Juraj Sprung1, David O Warner2, David S Knopman3, Ronald C Petersen4, Michelle M Mielke5, Clifford R Jack6, David P Martin7, Andrew C Hanson8, Darrell R Schroeder9, Scott A Przybelski10, Phillip J Schulte11, Mariana L Laporta12, Toby N Weingarten13, Prashanthi Vemuri14. 1. Department of Anesthesiology and Perioperative Medicine, Mayo Clinic College of Medicine and Science, Rochester, MN, USA. Electronic address: sprung.juraj@mayo.edu. 2. Department of Anesthesiology and Perioperative Medicine, Mayo Clinic College of Medicine and Science, Rochester, MN, USA. Electronic address: warner.david@mayo.edu. 3. Department of Neurology, Mayo Clinic College of Medicine and Science, Rochester, MN, USA. Electronic address: Knopman.david@mayo.edu. 4. Department of Neurology, Mayo Clinic College of Medicine and Science, Rochester, MN, USA. Electronic address: peter8@mayo.edu. 5. Department of Neurology, Mayo Clinic College of Medicine and Science, Rochester, MN, USA; Health Sciences Research, Division of Epidemiology, Mayo Clinic College of Medicine and Science, Rochester, MN, USA. Electronic address: mielke.michelle@mayo.edu. 6. Department of Radiology, Mayo Clinic College of Medicine and Science, Rochester, MN, USA. Electronic address: Jack.Clifford@mayo.edu. 7. Department of Anesthesiology and Perioperative Medicine, Mayo Clinic College of Medicine and Science, Rochester, MN, USA. Electronic address: martin.david@mayo.edu. 8. Health Sciences Research, Division of Biomedical Statistics and Informatics, Mayo Clinic College of Medicine and Science, Rochester, MN, USA. Electronic address: hanson.andrew@mayo.edu. 9. Health Sciences Research, Division of Biomedical Statistics and Informatics, Mayo Clinic College of Medicine and Science, Rochester, MN, USA. Electronic address: schroedd@mayo.edu. 10. Health Sciences Research, Division of Biomedical Statistics and Informatics, Mayo Clinic College of Medicine and Science, Rochester, MN, USA. Electronic address: Przybelski.Scott@mayo.edu. 11. Health Sciences Research, Division of Biomedical Statistics and Informatics, Mayo Clinic College of Medicine and Science, Rochester, MN, USA. Electronic address: Schulte.Phillip@mayo.edu. 12. Department of Anesthesiology and Perioperative Medicine, Mayo Clinic College of Medicine and Science, Rochester, MN, USA. Electronic address: laporta.mariana@mayo.edu. 13. Department of Anesthesiology and Perioperative Medicine, Mayo Clinic College of Medicine and Science, Rochester, MN, USA. Electronic address: Weingarten.toby@mayo.edu. 14. Department of Radiology, Mayo Clinic College of Medicine and Science, Rochester, MN, USA. Electronic address: Vemuri.Prashanthi@mayo.edu.
Abstract
PURPOSE: To investigate the association between episodes of critical care hospitalizations and delirium with structural brain changes in older adults. MATERIALS AND METHODS: We included Mayo Clinic Study of Aging participants ≥60 years old at the time of study enrollment (October 29, 2004, through September 11, 2017) with available brain MRI and 'amyloid' positron emission tomography (PET) scans. We tested the hypothesis that a) intensive care unit (ICU) admission is associated with greater cortical thinning and atrophy in entorhinal cortex, inferior temporal cortex, middle temporal cortex, and fusiform cortex (Alzheimer''s disease-signature regions); b) atrophy in hippocampus and corpus callosum; c) delirium accelerates these changes; and d) ICU admission is not associated with increased deposition of cortical amyloid. RESULTS: ICU admission was associated with cortical thinning in temporal, frontal, and parietal cortices, and decreases in hippocampal/corpus callosum volumes, but not Alzheimer''s disease-signature regions. For hippocampal volume, and 10 of 14 cortical thickness measurements, the change following ICU admission was significantly more pronounced for those who experienced delirium. ICU admission was not associated with an increased amyloid burden. CONCLUSIONS: Critical care hospitalization is associated with accelerated brain atrophy in selected brain regions, without increases in amyloid deposition, suggesting a pathogenesis based on neurodegeneration unrelated to Alzheimer''s pathway.
PURPOSE: To investigate the association between episodes of critical care hospitalizations and delirium with structural brain changes in older adults. MATERIALS AND METHODS: We included Mayo Clinic Study of Aging participants ≥60 years old at the time of study enrollment (October 29, 2004, through September 11, 2017) with available brain MRI and 'amyloid' positron emission tomography (PET) scans. We tested the hypothesis that a) intensive care unit (ICU) admission is associated with greater cortical thinning and atrophy in entorhinal cortex, inferior temporal cortex, middle temporal cortex, and fusiform cortex (Alzheimer''s disease-signature regions); b) atrophy in hippocampus and corpus callosum; c) delirium accelerates these changes; and d) ICU admission is not associated with increased deposition of cortical amyloid. RESULTS: ICU admission was associated with cortical thinning in temporal, frontal, and parietal cortices, and decreases in hippocampal/corpus callosum volumes, but not Alzheimer''s disease-signature regions. For hippocampal volume, and 10 of 14 cortical thickness measurements, the change following ICU admission was significantly more pronounced for those who experienced delirium. ICU admission was not associated with an increased amyloid burden. CONCLUSIONS: Critical care hospitalization is associated with accelerated brain atrophy in selected brain regions, without increases in amyloid deposition, suggesting a pathogenesis based on neurodegeneration unrelated to Alzheimer''s pathway.
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