14)=2.092
p=0.028
|
33%
|
|
|
|
|
Grasp reflex
|
T(14)=1.871
p=0.041
|
28%
|
|
|
|
|
Autonomic abnormality
|
T(14)=2.806
p=0.007
|
56%
|
|
|
|
BFCRS: Bush Francis Catatonia Rating Scale; ECT: electroconvulsive
therapy.
A stepwise logistic regression analysis of demographic and clinical parameters
identified the presence of grasp reflex (R2: 1.6; F=9.2;
df=1; p=0.009) as a predictor of late response. The presence of
other catatonia signs, symptom severity at baseline, age, or sex had no
influence on the time to response. In addition, treatment response was unrelated
to age or sex.
Maintenance electroconvulsive therapy
Seven patients received maintenance ECT due to a chronic, recurrent course of
catatonia. According to the BFCRS score and regular and detailed documentation,
all patients remained well and showed a stable long-term clinical course (see
[Table 3]).
Table 3 Overview of patients receiving maintenance
ECT
|
Pat ID
|
Gender
|
Age
|
Medication (in mg)
|
Maintenance treatment (MT) sessions
|
Symptoms before MT
|
Main residual symptoms
|
Stimu lation parameter
|
Frequency of stimulation
|
|
1a
|
w
|
47
|
Paliperidon Depot 75 mg Venlafaxin 150 mg
Mirtazapin 30 mg Valproat 2000 mg
|
12
|
Remitted
|
Rremitted
|
Bilateral 50%
|
6×2 weekly 4×4 weekly 1×2 &
1×3 monthly
|
|
1b
|
w
|
46
|
Venlafaxin 112.5 mg Mirtazapin 30 mg
Paliperidon 9 mg Lorazepam 1 mg
|
8
|
Remitted
|
Remitted
|
Bilateral 50%
|
6x weekly & 2×2 weekly
|
|
2
|
w
|
71
|
Clozapin 150 mg
|
20
|
Gegenhalten Grasp Reflex
|
Remitted
|
Bilateral 200%
|
5x weekly 13×2 weekly 4×3 weekly 1x
monthly
|
|
3a
|
m
|
19–24
|
Clozapin 225 mg
|
77
|
Mutism Immobility Stereotypy
|
Mutism Immobility Stereotypy Mannerism
|
Bilateral 40%
|
1 year weekly then intervals 2 days-5 months
|
|
3b
|
m
|
26–29
|
Venlafaxin 150 mg Fluvoxamin 50 mg Clozapin
100 mg
|
90 (still in treatment)
|
Mutism Immobility Stereotypy
|
Slight mutism Immobility Stereotypy
|
Bilateral 90%
|
Alternating 1–3 weekly
|
|
4a
|
m
|
48
|
Clozapin 400 mg
|
26
|
Immobility Mutism Negativism Autonomic Abnormality
|
Slight withdrawal Perseveration
|
Bilateral 100%
|
16x weekly 6×2 weekly 4×3 weekly
|
|
4b
|
m
|
49
|
Clozapin 400 mg Clomipramin 75 mg
|
6
|
Mutism Posturing Stereotypy Ambitendency Grasp reflex
Combativeness
|
Slight immobility Staring Stereotypy
|
Bilateral 100%
|
3x weekly 1×2 weekly 2×3 weekly
|
|
5a
|
w
|
70
|
Olanzapine 10 mg Amitriptyline 50 mg
|
6 (still in treatment)
|
Slight Immobility Echolalia Perseveration
|
Slight immobility Echolalia Perseveration
|
Unilateral 100%
|
9×4 weekly
|
|
5b
|
w
|
69
|
Olanzapine 5 mg
|
18
|
Slight Immobility Echolalia Perseveration
|
Slight immobility Echolalia Perseveration
|
Unilateral 150%
|
7x weekly 6×2 weekly 3×3 weekly 2×4
weekly
|
|
6
|
m
|
50
|
Clozapine 200 mg Aripiprazol 15 mg
Risperidone 3 mg Lorazepam 0.5 mg
|
8 (still in treatment)
|
Slight Excitement Echolalia Stereotypy Verbigeration
Perseveration Autonomic Obedience
|
Slight excitement Echolalia Stereotypy Verbigeration
Perseveration Autonomic Obedience
|
Bifrontal 170%
|
10×5 weekly
|
|
7
|
m
|
16
|
Clozapine 100 mg
|
43 (still in treatment)
|
Mutism Staring Catalepsy Stereotypy Withdrawal Autonomic
Abnormality
|
Mutism Staring Stereotypy
|
Bilateral 120%
|
40×1–2x weekly 1×3 weekly 1×4
weekly
|
ECT: electroconvulsive therapy.
