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catatonia en 14 a.

Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 41 (1), 2013, 69–74
Z. Kinder-Jugendpsychiatr.
F. Häßler
et al.: Catatonia
41 (1) © 2013
in a 14-Year-Old
Verlag Hans Huber,
Girl with
AG , renia
Bern - Tuesday, October 04, 2016 8:46:08 PM - IP Address:
A Case of Catatonia in a 14-Year-Old
Girl with Schizophrenia Treated with
Electroconvulsive Therapy
Frank Häßler1, Olaf Reis1, Steffen Weirich1, Jacqueline Höppner2,
Birgit Pohl3, and Johannes Buchmann1
Clinic for Child and Adolescent Psychiatry, Neurology and Psychotherapy, University of Rostock,
Germany, 2Clinic for Psychiatry and Psychotherapy, University of Rostock, Germany,
Clinic for Anaesthesiology, University of Rostock, Germany
Abstract. This article presents a case of a 14-year-old female twin with schizophrenia who developed severe catatonia following treatment
with olanzapine. Under a combined treatment with amantadine, electroconvulsive therapy (ECT), and (currently) ziprasidone alone she
improved markedly. Severity and course of catatonia including treatment response were evaluated with the Bush-Francis Catatonia Rating
Scale (BFCRS). This case report emphasizes the benefit of ECT in the treatment of catatonic symptoms in an adolescent patient with
schizophrenic illness.
Keywords: catatonia, schizophrenia, adolescence, ECT
Der Einsatz von EKT bei einer 14-jähigen schizophrenen Patientin mit Katatonie
Zusammenfassung. Es wird über den Fall einer 14jährigen schizophrenen Patientin berichtet, die nach der Behandlung mit Olanzapin
eine schwere Katatonie entwickelte. Unter einer kombinierten Therapie aus Amantadin, Elektrokrampftherapie (EKT) und gegenwärtig
Ziprasidon verbesserte sich ihr Zustand merklich. Schwere und Verlauf der Katatonie wurden mit der Bush-Francis Catatonia Rating
Scale (BFCRS) gemessen. Der Fallbericht betont die Nützlichkeit von EKT bei der Behandlung von katatonen Symptomen bei einer
adoleszenten schizophrenen Patientin.
Schlüsselwörter: Catatonia, Schizophrenie, Adoleszenz, EKT
Despite the first description of catatonia by Kahlbaum in
1874, our knowledge about the phenomenology, diagnosis,
etiology, and treatment of catatonia in childhood and adolescence is still scarce. One reason for this scarcity is that
in the past catatonia was frequently diagnosed under other
labels, such as catalepsy, stupor, and encephalitis lethargica
(Shorter, 2012). For adults, catatonia is a well-described
syndrome that appears to be underdiagnosed (Fink & Taylor, 2009). Both classification systems, DSM-IV (295.20)
and ICD-10 (F 20.2), acknowledge the association of catatonia with schizophrenia. In the upcoming version of DSM5 the direct tie between catatonia and schizophrenia is to
be eliminated. The DSM-5 consideration of a fifth digit for
a catatonia specifier might be an improvement. The addition of specifiers of this kind, however, has been criticized
DOI 10.1024/1422-4917/a000211
in the past (Fink, 2011). The DSM-5 classification acknowledges catatonia as an independent entity for the first
time (Fink, Shorter & Taylor, 2010). The current version
of DSM (DSM-IV) allows for a classification of catatonia
only as derived from affective, other psychiatric, or toxic
disorders as well as from organic diseases. Organic diseases as causes of catatonia are mentioned in ICD-10 (F06.1)
as well.
