Reminder of important clinical lesson

Temporal glioblastoma presenting as catatonia
Anouchka Franssen,1 Pascal Sienaert2
1

Universitair Psychiatrisch
Centrum KU Leuven,
Kortenberg, Belgium
2
Academic Center for ECT and
Neuromodulation (AcCENT),
Universitair Psychiatrisch
Centrum KU Leuven,
Kortenberg, Belgium
Correspondence to
Dr Anouchka Franssen,
​anouchka.​franssen@​
upckuleuven.​be
Accepted 26 June 2018

Summary
The objective of this article is to describe the possible
association of catatonia and temporal brain lesions. This
is a case presentation of a 57-year-old man presenting
with depression, with catatonia secondary to a temporal
glioblastoma. He was referred to hospital because
for a sudden deterioration in depressed state. He was
diagnosed with catatonia and treated successfully
with lorazepam. During his admission, he became
increasingly disinhibited, and an MRI scan revealed an
intracranial mass in the right temporal lobe, with uncal
herniation and a mass effect. Surgical resection of the
entire tumour was successful. Histological examination
revealed a glioblastoma multiforme requiring additional
chemoradiotherapy. Postoperatively, catatonic signs and
symptoms were not detectable. A postsurgical frontal
syndrome with disinhibition and logorrhoea was present
and gradually normalised over the course of several
weeks. Catatonia can be the presenting symptom of a
temporal brain tumour, and should therefore prompt the
physician to a thorough medical investigation.

Background

© BMJ Publishing Group
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re-use. See rights and
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To cite: Franssen A,
Sienaert P. BMJ Case
Rep 2019;12:e224017.
doi:10.1136/bcr-2017224017

Brain tumours are encountered only rarely in a
psychiatric hospital setting. However, psychiatric
symptoms can be the first signs of a malignant
cancer. Several causal mechanisms may be involved.
The symptoms can be caused by direct pressure of
brain tumour or metastases, immunological reactions, ectopic hormone production or hypoperfusion. The incidence of cancer and other somatic
illness is higher in older age groups, especially in
people older than 50 years,1 and should therefore
be considered in the evaluation of patients with
new-onset psychiatric symptoms. The early detection of malignancy is of utmost importance, since it
gives a chance of providing a curative intervention.
Brain tumours can present with a variety of
psychiatric symptoms, of which depression seems
to be the most common.2 There are few descriptions of brain tumours presenting with catatonia.3–6
We report a case of a 57-year-old man presenting
to the emergency room with catatonia.
We show that catatonia is a motor syndrome that
accompanies various psychiatric and medical conditions, including brain tumours. Irrespective of the
underlying cause of the catatonia, the principles in
catatonia treatment stay the same. Nevertheless,
it is vitally important to also treat the underlying
cause.
Catatonia is a severe and possibly lethal
syndrome with an excellent prognosis if recognised
and treated appropriately without delay. Despite

its frequent occurrence, it is often missed during
diagnosis. The emergence of a catatonic syndrome,
most frequently in the presence of a psychiatric
condition, should prompt the clinician to rule out
other medical conditions.

Case presentation

The patient was a 57-year-old man. He was brought
to the emergency room because of sudden deterioration of a depressive episode. He had no prior
psychiatric history. He had lost approximately 4 kg
in the past month. His self-care had become poor,
and he had developed nocturnal urinary incontinence. Interaction with the patient was becoming
increasingly difficult.
On admission, the man was found in a state of
self-neglect sitting slumped in a wheelchair. He
made limited eye contact and had a staring gaze
with a flattened facial expression. The patient’s
responses to questions were delayed, with fragments and half-phrases. Echolalia was present. He
spoke of ‘silly thoughts’. There were verbal stereotypies (“it will never get better”, “I won’t get out
of this”). There was increased motor activity, with
repetitive motor behaviour including reciprocation of the lower jaw, finger strumming and foot
tapping. He had an unstable walk, with increased
tendency to fall (the night before admission he fell
three times). On physical examination, rigidity and
catalepsy were observed.
A diagnosis of a depressive episode, with catatonia, was made, and the patient was admitted to
a psychiatric ward. Catatonic signs were evident:
multiple echophenomena, verbal stereotypies and
immobility. He also displayed discrete apraxia and
urinary incontinence.
Treatment with lorazepam 1 mg, four times
per day, resulted in a gradual improvement in the
clinical picture. The patient expressed feelings
of sorrow, loneliness and a fear of dying. Within
days, his behaviour became more disinhibited, with
sexual acts, sudden aggressive outbursts and endless
discussions about rules and regulations on the ward.
In addition, the patient had double vision.

