Citation

Divani AA, Phan JA, Salazar P, SantaCruz KS, Bachour O, Mahmoudi J, Zhu XH, Pomper M. J. Neurotrauma 2018; 35(1): 187-194.

Affiliation

Baltimore, United States ; mpomper@jhmi.edu.

Copyright

(Copyright © 2018, Mary Ann Liebert Publishers)

DOI

unavailable

PMID

28922962

Abstract

We present a longitudinal study of cerebral metabolism using [18F]fluorodeoxyglucose (FDG) positron emission tomography (PET) in a rat model of shockwave-induced traumatic brain injury (SW-TBI). Anesthetized rats received 5 or 10 shockwave pulses to the right anterior lateral or dorsal frontal regions using shockwave lithotripsy. Animals were scanned for FDG uptake at baseline, 3 hours post-injury, and 3 days post-injury, using a small animal PET/CT scanner. FDG uptake at all time points was quantified as the ratio of brain activity relative to peripheral activity in the left ventricle (LV) in the heart (Abrain/ALV) for the entire brain, each hemisphere, and four cortices (motor, cingulate, somatosensory, and restrosplenial). The mixed-designed models ANOVA for the hemispheric and global FDG uptake ratio showed a significant effect of the time-of-scan (P=0.038) and measured region (P=6.12e-09). We also observed a significant effect of the time-of-scan (P=0.046) and measured region (P=2.28e-09) for the FDG uptake ratio in four cortical regions. None of the measurements (global or local) showed a significant effect for the number of shockwave pulses (5 or 10) or shockwave location (lateral or dorsal frontal regions). Our data suggest that SW-TBI causes hypermetabolism on the impact side of the rat brain at 3 hours post-injury compared to the baseline measurements. However, the increase in FDG uptake by day 3 post-injury was not significant. Further studies on post-TBI metabolic changes are needed to understand better the pathophysiology of the injury.

Language: en

Keywords

METABOLISM; PET SCANNING; Rat; TRAUMATIC BRAIN INJURY