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TITLE OF CASE

Case of Frontal Glioblastoma with Catatonia

SUMMARY

This case highlights the need for thorough medical and neurological screening before making
any psychiatric diagnosis, even if the patient has classical syndromic presentation. This is a case
of 48 year old female presenting to our psychiatric OP with symptoms suggestive of catatonia.
She was treated at a private clinic as depression. As her symptoms deteriorated she was brought
to our hospital for further management. She was diagnosed with Catatonia during admission
assessment. A detailed neurological assessment later revealed slight weakness in right upper
and lower limb. Following this CT scan was done and was reported to have acute to subacute
infarct involving the bilateral frontal and basifrontal region, more pronounced in the left side.
MRI was subsequently done and was found to be suggestive of GLIOBLASTOMA MULTIFORME
involving bilateral cerebral hemisphere which was later confirmed by the histopathology report.

BACKGROUND

Catatonia is a psychomotor syndrome associated with several psychiatric and medical

conditions. There are two catatonia sub-types, a retarded or stuporous form with decreased
psychomotor behavior and an excited form, characterized by agitation, combativeness,
impulsivity and apparently purposeless overactivity. Catatonia can occur in a wide range of
psychiatric and medical conditions like mood disorders, schizophrenia , secondary to substance
use, stroke, infections, tumours, etc. This case highlights Psycho-Motor presentations which
later turned out to be Frontal Glioblastoma Multiforme with catatonic features. To the best of
our knowledge there were only two cases that have been reported earlier.

CASE PRESENTATION

A 48 year old married female from rural background, who had studied till primary school,
agricultural labourer, hailing from a Tamil speaking, lower socio-economic, nuclear family,
presented to our department. She presented with headache, slowness and inability to perform
her daily activities, reduced interaction, poor intake of food, poor self care for 1 month, worse
over the past 10 days, She also complained of weakness of right upper and lower limbs and
difficulty in walking for the past 1 week . It was insidious in onset and continuous in progression.
Patient is a known case of systemic hypertension on irregular medications with no past or family
history of psychiatric illness and with well adjusted premorbid personality.

Patient was apparently normal 1 month back, when she reported to have headache, dull aching
type, not associated with vomiting or blurring of vision. During this time, she was noticed to
keep to herself most of the time, not interacting much with her family members. She would
appear dull and was found to have difficulty in carrying out her day to day activities because of
 her slowness. Her self care started to deteriorate requiring assistance for the same. As she was
withdrawn, dull and had poor appetite, patient was taken to a near by private psychiatrist where
she was diagnosed with clinical depression and prescribed with oral medications (Olanzepine
5mg and Fluoxetine 20mg at bedtime and Lorazepam 1mg twice daily).

Gradually as patient’s symptoms worsened, she stopped going to work. She did not do her daily
household activities and was found to be lying on her bed most of the day, she would take only
liquids such as water, juice or milk. Her self care further deteriorated and she could not control
her bowel and bladder. She could no longer communicate verbally. During the same time, she
was noticed to have reduced usage of her right hand for her usual chores and was found to drag
her right feet while walking and thereby requiring assistance. As her condition was declining, she
was brought to our Outpatient department for further management.

She entered the room by dragging her right foot and required support by her attenders to sit for
the interview. She sat with drooping posture, leaning to her right side. Eye contact was made
but not maintained and her blinking was reduced. Rapport was established with difficulty.
Patient was verbally unresponsive to majority of questions and was responding only by nodding
her head and was abnormally still. She was obeying commands however when asked to write
she did not write anything and posturing was present. Her affect was dull however she was co-
operative throughout the interview. On detailed neurological examination, she was found to have
sluggish pupil response bilaterally and power of 4/5 on her right upper and lower limb, with flexor
plantar response bilaterally. On serial mental status examinations, sad mood and depressive
cognition was present. Her personal and social judgement was impaired with partial insight. She
was unco-operative for cognitive function tests

