Aims: Delirium superimposed on dementia (DSD) poses a significant diagnostic challenge in clinical practice and is associated with outcomes worse than delirium without dementia1,2. There is a need to develop strategies that more accurately differentiate between delirium, dementia, and DSD. The aims of this study were to describe the changes in cerebral glucose metabolism on fluorodeoxyglucose positron emission tomography (FDG-PET) in DSD and determine whether underlying neuropathology influences these changes.
Methods: Cerebral glucose metabolism was examined using FDG-PET imaging in two groups: acutely unwell inpatients experiencing delirium with a background of Alzheimer's dementia (DSD group, N = 20) and well outpatients with Alzheimer's dementia alone (AD group, N = 19). Using semi-quantitative analysis, regional cerebral glucose metabolism in the DSD group was compared to the AD group to identify specific brain regions affected in DSD.
Results: There was predominant cortical cerebral glucose hypometabolism in the DSD group compared with the AD group. This involved the lateral frontal, parietotemporal, inferior posterior temporal and visual cortices bilaterally. In contrast, most subcortical regions demonstrated similar levels of glucose metabolism between the groups.
Conclusions: Regional cerebral glucose metabolism in DSD does not represent an overlay of the changes that occur in delirium onto those that occur in AD3,4. This suggests that regional glucose hypometabolism in DSD may be influenced by other factors such as underlying neuropathology or acute illness. Neuropathology in AD predominantly affects the cortex of the brain, which may explain the cortical distribution of regional cerebral glucose hypometabolism in DSD.