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 Table of Contents    
Year : 2021  |  Volume : 63  |  Issue : 3  |  Page : 309-311
Catatonia associated with seizures due to parietal cavernoma

1 Department of Psychiatry, All India Institute of Medical Sciences, Raipur, Chhattisgarh, India
2 Department of Psychiatry, Adesh Medical College and Hospital, Mohri, Kurukshetra, Haryana, India
3 Department of Radiology, Adesh Medical College and Hospital, Mohri, Kurukshetra, Haryana, India

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Date of Submission28-Mar-2020
Date of Decision12-Aug-2020
Date of Acceptance23-Oct-2020
Date of Web Publication17-Jun-2021

How to cite this article:
Somani A, Sharma A, Goyal N, Gulia M. Catatonia associated with seizures due to parietal cavernoma. Indian J Psychiatry 2021;63:309-11

How to cite this URL:
Somani A, Sharma A, Goyal N, Gulia M. Catatonia associated with seizures due to parietal cavernoma. Indian J Psychiatry [serial online] 2021 [cited 2022 Nov 29];63:309-11. Available from:


Catatonia is a syndrome of specific set of motor abnormalities commonly found associated with psychiatric disorders and also with organic brain conditions such as parietal/temporal lobe disorders, closed head injury, dementia, encephalitis, and epilepsy.[1],[2] There are very few reports of catatonia associated with parietal lobe lesions.[1],[3] We, hereby, discuss a case of catatonia manifesting in a patient who had seizures due to cavernoma in the parietal lobe.

A 35-year-old male was brought to the emergency room (ER) in view of repeated episodes of generalized tonic-clonic seizures (GTCS). He had four episodes of GTCS before reaching the ER. He was shifted to the intensive care unit (ICU), was given injection midazolam, followed by a loading dose of sodium valproate. He did not have any seizures in ICU, regained consciousness by evening, accepted meals, and slept well at night. Next day, he was shifted to the ward. Within an hour of transfer, he showed abnormal behavior. While his eyes were open, he neither talked nor responded to gestures, had vacant looks, did not show any emotions toward family members, resisted their efforts to feed him by closing his mouth tightly, and fended off nursing staff too.

On evaluation by a psychiatrist, it was found that he had markedly decreased psychomotor activity, decreased blinking, held gaze for 30–40 s, and did not speak or open his mouth despite repeated efforts/instructions. His vital parameters were stable. Reports of blood counts, blood sugar, liver/kidney/thyroid function tests, serum electrolytes (sodium, potassium, chloride, calcium, and magnesium), viral markers, creatine phosphokinase level, and urine examination were all within normal limits. Noncontrast computerized tomography of the brain suggested a possible cavernoma with surrounding bleed in the right parietal lobe.

It appeared that the patient currently had catatonia. He scored 16 on the Bush-Francis catatonia rating scale (BFCRS) and was given 1 mg lorazepam injection intravenously which was repeated after 5 min. After 2 min of the second dose of lorazepam, he started to respond. He talked to his family members, followed commands, and accepted food and medicines. After 10 min, he scored only five on BFCRS. He was advised tablet lorazepam 2 mg once every 6 h for rest of the day and sodium valproate 1000 mg daily. By 4th day, he had complete resolution of catatonia. Mental status examination did not reveal features suggestive of any psychiatric illness. He was continued on sodium valproate 1000 mg and lorazepam 8 mg daily. Contrast-enhanced magnetic resonance imaging of the brain revealed a cavernoma in the lateral aspect of the right parietal lobe measuring 1.3 cm × 1.6 cm × 1.7 cm, extending superiorly up to corona radiata and inferiorly up to the posterior aspect of right basal ganglia. It was surrounded by chronic bleed, but there was no mass/edema effect [Figure 1], [Figure 2], [Figure 3], [Figure 4]. He was discharged on 6th day. Sodium valproate was continued and lorazepam was gradually tapered and stopped by the 15th day postdischarge. He is free of seizures and catatonia since then.
Figure 1: Transverse magnetic resonance imaging T2-weighted image showing lesion in the right parietal lobe which is heterogeneously hyperintense with peripheral hypointense rim giving “pop-corn appearance”, characteristic of cavernoma

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Figure 2: Coronal magnetic resonance imaging T2-weighted image showing cavernoma in the right parietal lobe

