Abstract
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Objectives Cerebral metabolic abnormality after acute traumatic brain injury (TBI) is heterogeneous regionally and temporally in patients (Wu et al., JNM, 2004) and experimental animals (Yoshino A, et al., Brain Res 1991). We applied integrated PET/MRI (iPET/MRI, Hitachi Metals/NEOMAX Company) to investigate immediate metabolic and morphological changes associated with acute TBI in rats.
Methods Four rats were subjected to impact-acceleration TBI produced with a weight 150-200g drop device under 2.0% isoflurane anesthesia. Body temperature was kept constant and monitored by MRI-compatible device. Immediately after TBI, 18F-fluoro- deoxy-glucose (FDG) (37MBq) was injected to tail vein. The iPET/MRI consists of DOI block detectors made of LGSO, optical fibers (80cm), PSPMTs for PET, RF coil (ϕ7.6cm) and 0.3T Nd-Fe-B permanent magnet for MRI (Yamamoto et al., ANM, 2010 in press). Simultaneous PET (list mode) and MR (fast low angle shot<FLASH> T1-weighted sequence, TR/TE=50/5msec) imaging was performed 30-60 min after injection of FDG for 10min. Five control rats were studied similarly without TBI.
Results Two rats could not survive from the TBI and showed brain contusion, ventricular hematoma, and subarachnoid hemorrhage evidenced by MRI and autopsy. Other two rats survived from the TBI without MRI lesions. Cerebral FDG uptake was predominantly decreased in brain stem and cerebellum compared with that of control rats.
Conclusions Cerebral glucose hypometabolism associated with normal MRI was documented in rats immediately after TBI. The iPET/MRI can be used for the rat experimental model of TBI to elucidate metabolic and morphologic pathology of TBI.
Research Support Program for Promotion of Fundamental Studies in Health Sciences of the National Institute of Biomedical Innovations, Japan (No. 06-35