Reversal of cerebral glucose hypometabolism on positron emission tomography with electroconvulsive therapy in an elderly patient with a psychotic episode. Issue 6 (12th January 2016)

• Record Type: Journal Article
• Authors: Hassamal, Sameer; Jolles, Paul; Pandurangi, Ananda
• Is Part Of: Psychogeriatrics. Volume 16:Issue 6(2016)
• Page Start: 376
• Page End: 381
• Publication Date: 2016-01-12
• Subjects: 18F‐fluorodeoxyglucose -- anxiety disorders -- dementia -- electroconvulsive therapy -- psychotic disorders; Geriatric psychiatry -- Periodicals; 618.9768905
• DOI: 10.1111/psyg.12174
• Languages: English
• ISSNs: 1346-3500

Abstract

Abstract: AB, a 74‐year‐old Caucasian woman, was admitted for acute onset of psychosis, anxiety, and cognitive impairment. Pharmacotherapy was unsuccessful and the patient was referred for electroconvulsive therapy (ECT). Pre‐ECT, 18 F‐fluorodeoxyglucose‐positron emission tomography (PET)/computed tomography showed extensive frontal, parietal, and temporal cortical hypometabolism suggestive of a neurodegenerative disease. After eight ECT sessions, the psychotic and anxiety symptoms as well as the cognitive impairment resolved. The rapid improvement in symptoms was more suggestive of a psychotic episode rather than dementia. Two days after the ECT course, 18 F‐fluorodeoxyglucose‐PET/computed tomography showed improvements in cerebral cortical hypometabolism, especially in the left parietal cortex, left temporal/occipital cortex. and bifrontal regions. At a follow‐up visit 2 months after the ECT course, the psychotic episode was still in remission, and 18 F‐fluorodeoxyglucose‐PET/computed tomography continued to show improved cerebral cortical hypometabolism in these areas. This case illustrated the effect of ECT in reversing cerebral glucose hypometabolism on PET. The improvement in cerebral glucose hypometabolism may represent the neurophysiological mechanism of ECT in the treatment of a psychotic episode. Improved cerebral glucose hypometabolism was present 2 months post‐ECT, which suggests that ECT caused sustained functional neural changes.