Symptoms of catatonia vary from positive motoric
symptoms, such as excitement, to negative motoric symptoms, such as immobility or stupor. More than 50% of all
patients suffering from catatonia display a combination of
immobility, mutism, withdrawal, negativism, posturing,
grimacing, and rigidity (Rosebush & Mazurek, 2010). Frequencies of catatonia among young patients admitted to
psychiatric facilities seem to be lower (0.6–17%) than rates
found in adults (7.6–38%) (Cornic, Consoli & Cohen,
Z. Kinder-Jugendpsychiatr. Psychother. 41 (1) © 2013 Verlag Hans Huber, Hogrefe AG, Bern
F. Häßler et al.: Catatonia in a 14-Year-Old Girl with Schizophrenia
Table 1
Similarities and differences of catatonia and NMS - Tuesday, October 04, 2016 8:46:08 PM - IP Address:
Motor symptoms
bizarre additional symptoms: posturing,
automatisms, negativism, rarely hyperkinesia (stereotypies)
only hypokinesia, rigidity, no major behavioral abnormalities
Affective symptoms
strong, intense and uncontrollable anxiety
less intense and more controllable anxiety
slower onset
sudden start of mental changes, motor rigidity, fever, and autonomous dysregulation
Pathophysiology of
motor symptoms
right posterior parietal cortical dysfunction blockade of D-2 receptors in striatum with
consecutive dysregulation of subcorticalcortical connections in the “motor loop”
Pathophysiology of affective symptoms
deficits in medial orbitofrontal cortical ac- emotional reaction to akinesia with abnortivity
mal subcortical-cortical modulation
first choice: benzodiazepines (BZP), e.g., Lorazepam 1–2 mg up to 20 mg/day
second choice in case of
nonresponding to BZPs
or in case of fever more
than 39 °C: ECT
third choice – if comorbid with schizophre- no neuroleptics
nia: neuroleptics, predominantly atypical
neuroleptics while maintaining BZPs
– if comorbid with affective disorders: no
2007). For childhood and adolescence, Wing and Shah
(2000) described five essential features of catatonia (1–5)
and three behavioral abnormalities (6–8):
1. Increased slowness affecting movement and verbal responses
2. Difficulties in initiating and completing actions
3. Increased reliance on physical or verbal prompting by
4. Increased passivity and apparent lack of motivation
5. Day-night reversal
6. Parkinsonian features
7. Excitement and agitation
8. Repetitive, ritualistic behavior.
To evaluate the severity and course of catatonia, including
treatment response, in adolescents, the Bush-Francis Catatonia Rating Scale (BFCRS) (Bush, Fink, Petrides, Dowling & Francis, 1996) is seen as the gold standard (Wong,
Ungvari, Leung & Tang, 2007). The BFCRS consists of 23
items with 17 items scored on a scale ranging from 0 to 3
and 6 symptoms being scored as either absent or present.
The BFCRS is well established in research and practice
(Takaoka & Takata, 2003). Nevertheless, the definition of
catatonia lacks coherence and clarity.
Benzodiazepines are the widely recommended first
choice of drugs for the treatment of catatonia (Francis,
2010; Ungvari, Caroff & Gerevich, 2010); second and third
choices for treatment are described in Table 1. Treatment
differs in third choices according to the comorbid disorder
of catatonic symptoms. In case a catatonia is associated
with a schizophrenic disorder, a cave has to be avoided,
because neuroleptics themselves have been shown to trigger catatonia. The so-called neuroleptic malignant syn-
drome (NMS) largely resembles catatonia and was extensively discussed in its relationship to catatonia. The most
commonly held opinion is that catatonia and NMS are two
entities on the same spectrum (Fink, 1996; Fink & Taylor,
2001). There are now five different hypotheses concerning
the nature of the link between the two diagnoses (Vesperini,
Papetti & Pringuey, 2010):
1. NMS is a drug-induced form of catatonia.
2. NMS is a drug-induced form of malignant catatonia.
3. NMS and malignant catatonia are the same.
4. Catatonia is a risk factor for NMS.
5. NMS is a heterogeneous syndrome that includes both
catatonic and noncatatonic responses to antipsychotic
For a clinician, it becomes difficult to distinguish between
these two conditions because many diagnostic criteria
overlap. In a retrospective investigation of clozapine, catatonia was diagnosed in 7.4% of patients while in a trial of
risperidone 5% of patients showed catatonic symptoms
(Ungvari et al., 2010). Both studies did not differentiate
between catatonia and NMS, a fact that might explain the
high rates of catatonic symptoms observed. About 20 cases
of NMS induced by olanzapine have been published (Srivastava, Borkar & Chandak, 2009). Confusion rises if aripiprazole is recommended for the treatment of catatonia
(Viktor & Tamas, 2010), which is also known to trigger
catatonic symptoms (Shepherd, Garza & De Leon, 2009).
For the clinician, the question often arises how to differentiate between symptoms induced by neuroleptics and noninduced symptoms, usually comorbid with an affective or
schizophrenic disorder. Table 1 gives an overview of some
characteristics we found in the literature (Lee, 2010; Nort-
Z. Kinder-Jugendpsychiatr. Psychother. 41 (1) © 2013 Verlag Hans Huber, Hogrefe AG, Bern - Tuesday, October 04, 2016 8:46:08 PM - IP Address:
F. Häßler et al.: Catatonia in a 14-Year-Old Girl with Schizophrenia
hoff, 1996, 2002; Rosebush & Mazurek, 2010), which can
help to differentiate between the two forms of catatonia.
