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Semi-quantitative Assessment Using [18F]FDG Tracer in Patients with Severe Brain Injury
Published on: November 9, 2018
Assessing subcortical, brainstem and cerebellar metabolic patterns using [18F]FDG PET-CT imaging in dementia with
Daniël S L Loewenstein1, Max van Grinsven2, Cécile de Pont3
1Department of Medical Imaging, Radboud University Medical Center, Geert Grooteplein Zuid 10, 6525 EZ, Nijmegen, The Netherlands. Daniel.loewenstein@radboudumc.nl.
Purpose:
Numerous clinical features of Dementia with Lewy Bodies (DLB) are attributed to dysfunction in subcortical anatomy. Despite this, [18F]FDG PET imaging as a diagnostic tool for DLB largely relies on the metabolic signature of the occipital lobe, precuneus, and posterior cingulate cortex. This study aimed to assess subcortical brain metabolism in patients with DLB using [18F]FDG PET imaging.
Methods:
Patients diagnosed with probable DLB were included from both a prospectively maintained regional database (n = 33), and the ADNI database (n = 43). Using statistical parametric mapping (SPM) analysis, metabolic activity was compared with a cohort of subjects exhibiting normal brain metabolism (n = 19). A sub-analysis was conducted with disease progression included as a covariate.
Results:
Hypermetabolism was observed in various subcortical regions, notably in the dentate nucleus, anterolateral thalamus, and regions of the superior cerebellar peduncle. Increased metabolism was also detected in the mesencephalic tectum, likely representing heightened activity in the superior colliculus. All findings were reproduced in the ADNI cohort and were found to be dependent on the DLB disease stage. Additionally, the well-established cortical hypometabolic signature of DLB pathology was evident, validating our methods and findings.
Conclusion:
Increased metabolic activity is evident in a variety of brainstem, cerebellar, and subcortical regions in patients with DLB. The dentatorubrothalamic tract, in particular, emerges as a structure of interest that connects these structures and potentially helps in understanding DLB pathophysiology. Correction for disease stage eliminated this pattern, suggesting a driver associated with disease progression.
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