Table 3.
Evaluations of glucose metabolism after ischemic brain injury with PET
| Types | Publication | Clinical or preclinical | Main parameters and results | New findings |
|---|---|---|---|---|
| Animal | Liang, 201866 | 9 SD rats of stroke (MCAO) | 18F-FDG uptake increased in part of contralateral brain | · Abnormal metabolic connectivity in acute ischemic stroke · Metabolism decreased in ipsilateral hemisphere and increased in contralateral cerebellum with voxel-wise analysis |
| Animal | Li, 2018 67 | 6 rats exposed to cerebral ischemia | Lower SUV in CIMT group compared to control group | · Evaluation of glucose metabolism based on CIMT · Assessment of glucose metabolism in different brain regions at baseline, before, and after treatment. |
| Animal | Joya, 2018 68 | 6 SD rats of stroke (MCAO) | 18F-FDG uptake showed the lowest value at day 1 and gradually rose | · Combined with MRI detection · Assessment of CCD after cerebral ischemia as a predictive factor of neurological outcome |
| Animal | Wu, 2017 69 | 54 SD rats of stroke (MCAO) | Higher SUV was exhibited in EA group in CPu, MCTX and SCTX | · Detection of glucose metabolism after EA treatment · Phosphorylation of AMPK increased |
| Animal | Han, 2015 70 |
SD rats of stroke (MCAO) | 18F-FDG uptake decreased and remained low for at least 14 days after ischemic stroke | · Evaluation of glucose metabolism based on HUK treatment · HUK increased angiogenesis in stroke rats |
| Animal | Hwang, 201571 |
10 SD rats of stroke (MCAO) | Cortical 18F-FDG uptake increased after liposomal delivery of angiogenic peptides compared with that of control and liposomes group | · Glucose metabolism after therapy of angiogenic peptides incorporated into liposomes ·Angiogenic peptide delivery facilitated glucose utilization |
| Animal | Arnberg, 2015 72 | 25 SD rats of stroke (M2CAO) | Increase of 18F-FDG uptake in the peri-infarct region | · Stroke model of M2CAO · Combined with MRI detection |
| Animal |
Jiang, 2014 73 | 36 SD rats of stroke (MCAO) | 18F-FDG uptake increased after post-stroke exercise | · Exercise therapy post-stroke · Exercise reverses hypometabolism caused by ischemia back to baseline from 7d to 2d on the ipsilateral brain |
| Animal | Wang, 2013 74 | 24 rats of stroke (MCAO) | 18F-FDG uptake ratio (lesion/normal) of cerebral ischemic area increased in the ESCs-treated group and iPSCs-treated group at 1 week after transplantation | · Treatment of iPSCs or ESCs · Treatment groups showed significantly higher 18F-FDG accumulations in the ipsilateral cerebral infarction |
| Animal | Walberer M, 2012 75 | 10 Wistar rats of stroke (MCAO) |
K1 and net influx rate constant Ki related to 18F-FDG uptake could predict tissue fate | · Unidirectional transport parameter K1 of FDG correlated well with rCBF at 60 minutes after the stroke · The infarct volume determined by MRI was well predicted by FDG-PET |
| Clinical observation | Stender, 2015 76 | 41 patients in the states of VS/ UWS/ MCS | Median global cortical CMRglc decreased in patients in the states of VS/ UWS/ MCS | · Averaged 42% of normal in VS/UWS, 55% of normal in MCS · ROC curve showed in MCS/ VS/ UWS patients can be differentiated with 82% accuracy based on cortical metabolism |
| Clinical observation | Soddu, 2015 77 | 11 VS/UWS and 4 locked-in patients | SUV (averaged over gray matter) was higher in healthy controls (5.5 ± 1.3) compared to VS/UWS patients (1.9 ± 1.3) | · Conjunction analysis with PET and fMRI show decreases in frontoparietal and medial regions in VS patients |
| Animal | Kim, 2019 78 | 18 SD rats of 5min CA | SUVdelta (SUV changes after CA) of forebrain regions were significantly decreased in good outcome group (p < 0.05) | · SUVdelta was firstly used to predict the outcome · Morris water maze test was applied to evaluate functional outcome |
| Animal | Putzu, 2018 79 | 10 rats of 8min CA |
CA altered 18F-FDG uptake in the range of −36% ~ +4% in different brain structure | · Focus on metabolism from cortex to brainstem, and deep structure · Autoradiography was applied |
| Animal | Li, 2015 80 | 6 beagle dogs of 6min CA | CMRglc decreased in whole brain, frontal cortex, cerebellum, and thalamus at 4 time-point |
· Comparison of glucose metabolism at 4 time points (baseline, 4h, 24h, 48h) · Assessment of hexokinase I (HXK I) and HXK II and glycolysis-related genes (GLUT3, HXK-I, GPI, PGK1, ENO2, and PKM2) |
| Animal | Zhang, 2015 81 | 44 miniature inbred pigs of 8min CA | Maximum value of SUV decreased in both VFCA and ACA groups compared to sham group at 24 h post-ROSC (parietal lobe, frontal lobe, brain stem and cerebellum) | · Grouping strategy based on different causes of cardiac arrest · Neurological deficit scores (NDS) and NSE/S100β were quantified |
| Clinical observation | Schaafsma, 2003 82 | 10 patients of CA | Reduction of 18F-FDG uptake was most marked for cortical gray matter (54% of normal) and least for cerebral white matter (70% of normal) | · Significant differences in PET data were not found between survivors and non-survivors |
| Clinical follow-up research | Rudolf, 1999 83 | 24 patients Post-CA comatose |
Cortical CMRglc in patients with PVS were significantly reduced when compared to patients in AVS | · Comparison of CMRglc in PVS and AVS patients · No significant correlation was found between the degree of evoked potential or EEG alterations and the reduction of glucose metabolism in VS patients |
| Clinical observation | Tommasino, 1995 84 | 15 unconsciousness patients of CA, TBI, Brain Ischemia | rCMRglc was significantly reduced to 3.70 +/− 61 in coma, to 3.45 +/− in VS, and to 2.33 +/− 0.34 mg/100 g/min in PVS patients | · Early clinical research · Comparison of glucose metabolism in patients of different coma levels |
SUV: standardized uptake value, CIMT: constraint-induced movement therapy, EA: electro-acupuncture, CPu: caudate putamen, MCTX: motor cortex, SCTX: somatosensory cortex, AMPK: AMP-activated protein kinase, HUK: human urinary kallidinogenase, iPSCs: induced pluripotent stem cells, ESCs: embryonic stem cells, (r)CMRglc: (region) cerebral metabolic rate of glucose, VS: vegetative state, PVS: persistent vegetative state, AVS: acute vegetative state, UWS: unresponsive wakefulness syndrome, NSE: neuron specific enolase, TBI: trauma brain injury, MCAO: middle cerebral artery occlusion, M2CAO: occlusion of the M2 branch of the MCA, CCD: crossed cerebellar diaschisis, MCS: minimally conscious state, VFCA: ventricular fibrillation cardiac arrest, ACA: asphyxial cardiac arrest