Reversal of cerebral glucose hypometabolism on positron emission tomography with electroconvulsive therapy in an elderly patient with a psychotic episode

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.