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. 2023 Jan;19(1):97-106.
doi: 10.1002/alz.12604. Epub 2022 Mar 15.

Regional cerebral hypometabolism on 18F-FDG PET/CT scan in delirium is independent of acute illness and dementia

Anita Nitchingham  1   2 , Jarett Vanz-Brian Pereira  2 , Eva A Wegner  2   3 , Vincent Oxenham  4   5 , Jacqueline Close  1   2   6 , Gideon A Caplan  1   2
Affiliations

Regional cerebral hypometabolism on 18F-FDG PET/CT scan in delirium is independent of acute illness and dementia

Anita Nitchingham et al. Alzheimers Dement. 2023 Jan.

Abstract

Introduction: Delirium is associated with new onset dementia and accelerated cognitive decline; however, its pathophysiology remains unknown. Cerebral glucose metabolism previously seen in delirium may have been attributable to acute illness and/or dementia. We aimed to statistically map cerebral glucose metabolism attributable to delirium.

Methods: We assessed cerebral glucose metabolism using 18 F-fluorodeoxyglucose positron emission tomography (FDG-PET) in sick, older patients with and without delirium, all without clinical dementia (N = 20). Strict exclusion criteria were adopted to minimize the effect of established confounders on FDG-PET.

Results: Patients with delirium demonstrated hypometabolism in the bilateral thalami and right superior frontal, right posterior cingulate, right infero-lateral anterior temporal, and left superior parietal cortices. Regional hypometabolism correlated with delirium severity and performance on neuropsychological testing.

Discussion: In patients with acute illness but without clinical dementia, delirium is accompanied by regional cerebral hypometabolism. While some hypometabolic regions may represent preclinical Alzheimer's disease (AD), thalamic hypometabolism is atypical of AD and consistent with the clinical features that are unique to delirium.

Keywords: 18F-fluorodeoxyglucose positron emission tomography; cerebral glucose metabolism; delirium; dementia; neuroimaging.

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Conflict of interest statement

Anita Nitchingham is supported by an UNSW Scientia Scholarship/Australian Government Research Training Program Scholarship (paid to Anita Nitchingham) and is a committee member of the Australasian Delirium Association (ADA) and Australian and New Zealand Society for Geriatric Medicine (ANZSGM) Scientific and Research Committee (both unpaid). Anita Nitchingham has received payment for educational content from the Australian Doctors Group (paid to Anita Nitchingham). Jarett Vanz‐Brian Pereira has no disclosures to report. Eva A. Wegner is an executive board member of the Australasian Association of Nuclear Medicine Specialists (unpaid). Vincent Oxenham is the Secretary of the College of Clinical Neuropsychologists in NSW (unpaid). Jacqueline Close is an investigator on grants funded by the National Health and Medical Research Council (NHRMC); Sydney Partnership for Health, Education, Research and Enterprise (SPHERE) Leading Better Value Care Programme; and Australian and New Zealand Hip Fracture Registry (all paid to the institution). Jacqueline Close has participated in educational events for General Practice New South Wales (paid to institution) and participates on a data and safety monitoring board (unpaid). Jacqueline Close is a current board member of Agency for Clinical Innovation and Clinical Excellence Commission (paid to Jacqueline Close). Gideon A. Caplan is an investigator on grants funded by the New South Wales Health Transitional Research Grants scheme, SPHERE, NHMRC and untied funding from the Harry Triguboff Foundation (all paid to the institution). Gideon A. Caplan receives royalties from a published textbook (paid to Gideon A. Caplan). Gideon A. Caplan has received personal payment for expert testimony from Allianz Australia, NSW Crown Solicitor's Office, Crown Solicitor Insurance for NSW, AXA, Norton Rose Fulbright, Avant Insurance, and AAI Limited (not related to this manuscript). Gideon A. Caplan received travel and accommodation support for speaking at the Alzheimer's Association International Conference in Los Angeles 2019 (payments were made to Gideon A. Caplan and the institution). Gideon A. Caplan is a committee member of the ADA and ANZSGM (unpaid).

Figures

FIGURE 1
FIGURE 1
Hypometabolic regions during delirium. Diagrammatic representation of hypometabolic regions in delirious patients compared to control. A, Left superior parietal cortex, (B) right superior frontal cortex, (C) right posterior cingulate cortex, (D) right infero‐lateral anterior temporal lobe, (E) bilateral thalami. Images generated using BrainPainter
FIGURE 2
FIGURE 2
18F‐fluorodeoxyglucose positron emission tomography (FDG‐PET) images. FDG‐PET during delirium compared to control. Top: axial; middle: sagittal; bottom: coronal slices. The delirium scan is an 89‐year‐old female with delirium but no dementia with acute gastroenteritis. The control scan is a cognitively intact 80‐year‐old male with pneumonia and acute kidney injury. Darker colors indicate lower metabolism. There is relative hypometabolism in the thalamus bilaterally (arrows) and also throughout the cerebral cortex in the delirious patient compared to cognitively intact control. During delirium, relative preservation of cerebellar FDG uptake is noted. See Appendix B in supporting information for further images
See this image and copyright information in PMC

References

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