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Delirium affects up to 40% of hospitalized patients over the age of 65 and is associated with a 3-fold increased chance of death, but the neural mechanisms responsible for delirium remain unknown
.
Delirium and dementia are distinct but interrelated causes of cognitive impairment
Due to the epidemiological and clinical overlap of delirium and dementia, it is of clinical interest to study their common pathophysiological mechanisms
.
However, histopathological studies suggest that cognitive decline following delirium is caused by mechanistically distinct pathways other than those classically associated with dementia, such as amyloid plaques, neurofibrillary tangles, and vascular damage
diagnosis
Decreased brain glucose metabolism, and as a biomarker, plays an important role in the pathophysiology of AD
.
Clinical trials targeting bioenergetic pathways in the human brain have shown some promising early results
Inadequate brain metabolism is also a feature of delirium
.
Cerebrospinal fluid (CSF) in elderly patients with delirium has increased levels of lactate and altered levels of key carbohydrate enzymes, suggesting suppressed aerobic metabolism
Two studies using FDG-PET to assess glucose metabolism during delirium found cortical hypometabolism
.
However, dementia and acute illness may have been important confounders in both studies
In this exploratory study, Anita Nitchingham and others at the University of New South Wales, Australia, sought to determine whether any part of the brain that is low in glucose metabolism is primarily attributable to delirium rather than acute disease or dementia
.
They used FDG-PET to compare distressed patients with delirium but no dementia diagnosis or symptoms to an acutely distressed control group without delirium but also without dementia
They used 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) to assess brain glucose metabolism in elderly 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
They found that patients with delirium showed hypometabolism in the bilateral thalamus and right upper frontal, right posterior cingulate, right medial-lateral anterior temporal, and left superior parietal cortex
.
Regional hypometabolism was associated with delirium severity and performance on neuropsychological tests
.
The significance of the study lies in the finding that in patients with acute disease but no clinical dementia, delirium is accompanied by regional cerebral hypometabolism
.
While some areas of hypometabolism may represent preclinical Alzheimer's disease (AD), hypometabolism in the thalamus is atypical of AD, consistent with clinical features specific to delirium
.
Delirium is associated with regional cerebral hypometabolism in patients with acute illness but no clinical dementia
Original source:
Nitchingham A, Pereira JV, Wegner EA, Oxenham V, Close J, Caplan GA.
Regional cerebral hypometabolism on 18F-FDG PET/CT scan in delirium is independent of acute illness and dementia .
Alzheimer's & Dementia.
Published online March 15, 2022: alz.
12604.
doi:10.
1002/alz.
12604