INVESTIGATIONS If relevant

Her Bush Francis Catatonia rating Scale (BFCR) scores were 5 suggestive of catatonia and Hamilton
Depression Rating Scale (HAM-D) scores were 20 suggesting moderate depression. In view of her
subacute onset of symptoms, catatonic symptoms and weakness on right limbs, CT brain was advised and
neurology opinion was sought. CT brain reported acute/subacute infarct involving the bilateral frontal
and basifrontal region, more pronounced on left side extending to rostrum and body of corpus callosum
on left side with mass effect and midline shift, also involving the left gangliocapsular region.(Fig.1)
Therefore neurologist had suggested for MRI brain. MRI revealed an intracranial mass involving both
frontal lobes, left basal ganglia and body of corpus callosum with peripheral enhancement. (Fig 2)

DIFFERENTIAL DIAGNOSIS If relevant

Initially a working diagnosis of Moderate Depressive Disorder was considered as per her Mental Status
Examination. The second differential was of Catatonia as evident by the catatonic features she had which
were rated on Bush Francis Catatonia Rating Scale. Drug induced Extra Pyramidal Syndrome was
considered in view of past history of antipsychotic medications. Following he neurological examination, a
differential of Cerebrovascular Accident or Space occupying lesion was considered, in view of the rapid
progression of her symptoms.

TREATMENT If relevant

As she had mild catatonic symptoms, scoring in areas of immobility/stupor, mutism and withdrawal. She
was started on oral dose of Lorazepam 2mg bd. Following which, patient minimal improvement in terms

Updated April 2023

 of accepting liquids orally and her other catatonia symptoms gradually improved. Brain imaging studies
were done and neurology opinion was sought. INJ MANITOL and LEVIPIL were started along with fluidsT
STROCIT PLUS, T CLOPILET, T ATOVASTATIN, T ECOSPIRIN were added. Following brain imaging reports,
neurosurgery opinion was sought an patient was transferred to their department for further
management. Patient underwent partial resection of the bifrontal tumour. Histopathology report
confirmed the diagnosis of Glioblastoma Multiforme. (Fig 3)

OUTCOME AND FOLLOW-UP

Post-surgery patient’s catatonic symptoms fully resolved. Her BFCR scores reduced from 5 to 1 and her
HAM-D scores improved from 20 to 17. There was minimal improvement in patient’s right sided
weakness. Patient was planned for Radiotherapy and Chemotherapy during follow-up. The overall
prognosis of the patient was noted as poor .

DISCUSSION Include a very brief review of similar published cases

Historically, catatonia as a distinct psychomotor disturbance was first recognised by Karl Ludwig Kahlbaum
in 1874 in his book “Catatonia or Tension Insanity “ which proved to be a milestone in establishing
catatonia as a separate entity but as a part of Schizophrenia . However, it is only in the most recent times
that our current classificatory systems recognize catatonia as a distinct disorder finding its place as an
independent diagnostic entity in the latest version of ICD 11 and has also been included in DSM-5.

Catatonia is prevalent in 5%-18% of psychiatric patients and 3.3% in neurology/neuropsychiatric units (1)
About 20-25% of individuals with catatonic syndrome have an underlying organic cause, with 70%
attributed to neurological conditions, primarily structural pathologies of the central nervous system (CNS).
Other neurological causes include encephalitis or CNS infections (25%) and seizure disorders (10%) (11). A
meta-analysis (16) found a mean prevalence of catatonia to be 9.2% among patients with psychiatric or
medical conditions, with higher prevalence in bipolar disorder compared to schizophrenia or major
depressive disorder. In patients with mania, catatonia is present in 31-62%, and in those with depressive
states, it ranges from 20 to 53% (15)

In our case, the patient initially presented with symptoms suggestive of depression which progressed with
her developing psychomotor disturbances as catatonia. Eventually the imagings revealed the underlying
Glioblastoma involving bilateral frontal lobes with extension in left basal ganglia and corpus callosum. The
histopathology report confirmed the diagnosis of Glioblastoma Multiforme.