Comprehensive reviews concerning this issue were given
by several authors (Lee, 2010; Takaoka & Takata, 2003; Ungvari et al., 2010) with varying results. Studies such as the one
by Carroll, Kennedy, and Goforth (2000) failed to discriminate between catatonia and NMS. Characteristics like those
listed in Table 1 might provide a first guideline, although the
differentiation between drug-induced and noninduced catatonia remains an open question in our view.
In case a catatonia is diagnosed for a patient also suffering
from schizophrenia, some issues should be considered (Fink
et al., 2010; Kruger, Bagby, Hoffler & Braunig, 2003). First,
the association of schizophrenia and catatonia appears only
to be moderate: Among adult catatonic patients about 28%
were also diagnosed with schizophrenia (Caroff, Mann,
Campbell & Sullivan, 2004). In younger patients this association appears to be even weaker. In 89 cases of children and
adolescents with catatonia analyzed by Takaoka and Takata
(2003), schizophrenia was present in 16.9%. Second, patients
with schizophrenic catatonia do not respond well to the treatment with benzodiazepines. A study by Ungvari et al. (2010)
reported response rates of 20–30% for schizophrenic patients, while more than 80% of catatonic patients suffering
from affective disorders reacted positively to benzodiazepines (Rosebush & Mazurek, 2010). Third, other beneficial
medical treatment options were reported for schizophrenic
patients, such as antiepileptic drugs or bromocriptine (dopamine agonist). Amantadine (antagonist of the NMDA type
glutamate receptor) was also reported to be beneficial (Lee,
2010; Rosebush & Mazurek, 2010; Takaoka & Takata, 2003).
In case schizophrenic children or adolescents do not
respond to medical treatment, or show a refractory to psychotropic medications, electroconvulsive therapy (ECT)
is considered to be an effective treatment alternative (Takaoka & Takata, 2003; Wachtel, Dhossche & Kellner,
2011). Recently, an overview was published regarding responses to ECT in catatonic adult patients (Caroff, Ungvari, Bhati, Datto & O’Reardon, 2007). The authors concluded that acute hypokinetic catatonia is extremely sensitive to ECT, achieving response rates of 67% to 100%.
Sienaert, Vansteelandt, Demyttenaere, and Peuskens
(2010) found no evidence of a deleterious effect of ultrabrief bifrontal or unilateral ECT on cognitive functioning. A study by Rey and Walter (1997) on children and
adolescents found overall efficacy rates of 80% for ECT.
For ECT in younger patients it is important to recognize
that, compared to adults, children show lower seizure
thresholds while ECT seizures last longer (Rey & Walter,
Case Report
The patient we report about is a 14-year-old female twin
(IQ 53) who at age 12 started to experience visual, haptic,
and imperative acoustic hallucinations. Since then she felt
anxious and observed, she shook herself and trembled over
her whole body. The patient’s thinking was confused, and
her thoughts were incoherent. Neurological status, laboratory findings, liquor cerebrospinalis, video-EEG, and cranial MRI remained normal. All findings failed to provide
evidence for an organic background to the psychotic symptoms. Developmental disorders were excluded by two experienced psychiatrists. Under combined treatment with
behavioral psychotherapy and an oral final dose of 600 mg
quetiapine retard, the symptoms of schizophrenia decreased significantly, allowing the patient to be discharged
from the hospital.
At age 13 psychopathological symptoms slowly returned. Especially acoustic hallucinations and symptoms
of anxiety cropped up. At the beginning of 2011, at age
14, our patient had to be treated again as an inpatient. At
this point in time, we were confronted with pronounced
mood variations and a distinctive affective instability
with ambitendencies. An increase of the quetiapine dose
(maximum 1200 mg) failed to provide substantial effects.
Therefore, we started to change medication to olanzapine
interleavingly. One day after the last application of quetiapine (300 mg) and under 20 mg olanzapine the girl became suddenly stiff showing a distinctive rigidity of the
extremities and the trunk, also developing a captocormia.
