Sir, 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.[12] There are very few reports of catatonia associated with parietal lobe lesions.[13] 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 4thday, 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 [Figures 1-4]. He was discharged on 6thday. Sodium valproate was continued and lorazepam was gradually tapered and stopped by the 15thday 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 cavernomaFigure 2: Coronal magnetic resonance imaging T2-weighted image showing cavernoma in the right parietal lobeFigure 3: Sagittal magnetic resonance imaging T1-weighted image showing heterogeneously hypointense lesion with multiple hyperintense foci within itFigure 4: Magnetic resonance imaging gradient recalled echo sequence showing peripheral and central areas of blooming within the lesionCatatonia has been reported in association with epilepsy and postictal state.[45] 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.[13] 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. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.