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Figure 3: Sagittal magnetic resonance imaging T1-weighted image showing heterogeneously hypointense lesion with multiple hyperintense foci within it

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Figure 4: Magnetic resonance imaging gradient recalled echo sequence showing peripheral and central areas of blooming within the lesion

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Catatonia has been reported in association with epilepsy and postictal state.[4],[5] However, the cause and effect relationship between catatonia and epilepsy is not clear. Repchak and Quinn have described three cases where patients manifested catatonia in the background of seizure disorder and two of them improved with antiepileptic treatment and simultaneous resolution of EEG features of seizures.[5] Repchak and Quinn have conceptualized catatonia in such cases as a possible preictal, ictal, postictal, or interictal phenomenon. Other possible explanations of catatonia in such cases could be seizure-induced neurotoxicity, forced normalization, or even due to anticonvulsant therapy.[5]

Cavernoma or cavernous angioma is a blood vessel malformation composed of a “mulberry-like” cluster of dilated thin-walled capillaries.[6] Cavernoma is believed to be present in 0.5% of the general population, of which 40% develop symptoms such as headache, epilepsy, repeated hemorrhages, or as symptoms of mass effect. There are reports of other cerebrovascular lesions such as cortical venous thrombosis, subarachnoid hemorrhage, subdural hematoma and aneurysms, and structural lesions of the parietal lobe such as biparietal infarct, right hemispheric infarct, arachnoid cyst, and neoplasms presenting as catatonia.[1],[3] Again, the cause and effect relationship between these lesions and catatonia is not clear. There are findings that suggest a possible role of parietal lobe dysfunction in the pathogenesis of catatonia. Researchers have found decreased regional cerebral blood flow (r-CBF) in the right parietal cortex in patients of catatonia compared to other psychiatric patients with the same illness but without catatonia.[7] In addition, measures for attention and visual-spatial abilities correlated significantly with r-CBF in the right parietal lobe.[8]

The index case emphasizes the importance of keeping a high index of suspicion for catatonia in a nonresponsive, mute, or combative patient who otherwise has a clear history of organic illness. This becomes even more important in cases where there is no apparent reason or motive behind noncooperation. Prompt identification and treatment of catatonia could save the patient from risks of increased morbidity and mortality.

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   References Top

Ahuja N. Organic catatonia: A review. Indian J Psychiatry 2000;42:327-46.  Back to cited text no. 1
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Dhossche DM, Stoppelbein L, Rout UK. Etiopathogenesis of catatonia: Generalizations and working hypotheses. J ECT 2010;26:253-8.  Back to cited text no. 2
Howard RJ, Low-Beer TS. Catatonia following biparietal infarction with spontaneous recovery. Postgrad Med J 1989;65:316-7.  Back to cited text no. 3
Quagliato L, Piedade R, Santana C, Cheniaux E. Catatonia and psychosis related to epilepsy: A case report. Clin Schizophr Relat Psychoses Fall; 12:142-4.  Back to cited text no. 4
Repchak AT, Quinn DK. Epileptic catatonia: A case series and systematic review. Psychosomatics 2016;57:217-25.  Back to cited text no. 5
Chirchiglia D, Della Torre A, Murrone D, Chirchiglia P, Marotta R. An unusual association of headache, epilepsy, and late-onset Kleist's pseudodepression syndrome in frontal lobe cavernoma of the cerebral left hemisphere. Int Med Case Rep J 2017;10:163-6.  Back to cited text no. 6
Northoff G, Steinke R, Czcervenka C, Krause R, Ulrich S, Danos P, et al. Decreased density of GABA-A receptors in the left sensorimotor cortex in akinetic catatonia: Investigation of in vivo benzodiazepine receptor binding. J Neurol Neurosurg Psychiatry 1999;67:445-50.  Back to cited text no. 7
Northoff G, Steinke R, Nagel DCzerwenka C, Grosser O, Danos P, Genz A, et al. Right lower prefronto-parietal cortical dysfunction in akinetic catatonia: A combined study of neuropsychology and regional cerebral blood flow. Psychol Med 2000;30:583-96.  Back to cited text no. 8

Correspondence Address:
Aditya Somani
Department of Psychiatry, All India Institute of Medical Sciences, Raipur, Chhattisgarh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/psychiatry.IndianJPsychiatry_268_20

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

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