Investigations

An extensive blood test (including virology, anti-Nmethyl-D-aspartate receptor antibody and sexually
transmitted diseases screening) revealed no abnormalities. In the clinical neurological examination,
the patient gave a functional impression with negativism, closed eyes and a persistent athetoid movement of the right arm after testing rigidity. The
electroencephalogram showed a regular rhythm
which excluded a non-convulsive seizure; however,

Franssen A, Sienaert P. BMJ Case Rep 2019;12:e224017. doi:10.1136/bcr-2017-224017

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Case report

Reminder of important clinical lesson

it also revealed an abnormality with lateralisation on the left
side. An MRI scan revealed an intracranial mass in the right
temporal lobe, with uncal herniation and a mass effect (figure 1).
The movement disorders observed on the right side could be
explained by the pronounced tumour mass effect exerting pressure on right cerebellar tracts.

Differential diagnosis

Diagnostic imaging revealed an intracranial mass. Differentiation between tumours and tumour-like lesions of the central

nervous system is essential for planning adequate treatment
and for estimating outcome and future prognosis. The classic
tumour-like lesion is an intracranial abscess. On MRI, pus within
the abscess typically shows restricted diffusion, whereas necrosis
in the centre of malignant tumours typically shows an increased
diffusion.7 As necrosis was visible in the MRI of our patient, a
malignant tumour was suspected (figure 2).
To differentiate between a primary or secondary tumour, CT
scans of the thorax and abdomen were obtained and revealed
no abnormalities. The diagnosis of a primary brain tumour was

Figure 2 MRI scan of the brain, preoperative, diffusion image shows increased diffusion in the centre of the tumour.
2

Franssen A, Sienaert P. BMJ Case Rep 2019;12:e224017. doi:10.1136/bcr-2017-224017

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Figure 1 (A) T2-weighted MRI scan reveals an intracranial mass, in the right temporal lobe, with uncal herniation and mass effect. (B) T2-weighted
MRI scan, after resection of the tumour. (C) T2-weighted MRI scan 1 year later shows relapse of the tumour in the frontotemporal lobe.

Reminder of important clinical lesson

made. A biopsy was required to confirm the type of tumour and
its histopathological characteristics.

Treatment

The patient’s catatonia was treated with lorazepam 1 mg, four
times per day which resulted in a gradual improvement in the
clinical picture. After the discovery of the brain tumour, the
patient was transferred to a neurosurgical ward. Neurosurgical
resection of the entire tumour was successful (figure 3). Histopathological examination showed a glioblastoma multiforme
that required additional radiotherapy and chemotherapy (in the
form of 60 Gy in fractions of 2 Gy, and temozolomide).

Outcome and follow-up

Postoperatively, catatonic signs and symptoms were not detectable. A frontal syndrome with disinhibition and logorrhoea
persisted which gradually normalised over the following weeks.
The frontal syndrome was considered to be the sequelae of parietotemporal oedema arising from the surgical intervention. The
patient could resume work part-time 5 months after the operation. Outpatient psychiatric and psychotherapeutic treatment
(because of postoperative depressive symptoms) aimed to attain
a stable euthymic mood. In supportive psychotherapy, special
attention was given to reactivation. Medication was not used.
One year later, the patient began to experience paroxysmal
dysosmia and panic attacks. The diagnosis of focal temporal
lobe epilepsy was made. Brain imaging showed relapse of glioblastoma multiforme in the frontotemporal lobe. Treatment
with antiepileptics (levetiracetam) and chemotherapy (lomustine) was initiated. During the course of treatment, follow-up
brain imaging 5 weeks later revealed further progression of the
disease. The patient died 4 months later.
Franssen A, Sienaert P. BMJ Case Rep 2019;12:e224017. doi:10.1136/bcr-2017-224017