Missing data
Seventeen of the patients and 25 of 31 ECT-series were assessed with the BFCRS
before and after treatment. In 3 patients and 6 ECT-series, BFCRS-total scores
were not available before or after the ECT-series. In 18 of 31 ECT-series,
patients had complete BFCRS-single items before or after the ECT-series. In 15
ECT-series, patients had complete BFCRS-single items before and after the
ECT-series.
Discussion
The present retrospective study aims to provide an overview of the ECT effect on
specific catatonia symptoms and to identify predictors of response. Our study
corroborates the overwhelming effect of ECT on catatonia. Response to ECT has been
achieved in 19 of 20 patients and in 30 of 31 ECT-series. Even the patient who did
not recover showed at least a moderate improvement in catatonia severity. There was
a better response to ECT for signs of motor inhibition, such as stupor and mutism,
while echophenomena, dyskinesia, stereotypy, and perseveration responded less well.
Regression analyses showed that the ECT effect in catatonia patients is independent
of age and sex and that the presence of a grasp reflex predicted a slow
response.
This naturalistic study focused on predominantly non-affective psychoses. We used
ICD-10 diagnostic criteria that consider schizophrenia the only non-organic mental
illness in which catatonia may occur. In addition, we included 2 patients with
severe bipolar disorder who otherwise qualified for catatonia. This decision was
based on prior work in catatonia by Northoff et al., Krüger et al., and
Taylor et al. [27]
[28]
[29].
With the new diagnostic criteria in DSM-5-TR and ICD-11, catatonia can be diagnosed
in a number of mental disorders (e. g., autism, depression), medical
conditions (e. g., autoimmune encephalitis), and substance-related effects
(e. g., intoxications) [34]
[35]. This change in criteria will broaden the
spectrum of catatonia, increase the prevalence and detection, and finally, will
require new studies evaluating treatment outcomes in these new conditions.
The small proportion of patients with affective disorders in our sample is clearly
related to the diagnostic procedure using ICD-10 criteria, in which catatonia is
diagnosed as a subtype of schizophrenia, while ICD-10 was blind to catatonia in mood
disorders.
Other studies have primarily included patients with catatonia due to affective
disorders, in whom acute retarded catatonia—the so-called Kahlbaum
phenotype—is the most frequent catatonia presentation [8]
[11]
[36]. However, there are also
studies with higher frequencies of psychotic disorders in their samples of catatonia
patients [37]
[38]
[39]. Clearly, the proportions
of catatonia with different comorbid mental disorders will change with the revised
diagnostic criteria in ICD-11 and DSM-5-TR.
The impressive effectiveness of ECT in the treatment of catatonia, with a response
rate of 95%, parallels previous reports [13]
[16]
[17]
[21]
[22]
[23]
[26].
One catatonia study reported lower response rates to ECT at 59% [25]. This study differed from our study in that
the patients had a high rate of comorbid neurological disorders, a long illness
duration, and a marked delay of ECT initiation.
In addition to the high effectiveness of ECT, the study provides evidence for a rapid
treatment response. After an average of 4.2 ECT sessions, patients have already
responded to the treatment. Similarly, rapid effects of ECT were also reported by
other catatonia studies, achieving response within 1–5 days [10]
[17]
[23]. Raveendranathan et al.
2012 [23] showed that 55% of the
patients with catatonia responded to ECT within four sessions. This fast response
was related to high symptom severity and a shorter illness duration before
treatment, as well as the presence of waxy flexibility and Gegenhalten. In contrast,
the presence of echophenomena was associated with a slower response [23]. A randomized controlled ECT trial reported
a slower response to ECT with an average of 8.87 ECT sessions, most probably due to
non-affective catatonia and a long illness duration before treatment [16]. To the best of our knowledge, our study is
the first to suggest the grasp reflex as a predictor of late response to ECT in the
treatment of catatonia. Grasp reflex is a frontal release sign and represents a
rather rare catatonia sign, but often occurs in neurodegenerative disorders [40]
[41].
