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TITLE OF CASE

Case of Frontal Glioblastoma with Depression and Catatonic features

SUMMARY

This case highlights the need for thorough assessment even in patients with Psychiatric
symptoms and or when given a Psychiatric diagnosis. This is a case of 48 year old female
presenting to our psychiatric OP with symptoms suggestive of catatonia. She was initially
treated at a private clinic as depression. As her symptoms deteriorated she was brought to our
hospital for further management. She was initially 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 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,
earning as daily wage worker, 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 in 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 patient’s symptoms worsened, she even stopped going to work. She was unable to do
her daily household activities and had difficulty getting up from her bed. She also had difficulty in
swallowing wherein she would take only liquids such as water, juice or milk. Eventually her self
care further deteriorated and started to defecate and urinate in her clothes. 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.

On presentation to the outpatient department, 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. Her affect was dull
however she was co-operative throughout the interview. On serial mental status examinations,
mild depressive cognition was present. Her personal and social judgement was impaired with
partial insight. On detailed neurological examination, she was found to have sluggish pupil response (?
Fundus) bilaterally and power of 4/5 on her right upper and lower limb, with flexor plantar response
bilaterally. (?catatonic Signs)

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 acute
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 as 5 on Bush Francis Catatonia Rating Scale. Drug induced Extra Pyramidal Syndrome -
Following neurological examination, a differential of Cerebrovascular Accident or Encephalitis was
considered, in view of the rapid progression of her symptoms.

Updated April 2023

 TREATMENT If relevant

On Bush-Francis Catatonia Rating Scale, she had a total score of 5, scoring in areas of immobility/stupor,
mutism and withdrawal. She was thereafter started on oral dose of Lorazepam 2mg bd. Following which,
patient started to show improvement in terms of accepting liquids orally and her other catatonia
symptoms gradually improved. Following brain imaging studies and neurosurgery opinion, patient was
then eventually transferred to their department and partial resection of the bifrontal tumour was done.
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. 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 with her life expectancy of 3-6 months post surgery.

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 as a clinical feature is prevalent in 5%- 18% of psychiatric patients and 3.3% in
neurology/neuropsychiatric units (1). Systematic reviews done over the past two decades found
that about 20-25% of the individuals with catatonic syndrome have an underlying organic cause
with roughly 70% of them due to a neurological condition among which structural pathologies of
CNS are the most common accounting to about 30%. The other neurological causes accounting to
25% due to encephalitis or other CNS infection, and 10% attributed to a seizure disorder(11).
Considering this high prevalence data, maintaining a high index of suspicion for neurological
disease where medical catatonia is on the differential, is recommended. (Association of Catatonia
and Affective disorders) Among the patients with affective disorders(Bipolar affective disorder and
Schizoaffective disorder, bipolar subtype, depression), 13-31% of patients were found to have
catatonic signs.(15) Among patients with mania catatonia was present in 31-62% and among
patients with depressive states it was 20-53%.(15) In a meta analysis by Solmi et al (16) the mean
prevalence of catatonia was 9.2% among patients with psychiatric or medical conditions. In their
findings catatonia was prevalent in schizophrenia, bipolar affective disorder, autism, depression
and mixed psychiatric illnesses . Catatonia prevalence was higher in BD, even more than in
schizophrenia or MDD

SOL was not considered - acute presentation ; No Vomiting/diplopia/seizures; Fundus was normal.

Space occupying lesions were not considered as the onset of symptoms were acute and was not associated
with vomiting, diplopia or seizures and fundus was normal. 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

Updated April 2023

a case report by Cheema et al, a left frontal and temporal lobe mass extending to right frontal lobe
confirmed as glioblastoma multiforme had presented as low mood, fatiguability , loss of interest and
insomnia poorly responding to antidepressant treatment for nearly 10 years. To the best of our knowledge,
a total of two cases with frontal lobe glioblastoma presented with psychiatric symptoms, one case
presented as depression with catatonic features and the other with catatonia alone. Other than frontal lobe
lesions, psychiatric symptoms of depression and catatonia have also been seen in temporal lobe lesions (9)

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. In another study by Franssen et al., the patient was diagnosed
with glioblastoma in right temporal lobe accompanied by uncal herniation and mass effect.
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). In our study, a butterfly shaped Glioblastoma Multiforme involving the
bilateral frontal and basifrontal regions, more pronounced on the left side extending the rostrum
and body of the corpus callosum is evident. 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. In this case report, a 45 year male with no
family or past history of psychiatric illness 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.

A recent critical literature review also highlighted that catatonia 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

● Catatonia is a common presenting feature of various CNS pathologies including stroke, infections,
infarction, and tumors.
● Appearance of catatonia 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.

Updated April 2023

 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
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:

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 10.1093/schbul/sbx157. PMID: 29140521; PMCID: PMC6101628.

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