Our patient showed severe states of uncontrollable anxiety, restlessness, drivenness, echolalia, verbigerations,
excitement, iterations, stereotypies, and a resistance to
passive movements. Her thinking and speaking were
completely confused and incoherent. Eventually, within
2 days, she developed a catatonic stupor with a waxy
flexibility (flexibilitas cerea). The creatinine kinase (CK)
increased within these 2 days to 1071 U/l (reference <
109 U/l), myoglobine increased to 171 ng/ml (reference
25–58 ng/ml). Other laboratory findings remained unchanged (liquor cerebrospinalis, parameters of coagulation and inflammation, liver enzymes, potassium, sodium, chloride), just as did temperature, blood pressure,
respiratory rate, diaphoresis, and other vegetative parameters. However, a constant trembling of the whole body
was remarkable. A repetition of EEG and cMRI did not
provide any new results. An intravasal application of biperidene to evaluate extrapyramidal side effects provided
no results. At this time, the hypothesis of an NMS was
built, despite the fact that an increase of the CK does not
provide a valid indicator (Lee, 2010). With the differential diagnosis of a NMS, all neuroleptics were removed
Table 2
Sum scores of the BFRCS during the catatonic stupor state
of the girl, starting with the first day of the rigidity (minimal
0, maximum 66); b = biperidene, d = diazepam, l = lorazepam, h = haloperidol
2 (b)
3 (d)
5 (l)
7 (l + h)
Z. Kinder-Jugendpsychiatr. Psychother. 41 (1) © 2013 Verlag Hans Huber, Hogrefe AG, Bern
F. Häßler et al.: Catatonia in a 14-Year-Old Girl with Schizophrenia - Tuesday, October 04, 2016 8:46:08 PM - IP Address:
Table 3
Course during treatment with ECT
ECT bitemporal
Energy set 10%
Charge delivered 49.3 mC
Current 0. 90 A
Stimulus duration 5.6 s
Pulse width 0.50 ms
Frequency 10 Hz
Epileptic seizure/duration
Bush-Francis Catatonia
Rating Scale
84 s
Lorazepam 2 × 2 mg
Haloperidol 3 × 5 mg i.v., Clexane 20 mg s.c.
No changes
121 s
No changes
No changes
29 s
+ Antibiotics and Iron
No changes
20 s
Moving to pediatric emergency unit, Amantadine 600 mg/day
Energy set 15%
Charge delivered 75.4 mC
Current 0.90 A
Stimulus duration 5.6 s
Pulse width 0.50 ms
Frequency 20 Hz
250 s
Amantadine 900 mg/day
No changes
108 s
No changes
No changes
152 s
No changes
No changes
210 s
No changes
No changes
145 s
No changes
Energy set 10%
Charge delivered 49.3 mC
Current 0. 90 A
Stimulus duration 5.6 s
Pulse width 0.25 ms
Frequency 10 Hz
51 s
No changes
32 s
Lorazepam 3 × 0.5 mg
Amantadine 2× 200 mg/day
In days with ECT without morning doses of any
No changes
54 s
No changes
No changes
32 s
Energy set 15%
Charge delivered 75.4 mC
Current 0. 90 A
Stimulus duration 5.6 s
Pulse width 0.50 ms
Frequency 20 Hz
97 s
No changes
Energy set 15%
Charge delivered 75.4 mC
Current 0. 90 A
Stimulus duration 4.2 s
Pulse width 0.50 ms
Frequency 20 Hz
Lorazepam 3 × 0.5 mg, Ziprasidone 2 ×
20 mg/day on days with ECT without morning
No changes
Lorazepam 3 × 0.5 mg, Ziprasidone 60 mg/day,
Amantadine 2 × 200 mg/day
on days with ECT without morning doses of
any drugs.
No changes
Z. Kinder-Jugendpsychiatr. Psychother. 41 (1) © 2013 Verlag Hans Huber, Hogrefe AG, Bern
No changes in medication, transfer back to the
clinic for child and adolescent neuropsychiatry - Tuesday, October 04, 2016 8:46:08 PM - IP Address:
F. Häßler et al.: Catatonia in a 14-Year-Old Girl with Schizophrenia
and the girl was treated solely with benzodiazepines (3 ×
10 mg diazepam). Within two days, the CK returned to a
normal degree, but the catatonic stupor and a significant
impairment of vigilance and communication abilities
with a pronounced staring remained. At this point, the
diagnosis was rechanged to catatonic schizophrenic stupor because catatonia had started as a mix of behavioral
symptoms, not only as hypokinesia (see Table 1). Neither
diazepam nor lorazepam (3 × 2 mg) improved the status
markedly. Because of the primary schizophrenia we started a reattempt with haloperidol (3 × 10 mg) as an ultima
ratio, but failed again. Table 2 shows the daily total scores of the BFCRS during this time.
On day 16 after the beginning of the rigidity, we commenced bitemporal ECT (Thymatron® System IV with
GenieTM IV EEG analysis software) with a cluster of daily treatments over 4 days. To reduce side effects, especially cognitive dysfunctions, we used ECT treatment
techniques that in adults have proved to result in smaller
short- or long-term memory deficits (Sackeim et al.,
2007). In particular, we stimulated her with brief pulse
form. An individual electrical dosage titration was done
at the beginning of the first ECT session. There were no
major effects, but an acute exacerbation of schizophrenic
symptoms was seen at the beginning of ECT. For that
reason, we started with an accompanying amantadine
therapy (3 × 200 mg). With this add-on we aimed at a
beneficial effect as reported by Carroll, Goforth, and
Thomas (2007). After the patient started to show signs of
malnutrition and a beginning pneumonia with light to
moderate febrile temperature, she was transferred temporarily to a pediatric emergency unit where antibiotics
were added to the treatment. No autonomic abnormalities
appeared further on.