In their large heterogeneous catatonia sample, Wilson et al. 2015 [42] reported a grasp reflex in only 14%
of the patients with confirmed catatonia. This speaks towards grasp reflex
identifying a group of subjects who will have a less favorable outcome of catatonia,
calling for more intense treatment strategies.
Although ECT is highly effective in treating catatonia, the relapse rate in the first
year after treatment response is high, even under continuation treatment with
antipsychotics [43]. There is some evidence
arguing for the maintenance of ECT combined with antipsychotics, which might be more
effective in the long-term treatment of schizophrenia than antipsychotics alone in
terms of catatonia symptoms, behavioral symptoms, social functioning, and
hospitalization rates [44]
[45]
[46].
Our study shows that patients who once responded to ECT also tend to respond to
subsequent ECT-series, indicating that the response to the first ECT-series might be
a predictor of response to future ECT-series. In recurrent catatonia, ECT might be
established as a first-line therapy whenever the first ECT series is effective.
Furthermore, our study provides insight into the treatment of patients with chronic
recurrent catatonia. In 7 patients, the use of maintenance ECT over several months
demonstrated a positive effect on catatonia severity according to the BFCRS-score
and detailed clinical documentation.
Our study should be interpreted in the light of several limitations. The
heterogeneous administration of antipsychotics may render interpretations of the
results more difficult than in studies administering only 1 substance. However, the
naturalistic design proved that all but 1 patient were treated with clozapine and
that half of them also required further psychopharmacology. The literature suggests
that the use of antipsychotics might maintain or worsen the catatonia state [36] and decrease the effect of ECT [47]
[48].
At the same time, clozapine is often administered and might be the most efficacious
and best-tolerated antipsychotic in combination with ECT due to lower dopamine
receptor blockade and modulation of the glutamatergic system [36]
[49].
There may have been an impact of antipsychotics on treatment outcomes as clozapine
doses were modified during the ECT-series. Furthermore, half of the patients were on
additional pharmacotherapy that was tapered off during the ECT-series in some cases.
Thus, a meaningful statistical correction for antipsychotic equivalent doses at one
specific time point was not possible. Furthermore, patients treated with lorazepam
during ECT had a very similar response (symptom reduction of 78%) in
comparison to patients without benzodiazepines (symptom reduction of
80%).
Another limitation of the study is the incomplete assessment of the BFCRS in a small
proportion of patients. However, clinical evaluations were carried out regularly and
precisely by experienced psychiatrists, who provided detailed documentation of the
course of catatonia in the case files.
The strength of the study is its sample, which includes a large proportion of
severely ill patients with catatonia and schizophrenia (90%) as the
underlying mental disorder. Most recent studies examining the effectiveness of ECT
included mixed samples with patients with unipolar or bipolar depression and only a
small proportion of patients with schizophrenia [11]
[26]
[50]. The patients in our sample were
well-characterized and received multiple sessions of ECT. As the observation period
was long, we were able to evaluate the ECT effect on different catatonia symptoms,
on patients who received therapy at different time points, and in patients with
chronic catatonia who received maintenance ECT.
Our study illustrates the strikingly high effectiveness of ECT in treating catatonia,
despite the fact that the majority of patients had schizophrenia as an underlying
diagnosis. The study demonstrates that ECT was effective in catatonia due to
schizophrenia and in patients on antipsychotic medication. For the first time, the
presence of a grasp reflex was indicated as a predictor of slow response. Thus,
these patients may require more intense treatment efforts.
Following the current guidelines, the use of benzodiazepines is still the first-line
treatment of catatonia [5]
[10]
[11].
Furthermore, non-invasive brain stimulation techniques such as repetitive
transcranial magnetic stimulation (rTMS) are promising treatment options for
catatonia that are still under investigation [6]
[51]. However, the relative
efficacy of rTMS is still unknown, while ECT clearly demonstrates efficacy across
varying levels of catatonia severity. Given the complications and life-threatening
conditions that can arise from catatonia, as well as the limited effectiveness of
benzodiazepines, an effective and fast-acting treatment is necessary. The present
study corroborates the impressive and rapid effect of ECT in catatonia, suggesting
that ECT should be considered early in the course of catatonia. High-quality data on
the effectiveness of ECT is still missing, and randomized controlled trials should
be performed to further validate the use of ECT in the treatment of catatonia.
Future studies should establish symptom profiles that may benefit most from rapid
ECT treatment.
