The Potential Roles of ¹⁸F-FDG-PET in Management of Acute Stroke Patients

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