To the best of our knowledge, a total of three cases with frontal lobe glioblastoma and one with temporal
glioblastoma presented with psychiatric symptoms [9,10,13], one case presented as depression with
catatonic features[13] and the other with catatonia alone [10].

This finding is similar to that of case report by Arora et al, wherein patient with catatonia was later found to
have butterfly glioma originating from the corpus callosum with bilateral medial frontal extensions [10]. A
45 year male had presented with 3 months duration of increased frequency of micturition and a month’s
history of forgetfulness, crying spells, decreased socialization and hallucinatory behavior with food refusal,
maintaining odd postures, urinary incontinence for 1 week. On Mental status examination patient was
uncooperative, mute, had posturing and negativism. Patient was given Inj. Lorazepam 2mg TID, however no
improvement was observed. The CT brain then revealed a large butterfly glioma involving genu and body of
corpus callosum extending into medial frontal lobe. The patient eventually succumbed to death.

Medial frontal lobe structures have been implicated in the pathophysiology of catatonia(10). Studies done
by Fink and Taylor and Northoff implicate the role of dysfunction of motor system involving frontal lobe and
basal ganglia in the mechanism of Catatonia. Taylor et al(1990), noted that the presence of catatonic
symptoms are an evidence for frontal lobe disease or dysfunction, and has proposed it to be due to
dopamine imbalance in the frontal lobe, basal ganglia and brain stem system.
Updated April 2023
Brain tumour presents with number of psychiatric co-morbidities of which depression and catatonia are
common with depression being the most common presentation. The tumours of frontal lobe commonly
presents as depression to psychiatry OPD. In a study by Cheema et al., a 53 year old male, a known case of
depression for 10 years, had presented with depressed mood, low energy, anhedonia and reduced
sleep.Despite various trials of antidepressants, he showed little improvement, and his functioning declined
to the point where he could not care for himself and experienced suicidal ideation, necessitating
hospitalization. Given his poor response to antidepressants and history of seizures, a CT scan followed by
MRI was done. The imaging revealed a mass in the left frontal and temporal lobes extending into the right
frontal lobe. Subsequent brain biopsy confirmed the presence of glioblastoma multiforme.

Other than frontal lobe lesions, psychiatric symptoms of depression and catatonia have also been seen in
temporal lobe lesions (9). In the study by Franssen et al., a 57-year-old man, initially presented with
symptoms of depression. His referral to the hospital was prompted by a sudden worsening of his depressive
state. Upon evaluation, he was diagnosed with catatonia and effectively treated with lorazepam. An
intracranial mass accompanied by uncal herniation and mass effect was discovered in the MRI scan and was
later confirmed as Glioblastoma Multiforme on Histopathology report. Numerous cases have documented
instances of catatonia occurring in temporal abnormalities, which includes temporal lobe infarction,
localised temporal encephalomalacia, surgical resection or lesions of temporal lobe (9).

A recent critical literature review also highlighted that catatonic disorder resulting from general medical
conditions should be considered in every patient with catatonic signs. Catatonia is associated with
significant morbidity and mortality if left untreated. With the early diagnosis and management of the
underlying condition, catatonic symptoms resolve and it further improves the prognosis. Thereby
necessitating the need for proper history, physical and neurological examination in the patients having
catatonic symptoms.

LEARNING POINTS/TAKE HOME MESSAGES 3-5 bullet points

● Acute onset of affective disorders warrant a through screening for medical and neurological
causes.
● Appearance of catatonia even in chronic depression should prompt clinicians to rule out
organicity/ non-psychiatric causes of catatonia especially neurological causes.
● Early diagnosis and intervention can significantly impact the outcome and prognosis of the
underlying medical condition.

REFERENCES

1.Hirjak D, Foucher JR, Ams M, et al. The origins of catatonia - Systematic review of historical texts
between 1800 and 1900 [published online ahead of print, 2022 Jun 13]. Schizophr Res. 2022;S0920-
9964(22)00208-0. doi:10.1016/j.schres.2022.06.003

2.Litofsky NS, Resnick AG. The relationships between depression and brain tumors. J Neurooncol
Updated April 2023
 2009;94:153–61. 10.1007/s11060-009-9825-4

3. Shetageri VN, et al. Case report: catatonia as a presenting symptom of Wilsons disease. Indian J
Psychiatry 2011; 53 Suppl 5:S93–S94.