Bitemporal ECT was continued three times a week for
the next six treatment episodes, then twice a week for
another four treatment episodes, and finally once per
week for two maintaining treatment episodes. Lorazepam
and amantadine treatment was continued over this time
period with the patient showing slow improvement of the
motor and the psychopathological state. After 12 treatments, the girl showed significant improvement; she
started to move (answered with little movement or tone)
and became more verbal. ECT was finished after 16 treatments. Catatonic symptoms were no longer evident,
though the visual, haptic, and imperative acoustic hallucinations returned, again associated with marked fear.
After careful consideration we decided to start again with
a neuroleptic therapy. With a dose of 40 mg (2 × 20 mg)
ziprasidone we saw an intermediate elevation of the CK,
with a maximum of up to 496 U/l. Under a dose of
20–40 mg ziprasidone our patient no longer hallucinated,
showing a markedly reduced anxiety with psychopathological and motor status being almost normal. Table 3
shows the course during treatment with ECT inclusive
technical parameters.
The patient reported here was a female adolescent with
mild mental retardation who exhibited severe catatonia.
She was successfully treated with amantadine HCL, ECT,
and is currently being treated solely with ziprasidone. Improvement was noted after 12 ECT episodes. In sum, she
received a total of 16 ECT episodes. Our case report is in
line with the investigation by Girish and Gill (2003). In
their study 14 patients with nonaffective, nonorganic catatonia who did not respond to benzodiazepines improved
rapidly under ECT. Catatonic symptoms in this study, however, disappeared more quickly than in our case. We observed a catatonic status with a prominent stupor combined
with waxy flexibility persisting over 7 weeks. Alterations
of excitement were first seen after the 12th ECT episode.
With regard to the young age of our patient initial seizure
thresholds (IST) were set at a lower level (49.3 mC and
75.4 mC), compared to IST in bilateral ECT in adults
(111.6 mC) as reported by Waarde, Verwey, and Mast
(2009). The treatment with antipsychotics is in line with
more recent strategies reported by Caroff et al. (2007) and
Rosebush and Mazurek (2010). However, the role of antipsychotic drugs in catatonia remains unclear to date and
has been studied insufficiently. We argue here that antipsychotics may be effective in some cases. They should, however, be handled with greatest care because they may rechallenge catatonic episodes (Lee, 2010). We agree with
Francis (2010), who proposed a cautious trial of these
agents and careful monitoring for catatonic symptoms.
Unfortunately, schizophrenic catatonia proves to be a severe condition in young people, with 10% mortality at 4year follow-up (Cornic et al., 2007), caused by either suicide (n = 2) or by medical conditions (n = 1). In other
words, the course of our patient remains uncertain, despite
the marked reduction of psychopathology and catatonic
symptoms. For severe cases of schizophrenic catatonic stupor refractory to pharmacological treatment, we suggest an
intensive and, if necessary, long-lasting ECT sequence –
even in adolescents. In our case we saw no memory impairment as measured with the Working Memory Index of the
Wechsler Scales for children. In sum, we regard ECT as a
valuable second-choice treatment option (see Table 1) in
adolescents with schizophrenic catatonic stupor.
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Initial Date Submitted
Date Revision Submitted
January 23. 2012
May 3, 2012
Disclosures of interest of Dr. Häßler concern the following
positions: Advisory Board for Eli Lilly GmbH Germany,
Janssen-Cilag, Research Support from Novartis Pharmaceuticals, Bayer Vital, Travel Grants from Novartis Pharmaceuticals, AstraZeneca Pharmaceutical, Bayer Vital,
consulting fees from Janssen-Cilag, Novartis Pharmaceuticals, Bayer Vital. All other authors declare that they have
no conflicts of interest concerning financial or personal involvement with other people or organizations that could
have had an interest in the outcome of the study.
Dr. Olaf Reis
Klinik für Psychiatrie, Neurologie,
Psychosomatik und Psychotherapie
im Kindes- und Jugendalter
der Universität Rostock
Gehlsheimer Straße 20
18147 Rostock
[email protected]
Z. Kinder-Jugendpsychiatr. Psychother. 41 (1) © 2013 Verlag Hans Huber, Hogrefe AG, Bern