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[P4–504]: NOVEL UNIQUE PATTERN OF CEREBRAL GLUCOSE HYPOMETABOLISM SEEN ON 2‐ 18 F‐FLUORO‐2‐DEOXYGLUCOSE POSITRON EMISSION TOMOGRAPHY IN DELIRIUM
Author(s) -
Caplan Gideon A.,
Haggstrom Lucy R.,
Nelson Julia A.,
Wegner Eva A.
Publication year - 2017
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2017.07.666
Subject(s) - delirium , dementia , positron emission tomography , neuroimaging , psychology , medicine , carbohydrate metabolism , neuroscience , psychiatry , disease
Background:Decreased cerebral glucose metabolism is seen in all types of dementia and is a reliable predictor of transition to mild cognitive impairment (MCI) and Alzheimer’s dementia (AD). Defective insulin signalling and resistance in the brain in AD led to the term, Type 3 diabetes for AD. Intranasal insulin has been shown to improve cognitive function in MCI and AD. Recent studies show that delirium is the major acute driver of dementia progression, and is associated with biochemical evidence of abnormal glucose metabolism in cerebrospinal fluid. There are no published studies of FDG PET scanning in delirium. Therefore we investigated cerebral glucose metabolism in delirium. Methods: We performed 2-18F-Fluoro-2-Deoxyglucose Positron Emission Tomography on patients during an episode of delirium and after resolution, 2-3 months later, using visual analysis and NeuroQ version 3.0 to assess the scans. Delirium was diagnosed by expert Geriatricians and confirmed with the Confusion Assessment Method and the Delirium Index was used to assess severity. Results: On PET scanning during delirium there was a unique pattern of widespread cortical glucose hypometabolism, with sparing of the sensorimotor cortex, which improved with resolution of delirium, in the whole brain, bilateral frontal, occipital and PCC, left parietal and temporal and right cerebellum (Range 1.4-5.0%; p<0.05). The improvement seen with resolution of delirium was similar in magnitude but opposite in direction to the change seen in AD over 1 year. These changes correlate with performance on neuropsychological tests for specific features of delirium, such as the WAIS-IV Digit Span Test forwards assessing Attention (Spearman’s r 1⁄40.65; p1⁄40.017). These PET scan changes are not seen on sick hospitalised older patients without delirium or dementia. Conclusions: Hospitalised patients with delirium exhibit marked widespread cortical glucose hypometabolism, in a different pattern to that seen in dementia, and not seen in older cognitively normal hospitalised patients. This hypometabolism improves with resolution of delirium.