4. Cardinal RN, et al. Psychosis and catatonia as a first presentation of antiphospholipid syndrome. Br J
Psychiatry 2009; 195:272.

5. Rogers JP, et al. Catatonia and the immune system: a review. Lancet Psychiatry 2019; 6:620–630.

6. Pustilnik S, et al. Catatonia as the presenting symptom in systemic lupus erythematosus. J Psychiatr
Pract 2011; 17:217–221.

7. Lander M, et al. Review of withdrawal catatonia: what does this reveal about clozapine? Trans
Psychiatry 2018; 8:139.

8.Benros, M. E., Laursen, T. M., Dalton, S. O., & Mortensen, P. B. (2009). Psychiatric disorder as a first
manifestation of cancer: A 10‐year population‐based study. International journal of cancer, 124(12),
2917-2922.

9.Franssen, A., & Sienaert, P. (2019). Temporal glioblastoma presenting as catatonia. BMJ Case Reports
CP, 12(3), e224017.

10. Arora M, Praharaj SK. Butterfly glioma of corpus callosum presenting as catatonia. World J Biol
Psychiatry. 2007;8(1):54-5. doi: 10.1080/15622970600960116. PMID: 17366353.

11. Carroll BT, Anfinson TJ, Kennedy JC, Yendrek R, Boutros M and Bilon A. Catatonic disorder due to
general medical conditions. The Journal of neuropsychiatry and clinical neurosciences 1994;6:122-33q

12.Northoff, G. (2004). Neuroimaging and neurophysiology. In S. N. Caroff, S. C. Mann, A. Francis, & G. L.

Fricchione (Eds.), Catatonia: From psychopathology to neurobiology (pp. 77–92). Washington, DC:
American Psychiatric Press.

13. Cheema FA, Badr A, Iqbal J. Glioblastoma multiforme presenting as treatment-resistant depression. The Journal
of Neuropsychiatry and Clinical Neurosciences. 2010 Jan;22(1):123-e26.

14. Petzold J, Severus E, Meyer S, Bauer M, Daubner D, Krex D, Juratli TA. Glioblastoma multiforme presenting as
postpartum depression: a case report. Journal of Medical Case Reports. 2018 Dec;12(1):1-4.

15. Takács R, Rihmer Z. Catatonia in affective disorders. Current Psychiatry Reviews. 2013 May
1;9(2):101-5.

16. Solmi M, Pigato GG, Roiter B, Guaglianone A, Martini L, Fornaro M, Monaco F, Carvalho AF, Stubbs B,
Veronese N, Correll CU. Prevalence of Catatonia and Its Moderators in Clinical Samples: Results from a
Meta-analysis and Meta-regression Analysis. Schizophr Bull. 2018 Aug 20;44(5):1133-1150. doi:
10.1093/schbul/sbx157. PMID: 29140521; PMCID: PMC6101628.

Updated April 2023

 FIGURE/VIDEO CAPTIONS

Fig 2: MRI BRAIN : Large heterogenous T2/FLAIR hyperintense, T1 iso to hypointense leision with irregular
peripheral enhancement in the genu, adjacent body of corpus callosum and adjacent both frontal lobes
and in left basal ganglia. Features suggestive of Glioblastoma Multiforme

Fig 1: CT BRAIN : Acute, subacute infarct involving left gangliocapsular region

Updated April 2023

 Fig 3: Histopathology : Sections studied show multiple fragments of infiltrating cellular tumour of
astrocytic origin showing sheet of tumour cells having mild to moderate pleomorphism. Background is
fibrillary and shows extensive areas of geographical necrosis and microvascular proliferation with few
vessels showing glomeruloid appearance. Features are of high grade astrocytic neoplasm- Glioblastoma-
WHO grade IV

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Updated April 2023