Discussion
Brain tumours may be accompanied by a number of comorbidities. While brain tumours may directly affect patients’ cognition,
mobility, communication, perception and other neurological
functions, these comorbidities may also greatly affect patients’
quality of life.2 8–10 Among these comorbidities, depression is
the most common.2 8 A substantially higher incidence of major
depressive disorder was found in adult patients with brain tumour
compared with other adult, ambulatory patients with cancer.11 12
Systematic reviews and longitudinal studies suggest that approximately 15%–20% of patients with glioma will develop clinical
major depressive symptoms during the first 8 months after diagnosis.13 14 The increased risk for depression may be maintained
up to a year after surgical intervention.15 Depression, thus, is
considerably more likely in patients with brain tumours than in
the general population (where the point prevalence is approximately 5%).2 8 9 13 14
Mood symptoms may be a forewarning of an evolving brain
tumour.16 17 Patients with a brain tumour may initially present
with psychiatric symptoms. In addition to depression, these
symptoms may include personality change, abulia, apathy, hallucinations, mania, panic attacks and amnesia.18 These symptoms
may be indistinguishable from such symptoms in patients with
psychiatric disorders without brain tumours. Some studies show
an increased incidence rate ratio for cancer in the months after
a first-time psychiatric inpatient or outpatient contact. For brain
tumours, an almost 19-fold increased incidence rate ratio during
the first month has been reported, but also the incidence rates of
small cell lung cancer have been found to increase sixfold during
the first month, indicating that certain cancers might mimic
psychiatric disorders.1
3

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Figure 3 MRI scan of the brain, postoperative, T1-weighted image with contrast shows complete removal of the tumour.

Reminder of important clinical lesson

Figure 4 MRI scan of the brain, preoperative, T1-weighted coronal
image shows the pressure on the thalamus and basal ganglia.
In our case, the patient presented with depression and catatonia. Catatonia is a syndrome of acute onset and a fluctuating
course, first described by Kahlbaum in 1874.19 In his original description, 12 of 26 cases had a diagnosis of depression,
while 14 of 26 had a somatic diagnosis (epilepsy, tuberculosis,
neurosyphilis). Catatonia is seen in the context of mood disorders and psychotic disorders, but is also found among the systemically ill with infections, endocrine and metabolic disorders, and
neurological disorders, including epilepsy.20 The neurobiology
of catatonia remains poorly understood. Due to ethical and practical concerns, functional neuroimaging studies have focused on
patients with catatonia many days after acute presentation and
treatment.21 22 The majority of studies have reported hypoactivity in cortical motor areas of the frontal and parietal cortices.23
Patients with catatonia have been found to have a dysfunction
of the ‘medial motor system’ which includes the supplementary
motor area, thalamus and basal ganglia, consistent with impairment in self-initiated movements.22 Such patients also showed
altered activation patterns and functional connectivity in the
orbitofrontal and medial prefrontal cortex.21 In our patient, the
intracranial mass exerted pressure on the thalamus and basal
ganglia which could explain the catatonic symptoms (figure 4).
Reviews by Fink and Taylor24 and Northoff25 support an
important role for dysfunction of the motor system involving
frontal lobe basal ganglia circuitry or for interference with this
system (through thalamic, parietal lobe, cerebellar or limbic
abnormalities) in the mechanism of catatonia. The same circuits
have been implicated in malignant catatonia and neuroleptic
malignant syndrome (NMS).26 Hyperthermia and autonomic
dysfunction in malignant catatonia and NMS may arise from
disrupted transmission between orbitofrontal structures and
lateral hypothalamus. γ-Aminobutyric acid and dopamine are
4

Learning points
►► Catatonia is a motor syndrome that accompanies various

psychiatric and medical conditions, including brain tumours.

►► Irrespective of the underlying cause of the catatonia, the

principles in catatonia treatment stay the same. Nevertheless,
it is also very important to treat the underlying cause.
►► The emergence of a catatonic syndrome, most frequently in
the presence of a psychiatric condition, should prompt the
clinician to rule out medical conditions.
Acknowledgements Thanks to Professor Max Fink for his comments on a
previous version of this manuscript.
Contributors AF: conduct, reporting, acquisition of data, analysis and
interpretation of data. PS: review, guidance and interpretation of data.
Funding The authors have not declared a specific grant for this research from any
funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.

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Reminder of important clinical lesson
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