Table 2.
Possible mechanisms of increased 18F-FDG utilization in penumbral areas.
| Cellular mechanisms | Time course | |
|---|---|---|
| Increased FDG transport | ||
| GLUT1 upregulation | Increased 18F-FDG transport across the blood-brain barrier | Acute |
| GLUT3 upregulation | Increased 18F-FDG uptake by neurons | Acute |
| GLUT5 upregulation | Increased 18F-FDG uptake by microglia cells | Subacute to chronic |
| Increased FDG phosphorylation | ||
| Hexokinase upregulation | Increased 18F-FDG-6P “trapping” in cells | Acute |
| Neuroinflammation | ||
| Microglia activation | Increased 18F-FDG uptake by activated cells | Acute |
| Leukocyte migration | Increased 18F-FDG uptake by activated cells | Sub-acute |
| Macrophage migration | Increased 18F-FDG uptake by activated cells | Sub-acute |
|
| ||
| Physiologic associations | ||
|
| ||
| Peri-infarct speeding depression-like depolarization (PID) | Increased metabolic demand | Acute to sub-acute |
| Neuronal regeneration | Increased metabolic demand | Acute to sub-acute |